Uncle Wiggily’s Weblog

  • 12:22:13 am on May 1, 2008 | 1


    The endovascular AAA repair is typically performed under high lumbar or low thoracic epidural anesthesia with MAC. LIDOCAINE is often a good choice as these patients will typically not have difficulty with postoperative pain.

    PREPARATION requires adequate IV access and arterial line. Infusions for resuscitation should be available including NTG and phenylephrine drips. Epidurals will be removed six hours after the last dose of heparin is given. Intraoperative fluid requirements are typically low at approximately 2500 in one recent series.

    Studies have demonstrated that RA is as safe as GA for endovascular AAA repair. Parameters evaluated include duration of anesthesia care, cardiovascular instability, incidence of desaturation, need for cardiovascular infusions and systemic inflammatory response.

    One other study has demonstrated more stability with regards to MAP and MPAP using epidural anesthesia. There was no significant difference with regards to HR, SPAP or DPAP.

    It is possible to perform endovascular repairs using only field block local anesthetic agents but the advantages have yet to be demonstrated.


    Abdominal aortic aneurysms are the most common type of arterial aneurysm. Approximately 5% of people older than 60 years will develop an AAA and the M:F ratio is 3:1. Risk factors include smoking, HTN and a family history of aneurysm. AAA are caused by atherosclerosis in 90% of all patients and 5% of aneurysms are inflammatory.

    AAAs are usually asymptomatic. Aneurysm expansion or rupture may cause severe back, flank or abdominal pain and shock. Distal embolization, thrombosis, and duodenal or ureteral compression can produce symptoms.

    PHYSICAL EXAMINATION Almost all AAAs greater than 5 cm are palpable as a pulsatile mass at or above the umbilicus. Most AAAs range from 3-15 cm in diameter.

    Small aneurysms can be followed using ultrasound or CT scan every 6 months.

    Indications for repair include symptomatic aneurysms of any size, aneurysms exceeding 5 cm, those increasing in diameter by more than 0.5 cm per year and saccular aneurysms.


    Morbidity and mortality is primarily attributed to cardiac events. Myocardial infarcts cause 55% of all perioperative deaths and 75% with MI will die. Overall perioperative mortality is 2-3%.

    Half of the AAA patients have significant (over 50% stenosis) CAD and 33% have severe stenosis (over 70%). Patients with normal EKG and history still will have significant CAD 15% of the time.

    PAC may be monitored for V waves (papillary ischemia and MR), large A waves (decreased ventricular compliance) or sudden increase in PA or PAWP. Only 10% of TEE RWMA is detected by PAC. PAWP is BETTER than CVP for volume status as right heart is more compliant and sensitive to only large changes in volume. Normal PAWP is 5-12 mm Hg.

    ARF is more likely with suprarenal clamp and mortality is at 30%. Operative mortality is 19% if preoperative creatinine is greater than 2.

    SPINAL CORD ISCHEMIA occurs secondary to decreased intercostal flow with infrarenal clamps and aortic hypotension with thoracic clamping which produces a steal phenomenon to the distal aorta. The artery of Adamkiewicz is primary supply to lumbar enlargement at the TL junction. Thirty minutes of cross clamping is considered to be the maximal amount of time allowed prior to ischemia development.

    Paraplegia is the most feared complication following repair of the high aortic aneurysm. Various series place the risk of paraplegia between 5-30%.

    Fluid administration should include MIVF plus blood loss plus insensibles at 8-10 mL/kg/hour for large incisions.

    NECESSARY PREPARATION includes arterial line, PA cathter or 8.5 F cordis, thoracic EPIDURAL placement for post-operative analgesia, four channel pump with carrier fluid and INFUSIONS

    NTG up to 1.5 mcg/kg/min
    NEO up to 1 mcg/kg/min
    SNP 1-10 mcg/kg/min

    Inotropic agents such as dobutamine or dopamine may also be necessary. DuraMorph, mannitol, Lasix, heparin and sodium bicarbonate should also be available. Upper warmers are necessary but lower warmers may be contraindicated. Blood products should be available in the room.

    EMERGENCE will often require the use of labetalol or NTG for blood pressure control. The use of epidural anesthetics may circumvent this need but even these patients may require brief assistance with esmolol or hydralzine at the minimum.

    Pulmonary changes following upper abdominal surgery include

    VC decreases 25-50%
    VT decreases 20%
    RV increases 13%
    FRC decreases 20%
    ERV decreases 60%

    The decrease in VC is most persistent and may affect patients for up to 1-2 weeks.


    Abdominal compartment syndrome is a condition of elevated abdominal pressure which leads to impairment of organ function. Intra-abdominal hypertension is diagnosed with pressures over 12 mmHg.

    IAH usually develops following abdominal trauma and risk factors include primary fascial closure, use of surgical packing, coexisting pelvic injury, intraperitoneal or retroperitoneal bleeding, bowel distension and multiple transfusions. The incidence following abdominal trauma ranges between 14-33%. IAH can have other etiologies including ascitis, sepsis, pneumoperitoneum and pancrancreatitis.

    ACS will have various deleterious effects on the patient including compromised respiratory function, impaired cardiac output (worse in the hypovolemic patient), increased intracranial pressure (through increased mediastinal pressures), decreased GI perfusion and decreased RBF and GFR (which is NOT amenable to augmentation of cardiac output).

    Bladder pressure is considered the most accurate method of DIAGNOSIS. Catheters are transduced after slightly distending the bladder with 50-100 mL of fluid.

    TREATMENT is accomplished by aggresive fluid resuscitation to optimize peripheral oxygen delivery. Decompressive laparotomy is considered the definitive treatment for ACS and if performed early may decrease the high mortatlity associated with this condition. Most of the existing literature recommends decompression when critical IAP is reached (25 mmHg or higher).


    Optimal management of pH and PaCO2 for patients undergoing hypothermic bypass remains controversial. The two strategies for management include the modern ALPHA-STAT (temperature uncorrected) method used at UNC and the older pH-STAT method (temperature corrected).

    pH-STAT method aims at keeping constant pH at 7.40 and PaCO2 40 at any given temperature. With the pH-stat strategy, the blood gas values are corrected by nomogram and the patient is treated as if he were a HIBERNATING animal. The intracellular state becomes slightly acidotic as CO2 is added through the gas exchanger because the patient’s cold blood is actually alkalotic.

    ALPHA-STAT method aims at a keeping a constant ratio of [OH]:[H] at 16:1. This is based on the premise that pH of blood is regulated to keep the stage of dissociation of imidazole moiety (the ALPHA of imidazole) constant. With this strategy, the blood gas values are NOT corrected regardless of temperature and the patient is treated as if he were a POIKLOTHERM (such as the turtle). The intracellular state remains neutral.

    Studies indicate that ALPHA-STAT provides better preservation of myocardial function. Cerebral autoregulation is also better maintained while it becomes pressure dependent with the pH-stat strategy.


    As the temperature of the blood decreases, the solubilty of oxygen and carbon dioxide increases which consequently LOWERS their partial pressures.

    For the HYPOTHERMIC patient, an ABG that is warmed to 37 degrees will FALSELY elevate the PCO2 (4.5% per degree) and decrease the pH (0.015 units per degree). The PO2 will also be falsely elevated (6% per degree) so the end results are both falsely discouraging and encouraging.

    Remember the following scenario in the trauma resuscitation: the cold patient may not be as acidotic as they appear – but they are likely not as well oxygentated as they appear by ABG analysis.

    The hypothermic patient’s gas read after warming to 37 degrees is known as temperature uncorrected value (this is the modern alpha stat protocol used at UNC). When the results are corrected for the patient’s temperature by computer nomogram, the results are said to be temperature corrected.


    Class I indications for catheter ablation include: AVNRT, WPW syndrome, unifocal atrial tachycardia, atrial flutter (especially common RA forms), symptomatic SVT, atrial fibrillation, AV junction ablation for poorly controlled ventricular rates secondary to drug inefficacy or drug intolerance, ventricular tachycardia, symptomatic monomorphic VT (first-line therapy in idiopathic VT if patient preference – generally performed for drug or device intolerance or inefficacy in structural heart disease).

    Other indications include symptomatic drug-refractory (inefficacy or intolerance) idiopathic sinus tachycardia and junctional ectopic tachycardia.


    Absorption atelectasis refers to the tendency for airways to collapse if proximally obstructed. Alveolar gases are reabsorbed. This process is accelerated by nitrogen washout techniques. Oxygen shares alveolar space with other gases, principally Nitrogen. Nitrogen is poorly soluble in plasma, and thus remains in high concentration in alveolar gas. If the proximal airways are obstructed, for example by mucus plugs, the gases in the alveoli gradually empty into the blood along the concentration gradient, and are not replenished: the alveoli collapse, a process known as atelectasis. This is limited by the sluggish diffusion of Nitrogen. If nitrogen is replaced by another gas, that is if it is actively “washed out” of the lung by either breathing high concentrations of oxygen, or combining oxygen with more soluble nitrous oxide in anesthesia, the process of absorption atelectasis is accelerated. It is important to realize that alveoli in dependent regions, with low VQ ratios, are particularly vulnerable to collapse.


    NONINVASIVE testing is indicated for (1) any single major predictor, (2) intermediate predictor and poor function or high risk surgery or (3) poor function and high risk surgery.

    CATHETERIZATION is indicated for (1) risk indicated by noninvasive test, (2) unresponsive angina, (3) unstable angina before intermediate or high risk surgery or (4) equivocal noninvasive testing before intermediate or high risk surgery.

    NONINVASIVE testing includes exercise tolerance testing, dipyridamole thallium scans and DSE. ETT is the test of choice if no contraindications exist. ETT is preferable for evaluating funtional capacity and detecting ischemia by ST segment changes and correlated HD responses. Dipyridamole testing is contraindicated in patients with severe bronchospasm or carotid disease.

    Potential outcomes include delayed surgery for unstable conditions, increased medical therapy, coronary interventions, more invasive intraoperative monitoring, planned ICU admission following surgery and changing outpatient procedures to inpatient surgery.

    decompensated CHF
    significant dysrhythmias
    unstable coronary syndrome
    severe valvular disease

    Significant dysrhythmias include severe AV block, supraventricular dysfunction with RVR and symptomatic ventricular dysrhythmias.

    mild angina
    history of MI or CHF
    diabetes meilletus
    creatinine over 2

    emergent surgery
    surgery for the elderly
    aortic or major vascular surgery
    peripheral bypass surgery
    long surgery with fluid shifts

    carotid endarterectomy
    abdominal or thoracic surgery
    orthopedic surgery
    ENT surgery
    prostate surgery

    POOR FUNCTION is indicated by the inability to perform over four MET where 1 MET requires only basal oxygen consumption.

    POOR prognosis
    1 watches TV at basal oxygen
    2 dress without rest, walk 2 mph
    3 level ground walking

    MODERATE prognosis
    4 cart golfing or bowling
    5 eight stairs, walk 4 mph
    6 stairs with groceries

    GOOD prognosis
    7 running or bag golfing
    8 jogging 8 mph
    12 vigorous stationary biking
    16 scuba diving


    ACE inhibitors have a major role in preventing deterioration in LV function and are useful for HTN, CHF history and for patients with proteinuria and DM nephropathy. They inhibit conversion of angiotensin I to angiotensin II (in the lung) and consequently preventing the multiple effects of angiotensin II as well as inhibiting the breakdown of the vasodilator bradykinin.

    RENIN is released by the juxtaglomerular cells in response to decreased renal perfusion, decreased sodium to the macula densa and sympathetic activity. Renin then generates ANGIOTENSIN I which is then cleaved by ACE to ANGIOTENSIN II. ANGIOTENSIN II increases the release of ALDOSTERONE from the adrenal medulla and has direct effects on arteriolar wall tone. ANGIOTENSIN II also has the indirect effects of increasing the release of NE and preventing its reuptake.

    Interupting this cycle will first decrease AFTERLOAD (loss of angiotensin-II and NE) and subsequently decrease PRELOAD through loss of aldosterone mediated sodium and water retention and increased vasodilation because of higher concentrations of bradykinin.

    SIDE EFFECTS of concern during the perioperative period include refractory hypotension and postoperative renal dysfunction. All ACE inhibitors can also cause angioedema (0.1-0.2%), dizziness, proteinuria, rash, tachycardia, HYPERKALEMIA and HA. The drugs are contraindicated during pregnancy (category X).

    BENZAPRIL (Lotensin) is given daily in doses between 10 and 80 mg

    CAPTOPRIL (Capoten) is given in doses between 25-100 mg twice or three times each day

    ENALOPRIL (Vasotec) is given at doses up to 40 mg per day either once or divided bid

    FOSINOPRIL (Monopril) is given at doses between 10 and 80 mg once each day

    LISINOPRIL (Prinvil, Zestril) is given in doses between 10 and 80 mg once each day

    QUINAPRIL (Accupril) is given in doses up to 80 mg each day

    RAMIPRIL (Altace) is given in doses up to 20 mg per day in one or two divided doses

    Many combinations of ACE inhibitors with diuretics (HCTZ) are also available for obvious reasons.

    Agents classified as ANGIOTENSIN RECEPTOR ANTAGONISTS (A2RB) are commonly used alone or in combination with benefits similar to those of the traditional ACE inhibitors but without the side effect of cough. Such A2RB drugs include LOSARTAN (Cozaar, Hyzaar) and IRBESARTAN.


    Considered to be an NSAID by some, the action of acetominophen is thought to be secondary to a inhibition of prostaglandin synthesis within the CNS. Acetominophen is analgesic and antopyretic but has no anti-inflammatory activity.

    A small proportion of acetominophen is metabolized to a hepatotoxic metabolite. With large ingestions, hepatic GLUTATHIONE may be depleted which is necessary for further metabolism of this toxin. Alcoholics are apparently more susceptible to the hepatotoxic effects of acetominophen.

    DOSING Rectal dosing for pediatric patients is at 30-40 mg per kg. Peak analagesic effects may not be seen for up to three hours. PO dosing is at 15 mg per kg for the pediatric patient and typically up to 1000 mg for the adult (which is 15 mg per kg for a 70 kg adult).

    It is generally recommended that doses not exceed 4 GRAMS per day although doses up to 6 grams per day for 3-4 days may be acceptable.


    Acetazolamide (Diamox) is an enzyme inhibitor that acts specifically on CARBONIC ANHYDRASE, the enzyme that catalyzes the reversible reaction involving the hydration of carbon dioxide and the dehydration of carbonic acid.

    In the eye, this inhibitory action of acetazolamide decreases the secretion of aqueous humor and results in a drop in intraocular pressure, a reaction considered desirable in cases of glaucoma and even in certain nonglaucomatous conditions.

    Evidence seems to indicate that acetazolamide has utility as an adjuvant in the treatment of certain dysfunctions of the central nervous system (epilepsy). Inhibition of carbonic anhydrase in this area appears to retard abnormal, paroxysmal, excessive discharge from central nervous system neurons.

    The DIURETIC effect of acetazolamide is due to its action in the kidney on the reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. The result is renal loss of HCO3 ion, which carries out sodium, water, and potassium. Alkalinization of urine, resolution of METABOLIC ALKALOSIS and promotion of diuresis are the result. Alteration in ammonia metabolism occurs due to increased reabsorption of ammonia by the renal tubules as a result of urinary alkalinization.

    ADVERSE REACTIONS occurring most often early in therapy include paresthesias, particularly a tingling feeling in the extremities, hearing dysfunction or tinnitus, loss of appetite, taste alteration and gastrointestinal disturbances such as nausea, vomiting and diarrhea, polyuria and occasional instances of drowsiness and confusion.

    Metabolic acidosis and electrolyte imbalance may occur.

    DOSAGE for glaucoma is 125-250 mg PO/IV as often as every four hours. Treatment for altitude sickness occurs at 250-500 mg PO bid with the first dose given 48 hours prior to ascent.

    For URINARY ALKALINIZATION the dose is 5 mg/kg PO/IV which may be repeated 2-3 times each day. A typical dose for diuresis in the face of alkalosis is at 250 mg IV.


    The pKa is the pH at which a weak acid or base is 50% in its ionized form and 50% in its nonionized form

    ACIDIC drugs are highly ionized at a high or alkaline pH. These include (1) barbiturates, (2) etomidate is unstable at physiologic pH and is prepared with propylene glycol (pH 6.9) contributing to a high incidence of pain on injection and (3) midazolam (pK 6.15) is prepared at a pH of 3.5 to maintain closure of the imadazole ring providing water solubility.

    BASIC drugs are susceptible to ion trapping in the fetus. Basic drugs are highly ionized at a low acid pH. These include (1) alfentanil is the least basic of the opioids with a pKa of 6.8 conferring that 90% is nonionized at a physiologic pH and (2) ester local anesthetics generally have higher pKa values (8.5-8.9) than the amide anesthetics and are therefore less basic at physiologic pH such that there is more ionized drug present equating to slower onset. Chloroprocaine is the exception with a high pKa and fast onset most likely secondary to high concentrations used.


    For the 2000 ACLS recommendations and alogorithm formulations all acceptable evidence has been integrated, sometimes with the assistance of experts, into a final class of recommendations. Using this methodology, recommendations are classified into 5 CATEGORIES.

    CLASS I recommendations are definite indications supported by excellent evidence proving efficacy.

    CLASS IIa recommendations are acceptable and useful and supported by good to very good evidence.

    CLASS IIb recommendations are acceptable and useful with fair to good evidence in support of the therapy but not strongly favored by weight of evidence and expert opinion.

    CLASS INDETERMINATE recommendations indicate that available evidence is insufficient to support benefit from the therapy.

    CLASS III recommendations are unacceptable with no documented benefit and the potential to cause harm to the patient.


    The ACLS survey involves eight steps (primary and secondary surveys) which involve concomitant assessment and management.

    The PRIMARY SURVEY includes the more familiar (1) AIRWAY, (2) BREATHING, (3) CIRCULATION and (4) DEFIBRILLATION for ventricular fibrillation and pulseless tachycardia.

    The SECONDARY SURVEY includes (1) advanced AIRWAY management, (2) advanced BREATHING assessment by confirming tube placement, (3) advance CIRCULATION management by obtaining intravenous access, evaluating rhythm and giving appropriate medications for dysrhythmias and hypotension, and (4) DIFFERENTIAL considerations which includes searching for and treating reversible etiologies for the cardiac event.

    VT: synchronized cardioversion, amiodarone, rapid DDX

    VF or PULSELESS VT: defibrillation, vasopressin, epinephrine then amiodarone

    ASYSTOLE: epinephrine, atropine, pacing, 5H5T


    ACROMEGALY is due to excess secretion of GH in the adult most often from an adenoma in the anterior pituitary gland. DIAGNOSIS is made by GH levels over 3 ng/mL or failure of the GH to decrease 1-2 hours after glucose ingestion.

    SYMPTOMS include enlarged sella turcica, HA, visual field defects and rhinorrhea. Excess GH produces PROGNATHISM, soft tissue overgrowth, connective tissue overgrowth (recurrent laryngeal nerve palsy), peripheral neuropthy (carpal tunnel), visceromegaly, glucose intolerance, osteoartritis, hyperhydrosis and skeletal muscle weakness.

    The incidence of HTN and ischemic heart disease is increased and stress testing may be indicated. Lung volumes might be high and VQ mismatch is increased.

    THERAPY is by adenoma resection but when the tumor has extended beyond the sella turcica, suppressive therapy with BROMOCRIPTINE might be the most appropriate option.


    FACTOR VIIa or NovoSeven was initially developed for the treatment of hemophilia patients. Factor VIIa binds with any exposed tissue factor TF to begin the cascade for the production of thrombin.

    In essence, FACTOR VIIa may enhance platelet surface THROMBIN production in patients with hemophilia or other factor related coagulopthy (including patients on coumadin) and those with quantitative or qualitative platelet disorders.

    FACTOR VIIa is being studied for use in trauma patients, liver transplant patients, DIC and patients with transfusion related coagulopathy. It is likely that factor VIIa is less beneficial in those patients with hypothermia and acidosis. The cost of administration is approximately six thousand dollars (2007).

    DOSING described in the literature ranges between 80-150 mcg per kg.
    The duration of action is appriximately four hours.


    The latest ACLS protocols recommend early ambulatory 12-lead EKG and triage for the patient with chest pain into one of three categories:

    nondiagnostic EKG

    Initial MANAGEMENT for ALL patients includes 12-lead EKG, IV placement, laboratory assessment, CXR and the four cornerstones of therapy: (1) OXYGEN at four LPM, (2)
    ASPIRIN 160-325 mg PO, (3) NTG SL (up to three tablets at five minute intervals) for those with SBP above 90 mmHg – can be used in combinnation with NTG paste at one inch each six hours and (4) MORPHINE at 2-4 mg IV for those with pain not treated with NTG.

    ST ELEVATION patients are the only subset that benefit from acute reperfusion therapy. FIBRINOLYTIC therapy is a CLASS I treatment for those less than 75 years of age (less risk for hemorrhage) and with onset of symptoms LESS THAN 12 hours prior to intervention.

    PCI (stenting and angioplasty) is an equivalent CLASS I intervention but is the treatment of choice for those with cardiogenic shock or contraindications to fibrinolysis.

    Two OTHER subsets of patients without ST elevation that may benefit from fibrinolytics include posterior infarctions presenting only with ST depression in V1-4 and those with hyperacute T waves that often precede ST elevation.

    ADJUNCTIVE therapies for those with ST ELEVATION include (1) BETA BLOCKADE for those without contraindications, (2) IV NTG which is Class I for the first 24-48 hours for those with CHF, large anterior infarcts, persistent ischemia or hypertension, (3) HEPARIN for those receiving fibrinolytics and those with planned stenting or angioplasty and (4) ACE inhibitors for those with CHF and systolic dysfunction to be given only after at least SIX HOURS past acute presentation (and after fibrinolytic therapy).

    Patients with ST DEPRESSION or dynamic T wave inversion should be treated with adjunctive therapies including heparin, ASA, GLYCOPROTEIN INHIBITORS, IV NTG and ß blockade. Stable patients are admitted for observation while unstable patients should undergo catheterization to consider possibilities of revascularization by PCI or CABG.

    Pateints with NONDIAGNOSTIC EKG should be admitted for monitoring and serial laboratory assessment. Those who meet criteria for unstable or new onset ANGINA and those with elevated TROPONIN (sensitive after 3-4 hours) should be treated as described above for ST depression.


    Epiglottitis is an inflammation of the mucosa of the supraglottic structures usually caused by Hemophilus influenza type B but also occassionally caused by Group A Streptococcus pyogenes. It is a true pediatric emergency, the rapid progression of which may be an unpredictable and fatal airway obstruction. Restoration of a secure airway is priority number one.

    Expectant intubation under anesthesia is the most common treatment until antibiotic therapy is initiated and signs of systemic toxicity subside. In children, intubation is mandatory. There is rarely a preceding upper respiratory illness and the child usually appears quite toxic with fever. Epiglottitis is NOT age dependent but is dependent on contact with the H flu disease which occurs most commonly in the early school-age population.

    In the child without IV access, mask inductions with gentle laryngoscopy is appropriate. Tracheostomy sets and surgeons should be immediately available.


    It is pertinent that EMS personnel identify stroke victims as early as possible. Commonly used scales include the Cincinnati Prehospital Stroke Scale (72-85% PPV) which simply assesses for facial droop, arm drift and abnormal speech.

    The FOUR CLASSES of stroke include ISCHEMIC stroke (70-80% of all strokes that are secondary to cerebral thrombosis or cerebral embolism) and HEMORRHAGIC stroke (caused by intracerebral or subarachnoid hemorrhage).

    Airway, breathing and circulation are supported as usual. Patients may be placed in the recovery position while comatose patients require intubation. Arrhythmias and changes in blood pressure are common but hypotension and shock are rarely caused by stroke.

    NONCONTRAST CT should be completed and read within 45 minutes from hospital arrival. Edema and hypodensities are not seen until 6-12 hours after ischemic stroke. Approximately 5% of all patients with hemorrhagic stroke will have normal appearing noncontrast scans. When suspicion is very high for hemorrhage, a lumbar puncture should be performed to rule out hemorrhagic stroke.

    Therapy with ALTEPLASE (tPA) should be administered within 60 minutes of hospital arrival for those meeting the following criteria.

    1) age older than 18 years with major stroke symptoms
    2) onset of symptoms clearly within the previous 180 minutes
    3) absence of ICH on noncontrast CT
    4) absence of obvious improvement in symptoms prior to therapy
    5) absence of internal bleeding within the last 21 days or major surgery within the previous 14 days
    6) platelets counts over 100K
    7) absence of heparin administration within the previous 48 hours (or elevated PTT) or recent use of coumadin (PT over 15) or other anticoagulants
    8) SBP less than 185 mmHg and DBP less than 110 mmHg

    BP can be frequently managed by nitroglycerin and labetalol.

    ALTEPLASE is given at 0.9 mg per kg (maximum 90 mg) with 10% as an intitial bolus and the remainder over the next 60 minutes. Blood pressure should be carefully monitored and patients should be observed for evidence of bleeding or DIC.


    ATN is characterized by a spot urine concentration over 40 mEq/L and fractional excretion of sodium greater than 1% because necrosed tubules do not efficiently reabsorb sodium.

    FENA (%) is calculated by [(UNa / PNa) ÷ (UCr / PCr)] x 100. FENA may be less reliable if the patient is elderly, received diuretics or has preexisting renal disease.

    Urine sodium is less reliable if loop diuretics have been used in the preceding 24 hours.

    ATN is the most common intrinsic renal disease leading to ARF. Prolonged renal hypoperfusion is the most common cause of ATN. Nephrotoxic agents such as aminoglycosides, heavy metals, radiocontrast media, ethylene glycol, FK 506 and cyclosporine represent exogenous nephrotoxins.

    ATN may also occur as a result of endogenous nephrotoxins, such as intratubular pigments (hemoglobinuria), intratubular proteins (myeloma), and intratubular crystals (uric acid).


    Addison’s disease is a primary disease of the adrenal gland with inadequate secretion of both glucocorticoid & mineralocorticoid.

    Most common ETIOLOGIES include autoimmune (80%), TB & HIV. Other causes include adrenal hemorrhage, metastatic cancer, ketoconazole, etomidate, sarcoidosis and hemochromatosis.

    Addison’s disease is technically differentiated from secondary (pituitary) and tertiary (hypothalamic) causes of adrenocortical insufficiency.

    SIGNS include weakness, weight loss, orthostatic hypotension, increased pigmentation, nausea, vomiting, diarrhea, salt craving and depression.

    LABORATORY FINDINGS include hyponatremia, hyperkalemia, hypoglycemia, metabolic acidosis and anemia.


    Adenosine is an endogenous nucleoside with antiarrhythmic activity slowing conduction through the AV node and restoring NSR in patients with acute PSVT.

    Adenosine is indicated for SVT (WPW patients) and as a diagnostic tool for any patient with a narrow complex tachycardia. Through AV node blockade it also may elucidate the DX of atrial flutter with a RVR and differentiate this rhythm from SVT.

    1) acute PSVT
    2) DDX SVT with abberancy and VT
    3) unmasking delta waves in WPW
    4) afterload reduction in low output
    5) controlled hypotension
    6) pharmacologic stress testing

    Adenosine does NOT convert AF or VT to NSR with the rare exception of adenosine-sensitive VT.

    DOSING for adults at 6-12 mg rapid IV push. PEDIATRIC dosing ranges from 50-500 mcg/kg IV push prefarably through a central vein. The drug is available as 3 mg per mL or 300 mcg per 0.1 mL. NEONATES receive a maximum dose of 250 mcg/kg.

    Dosing for controlled hypotension is between 40-500 mcg/kg/minute.

    PHARMACODYNAMICS Adenosine slows conduction time through AV node blockade. It may decrease PVR, cause arrhythmias (heart block or asystole), angina, hypotension and depressed LV function. It may cause dyspnea and bronchospasm in patients with RAD occasionally requiring intubation.

    When there is uncertainty about diagnosis of VT versus SVT, adenosine may be tried but a response does not reliably differentiate the two diagnoses and there is a 1% risk of converting to VF.

    PHARMACOKINETICS Onset of action is within 20 seconds and peak effects occur within 20-30 seconds. Prolonged bradycardia may occur in patients with toxic concentrations of calcium channel blockers. The action of adenosine is antagonized by methylxanthines and potentiated by blockers of nucleoside transport such as dipyridamole.


    Adrenal crisis or ADDISONIAN physiology is commonly diagnosed in the ICU patient with the clinical findings of sepsis but without a source for infection (negative blood for bacteria and fungi, negative CSF and CT scans, negative cardiac echocardiography). Several factors may predispose the ICU patient to a primary insufficinecy including surgical stress, circulatory failure, sepsis, coagulopathy and HIV.

    CLINICAL The most prominent finding is hypotension that is refractory to vasopressors. Other features include HYPONATREMA and HYPERKALEMIA, weakness and hyperpigmentation all of which are not specfic enough to readily lead to a diagnosis. In mild cases, the hemodynamic changes are similar to hypovolemia with low cardiac output. More severe cases resemble septic shock (for which they are often superimposed).

    DIAGNOSIS The gold standard for diagnosis is the ACTH stimulation test involving measure of the cortisol levels one hour after injection. Rapid screening for adrenal crisis can be accomplished by measuring the urine potassium content.

    TREATMENT Decadron will not interfere with the plasma cortisol assay and can be given as 10 mg IV (equvalent to 270 mg of hydrocortisone). Continued empiric therapy should continue as hydrocortisone 100 mg every six hours until test results are available.


    Adverse drug reactions can be categorized as anaphylactic, anaphylactoid and miscellaneous reactions.

    The most common agents responsible for ADRs include analgesics, antibiotics, sedatives and antipsychotics. Additives, including the preservatives sulfite and paraben, may also cause ADRs. A number of other agents, such as local anesthetics, narcotics, mannitol, dextran, protamine and blood products have been implicated as well.

    SCh has been associated with a number of adverse effects, including fasciculations, myalgia, potassium release, changes in HR, increases in intragastric and intraocular pressures and MH. In addition, NMB-specific immunoglobulin E antibodies have been noted to be responsible for anaphylaxis to SCh and other neuromuscular blockers. Finally, non-IgE mediated reactions, including those secondary to histamine release, have also been associated with NMB.

    A few reports of ADRs have been associated with THIOPENTAL. Although anaphylactic reactions are exceeedingly rare, estimated at about 1:30K injections by one report, fatalities have been reported. Of interest, some patients have experienced severe reactions even after 4-5 uneventful exposures to thiopental.

    As many drug reactions are allergic in nature, neither dose nor rate play much of a role. However, in what Sanchez Palacios et al terms pseudoallergic reactions, which the authors define as ADRs due to the release of histamine and other mediators but not related to IgE antibodies, the dose of the agent appeared important. Morphine and muscle relaxants, especially the benzylisoquinoline types (curare, metocurine, atracurium), which cause histamine release, were implicated in these reactions. Other muscle relaxants associated with this form of ADR include succinylcholine, vecuronium, pancuronium, alcuronium and galamine.

    Some agents have been associated with ADRs based primarily on their rate of administration. These include: (1) vancomycin, which causes a histamine-like reaction characterized by facial and neck erythema, (2) phenytoin, which causes hypotension due to cardiotoxicity, and (3) aminoglycosides, which may cause renal and ototoxicity directly related to peak serum levels.


    PHARMACOKINETICS Changes manifest as prolongation of elimination half-times of drugs. This can reflect decreased clearance or increases in the Vd.

    PHARMACODYNAMICS MAC requirements are decreased in the elderly. Plasma concentrations of NDMRs necessary to produce comparable degrees of twitch response suppression are similar in young and elderly patients. Likewise, the plasma concentration necessary to produce equivalent pharmacologic effect of thiopental or etomidate is the same, however the dose is reduced in the elderly. This is due to an reduced initial volume of distribution, resulting in a higher plasma concentration after any given dose in the elderly, a larger volume of distribution at steady state and a reduced clearance, rather than a pharmacodynamic explanation. There is also a reduced affinity of ß receptors for adrenergic agonists with aging.

    EVALUATION Elderly patients are likely to be taking several different drugs that may contribute to adverse drug interactions.

    REGIONAL Elderly patients may be more sensitive to spinal anesthesia, manifesting as prolonged duration of action (perhaps reflecting decreased absorption) and exaggerated reductions in blood pressure. Doses of local anesthetics for epidural anesthesia (and probably spinal) are decreased (25-50%) in aging, perhaps reflecting progressive occlusion of intervertebral foramina with connective tissue resulting in greater spread of local anesthetics.

    GENERAL Changes associated with aging can cause mechanical problems during general anesthesia. There is no evidence that any specific drug is preferable to another in elderly patients. The initial doses of muscle relaxants should be reduced because of reduced muscle mass. Atracurium clearance is largely independent of hepatic and renal mechanisms and its duration of action is not significantly influenced by aging. Vecuronium shows detectable but modest prolongation of duration of action in the elderly. The incidence of cardiac dysrhythmias may be greater with anticholinesterases in the elderly.


    Old age can be conventionally defined as over 65 years of age. Elderly patients are more vulnerable to adverse effects of anesthesia because of their generalized decline in organ function which may manifest only with the added stress of the perioperative period. Although morbidity and mortality of surgery in elderly patients is higher, these problems are usually due to concomitant diseases rather than aging itself. Psychological, physiologic and pharmacologic changes must be taken into account when anesthetizing elderly patients.

    PHYSIOLOGIC Elderly patients have a generalized decline in organ function characterized as a decreased margin of reserve for adaptation, especially with acute stresses during the perioperative period.

    CNS There is a progressive decline in CNS activity and loss of neurons. Conduction velocity in peripheral nerves slows, and there may be reduced numbers of fibers in spinal cord tracts. These may manifest as decreased dose requirements for drugs (MAC).

    CARDIOVASCULAR Systolic BP increases with age reflecting poorly compliant arterial walls. Heart rate decreases, suggesting an increase in activity of the parasympathetic nervous system. Drug-induced heart rate changes are less severe and reflex-induced increases via the carotid sinus to hypotension are attenuated in elderly patients. Cardiac output decreases about 1% per year after age 30, reflecting decreases in oxygen requirements. Cerebral, coronary, and muscle blood flow are maintained, therefore they receive a greater percentage of blood flow in the elderly. Stroke volume is unaffected by aging, although the ability to increase myocardial contractility in response to stress is impaired

    PULMONARY changes are characterized by deterioration of gas exchange and changes in breathing mechanics. PaO2 decreases about 0.5 mmHg per year after age 20 and the Aa gradient increases. These are due to V/Q mismatching due to decreased cardiac output and degenerative changes (loss of alveolar septae) in the lungs. Aging alone does not alter PaCO2, although the Aa gradient for CO2 may increase due to increased physiologic dead space. Mechanical ventilatory function is impaired because of decreased elasticity of the lungs and increased stiffness of the thorax. Vital capacity and FEV1 decrease (about 1% per year) with aging and residual volume and FRC increase. Maximum breathing capacity is substantially reduced. Pneumonia occurs with increased frequency and there is increased incidence of aspiration of secretions in the elderly.

    RENAL Aging is associated with progressive declines in renal blood flow (parallels reductions in cardiac output), GFR and urine concentrating ability. Ability to conserve sodium is reduced, making elderly patients vulnerable to hyponatremia, whereas decreased renin activity with associated reductions in aldosterone may contribute to hyperkalemia. Despite reduced renal function, plasma creatinine levels do not increase reflecting decreased muscle mass.

    HEPATIC blood flow decreases. There is also decreased activity of hepatic microsomal enzymes. Reduced hepatic blood flow is important in the delayed drug clearance that is often observed. Production of albumin is decreased with resultant decreased drug binding.

    GASTROINTESTINAL There is a general decrease in motility and delayed gastric emptying. GE sphincter tone is frequently decreased making elderly patients at increased risk for aspiration.


    There are three basic ANATOMIC changes that affect lung function in the elderly.

    1) stiffening of the thorax from changes in the ribs, sternum, cartilages and spinal column so that chest cage is less expansible for any expanding force
    2) muscles become weaker
    3) parenchyma becomes MORE COMPLIANT with lost elastic recoil

    The upper airway is less affected than the larynx and the tracheobronchial tree.

    The functional changes that result from these anatomic changes are best understood by considering the FOUR independent volumes that comprise the TLC. The term capacity refers to the sum of two or more volumes. The four building blocks of gas space are IRV, VT, ERV and RV.

    A newer volume described by a functional test is the closing volume (CV) that usually is a fraction of the ERV but in elderly may actually include all of the ERV and some of the tidal volume. The closing capacity (CC) refers to the closing volume plus residual volume.

    The TLC increases rapidly after birth to a maximum of 6-7 liters by maturity. It gradually declines after maturity as a result of decrease in height and disc shrinkage. The RV (like TLC) also increases until maturity but after a plateau will continue to increase with age. The tidal volume, while operating above an increasing FRC (which is ERV plus RV) maintains an average value of about 6-7 mL/kg. The CC (reflecting the minimal lung volume before small airways begin to close) lies within the ERV through youth but encroaches TV in the erect 60 year old. As a result, the vital capacity (ERV plus TV plus IRV) declines progressively with age. The overall respiratory function decreases at about 10% (range 5-20) per decade of life.

    Gas exchange is affected by (1) DIFFUSION of the gases across alveolar walls and within air spaces, (2) MATCHING of ventilation and perfusion and (3) SHUNTING of venous blood past the alveolar units.

    While PAO2 remains constant, a decrease in PaO2 with age will increase the A-a gradient. Numerous studies demonstrate that arterial O2 tension will decrease about 4-5 mmHg with each decade of life over twenty. There may be a small decrease in ETCO2 with age (reflecting the dead-space effect of any VQ mismatch) but PaCO2 remains fairly constant in older healthy individuals.

    Arterial oxygen falls primarily because of increased VQ mismatch and this mismatch is often attributed to a nonuniform loss of pulmonary elastance. While there still remains a balance of lung zones above and below V/Q = 1, there is a broader bell-shaped curve with an increase in mismatched units. While diffusion (as measured by carbon monoxide studies and reported as DLCO) does decrease, there is little evidence that this contributes to falling oxygen tension. Likewise, true shunting of the venous blood does not contribute to increasing A-a gradients and there is no good evidence that physiologic shunting (about 4-5% of cardiac output) increases with age.

    Elderly patients do exhibit a blunted response to hypoxemia and hypercarbia. These normal physiologic reflexes are even more severely blunted with the effect of anesthesia but often it is difficult to differentiate pharmacodynamic and pharmocokinetic causes.


    INDICATIONS include (1) arrest due to VT/VF not due to transient or reversible cause, (2) spontaneous sustained VT, (3) syncope of undetermined origin with sustained VT/VF induced at EPS when drug therapy is not effective or tolerated, (4) ischemic cardiomyopathy and depressed LV function and (5) nonsustained VT with CAD, previous MI, LV dysfunction and inducible VT/VF at EPS not suppressed by class I antidysrhythmic.

    An ICD is composed of two components, the pulse generator and the leads. The pulse generator generates the shock and houses the battery and circuitry for pulse pacing, signal filtering and analysis and data storage. The leads transmit electrical signals from the heart for analysis and from the pulse generator to deliver pacing signals and defibrillating shocks.

    The greatest alteration in ICD lead design was the change from contoured epicardial to transvenous leads. This design change eliminated the need for a thoracotomy to place the leads, thereby decreasing implant morbidity and improving long term lead reliability.

    The nomenclature for the ICD is as follows:

    POSTION I: chamber shocked (either none, atrium, ventricle or dual)
    POSTION II: antitachycardia pacing chambers (same as I)
    POSTION III: tachycardiadetection (eith electrogram or hemodynamic)
    POITION IV: antibradycardia pacing chambers (same as I)

    Newer devices can deliver tiered therapy (essential by pacing and then increasing shocks). Devices measure R-R interval over time. Pacemakers can function in presence of ICD as long as electrodes are bipolar. Most ICDs have backup VVI pacing to protect against post-shock bradycardia.

    DEACTIVATION has been recommended by some authors as extraneous signals, such as myopotentials from shivering, fasciculations from SCh, and electrocautery may cause the ICD to inappropriately discharge.

    DEACTIVATION is best accomplished with a programming device. The use of a magnet over the Medtronic, St Jude or Biotronik pulse generator will accomplish the same result. The magnet can then be removed to resume function. Guidant ICD devices require a 30 second holding pattern with audible tones to deactivate and subsequently reactivate the detection capabilities.

    Partial deactivation can also be programmed in third or higher generation ICDs, where the anti-bradycardia pacing functions are retained, but the defibrillating functions are deactivated.

    While no specific anesthetic techniques have been advocated during the PLACEMENT of an ICD or in patients with ICDs, there has been one case report in which isoflurane appeared to significantly LOWER the defibrillation thresholds for an ICD.

    During the initial implantation of an ICD, the patient received isoflurane and thresholds were obtained. Post-implantation testing using midazolam and fentanyl, however, revealed significantly higher DFTs, necessitating a third operation without isoflurane to obtain an adequate and subsequently verifiable DFT. Of note, the authors observed that the discontinuation of isoflurane intraoperatively resulted in a DFT rise within 25 minutes.

    While GA was once the standard anesthetic regimen for implantation of ICD devices, with reductions in the size and technical difficulty of placing ICDs, the use of local anesthesia and conscious sedation has increased dramatically. Such anesthetic techniques have been noted to reduce some complications and costs.


    There are two primary nerves which innervate the larynx and both are derived from the VAGUS.

    The SUPERFICIAL LARYNGEAL divides into TWO branches. The INTERNAL LARYNGEAL is purely sensory with fibers from the tongue to the vocal cords. The EXTERNAL LARYNGEAL is purely MOTOR but innervates only the cricothyroid muscle (which tenses and ADDUCTS the cords) and part of the transverse arytenoid muscle.

    The second nerve of the larynx is the RECURRENT LARYNGEAL (again a branch of the vagus) which innervates ALL muscles of the larynx (exept the cricothyroid and part of the transverse arytenoid muscle) and ALSO provides sensory innervation to that portion below the vocal cords including part of the trachea.

    The cricothyroid muscle adducts the cords – it is the only TENSOR of the larynx. Transection of one RLN innervating all other muscles incuding adductors and abductors leaves the external laryngeal unopposed and a flaccid cord in the closed position. Patients with RLN injury may complain of hoarseness and may be at increased risk for aspiration. Bilateral RLN injury causes aphonia and cords may flap together during inspiration leading to complete airway obstruction.

    Some experts advocate direct or fiberoptic inspection of the cords with a deep extubation following THYROIDECTOMY to rule out any neurologic injury.


    NASAL PREP The nasal passages should be treated with a topical vasoconstrictor to shrink the nasal mucosa. The mucosa can be anesthetized and vasoconstricted with a mixture of lidocaine and phenylephrine or xylometazoline.

    The applicators are gently inserted into each nostril and gently advanced until they reach the posterior wall of the nasopharynx. It is advisable to prepare both nares.

    Nasal airways are dilated with trumpets that have been lubricated with lidocaine jelly or viscous lidocaine (both are 2% concentration).

    ORAL ANESTHESIA The mouth can be anesthetized with lidocaine spray, ointment on a tongue depressor or viscous lidocaine to swish and spit. Hurricaine spray (with 20% benzocaine) is also available but must be cautiously utilized.

    The airway can be anesthetized by with 5 mL of 4% lidocaine solution by nebulizer with a small risk of bronchoconstriction (AA 2007).

    SUPERIOR LARYNGEAL NERVES (branches of the VAGUS nerve) provide sensory innervation to the epiglottis, arytenoids and vocal cords. They are blocked as they pass into the larynx through the thyrohyoid membrane. The skin of the neck is retracted caudad over the thyroid cartilage. A syringe containing 2.5 mL of lidocaine 0.5-1% with a 25g needle is used. The needle is inserted until it rests on the lateral portion (the GREAT CORNU) of the hyoid bone. It is then withdrawn slightly and walked off the hyoid bone in an INFERIOR direction. The needle is then advanced and passed through the thyrohyoid membrane which should be felt as a slight resistance. The syringe is then aspirated and the lidocaine is injected.

    Hypotension and bradycardia are rare complications of the SLN block (incidence 2.7%). Prophylactic anticholinergics are recommended and may be useful as antisialogues as well.

    The TRANSTRACHEAL BLOCK provides rapid anesthesia of the entire trachea between the carina and vocal cords (innervated by the recurrent laryngeal nerves). It requires only a 5-10 mL syringe, 23g needle and hemostat for needle control.

    Alternatively, an 18g angiocath can be used with the needle removed to be utilized for JET ventilation if necessary.

    Complications of the transtracheal block include bleeding, tracheal injury and SQ emphysema.

    The transtracheal block should be performed approximately one minute prior to the start of the bronchoscopy. Three mL of 2% lidocaine are drawn into a syringe. The cricothyroid membrane is identified, and the syringe is directed posteriorly and perpendicular to the floor. The needle is in the trachea when a sudden loss of resistance is felt. The position is confirmed by aspirating air through the syringe. Lidocaine is then injected rapidly and the needle withdrawn. The patient will cough, drawing the LA down to the carina and then spraying it over the entire trachea up to the vocal cords.

    Such procedures may require up to 9 mg/kg of lidocaine though radioisotope studies demonstrate much of the lidocaine is swallowed and easily cleared by a high first pass metabolism.


    Mouth opening (largely a function of the TMJ) is of prime importance to allow the insertion of a laryngoscope blade and subsequent glottic visualization. Adults should be able to open their mouths so that there is a 3-4 cm distance between upper and lower incisors (two large fingerbreadths).

    The distance from the inner surface of the mandible to the hyoid bone during neck extension should be at least two large fingerbreadths in adults. The THYROMENTAL distance should be at least 6 cm or three large fingerbreadths. The laryngoscope displaces the tongue into this space and exposure of the glottis may be inadequate if the space is narrowed or noncompliant. The sternomental distance should be over 12.5 cm. This test independently has the best likelihood ratio of 5.7 for predicting difficult airways.

    The oropharyngeal classification of the airway (first suggested by MALLAMPATI in 1983 and tested in a prospective study in 1985) has become the standard basic assessment tool for anesthesiologists.

    In the original description of the method, the patient assumes the sitting position, opens the mouth maximally and extends the tongue. The patient does not phonate and head position is not specified. The visibility of the oral and pharyngeal structures are then rated according to a THREE point scale.

    Class 1 – faucial pillars, soft palate and uvula visualized
    Class 2 – faucial pillars and soft palate visualized, but uvula is masked by the base of the tongue
    Class 3 – only soft palate visualized

    Note the original Mallampati test utilized a three-class scale. Many anesthesiologists use a four-class scale later popularized by Samsoon and Young. This scheme essentially duplicated the Mallampati Class 1, but differed as noted below.

    Class 2 – soft palate, fauces, uvula
    Class 3 – soft palate, base of uvula
    Class 4 – soft palate not visible at all

    In the Mallampati 1985 study patients were given a standardized GA induction and laryngoscopy was attempted in a standardized fashion with a Macintosh 3 blade. The quality of visualization of the larynx was then assessed on a four point scale.

    Grade 1 – full glottic view
    Grade 2 – glottis partly exposed
    Grade 3 – glottis not exposed (corniculate cartilages visualized)
    Grade 4 – corniculate cartilages could not be exposed

    If we predict a difficult airway with a Mallampati Class 3, then the original data revealed a SENSITIVITY of just 50% and a SPECIFICITY of 99%. This means the test successfully identified easy airways but missed significant numbers of difficult airways.

    Tse et al (more recent study) found the test to perform less well with a sensitivity of 66% and specificity of just 65%. The PPV was only 22%, meaning there were a large number of false positives relative to the number of true positives. Treating all positive airways would therefore cause significant overtreating of patients with actually easy airways.

    Assessment as a Mallampati class ZERO airway has recently been proposed when the epiglottis is seen on mouth opening and tongue protrusion.


    In comparison with other colloidal solutions and crystalloid solutions, human albumin solutions are expensive. Volume for volume human albumin solution is twice as expensive as hydroxyethyl starch and over thirty times more expensive than crystalloid solutions. It is estimated that approximately 90% of administered albumin remains in the intravascular space after 1-2 hours (compared with only 25% for NS).

    In critically ill patients and patients with sepsis, 5% albumin has been demonstated to expand the extracellular space (plasma AND interstitial volume) by twice the volume infused. This in comparison to NS which expands the extracellular volume by the same amount as that infused but with a predilection for the interstitial volume over the plasma volume (in a 3:1 ratio).

    There is no evidence that albumin reduces mortality and a strong suggestion that it may increase the MORTALITY rates in patients with hypovolemia, burns and hypoproteinemia. Albumin is believed to have anticoagulant properties, inhibiting platelet aggregation and enhancing the inhibition of factor Xa by antithrombin III.

    The SAFE study is the largest randomized controlled trial to date evaluating the safety of albumin (NEJM 2004 350:2247). In this trial, 6997 critically ill subjects were randomized to receive either 4% albumin or normal saline for the treatment of hypovolemia. The results presented by the Principal Investigator at the BPAC meeting on March 2005 indicate that for patients in the general ICU population requiring fluid resuscitation, the mortality rate of those who receive albumin is the same as for those who receive saline (relative risk of mortality 0.99).

    Secondary analyses of prespecified subgroups of patients with adult respiratory distress syndrome, severe sepsis and trauma were consistent overall with this finding. Two additional findings deserve mention. First, results of an exploratory analysis of trauma patients with concomitant traumatic brain injury showed increased mortality in the albumin treatment arm (relative risk of mortality 1.36). Second, a higher survival rate was observed in the albumin treated patients with severe sepsis, but since this finding was not statistically significant, its clinical significance remains uncertain.

    Administration sets include 15 micrometer FILTERS to prevent infusion of air, bacteria, fungi and albumin microaggregates.


    In adults, there is evidence that MDI will more effectively distribute the drug than nebulization. In the uncooperative patient, DOSING for adults is at 2.5 mg and pediatric patients may be treated with 0.05-0.15 mg/kg in normal saline.

    In severe status asthmaticus, continuous nebulizations may be administered at 40-80 mg per hour and are generally given intermittently once weaned to 10 mg per hour. For status, there is good evidence that continuous nebulization is superior to intermittent dosing.


    SIDE EFFECTS of all of the beta agonists include tachycardia, increased QT interval, dysrhythmia, hypertension and hypotension. Less common side effects include hypokalemia, tremor and worsening of VQ inequalities.


    ETOH produces widespread nonspecific effects on cell membranes but there is evidence that many effects are mediated by actions on the receptor for the inhibitory neurotransmitter GABA. A shared site of action for alcohol, benzodiazepines and barbiturates explains the ability to produce cross tolerance.

    SYMPTOMS In the naive patient, a blood alcohol level of 25 mg/dL will impair cognition and result in incoordination. At levels greater than 100 mg/dL signs of vestibular and cerebellar dysfunction (nystagmus, dysarthria, ataxia) increase. Autonomic dysfunction may result in hypotension, hypothermia, stupor and ultimately coma. Blood levels greater than 500 mg/dL are typically fatal primarily due to depression of ventilation. The maximum survived BAC include 1510 mg/dL in an alcoholic and 1127 mg/dL in a naive patient.

    The critical aspect of treatment is maintenance of ventilation though hypothermia and hypoglycemia may also warrant therapy. THIAMINE at 100 mg IV/IM should be given prior to administration of glucose. HEMODIALYSIS effectively removes alcohol in patients who deteriorate despite conventional therapy. HD may decrease alcohol levels by 60-100 mg/dL/hour.

    CARDIOVASCULAR effects secondary to acute intoxication include possible atrial fibrillation, prolonged PR and QTc intervals and AV block. Hypothermia alone may be associated with bradycardia, widened QRS and prolonged PR interval. Many leads may also show classic OSBORN WAVES or J WAVES seen at the junction of the QRS complex and the ST segment. Below 28 degrees, ventricular irritability increases and dysrhythmias can occur. Fibrillation usually happens between 25-30 degrees.

    METABOLIC disturbances may include lactic or ketoacidosis, hypokalemia, hypomagnesemia and hyperosmolality.

    WITHDRAWAL is usually not noted until 6-8 hours after an abrupt decrease in consumption but symptoms are not typically severe until after 24-36 hours. SEIZURES may occur 6-48 hours into withdrawal and delerium tremons does not occur until 2-4 days into withdrawal. TREATMENT is by resumption of alcohol intake, benzodiazepines, beta blockade and alpha 2 agonists (clonidine).

    DISULFIRAM is given to alcoholic patients to inhibit aldehyde dehydrogenase activity which serves to increase acetylaldehyde concentrations with consumption of alcohol. Symptoms of disulfiram reactions include flushing, vertigo, diaphoresis, nausea and vomiting. Patients treated with DISULFIRAM may present with a baseline sedation or hepatotoxicity. Disulfiram may result in a potentiation of the effects of benzodiazepines.

    Acute unexplained HYPOTENSION during GA may reflect inadequate stores of norepinephrine owing to disulfiram induced inhibition of dopamine beta hydroxylase. This hypotension may be responsive to ephedrine but phenylephrine may produce more predictable results.


    Tremulousness which tends to occur early is the most common clinical manifestations of alcohol withdrawal. Tremulousness typically begins 6-8 hours after decreasing alcohol intake. Patients will typically demonstrate a clear sensorium but may complain of nausea, anxiety or insomnia. Symptoms typically abate in 24-36 hours and most patients will recover without additional incident.

    Approximately 25% of patients progress to more severe sequelae, although it is impossible to predict which patients are at risk.

    SEIZURES occur in approximately 10% of alcoholic patients but they may not be caused by withdrawal and physicians should rule out other causes such as trauma, metabolic causes (hypomagnesemia, hypoglycemia and hyponatremia), and idiopathic epilepsy. Most seizures attributable to withdrawal occur 6-48 HOURS after decrease in alcohol intake. Seizures typically are short, generalized tonic-clonic seizures and 40% are limited to a single event. Status epilepticus and recurrent seizures lasting more than 6 hours are highly suggestive of a cause other than alcohol withdrawal.

    HALLUCINATIONS occur in almost 25% of alcohol withdrawal cases, are typically visual in nature and occur 8-48 hours after decrease in alcohol intake. Hallucinations may last 1-6 days. Alcoholic HALLUCINOSIS is a unique disorder of chronic alcoholics that consists of auditory hallucinations with an otherwise clear sensorium and is differentiated from hallucinations within the continuum of withdrawal.

    DELIREUM TREMENS occurs in only 5% of alcohol withdrawal patients, but it carries a 10-15% mortality rate. Approximately 30% of patients developing seizures will progress to develop DT. Trauma patients will exhibit DT within 48 hours after injury but this may be delayed for 4-5 days.

    DT is characterized by a confused, disoriented and disheveled appearance with constant movement, picking at bed sheets, fighting against restraints and incontinence. The tremor can become so pronounced that even simple eating and grooming tasks become impossible.

    Dehydration, vomiting, hyperthermia, electrolyte imbalances and aspiration can quickly progress to death unless aggressive interventions are made. Concomitant illness, trauma, seizure disorder or medication administration may mask or modify this typical presentation.

    Death is most often caused by cardiac dysrhythmia, which may be related to the profound hypomagnesemia and hypokalemia seen in patients with DT. Other considerations in the DDX include other causes of hyperadrenergic state and delirium, including cocaine or amphetamine intoxication, ingestion of PCP or monoamine oxidase inhibitors, lithium overdose, severe infection, hypoxia and trauma.

    Wernicke-Korsakoff encephalopathy is occasionally seen in the alcoholic patient. WKE is attributed to thiamine deficiency.

    Consideration must be given to anesthetic administration in these patients because (1) hypotension may necessitate lower anesthetic doses, (2) inotropic agents may be needed to offset the hemodynamic depression of acute intoxication, (3) these patients are at much greater risk for aspiration, and (4) underlying liver disease may alter the pharmacokinetics of various anesthetic agents.


    Alfentanil is an analogue of fentanyl that is 5-10 times less potent and has one-third the duration of action of fentanyl. Alfentanil has 10 times the potency of morphine. It is a weaker BASE than other opioids with a pKa of 6.8. As such 90% of unbound plasma alfentanil is NONIONIZED at a physiologic pH.

    A unique advantage of alfentanil (compared with fentanyl and sufentanil) is the more RAPID onset of action after IV administration. It is used less commonly since the introduction of remifentanil.

    DOSING Induction dose of 50-300 mcg/kg over 3 minutes. To avoid chest rigidity, neuromuscular blockers should be administered with IV induction doses. Anesthesia supplement doses range from 0.05-1.25 mcg/kg/min.

    Alfentanil can be used as a sole anesthetic at 1-8 mcg/kg/min.

    Epidural boluses are dosed at 500-1000 mcg (10-20 mcg/kg) and infusions may be dosed at 100-250 mcg/hour (2-5 mcg/kg/hour).

    PHARMACOKINETICS The onset of action is within 1-2 minutes and duration of action is between 10-15 mintues. Duration of action for IM dosing is between 10-60 minutes. Terminal elimination half life is at 84-90 minutes primarily due to a small Vd.

    The Vd of alfentanil is 4-6 times smaller than that of fentanyl reflecting a lower lipid solubility. Despite this low solubility, the high nonionized state at physiologic pH makes the opioid quick to cross the blood brain barrier.



    Allergic or hypersensitivity reactions can be categorized into four basic categories.

    1) ANAPHYLACTIC TYPE reactions are typified by anaphylaxis and some forms of bronchial asthma. The mechanism or reaction is through formation of IgE (cytotropic) antibody, immediate release of vasoactive amines and other mediators from basophils and mast cells, followed by recruitment of other inflammatory cells.

    One large study in France revealed that 57% of all intraoperative adverse drug reactions are TYPE 1 reactions. The estimated incidence of perioperative ANAPHYLAXIS is 1 in 4500 (females more commonly affected at 1.6:1).

    2) CYTOTOXIC TYPE reactions are typified by autoimmune hemolytic anemia, erythroblastosis fetalis and Goodpasture syndrome. The mechanism is through formation of IgG and IgM which binds to antigen on target cell surfaces leading to phagocytosis of target cell or lysis of target cell by C8,9 fraction of activated complement or antibody-dependent cellular cytotoxicity.

    3) IMMUNE COMPLEX diseases include arthus reaction, serum sickness, SLE and certain forms of acute glomerulonephritis. Antigen-antibody complexes will activate complement and attract neutrophils which release lysosomal enzymes and other toxic moieties.

    4) CELL-MEDIATED (delayed) hypersensitivity includes tuberculosis, contact dermatitis and transplant rejection. Mechanism is through sensitized T lymphocytes which release lymphokines and induce T cell-mediated cytotoxicity.

    The incidence of drug allergy is 5% in the US population. More than 90% of the allergic reactions to IV medications occur within 3 minutes of administration.

    Approximately 80% of all intraoperative allergic reactions are secondary to neuromuscular blockers (usually benzylisoquilinium derived). Allergies to local anesthetics are very rare (more common with esters) but true allergies exist which may be categorized as a type 1 or type 4 reactions.


    Alveolar oxygen is calculated by the following formulas.

    PAO2 = PIO2 – (PaCO2/RQ)

    where RQ is the respiratory quotient that defines the proportional exchange of CO2 and O2 across the interface (VCO2/VO2 is normally 0.8).

    Note that a high FAT diet will DECREASE the RQ as less CO2 is liberated by metabolism of lipid nutrients. A diet rich in CARBOHYDRATES will INCREASE the RQ towards 1.

    PIO2 is calculated by the additional formula.

    PIO2 = FiO2 (PB – PH2O) or
    PIO2 = FiO2 (760 – 47)

    An academic point to consider is that PPV increases the airway pressure above ambient barometric. The Aa gradient could therefore increase with PPV but this has not been demonstrated.

    An A-a gradient is normally less than 20 mmHg at a room air FiO2 of 0.21. The magnitude of the gradient is not linear with FiO2 and at FiO2 of 1.0 the normal A-a gradient is just less than 100 mmHg. This is thought to be secondary to a loss of effective HPV at higher oxygen levels.

    Increasing age will increase the gradient by decreasing arterial content. The PaO2 on room air falls by 4-5 mmHg for each decade over the age of twenty.

    The nonlinear relationship of the gradient has led to other methods of measuring the efficiency of gas exchange.


    In the ICU SETTING, the A-a gradient can be used to easily differentiate between hypoventilation (normal gradient) and pulmonary disorder (increased gradient) in the hypoxic patient.

    Commonly used extubation criteria in the ICU may include PaO2 over 60 with an FiO2 less then 0.4 and an A-a gradient of less than 300 mmHg.


    ARICEPT is a reversible inhibitor of acetylcholinesterase which may prolong the effects of SCh. The drug may also antagonize blockade by the non-depolarizing agents. The half-life is 70 hours.

    Galantamine or RAZADYNE is another medication with an identical mechanism of action. The half-life of the drug is approximately eight hours.

    Some mice studies have suggested potential links between progression or early development of AD and volatile agents (JAMA 2007).


    AMICAR or aminocaproic acid acts as an INHIBITOR of FIBRINOLYSIS. The inhibitory effects of aminocaproic acid appear to be exerted principally via inhibition of plasminogen activators and to a lesser degree through antiplasmin activity.

    Renal excretion is the primary route of elimination, whether AMICAR is administered orally or IV. About 65% of the dose is recovered in the urine as unchanged drug and 11% of the dose appears as a metabolite. Renal clearance approximates endogenous creatinine clearance. The total body clearance is 169 mL/min. The elimination half-life for AMICAR is approximately two hours.

    AMICAR is useful in enhancing HEMOSTASIS when fibrinolysis contributes to bleeding. In life-threatening situations, whole blood transfusions, fibrinogen infusions and other emergency measures may be required.

    Fibrinolytic bleeding may frequently be associated with surgical complications following heart surgery with or without bypass, TURP coagulopathy, portacaval shunts, hematologic disorders such as aplastic anemia, abruptio placentae, hepatic cirrhosis and neoplastic disease such as carcinoma of the prostate, lung, stomach and cervix. Amicar has also been used to reduce bleeding during idiopathic scolioisis repair.

    When there is UNCERTAINTY as to whether the cause of bleeding is primary fibrinolysis or DIC, this distinction must be made before administering aminocaproic acid.

    The following TESTS can be applied to differentiate the two conditions.

    1) platelet count is usually decreased in DIC but normal in fibrinolysis
    2) protamine paracoagulation test is positive in DIC – a precipitate forms when protamine sulfate is dropped into citrated plasma. This is negative in the presence of fibrinolysis.
    3) the euglobulin clot lysis test is abnormal in primary fibrinolysis but normal in DIC

    DOSAGE Amicar is administered by infusion utilizing water, NS, D5W or LR. Rapid injection is NOT recommended.

    For the treatment of acute bleeding syndromes due to elevated fibrinolysis and for prophylactic protocols during CPB, it is suggested that 20 mL (5 grams) is administered during the first hour through a carrier line, followed by a continuous infusion at the rate of 4 mL (1 gram) per hour. This method of treatment would ordinarily be continued for about 8 hours or until the bleeding situation has been controlled.

    SIDE EFFECTS induce hypotension, bradycardia and arrhythmias. The medication may be contraindicated in the patient with history of PE or DVT.

    Aminophylline is the IV form of theophylline used for refractory bronchospasm most often when it is difficult to deliver direct acting ß agonists to the lower airway.

    The MECHANISMS of action include release of NE (direct ß agonist) and inhibition of the phosphodiesterase catalyzed breakdown of cAMP.

    DOSING is by loading 6 mg/kg IV over 20-30 minutes followed by maintenance IV infusions (1 g in 250 mL D5W for 4 mg/mL) at doses between 0.5-1 mg/kg/hour.

    SIDE EFFECTS include dysrhythmias and antagonism of the barbiturates. Multiple medications increase serum concentrations to toxicity: ketoconazole, rifampin, carbamazepine, isoniazid, phenytoin, macrolides, zafirlukast and cimetidine.

    AMIODARONE is primarily a class III antiarrhythmic indicated for VF, pulseless VT, stable VT, wide complex tachycardia of unknown origin, refractory atrial fibrillation & flutter, PSVT and PSVT with reentrant tachycardias including patients with WPW.

    DOSING The latest ACLS guidelines recommend 300 mg of amiodarone IV push (before lidocaine) following epinephrine for shock refractory VF or pulseless VT. A second dose at 150 mg may be given for persistent VF/VT but the total cumulative dose should not exceed 2.2 grams over 24 hours.

    The PEDIATRIC dose for refractory VF/VT is at 5 mg per kg IV/IO.

    Although only fair evidence exists regarding its antiarrhythmic properties, amiodarone has greater support than other agents used in the VF/VT algorithm which include lidocaine, magnesium (if hypomagnesemic) & procainamide.

    As a maintenance antiarrhythmic after a return of the spontaneous circulation, a slow infusion at 1 mg per minute for 6 hours (360 mg) followed by a continuous infusion at 0.5 mg per minute for the next eighteen hours (540 mg) may be benficial.

    For STABLE VT (monomorphic and polymorphic) amiodarone has been recommended as a Class IIa (acceptable and useful) agent. For wide complex tachycardia with low EF, amiodarone has been promoted as a class IIb drug ahead of lidocaine and adenosine.

    Amiodarone may also be useful for ATRIAL FIBRILLATION with RVR that is refractory to diltiazem. It can be infused concominantly with diltiazem.

    DOSING for all diagnoses other than VF and pulseless VT is at 150 mg over 10 minutes which may be followed by infusions at 1 mg/min. Pediatric dosing may start at aliquots of 1 mg/kg.

    PHARMACODYNAMICS Amiodarone is both an antiarrhythmic (class I and III properties) as well as a potent vasodilator. It acts directly on the myocardium to prolong action potential duration and increase the refractory period of cardiac fibers including accessory pathways (class III). Amiodarone is a weak sodium channel blocker (class I) slowing the upstroke velocity of phase 0 which reduces the rate of membrane depolarization.

    It noncompetitively inhibits alpha and ß receptors. It possesses vagolytic and CCB-like properties. Amiodarone decreases coronary and peripheral vascular resistance, LVEDP and SBP.

    Amiodarone may potentiate warfarin anticoagulants. It may cause bradycardia or even sinus arrest in patients receiving ß-blockers, CCB or lidocaine. Amiodarone can lead to interstitial PNEUMONITIS, alveolitis or pulmonary fibrosis. It may also cause thyroid dysfunction and thyrotoxicosis.


    AFE is estimated to occur once per every 20K pregnancies, the wide estimation of incidence is due in part to its variable presentation, with nonfatal or subclinical episodes rarely reported. When symptomatic, a high incidence of mortality has been reported. In two series, 61-86% of symptomatic patients resulted in maternal fatalities. One study noted that when survival did occur in symptomatic patients, only 15% remained neurologically intact. Only 39% of fetuses in utero at the time of a symptomatic AFE event will survive.

    SYMPTOMS Classically described as a profound and unexpected state of shock followed by cardiovascular collapse, the syndrome has been associated with a number of precursor signs and symptoms. The most common PRESENTING symptoms, in descending order:

    respiratory distress 51%
    hypotension 27%
    coagulopathy 12%
    seizures 10%

    Seizures will occur in approximately 30% of individuals when AFE occurrs prior to delivery. If symptoms present after delivery, an isolated coagulopathy manifesting as hemorrhage is the presenting symptom in 54% of all cases.

    Many report that symptoms occur in a BIPHASIC pattern with pulmonary symptoms and right heart failure leading to hypoxemia and left heart failure with concomitant hypotension. The wide variation in timing, symptoms and subsequent course, suggests that a high index of suspicion should be maintained at all times.

    DDX for such a variety of symptoms are broad and consist of hemorrhage, eclampsia, VAE, sepsis, anaphylaxis, MI, total spinal anesthesia and LA toxicity.

    TREATMENT consists of supportive care for mother and the newborn infant. Right heart failure may require vasopressin, NE or dobutamine infusions. Urgent cesarean may be necessary.


    Chronic amphetamines are often prescribed for narcolepsy and ADHD. The medications may be safely continued through the perioperative period according to one review (AA 2006 103:203).


    Amrinone or INOCOR is a bipyridine which produces positive INOTROPIC and VASODILATOR effects. This results in increased CO and decreased LVEDP. HR may increase with a concomitant decrease in BP. Milrinone is often PREFERABLE to amrinone because of its greater TI and shorter elimination half-life.

    MECHANISM Amrinone inhibits the PHOSPHODIESTERASE III enzyme resulting in an increase of cAMP and increased calcium to the myocardium. Inotropic effects are not prevented by alpha or ß blockade or depletion of catecholamines. Amrinone can be used concurrently with digitalis therapy.

    DOSING begins with a loading dose of 0.75 mg/kg over 2-3 minutes. The load may be repeated after 30 minutes and followed by an infusion at 2-20 mcg/kg/min. Onset of action is within 2-3 minutes and peak effects are achieved within 10 minutes. Postive inotropy can be observed for several hours after discontinuation. The elimination half time is about 6 hours and is primarily through renal excretion.

    The drug is diluted as 500 mg in 500 mL of NS. Maximum daily dose of 10 mg per kg.

    SIDE EFFECTS can include hypotension due to vasodilation. Chronic administration has resulted in thrombocytopenia and hepatic dysfunction.


    GABAPENTIN is commonly dosed at 300 mg BID to TID. Primary side effects include dizziness, somnolence, confusion and ataxia.

    … or LYRICA is

    STIMULANTS commonly used to offset sedation secondary to the opioids include Provigil


    ketorolac 15-30 mg IV q4-6
    ibuprofen 200-800 mg PO qid
    naproxen 250-500 mg PO bid
    celecoxib 100-200 mg PO bid
    rofecoxib 12.5-50 mg PO qd
    meloxicam 7.5 mg PO qd-bid
    Tylenol 1000 mg PO qd


    ketorolac 0.5 mg/kg IV qid
    Tylenol 35 mg/kg PR
    oxycodone 0.05-0.15 mg/kg PO
    hydrocodone 0.1-0.2 mg/kg PO


    3-6 years 5 mL every 4-6 hour
    7-12 years 10 mL every 4-6 hour

    Elixir contains 120 mg and 12 mg per 5 mL. Dosing for CODEINE in patients older than one year of age is at 0.5-1 mg/kg PO/SC/IM every 4-6 hours.


    The incidence of drug allergy is 5% within the US population. The INCIDENCE of perioperative anaphylaxis is 1:4500 (F:M 1.6:1) while the incidence of anaphylactoid reactions may be as high as 1:1000. MORTALITY rates for true anaphylaxis ranges between 3-6%.

    SYMPTOMS include hypotension, tachycardia (histamine stimulates adrenal catecholamines), pulmonary HTN, cardiac arrest, dyspnea, bronchospasm, laryngeal edema, pulmonary edema, urticaria, perioral and periorbital edema. It is possible to present with a solitary symptom and anaphylaxis may be indistinguishable from primary bronchospasm.

    PRIMARY TREATMENT involves maintaining the airway with oxygen and discontinued use of anesthetics and suspected offending agents. Intravascular volume should be restored with crystalloid and epinephrine (the cornerstone of successful treatment) should be utilized.

    A characteristic of anaphylaxis is the failure to respond to vasopressors other than EPINEPHRINE. Dosing should begin at 5-10 mcg (or 0.1 mcg/kg) IV and escalate RAPIDLY to clinical response. Infusions at 5-10 mcg per minute can also be started. Cardiovascular collapse requires larger doses of 0.1 to 1 mg IV. Higher dosing is often required in the perioperative setting because of the sympatholytic effects of general and regional anesthesia. In SEVERE resistant cases, atropine 1-2 mg IV and GLUCAGON 1-5 mg followed by infusions at 1-2 mg/hour may be required. Glucagon will increase the intracellular cAMP independently of beta adrenergic receptors.

    When IV access is not available, epinephrine can be given SQ at a dose of 0.5-3 mg or through the ETT at 50-100 mcg. Starting with code doses of epinephrine may ironically cause life-threatening hypotension, myocardial ischemia and stroke.

    SECONDARY TREATMENT includes (1) corticosteroids such as 0.25-1 g hydrocortisone or 1-2 g methylprednisilone, (2) H1 antagonists such as 0.5-1 mg per kg of diphenhydramine [H2 antagonists are not recommended though they are part of prophylaxis for anaphylactoid reactions (Audio Digest December 2003)], (3) catecholamine infusions consisting of epinephrine at 4-8 mcg/minute or norepinephrine at 4-8 mcg/minute, (4) aminophylline at 5-6 mg per kg over twenty minutes for persistent bronchospasm and (5) sodium bicarbonate at 0.5-1 mEq per kg for persistent hypotension with acidosis

    POSTOPERATIVE tryptase levels can assist with the diagnosis. Peaks occur between 30 minutes to 5 hours and will remain elevated for several days to weeks depending on the severity of the event. Other confirmatory tests include histamine levels and specific IgE levels.

    Postoperative skin testing and in vivo tests may be performed by an allergist with complete resuscitation equipment available.

    Common ETIOLOGIES for intraoperative anaphylaxis include neuromuscular blocking agents (69% of all cases). latex (12%), antibiotics (8%), colloids (3%), hypnotics (3.7%), opioids (1.4%) and others. Of the NMB agents, the distribtion includes rocuronium (29%), SCh (23%), atracurium (21%), vecuronium (17%), pancuronium (6%), mivacurium (3%) and cisatracurium (0.3%). Approxiamtely 1% will have anaphylaxis with isosulfan blue or Lymphozuran.

    Muscle relaxants account for most anaphylactic reactions in adults though LATEX anaphylaxis is more common in children.


    The incidence of intraoperative anaphylactoid reactions may be as high as 1:1000 (compared to 1:5000 for intraoperative anaphylaxis).

    Anaphylactoid reactions are often due to a direct effect of a drug on MAST cells and BASOPHILS that stimulate the release of histamine. Conceptually, BASIC drugs (such as d-tubocurarine, succinylcholine, thiobarbiturates, trimethaphan or polymyxin) displace another basic molecule (histamine) from the blood cells.

    The principle factors that predispose a patient to anaphylactoid responses include genetic features of atopy, abnormalities of the complement system and frequent exposure to the drug in question.

    The manifestations are often INDISTINGUISHABLE from anaphylaxis (type 1 reactions) or activation of the complement system (type 3 reactions) but the simple release of histamine is not dependent on prior exposure to the drug or presence of specific antibodies. It is likely that subclinical anaphylactoid reactions occur with high frequency but the amount of histamine released depends on the dose and rate of administration.

    Most common ANAPHYLACTOID reactions occur with ASA or other NSAIDS and radiocontrast dye. The incidence of radiocontrast reactions is between 5-8%. These may become less frequent as low osmolality agents become more popular.

    Unlike the nature of true allergic reactions, PRETREATMENT of patients with known anaphylactoid reactions are effective. See more information under LATEX ALLERGY. H1 and H2 blockers and steroids are NOT effective at blunting immune mediated IgE reactions (TYPE 1 reactions).


    The PHYSIOLOGIC CHANGES occurring secondary to ANEMIA are worth contemplation.

    1) increased 2,3 DPG which shifts the oxyhemoglobin curve to the right fascilitating unloading
    2) increased P50
    3) increased cardiac output mediated by tachycardia if anemia is acute or low grade chronic
    4) increased coronary flow due to decreased viscosity, increased myocardial demand and vasodilation
    5) increased oxygen extraction and a decreased mixed venous oxygen
    6) decreased viscosity
    7) decreased blood solubility of the volatile agents

    One study of otherwise normal pediatric patients for scoliosis repair demonstrated adequate oxygen delivery with normovolemic hemodilution to 3 g/dL (Anesth Analgesia 1995 80:219-25).


    Classically anesthesia is composed of unconsciousness, analgesia and muscle relaxation. In the modern era a fourth principal component is sometimes added to the definition, autonomic reflex stability. The meanings of analgesia (insensitivity to pain) and muscle relaxation (absence of movement, adequate reduction in muscle tone to allow surgery) are fairly straightforward. Autonomic stability refers to normal and stable vital signs, principally BP and HR, though respiratory parameters and neuroendocrine responses to surgical stimulation may be included.

    The term DEPTH of anesthesia seems simple but in fact is quite difficult to define. Anesthetic agents may affect each of the components of the anesthetic state differently. For example, opioids produce analgesia at doses that produce only modest degrees of sedation, and certainly at doses well below those causing unconsciousness. Even at very high doses, muscle relaxation is not produced. Therefore, under opioid-based anesthesia, it may be very difficult to find a single physiologic parameter that reflects depth of anesthesia. Conversely, IV anesthetics such as propofol may produce unconsciousness but little analgesia. Inhalation anesthetics probably produce all the components of anesthesia, but at different concentrations.

    It is easier to measure autonomic stability and muscle relaxation using ordinary hemodynamic and neuromuscular blockade monitors. These same surrogates are often used to assess adequacy of analgesia. Therefore modern technologies for monitoring depth of anesthesia usually focus on the most difficult parameter, consciousness. It must be emphasized that depth of anesthesia and consciousness monitoring are not synonyms.


    Volatile agents may have important cardioprotective properties against myocardial ischemia and reperfusion injury. Protection against reversible and irreversible myocardial injury is not easily explained by simple alterations in myocardial oxygen supply and demand. Previous clinical investigations have not found evidence for a preferred anesthetic in patients with CAD. Early lab findings went largely unresolved with the appearance of having few if any direct implications for humans.

    ISCHEMIC PRECONDITIONING Single or multiple brief periods of ischemia can be protective against subsequent prolonged ischemic insult. IPC results in finite periods in which the myocardium is protected. An early phase or window of IPC persists for 1-2 hours before disappearing and then reoccurring 24 hours later. This second or late window of preconditioning may last for as long as 3 days. A variety of ligands and multiple receptors coupled to G proteins are primarily responsible for activation of an intracellular signal transduction pathway that involves protein kinase C, mitogen-activated protein kinases, protein tyrosine kinases, reactive oxygen species and nitric oxide synthase. Central to this process is the role of the mitochondrial adenosine triphosphate-sensitive potassium (KATP) channel. Opening of this channel is critical for the beneficial cardioprotective effects of IPC.

    ANESTHETIC PRECONDITIONING Volatile anesthetics have been shown to directly precondition or indirectly enhance IPC, resulting in cardioprotection against myocardial infarction with the KATP channel playing an important role. Pharmacological preconditioning produced by volatile agents, including isoflurane, desflurane, and sevoflurane, is remarkably similar to IPC and shares many of the same signal transduction elements.



    perfusion volume
    acid-base status


    airway maintenance
    circulation – perfusion
    neurologic – relaxation
    renal – urine output
    position – head, trunk, limbs
    thromboembolism prophylaxis


    The risk of anesthetic related mortality has decreased sharply over the past twenty years. Mortality rates are still slightly higher for the pediatric age groups. Overall risk of mortality directly related to anesthesia is likely as low as 1 in 68,000 anesthetics.


    cardiac arrest 1:10,000
    mortality 1:13-47,000
    CNS injury
    PNS injury
    anaphylaxis 1:4500
    anaphylactoid 1:1000
    dental injury 1:500
    awareness 1-2:1000
    pediatric mortality 1:200,000
    pediatric aspiration 1:10,000

    winning the lottery
    struck by lightening

    The annual mortality rate totally attributable to anesthesia in Japan was 0.21 per 10,000 or 1 death per 47,619 anesthetic cases (Acta Anaes Scand 2003 47:809). A review of over two million anesthetics was performed over a five year period in Japan. The average incidence cardiac arrest during surgery due to all etiologies and that totally attributable to anesthesia was 7.12 and 1:10,000 cases, respectively. The average mortality per year in the operating room or within 7 postoperative days due to all etiologies and that totally attributable to anesthesia was 7.18 and 0.21 per 10,000 cases, respectively. The two principal causes of cardiac arrest during anesthesia and surgery due to all etiologies were massive hemorrhage (32%) and surgery (30%). Those totally attributable to anesthesia were drug overdose or selection error (15%) and serious arrhythmia (14%). Preventable human errors caused 53% of cardiac arrest and 22% of deaths in the operating room totally attributable to anesthesia.

    The 10 major causes of cardiac arrest totally attributable to anesthesia during surgery were

    overdose or selection error (15%)
    serious arrhythmia (14%)
    MI, ischemia, coronary spasm (8%)
    airway management (7%)
    high spinal (7%)
    inadequate vigilance (7%)
    hemorrhage, hypotension (5%)
    overdose of anesthetics (3%)
    suffocation, aspiration (3%)
    disconnection of circuit (2%)

    The Pediatric Perioperative Cardiac Arrest Registry or POCA published in Anesthesiology 2000 revealed anesthetic cardiac arrest at an incidence of 1.4:10,000. One third of all of these patients were ASA PS 1 or 2. Medication errors were the most common cause for cardiac arrest. Arrest secondary to MH or anaphylaxis was not reported in this survey of over one million GA. Incidence was highest in children less than one month.


    The FOUR stages of anesthesia as described by Guedel in a 1937 text on inhaltional anesthesia. The distinct stages are infrequently differentiated on induction as the IV induction agents take us quickly through stage three.

    STAGE I begins with induction and ends with loss of consciousness. Patients still follow commands but are analgesic with mildly painful stimuli. Pupils are small and divergent. Patients may open their eyes on command. Muscle tone and reflexes are intact.

    STAGE II lasts from LOC to beginning of rhythmic breathing. The period is characterized by uninhibited excitation and potentially injurious responses to noxious stimuli including uncontrolled movement, vomiting, laryngospasm, HTN, tachycardia and tachpnea. The pupils are usually dilated and divergent and respiration is usually irregular. Pharyngeal and laryngeal reflexes are depressed but are very reactive to noxious stimuli.

    STAGE III lasts from onset of rhythmic breathing to respiratory arrest and consists of four progressive planes. Inhalation is separated from exhalation by a slight pause. Abdominal muscles become parlayzed and breathing is entirely diaphragmatic. Stage III is the target depth of anesthesia noted for the TRIAD of akinesis, analgesia and amnesia as well as loss of sympathetic response to painful stimuli.

    STAGE IV extends from diaphragmatic paralysis to cardiac arrest. The stage is marked by shallow respirations and dilated nonreactive pupils. Hypotension progresses to total circulatory failure.


    Chronic stable angina includes patients with prior myocardial infarction, prior revascularization, coronary atherosclerosis or noninvasive evidence of myocardial ischemia. Typical symptoms include chest pressure, heaviness and/or pain, with or without radiation of the pain or shortness of breath.

    TREATMENT Monotherapy with a beta blocker or a nitrate is the first choice for patients with stable angina if there are no contraindications. If monotherapy fails to produce improvement, the combination of a beta blocker and a nitrate may relieve symptoms and mitigate ischemia. If combination therapy fails to relieve symptoms, invasive approaches to treatment should be considered.


    Unstable angina represents a clinical spectrum of coronary artery disease that lies between stable angina and acute myocardial infarction. Unstable angina typically presents with a prolonged episode of substernal chest pain or as stable angina that has been increasing in frequency, severity or duration.

    The DIAGNOSIS of unstable angina depends on clinical history, physical examination and a 12-lead ECG. Compared with patients with stable angina, those with unstable angina are more likely to have multivessel disease and progression of atherosclerosis. Pain may be accompanied by reversible, horizontal or down-sloping ST-segment depression or deep symmetric T-wave inversion. Factors that may precipitate unstable angina include:

    1) lung disease (COPD)
    2) anemia (occult GI bleeding)
    3) fever
    4) hyperthyroidism
    5) uncontrolled hypertension
    6) arrhythmias

    If no precipitating factors are found, unstable angina is most likely due to significant atherosclerotic coronary artery disease with PLAQUE DISRUPTION. Plaque disruption leads to platelet aggregation, thrombus formation and decreased coronary blood flow.

    TREATMENT All patients with suspected unstable angina should be started on ASA at 80-324 mg/day unless contraindicated. For patients who have aspirin hypersensitivity or recent bleeding, TICLODIPINE (Ticlid) at 250 mg twice a day or CLOPIDOGREL (Plavix) 75 mg once a day should be considered (see other listing).

    Those patients who are newly diagnosed with unstable angina should also be given sublingual nitroglycerin for treatment of individual episodes and treated with either a beta-blocker or long-acting nitrates as prophylactic therapy. Patients who exhibit evidence of autonomic instability, such as inappropriate tachycardia or hypertension, should be treated with beta-blockers as the initial therapy. Therapy is usually initiated with one major antianginal drug, preferably a long-acting preparation and a second agent is added if there are recurrent symptoms on optimal doses of the first agent. The first two classes used should be nitrates and beta-blockers followed by calcium antagonists.

    Patients with ongoing angina should be admitted to a telemetry unit. Heparin should be initiated with an initial bolus dose of 80 units/kg followed by a continuous infusion of 18 units/kg/h, titrated as needed to achieve a PTT of 1.5-2.5 times the control. Heparin is usually continued for 3-5 days or 48 hours after the last episode of angina. Sublingual nitroglycerin should also be given in the emergency room. If the pain episode is controlled with this therapy, the patient should then be converted to longer-acting oral forms of nitrates with the addition of a beta-blocker if possible. If the pain persists despite SL nitrate therapy intravenous nitrates should be started. An initial nitroglycerin infusion rate of 10-30 mcg/min is recommended with upward adjustments at intervals of 10 to 30 minutes until the ischemic symptoms disappear. A maximum dose level of 40 mcg/min is advised. The systolic blood pressure should not fall below 90 mmHg or 30% below the starting mean arterial pressure if significant hypertension is present.

    Unless contraindicated, CATHETERIZATION is done if one or more of the following high-risk indicators are present:

    1) prior revascularization
    2) CHF
    3) depressed LV function
    4) ventricular arrhythmia
    5) persistent or recurrent pain
    6) study indicating high risk

    Patients with one or more recurrent, severe, prolonged (longer than 20 minutes) ischemic episodes should be considered for early cardiac catheterization.


    Newer agents classified as angiotensin II receptor blockers (A2RB or ARB) are commonly used alone or in combination with diuretics with benefits similar to those of the traditional ACE inhibitors but without the side effect of cough. Cough is attributed to bradykinin potentiation that is common with traditional ACE inhibitors. All A2RB can also cause dizziness, rash, HYPERKALEMIA and headache.

    LOSARTAN (Cozaar, Hyzaar)

    CANDESARTAN (Atacand)

    IRBESARTAN (Avapro, Avalide)

    OLMESARTAN (Benicar)

    TELMISARTAN (Micardis)

    VOLSARTEN (Diovan)

    The incidence of intraoperative hypotension in patients on A2RB may be as high as 75% and is seen in patients on A2RB for HTN and ischemic CHF. Generally, hypotension may be managed with fluid and pressors though 20% of these patients may require vasopressin analogues. It may be advised to withhold these drugs for the ten hours prior to induction.


    Unequal pupil size (0.3 to 0.5) can be demonstrated in 20% of the population and is usually the result of a defect in the efferent nervous pathways.

    From a CLOCKWISE progression along the right ankle:

    SAPHENOUS NERVE (L2-4) is a terminal branch of the femoral and is the only innervation NOT part of the sciatic system. Supplies superficial sensation to the anteromedial aspect and is most commonly blocked just anterior to the MEDIAL malleolus.

    DEEP PERONEAL NERVE (L4 – S2) runs in the anterior leg as a continuation of the common peroneal. Innervates toe short extensors, enters the ankle lateral to the flexor hallucis longus and medial to the extensor digitorum longus tendons, provides sensation to the medial half of the dorsal foot (especially the first and second digits). Blocked at level just above the malleoli and LATERAL to the dorsalis pedis artery.

    SUPERFICIAL PERONEAL NERVE (L4 – S2) is also a branch of the common peroneal which descends toward the ankle in the lateral compartment, entering the ankle just lateral to the extensor digitorum longus. Provides most of the cutaneous sensation to the dorsum of the foot and is located lateral to the extensor digitorum longus at the level of the lateral malleolus.

    SURAL NERVE consists of a branch from the tibial nerve and one from the common peroneal nerve. Enters the foot between the Achilles tendon and the lateral malleolus and provides sensation to the lateral foot. It is blocked quite superficially between the lateral malleolus and the Achilles tendon.

    TIBIAL NERVE or POSTERIOR TIBIAL NERVE (L4 – S3) is a direct continuation and enters the foot posterior to the medial malleolus, branching into lateral and medial plantar nerves. Provides sensation to the heel, medial sole, and part of the lateral sole. Blocked posterior to the posterior tibial artery at the level of the medial malleolus.

    PROCEDURE The patient is best positioned in the supine position with the knee flexed and sole of the foot on the bed.

    Appropriate needles include 25 g injection or 22 g regional. A 5 mL dose of LA per nerve is sufficient and short blocks (1 to 1.5% lidocaine) or long blocks (0.5% bupivicaine) can be provided.

    MAXIMUMS Thirty mL of plain 1% lidocaine (300 mg) or 35 mL of plain 0.5% bupivicaine (175 mg).

    Epinephrine should NOT be used, especially if the block is circumferential. Patients are often able to walk with assistance after outpatient surgery.


    Ankylosing spondylitis is a systemic disease characterized by ossification of ligaments, cartilage and the disc space of the axial spine. An AD disease seen mostly in males, AS is associated with HLA-B27 (90% of all patients) and has an onset in the third to fourth decades of life. Usual therapy includes PT to maintain mobility and potent NSAIDS. Symptoms are chacterized by morning stiffness that improves with exercise.

    ANESTHESIA Difficult airways secondary to atlanto-axial instability, kyphosis, TMJ and cricoarytenoid involvement are possible. Cardiac conduction defects, cardiomyopathy and aortic root disease may occur in 1-4%. Decreased pulmonary function from rigid rib cage, pleuritic involvement, APICAL CAVITARY LESIONS with pleuritic thickening mimicking TB is possible. Radiculopathies and chronic back pain are common. Examination of the spine may reveal skeletal muscle spasm, loss of lordosis and decreased mobility involoving the entire vertebral column. CERVICAL CORD COMPRESSION may occur from atlanto-axial involvement. Renal disease is possible.

    Patients may have a FROZEN NECK that will not extend at the atlanto-occipital joint. Mouth opening may be limited. The larynx may be affected if the patient has a hoarse voice. ROM of the extremities may be limited and have implications for positioning during surgery. Evaluation of the CXR, EKG and possibly cardiac echo and PFT should be considered based on history and symptoms. REGIONAL techniques may be challenging or impossible in these patients.

    SBE prophylaxis may be indicated for aortic root disease.


    AMOXICILLIN for pediatric OM is given at 80-90 mg/kg/day divided by two or three doses each day.

    AMPICILLIN sulbactam (Unasyn) is given at 1.5-3 grams every 6-8 hours. Pediatric patients receive 25 mg per kg up to 50 mg per kg. Ampicillin or a third-generation cephalosporin is most often used for enterococcus coverage.

    CEFAZOLIN (Ancef or Kefzol) is dosed from 0.5-1.5 grams IV or IM three or four times a day. The pediatric dose is up to 25 mg/kg every six hours but generally only 10 mg/kg per dose.

    CEFOXITIN (Mefoxin) is a second generation cephalosporin commonly used preoperatively in the pediatric patient. Adults may receive 1-2 grams every six to eight hours. Pediatric patients may receive up to 40 mg per kg every six hours to 12 grams per day maximum.

    CEFTRIAXONE typically dosed at 50 mg/kg IV or IM

    CEFUROXIME is commonly used before cardiac surgery at 1.5 grams for adults and 30 mg/kg in the pediatric patient.

    CIPROFLOXACIN (Cipro) is given at 200-400 mg IV every 12 hours.

    CLINDAMYCIN is typically dosed at 600 mg IV. 900 mg is often given but typically reserved for ID consult. Pediatric patients are given 10 mg per kg IV every six hours.

    GENTAMYCIN is dosed at 1.5 mg/kg to a maximum of 80 mg. Children less than 5 years of age receive 2.5 mg/kg IV or IM.

    LEVAQUIN should be used with care in the patient with decreased renal function and those with altered mental status.

    VANCOMYCIN is is given as 1 gram twice a day for adults and 10 mg/kg every six hours for the pediatric patient.


    GNB account for 55-85% of NOSOCOMIAL PNEUMONIA, and GPC account for 20-30%. GNB rarely causes community-acquired pneumonia. All empiric treatment regimens should include coverage for a group of core organisms that includes aerobic GN bacilli (Enterobacter spp, Escherichia coli, Klebsiella spp, Proteus spp, Serratia marcescens and Hemophilus influenzae) and GP organisms such as Streptococcus pneumoniae and Staphylococcus aureus.

    In patients with mild or moderate infections and no specific risk factors for resistant or unusual pathogens, monotherapy with a second-generation cephalosporin such as cefuroxime, a non-pseudomonal third-generation cephalosporin such as ceftriaxone or a beta-lactam and inhibitor combination such as ampicillin/sulbactam, ticarcillin/clavulanate or piperacillin/tazobactam may be appropriate. For patients in this low-risk category who have an allergy to penicillin, it is appropriate to initially use a fluoroquinolone (ciprofloxacin or levofloxacin), clindamycin and aztreonam.

    Patients with mild or moderate infections with specific risk factors should have broadened empiric coverage. In patients with witnessed aspiration or in those who have had recent thoracoabdomial surgery, it may be advisable to cover anaerobes by adding clindamycin, although use of a beta-lactam alone may be sufficient. Patients with coma, head trauma, recent infections with influenza virus, diabetes, or chronic renal failure, or who are IV drug abusers, are at risk for infections by Staphylococcus aureus and may require the addition of vancomycin to cover methicillin-resistant strains until sensitivities are known.


    Several types of ABX have been shown to enhance NM blockade. The effect is related to prejunctional and postjunctional membrane STABILIZATION.

    Most prominent of the antibiotics are AMINOGLYCOSIDES with neomycin and streptomycin being the most potent. Reversal of their blockade is inconsistent with calcium chloride or anticholinesterases.
    Lincosamines, clindamycin and lincomycin, also have effects that cannot be reversed with calcium or anticholinesterases.

    TREATMENT is difficult and consists of high suspicion, reversal with anticholinesterase and mechanical support until the ABX block wears off. Calcium has limited action. Prejunctionally calcium may compete with the ABX to reverse inhibition and facilitate release of acetylcholine. Postjunctional effect of calcium may cause the membrane to be stable to the effects of acetylcholine – thus, the unpredictable effect.

    SIDE EFFECTS of the anticholinergics include central and systemic effects. The organs most affected are those with the greatest parasympathetic innervation. Contrast these DRY symptoms with the symptoms of cholinergic crisis and OP toxicity or the WET SLUDGE symptoms.

    LES relaxation theoretically increases risk of aspiration as does decreased gastric motility.

    INCREASED IOP via mydriasis and cycloplegia can cause potential problem with glaucoma patients. It is unlikely with doses used for premedication.

    BRONCHODILATION results in increased dead space.

    DRYING and thickening of secretions with theoretical increase in airway resistance can be a potential problem with CF patients.

    Interference with sweating and temperature control mechanisms can be a concern in a FEBRILE child.

    TACHYCARDIA (AGS) is more likely with IV rather than IM administration. SA rate and AV conduction are increased. NOTE that initial small doses of atropine can actually slow HR due to peripheral agonist effects.

    Urinary RETENTION is most problematic in elderly men.

    Large doses can block NICOTINIC receptors and lead to skeletal muscle WEAKNESS and orthostatic HYPOTENSION. Note that excess acetylcholine with cholinergic crisis can actually cause PARALYSIS.


    CENTRAL ANTICHOLINERGIC SYNDROME presents with delirium, restlessness, confusion and obtundation that is potentiated by inhalation anesthetics. CAS is most likely with scopolamine and atropine but other drugs may be implicated.


    TREATMENT is with PHYSOSTIGMINE, which is the only tertiary amine anticholinesterase at 1-2 mg or 15-60 mcg/kg.

    DDX for anticholinergic toxicity includes hypoxemia and hypercarbia, thyrotoxicosis, MH, sepsis and pheochromocytoma. Many will often confuse symptoms of anticholinergic excess with the diametrically different findings of excessive cholinergic tone due to anticholinesterase poisoning.

    Consider the following DISTINCTIONS. Anticholinergic toxic patients typically have normal blood gases. Pupillary reflexes are usually intact with other diagnoses but pupils may be dilated with MH. Most of the other DX are characterized by sweating which is absent with DRY anticholinergic toxicity. Other DX may present with ventricular arrhythmias where the anticholinergic toxicty generally presents with tachycardia alone.

    For patients without CNS toxicity, the TREATMENT is primarily supportive as most symptoms are time limited. If tachycardia is problematic (causing ischemia or presenting in patients with mitral or aortic stenosis or IHSS), then ß-blockers or CCB may be useful.

    OP = cholinergic = SLUDGE & miosis
    anticholinergic = dry & myDRYatic


    The frequently prescribed contemporary antidepressants include the SSRI medications, SNRI (serotonin and NE reuptake inhibitor such as Effexor) and newer non-SSRI drugs.

    The acute injection of METHYLENE BLUE in the presence of an SSRI has been shown to increase CNS levels of serotonin by more than 2-fold in rats. In 1986, Naylor, using PO methylene blue 300 mg/day, reported a reduction in the duration and severity of depression in patients with bipolar affective disorder. It has been postulated that use of methylene blue in a patient on SSRI medication may preceipitate acute SEROTONIN SYNDROME.

    Prozac (fluoxetine)


    The cardiac antidysrhythmic drugs are classified based on their electrophysiologic and electrocardiographic effects.

    CLASS I drugs block the fast, inward sodium ion current and can decrease the rate of phase 0 depolarization. These drugs are considered to be membrane stabilizers. All of the class I drugs depress automaticity, depress conduction in bypass tracts and have a depressant effect on phase 0 depolarization at rapid heart rates.

    CLASS IA (quinidine, procainamide, disopyramide) drugs depress phase 0 depolarization, prolong the action potential duration and slow conduction velocity.

    CLASS IB (lidocaine, mexiletine, phenytoin) shorten the action potential and have little effect on phase 0 depolarization.

    CLASS IC (flecainide, lorcainide) drugs markedly depress phase 0 depolarization, minimally affect the action potential duration and profoundly slow conduction velocity.

    CLASS II drugs are comprised of the beta antagonists. The rate of phase 4 depolarization is decreased and the rate of SA node discharge is decreased. The rate of conduction of cardiac impulses through the AV node is slowed as reflected by a prolonged PR interval on EKG.

    CLASS III drugs include amiodarone, sotalol and bretylium. Amiodarone prolongs the effective refractory period in all cardiac tissues including SA node, atrium, AV node, His-Purkinje system, ventricle and accessory bypass tracts.

    CLASS IV drugs include the calcium channel blockers which inhibit the flux of calcium ions across the slow channels of vascular smooth muscle and cardiac cells. This effect is manifested as a decreased rate of spntaneous phase 4 depolarization.

    The resting potential of normal cardiac cell membranes is about negative 90 millivolts and is designated by phase 4. Depolarization and reversal of the transmembrane potential is designated phase 0 whereas the three phases of repolarization are labeled 1, 2 and 3.


    Two platelet aggregation inhibitors commonly used as prophylaxis following PCI include TICLOPIDINE (Ticlid) and CLOPIDOGREL (Plavix). These medications greatly enhance patency when used for six months after stenting and early discontinuation should be thoroughly discussed with surgical and cardiology consult. The glycoprotein receptor inhibitors are similar agents that are not available in oral formulations despite extensive study.

    CILOSTAZOL (Pletal) is a reversible antiplatelet drug

    MECHANISM Both agents interfere with the ADP-induced binding of fibrinogen to the platelet membrane at specific receptor sites. Platelet adhesion and platelet to platelet interactions are subsequently inhibited. The agents also affect blood viscosity and reduces fibrinogen concentrations, which is of benefit to patients with vascular disease. The inhibitory effects on platelet aggregation are irreversible. They begin within 24-48 hours and reach a maximum at 5-6 days of therapy. Antiplatelet activity persists for at least 72 hours after discontinuation of therapy. Platelet function returns to normal within 1-2 weeks as new platelets replace the affected ones.

    SURGERY Package inserts explain that if patients are to undergo surgery and the antiplatelet effects are not desirable, CLOPIDOGREL should be discontinued 7 DAYS prior and TICLOPIDINE should be discontinued 10-14 DAYS prior to surgery.

    The INDICATIONS for these medications include treatment of acute MI, prophylaxis following percutaneous stent placement, unstable angina, sickle cell disease and claudication.

    The most serious ADVERSE EFFECTS of the medications include life-threatening agranulocytosis, aplastic anemia, pancytopenia or thrombotic thrombocytopenic purpura (TTP). Other hematologic events include bone marrow suppression, eosinophilia, neutropenia, secondary malignancy (leukemia), thrombocytopenia and thrombocytosis. Severe hematologic events are most likely to occur during the first 3 months of treatment. Only a few cases have occured after 3 months.


    Aortic cross clamping is most often utilized for surgery of the aorta and during CPB to keep pumped blood flowing in the forward direction. The physiologic changes are minimized during thoracic procedures because of one of several shunts that may be utilized.

    VOLUME status should be MINIMIZED 30 minutes PRIOR to clamping. The PHYSIOLOGY of clamping includes increased preload (secondary to passive recoil distal to clamp), increase in aortic impedence (afterload), increase in catecholamines and CO which may increase or decrease.

    HTN is much more common with aortic clamping for the aneurysm patient in contrast to the patient being clamped for occlusive repair (aortobifemoral grafts).

    An increase in volatile agent with or without vasodilator may be needed to decrease afterload and increase cardiac output while decreasing stress on the LV. The physiologic increase in afterload may produce ischemia requiring the use of nitroglycerin.

    Suprarenal or infrarenal clamps may decrease GFR and it has been demonstrated that UOP may not be reflective of GFR. Mannitol 12.5 grams can be given before clamping and dopamine or fenoldapam may be considered with existing renal disease or suprarenal clamping. Mannitol has the additional benefit of free radical scavenging at time of reperfusion. Lasix is of questionnable value.

    UNCLAMPNG causes a sudden decrease in SVR and blood pressure which is mediated by anoxic vasodilation or ischemic dilators. Declamping shock may be seen as the mediators reach the arterial system. Volume loading 30 minutes prior to unclamping may blunt the hypotensive response and volume can be administered while simultaneously infusing SNP or NTG (which permit greater volume loading). PCWP can be gradually brought up to 20 mm Hg (as many recommend) proir to unclamping. It is helpful to decrease vasodilators or volatile agents five minutes prior to unclamping.

    Other causes of hypotension should be considered including myocardial ischemia or failure (indicated by high filling pressures) or hemorrhage (indicated by low filling pressures).

    ANATOMY The celiac artery comes off the aorta above the SMA which comes off just above the renal arteries. The celiac branches into the common hepatic and the splenic arteries. Remember that the SMA is the nutcracker above the renal veins. The IMA branches off just above the bifurcation to the common iliac arteries.


    Traumatic aortic rupture usually results in imminent death (70-90% incidence) but those that are salvageable must be operated on immediately. Those that survive tend to have lacerations near the ligamentum arteriosum and it is the continuity of an intact adventitial layer that prevents immediate death.

    DIAGNOSIS is made by aortogram when suspicion is high or the study is indicated by widened mediastinum. 10-17% of those with widened mediastinum will have positive findings on aortogram. Adjunctive radiographic signs include fractures of the first and second ribs, obliteration of the aortic knob, tracheal deviation to the right, depression of the left mainstem bronchus and deviation of an NG tube to the right on radiograph.

    ANESTHESIA Lesions are typically approached through a left thoracotomy and one lung ventilation is desirable. Blood pressure control during induction may be achieved with esmolol and nitroprusside. Partial cardiac bypass is usually required which will shunt aortic blood across the lesion usually from the LA or pulmonary vein to the femoral artery. See more information under TAAA – REPAIR.


    AR is usually secondary to cogenital defect, dissection of annulus or bacterial endocarditis. Acute AR causes sudden increases in filling pressure and pulmonary edema. Chronic AR causes progressive dilation of the LV which eventually leads to CHF. If the pulse pressure is not at least 50% of SBP or the DBP is greater than 70, significant AR is unlikely.

    When moderate or severe AR is present (3-4 plus or greater than 6 liters per minute of regurgitation), the primary compensation is an increase in SV. This mechanism can only be maintianed if preload is adequate and SVR is normal or decreased. Because AR occurs in diastole, the severity is increased as the HR slows. Modest decreases in contractility are well tolerated but provide no advantage. Vasodialtors are helpful in some patients but (because the DBP is already low – typically at 30-50 mmHg) vasodilators are associated with risk for ischemia.

    HR high normal at 85-100
    NSR if possible
    normal or increased preload
    normal or decreased SVR
    normal inotropy


    Symptomatic AS (angina, syncope, CHF) begin late in the course when gradient exceeds 50 mmHg equivalent to peak velocity of 3.5 meters per second) and valve area is less than 1 cm squared (normal 2-3 cm squared). Catheterization will underestimate gradients by 5-20 because LV and aortic pressures are not measured simultaneously.

    With moderate to severe disease the LV is hypertrophied and noncompliant. NSR and high filling pressures are required to adequately distend the LV during diastole. Atrial systole contributes 40-50% to stroke volume in these patients. Vasodilation does not reduce the work of the LV because of the fixed resistance at the valve. Vasodilation DOES reduce CPP and will likely provoke ischemia. Modest decreases in contractility are generally well tolerated even with history of CHF. Augmentation of contractility or increased HR may induce ischemia even in absence of CAD.

    It is reported that with appropriate care, the AS patient is at minimal risk during noncardiac surgery though patients with CRITICAL AS may have perioperative mortality rates of ten percent.

    NSR at HR 70-85
    increased preload
    normal or increased SVR
    normal or decreased inotropy


    When a patient becomes apneic while breathing air, alveolar gas reaches equilibrium with mixed venous gas within a few minutes. This involves a rise of alveolar PCO2 from 40 to 46 mmHg and a fall of PO2 from 105 to 40 mmHg.

    These changes correspond to an uptake of 230 mL of oxygen but the output of only 21 mL of carbon dioxide. This assumes alveolar gas is not replenished from outside. What actually happens to the blood gases depends upon the patency of the airway and the composition of ambient gas if the airway is patent.

    OCCLUSION Equilibrium is rapidly established between alveolar and mixed venous PCO2. Thereafter, arterial, alveolar and mixed venous PCO2 remain close, and with recirculation of the blood, increase at a rate of 3-6 mmHg per minute. Alveolar PO2 decreases close to the mixed venous PO2 within about a minute and then decreases further as recirculation continues.

    The lung volume falls by the difference between O2 uptake and CO2 output. Gross hypoxia supervenes after about 90 seconds if apnea with airway occlusion follows breathing at the FRC.

    PATENT AIRWAY with AIR as the ambient gas. Instead of lung volume falling by net gas exchange rate, a volume of ambient gas is drawn in by mass movement down the trachea. If ambient gas is air, the oxygen in it will be removed but the nitrogen will accumulate and rise above normal concentration until gross hypoxia supervenes in about 2 minutes. Note that CO2 elimination cannot occur as there is mass movement of air down the trachea. Measured at the mouth, there is O2 uptake but no CO2 output and the respiratory exchange ratio is zero.

    PATENT AIRWAY with OXYGEN as the ambient gas. Oxygen is continuously removed from alveolar gas but is replaced. No nitrogen is added to alveolar gas and the alveolar PO2 only falls as fast as the PCO2 rises. The patient will not become seriously hypoxic for several minutes. If the patient had been breathing oxygen prior the respiratory arrest, the starting alveolar PO2 would be about 660 mmHg and about 100 MINUTES of apnea theoretically could be tolerated provided the airway remained clear and 100% O2 was supplied. Obviously, PCO2 values as high as 140 mmHg could occur.


    Aprepitant (Emend) is

    Aprotinin or TRASYLOL is a natural broad spectrum PROTEINASE INHIBITOR that modulates the systemic inflammatory response associated with CPB. Through its inhibition of multiple mediators (kallikrein, PLASMIN and others) it attenuates the inflammatory response, fibrinolysis and THROMBIN generation.

    REMEMBER Thrombin activates the conversion of fibrinogen to fibrin. Heparin activates antithrombin III which inhibits this conversion. Plasmin, on the other hand, promotes fibrinolysis (or the breakdown of fibrin to the various split products).

    ANAPHYLACTIC or anaphylactoid reactions are possible with aprotinin use. Effects may be mild but fatal hypersensitivity may be exhibited during the first exposure to a test dose. Incidence of hypersensitivity to a repeat dose is reported at 2.7% but the incidence decreases after six months post exposure.

    A TEST DOSE of 1 mL (1.4 mg) should be given ten minutes prior to a loading dose. The loading dose is given over 20-30 minutes and a matching dose is administered with the pump priming solution. High and low dose regimens have been evaluated with little benefit seen with higher dosage protocols.

    LOW DOSING after test dose is given as 100 mL (140 mg) followed by the pump priming dose of 100 mL and a constant infusion should follow at 25 mL per hour. To avoid the physical incompatibility of aprotinin and heparin, each agent is added during recirculation of the pump prime to assure dilution.

    MONITORING is effected because aprotinin alone may prolong the ACT used for heparin monitoring. It has been noted that KAOLIN based ACT are not affected to the same degree as diatomaceous earth based ACT. While protocols vary, a minimal celite ACT of 750 seconds or a kaolin based ACT of 480 seconds is recommended in the presence of aprotinin.

    Reversal of haparin with protamine should be based on the total dose of heparin used and not the measured ACT. 1 mg of protamine neutralizes 90 units of heparin and represents the maximum dose that should be necessary.

    Metabalysis reveals benefits including lowered blood loss by 53%, reduced reoperations for bleeding, reduced donor units by as much as 60%, decreased platelet transfusions by as much as 80%, reduced hospital stay, decreased OR and closure time and reduced overall lifetime costs. One more recent and controversial studies reveal increased risk of renal failure, CVA, CHF and MI (NEJM 2006).


    The acute respiratory distress syndrome is a diffuse inflammatory process that involves both lungs. Erythrocytes, leukocytes and proteinaceous debris accumulate and eventually obliterate the alveolar airspaces. Consolidation originates from activation of circulating neutrophils.

    The systemic inflammatory response can be triggered by sepsis (40% will develop ARDS), multiple transfusions, pulmonary contusions, aspiration, increased ICP, pneumonia, CPB, pancreatitis, long bone fractures and drug overdose. The mortality after ARDS develops is generally tripled for any given inciting event.

    CLINICAL Early signs include tachypnea, rales and hypoxemia in a patient with one or more of the known predisposing conditions. The PaO2:FiO2 RATIO is usually less than 200. Hypoxemia is typically worse than expected from CXR but within 24 hours the CXR reveals bilateral airspace infiltrates that may be more prominent in the periphery.

    DDX includes cardiogenic pulmonary edema, pneumonia and PE. Fever and leukocytosis can be a feature of all the DX including LV failure after MI or myocarditis. Bilateral disease is seen occasionally with pneumonia but rarely with PE. Effusions are unlikely with ARDS, possible with pneumonia and PE and common with LV failure.

    The CXR is NOT RELIABLE for distinguishing ARDS and CARDIOGENIC EDEMA. Often, the presence of predispostion may be the best or only means of differentiating the two entities.

    WEDGE PRESSURE can sometimes be used to differrentiate ARDS and pulmonary edema. PAOP is generally lower than 18 mmHg in the ARDS patient. More accurately, the pulmonary capillary pressure can be estimated by Pc = PAOP + 0.4 (mean PA – PAWP). Capillary pressures are normal with ARDS.


    Because there is no specific treatment, therapy revolves around

    1) reducing iatrogenic lung injury
    2) reducing lung water
    3) maintaining oxygenation

    It is important to remember that only 15-40% of deaths in ARDS are caused by respiratory failure itself. The majority are caused by multiorgan failure.

    MANIFESTATIONS of ARDS include a decreased FRC, increased right to left shunt, increased secretions and decreased lung compliance measured as less than 40 mL per cmH2O.

    Regions of infiltrated lung interspersed with normal lung (30% of tissue) complicate management as these normal alveolar beds receive most of the delivered Vt.

    In general, PIP should be kept below 35 mmHg by using Vt of 7-10 mL/kg. FiO2 should be kept below 0.5 and PEEP should be used only if oxygen can not be reduced below 60%. Oxygenation should be adequate with saturation above 90%.

    Diuretics and PEEP are not capable of reducing lung water. PEEP may actually lead to more lung water and PEEP should not be considered a therapy for ARDS. PEEP is instead a method of reducing iatrogenic lung injury by allowing ventialation with lower inflation volumes and lower levels of toxic oxygen.

    Tissue oxygenation can be evaluated by measuring oxygen uptake (should be greater than 100 mL/minute/m2 or 2 mL/kg), venous lactate (should be less than 4) and gastric intramucosal pH (should be greater than 7.32).

    In order to maintain oxygenation, preload should be maintained remembering that CVP and PCWP may be overestimated in presence of PPV (especially with PEEP). Cardiac index should be above 3 and volume infusion may be indicated if low.

    If volume is not indicated, than dobutamine may be used to augment output. Dopamine should be avoided because of its propensity to constrict pulmonary veins. Vasodilators should also be avoided because of their ability to increase pulmonary shunt adding to the primary gas exchange abnormalities of ARDS.


    Argatroban is a direct thrombin inhibitor useful as an adjunct to PCI and for patients with heparin induced thrombocytopenia who must be anticoagulated for bypass procedures.

    see Wikipedia article


    Infusions to have available include dopamine, epinephrine, calcium chloride and nitroglycerin.

    Medications to have available include phentolamine, magnesium and albumin in addition to the typical bypass medications.


    Arthrogryposis is a general term that describes multiple joint contractures of prenatal onset. It may be associated with a variety of diseases and may be the result of fetal myopathy, neuropathy or severe oligohydraminos. An AD form of the disease has also been described.

    Patients may have associated ptosis, cleft lip or palate, micrognathia and trismus. Patients may be at risk for hypoventilation and aspiration. A variety of congenital heart defects are occassionally associated with the condition and severe respiratory disease may lead to cor pulmonale.

    Arthrogryposis is NOT associated with MH though hypermetabolism and hyperthermia are occassionally associated with anesthesia.


    These standards apply to all anesthesia care although, in emergency circumstances, appropriate life support measures take precedence. These standards may be exceeded at any time based on the judgment of the responsible anesthesiologist. They are intended to encourage quality patient care, but observing them cannot guarantee any specific patient outcome. They are subject to revision from time to time, as warranted by the evolution of technology and practice. They apply to all GA, RA and MAC.

    This set of standards addresses only the issue of basic anesthetic monitoring, which is one component of anesthesia care. In certain rare or unusual circumstances, 1) some of these methods of monitoring may be clinically impractical, and 2) appropriate use of the described monitoring methods may fail to detect untoward clinical developments. Brief interruptions of continual monitoring may be unavoidable. Under extenuating circumstances, the responsible anesthesiologist may waive the requirements marked as optional – though it is recommended that when this is done, it should be so stated (including reasons) in the patient’s medical record. These standards are not intended for application to the care of the obstetrical patient in labor or in the conduct of pain management.

    STANDARD ONE Qualified anesthesia personnel shall be present in the room throughout the conduct of all GA, RA and MAC.

    Because of the rapid changes in patient status during anesthesia, qualified anesthesia personnel shall be continuously present to monitor the patient and provide anesthesia care. In the event there is a direct known hazard (such as radiation) to the anesthesia personnel which might require intermittent remote observation of the patient, some provision for monitoring the patient must be made. In the event that an emergency requires the temporary absence of the person primarily responsible for the anesthetic, the best judgment of the anesthesiologist will be exercised in comparing the emergency with the anesthetized patient’s condition and in the selection of the person left responsible for the anesthetic during the temporary absence.


    STANDARD TWO During all anesthetics, the patient’s oxygenation, ventilation, circulation and temperature shall be continually evaluated.

    OXYGENATION To ensure adequate oxygen concentration in the inspired gas and the blood during all anesthetics.

    1) inspired gas – during every administration of general anesthesia using an anesthesia machine, the concentration of oxygen in the patient breathing system shall be measured by an oxygen analyzer with a low oxygen concentration limit alarm in use (optional).
    2) blood oxygenation – during all anesthetics, a quantitative method of assessing oxygenation such as pulse oximetry shall be employed (optional).
    3) adequate illumination and exposure of the patient are necessary to assess color (optional).

    VENTILATION To ensure adequate ventilation of the patient during all anesthetics.

    Every patient receiving GA shall have the adequacy of ventilation continually evaluated. Qualitative clinical signs such as chest excursion, observation of the reservoir breathing bag and auscultation of breath sounds are useful. Continual monitoring for the presence of expired carbon dioxide shall be performed unless invalidated by the nature of the patient, procedure or equipment. Quantitative monitoring of the volume of expired gas is strongly encouraged (optional).

    When an ETT or LMA is inserted, the correct positioning must be verified by clinical assessment and by identification of carbon dioxide in the expired gas. Continual end-tidal carbon dioxide analysis, in use from the time of endotracheal tube/laryngeal mask placement, until extubation/removal or initiating transfer to a postoperative care location, shall be performed using a quantitative method such as capnography, capnometry or mass spectroscopy (optional).

    When ventilation is controlled by a mechanical ventilator, there shall be in continuous use a device that is capable of detecting disconnection of components of the breathing system. The device must give an audible signal when its alarm threshold is exceeded.

    During RA and MAC, the adequacy of ventilation shall be evaluated, at least, by continual observation of qualitative clinical signs.

    CIRCULATION To ensure the adequacy of the patient’s circulatory function during all anesthetics.

    Every patient receiving anesthesia shall have the electrocardiogram continuously displayed from the beginning of anesthesia until preparing to leave the anesthetizing location (optional). Every patient receiving anesthesia shall have arterial blood pressure and heart rate determined and evaluated at least every five minutes (optional).

    Every patient receiving GA shall have, in addition to the above, circulatory function continually evaluated by at least one of the following: palpation of a pulse, auscultation of heart sounds, monitoring of a tracing of intra-arterial pressure, ultrasound peripheral pulse monitoring or pulse plethysmography or oximetry.

    BODY TEMPERATURE To aid in the maintenance of appropriate body temperature during all anesthetics.

    Every patient receiving anesthesia shall have temperature monitored when clinically significant changes in body temperature are intended, anticipated or suspected.

    Note that CONTINUAL is defined as repeated regularly and frequently in steady rapid succession whereas CONTINUOUS means prolonged without any interruption at any time.


    These standards apply to postanesthesia care in all locations. These standards may be exceeded based on the judgment of the responsible anesthesiologist. They are intended to encourage quality patient care, but cannot guarantee any specific patient outcome. They are subject to revision from time to time as warranted by the evolution of technology and practice.

    Under extenuating circumstances, the responsible anesthesiologist may waive the requirements marked as optional – though it is recommended that when this is done, it should be so stated (including reasons) in the patient’s medical record.

    STANDARD ONE All patients who have received GA, RA or MAC shall receive appropriate postanesthesia management.

    A PACU or an area which provides equivalent postanesthesia care shall be available to receive patients after anesthesia care. All patients who receive anesthesia care shall be admitted to the PACU or its equivalent except by specific order of the anesthesiologist responsible for the patient’s care. The medical aspects of care in the PACU shall be governed by policies and procedures which have been reviewed and approved by the Department of Anesthesiology.

    The design, equipment and staffing of the PACU shall meet requirements of the facility’s accrediting and licensing bodies.

    STANDARD TWO A patient transported to the PACU shall be accompanied by a member of the anesthesia care team who is knowledgeable about the patient’s condition. The patient shall be continually evaluated and treated during transport with monitoring and support appropriate to the patients condition.

    STANDARD THREE Upon arrival in the PACU, the patient shall be re-evaluated and a verbal report provided to the responsible PACU nure by the member of the ACT who accompanies the patient.

    The patient’s status on arrival in the PACU shall be documented. Information concerning the preoperative condition and the surgical/anesthetic course shall be transmitted to the PACU nurse. The member of the ACT shall remain in the PACU until the PACU nurse accepts responsibility for the nursing care of the patient.

    STANDARD FOUR The patient’s condition shall be evaluated continually in the PACU.

    The patient shall be observed and monitored by methods appropriate to the patient’s medical condition. Particular attention should be given to monitoring oxygenation, ventilation, circulation and temperature. During recovery from all anesthetics, a quantitative method of assessing oxygenation such as pulse oximetry shall be employed in the initial phase of recovery (optional). This is not intended for application during the recovery of the obstetrical patient in whom RA was used for labor and vaginal delivery.

    An accurate written report of the PACU period shall be maintained. Use of an appropriate PACU scoring system is encouraged for each patient on admission, at appropriate intervals prior to discharge and at the time of discharge.
    General medical supervision and coordination of patient care in the PACU should be the responsibility of an anesthesiologist.

    There shall be a policy to assure the availability in the facility of a physician capable of managing complications and providing CPR for patients in the PACU.

    STANDARD FIVE A physician is responsible for the discharge of the patient from the PACU.

    When discharge criteria are used, they must be approved by the Department of Anesthesiology and the medical staff. They may vary depending upon whether the patient is discharged to a hospital room, to the ICU, to a short stay unit or home.

    In the absence of the physician responsible for the discharge, the PACU nurse shall determine that the patient meets the discharge criteria. The name of the physician accepting responsibility for discharge shall be noted on the record.


    The ASA physical status classification and associated mortality rates are as follows.

    I healthy (0.06 – 0.08%)
    II mild systemic disease including mild diabetes, controlled HTN, obesity, smoking (0.27 – 0.4%)
    III severe systemic disease, not incapacitating including angina, COPD, uncontrolled HTN and prior myocardial infarction (1.8 to 4.3%)
    IV severe systemic disease that is a constant threat to life
    including CHF, unstable angina and renal failure (7.8 – 23%)
    V moribund, not expected to live 24 hrs irrespective of
    operation including ruptured
    aneurysm, intracranial
    hemorrhage with elevated ICP
    (9.4 – 51%)
    VI brain-dead patient whose
    organs are being harvested

    Mortality rates quoted do not correspond with anesthesia mortality. Mortality directly related to anethesia is suspected to be as low as 1:400K (or 0.000002%).

    The range of the mortality rates are based on two large studies done during the sixties.


    These standards apply to all patients who receive anesthesia or MAC. Under unusual circumstances, such as extreme emergencies, these standards may be modified. When this is the case, the circumstances shall be documented in the patient’s record.

    STANDARD An anesthesiologist shall be responsible for determining the medical status of the patient, developing a plan of anesthesia care and acquainting the patient or the responsible adult with the proposed plan.

    The development of an appropriate plan of anesthesia care is based upon: (1) reviewing the medical record, (2) interviewing and examining the patient to discuss the medical history, previous anesthetic experiences and drug therapy as well as to assess those aspects of the physical condition that might affect decisions regarding perioperative risk and management, (3) obtaining and/or reviewing tests and consultations necessary to the conduct of anesthesia, (4) determining the appropriate prescription of preoperative medications as necessary to the conduct of anesthesia

    The responsible anesthesiologist shall verify that the above has been properly performed and documented in the patient’s record.

    One recent study (AA 2001) reported that only ASA classifications correlated well with postoperative morbidity in the geriatric population.
    The authors concluded that testing should be directed by the history and physical examination even in the geriatric population.

    See other information under PREOPERATIVE TESTING.


    Although comparative studies are insufficient to evaluate the peripartum impact of conducting a focused history (reviewing medical records) or a physical examination, the literature reports certain patient or clinical characteristics that may be associated with obstetric complications. These characteristics include, but are not limited to, preeclampsia, pregnancy-related hypertensive disorders, HELLP syndrome, obesity and diabetes. The consultants and ASA members both strongly agree that a directed history and physical examination, as well as communication between anesthetic and obstetric providers, reduces maternal, fetal and neonatal complications.

    RECOMMENDATIONS The anesthesiologist should conduct a focused history and physical examination before providing anesthesia care. This should include, but is not limited to, a maternal health and anesthetic history, a relevant obstetric history, a baseline blood pressure measurement, and an airway, heart, and lung examination, consistent with the ASA Practice Advisory for Preanesthesia Evaluation. When a neuraxial anesthetic is planned or placed, the patient’s back should be examined. Recognition of significant anesthetic or obstetric risk factors should encourage consultation between the obstetrician and the anesthesiologist. A communication system should be in place to encourage early and ongoing contact between obstetric providers, anesthesiologists and other members of the multidisclipinary team.


    ASD comprise 10% of the lesions found in the pediatric population but will be the most common undiscovered lesion in the adult population. Unlike VSDs, ASDs occur 2-3 times more commonly in females. Osium SECUNDUM is the most common (80%) type of ASD requiring repair. It results from resorption of the septum primum or a short septum primum that is incapable of fusing with the secudum to fuse the foramen ovale. SECUNDUM lesions often close spontaneously and may be associated with MVP. Though conventionally thought to close less often than VSDs, recent evidence argues otherwise. PRIMUM lesions (15%) may be associated with regurgitation and usually do not close spontaneously. SINUS VENOSUS (10%) lesions also do not often spontaneously close and may be associated with anomalous pulmonary venous return.

    Because of the lower pressure gradients between the atria, left to right shunting and an augmentation of pulmonary flow is less pronounced and the risk of developing Eisenmengers physiology is low in all but the largest defects – generally over 2 cm in diameter (or about 3 sq cm). ASDs in children may be picked up by evaluation for cyanotic episodes during prolonged crying episodes or if pulmonary flow is increased to the point of causing a loud systolic murmur with a fixed and widely split second heart sound – a result of delayed pulmonic valve closure. Small to moderate SHUNTS with Qp:Qs less than 1.5 are usually well tolerated, but larger shunts with Qp:Qs over 3 result in fatigue, dyspnea and right heart failure due to volume overload. Many patients with small ASDs may have no clinical findings until the third decade of life or later. Only 10% of all uncorrected ASDs will develop Eisenmenger physiology.

    There are many reports of virtually asymptomatic patients with moderate lesions surviving into the 8th or 9th decade though patients with very large lesions will often succumb to RV failure or atrial arrhythmias by the 3rd or 4th decade of life. Retrospective and prospective studies have demonstrated increased survival in older patients (over 40 years) treated surgically versus medically. Late repairs usually do not reduce the incidence of rhythm disturbances and may be combined with Maze procedures.

    The Amplatzer device approved by the FDA in December 2001 has been used children as young as 4 months of age for lesions measuring up to 34mm in diameter – patients are generally hospitalized overnight and discharged on aspirin to be continued for six months.


    Ostium secundum is the most common (80%) type of ASD requiring repair. It results from resorption of the septum primum or a short septum primum that is incapable of fusing with the secudum to fuse the foramen ovale.

    Three other types of ASDs include patent foramen ovale (which are typically closed only in patients undergoing VSD closure or other heart surgery), sinus venosus (which is often accompanied by partial anomalous venous return) and the common atrium.

    Small to moderate SHUNTS (Qp:Qs less than 1.5) are usually well tolerated, but larger shunts (Qp:Qs over 3) result in fatigue, dyspnea and right heart failure due to volume overload. Many patients with small ASDs may have no clinical findings until the third decade of life or later.

    Physical findings in the healthy young patient include systolic murmur at the pulmonic area (resulting from relative tricuspid stenosis) and a fixed splitting of the second heart sound.

    INDUCTION technique for the adult with left-to-right shunt is not critical and can be done with most any agent. The more afflicted patient with pulmonary HTN and RV failure can be induced with high dose fentanyl or ketamine.

    Most relatively healthy children may be induced by inhalational techniques. The volatiles do carry the theoretical disadvantage of decreasing CO and SVR and potentially reversing the left-to-right shunt. This usually will not occur in the absence of significant pulmonary HTN.

    If severe PVOD and RV failure are present, an IV technique or ketamine at 8 mg/kg IM can be used to allow for IV canulation. Ketamine is capable of worsening PVR (unique amongst the anesthetic agents).

    In general, one wants to maintain preload, keep PVR high (low oxygen, avoid hyperventilation) and keep SVR low (volatiles, NTG, PDE inhibitors).

    POSTOPERATIVE care for these patients is generally simple. Extubation can be performed early in the postoperative period in most instances.

    An acute increase in LA pressure is usually accompanied by a RA decrease which may make utilization of the CVP hazardous in guiding fluid replacement. Overtransfusion may be a special problem in the early postoperative period and LA LINES may be indicated for optimal management.

    Supraventricular dysrhytmmias are common and possibly related to atriotomy. The incidence increases with age.

    See related information under PATENT FORAMEN OVALE.


    ASYSTOLE is characterized by a pulseless patient WITHOUT presence of VF or VT. Variations of asystole include P-wave asystole and agonal or idioventricular complexes that occur at a rate of less than six per minute.

    CPR should be started immediately and continued throughout the resuscitation. Patient should be intubated and IV access should be obtained. ETT placement is verified and a second lead ECG should be checked to verify the absence of electrical activity. Electrical activity of any kind should direct care to the PEA algorithm.

    TRANSCUTANEOUS PACING may be helpful if done early with EPINEPHRINE but reports of success are anecdotal. Patients that may respond to TCP include those with sudden bradyasystolic arrest, Stokes-Adams attack, asystole due to vagal discharge, stunning after defibrillation and patients asystolic secondary to drug overdose.

    CPR should continue as TCP is initiated at the maximum energy output for the device. The pacer should periodically be turned off to examine tracings for VF or VT.

    CAUSES of asystole as similar to those causing PEA. The MNEMONIC for the differential reads as 5H-5T.

    hydrogen ion (acidosis)
    hyperkalemia or hypokalemia
    digoxin, CCB, TCA, ASA & ß blockers
    tension pneumothorax
    thrombosis (coronary)
    thrombosis (pulmonary)

    EPINEPHRNE is given in 1 mg boluses every 3-5 minutes. Higher doses of epinephrine up to 5 mg can also be used but are discouraged by the latest ACLS recommendations. ETT doses can be given at 2-2.5 times the IV dose, flushed with 10 mL of saline and followed by 3-4 forceful ventilations. Note that VASOPRESSIN is NOT indicated as it is for VF and VT.

    ATROPINE is given in 1 mg boluses (by 2006 guidelines) every 3-5 minutes up to a maximum dose of 0.03-0.04 mg/kg. This maximum dose extrapolates as 2-3.5 mg maximum for a normal sized adult.

    SODIUM BICARBONATE at 1 mEq/kg may be useful for the asystolic patient with hyperkalemia, TCA overdose and upon return of spontaneous circulation after a long arrest interval.

    Asystole differs from PEA in that the use of TCP and atropine are not always indicated for PEA.


    Atracurium is a benzylisoquinolinium nondepolarizing neuromuscular blocking drug with an onset of action at 2-5 minutes and an duration between 35-45 minutes (slower onset and longer duration than cisatracurium).

    DOSING for intubation is typically 0.5 mg/kg (2.5 times the ED95) which is more than that required of cisatracurium. Atracurium is refrigerated and provided at a concentration of 10 mg/mL.

    METABOLISM is by TWO primary mechanisms. Hoffmann elimination and hydrolysis by NON-SPECIFIC plasma cholinesterases both produce LAUDANOSINE as the major metabolite. Hepatorenal function is NOT important as it is for 20% of cisatracurium metabolism.

    HOFFMANN elimination is a spontaneous, base catalyzed, degradation at normal body temperature and pH at the quaternary nitrogen of the alpha side chain of atracurium, which yields laudanosine as the primary metabolite. Electrophilic acrylates may also be formed by Hoffman elimination. Hoffman elimination is slowed by acidosis or decreases in body temperature. Ester hydrolysis, on the other hand, is enhanced with acidosis.

    LAUDANOSINE levels peak within two minutes of injection and remain at approximately 75% peak for fifteen minutes. Levels are HIGHER than those produced by cisatracurium. Laudanosine is inactive at the NMJ but can act as a CNS stimulant possibly increasing MAC and possibly leading to seizure activity.

    One controversial report of problems including death following atracurium use in the neonate have been published (Paed Anaesthesia 2001 11:631).


    Atrial fibrillation is the most frequently encountered cardiac arrhythmia with a prevalence of 2%. In patients older than 65 years old, the prevalence is 5%. Overall, approximately 15-25% of all strokes in the US can be attributed to AF. Patients are categorized clinically based on whether AF is paroxysmal, persistent (can be converted to sinus rhythm) or chronic (unable to cardiovert or maintain SR despite antiarrhythmic agents). Patients can be divided further into groups according to the presence or absence of underlying heart disease.

    SYMPTOMS AF may manifest only as fatigue caused by impaired cardiac output or the patient may have no symptoms at all. Palpitations, SOB or chest pain can occur and syncope may infrequently accompany AF. Symptoms of ischemia and angina may be caused by the rapid ventricular rate. Paroxysmal AF may cause symptoms that abate and recur in an unpredictable manner.

    ETIOLOGY Precipitating causes, such as hyperthyroidism, electrolyte abnormalities (hypomagnesemia…), hypoglycemia and drug toxicity should be excluded. Stimulant abuse, excess tobacco, alcohol abuse or withdrawal, caffeine, chocolate, OTC cold remedies and the use of street drugs should be considered.

    AF may be associated with respiratory illness and pulmonary embolus. AF complicates acute myocardial infarction in 5-10% of cases. The causes of AF in AMI are thought to be due to any number of factors, such as atrial infarction, atrial ischemic injury, atrial distension, or, perhaps, pericarditis. AF is also associated with MITRAL VALVE disease, WPW, pericarditis, LVH, hypertrophic cardiomyopathy, CAD, aortic stenosis and ASD. Patients with mitral STENOSIS are most intolerant of the loss of atrial kick.

    EXAMINATION The pulse is characterized by an irregular-irregular timing and amplitude. The rapid ventricular rate may cause hypotension and pulmonary congestion. The patient should be examined for hypertension, rheumatic fever, VALVULAR disease, pericarditis, coronary artery disease, hyperthyroidism or chronic obstructive pulmonary disease. Murmurs and cardiac enlargement should be sought. Peripheral bruits may be a marker for associated coronary artery disease.

    EVALUATION 12-lead EKG should reveal irregular RR intervals with no apparent P waves. The ventricular rate is irregularly, irregular and the ventricular response rate is usually 130-180. Further evaluation includes CXR, electrolytes, ABG (hypoxia or carbon monoxide intoxication may lead to an irritable myocardium), TEE, free T4, TSH and appropriate drug levels (such as theophylline).


    The TWO PHASES of treatment include rate control followed by cardioversion.

    UNSTABLE AF (acute hypotension, angina, CHF) is treated by immediate synchronized DC cardioversion if duration is known to be less than 48 HOURS. Patients often respond to lower energy cardioversion and 50 JOULES is an often recommended starting point. Anesthesia or sedation and supplemental oxygen should be initiated if time permits. After cardioversion, rhythm should be stabilized with an oral antiarrhythmic.

    For patients with UNSTABLE AF of unknown duration, ventricular rate should be slowed with DILTIAZEM or AMIODARONE. Amiodarone may pharmacologically cardiovert those in AF and should therefore be used cautiously in patients at risk for atrial thrombus. DIGOXIN is appropriate for rate control but may take four hours before clinical response is observed.

    Digoxin, CCB and beta blockade are contraindicated in the WPW patient with AFIB. PROCAINAMIDE or cardioversion are the therapies of choice.

    Patients with unstable AF should then be anticoagulated for subsequent cardioversion.

    If TEE has excluded the presence of an atrial thrombus, the patient may be cardioverted to sinus rhythm without anticoagulation. If TEE reveals an atrial thrombus, WARFARIN should be administered for 3 weeks before the cardioversion at an INR of 2-3. After successful cardioversion, warfarin is continued for another 4 weeks.

    More rapid cardioversion is permitted if HEPARIN is administered for 24 hours.

    For patients with STABLE AF, acute RATE CONTROL (diltiazem, beta blockers) is the primary goal and cardioversion (amiodarone, ibutilide, procainamide or electrical cardioversion) may be considered if duration of fibrillation is known to be less than 48 hours. Ventricular rate should usually be brought to below 100 beats per minute.

    DILTIAZEM (Cardizem) is the most commonly utilized rate control agent because of rapid onset of action. Dosage is 0.25 mg/kg (20 mg) IV bolus over 2 minutes followed by an infusion of 5-15 mg per hour. The bolus may be repeated with 0.35 mg/kg if needed. Verapamil (Calan) 2.5-5 mg IV every 4-6 hours is also effective. Calcium channel blockers are contraindicated in CHF or high grade atrioventricular block and must be used cautiously in those on beta blockade.

    BETA BLOCKERS may also be useful for acute rate control. Relative contraindications include asthma, obstructive lung disease and heart failure. PROPRANOLOL is given at 1-4 mg IV (1 mg per minute). Maintenance doses are 10-30 mg PO tid-qid. METOPROLOL (Lopressor) is bolused in 1-5 mg IV doses and can be continued at 25-100 mg PO bid.

    DIGOXIN is appropriate only in patients with left ventricular systolic dysfunction. Up to 4-6 hours are required before rate control can be accomplished. Digoxin does NOT promote conversion to NSR. Loading doses are at 0.5 mg IV/PO followed by 0.25 mg IV every 4 hours for 2-3 doses followed by 0.125-0.25 mg per day IV/PO.

    Subsequent management of STABLE AF (after the ventricular rate has been controlled) includes restoration of NSR to improve cardiac output and reduces the risk of systemic embolization. Cardioversion should only take place after the possibility of thrombus is ruled out. Patients can be cardioverted by IV loading of an antiarrhythmic drug (procainamide or ibutilide) or an oral agent, such as quinidine or disopyramide. If pharmacologic conversion is ineffective, elective synchronized cardioversion should be initiated.


    Atrial flutter is characterized on the ECG by an absolutely regular rate of 250-320 deflections per minute with a variable block that is usually 2:1. The deflections are known as F waves that appear in a sawtooth pattern.

    Atrial flutter differs from paroxysmal SVT in that the atrial rate is faster and carotid sinus massage is ineffective but can possibly increase the degree of AV block.

    THERAPY follows the same ACLS guidelines as described for atrial fibrillation.

    Chronic suppression of atrial flutter is typically done with digoxin, quinidine or procainamide.


    SINUS BRADYCARDIA in adults is treated with 0.5-1 mg IV or IM with a maximum cumulative dose of 3 mg for an average adult.

    CHILDREN receive 10-20 mcg/kg IV (minimum dose 0.1 mg or 0.25 mL). IM and PO dosing is at 20 mcg/kg.

    Patients with third-degree block and Mobitz type 2 second-degree block should NOT receive atopine as it may result in a paradoxical slowing of the ventricular escape rates.

    REVERSAL doses are at 10-15 mcg/kg when given concomitantly with an anticholinesterase.

    INFANTS Experts recommend 10 mcg/kg IV prior to laryngoscopy in all infants less than 6 MONTHS of age regardless of whether or not SCh is used. It may also be useful in older chidren for bronchodilation or prior to SCh administration. The incidence of severe bradycardia during inhalation induction is 0.36% in normal children though it is 3.6% in the Down syndrome population such that many receommend pretreatment with IM atropine and allowing for the effect prior to administration of the volatile.

    PHARMACOKINETICS Atropine is a tertiary amine. It has an alpha half-life of 1 minute and ß half-life of 2.3 hours.

    PHARMACODYNAMICS Atropine competitively antagonizes the action of ACh at the MUSCARINIC receptor.

    Atropine decreases salivary, bronchial and gastric secretions. It decreases GI tone and motility and decreases pressure at the LES. Atropine increases IOP secondary to pupillary dilation. Large doses may increase body temperature and the drug should be used cautiously in patients with fever.

    Atropine may cause transient DECREASES in HR with initial dosing secondary to a weak peripheral muscarinic cholinergic AGONIST effect.

    Atropine is a TERTIARY amine that crosses the blood-brain barrier. Glycopyrrolate is quaternary.

    AUROY ET AL 2002

    Major Complications of Regional Anesthesia (Anesthesiology 2002; 97:1274)


    Autodonation refers to the elective withdrawal of whole blood prior to cardiopulmonary bypass, with the concurrent administration of a crystalloid or colloid solution to maintain normal circulating blood volume. This blood is stored and then retransfused after separation from CPB and the timely administration of protamine.

    This is a variant of intraoperative isovolemic hemodilution, with the goals of (1) decreasing the need for postoperative erythrocyte transfusion, (2) restoring normal concentrations of clotting factors and platelet function by decreasing the exposure of the harvested blood to the foreign extracorporeal membrane surfaces and (3) lowering the hematocrit in those rare cases where the preoperative value exceeds 46%.

    There is ample evidence from the British literature that hematocrit values over 46% increase the risk of myocardial thrombosis and stroke.

    But are these goals achieved? The literature conflicts but generally the hemostatic effects achieved with just one unit of autodonated whole blood proves insufficient to alter the need for blood or blood components after surgery, especially if examined over large groups of patients. On a case by case basis, there may be individual patients who may limit their exposure to blood products in this fashion. These benefits ignore the extra time, equipment and costs of the autodonation process however.

    It must be recognized that the process of isovolemic hemodilution is not without potential serious adverse effects. The cardiovascular system must respond to hemodilution by increasing cardiac output (by either stroke volume or HR) in order to maintain oxygen delivery. This is complicated by effects on peripheral resistance, blood viscosity and the oxyhemoglobin dissociation curve. In addition, effects on colloid osmotic pressure, intrapulmonary shunt, extravascular lung water and tissue edema have been documented and reviewed.

    Thus, while theoretically appealing, the results of autodonation often fall short of its promise. In addition, the clinician must recognize and be vigilant for the risks and limitations of hemodilution in the pre-CPB period. It appears most centers are currently relying on protocols which infuse antifibrinolytics (Amicar, aprotinin) and minimizing time on CPB as alternative hemostatic strategies.


    AH occurs in 85% of patients with cord lesions above T6 and is rare with lesions below T10. It can occur in patients without complete transections including patients with spina bifida cystica. AH results from the absence of central inhibition on the sympathetic neurons below the cord lesion.

    Noxious stimuli (bowel, bladder or uterine contractions) will transmit impulses through the dorsal nerve root. Bladder distension is the most common stimulus. Afferents will synapse with sympathetic neurons and the impulse is propagated both cephalad and caudad in the sympathetic chain without inhibition.

    AH results in vasoconstriction below the cord lesion and global HTN. Reflex arcs involving baroreceptors (carotid sinus and aortic arch lead to bradycardia and vasodilation above the cord lesion although these compensatory mechanisms are insufficient in patients with high lesions. Seizures, intracranial or SAH, CHF, pulmonary edema and myocardial ischemia can occur.

    Patients with spinal cord injury often have low baseline pressures and some degree of hemodynamic instability. It is prudent to make use of an arterial catheter for BP titration. Various methods of controlling HTN associated with AH should be available and understood:

    1) afferent limb blockade: SA is more effective than epidural block
    2) ganglionic blockers: trimethaphan , pentolinium, hexamethonium, volatiles
    3) adrenergic blockers: guanethidine
    4) alpha blockers: phentolamine, phenoxybenzamine (which may be used as prophylaxis as it is for pheochromocytoma)
    5) direct vasodilators: SNP, volatile anesthetics, hydralazone



    FIRST DEGREE AV block usually results from conduction delay within the AV node, but rarely, intra-atrial delay or delay within the His-Purkinje system (in conjunction with BBB) may be responsible. The ECG reveals a PR interval greater than 200 milliseconds (five small blocks). The PR interval is measured from the beginning of the P wave to the beginning of the Q wave or R wave if a Q wave is not present.

    Etiologies include increased vagal tone, drug effect, electrolyte abnormalities (either high or low potassium or magnesium), ischemia and conduction system disease. First degree block is usually asymptomatic but may exacerbate failure from loss of AV synchrony.

    Asymptomatic patients require no therapy. In symptomatic patients, dual-chamber pacemaker therapy can be considered in the absence of treatable causes.


    SECOND DEGREE AV block is present when some atrial impulses are not conducted to the ventricle when the AV node should not be refractory. Two types of second degree block are recognized based on the pattern of impulse conduction and distinctions between type I and type II are important, as they carry different prognostic implications.

    MOBITZ TYPE I (Wenckebach) block demonstrates progressive delay in AV conduction with successive atrial impulses, as evidenced by PROGRESSIVE PR interval prolongation, before the block of an atrial impulse. The characteristic ECG pattern is of QRS complexes occurring in regular groupings (grouped beating) separated by the blocked beat. The RR interval progressively shortens before a blocked P wave. The site of conduction block almost always is within the AV node.

    Etiologies include increased vagal tone, antiarrhythmic drug effects, electrolyte abnormalities, myocardial ischemia (typically in an inferior or posterior distribution) and conduction system disease.

    Mobitz TYPE I block (especially with a normal QRS) is BENIGN and usually does not portend development of complete heart block. These rhythms may be common in well trained athletes.

    Symptomatic TYPE I AV block is managed initially with atropine 0.5 mg IV every 2 minutes to a maximum of 0.04 mg/kg or approximately 2.5 mg. For persistent symptoms, permanent pacemaker therapy should be instituted.

    MOBITZ TYPE II block is characterized by abrupt AV conduction block without evidence of conduction delay in preceding conducted impulses. The ECG demonstrates no change in PR intervals preceding a nonconducted P wave. The site of block is localized most often to the His-Purkinje system.

    Etiologies include conduction system disease, antiarrhythmic drug effects, anterior myocardial ischemia and increased vagal tone. Type II block, especially in the setting of BBB, often antedates the development of complete heart block. Symptoms may include fatigue, palpitations and syncope.

    Unstable patients should be treated initially with temporary transvenous pacemaker insertion followed by permanent pacemaker implantation. Because of the propensity for progression to complete block, asymptomatic patients can also be treated with permanent pacemaker implantation.

    ATROPINE should NOT be used to treat Mobitz type II block associated with BBB, as this can exacerbate the degree of block by accelerating the sinus rate.

    2:1 AV block may be caused by either type I or type II mechanisms. The concomitant presence of bundle branch block or fascicular block suggests the presence of type II second-degree AV block.


    THIRD-DEGREE (complete) AV block is present when all atrial impulses fail to conduct to the ventricle and the prevailing ventricular escape rhythm is slower than the atrial rate.

    This pattern is distinct from AV dissociation, typically a benign condition, which is present when the ventricular rate exceeds the atrial rate. The site of block in complete AV block may be the AV node (as occurs in congenital heart block) or within the His-Purkinje system (typical for acquired heart block).

    Etiologies of acquired complete AV block include ischemia or infarction, drug toxicity, idiopathic degeneration of the conduction system, infiltrative diseases (amyloidosis, sarcoidosis, metastatic disease), rheumatologic disorders (polymyositis, scleroderma, rheumatoid nodules), infectious diseases (Chagas disease, Lyme disease), calcific aortic stenosis or endocarditis.

    Symptoms depend on the degree of bradycardia of the underlying escape rhythm and include lightheadedness, dyspnea, CHF, angina and syncope.

    In the absence of reversible causes of complete heart block, permanent pacemaker therapy is indicated for acquired complete heart block. Congenital complete heart block with significant bradycardia (less than 45 bpm) can be treated with permanent pacemaker implantation to prevent a malignant ventricular arrhythmia.


    PATHOPHYSIOLOGY Aortic valve regurgitation leads to chronic volume overloading resulting in eccentric ventricular hypertrophy. LVESV and LVEDV increase but LVEDV increases to a greater extent resulting in greater SV without an increased EF. The diastolic slope is little changed and compliance is only slightly decreased but the entire PV loop is shifted to the right. This is known as creep. As AR progresses and systolic dysfunction evolves, preload reserve is exhausted and wall stress elevates secondary to an increase in ventricular radius.

    Myocardial oxygen CONSUMPTION is increased by the large mass of myocardium, enormous volume work (which is less demanding than pressure work) and wall stress (which is increased in diastole as well as systole). Myocardial oxygen DELIVERY is compromised by the low diastolic pressures (worsened by bradycardia).

    BRADYCARDIA is DETRIMENTAL because regurgitant volume per beat is greater lowering DBP and larger SV will increase wall tension and per beat oxygen consumption. A HR between 75-85 appears ideal.

    Increased afterload is detrimental because it increases regurgitant volume per beat. Nevertheless, vasodilators seem only to benefit those with low EF, decreased forward output and high arterial pressures – other patients may suffer because of a consequent decrease in preload.

    ANESTHETIC TECHNIQUE Maintain SR (not as important as with AS), HR between 75-85, avoid increase in afterload, maintain PCWP between 10-15 to assure optimal LVEDV and maintain contractility.

    NSR at HR 85 or high normal
    normal or increased preload
    normal or decreased SVR
    normal inotropy

    In patients with depressed ventricular function and exhausted preload reserve, the peak A pressure will be 20-25 when preload is optimized. Nitroprusside (0.15-0.3 mcg/kg/min) is beneficial to these patients but can reduce preload as well. Etomidate may be useful for induction.

    Bradycardia with hemodynamic compromise should be treated promptly. A small dose of pancuronium can be helpful if vecuronium was used and atropine or glycopyrrolate is also appropriate. Ephedrine will be a poor choice because of consequent afterload increase.

    HYPOTENSION should not be routinely treated with vasopressors because regurgitant fractions could increase. If HR and SV are optimized, DA at less than 5 mcg/kg/min or dobutamine at less than 10 mck/kg/min can augment CO without increases in afterload.

    POSTOPERATIVE Impedence to ejection will be increased by the compotent valve. Although there is an increase in LV pressure generation, wall stress does not increase because of the decrease in ventricular radius. Inotropic support is often necessary with low doses of epinephrine (0.015-0.03), DA (1-5) or dobutamine (5-10) all of which should produce only minimal vasoconstriction. Atrial systole is more important postoperatively because all of the LV diastolic filling must occur through the mitral valve with an atrial kick.


    Angina, syncope and CHF of aortic stenosis begin late in the course when GRADIENT exceeds 50 mmHg. This is equivalent to peak VELOCITY of 3.5 m/s and valve AREA of less than 1 cm squared. Cath will underestimate gradients by 5-20 because LV and aortic pressures are not measured simultaneously.

    With moderate to severe disease the LV is hypertrophied and noncompliant. NSR and high filling pressures are required to adequately distend the LV during diastole. Atrial systole contributes 40-50% to stroke volume in these patients. Vasodilation does not reduce the work of the LV because of the fixed resistance at the valve. Vasodilation DOES reduce CPP and will likely provoke ischemia. Modest decrease in contractility is generally well tolerated even with history of CHF. Augmentation of contractility or increased HR may induce ischemia even in absence of CAD.

    NSR at HR 70-85
    preload increased
    SVR normal or increased
    inotropy normal or decreased

    Pertinent TEE evalutions include review of the LVOT, valve anatomy and ascending aorta, measurement of the valve diameter and estimation of the peak and mean gradients. The best views for evaluation include (1) ME AV SAX 60 degrees for three cusp views, to measure area by planimetry and to evaluate for AI with color, (2) ME AV LAX 130 degrees to measure LVOT diameter and evaluate for subvalvular and supravalvular pathology – DOMING of the cusps in this view is enough to make a qualitative diagnosis of stenosis, (3) TG LAX 120 degress obtained by rotating from the TG SAX 0 degree view, and (4) DEEP TG LAX 0 degrees. Both TG views can be used for CWD and PWD velocity measurements.

    VELOCITY is measured by CWD of the TG LAX 120 degree or the DEEP TG LAX 0 degree view maintaining less than 20 degrees between the beam and direction of the LVOT. The pressure GRADIENT is calculated by four times velocity squared (in meters per second). The MEAN VELOCITY is obtained by tracing the CWD outflow velocity profile. Peaks above 64 mmHg and means above 50 mmHg are considered severe. The AREA of the valve is calculated by application of the continuity equation. The area of the LVOT is measured during systole utilizing the midesophageal long-axis view and 0.785 times the diameter squared. Instantaneous velocities are measured by PWD at the LVOT and AV. The area is then calculated by the following continuity formula:

    vel x area = vel x area

    Unique surgical problems that may be encountered include (1) aortic dissection requiring replacement of the entire aortic root, (2) sewing the valve over a coronary ostium leading to ischemic dysfunction and (3) inadequate removal of air in the heart leading to air embolism in the coronary and possibly cerebral vessels.

    After repair, once ventilation has resumed, the surgeon attempts to free AIR from the ventricle. TEE can be used to visually inspect the adequacy. Patients with good function prior to surgery are easily weaned from bypass and often require vasodilators for profound HTN that can develop off bypass. Surgeons generally want pressures to be LOW between bypass and delivery to the ICU.

    The mortality rate for AVR is approximately 4 percent. In general, patients with moderate AS have minimal additional risk during noncardiac procedures.


    These defects result in a communication between all four heart chambers as well as abnormalities in both of the AV valves. Similar to large VSD lesions, the CAVC results in large left-to-right shunts, transmission of the systemic pressures to the RV and PA and volume overload to both right and left ventricles. As with large VSD, there is also a predisposition to early development of PVOD.

    In some CAVC defects the presence of severe MR results in demonstratable regurgitation directly into the RA (worsening the left-to-right shunt). Severe MR also increases the volume work of the left ventricle.

    Pertinent preoperative evaluation includes assessment of regurgitation, tethered or crossed chordae and ventricular function.

    SURGERY is usually performed through the right atrium. One or more pericardial patches are used to close the AV canal. 30% of the patients with complete AV canals require surgery by 1 year of age. 70% will require surgery by 2 years of age. In the past, patients were treated initially with PA banding to be followed by complete repair at an older age.

    ANESTHETIC preparation requires preparation of infusions including DA, phenylephrine, NTG and SNP. Epinephrine, prostacyclin, milrinone, calcium and albumin boluses should also be available.

    Heart rate, contractility and preload should be maintained to assure adequate cardiac output. Avoid decreases in the PVR-SVR ratio as well as large increases in PVR. An increase in pulmonary flow will necessitate an increase in cardiac output and a decrease in pulmonary flow will result in a right-to-left shunt.

    In instances where a right-to-left shunt preexists, ventilatory measures to decrease PVR should be used (oxygen and hyperventilation). In addition, SVR must be maintained or increased.

    Management in general is similar to that of the child with a large VSD. However, the child with a CAVC may also have severe MR and a highly reactive pulmonary vasculature.

    POST BYPASS Closure will usually result in some immediate decrease in pulmonary pressures. Near normal PAP may result in the child without PVOD. Therapy to reduce PVR and to increase contractility in the post-CPB period may occasionally be necessary to avoid RV afterload mismatch (prostacyclin or milrinone).

    Separation from bypass may be complicated by inadequate closure, conduction block and persistent mitral regurgitation. Diagnosis can be made with TEE and LA pressure lines. The presence of large V waves on the pressure tracing from a LA catheter may aid in assessing the degree of mitral regurgitation. Occasionally, patch placement will reduce the size of the LV and subsequently reduce stroke volume.


    General INDICATIONS for the awake intubation include known difficult airway and suspected difficult airways in the face of:

    risk of aspiration
    cardiovascular instability
    cervical spine instability
    MH susceptability

    Other advantages include the ability to undertake neurologic examination after intubation and allowing for patient self positioning.


    Awake intubation implies that the neonate will have direct laryngoscopy and be intubated without any prior medication. This technique is still occasionally employed in limited circumstances. Three surveys of anaesthetic practice have been published. In 1991, the Hospital for Sick Children in Toronto reported that 44 of 100 of anaesthetics for pyloromyotomy used awake intubation and, in 1994, a postal survey of 153 paediatric anaesthetists in the UK, North America, Europe and Australasia reported a 5% incidence of awake intubation for pyloromyotomy (Paed Anaes 2001:11:135-45).

    Attempts to awake intubate an adult without adequate analgesia result in intense pain associated with the stimulation of both visceral and somatic pathways. While the presence or absence of pain is more difficult to assess in the neonate, awake intubation causes a variety of physiological changes including changes in BP, HR, oxygenation and raised anterior fontanel pressure.

    From the data available, it would appear that awake intubation is associated with physiological changes that may put neonates at risk of intracranial haemorrhage and hypoxia. A struggling baby is also less likely to be successfully intubated at one attempt and the time required for intubation is longer, increasing the chance of supraglottic airway damage. Painful experiences in the neonatal period can lead to long-term behavioural changes. Anaesthesia for intubation can provide safe, stable, stress free and painfree intubation in a vulnerable population. We therefore believe that it should be considered as routine to prevent the detrimental effects associated with awake intubation.

    Safety should always be the priority in neonatology and there are situations where a neuromuscular blocker may not be advisable, for example, in those circumstances where congenital abnormalities, such as in Pierre-Robin sequence, predict a difficult intubation or a difficult airway.


    Awareness during GA appears to be a ubiquitous phenomenon that occurs at an incidence of 1-2 cases per 1000, irrespective of geographic location and potential differences in anesthetics and techniques (AA 2004 99:833-9). Of 20 million general anesthetics performed each year, 20-40K cases of awareness may be expected. In the ASA closed claims analysis, awareness accounted for 1.9% of all suits. The majority of these claims involve women, ASA 1-2 for elective surgery.

    Particular surgical patient populations, such as those individuals requiring GA for obstetric, major trauma and cardiac surgery are known to experience a high incidence of awareness that is variably reported between 7-40%.

    Most clinicians define awareness as the spontaneous recall of events occurring during GA and surgery. This is known as EXPLICIT memory. There are numerous studies documenting that the registration or retention of mental images or information under GA also can occur without conscious recollection. This is known as IMPLICIT memory.

    Clinical SIGNS suggestive of awareness are generally motor and autonomic. Eyelid motion, swallowing, increased spontaneous respiratory effort, coughing, facial grimacing and extremity or head motion are signs often assumed to indicate inadequate amnesia. HTN, tachycardia, mydriasis, tearing, sweating or salivation may also indicate too light a level of anesthesia. Monitoring for muscle activity as an indicator of awareness is useful because muscle movements usually occur before awareness occurs. Motor signs also frequently occur prior to hemodynamic or autonomic indications of possible awareness.

    FACTORS that may contribute to awareness include:

    inadequate anesthetic technique
    no premedication
    short-acting IV induction agent
    excessive or unnecessary NMB
    difficult or prolonged intubation
    equipment failure
    ASA physical status IV or V
    obstetric procedure
    morbid obesity
    cardiac surgery
    inexperience of anesthesiologist
    autonomic blockade
    anesthesia at high altitude
    increased anesthetic required

    The ASA Practice Advisory currently recommends discussing this topic only with high risk patients.


    The brachial plexus is derived from the cervical roots C5-8 and the thoracic root T1. The plexus runs to the axilla passing between the clavicle and the first rib. In the axilla the plexus forms THREE CORDS (posterior, lateral and medial) which surround the axillary artery. The musculocutaneous nerve arises first and is often incompletely anesthetized during an axillary block. It is also important to realize that the LA more easily reaches the medial and lateral cords with the posterior cord (RADIAL) less easily blocked. The radial nerve primarily supplies a posterior band but also the lateral portion of the antecubital fossa.

    PROCEDURE The patient is positioned with the arm held at 90 degrees to the body, elbow flexed at 90 degrees, forearm elevated on a pillow and hand supine. Researchers concur that THREE nerves (median, radial and musculocutaneous but not the ulnar) must be electrolocated to obtain complete forearmand hand analgesia in at least 90% of patients within 20-30 minutes. It is useful to identify these nerves as proximal as the pulsation can be appreciated (the teres major and the lattisimus dorsi meet the humerus at point where the CORDS are in greatest approximation). The MEDIAN nerve is in a superior position, the ULNAR inferior and the RADIAL is deep and inferior to the axillary artery.

    The modus operandi for TRIPLE-INJECTION block (Reg Anes Pain Med May 2006): (1) the first skin-puncture site is just superior to the artery with a SQ injection of 3-5 mL to block the intercostobrachial (T2) – this is alternatively blocked with a skin wheal injected across the upper axilla and lateral chest wall in the distribution of a tank top sleeve, (2) puncture the fascia and slowly increase stimulating current until hand or forearm flexion and pronation are obtained (MEDIAN) – the needle is adjusted and half-volume LA injection is perfomed, (3) the needle is withdrawn to the subcutis and reinserted upward toward the coracobrachial muscle until stimulation synchronous elbow flexion (MUSCULOCUTANEOUS) is observed for LA injection of 5-8 ml, and (4) the needle is withdrawn completely and reinserted approximately 2 cm inferior to the artery through anesthetized skin – puncture the fascia and slowly increase stimulating current to achieve finger and wrist extension (RADIAL) to inject the remaining LA volume – elbow extension and finger flexion should be ignored and the needle advanced deeper and slightly behind the artery)

    MEDICATIONS may include bupivicaine, lidocaine or mepivicaine. Lidocaine and mepivicaine produce 2-3 hours of anesthesia without epinephrine and 3-5 hours with epinephrine. Plain bupivicaine produces 4-6 hours of anesthesia while the addition of epinephrine extends the duration to 8-12 hours. In COMBINATION, 20 mL of 2% mepivicaine can be used with 20 mL of 0.5% ropivicaine to provide 400 mg mepivicaine (700 mg maximum with epinephrine) and 100 mg of ropivicaine (200-300 mg maximum with epinephrine).

    SEQUENCE OF BLOCK Consequent to the construction of the peripheral nerves, the muscles are blocked first and the patient will be unable to raise the arm off the table. Secondarily blocked are the fibers sensitive to sharpness – the radial nerve is the sole innervation to the anatomical snuff box, the ulnar nerve to the pinky and the median nerve to most of the palmar surface. Motor function in the hand may also be used to assess the block of the median nerve (which opposes pinky and thumb), the ulnar (which spreads the fingers) and the radial (which extends the fingers and wrist).



    life threatening withdrawal

    The self-inflating transport bags or CPR bags are available in three sizes for transport and emergency ventilation.

    INFANT BAGS are recommended for children under seven kilograms. They provide a maximum tidal volume of 175 mL. Total volume of the bag is 240 mL and resevoir volume is 600 mL. The infant unit provides 100% oxygen at 4 liters of FGF with the reservoir bag in place.

    CHILD BAGS are recommended for children between 7-30 kilograms. They provide a maximum tidal volume of 360 mL. Total volume of the bag is 500 mL and resevoir volume is 2500 mL. The child unit provides 100% oxygen at 10 liters of FGF with the reservoir in place and 85% oxygen without the use of the reservoir.

    ADULT BAGS provide a maximum tidal volume of 900 mL with one hand bagging and 1500 mL with two hands on the distensible bag. Total volume of the bag is 1600 mL and resevoir volume is 2600 mL. The adult apparatus requires 10 liters of FGF to provide 100% oxygen with a resevoir in place and at typical respiratory rates and tidal volume.

    The DEAD SPACE of the apparatus itself is only 7 mL. RESISTANCE through the apparatus is measured at 2.1 cmH2O for expiration at 50 LPM and 2.9 cmH2O for inspiration at 50 LPM.


    The Bainbridge reflex responds to changes in RA or central venous pressure via stretch receptors present within the RA wall and cavoatrial junction. Increases in intravascular volume or right-sided filling pressures stimulate these receptors which send their impulses through VAGAL AFFERENTS to inhibit parasympathetic activity and to increase HR. The changes in HR, however, are dependent on the underlying rate prior to stimulation, and relatively fast heart rates are less sensitive to further increase.

    There is also a direct effect of stretching on the SA node, which leads to enhanced automaticity and increased HR which complements the Bainbridge reflex.

    CLINICALLY the inhibition of this reflex may be seen if volume status suddenly drops (as with onset of neuraxial anesthesia and venous pooling) and the patient suddenly becomes bradycardic which may potentiate the fall in arterial blood pressure from a drop in preload (Mueller). There is obviously some resistance to this response from the more commonly appreciated baroreceptor reflex.


    A pentobarbital coma is generally seen as a tertiary effort to control elevated ICP. The CMRO2 for the brain is 3-3.5 mL/100g/minute – 55% of which is for electrophysiologic activity and 45% for cell homeostasis.

    Burst suppression is ideally titrated to one burst of activity every six seconds (one EEG screen).

    EEG waves are classified according to frequency.

    DELTA 0-3 Hz anesthesia
    THETA 4-7 Hz deep sleep
    ALPHA 8-13 Hz resting awake
    BETA > 13 Hz mentation


    The baroreceptor reflex, also called the carotid SINUS reflex, responds to changes in blood pressure via circumferential and longitudinal stretch receptors present in the carotid SINUS and aortic ARCH. Remember that sinuses respond to pressure but bodies do not.

    Increases in blood pressure stimulate these two receptor regions, which send impulses along the afferent limbs of the GLOSSOPHARYNGEAL nerve (nerve of Hering) and the VAGUS nerve, respectively, to the nucleus solitarius in the medullary cardiovascular center.

    This center actually comprises two functional areas: a lateral and rostrally located pressor center and a central and caudally located depressor center, in which hypothalamic and limbic system inputs are then integrated.

    The response to HYPERTENSION is (1) decreased sympathetic activity, which, in turn, decreases contractility, HR and vascular tone and (2) increased parasympathetic activity, which also decreases heart rate and further depresses contractility.

    Typically, these receptors begin to respond at systolic pressure in excess of 170 mm Hg. This set point shifts upward in patients with chronic or poorly controlled hypertension.

    DECREASES in blood pressure have the reverse effect and thus these receptors play an important role in the response of the cardiovascular system to acute blood loss and shock. Nevertheless, at pressures lower than 50-60 mm Hg, the baroreceptors lose much of their functional capacity.

    Interplay with the BAINBRIDGE reflex during periods of acute hypotension seem to counterbalance atleast the tachycardic response to acute hypotension.

    The baroreceptor reflexes are blunted during GENERAL ANESTHESIA and for two hours following GA. It has been demonstrated that the response to hypotension recovers more quickly than the response to hypertension (AA 2001).


    HURRICAINE is a compound containing 20% benzocaine that is useful as a topical anesthetic but has been associated with methemoglobinemia with only minimal application.

    The TOXIC dose of benzocaine is 100 mg or only 0.5 mL of the 20% spray. One half-second spray delivers approximately 0.15 mL or 30 mg and therefore more than 3 quick sprays is often ill advised.

    CETACAINE is a slightly less toxic compound containing benzocaine 14%, tetracaine 2% and butyl aminobenzoate 2%.

    The active ingredient in both Cepastat and Chloraseptic is PHENOL or carbolic acid. Phenol has ill effects only in overdosages. It is also used for neurolytic blocks.


    Withdrawal from benzodiazepines may be as severe as withdrawal from alcohol and is most common in patients taking higher than recommended doses for anxiety.

    The variability in time course and severity of withdrawal is dependent on the half-life of the drug involved. Withdrawal from short-acting agents (ALPRAZOLAM or Xanax) can precipitate severe symptoms in as little as 24 hours. Withdrawal from DIAZEPAM, with its long half-life and active metabolites, may require 8 days or longer and persist for months.

    SYMPTOMS The early signs of withdrawal are similar to those of alcohol withdrawal – characterized by CNS stimulation and autonomic hyperactivity. Patients exhibit anxiety, irritability, dysphoria, insomnia, nausea, palpitations, tremor and diaphoresis. An underlying anxiety disorder may become evident and cause symptoms such as paresthesias, tinnitus, vertigo and metallic taste to develop. As withdrawal worsens, patients may develop emesis, tachycardia, hypotension and hyperthermia.
    Symptoms can be precipitated by the use of flumazenil and flumazenil has been reported to cause severe withdrawal syndromes, seizures and death.

    TREATMENT is similar to that of alcohol withdrawal. Replacement therapy typically is carried out with the abused drug at a dosing level that relieves the withdrawal syndrome. Alternatively, a longer-acting benzodiazepine may be used. Then, a gradual reduction in dosing over several weeks completes the recovery. In patients with severe withdrawal, IV diazepam can be used to quiet the symptoms and relieve seizures. Barbiturates may also be used. If withdrawal is precipitated by flumazenil, supportive care should be given because the relatively short half-life of flumazenil will be overcome by the longer half-life of the abused benzodiazepine.


    Three SUBSETS of the beta-blockers now exist including the non-selective, ß2 selective and those with intrinsic sympathomimetic activity (ISA).

    The ß2 SELECTIVE agents (remember AME for atenolol, acebutolol, metoprolol and esmolol) are less likely to cause bronchospasm but advantages are lost at higher doses. Those agents with ISA (acebutolol, carteolol, penbutolol and pindolol) are less likely to increase serum triglyceride levels and less likely to decrease concentrations of HDL.

    Two agents (carvedilol and labetalol) have alpha as well as ß-blocking properties. Sotalol is a beta-blocker as well as potassium-channel blocker.

    INDICATIONS for ß-blockers include hypertension and angina pectoris. Atenolol, metoprolol, propranalol and timolol probably decrease mortality following myocardial infarction. Atenolol and bisoprolol have been demonstrated to decrease perioperative and late cardiac mortality after noncardiac surgery in those at risk. Only sotolol (which delays ventricular repolarization) is approved for rate control in those with chronic atrial fibrillation. Bisoprolol, carvediol and metoprolol have all demonstrated the ability to decrease mortality and curb hospitalizations for patients with mild to severe heart failure.

    ADVERSE EFFECTS can usually be minimized by slowly titrating upward. The ß-blockers can be associated with hypotension, bradycardia and heart block, bronchospasm and aggravation of CHF. They may mask symptoms of hypoglycemia in the diabetic patient and they may promote development of type II diabetes. Fatigue, depression, impotence, Raynaud’s phenomenon, insomnia and delirium are other possible side effects.


    Effective beta blockade is suggested by a resting heart rate between 50-60 without evidence of CHF or AV block on EKG.

    THERAPY for overdose may include atropine at 0.4-0.6 mg, isoproterenol at 2-5 mcg per minute, dobutamine or calcium chloride.

    Glucagon or insulin euglycemia are two other therapies for patients refractory to other treatment.

    Dopamine will typically result in excessive SVR due to unopposed alpha stimulation and is therefore ill advised for the overdosed patient.


    Several studies have demonstrated the benefit to the adminstration of perioperative ß blockers (atenolol and bisoprolol) in decreasing the incidence of post-operative myocardial events and cardiac death as late as two years after noncardiac surgery.

    Smaller studies have demonstrated less lability and a decreased incidence of intraoperative ischemia with a single dose of ß blockers given during the premedication or induction period. The risks of ischemia associated with tachycardia are not correlated with HR of less than 110 BPM (Stoeltings Coexisting Disease).


    In general there exists an inverse relationship between the number of beta receptors and plasma catecholamine levels.

    Hypertensive patients with increased catecholamine levels are known to have decreased receptor numbers AND decreased receptor sensitivity. Chronic use of ß-agonists (and even short-term use over 1-6 hours) may cause down-regulation of receptor numbers in a way similar to that seen in the chonic hypertensive.

    This DOWN-REGULATION is reversible upon lowering of plasma catecholamine levels or discontinuation of the ß-agonists.


    The BEZOLD-JARISCH reflex is initiated by left ventricular mechanoreceptors secondary to noxious ventricular ischemia including ischemia and reperfusion following ischemia. It results in increased parasympathetic activity causing bradycardia, hypotension and coronary artery vasodilation (Anesthesiology 2003).


    IVRA is usually produced using 0.5% lidocaine although 0.2% ropivicaine and even 0.25% bupivacaine have been described in small studies. Less than 50 mL should be used in the arm and up to 80 mL can be used in the lower extremity. For UE blocks, the antecubital fossa is more easily cannulated and may provide better results than distal vein cannulation (J Trauma 1995 39:726). Local infiltration by the surgeon can provide postoperative analgesia when desired as the effects of the Bier blocks are quickly lost as the tourniquet is released. Studies have demonstrated that the average volume of the UE is 170 mL.

    TIME constraints are secondary to maximum tourniquet time but Bier blocks can be used for procedures lasting up to 90-120 minutes. Histologic studies generally show early changes after 1 hour but muscle degeneration and cell necrosis occurs at 2-3 hours. Functional studies show that most patients tolerate 2 hours of tourniquet ischemia with no sequelae.

    At the conclusion of surgery, if the tourniquet has been inflated for more than 40 MINUTES, the cuff can be deflated as a single maneuver but most recommend incremental deflation at ALL time intervals. If surgery is completed between 20-40 minutes after block placement, the cuff is deflated incrementally over 5 minutes to delay the sudden absorption of the local anesthetic into the circulation.

    If the interval between block placement and completion of the procedure is less than 20 minutes, the cuff should remain inflated until 20 minutes have elapsed at which time the cuff may be deflated in the stepwise manner described above.


    The bispectral index is a variable derived from the EEG that is a quantifiable measure of the sedative and hypnotic effects of anesthetic drugs on the CNS. Bispectral index decomposes the EEG signal into its component sine waves using FOURIER transformation.

    BIS monitoring may be particularly useful in only a few specific situations: during TIVA and to rule out anesthetic overdose in patients with hypotension.

    Glass demonstrated that reductions in BIS correlated well to increasing sedative effect as assessed by clinical scoring scales and provided excellent prediction for loss of consciousness with a variety of anesthetic agents. BIS values were better than or equal to measured drug concentrations in correlating with sedation assessment. Significant memory impairment (loss of free recall) occurs at BIS values greater than values where the patient becomes unconscious.

    In a recent investigation, the ability of both BIS and A-Line Autoregressive Index (based upon the MLAEP) to detect propofol-induced changes in responsiveness, consciousness and response to stimulation were compared in volunteers. BIS, AAI, and propofol effect-site concentration were accurate indicators of sedation and loss of consciousness. Interestingly, hemodynamic parameters had poor correlation to sedation state and were unable to predict loss of consciousness. The accuracy of BIS or AAI to assess consciousness (measured by changes in sedation scale or loss of eyelid reflex) was reflected in a high predictive probability measurement. Individual threshold values were tested as cut-off points to define loss of consciousness. For example, BIS values less than 60 were extremely accurate to detect unconsciousness, with a measured sensitivity of 0.99 and specificity of 0.81 to determine loss of consciousness. The OAA/S is a simple assessment of response to graded stimuli such as the patient’s spoken name, gentle shaking of the patient, or painful trapezius muscle squeeze.

    Blood pressure and heart rate are frequently used as indicators of the adequacy of anesthetic state. Although this may have some validity in situations of identifying responses to surgical stimulation, it appears that blood pressure and heart rate are not accurate indicators for transitions between consciousness and unconsciousness. In one investigation, the isolated forearm technique was used to define the relationship between BIS and the ability to detect the loss and return of consciousness following induction doses of either propofol or thiopental. In this study, there was no correlation between hemodynamic measures and return of consciousness, whereas BIS was effective in tracking the effects of both agents.

    Although the above investigations support the validation of BIS and AAI as accurate indicators of sedation state and consciousness, many anesthesia professionals emphasize lack of movement as the primary indicator of adequate anesthesia. Although there is a relationship between BIS values and the probability of movement, this correlation is very dependent upon the combination of anesthetic agent and lacks aspecific threshold value to identify patients likely to move. In the study reviewed above, neither BIS, AAI or propofol concentration could predict patient response to noxious stimulation. However, both BIS and AAI exhibited transient increases indicative of EEG arousal responses to stimulation. A variety of studies now support the concept that the movement and unconsciousness endpoints of the anesthetic state are distinct in their dose-response relationships and anatomic substrate. Because movement is primarily a response mediated at the spinal cord, current consciousness monitoring technologies that utilize cerebral cortical signals (EEG or MLAEP) are unlikely to reliably predict movement.

    One recent study (AA 2002) of BIS use in pediatrics demonstrated the ability to use lower concentrations of the volatile agents but no change in recovery parameters.





    premature 100 mL/kg
    term infant 90 mL/kg
    3-12 months 80 mL/kg
    over 1 year 70 mL/kg
    adult male 70 mL/kg
    adult female 65 mL/kg

    For the pediatric patient, 10 mL/kg of packed RBC will increase the hemoglobin by 1 g/dL. One UNIT of packed RBC will increase the hemoglobin of the adult by 1 g/dL.

    ALLOWABLE blood loss formula (multiplying by 3 is the alternative to dividing by mean HCT):

    BV x (preop HCT – target HCT) x 3

    POSTOPERATIVE blood loss through surgical drains that should likely lead to reoperation includes 10% blood loss in any given hour or 20% blood loss over any four consecutive hours.


    Although long-term cardiac risk studies have focused on DBP or pulse pressure as a measure of vascular overload or stress, short-term clinical monitoring in the ICU or operating room has focused on the measurement of MAP or SBP. In part, the difference stems from the suggestion that MAP is less subject to technical problems and that little additional information on acute hemodynamic changes is added beyond a knowledge of systolic pressures.

    MAP is usually equal or slightly overestimated by the indirect measurement. SBP is the next most accurate measurement by oxcillatory measures while the DBP by indirect measurement is the least likely to be accurate.

    SBP will be equal or underestimated by indirect measurement in the normotensive patient. SBP overshoot is common by direct methods of measurement because most of the systems we use in the operating room are underdamped. Systems must have high natural frequencies (equal to ten harmonics of the heart rate) in order to accurately depict the arterial waveform. High frequency systems are more forgiving over a range of damping coefficients.

    DBP is usually slightly overestimated by the indirect method of measurement.

    When major disagreements between these modalities occur, check the patient for signs and symptoms of circulatory adequacy (dysrhythmias, shock), patient factors for regional arterial pressure gradients (peripheral vascular disease, embolic disease, patient position, rapid rewarming from bypass) and technical factors in the monitoring (extrinsic cuff compression, shivering, movement of transducers).

    It is known that patients with severe sclerosis may exhibit pseudohypertension by as much as 50 mmHg by indirect BP measurement. Approximately 20% of all patients with vascular disease will have discrepancies of greater than 20 mmHg when comparing left and right upper extremeties and this discrepancy may be dynamic in nature.

    In both adults and children, cuffs that are too wide or too loosely applied, underestimate the blood pressure. Cuffs that are too narrow will give an artificially high measurement.

    In ADULTS, the cuff bladder:
    1) width should be 1/3 to 1/2 the limb circumference
    2) length should be twice the width of the cuff bladder (approximately 80% of the limb circumference) but not quite enough to completely encircle the limb

    In CHILDREN, since their build varies markedly at each age, the cuff bladder should have:
    1) width of 2/3 of the length of the upper arm or thigh
    2) length of 3/4 of the circumference of the extremity

    Given the option between a blood pressure cuff that is too small or too large, in general, the larger cuff should be utilized.

    10 mmHg = 13 cmH2O


    RAPID MECHANISMS of control include baroreceptors (blunted by volatiles), atrial reflexes (stretching evokes vasodilation and tachycardia) and the Cushing reflex (medullary vasomotor center ischemia results in intense sympathetic response). Norepinephrine is the primary vasoconstrictor at the alpha receptors while epinephrine is the primary dilator at the beta receptors.

    MODERATELY RAPID mechanisms include at least three hormonal mechanisms (catecholamines, renin-angiotensin and ADH). There are also two intrinsic mechanisms (capillary fluid shift and stress relaxation of blood vessels) important to moderately rapid control.

    LONG TERM regulation includes the renal-body fluid system and also the renin-angiotensin system and the interaction with aldosterone concentrations and fluid and electrolyte balance.


    Placement of the esophageal bougie may place extrinsic pressure on the left mainstem bronchus resulting in lung collapse and atelectasis simulatiing a right main-stem intubation. Other considerations in this presentation include mucous pluggin, pneumothorax, foreign body aspiration and severe air space disease.


    Choice of technique should be based on the surgical site and on the experience of the anesthesiologist performing the block. The anatomy of the brachial plexus progresses from roots to trunks, divisions, cords and terminal branches.

    INTERSCALENE should be used for surgery of the clavicle, shoulder and upper arm. Paravertebral or intercostal blocks may be necessary for more extensive surgery. ADVANTAGES include clear landmarks, lower required volumes of LA, low likelihood of PTX and convenience of placement in the patient with an immobilized arm. This block preferentially reaches the caudad part of the cervical plexus (C3-4) as well as the superior and middle trunks of the brachial plexus (C5-7). The primary DISADVANTAGE is that the ISB often MISSES the inferior trunk from which the median and ULNAR nerves originate and is therefore not useful for surgery of the hand. There is also the possilbility of vertebral artery, epidural, subdural or spinal injection and the block should generally be avoided in patients with severe pulmonary disease.

    SUPRACLAVICULAR and SUBCLAVIAN perivascular techniques are more suited for surgery of the upper arm, elbow, forearm and radial aspect of the hand. Both techniques are fairly reliable at completely blocking ALL NERVES of the brachial plexus because of the tightly bundled arrangement of the DIVISIONS near the site of injection. This is the MOST EFFECTIVE block for all portions of the upper extremity. ADVANTAGES include easily identifiable landmarks, convenience of the block in the patient with an immobilized arm and smaller required volumes of LA when compared to the axillary block. The only DISADVANTAGES include the possibility of pneumothorax (incidence up to 6% although many will use this approach for all patients including those for outpatient procedures), phrenic nerve block (40-60%) and stellate ganglion block (70-90%).

    Some practitioners may combine the axillary and interscalene blocks (known as the AXIS BLOCK) to approximate the supraclavicular block without risk of pneumothorax. One must be willing to use almost 60 mL of LA for this combination and the axillary block should always be performed first for obvious reasons.

    INFRACLAVICULAR BLOCKS are useful as an alternative to the axillary block in patients that are unable to abduct the arm. It is useful for procedures on the elbow, forearm and hand. Many centers use this block for those requiring prolonged anesthesia. There is a lower incidence of pneumothorax when compared to the supraclavicular block. The disadvantage (similar to that of ISB) is the greater possibility of SPARING of the ULNAR nerve.

    AXILLARY techniques are best suited for surgery of the forearm and hand, especially when the area is innervated by the median and ulnar nerves. Here, the LA more easily reaches the medial and lateral cords with the posterior cord (and RADIAL nerve) less easily blocked. The axillary block is clearly the safest of all of the brachial plexus blocks and is clearly the easiest to perform in children.

    DYSTHESIAS following any of the brachial plexus blocks is reported to be between 0.1-1.9%. The DDX for dysthesias include crush injury, tourniquet pressure, retractor use during surgery, tight casts or dressings, positioning complications and undiagnosed preexisting conditions including injury, diabetic or alcoholic neuropathy.


    Individual nerves may be blocked alone or as required by failure of one of the bundled brachial plexus blocks.

    The MUSCULOCUTANEOUS is the most proximal branch of the brachial plexus and the most common nerve missed by an axillary block. This occurs because the MCN has already left the sheath and lies within the coracobrachialis muscle. It provides sensory innervation to the lateral aspect of the forearm (by the lateral cutaneous nerve of the forearm). Inadequate block of the MCN can be rescued by either (1) injection of 5-8 mL of LA into the coracobrachialis muscle at the time of the axillary block or (2) injection of LA behind the brachial artery (facilitated by superior displacement of the biceps muscle) at the mid-humerus.

    The RADIAL provides sensory innervation to the radial aspects of the dorsal wrist and the dorsolateral 3.5 digits. The most reliable places for rescue blocks of the radial nerve are at the musculospiral groove (between the heads of the triceps muscle), the radial head (medial to the lateral epicondyle) and the distal forearm (medial to the radial artery).

    The MEDIAN provides sensory innervation to the palmar aspects of the thumb, index finger, middle finger and the radial half of the fourth digit. It also provides innervation to the nail beds of many digits. A rescue block is best performed at either the elbow (medial to brachial artery in the antecubital fossa) or at the wrist (midline, deep to the palmaris longus tendon).

    The ULNAR provides sensory innervation to the ulnar side of the hand, the fifth digit and half of the fourth digit. It is the second most commonly missed nerve by a correctly performed axillary block. A rescue block can be performed either at the elbow (just lateral to the medial epicondyle in the ulnar groove) or at the wrist (lateral to the ulnar artery).


    RADIAL nerve C5-8
    MEDIAN nerve C6-T1
    ULNAR nerve C8-T1

    RADIAL: wrist extension, finger and thumb extension, thumb abduction

    MEDIAN: pronation, wrist flexion, finger and thumb flexion, opposition of thumb and little finger, lateral palmar sensory

    ULNAR: wrist flexion, finger abduction and adduction, thumb flexion, thumb adduction, palmar and dorsal fourth and fifth sensory

    PRONATION is by the median nerve to the pronator quadratus and pronator teres muscles.

    WRIST FLEXION is by median and ulnar nerves to the flexor carpi radialis and ulnaris respectively.

    WRIST EXTENSION is by the radial nerve.

    FINGER FLEXION is primarily by median innervation but also by ulnar to the third and fourth lumbricals and the interossei muscles.

    FINGER and THUMB EXTENSION is solely by radial innervation.

    FINGER ABDUCTION and ADDUCTION is by ulnar innervation.

    THUMB FLEXION is by median and ulnar to the flexor pollicis brevis and median alone to the opponens pollicis.

    THUMB ABDUCTION is by radial and median innervation.

    THUMB ADDUCTION is by ulnar to the ADDUCTOR POLLICIS and it is this innervation that is commonly monitored for adequacy of neuromuscular blockade.

    OPPOSITION of the THUMB and little finger is primarily by median innervation but also somewhat reliant on ulnar innervation to the opponens digiti minimi.


    RADIAL nerve C5-8
    MEDIAN nerve C6-T1
    ULNAR nerve C8-T1

    PALMAR innervation to the lateral portion of the hand is by the median nerve while the ulnar nerve innervates the palmar fifth and half of the fourth digit.

    DORSAL innervation is by the superficial radial nerve excluding the medial fingertips which are innervated by the median nerve and the lateral fifth and half of the fourth digits that are innervated by the ulnar nerve.


    Bradycardia is often associated with sinus node dysfunction and may include sinus bradycardia, sinus pause, sino-atrial block and sinus arrest. These rhythms may or may not be symptomatic and may result in the emergence of alternative pacemakers. Anesthetic intervention, including medications, laryngoscopy and the onset of spinal anesthesia, may create the autonomic imbalance which is often responsible for these changes.

    SYMPTOMATIC bradycardia is manifested as lightheadedness, dizziness, near or frank syncope, manifestations of cerebral ischemia, limitations in exercise tolerance, DOE and CHF. A commonly overlooked cause of reduced CORONARY perfusion is bradycardia which encourages diastolic runoff and may result in a wide pulse pressure and reduced DBP. In addition, the increased SV required with bradycardia will increase volume and pressure and further reduce CPP.

    A number of DRUGS are noted to have an effect on the sinus node or perinodal tissue causing bradycardia.

    calcium channel blockade
    induction agents
    steroid neuromuscular blockers
    H2 blockers

    THERAPY for bradydysrhythmias should be dictated by the clinical circumstances. Should hemodynamic compromise or hypoperfusion (such as ECG evidence of ischemia) occur, treatment is indicated.

    ß1 agonists (isoproterenol) and antimuscarinic agents (atropine, glycopyrolate) can increase the rate, however, atropine may be of only limited value in managing hemodynamically significant dysrrhythmias in the setting of sick sinus syndrome and calcium channel or ß-blocker toxicities.

    Although the use of calcium chloride (100-500 mg IV) has been noted to be of some value in reversing the peripheral dilation associated with CCB toxicity, HR increases may not be observed. Most recently, calcium with digoxin was noted to be more effective in raising SBP and preventing malignant arrhythmias than calcium alone. This may prove to be the combination of choice in such CCB toxicities.

    In an provocative case report, it has been suggested that CCB toxicity may also be treated with benzodiazepine antagonists. Noting that myocardial benzodiazepine receptor ligands exist and appear to affect calcium-channel activity (consistent with a report of a benzodiazepine overdose resulting in first degree AV block) the authors suggested that FLUMAZENIL may be a useful adjunct in the management of CCB toxicity. Further work will need to be done to demonstrate the effectiveness of this treatment modality.

    In the setting of beta blocker toxicity, GLUCAGON (IV dose of 2-4 mg) may be the inotrope of choice, although severe nausea and emesis may occur and protection against aspiration should be instituted.

    Should it be necessary, cardiac pacing is effective and may be initiated by transesophageal or transvenous routes. Patients with preexisting bradydysrhythmias associated with sinus node dysfunction may be best managed by the insertion of a prophylactic temporary pacemaker prior to surgery.


    The ACLS treatment sequence for symptomatic bradycardia is listed in order of increasing clinical severity. For severly symptomatic patients, multiple modalities are required simultaneously – atropine, TCP, catecholamine infusions and alerting cardiology for the need for transvenous pacing.

    1) atropine at 0.5-1 mg IV
    2) transcutaneous pacing
    3) dopamine at 5-20 mcg/kg/minute
    4) epinephrine at 2-10 mcg/minute
    5) isoproterenol at 2-10 mcg/minute

    ATROPINE is not indicated for patients with transplanted hearts, third degree AV block and wide-complex ventricular escape beats or Mobitz type II second degree AV block. Atropine may accelerate atrial rates and produce increased AV nodal block in those with type II second degree or third degree AV blocks. Atropine should also be used cautiously in those with suspected acute MI as atropine may exacerbate ischemia or induce VT or VF in these patients.

    The maximum dose is 2 mg for the typical 70 kg patient.

    TRANSCUTANEOUS PACING should not be delayed for the symptomatic patient and is more desirable in the patient with blocks at or below the His-Purkinje level. Analgesics or sedation may be required for the patient to tolerate TCP.

    DOPAMINE infusions are quickly titrated once maximum doses of atropine are infused.

    EPINEPHRINE infusions are the drug of chioce for the patient with severe bradycardia and hypotension. Epinephrine is also indicated when higher doses of dopamine are not effective. One mg in 500 mL of NS produces a concentration of 2 mcg per mL.

    ISOPROTERENOL should be used very carefully in any patient. At low doses it is considered a class IIb (possibly helpful) intervention. Isoproterenol is generally considered only a temporizing measure until TCP or transvenous pacing is available. As a vasodilator, isoproterenol is relatively contraindicated in the hypotensive patient which includes most patients with bradycardia.


    Electrical silence by EEG is established in addition to one or more tests to confirm the absence of brain stem reflexes (pupillary, vestibulo-ocular, corneal and gag reflexes). The limbs are most often flaccid although movement may occur through spinal cord reflexes in response to pain.

    The APNEA test will demonstrate that there is no respiratory effort with an arterial CO2 of at least 60 mmHg.

    Body temperature must be maintained above 32 degrees and there must be no possibility of drug intoxication or neuromuscular blockade (which is occasionally confirmed by peripheral nerve stimulation).


    Plasma concentrations of BNP are markedly higher in patients with clinically diagnosed CHF (including patients with right heart failure due to cor pulmonale) compared to those without CHF (mean 675 versus 110 pg/mL). Intermediate values were found in the patients with baseline LV dysfunction without an acute exacerbation (346 pg/mL). A plasma BNP over 100 pg/mL diagnosed CHF with a sensitivity, specificity and predictive accuracy of 90, 76 and 83% respectively. Choosing values of 125 or 150 pg/mL decreased sensitivity, increased specificity and did not change overall predictive accuracy. The predictive accuracy of plasma BNP for CHF was equivalent to or better than other parameters such as cardiomegaly on CXR, history of CHF or rales on examination. It was found that plasma concentration of BNP correlated with NYHA functional class, ranging from 244 to 817 pg/mL for class I to IV (Arch Int Med 2004 and J Postgrad Med 2003).

    Elevations in plasma BNP can establish the presence of CHF due to diastolic dysfunction with similar accuracy to systolic dysfunction. However, the values do not differentiate between systolic and diastolic dysfunction. Based upon these data, BNP was approved by the FDA as an aid for CHF diagnosis. Plasma BNP concentrations are also elevated in patients with pulmonary hypertension and right ventricular dysfunction. In such patients, they correlate positively with mean pulmonary artery pressure, total pulmonary resistance and right ventricular mass. A high level of plasma BNP and a further increase in plasma BNP during follow-up may have a strong, independent association with increased mortality in patients with primary pulmonary hypertension. The cost for a BNP test is about $20 and it has been suggested that measurement of BNP levels should be part of the diagnostic approach to patients with CHF.

    The plasma concentrations of BNP fall after effective pharmacologic therapy of CHF. The magnitude of this effect was illustrated in a report of 102 patients with severe CHF who were studied at baseline and three months after optimized medical therapy including ACE inhibitors, beta blockers, and digoxin. Optimized medical therapy was associated with significant reductions in plasma BNP (917 at baseline to 285 pg/mL) levels. These findings suggest that measurement of plasma BNP may be helpful in titrating therapy. This issue was addressed in another trial of 69 patients with impaired left ventricular function and clinical CHF who were randomly assigned to medical treatment guided by plasma BNP concentrations (goal less than 200 pmol/L) or standard clinical assessment. At six months, a first cardiovascular event occurred less frequently in those undergoing BNP guided therapy (27 versus 53% for clinical assessment).


    Primary brain tumors arise from CNS tissue and account for almost one half of all cases of intracranial neoplasms. The remainder of brain neoplasms are caused by metastatic lesions. In adults, two thirds of primary brain tumors arise from supratentorial structures, while in children, two thirds of brain tumors arise from infratentorial. Gliomas, metastases, meningiomas, pituitary adenomas and acoustic neuromas account for 95% of all brain tumors.

    The cumulative effects of tumor invasion, peritumor edema and hydrocephalus may elevate ICP and impair cerebral perfusion. Intracranial compartmental rise in ICP may provoke shifting or herniation of tissue under the falx cerebri, through the tentorium cerebelli, or through the foramen magnum.

    Most primary brain tumors do not metastasize. Of those neural element tumors that do, intraparenchymal metastasis generally precedes distant hematogenous dissemination via the arterial system.



    Bretylium was once a recommended Class IIb (acceptable and useful, fair to good evidence but not strongly favored by weight of evidence and expert opinion) therapy following defibrillation for refractory VF and pulseless VT. Bretylium has now been OMMITTED from this algorithm.

    In part, this stems from the natural sources for bretylium being almost exhausted, the limited information confirming its benefit, and the high incidence of side effects, in particular hypotension, in the postresuscitation setting.

    In lieu of bretylium, AMIODARONE (another Class IIb drug) is one of several recommended antiarrhythmic medications for the patient with refractory VF or pulseless VT.


    Bromocriptine is an ergot derivative that directly stimulates the dopamine 2 receptors but is an antagonist at the dopamine 1 receptor. Bromocriptine is effective in the treatment of acromegaly because of a paradoxical inhibitory effect of dopamine agonists on secretion of GH. Bromocriptine also suppresses the excess prolactin secretion from a prolactinoma (the most common of the hypersecretory pituitary tumors) and that which is often associated with GH hypersecretion or any of the pituitary tumors. By what is known as the stalk effect, various pituitary tumors may prevent dopamine from traversing the stalk which is necessary for the inhibtion of prolactin secretion from the adenohypophisis.

    SIDE EFFECTS include auditory hallucinations, hypotension and dyskinesia. The doapmine agonists may also cause pleuropulmonry fibrosis occasionally with pleural effusions.


    The endobronchial blocker is useful for one lung ventilation in patients for which postoperative ventilation is anticipated as an alternative to the Univent tube. With certain endobronchial blockers including the Arndt endobronchial blocker, CPAP may be applied through the blocker using a specialized adaptor.

    In order to perform this technique with a conventional Fogarty catherter, the bronchus on the operative side is initially intubated with an ETT. A left main stem intubation can occasionally be performed by turning the patients head to the estreme right during advancement of the ETT. A guide wire is then advanced into that operative bronchus through the ETT, which is then removed. The blocker is advanced over the guide wire into the bronchus, after which another ETT is reinserted into the trachea alongside the blocker catheter. Under fiberoptic visual guidance the catheter balloon is then positioned in the proximal mainstem bronchus.

    This traditional technique places the endobronchial catheters outside of the ETT. The use of adapters provided in the Arndt kits allow the administration of oxygen and ventilation during the placement of a bronchial blocker through an indwelling ETT. The loop of the blocker is positioned around the FOB ideally before attaching the adapter to the in situ ETT. This new technique diminishes the risk of hypoxemia during blocker placement and, with fiberoptic guidance, repositioning of the blocker may be performed during surgery.

    The 9 FRENCH adult blocker is most optimally placed with the use of a pediatric bronchoscope with an outer diameter of 3.0 to 3.5. An ETT sized 8.0 to 8.5 is ideal but tubes as small as 7.5 may be utilized to accomadate both the bronchoscope and the blocker. The high-volume, low-pressure balloon is designed to accommodate up to 15 mL of air but typically 5-8 mL is all that is required.

    The 5 FRENCH pediatric blocker is optimally placed with a smaller bronchoscope with an OD of 1.8 to 2.0 and may be placed through a tube as small as 4.5 to 5.0.

    CPAP can be applied through the central lumen of the blocker using an adapter included in the blocker kit. Any conventional CPAP circuit can then be utilized.


    LF-P 2.2 3.0 ETT
    LF-DP 3.1 4.0 ETT
    3.5 4.5 ETT
    LF-GP 3.8
    LF-2 4.0 5.0 ETT

    The Olympus LF-P (ultrathin bronchoscope) is a 2.2 mm OD bronchoscope (without a suction port) that is compatible with endotracheal tubes as small as 3.0 mm ID and double lumen tubes as small as 28 French. The LF-P may also be used in the pediatric sized Univent tubes (3.5 and 4.5 ID). The working length of the LF-P is 60 cm.

    The Olympus LF-DP is a self-powered 3.1 mm OD bronchoscope with a 1.2 mm suction port that is compatible with endotracheal tubes as small as 4.0 mm ID and double lumen tubes as small as 32 French. The working length of the LF-DP is 60 cm.

    The 3.5 mm OD bronchoscope may be used in endotracheal tubes as small as 4.5 mm ID.

    The Olympus LF-2 is a 4.0 mm OD bronchoscope with a 1.5 mm suction lumen that may be used in endotracheal tubes 5.0 ID or larger, 37 French or larger double lumen tubes and all of the adult sized Univent tubes (greater than 4.5 ID). The working length of the LF-2 is 60 cm.

    The depth of field for most of the Olympus bronchoscopes ranges from 3-50 mm.


    The INCIDENCE of intraoperative bronchospasm is said to be between 0.8 and 25% in patients with asthma and between 0.16 and 6% in those without the diagnosis.

    Factors that DO NOT correlate with risk include sex, smoking history, emergency surgery and presence of upper respiratory infection.

    The diagnosis of bronchospasm in the OR is often a diagnosis of exclusion. All other causes for increased airway pressures should be considered (DDX – HIGH AIRWAY PRESSURE).

    Nonbronchospastic wheezing may be caused by obstruction of the endotracheal tube, negative pressure expiration, tension pneumothorax, pulmonary edema, pulmonary aspiration and pulmonary embolism.

    TREATMENT Typically administered inhalation therapy includes albuterol 2.5 mg and ipratroprium 500 mcg. Ipratroprium is generally more effective for the patient with emphysematous disease. Commonly used steroid regimens include SoluMedrol at 2 mg/kg IV or IM and continued at 0.5-1 mg/kg. Alternatives to conventional therapy includes 0.3 mg SQ epinephrine (0.3 mL of 1:1000), magnesium sulfate (2 grams over 20 minutes), helium at concentrations of 60 to 80% and ketamine (with infusion doses from 1-2.5 mg/kg/hour). IV lidocaine increases airway tone and may worsen bronchospasm (AA May 2007).

    See more information in the 2001 IARS review lectures.


    Brugada syndrome is characterized by a distinctive EKG pattern (RBBB and ST segment elevation in precordial leads) and a high risk of cardiac arrest and malignant dysrhythmia. The genetic basis is a molecular defect of the cardiac Na channel and the pattern of inheritance is AD. Many factors during GA (medications, bradycardia, temperature changes) can precipitate malignant dysrhythmias in these patients.

    Many drugs can have proarrhythmic effect. In patients with Brugada syndrome, Class I antiarrhythmic sodium channel blockers (specifically procainamide) can induce ST segment elevation because they interact directly with the receptors affected by the syndrome. The muscarinic and alpha receptor agonists cause an increase in ST segment elevation in the general population and in many cases of Brugada syndrome. Psychotropic drugs also have electrophysiologic effects: amitriptyline induces cardiac sodium channel blockade but also causes the reduction in the inward sodium current and a prominent outward current. Phenothiazines modify the action potential of cardiac myocytes, an effect similar to that reported for quinidine. Fluoxetine depresses sodium and calcium channel activation producing a shortening in action potential duration. The final effect of all these drugs is a reduction in action potential duration.

    Recently it has been reported that epidural bupivacaine administration could induce the ECG characteristic pattern of Brugada syndrome. Bupivacaine binds to the sodium channel and produces a depression of the rapid phase of depolarization in Purkinje fibers. Volatile anesthetics can also interfere with QT interval in patients without Brugada syndrome. A prospective double-blind randomized study found a significant increasing QT interval during induction with isoflurane, no changes with sevoflurane and significant shortening with halothane.

    The ECG pattern should alert the clinician to suspect possible Brugada syndrome. If this finding is confirmed further investigation is justified. There is a degree of genetic heterogeneity and some patients affected by the syndrome do not show the typical ECG pattern. Follow-up data indicate that the risk of ventricular tachyarrhythmia is minimal in the absence of a resting ECG abnormality and the absence of adverse events reported during anesthesia should be reassuring. For these patients many situations that could precipitate ventricular fibrillation happen during anesthesia. Even if the few reports did not detect any arrhythmic problem, it is difficult to draw a firm conclusion, especially because of the heterogeneous nature of the mutation leading to Brugada syndrome. Risk stratification criteria currently do not allow identification of patients who run the risk of malignant arrhythmias and surgical patients probably need different criteria for this stratification. It is our opinion that with an adequate anesthetic plan the risk during major or minor procedures should be the same. During major procedures the risk may be increased for the longer procedure time.

    Even if there were no reported problems during surgery, general, regional or local anesthesia should be carefully managed and should include monitoring ST segment on ECG, measuring invasive arterial blood pressure and body temperature, keeping an external defibrillator ready in the operating room and, if possible, avoiding drugs that could trigger arrhythmias. Anesthesiologists should consider the risk/benefit ratio of arterial cannulation, especially for short surgery procedures or for regional and local anesthesia.


    CAUDAL blocks are rarely performed in patients older than 10 years of age with doses from 37.5-150 mg (15-30 mL of 0.25 or 0.5% solution). Children receive 0.4-0.7-1.25 mL/kg (corresponding to L2-T10-T7 levels of anesthesia).

    BRACHIAL PLEXUS blocks through various techniques require 75-250 mg (30-50 mL of 0.375 to 0.5% solution). Children require 0.5-0.75 mL/kg with higher doses (over 2 mg/kg) requiring epinephrine to decrease systemic toxicity.

    STELLATE GANGLION blocks require 10-20 mL of 0.25% solution (25-50 mg) with or without epinephrine.

    PSOAS OR LUMBAR PLEXUS blocks generally require 25-30 mL of 0.25-0.5% solution.

    EPIDURAL BOLUS doses are given in doses ranging from 50-150 mg (0.175 to 0.75% solution). Children may be bolused with doses between 0.5-2.5 mg/kg.

    EPIDURAL INFUSION are generally given at 6-12 mL per hour (0.0625 to 0.125% solution with or without narcotics). Childrens infusions range between 0.2-0.35 mL/kg/hour.

    SPINAL anesthesia requires doses between 7-29 mg (0.5 or 0.75%). Children may be given 0.5 mg/kg with a minimum of 1 mg. Baricity of hyperbaric solution is 1.0227 and that of isobaric solution is 0.9988.

    For THA, it is common to use up to 15 mg with 20 mcg fentanyl and up to 0.3 mg of Duramorph – the isobaric form will allow for injured limbs to be non-dependent during injection and will limit the cephalad spread of the subarachnoid block.

    MAXIMUM DOSE is at 2 mg/kg without epinephrine (approximately 175 mg) or 2-3 mg/kg with epinephrine (about 225 mg).


    BUPIVICAINE is an amino amide local anesthetic with pKa of 8.1 and a commercial preparation pH of 4.5 to 5.5. It is a slow onset, long duration and highly toxic local anesthetic agent. The TOXIC DOSE is thought to be approximately 2.5-3 mg/kg. The observed toxicity is probably also related to use of epinephrine.

    CLINICAL uses include infiltration at the 0.25% concentration with the duration of action between 2-4 hours or greater.

    EPIDURAL analgesia and anesthesia are performed between a 0.25% and 0.75% concentration with 2-5 hour duration of action. At 0.25% the agent is uniquely suited to obstetric analgesia as it provides intense analgesia with minimal motor block, allowing the parturient to be active during the second stage of labor. Epidural anesthesia is performed at the 0.5% concentration as with all bupivacaine blocks, intensity of motor block is variable. Some practitioners use the 0.75% concentration to provide a more intense motor block for certain types of procedures.

    SPINAL anesthesia is performed with the 0.75% concentration combined with 8.75% dextrose for hyperbaric spinal anesthesia and is also performed with isobaric or plain bupivacaine in concentrations ranging from 0.125% to 0.75% with satisfactory results. It should be noted that this agent is not approved in the United States for isobaric spinal anesthesia use although the isobaric concentration is commonly utilized to achieve greater cephalad spead of the subarachnoid block.

    PERIPHERAL conduction block is performed with the 0.25% to 0.50% concentrations, depending on the amount of motor block sought.

    The CV toxicity of bupivicaine is related to the HIGH PROTEIN BINDING and lipid solubility of the agent. The results of this combination is a very limited prodrome with very short interval between first signs of CNS disturbance and massive CV collapse. This CV collapse is complicated by the specific lipid solubility in the tissue of the conduction system with a reentrance activation associated with intractable VT and VFIB. These arrhythmias are resistant to the use of lidocaine and cardioversion. Success has been observed with BRETYLIUM, AMIODARONE and insulin glucose therapy. Prolonged CPR is often necessary and CPB has been instituted to salvage the patient during the metabolism of the agent.

    INFANTS may be at increased risk for toxicity because of lower levels of binding proteins and diminished clearance.

    The 0.75% concentration is not used in OBSTETRICS because of the associated mortality with the use. It is clear that the toxicity associated with bupivacaine is magnified by respiratory acidosis, hypoxia and the associated effects of progesterone.


    THIOPENTAL for burst suppression or isoelectricity requires bolus doses of 5-10 mg/kg and infusions of 4-6 mg/kg/hour.

    PROPOFOL initial 1 mg/kg, followed by 0.5 mg/kg if needed and maintenance of suppresion with 50-70 mcg/kg/min infusion.

    The classic EEG pattern shows 4 second epileptiform inerval followed by a 10 second interval of quiesence.

    Butorphanol is a synthetic agonist-antagonist with analgesic potency 3.5-7 times that of morphine or 30-40 times that of meperidine. Butorphanol has a ceiling effect for respiratory dpression and analgesia at high doses over 30-60 mcg/kg.

    DOSING by IV administration is between 0.5-2 mg (0.01-0.04 mg/kg) every 3-4 hours. Common IM doses range between 1-4 mg. Nasal dosing is at 1-2 mg every 3-4 hours or 20-25 mcg/kg for pediatric patients. Epidural bolus dosing is between 1-2 mg (0.02-0.04 mg/kg). The medication is supplied at either the 1 or 2 mg per milliliter concentration.

    PHARMACOKINETICS Duration of action is between 2-4 hours after IV dosing, 3-4 hours after IM or epidural dosing and 4-5 hours after nasal administration.

    PHARMACODYNAMICS Analgesic doses increase sytemic blood pressure, pulmonary blodd pressure and cardiac output.

    Butyrophenones are one category of antipsychotic medications that include haloperidol and droperidol. The medications are contraindicated in patients with Parkinson’s disease.


    Several 1970-80 randomized trials demonstrated that surgical therapy may be preferable to medical therapy in patients with stenosis of the left main coronary or in patients with three-vessel disease and left ventricular dysfunction, but there appears to be no clear benefit of surgery for other patients with CAD.


    Possible advantages of OPCAB surgery are more likely to be found in high-risk patients with significant comorbidities. Mortality appears to be lower in some series, but not all. In elderly patients, results are improved with OPCAB surgery: mortality and postoperative complication rates are lower; the incidence of a low postoperative CO is reduced from 32% to 10%; and strokes are reduced from 9% to 1%. Emergency surgery or surgery performed on patients with impaired ventricular function have shown encouraging results. Available reports show only some trend toward possible renal protection, but there is probably no difference for patients on dialysis. The results concerning IDDM patients show no improvement in comparison with conventional surgery (BJA 2004).

    Surgical access to the LAD is relatively easy but, in order to work on the posterior or lateral walls, the heart must be lifted and tilted out of the pericardial cradle. The heart is tilted in a vertical position with the apex at its zenith; the atria are then situated below the corresponding ventricles, and the blood must flow up into the ventricular cavities. Filling pressures measured in the atria are increased much more than the corresponding ventricular EDP, and must be maintained at a higher than normal level to maintain ventricular filling. The most profound disturbances are observed during lateral wall exposure for anastomosis on the circumflex artery because the heart is then lifted more extensively than for surgery on the LAD. A vertical position of the heart induces distortions of the mitral and tricuspid annuli, as the intracardiac structures are folded primarily at the AV groove. This may result in significant MR and TR. The sudden appearance of large v waves (30 mmHg), without signs of LV failure illustrates this mechanism. To improve surgical access to the lateral and posterior walls of the heart, the operating table is tilted to the right or positioned in the Trendelenburg position, respectively. Leg elevation appears the most efficient technique to improve preload. CO is increased with leg elevation, but not in the head-down position.

    Coronary cross-clamping to ensure bloodless anastomotic conditions results in brief periods of myocardial ischaemia, usually manifested by ST-segment elevation and new RWMA on echo. Severe ischemia during clamping of a non-occlusive RCA can result in dangerous arrhythmias such as complete AVB attributable to interruption of the blood flow in the AV node artery. Techniques are available in order to reduce the consequences of coronary interruption: improvement in myocardial oxygen balance, ischemic and pharmacological preconditioning, pharmacological prophylaxis and surgical shunting. It is advisable to keep a MAP 70 mmHg allowing a safety margin above the critical CPP by administration of a vasopressor like phenylephrine or NE. The aim is an overall equilibrium, where a low CO is tolerated in so far as it meets the demands as shown by an SvO2 > 60%. In order to prevent increased myocardial oxygen demand when ischemia is threatening, ß stimulants are best avoided until complete revascularization. A CCB such as diltiazem may has some theoretical advantages over ß-blockers in the intraoperative period. It has been shown that, for the same decrease in HR, diltiazem lowers PAP, whereas esmolol tends to increase it. In addition to reducing AV conduction and HR as ß blockers do, CCB offer the advantage of inducing vasodilation in arterial conduits. Patients suffering from CAD are at particular risk of ischemia when their MAP is less than the HR (the Buffington ratio).

    The targeted ACT is usually kept at 250–300 as in major vascular surgery. This is reached by administration of heparin 100–200 units/kg before section of the internal mammary artery. Heparin reversal with protamine is optional and some have reported a hypercoagulable state after off-pump procedures.


    The national mortality rate from CABG in the US was approximately 3% in 1998. The mortality was higher if the surgery was accompanied by a valve replacement (7% with AVR and 12% with MVR), if the surgery was emergent (6% and 13.5% for repeat emergent), for repeat surgeries (5.4% for elective repeat), for females (3.9 versus 2.3%) and for the elderly (4.1% for those in their seventies and 6.7% for those in their eighties). It should be also noted that for patients with a major clinical predictor of cardiac risk such as unstable angina or evolving MI, the cardiac surgical intervention is likely to be performed emergently or urgently, thus raising the mortality and morbidity of CABG.

    Several retrospective reviews indicate that those who survive CABG may have a reduced cardiac risk at the time of a subsequent noncardiac surgery and that this reduced risk may be comparable with that of those with no CAD. In the largest such review, Eagle et al showed from a review of 1961 patients in the Coronary Artery Surgery Study database that prior surgical revascularization is associated with a lower MI rate (0.8 versus 2.7%) and death rate (1.7 versus 3.3%) in subsequent high-risk noncardiac surgeries, compared with medical therapy alone.


    Doses of CAFFEINE at 10 mg per kg given immediately after induction will decrease risks of brief and prolonged apnea during the recovery period for premature infants. In general, caffeine is recommended for infants less than 44 WEEKS postconception though many recommend monitoring all former premature infants at (1) less than 50 weeks postconception for a minimum of 24 hours following general anesthesia and (2) less than 60 weeks postconception for a minimum of 12 hours following general and regional anesthesia.

    Caffeine is provided free of sodium benzoate as CAFCIT which is dosed at 1 mL per kg. One mL contains 10 mg of caffeine base or 20 mg of caffeine citrate.

    The half-life is inversely related to gestational age. The half-life in the term neonate is 3-4 days while the half-life in the nine month old and adult is approximately 5 hours.

    A Cochrane Review found some evidence that postoperative caffeine reduces apnea, bradycardia and cyanosis after anesthesia but the importance of this is unclear.


    The CCB are divided into the dihydropyridine derivatives (amlodipine, felodipine, isradipine, nicardipine, nifedipine, nimodipine) and the non-dihydropyridine medications (diltiazem, verapamil). The dihydropyridine drugs are associated with reflex tachycardia, pedal edema and gingival hyperplasia. The non-dihydropyridine drugs are associated with AV conduction delay (especially in conjunction with beta-blockers), worsening LV systolic function, gingival hyperplasia and increased levels of digoxin, sulfonylureas and theophylline.


    decreased MAP N = V = D
    tachycardia N > V > D
    prolonged PR D > V > N
    decreased CO V = D > N
    increased PAOP N = V = D
    decreased PVR N > V = D

    Recall that we are fond of saying that most of the volatile agents behave as nifedipine. Enflurane behaves as diltiazem and halothane behaves as verapamil.

    INDICATIONS The drugs may be used to treat SVT, rapid ventricular response to atrial dysrhythmias, essential HTN, angina, coronary and peripheral vasospasm. Nimodipine may be useful in the treatment or prophylaxis of cerbral vasospasm.

    In the OR setting, diltiazem is most often utilized though verapamil has the advantage of a slighty shorter duration of action. Nifedipine is known to increase mortality after MI and should not be used for its antihypertensive effects in the perioperative setting.

    TOXICITY may be treated with mixed alpha and ß agonists, pacemaker placement, calcium infusions, flumazenil or insulin euglycemia.

    CCB may potentiate the effects of SCh and NDMB. Antagonism of blockade may also be impaired due to diminished release of acetylcholine.


    DOSING Replaced at 500-1000 mg bolus doses (maximum of 100 mg per min). Given for hyperkalemia (WITH cardiovascular compromise) as 1000 mg over three minutes. The pediatric dose is 10-25 mg per kg. Infusions at the conclusion of cardiopulmonary bypass may range from 5-20 mg/kg/hour. Calcium chloride 10% contains 27 mg (1.36 mEq) of elemental calcium per mL.

    PHARMACOKINETICS Onset of inotropic action begins within 30 seconds and duration of action is between 10-20 minutes.

    INTERACTION/TOXICITY Calcium chloride should not be followed by sodum bicarbonate or given with blood products because of the risk of crystallization.


    DOSING Replacement at 500-2000 mg IV (repeat every six hours as needed). Pediatric dosing at 200-500 mg/kg/day either as a continuous infusion or divided QID. 10% calcium gluconate contains 9 mg (0.46 mEq) of elemental calcium per mL and is therefore about one third as potent as calcium chloride.


    Calcium gluconate is less irritating to the veins (because of a lower osmolarity) and may be preferred if infusions must be given by peripheral vein. Provides three times LESS calcium than an equal volume of 10% CaCl. It is less often used for treatment of hyperkalemia.


    Both absorbents chemically neutralize CO2 (an acid after combining with water to form carbonic acid) by reaction with a base. Both are important in the humidification of the anesthesia circuit.

    active BaOH2 NaOH
    CaOH2 80% 94%
    BaOH2 20%
    NaOH 5%
    KOH 1%
    density high low
    efficiency less more
    water yes none
    regenerate none yes

    SODA LIME is composed of 4% sodium hydroxide, 1% potassium hydroxide, 14-19% water, 0.2% silica and 80% calcium hydroxide.

    CO2 + H2O <> H2CO3

    H2CO3 + 2NaOH <>
    Na2CO3 + 2H2O + heat

    Na2CO3 + Ca(OH)2 <>
    CaCO3 + 2NaOH

    Soda lime contains silica to give hardness to the granules and minimize formation of alkaline dust which is an irritant to the airways. Baralyme does not need silica because barium hydroxide is inherently harder than sodium hydroxide.

    Sevoflurane is unstable in soda lime, producing COMPOUND A (lethal at 130-340 ppm and capable of causing renal injury at 25-50 ppm in rats). Compound A concentrations of 25-50 ppm are easily achievable in normal clinical practice.

    BARALYME is a more simple compound composed of 20% barium hydroxide and 80% calcium hydroxide.

    Ba(OH)2 + 8H20 + CO2 <>
    BaCO3 + 9H2O + heat

    9H2O + 9CO2 <> 9HCO3

    9H2CO3 + 9Ca(OH) <>
    CaCO3 + 18H2O + heat

    Barlyme does not contain water because its water is derived from the bound water crystallization in the octahydrate salt of the barium hydroxide. Baralyme gives more reliable performances in dry environments and is generally thought to be more stable than soda lime.

    CARBON MONOXIDE is produced by baralyme more readily than with soda lime. It is more easily produced with
    D > E > I > H > S. CO production is more pronounced in dry absorbent and FGF should be turned off between cases to prevent excessive drying.


    Carbon dioxide is transported in the blood primarily as CARBONIC ACID. 95% of the CO2 enters the RBC where 30% is bound to proteins as carbamino compounds and 65% is hydrolyzed to carbonic acid. The other 5% is transported as dissolved CO2. The normal CO2 tension of the venous return is 46 mmHg.

    A small amount of CO2 is bound to hemoglobin as carboxyhemoglobin. The HALDANE EFFECT describes the greater affinity of CO2 and Hgb in the presence of lower oxygen tension. Deoxygenated hemoglobin has a higher affinity for the H ions produced when carbonic acid dissociates AND a greater propensity to form carbaminohemoglobin.


    Carbon monoxide exerts its toxic effects through tissue hypoxia. The hemoglobin molecule has an affinity for CO that is 240 times greater than its affinity for oxygen. CO and Hb form carboxyhemoglobin, which is incapable of carrying oxygen. Carbon monoxide also shifts the oxyhemoglobin dissociation curve to the LEFT by interfering with the release of oxygen that is already associated with hemoglobin.

    CO further potentiates tissue hypoxia by poisoning the cytochrome oxidase system leaving the cells with nothing more than anaerobic metabolism.

    SYMPTOMS depend on the amount of carboxyHb present and the patient’s activity level, tissue oxygen demands and Hb concentration. Exposure to low concentrations of CO causes irritability, altered visual and motor skills, headache, nausea, vomiting and predisposes to angina.

    Severe poisoning may result in seizures, coma, respiratory failure and death. The classic cherry red color results from the bright red cast of carboxyHb. In patients with severe poisoning, however, cyanosis may predominate. The diagnosis is confirmed with a %COHb level. Exogenous CO poisoning should be considered when the %COHb level is greater than 3%. Measurements of PaO2 may be normal.

    TREATMENT consists of removing the offending agent and providing a high oxygen enriched environment. The half-time of CO elimination can be shortened from 5 hours to 40-90 minutes by hyperventilation of the lungs with 100% O2. Ventilation may require mechanical support.

    Other treatment modalities include hyperbaric O2, transfusion, diuretics and steroids for the treatment of complicating cerebral edema.

    The application of HYPERBARIC therapy rapidly dissociates the carbon monoxide and hemoglobin molecules. Classic studies frequently quoted note that the half-life of COHb decreases from 5 hours while breathing room air, to 90 minutes under normobaric 100% oxygen and 23 minutes under hyperbaric 100% oxygen at 3 ATA.

    CO can be formed through a reaction of isoflurane, desflurane and enflurane with DRIED carbon dioxide absorbents (baralyme produces more CO than soda lime).


    HEMABATE is the tromethamine salt of the methyl analogue of naturally occurring prostaglandin F2 alpha. The drug stimulates uterine contractions at all stages of pregnancy (in contrast to oxytocin). The use of carboprost is usually limited to those patients failing to respond to oxytocin, uterine massage and the ergot methylergonivine.

    DOSING by deep IM injection is at 250 mcg. This dose may be repeated at 15-90 minute intervals if necessary.

    The drug should be used with caution for patients with ASTHMA, hypertension, cardiovascular, pulmonary, renal or hepatic disease.


    Carcinoid tumors are the most common neoplasms of the small intestine (may mimic appendicitis and may occur in the appendix) but may also occur in the bronchi. DX is supported by increased urinary secretion of 5-hydroxyindoleacetic acid which is the the degradation product of serotonin.

    Carcinoid SYNDROME is present when vasoactive substances (serotinin, kallikreins, histamine) are released from the cells of carcinoid tumors. The syndrome develops in only 5% of those with carcinoid tumors. The syndrome does not develop from tumors of the appendix.

    SYMPTOMS of carcinoid syndrome include bronchoconstriction, tricuspid regurgitation and pulmonary stenosis, PAC and SVT, cutaneous flushing or cyanosis, chronic abdominal pain, diarrhea, hepatomegaly, hyperglycemia and decreased plasma albumin.
    Patients with metastatic liver lesions often are more symptomatic.

    ANESTHETIC management may include the preoperative use of a drug which blocks the effects of vasoactive substances such as OCTREOTIDE or somatostatin. H1 and H2 blockers may be considered for symptoms. Ondansetron has been useful for GI symptoms alone.

    Hypotension may stimulate the release of these vasoactive substances and it is wise to avoid deep anesthesia, drug-induced histamine release and sympathetic blockade. It is also wise to avoid additional sympathetic stimulation as catecholamines are known to activate the kallikreins.


    During DIASTOLE (following S2), the ventricles fill by passive flow followed by a more vigorous, muscular ejection. The PASSIVE stage occurs quickly to distend the ventricular walls, causing a vibration which results in an S3. The ACTIVE stage occurs so late in diastole that it is often confused with a split S1 (asynchrony of the systolic closure of the mitral and tricuspid valves). The ACTIVE phase tends to vibrate the valves, papillae and ventricular walls, causing an S4. Both S3 and S4 tend to be quiet and difficult to hear in the otherwise normal patient.

    The presence of an S3 often denotes a loss of ventricular compliance (hypertensive disease and CAD) or an increase in stroke volume observed in high output states (profound anemia, pregnancy and thyrotoxicosis). The presence of an S3 may be the earliest clue of LV failure and an indication of possible postoperative complications in the setting of noncardiac surgery.

    An S4 is more audible when LV filling is impaired as with aortic stenosis, HTN, myocardial ischemia and almost all instances of acute MI. One study concluded that a clearly audible S4 detected 1 month after the onset of an MI, increased the risk of adverse cardiac events, including death, worsening angina, heart failure and repeat MI.


    Samuel Levine developed the classification system for grading murmurs over 60 years ago. It is easier to discriminate systolic murmurs than diastolic ones.

    1/6 barely audible
    2/6 soft but readily heard
    3/6 prominent but not loud
    4/6 loud, associated with a thrill
    5/6 audible with a stethoscope partially off the chest, may have a palpable thrill
    6/6 extremely loud, audible with a stethoscope removed from the chest, may have a palpable and visible thrill

    Murmurs can also be classified in regard to their timing and duration, pitch, intensity, pattern, quality, location, radiation and variation to respiratory phases.

    INNOCENT or functional murmurs often occur in young healthy people and are usually midsystolic, no louder than a grade 2/6 or 3/6, of medium pitch, blowing, brief and often accompanied by the splitting of the S2. Such murmurs are best heard in the recumbent position and often disappear when the patient sits or stands. Two common innocent murmurs:

    1) second LIS murmurs may be caused by vibrations within the main pulmonary artery
    2) apex and LLSB murmurs may be caused by vibrations of the pulmonary leaflets

    Associated findings often help distinguish an innocent from a pathologic murmur. Single or multiple clicking sounds can indicate pathologic stenotic or prolapsing valves. Pulmonic stenosis gives a sharp early systolic click at the second left interspace. A sharp click at the RUSB can indicate aortic stenosis. A click at the cardiac apex that occurs mid to late systole is common with MVP.

    Remember that all murmurs are not the result of valvular defects. High output demands that speed blood flow (anemia, thyrotoxicosis, pregnancy), diminished myocardial contractile ability and structural defects (myocardial septa) are sometimes responsible. In addition to physical examination, echocardiography is now utilized to distinguish etiology.



    1) volume load
    2) chrono/inotropes
    3) vasodilators with nL vol
    4) inhalation agents (for LVOTO)
    5) calcium
    6) beta-blockers (for LVOTO)
    7) PDE-III inhibitors
    8) glucagon ?


    1) inhalation agents
    2) hypovolemia
    3) vasodilators s adeq volume
    4) dysrhythmias
    5) ischemia
    6) calcium channel blockers
    7) high MAP

    A normal cardiac output ranges from 3 to 9 liters per minute. A normal cardiac index ranges from 2.1 to 4.9 liters per minute per meter squared.


    RIGHT HEART: performed via basilic, cephalic or femoral vein. Umbilical venous catheters tend to pass directly into the left atrium.

    LEFT HEART: performed via brachial or femoral artery. Infants can be accessed through the right heart. Umbilical artery is too tortuous. Volumes can be estimated and calculations made.


    CARDIAC OUTPUT is determined by thermodilution or the Fick method (both measure forward CO which is equal to total CO only without regurgitation). Thermodilution measures pulmonary flow but is not accurate at low CO, with TR or with left-to-right shunts. Fick is based on relationship of O2 uptake/AV O2 difference [VO2 = CO (A-V)]. O2 uptake can be calculated based on expired oxygen or taken from tables based on BSA or HR and age. AV O2 difference is calculated by measuring O2 contents: (saturation percent x Hgb x 1.36) + (0.003 x O2 partial pressure). The Fick method is most accurate at LOW CO when the AV difference is great. It is also accurate with intracardiac shunts.

    RESISTANCE can be calculated such that SVR = (MAP-CVP)/CO x 80.


    Normal DIASTOLIC FUNCTION is depedent on normal distensibility and compliance. Both intrinsic and extrinsic factors affect diastolic function.

    COMPLIANCE is defined as the ratio of volume change to the consequent pressure change or as the slope of the pressure-volume relationship. Decreased compliance is indicated by an increase in steepness of the pressure-volume plot. There is normally a gradual decrease in compliance (the slope becomes steeper) at higher volumes. Pathologic decreases in compliance may arise from HTN, aortic stenosis or cardiomyopathy. Compliance may also appear to be decreased if the ventricle is forced to operate on the steeper portion of the curve – by utilization of the preload reserve.

    A decrease in DISTENSIBILTY is defined as an increased diastolic pressure at a given volume and is represented by a curve that is shifted upward but maintains the same slope.

    Ischemia may cause a decrease in distensibility because of the lack of energy required for normal relaxation. The ischemic patient will exhibit loss of diastolic function (distensibility) before loss of systolic function. Ischemia is thought to be first manifest by diastolic dysfunction.

    Extrinsic causes of decreased distensibility include limitations to ventricular expansion during diastole which may be secondary to diseased or fluid-filled pericardium or distension of the right ventricle causing a leftward septal shift.

    Normally the RVEDP is 1-2 mmHg higher than the mean RAP, and the LVEDP is 2-3 mmHg higher than the mean PAWP. These differences are explained by the small volumes that are added to the ventricles during atrial systole. When COMPLIANCE of the LV is poor the A WAVE will be large and the volume added to the ventricle by atrial systole will cause a greater increase in actual EDP. Thus, in patients with poor compliance, the PEAK (A wave) pressure of the LAP or PAWP will be a better measure of LVEDP.

    In patients who chronically function on the steep portion of the compliance curve, a large A wave, LAE and S4 gallop are prominent findings.

    In patients with MR, the presence of large V WAVES will cause the mean LAP or PAWP to overetimate the actual LVEDP.


    Oxygen saturation measurements (catheterization data) are essential for evaluation of shunts (step-up or step-down). 14 locations are typically sampled.

    Shunts are QUANTIFIED by comparison of Qs and Qp (calculated by the Fick method).

    Qp = VO2 / (PVO2 – PAO2)
    Qs = VO2 / (SAO2 – MVO2)

    PVO2 must be measured directly or assumed to be 95-98%. When left-to-right shunt exists PAO2 will be higher than MVO2 and MVO2 must be separately calculated:

    MVO2 = 0.75 SVC O2 + 0.25 IVC O2

    The magnitude for a L to R shunt is (Qp – Qs) while the magnitude of a R to L shunt is (Qs – Qp). The Qp/Qs is also a useful calculation derived from saturation data alone (O2 uptake cancels out).

    (SAO2 – MVO2) / (PVO2 – PAO2)

    A Qp/Qs ratio greater than 2 constitutes a large L to R shunt while a ratio less than 1 indicates a R to L shunt.


    EXERCISE ECG is useful in establishing the diagnosis of CAD. The PPV is 8-20% and NPV is 90-100%. Exercise that is sufficient to increase the HR to 85% of the predicted maximum is necessary for optimal sensitivity at 75%. Inability to exercise, resting ECG abnormalities, female gender and medications (digoxin, ß-blockers) adversely affect the accuracy of a stress exercise ECG.

    1) ST depression over 1 mm
    2) ST elevation over 2 mm in multiple leads
    3) inability to exercise for more than two minutes
    4) decreased systolic BP
    5) CHF symptoms or sustained ventricular arrhythmias
    6) prolonged interval before ischemic changes resolve

    Patients who have a markedly positive test result should undergo catheterization though 10% of these will have no CAD. In patients with known CAD, the ability to complete 7 minutes of a standard Bruce exercise protocol without significant ST depression is associated with an excellent prognosis with medical therapy.

    Stress perfusion imaging with THALLIUM or SESTAMIBI (Cardiolite) has been reported to increase the sensitivity for detection of significant CAD to 80% and specificity to 90%. The scan has a PPV for MI or death of 4-20% and a NPV of 99%. Stress perfusion imaging also allows the diagnosis of multivessel disease, localizes ischemia and permits a determination of myocardial viability. Given the increased cost compared with exercise stress testing, these techniques should be reserved for patients with ECG abnormalities at rest (LBBB, LVH or baseline ST depression).

    Stress perfusion imaging can be performed with IV adenosine, dipyridamole or dobutamine. A markedly positive study may demonstrate multiple areas of ischemia, LV dilatation or uptake of tracer in the lungs. Patients with any of these study results should be evaluated by angiography. False-negative tests can occur when there is ischemia in multiple coronary distributions (balanced ischemia), such as in some patients with three-vessel CAD.

    Exercise and pharmacologic stress ECHOCARDIOGRAPHY is useful in the diagnosis of CAD. The test has a PPV of 9-25% and a NPV of 93-100%. Dobutamine, with or without atropine, can be used to induce pharmacologic stress in patients who are unable to exercise. Patients with multiple regions of inducible ischemia should be referred for an invasive study.


    SYSTOLIC FUNCTION is not synomous with contractility. Normal systolic function is the ability of the ventricle to generate SV with varying degrees of preload, afterload and contractility.

    EJECTION FRACTION is the index most commonly used to to describe global systolic function. the normal value is from 50 to 80%.


    An increase in PRELOAD has small effect on EF because the numerator (SV) and denomenator are increased. A 20% increase in preload will increase the EF by only 9%.

    An increase in AFTERLOAD (with other factors constant) will diminish EF by increasing LVESV. Ventricles with decreased contractility will be more adversely affected by an increase in afterload.

    EF is not a sensitive index for CAD because of regional abnormalities may exist without global dysfunction. EF is diminished in all patients with three vessel disease but will be diminished in one or two vessel disease ONLY in the presence of previous MI.

    EF may overestimate systolic function in patients with MR because of the unique volume loading conditions in these patients. The mitral valve provides a low-impedence outflow tract to ventricular ejection.

    STROKE WORK is another good index of systolic function that differs in two ways. SW (the area within the pressure-volume loop) is not affected by afterload but is greatly affected by changes in preload.


    VALVULAR LESIONS can be evaluated by calculating valve areas from flow across the valve and a measured pressure gradient. Total flow (best obtained from angiographic analysis) is utilized as forward flow will underestimate area and exagerate degree of stenosis if regurgitation exists.

    It is important when evaluating stenosis that pressure gradient alone is not evaluated. At low CO it is possible for a critical stenosis to demonstrate a small gradient.

    The MEAN PRESSURE GRADIENT IS DIRECTLY RELATED TO THE SQUARE OF FLOW (recall that the gradient across a valve is approximately four times the PEAK velocity squared). Thus if CO doubles, the mean pressure gradient will increase by a factor of four.

    The MEAN PRESSURE GRADIENT IS INVERSELY RELATED TO THE SQUARE OF THE VALVE AREA. Thus if valve area is reduced by one half, the gradient will increase by a factor of four.

    MITRAL STENOSIS Normal valve area is 4 to 6 cm2. A valve area of 1 is severe and requires a LA pressure of 25 mmHg to maintain minimal CO.

    AORTIC STENOSIS Normal valve area is 2.6 to 3.5. Symptoms of angina, syncope and CHF occur at 0.8 (correlating with a gradient of 50 mmHg) and severe AS occurs at less than 0.5.

    MITRAL REGURGITATION is evaluated qualitatively (1 to 4+) or quantitatively with greater than 60% regurgitation being considered severe. V WAVES are not a direct assessment of the degree of MR. V waves may be abolished by nitroprusside. High inotropy can decrease LV size, reducing MV annulus thus decreasing MR. TR is likewise evaluated and the RA trace takes on the appearance of the RV with severe TR.

    AORTIC REGURGITATION likewise is considered severe at greater than 60%.


    PRELOAD refers to the end-diastolic fiber length or volume. An increase in fiber length enhances the velocity of shortening for a given afterload. With afterload constant, an increase in preload results in increased stroke volume.

    AFTERLOAD refers to the stress (force per unit area) encountered by ventricular fibers after the onset of shortening. Afterload is constantly changing during ventricular ejection because pressure, radius and thickness are changing as ejection progresses. STRESS = (pressure x radius) / (2 x wall thickness). Afterload has both pulsatile and nonpulsatile components. For a given contractile state, an increase in afterload results in a larger LVESV.

    CONTRACTILITY is defined as the state of cardiac performance independent of preload and afterload. An increase in contractility with preload and afterload constant results in augmented stroke volume because of a decrease in LVESV with LVEDV (preload constant).

    The concepts are unified by a pressure (y) – volume (x) loop with the seven o’clock position representing the beginning of diastolic filling (AV valves open). The area represents stroke WORK.

    The ability of the ventricle to maintain SV in face of an increased afterload by increasing preload is defined as PRELOAD RESERVE. This reserve is exhausted once the sarcomeres are stretched to their maximum diastolic length.


    ETIOLOGIES include infection, infiltrative disease and chronic alcohol abuse.

    ANESTHETIC goals are similar to those for CHF by other etiologies.

    HR normal to high
    rhythm sinus
    preload normal or increased
    SVR decreased
    inotropy icreased


    Idiopathic hypertrophic subaortic stenosis or asymmetric septal hypertrophy is usually a genetic disease characterized by abnormal myocytes and hypertrophy developing a priori and not in response to pressure or volume overload. This includes non-uniform ventricular hypertrophy, subaortic obstruction to the LVOT and occasionally mitral insufficiency.

    Features of HOCM include poor ventricular filling related to impaired diastolic relaxation and reduced compliance, late systolic subvalvular obstruction and mitral insufficiency that develops late in systole. There is also evidence of abnormally small coronaries making ischemia a possibility.

    SYMPTOMS include angina, syncope, tachyarrhythmias and CHF. The ECG often shows LVH and strain patterns. Abnormal Q waves are possible. Arrhythmias as well as sudden death are not uncommon.

    Medical TREATMENT is often by ß blockade, CCB and recently by DDD pacing which may benefit the patient by delaying septal contraction until after contraction of the apex. Surgical correction may include myomectomy or MV replacement.

    PATHOPHYSIOLOGY During systole, the LVOT is narrowed by opposition of the hypertrophied septum to the anterior leaflet of the mitral valve. Blood is ejected rapidly through this area, creating a Venturi effect, pulling the mitral valve even closer to the septum. This is referred to as SAM or systolic anterior motion of the mitral valve.

    The timing and duration of septal-leaflet contact determine the severity and clinical significance of the obstruction. Early prolonged contact can generate high pressures gradients. If the apposition occurs later, it is of less importance since most of the SV has already been ejected.

    ANESTHESIA During anesthesia, attempts should be made to minimize apposition of septum and leaflet. This can be done by maneuvers that preserve SV, including reduced contractility using halothane, ß BLOCKADE and CCB, augmenting PRELOAD prior to induction and maintaining afterload with vasoconstrictors.

    Increased contractility, increased HR or decreases in preload or afterload as with RA are detrimental due to reduction in LV volume and increased septal-leaflet contact.

    CARDIAC SURGERY When separating from bypass, avoid inotropes and first consider vasoconstrictors. HCM may coexist with AS and may explain difficulties separating from bypass after a seemingly uncomplicated AVR.


    Cardioplegia formulations vary but always are cold, contain potassium and may contain glucose as an energy substrate, buffering agents, albumin or manitol for osmotic activity, citrate to reduce the calcium concentration and NTG to improve the distribution of the solution. This solution is mixed with either crystalloid or oxygenated blood and is infused into the aortic root after the cross clamp is applied proximal to the aortic cannulation.

    The cardioplegia may be injected through a separate circuit of the bypass machine or manually using a pnuematic infusion device.

    Direct injection is not possible in patients with aortic insufficiency and the aorta must be opened with cardioplegia injected directly into the coronary ostia with small perfusion cannulas.

    Cardioplegia can also be injected retrograde through the coronary sinus. This is particularly helpful in patients with severe stenosis or multiple severe lesions but is often used routinely for valve and coronary procedures.

    During injection, the anesthesiologist should monitor the EKG for return of electrical activity, the PA pressure and the appearance of the heart for distension.

    Depending on the duration of ischemia necessary, reinjection every 20 minutes may be necessary to maintain hypothermia and diastolic arrest and to wash out products of metabolism.


    There are several INDICATIONS for cardioversion – most of which are unstable tachdysrhythmias. Elective cardioversion is most often provided for correction of persistent atrial fibrillation or flutter.

    EMERGENT use of cardioversion is indicated for any hemodynamically unstable sustained ventricular tachyarrhythmia or when a hemodynamically stable and sustained ventricular tachycardia is not promptly restored following drug therapy. It also should be considered when sustained SVT precipitates angina, heart failure or hypotension. Cardioversion is seldom indicated with heart rate less than 150 bpm.

    1) ventricular tachycardia
    2) paroxysmal SVT
    3) atrial fibrillation
    4) atrial flutter

    Incremental energy delivery progresses from 100 to 360 joules. SVT and atrial FLUTTER often respond to energy levels as low as 50 joules. Polymorphic VT should be treated with a minimum of 200 joules. PEDIATRIC cardioversion takes place with 0.5-1 joule per kg and may increase to 2 joules per kg if necessary.

    Adhesive pads or paddles can be used at the right sternal border and apex. Twenty-five pounds of pressure should be applied to the paddles. Units should be set back to the SYNCHRONIZED mode after each delivery as the default is typically unsynchronized. Synchronization delivers energy to coincide with the R wave thus minimizing risk of VT or VF.

    If delays in synchronization occur or if clinical condition is critical, patients should be immediately treated with unsynchronized shocks or DEFIBRILLATION.

    Serial cardioversion are not appropriate for recurrent (hourly or daily) paroxysmal atrial fibrillation, a situation common following cardiac surgery. These arrhythmias are best managed with removal of potential precipitants or the use of antiarrythmic therapy.

    Cardioversion is INEFFECTIVE in terminating multifocal atrial tachycardias, as well as tachycardias associated with DIGITALIS toxicity (may lead to refractory ventricular fibrillation).

    ANESTHESIA REQUIREMENTS for elective cardioversion are usually quite simple. Patients who are unstable require intubation and ventilation with 100% oxygen although intubation should not delay cardioversion.

    Elective cardioversion is usually performed with light anesthesia (propofol, methohexital or etomidate) and NC oxygen. Propofol is more likely to cause a persistent hypotensive response and is more likely to cause bradycardia and apnea than etomidate. Midazolam is also appropriate but is less practical because of greater interindividual variability in dosing requirements.

    Patients should be NPO for six hours (as with all elective anesthetic cases) and a complete set up for airway management and emergency pacing should be available.

    COMPLICATIONS of cardioversion include failure to convert, asystole, hypotension, respiratory depression, gastric aspiration and difficult airway management. Skeletal fractures have been reported in elderly patients.



    The cauda equina is formed by nerve roots caudal to the level of spinal cord. CES may result from any lesion that compresses CE nerve roots. These nerve roots are particularly susceptible to injury, since they have a poorly developed epineurium. When well developed, the epineurium protects against compressive and tensile stresses. The microvascular systems of nerve roots have a region of relative hypovascularity in their proximal third. Increased vascular permeability and subsequent diffusion from the surrounding CSF supplement the nutritional supply. This property of increased permeability may be related to the tendency toward edema formation of the nerve roots, which may result in edema compounding initial and sometimes seemingly slight injury.

    SYMPTOMS include (1) LBP, (2) acute or chronic radiating pain usually bilateral but possibly unilateral, (3) unilateral or bilateral LE motor or sensory abnormality, and (4) bowel or bladder dysfunction which is usually with associated perineal anesthesia. Bladder dysfunction may present as incontinence, but often presents earlier as difficulty starting or stopping a stream of urine.

    EXAMINATION may reveal (1) pain often localized to the low back, (2) loss or diminution of LE reflexes, (3) pain in the legs or radiating to the legs, (4) sensory abnormality present in the perineal area or lower extremities, (5) muscle weakness present in muscles supplied by affected roots with wasting possible if CES is chronic, (6) poor anal sphincter tone, (7) anesthetic areas may show skin breakdown, (8) alteration in bladder function assessed empirically by obtaining urine via catheterization.

    Hyperactive reflexes may signal spinal cord involvement and exclude the diagnosis of CES. Babinski sign or other signs of upper motor neuron involvement also suggest a diagnosis other than CES and possibly a diagnosis of spinal cord compression.

    THERAPY Early surgical, neurologic or orthopedic consultations are recommended, depending on the suspected etiology of CES. Steroids may be recommended in acute or traumatic CES. Steroids have anti-inflammatory properties and may decrease edema around nerve root segments. Methylprednisolone is most often used at the dose employed in traumatic spinal cord injuries, but no studies exist to support this regimen.


    Caudal analgesia can be provided for children generally up to ten years of age. The spinal cord of the infant ends at L3 whereas it ends at about L1-2 in the adult. The dural sac of the infant ends at S3 whereas it ends at S1 in the adult.

    A 22 gauge angiocath is typically utilized to lessen risk of epidermoid tumor formation. Alcohol swabs and sterile gloves are all that are absolutely required for sterility. The sacral hiatus is identified and the lateral CORNUA are palpated. The bevel is usually directed anteriorally to avoid intraosseous or IV injection. The needle is advanced at a 45-60 degree angle until a pop is felt as the sacrococcygeal membrane is pierced. The angle is then lowered to 15 degress and the needle is advanced an additional 1-2 mm. Negative aspiration is verified. Saline may be injected to assure a memorable feel of resistance. Air is generally not recommended.

    BUPIVICAINE 0.125 or 0.25% with epinephrine is typically utilized. Volumes range from 0.5 mL per kg (sacral analgesia) to 1.25 mL per kg (mid-thoracic blocks). The TAKASAKI formula (0.056 mL/kg/segment) has proven reliability.

    The maximum dose of bupivicaine with epinephrine is 3 mg per kg and 1.25 mL per kg calculates to a dose of 3.125 mg per kg. Some authorities state that up to 3.75 mg per kg may be used in the infant despite the fact that infants may be more susceptible to CV toxicity. This safety has been demonstrated in animal and pediatric pharmocokinetic models.

    TWENTY minutes are required for complete efficacy. When caudals are placed preoperatively, the block may be repeated after a two hour interval without worry about LA toxicity.

    TEST DOSES Epinephrine will not reliably produce tachycardia in children unless preceded by atropine (10 mcg/kg) which simply attenuates the predominant parasympathetic tone of the infant. IV (and intraosseous) LA will produce T wave ELEVATION (greater than 25% in lead II) on the ECG which is likely not related to adrenergic effect. Some argue that this is actually a combined effect of LA and epinephrine.

    Contrast this with the T wave DEPRESSION that may be seen in the elderly or deeply anesthetized patient as a result of LA IV injection

    MORPHINE Many authors advocate the use of PF morphine at 50 mcg per kg without significant risk of respiratory depression. At 30 mcg per kg, the incidence of PONV and pruritis may be as high as 40%.

    CLONIDINE may be utilized at 1-3 mcg per kg with lower doses being acceptable for ambulatory surgery. Doses of 3 mcg per kg will cause sedation in the PACU but should not cause any marked respiratory depression.

    Clonidine is NOT recommended in children less than six months of age due to three case reports of apnea in the PACU that may be related to the use of clonidine.

    There is a 50% incidence of MOTOR BLOCK with 0.25% bupivicaine and 8% incidence with 0.125% after one hour (Anes 69:102-5). The incidence of urinary RETENTION is extremely rare without the use of opioids. HYPOTENSION may occur in children older than eight years of age.

    COMPLICATIONS include SQ injection, bloody taps, dural puncture (incidence 0.3%), IV injection (incidence 0.4%), breakage of the needle, perforation of the rectum, hematoma, sepsis and urinary retention (extremely rare). The differential for the dural puncture include IV injection, anaphylaxis and transient elevated intracranial pressure that may occur with 10 mL of LA injected to the epidural space.

    See related information under EPIDURAL – PEDIATRIC.


    Caudal anesthesia is typically provided by using 1 mL per kg of a 0.375% levobupivicaine solution with 1:200K epinephrine. The pharmocokinetics of such high doses have demonstrated safety in the neonatal population that is supported by infant and animal models.


    Autoregulation and brain metabolism (the INTRINSIC factors) are one of the THREE categorical physiologic factors determining CBF.

    Cerebral autoregulation refers to the maintenance of a constant CBF despite wide variations in CPP. The CPP is equal to the MAP minus the ICP or RA pressure, whichever is greater. The brain vasculature utilizes pressure autoregulation, as does the vasculature of other vital organs (spinal cord, heart, kidneys). Autoregulation is a local phenomenon.

    When MAP increases, the cerebral vessels constrict and during decreases in MAP, the cerebral vessels dilate, keeping CBF constant. This autoregulation occurs from a MAP 50 mmHg to 150 mmHg. Autoregulation occurs within 30-120 seconds. Two theories – myogenic and metabolic – exist to explain the mechanism of autoregulation.

    Autoregulation can be LOST with hypoxia, ischemia, hypercapnia, trauma, brain tumors and some anesthetic agents.

    HTN shifts the autoregulation curve (MAP/CBF) to the RIGHT. The shape of the curve is unchanged. The lower and upper limits of autoregulation are higher than in normotensive patients. Newborns and infants have lower systemic blood pressures and their autoregulatory curve is shifted to the left.

    LUXURY PERFUSION is blood flow in excess of metablic need. It is most often seen in tissues surrounding tumor or infarcted areas.

    INTRACEREBRAL STEAL is a paradoxic response to CO2 in which hypercapnea decreases blood flow in an ischemic area. Because chronically ischemic areas are maximally dilated, they are unable to dilate further in response to hypercapnea.

    INVERSE STEAL or ROBIN HOOD syndrome (also a paradoxic response) involves hypocapnea leading to increased flow to ischemic areas of the brain. Vasoconstriction occurs in adjacent normal arterioles causing a local increase in perfusion to the maximally dilated ischemic areas. Hence, stealing from the rich and giving to the poor when resources are limited. Remember, Robin Hood runs very fast and is usually hypocapnic.


    Various medications may have profound influences on CBF by altering MAP, direct effects on vascular resistance and influence on the CMRO which subsequently manipulates one of the primary intrinsic mechanisms for determining flow.

    barbiturates – –
    propofol – –
    etomidate – –
    KETAMINE + +
    droperidol 0 0
    lidocaine – –
    morphine -/0 -/0
    fentanyl – –
    alfentanil 0 0
    sufentanil -/0 -/0
    remifentanil – ?
    diazepam – –
    midazolam – ?
    flumazenil + +/0
    HALOTHANE +++ –
    enflurane ++ –
    sevoflurane -/0 –
    nitrous oxide + +

    CMR depression: I=E > D=S > H
    CBF increase: H > E=I=D > S

    The volatile agents are said to be uncoupling agents as they uncouple the normal relationship between CMR and CBF. All agents over 0.6 MAC will increase CBF. Halothane is the most offensive and weakest volatile agent in protecting the neural tissues. Nevertheless, nitrous oxide may be more detrimental with a profile similar to ketamine. Volatiles do not influence the normal response to changes in PaCO2.

    CRITICAL blood flows to prevent ischemia varies between inhalation agents. In general, evidence of ischemia is not present until CBF falls to 22 mL/100g/minute. The ischemic threshold with isoflurane is the lowest at 10 mL/100g/min and halothane has the highest threshold at about 20 mL/100g/min. Isoelectricity occurs at 15 but irreversible damage does not occur until blood flow falls to 6 mL/100g/min.


    Normal CBF is equal to CPP divided by cerebral vascular resistance. CPP is defined as the MAP minus the ICP or CVP (whichever is greatest) and is usually 100 mmHg. Normal CBF averages 50 mL/100 g/minute (80 in the gray matter and 20 in the white matter).

    The THREE physiologic factors that determine CBF include:

    1) determinants of CPP
    2) intrinsic factors determining vascular resistance – autoregulation and the coupling of metabolism with cerebral vascular resistance
    3) extrinsic factors

    The four EXTRINSIC factors which determine CBF include:

    1) arterial CO2 tension
    2) temperature
    3) viscosity
    4) autonomic regulation

    Various medications may have profound influences on CBF by altering MAP, direct effects on vascular tone and influencing the metabolic rate which manipulates one of the primary intrinsic mechanisms for determining flow. See other details under INTRACRANIAL HYPERTENSION.


    STROKE occurs at a 5.5% incidence in the CEA perioperative period (disabling stroke at 0.9% and non-disabling stroke at 4.5%). About 30% of all strokes occur intraoperatively and may be more common in the GA population (according to one large metanalysis).

    DEATH occurs with an incidence of 1.1% and may be secondary to cerebral or myocardial adversity.

    DELAYED EMERGENCE is more common after GA for CEA. Once common causes of delayed emergence are eliminated (hyperglycemia, hypoglycemia, hypothermia, anesthetic overdose, hypercarbia, hypoxemia), the possiblilty of intraopertive ischemic event should be evaluated. Necessary studies may include Doppler evaluation (leading to prompt reexploartion if flow is not detected), CT scan or cerebral angiography.

    The incidence of BP derangements is over 60% following CEA. RA is more often associated with hypotension while GA is more often complicated by hypertension.

    HTN is seen more commonly than hypotension. Causes include hypervolemia, hypoxemia, hypercarbia, pain and full bladder. Another common cause may be blunting of the carotid baroreceptor secondary to carotid SINUS dysfunction caused by surgical trauma or chemical denervation. BP usually peaks 2-3 hours after surgery.

    HYPOTENSION may be secondary to hypovolemia, residual anesthetics, dysrhythmias and myocardial ischemia. Another possible cause is an increased sensitivity of the carotid SINUS after plaque removal. The baroreceptor reflex can be (in essence) up-regulated as it has been shielded in the preoperative period leading to vagally mediated bradycardia and hypotension.

    MYOCARDIAL INFARCTION occurs at an incidence of 1.1%. Perioperative MI is possibly more likely after GA but results are not significant according to one large metanalysis. Myocardial events are obviously more common in those with hypertension, angina or history of MI.

    Postoperative RESPIRATORY insufficiency may be secondary to vocal cord paralysis (from traction on the laryngeal nerves) or hematoma formation at the operative site. Tension pneumothorax can result from air dissecting through the wound and the mediastinum to the pleura.

    CHEMORECEPTOR function (the function of the carotid BODY) is irreversibly suspended in most patients for up to TEN months. There is a lack of circulatory response to hypoxia and an increase in resting PaCO2 of about 6 mm Hg. This complication is obviously most important in the patient undergoing recent contralateral CEA.


    The value of regional versus GA for CEA continues to be controversial. Some studies have indicated advantages of RA which include shorter operating time, fewer shunts, quicker recognition of shunt dysfunction, less stroke and cardiac morbidity and a lower incidence of perioperative hypertension.

    PREPARATION for a typical CEA under RA includes NTG or SNP infusions which are most useful in the immediate postoperative period and phenylephrine infusions to raise MAP if necessary to improve perfusion across the circle of Willis.

    Levobupivicaine 0.5% with epinephrine is most useful for cervical plexus blocks if time will permit the agent to take action. Sedation may be provided with any of the available agents (fentanyl, midazolam, propofol or remifentanil).

    See other information under CERVICAL PLEXUS BLOCK.

    The reported rate for unplanned conversion to GENERAL anesthesia is only 3%. There are nevertheless several indications for which GA would be advisable: patient refusal for regional anesthesia, claustrophobia and high carotid lesions making surgical exposure more difficult. GA is most often maintained with isoflurane because of the associated lower critical CBF. High or high-normal perfusion pressures are useful during cross-clamp if not complicated by cardiac dysfunction.


    Perfusion during clamping may be monitored with EEG under GA or neurologic assessment with RA. There is no evidence that EEG monitoring affects outcome.

    When there is evidence of ischemia during carotid clamping (1) the case may be cancelled, (2) a shunt may be placed or (3) the BP may be pharmacologically raised before the clamp is reapplied.

    Many surgeons will routinely place shunts. Many surgeons will request the blood pressure be maintained at 20% above baseline during carotid occlusion but this obviously may have deleterious effects on myocardial perfusion. Simply clamping the carotid has been shown to produce segmental wall motion abnormalities in up to 25% of those patients with no other change in hemodynamics.

    With GA, the EEG is ultimately monitored by a neurophysiologist as consult. Ischemic changes are indicated by a dropout in the higher frequency waves read as generalized diffuse slowing.


    The CELIAC plexus is the largest of the three great plexuses of the sympathetic system in the chest and abdomen. The other plexuses include the cardiac and hypogastric. All of these units contain VISCERAL ARRERENT and EFFERENT fibers in addition to some parasympathetic fibers that pass through these ganglia after originating in cranial or sacral areas. Sympathetic afferents signal pain from the viscera. The celiac plexus provides innervation from the LES to the splenic flexure of the colon. The afferent and efferent fibers are derived from T5-12 via the greater, lesser and least splanchnic nerves.

    TECHNIQUE A knowledge of the surrounding structures is important for correct needle placement. The plexus lies in close relation to the L1 vertebrae. The vena cava lies anteriorly to the right and on the left anteriorly is the aorta. The kidneys lie laterally with the pancreas anterior. The number of ganglia varies from one to five and the size is 0.5 to 4.5 cm in diameter. Left-sided ganglia are usually lower than those on the right.

    Bony surface landmarks can be reliably utilized for needle placement. With the patient in the prone position with a pillow beneath the abdomen, lines are drawn connecting the spine of T12 with points 7 to 8 cm lateral at the lower edges of the 12th ribs. These lines form a flattened isosceles triangle, the equal sides of which serve as directional guides for the needles. A 20-gauge 10-15 cm needle is inserted on the left side through a skin wheal at a 45-degree angle toward the body of T12 or L1. Bony contact should be made at an average depth of 7 to 9 cm. The needle is then withdrawn and is reinserted to allow the tip to slide off the vertebral body anterolaterally. The needle is advanced 1.5 to 2 cm past this point – aortic pulsations can be felt as they are transmitted along the needle when it is correctly placed. Once this depth is ascertained, the right-sided needle is inserted in a similar fashion to a depth of 1-1.5 cm farther.

    When the needles are in position, observation for leakage of blood, urine, or cerebrospinal fluid is made prior to careful aspiration. A 3-5 mL test dose of local anesthetic is given prior to injection of 20 to 25 mL of solution through each needle.

    SIDE EFFECTS associated with celiac plexus block include hypotension, spinal, epidural or IV injection, pneumothorax, puncture of viscera (kidney, ureter, gut) and retroperitoneal hematoma. Theoretically, paraplegia may result from drug-induced spasm of the artery of Adamkiewicz.

    The celiac plexus block can be combined with intercostal block to provide anesthesia for intra-abdominal surgery. Because it results in blockade of the autonomic nervous system, this block may help to reduce stress and endocrine responses to surgery.


    Intraoperative blood salvage with a device such as the Cell Saver is useful for recovery and processing of blood shed during surgery. In children, it is used most extensively in orthopedic and cardiac cases correction but it may be useful in a variety of adult surgical procedures. There have been reports of the development of COAGULOPATHY after the infusion of Cell Saver processed packed red blood cells. This occurrence is rare, but several contributing risk factors have been identified.

    When extremely dilute blood is being processed, leukocyte and platelet activation may lead to a coagulopathy similar to DIC on reinfusion – called the salvaged blood syndrome. Normally, when adequate numbers of red blood cells are present in the aspirated blood, they form a protective layer along the sides of the salvage bowl. When blood contacting the sides of the salvage bowl is dilute, however, platelets and leukocytes adhere to the side of the collection bowl, subsequently releasing cytokines, which activate the coagulation cascade.

    When excess amounts of irrigating saline are used intraoperatively, a suction separate from the Cell Saver should be used to avoid excessive hemodilution of the scavenged blood. Complying with recommended maximum suction limits (less than 300 mmHg) also may help to decrease red blood cell destruction and release of inflammatory mediators.

    Another contributing factor is activation by cellular debris. When using a Cell Saver for orthopedic procedures, increased washing is recommended to remove extraneous bone fragments and tissue that can activate the coagulation cascade. Although no convenient investigative method has been validated as an indicator of cleanliness of the salvaged erythrocytes, one in vitro study suggests that residual potassium concentration may be an indicator of quality after washing with a contemporary intraoperative salvage system.

    The use of intraoperative thrombin, (Gelfoam) fibrin glue, and microfibrillar collagen have the potential for initiating a consumptive coagulopathy when aspirated with blood to be processed by the Cell Saver. It is recommended that these agents not be used when intraoperative blood salvage is used.


    Often performed with spinal anesthesia utilizing 5% lidocaine with dextrose at a dose of 50 mg. Lidocaine is usually diluted with CSF althouqh neurotoxicity is virtually unheard of in the OB population. Patients may remain in the sitting position for approximately 5 minutes to achieve a true saddle block.


    Although the etiology for most aneurysms is congenital they can also develop secondary to degenerative hypertensive changes. Some heriditary conditions are associated with cerebral aneurysms such as Ehlers-Danlos syndrome, coarctation of the aorta, polycystic kidney disease, AV malformations, fibromuscular dysplasia and sickle cell disease.

    Predisposing factors for RUPTURE of aneurysms include use of tobacco, abuse of alcohol, pregnancy, strenuous activity and hypertension.

    LOCATION Most aneurysms are close the circle of Willis. 39% are at the junction or the anterior communicating artery and the anterior cerebral artery, 30% are along the carotid artery, 22% are along the middle cerebral artery and 8% are in the posterior circulation.

    Rupture of cerebral aneurysms cause 80-90% of all cases of SAH.



    Cerebral oximetry utilizes near infrared trchnology to assess oxygenation of the frontal cortex. The technology provides data derived from arterial, capillary and primarily venous saturations. It may elucidate cerebral vasospasm that is possible in a cold stressed patient with Raynaud’s phenomenon.


    CP includes a constellation of nonprogressive disorders characterized by central motor deficits usually resulting from anoxic or hypoxic cerebral damage. The incidence ranges between 2-4:10,000 live births. Known etiologies include genetic abnormalities, metabolic defects, birth trauma, cerebrovascular malformations, neonatal infections, toxins, prematurity, kernicterus and hypoglycemia.

    SYMPTOMS CP is classified as spastic, extrapyramidal, atonic or mixed. Most common is the spastic variety. Extrapyramidal patients may display choreoathetosis and dystonia. Cerebral ataxia is characteristic of atonic CP. Varying degrees of MR, speech defects and seizure disorders can accompany CP.

    MEDICAL THERAPY Patients are often treated with a variety of medications for spasticity and seizure disorders and the anesthetic implications of these medications should be understood. Commonly used drugs for spasticity include dantrolene, benzodiazepines and baclofen. Incapacitating athetosis is treated with levodopa and dystonia is treated with carbemazepine and trihexyphenidyl. Seizures are often treated with phenobarbital, phenytoin, clonazepam, carbemazepine and valproate.

    ANESTHESIA Most patients with CP require tracheal INTUBATION for history of GER and poor function of laryngeal and pharyngeal reflexes. Some report that patients with CP may have an exaggerated hyperkalemic response with SUCCINYLCHOLINE but in general, succinylcholine may be safely given.

    Patients with SEIZURE DISORDERS warrant avoidance of those few anesthetic agents which may promote seizures – enflurane, etomidate (controversial), ketamine, methohexital, PROPOFOL and meperidine. Interestingly, most of these PROCONVULSANTS will raise the seizure threshold in normal patients and are proconvulsants only in those with seizure disorders. Without exception, patients should take their anticonvulsant medications on the day of surgery although most all anticonvulsants have long half lives (24-36 hours) and patients that are adequately treated are at minimal risk for a 24 hour period without treatment. Epidural anesthesia is not contraindicated in these patients, but in those with poorly controlled seizures it may be advisable to utilize chloroprocaine instead of lidocaine or bupivicaine.

    Patients may be particularly prone to hypothermia and may recover more slowly from GA. Patients with CP may be at greater risk for pulmonary complications following anesthesia.


    CSW is the renal loss of sodium during intracranial disease leading to hyponatremia and a decrease in extracellular fluid volume. Patients are clinically volume depleted and urine output is usually excessive. (Crit Care Clinics 2001 17:1)

    LAB EVALUATION An elevated potassium is incompatible with SIADH but suggestive of CSW. Serum urate is decreased with SIADH but usually normal with CSW. Urine sodium is markedly elevated with CSW but variable with SIADH.

    THERAPY is by volume replacement and maintenance of a positive salt balance. Sodium should not be restored faster than 0.7 mEq per liter per hour or 20 mEq per liter per day.


    Normal Findings

    CSF Glucose
    Children and Adults: 50-80 mg/dl
    Normal newborn: >60% of simultaneous Serum Glucose
    Normal infant: >50% of simultaneous Serum Glucose

    CSF Protein
    Children and Adults: 20-45 mg/dl
    Normal term newborn: <70 mg/dl
    Normal term newborn: <40 mg/dl

    CSF Chloride 116-122

    CSF Opening Pressure 100-200

    CSF Leukocytes
    No Neutrophils and under 6 Lymphocytes
    Normal term newborn: <10 WBCs/ml (<10% Neutrophils)

    Bacterial Meningitis

    CSF Glucose much less than 50
    CSF Protein much greater than 45
    CSF Leukocyte: Markedly increased Neutrophils
    CSF Opening Pressure: increased >200

    Viral Meningitis

    CSF Glucose: Normal
    CSF Protein > 45
    CSF Leukocytes: Increased CSF Lymphocytes
    CSF Opening Pressure: Normal or increased

    Fungal Meningitis

    CSF Glucose < 50
    CSF Protein > 45
    CSF Leukocytes: Monocytes increased
    CSF Opening Pressure: Increased

    Tuberculosis Meningitis

    CSF Glucose < 50
    CSF Protein > 45
    CSF Leukocytes
    Early: Neutrophils increased
    Later: Lymphocytes increased

    Intracranial Hemorrhage

    CSF Glucose: Normal or decreased
    CSF Protein: >45
    CSF Red Blood Cells: Increased
    CSF Opening Pressure: Increased >200


    CSF Glucose: Normal or decreased
    CSF Protein: Normal or increased
    CSF Leukocyte: Normal or increased Lymphocytes
    CSF Opening Pressure: Increased >200


    CSF Glucose: Normal
    CSF Protein: >45
    CSF Leukocytes: Monocytes increased
    CSF Opening Pressure: Normal or increased


    CSF Glucose: Normal
    CSF Protein much greater than 45
    CSF Leukocytes: Lymphocytes normal or increased
    CSF Opening Pressure: Normal


    Intravascular injection of local anesthetic may occur either into a vein or artery. Systemic toxicity of local anesthetics results in either central nervous or cardiac effects. The CNS effects vary from sedation to tinnitus to seizures, depending on the blood level. Grand mal seizures have been reported after 2.5 mg of bupivicaine into the vertebral artery. Cardiac effects generally occur at higher blood levels than CNS effects. Conduction blockade and myocardial depression progressing to refractory arrhythmias and cardiac arrest at higher levels may occur.

    The vertebral artery is very close to the site of desired injection. It lies in the vertebral canal, which is only about 0.5 cm below the tip of the transverse process. Since the vertebral artery has direct supply to the brain, only a small amount of local anesthetic needs to be injected to cause CNS effects. Therefore, it is important to remain in constant communication with the patient during injection to help detect early signs of CNS toxicity such as perioral numbness, disorientation or tinnitis. Aspiration should be done frequently. If injection is performed slowly, and patient contact is maintained, progression of toxicity from CNS to cardiac is very unlikely.

    Toxicity may be reduced in the CNS by giving the patient IV benzodiazepines prior to performing the block. This may also potentially raise the seizure threshold. Caution must be exercised in the use of benzodiazepines, because oversedation may make the patient uncooperative and the sedation caused may be difficult to differentiate from early CNS toxicity of local anesthetics. If CNS toxicity does occur, the patient should be given oxygen by mask and observed. If progression to seizure activity occurs, this can be treated with THIOPENTAL in a dose of 2 mg/kg. The patient may also require succinylcholine and tracheal intubation to maintain adequate oxygenation. The decision as to whether to proceed with the surgery under these conditions must be made by both the surgeon and the anesthesiologist.

    Besides IV injection, subdural injection may also occur. If the needle is placed too far, a dural sleeve around the nerve root may be entered. Local anesthetic injected here may cause subarachnoid block. This may be seen as unconsciousness and hypotension. Pressure support and endotracheal intubation may be necessary. This will resolve when the local anesthetic is metabolized from the CNS.

    An additional complication of cervical block is hematoma formation. This may occur if the needle enters a large blood vessel. Usually, local compression will alleviate the problem, but occasionally, the hematoma will progress, and rarely airway compromise may result.

    Because of the fact that the phrenic nerve is composed of cervical nerves 3-5, unilateral PHRENIC nerve palsy is possible and common with this block. This should not present a problem unless the patient has severe pulmonary disease and is dependent on diaphragmatic function for adequate respiration. Cervical plexus block should arguably be avoided in these patients with severe respiratory dysfunction.


    Sensory blockade for regional CEA is required in the C2-4 dermatomes. Cervical plexus blocks may also be useful for superficial neck procedures, thyroglossal duct excision and lymph node dissection.

    The anterior rami of C2-4 form the cervical plexus (C1 is primarily motor). The cervical plexus is comprised of the cutaneous branches of the plexus, the ansa cervicalis complex, the phrenic nerve (C3-5), contributions to the accesory nerve (which innervates SCM and trapezius muscles) and direct muscular branches.

    The SUPERFICIAL block is accomplished by superficially infiltrating along the middle third of the posterior border of the sternocleidomastoid. The needle is fanned to deposit a total of 15 mL of LA. Nerves blocked at this location include lesser occipital, greater auricular, transverse cervical and supraclavicular nerves. Additional LA infiltration along the angle of the MANDIBLE may be useful in blocking contributions of the trigmeminal nerve to the lateral neck.

    A blunt tipped 22 gauge regional needle inserted without a syringe attached may be useful to appreciate the fascial penetrations deep to the sternoceidomastoid. A 1 inch 25 guage needle or a longer Quinke needle can then be used to fan along the SCM and mandible.

    DEEP CERVICAL is generally not needed but may provide more of a motor block that fascilitates surgical exposure. The block is performed with three injections along a line drawn from CHASSAIGNAC’S tubercle (transverse process of C6) to the mastoid process. This tubercle is palpable lateral to the cricoid cartilage (where the EJ crosses the border of the SCM). Actual injections are made along a line drawn parallel and 1 cm posterior to the reference line.

    The C2 process is found 1 to 2 cm caudal to the mastoid process. C3 and C4 are subsequently found 1.5 cm caudal to the superior process. Needles should be perpendicular but slightly POSTERIOR and
    CAUDAD (to avoid entry directly into the intervertebral foramina). The needle is walked off the process in a CUADAD direction. 5 mL of LA can be deposited at each of the three levels but 3 mL should be satisfactory.

    Surgeons will commonly need to supplement LA as deeper dissection takes place. The contents of the carotid sheath are innervated by the glossopharyngeal (IX) and vagus (X) nerves.

    LOCAL ANESTHETICS include 0.5 to 0.75% levobupivicaine (bupivicaine) for 2-6 hours duration or 1 to 1.5% lidocaine or mepivicaine for 1-1.5 hours duration or 1-3 hours duration if epinephrine is used. Mixtures of 2% lidocaine and 0.5% bupivicaine are also commonly used.

    MAXIMUMS About 35 mL of plain 0.5% levbupivicaine (40 mL with epinephrine). About 30 mL of plain 1% lidocaine or mepivicaine (50 mL with epinephrine).

    For the patient with carotid disease, care must be taken to prevent possible dislodgement of atheromatous plaques.



    Cervical disc disorders include herniated nucleus pulposus, degenerative disc disease and internal disc disruption. HNP implies extension of disc material beyond the posterior margin of the vertebral body. Most of the herniation is made up of the annulus fibrosus. DDD involves degenerative annular tears, loss of disc height and nuclear degradation. IDD describes annular fissuring of the disc without external disc deformation. Cervical radiculopathy can result from nerve root injury in the presence of disc herniation or stenosis, leading to sensory, motor or reflex abnormalities.

    The disc consists of eccentrically located nucleus pulposus and surrounding annulus fibrosus separating each segmental level. No disc exists between C1 and C2 where only ligaments and joint capsules resist excessive motion. Disc degeneration and/or herniation can injure the spinal cord or nerve roots and result in stenosis and/or myofascial pain.

    Manifestations of HNP are divided into subcategories by type: disc bulge, protrusion, extrusion and sequestration. Disc bulge describes generalized symmetric extension of disc margin beyond the margins of the adjacent vertebral endplates. Disc protrusion describes herniation of nuclear material through a defect in the annulus, producing a focal extension of the disc margin. Extrusion applies to herniation of nuclear material resulting in an anterior extradural mass attached to the nucleus of origin, often via a pedicle. Disc sequestration refers to separation of material from the disc, which ultimately comes to lie in the spinal canal.

    Herniation typically occurs secondary to posterolateral annular stress. Herniation rarely results from a single traumatic incident. Acute traumatic cervical HNP serves as a major etiology of central cord syndrome. The C6-C7 disc herniates more frequently than discs at other levels.

    A rare trauma-induced high cervical (C2-C3) HNP syndrome manifests nonspecific neck and shoulder pain, perioral hypesthesia, more radiculopathy than myelopathy, and more upper limb motor and sensory dysfunction than lower limb symptomology. Decreased middle and/or lower cervical spine mobility from spondylosis, with consequent overload at higher segments, may precipitate high cervical disc lesions in older patients. A retro-odontoid disc may result from an upwardly migrating C2-C3 HNP. Some case reports describe cervical HNPs causing Brown-Séquard syndrome, as well as atypical nonradicular symptoms in patients with congenital insensitivity to pain.

    Cervical radiculopathy results from mechanical nerve root compression or intense inflammation (chemical radiculitis). Specifically, nerve root compression may occur at the intervertebral foraminal entrance zone at the narrowest segment of the root sleeve anteriorly by disc protrusion and uncovertebral osteophytes and posteriorly by superior articulating process, ligamentum flavum and periradicular fibrous tissue. Decreased disc height, as well as age-related foraminal width decrease from inferior z-joint hypertrophy may impinge subsequently on nerve roots. The cervical region accounts for 5-36% of all radiculopathies encountered. Incidence of cervical radiculopathies by nerve root level is as follows: C7 (70%), C6 (19-25%), C8 (4-10%), C5 (2%).


    The patient with RADICULAR pain often displays a decreased cervical range of motion. Pain is exacerbated from neck extension and rotation or from Spurling maneuver (neck is extended, laterally bent and held down) designed to elicit radicular symptoms. Pain improves with neck flexion or abduction of the symptomatic upper limb over the top of the head (abduction sign). Decreased SENSATION to pain, light touch or vibration may be present in the distal upper limb. Proximal limb weakness manifests when significant motor root compromise exists but must be differentiated from pain-related weakness. The seventh (60%) and sixth (25%) cervical nerve roots are the most commonly affected.

    PALPATION Tenderness usually is noted along the cervical paraspinals and usually is more pronounced along the ipsilateral side of the affect nerve root. Muscle tenderness may be present along muscles where the symptoms are referred.

    MOTOR Manual muscle testing detects subtle weakness in a myotomal distribution. Place the limb in the antigravity position and the force applied just proximal to the next distal joint – eg the extensor carpi ulnaris muscle should be tested with the forearm in full pronation and resting on a table or supported and then resisting against the dorsum of the fifth metacarpal bone in the direction of flexion toward the radial side.

    C5 weak shoulder abduction
    C6 weak elbow flex & wrist exten
    C7 weak elbow exten & wrist flexion
    C8 weak thumb extension & ulnar deviation of the wrist

    SENSORY Dermatomal decrease or loss of sensation should be noted in patients with clear radiculopathy. Patients with radiculopathy may have hyperesthesia to light touch and pin prick examination.

    DTR or more properly muscle stretch reflexes since the reflex occurs after a muscle stretch is obtained (most commonly by tapping the distal tendon of a muscle), are helpful in the evaluation of patients presenting with limb symptoms suggestive of a radiculopathy. The examiner must position the limb properly when obtaining these reflexes and the patient needs to be as relaxed as possible. Any grade of reflex can be normal, so it is the asymmetry of reflexes, which is most helpful. The BICEPS BRACHII reflex (C5-6) is obtained by tapping the distal tendon in the antecubital fossa. This reflex occurs at the C5-6 level. The BRACHIORADIALIS reflex (C5-6) that can be obtained by tapping the radial aspect of the wrist. The TRICEPS reflex (C7-8) can be obtained by tapping the distal tendon at the posterior aspect of the elbow with the elbow relaxed at about 90° of flexion. The PRONATOR reflex can be helpful in differentiating C6 and C7 nerve root problems. If it is abnormal in conjunction with an abnormal triceps reflex, then the level of involvement is more likely to be C7. This reflex is performed by tapping the volar aspect of the distal radius with the forearm in a neutral position and the elbow flexed. This results in a stretch of the pronator teres resulting in a reflex pronation.

    Patients with MYELOPATHY may demonstrate

    LE hypertonia
    LE hyperreflexia
    toe up Babinski reflexes
    Hoffman reflexes
    difficult tandem walking

    PROVACATIVE The foraminal compression or SPURLING test is performed by extending the neck and rotating the head and then applying downward pressure on the head. The test is considered positive if pain radiates into the limb ipsilateral to the side that the head is rotated to. The Spurling test is very specific, but not sensitive, in diagnosing acute radiculopathy. Manual cervical distraction can be used as a physical examination test. With the patient in a supine position, gentle manual distraction often greatly reduces the neck and limb symptoms in patients with radiculopathy. LHERMITTE sign is performed by flexing the neck and asking the patient about symptoms of electriclike sensation radiating down the spine.


    ANTERIOR LAMINECTOMY and FUSION procedures generally do not require invasive monitors. Airway considerations include evaluation for reproducible radicular or myelopathic sysmptoms.


    Emergent cesarean may be required for fetal distress, abruption, uterine rupture, cord prolapse and maternal cardiopulmonary arrest.

    Patients are quickly evaluated, given aspiration prophylaxis, placed in a left uterine displacement position with oxygen while IV access is secured.

    For the anticipated easy airway, GA is usually preferred. Other patients may receive SAB in the lateral position. SAB in the presence of a failed epidural should be performed with caution and likely should NOT be performed in the patient with a difficult airway. Difficult airway equipment should be available in all circumstances. FAILED INTUBATIONS occur in 0.05% (1:2230) of all surgical cases and 0.2% (1:500) of all obstetric cases (four times the overall incidence).

    OXYTOCIN at 20-40 units in one liter of IVF is most often utilized and side effects are often limited to minor ADH effects. Boluses of oxytocin will often precipitously decrease MAP.

    HEMABATE (15-meth-PGF2alpha) at 250 mcg IM or directly in the myometrium may be repeated every 15-30 miunutes. Side effects include possible BRONCHOSPASM, VQ mismatch and hypoxemia. Other side effects include diarrhea and fever.

    METHERGINE (methylergonovine) is an ergot given at 200 mcg IM or in 20 mcg IV boluses. It is provided in 1 mL (200 mcg) vials. Side effects include HYPERTENSION, CVA and seizures.


    General techniques for section include preparation by large bore IV placement, aspiration prophylaxis and left uterine displacement. Preoxygenation is crucial as maternal desaturation takes place rapidly by increased oxygen consumption and decreased FRC.

    RSI with cricoid pressure
    STP at 3-4 mg per kg or
    PROPOFOL at 2-2.5 mg/kg
    KETAMINE 1-2 mg per kg
    SCh 1-1.5 mg per kg
    intubation with a 6.5 ETT

    FAILED INTUBATIONS occur in 0.05% (1:2230) of all surgical cases and 0.2% (1:500) of all obstetric cases (four times the overall incidence). Depolarizing and NDMB will cross the placenta to varying degrees. Compared with STP, propofol for cesarean is associated with high umbillical vein concentrations, muscular hypotonus and lower neonatal Apgar scores at 1 and 5 minutes.

    MAINTENANCE before delivery:
    50% nitrous oxide
    0.75 MAC of volatile agent

    The PaCO2 should be kept at 30-32 mmHg as an approximation of the normal PaCO2 in the term paryrient. Mivacron may be the preferred relaxant as successive doses of succinylcholine may produce bradycardia and phase two block.

    Maintenance AFTER DELIVERY:
    70% nitrous oxide
    less than 0.5 MAC of volatile agent
    or propofol for severe atony

    Versed, morphine or fentanyl are also beneficial after delivery.

    OXYTOCIN at 20-40 units in one liter of IVF is most often utilized and side effects are often limited to minor ADH effects. Boluses of oxytocin will often precipitously decrease MAP.

    HEMABATE (15-meth-PGF2alpha) at 250 mcg IM or directly in the myometrium may be repeated every 15-30 miunutes. Side effects include possible BRONCHOSPASM, VQ mismatch and hypoxemia. Other side effects include diarrhea and fever.

    METHERGINE (methylergonovine) is an ergot given at 200 mcg IM or in 20 mcg IV boluses. It is provided in 1 mL (200 mcg) vials. Side effects include HYPERTENSION, CVA and seizures.


    SAB is usually achieved with 1.6 mL (12 mg) of hyperbaric 0.75% bupivicaine and 0.1 mg of Duramorph. Fentanyl may prolong the duration of block. Blocks may be higher than seen in the general population because of SA space compression by the engorged epidural veins. A sensory level of T4-6 is required for adequate analgesia. Alternatives to bupivicaine include tetracaine and lidocaine.

    Hypotension is LESS often observed in the laboring patient most likely secondary to an autotransfusion of 300 mL of uterine blood.

    SAB AFTER FAILED EPIDURAL Caution must be exercised because of a possible increased compression of the SA space. One series reports 11% incidence of high spinal following failed epidural. Management includes lowering the SA dose by 20% and maintaining a head up position or repeating the epidural.

    EPIDURAL for CESAREAN is accomplished with 15-30 mL of 2% lidocaine with 1:200K epinephrine. Alternatively, 0.5-0.75% levobupivicaine or 3% chloroprocaine may be used depending how much time is allowed to achieve the block.

    Bicitra should be given prior to initiating the surgical block. An existing catheter should be checked for depth and a negative aspiration and negative test dose should be documented. Duramorph 3-4 mg is administered following cord clamp.

    OXYTOCIN at 20-40 units in one liter of IVF is most often utilized and side effects are often limited to minor ADH effects. Boluses of oxytocin will often precipitously decrease MAP.

    HEMABATE (15-meth-PGF2alpha) at 250 mcg IM or directly in the myometrium may be repeated every 15-30 miunutes. Side effects include possible BRONCHOSPASM, VQ mismatch and hypoxemia. Other side effects include diarrhea and fever.

    METHERGINE (methylergonovine) is an ergot given at 200 mcg IM or in 20 mcg IV boluses. It is provided in 1 mL (200 mcg) vials. Side effects include HYPERTENSION, CVA and seizures.

    The CLG (2006) allows 8 ounces of clears no later than 8 hours prior to scheduled cesarean section.


    parasternal mediastinoscopy

    In the asymptomatic patient, only TEF and Beckwith Weideman syndrome require thorough cardiac evaluations with echocardiography. The congenital heart diseases may be conceptualized to fall into one of four categories.

    CYANOTIC with NORMAL PBF occurs with mixing of arterial and venous blood in common cardiac chambers and patients present with cyanosis and polycythemia in older children.

    1) single ventricles
    2) hypoplastic RV
    3) double outlet RV
    4) TGA with ASD or VSD

    PBF will be preload dependant and sinus rhythm will promotes PBF. An increased PVR will decrease CO. Careful attention to IV lines will prevent venous air bubbles from embolizing to the systemic circulation. A faster effect of the IV agents is typically observed.

    CYANOTIC with DECREASED PBF occuring secondary to obstruction of pulmonary blood flow leading to shunting at the atrial and/or ventricular level. Patients present with cyanosis and CHF as well as polycythemia in older children.

    1) tricuspid atresia
    2) tetralogy of Fallot
    3) pulmonary atresia

    PBF will depend upon an adequate systemic BP. An increase in SVR will improve oxygenation. Both systemic and PBF will depend upon the relative resistance of PVR and SVR. An increase in PVR will increase the degree of cyanosis. A reduced uptake and excretion of the volatile agents is typically observed. A faster onset of action with the IV agents is typically observed.

    ACYANOTIC with INCREASED PBF occurs secondary to left to right shunt at the atrial, ventricular or great vessel level leading to preferential flow to the low resistance pulmonary bed. Patients with simple PDA and ASD may appear clinically normal. Patients with large VSD may present with CHF.

    1) ASD
    2) VSD
    3) PDA
    4) aortopulmonary window

    RV overload will result in poor tolerance of negative inotropic agents including volatiles. An increase in PVR can reverse shunt from a congestive shunt towards a cyanotic right to left shunt. A slower onset with the IV agents is typically observed.

    ACYANOTIC with obstructed blood flow may occur without shunting. Pateints present with CHF.

    1) pulmonary stenosis
    2) aortic stenosis
    3) coarctation of the aorta

    Ventricular failure will result in poor tolerance of the negative inotropes. Tachycardia is poorly tolerated in these patients. A rapid uptake of the volatile agents is typically observed.


    RASTELLI: surgery for various types of heart defects (TGA, VSD with significant pulmonary artery stenosis). It is usually performed in older infants and consists of closing the VSD with a synthetic patch in such a way that the blood flows from the left ventricle through the VSD and out to the aorta. The pulmonary valve which comes off the left ventricle is usually sewn shut. A tube containing a valve (valved conduit or pulmonary artery homograft) is then connected from the right ventricle (after making a hole in it) to the main pulmonary artery.

    MUSTARD or SENNING: atrial (venous) switch operation diverts systemic venous return into the left ventricle through the mitral valve and thence through the left ventricle and pulmonary artery, while the pulmonary venous blood is diverted through the tricuspid and right ventricle to the aorta. Because midterm results of atrial switch procedures disclosed numerous problems involving late right ventricular failure, tricuspid insufficiency, and arrhythmias, most centers have abandoned the use of the atrial switch approach in favor of the more anatomical arterial switch operation.

    FONTAN: in most centers, Fontan procedure is divided into two stages, an initial SVC-PA anastomosis (bidirectional GLENN shunt or hemi-Fontan procedure, followed later by completion of the Fontan procedure directing flow from the inferior vena cava to the amalgamation of the superior vena cava and the branch pulmonary arteries. At first-stage operation, prior systemic-pulmonary shunts are eliminated and any areas of distortion or narrowing of the pulmonary arteries are repaired, particularly if a prior pulmonary artery banding was performed to limit pulmonary blood flow.

    NORWOOD: procedure for left hypoplastic heart disease (as with critical aortic stenosis) in which an initial single-ventricle repair in which the main pulmonary artery is anastomosed to the aorta with creation of a systemic-to-pulmonary arterial shunt, followed later by a Fontan-type operation that creates an atriopulmonary connection, with or without a prior superior cava-pulmonary connection. The single-ventricle repair results in functional sacrifice of the left ventricle and the right ventricle supporting the systemic circulation without a pulmonary ventricle.

    RASHKIND: rupturing the valve of the foramen ovale by balloon catheter during transseptal catheterization of the left side of the heart.


    The chemoreceptor reflex responds to changes in pH status and blood oxygen tension at an arterial partial pressure of oxygen (PaO2) of less than 50 mm Hg via receptors in the carotid and aortic BODIES (versus the carotid sinus and atrial receptors of the baroreceptor reflex).

    Conditions of acidosis and hypoxia stimulate these receptors, especially those within the carotid body, which also send their impulses along the glossopharyngeal and vagus nerves to the chemosensitive area of the medulla, located bilaterally just beneath its ventral surface. This area responds by stimulating respiratory centers to increase ventilation and also by increasing PARASYMPATHETIC activity, which produces significant bradycardia and decreased contractility. If hypoxia persists, direct central nervous stimulation will lead to improved ventricular performance independent of parasympathetic activity.


    TOXICITY of various CTX agents are described. The TWO agents to be concerned about in the perioperative period are 5-FU (for the possibilty of ectopy) and BLEOMYCIN (for susceptibility to oxygen toxicity).

    5-FLUOROURACIL and ARA-C may cause hemorrhage enteritis, diarrhea, myelosuppression and ectopy.

    6-MERCAPTOPURINE (a purine analogue) is associated with pulmonary, renal and hepatic (bile stasis) toxicity.

    ADRIAMYCIN may cause cardiac toxicity. Risk factors include total cumulative dose over 550 mg/m2, concomitant cyclophosphamide therapy, prior history of heart disease and age over 65 years.

    BLEOMYCIN may cause pulmonary toxicity with incidence of 5-10%. Risk factors include total cumulative dose over 200 mg, concomitant thoracic radiation therapy and age over 65 years. Patients are at much greater risk for oxygen toxicity. Mucocutaneous reactions are the most common side effect but are much less serious in nature.

    CARBOPLATIN is a compound related to cisplatin that is much less toxic to the renal and nervous system but may be associated with myelosuppression.

    CISPLATIN may cause renal toxicity and neurotoxicity (specifically ototoxicity).

    CYCLOPHOSPHAMIDE (Cytoxan) may cause myelosuppression, hemorrhagic cystitis, water retention, pulmonary fibrosis and plasma cholinesterase inhibition.

    CYTOSINE ARABINOSIDE is associated with pulmonary toxicity.

    DOXORUBICIN (an antibiotic) is associated with cardiac and hepatic toxicity.

    ETOPOSIDE or VP-16 is primarily associated with myelosuppression. Tumor lysis syndrome (TLS) is also possible with concurrent hyperkalemia, hyperphosphatemia, hyperuricemia and hypocalcemia. Uric acid nephropathy, ARF due renal tubular obstruction, metabolic acidosis & nephrolithiasis can also occur with this medication.

    IFOSFAMIDE is associated with renal and neurologic toxicity.

    ASPARIGINASE (an enzyme) is associated with neurologic and hepatic toxicity as well as urticaria, anaphylaxis and decreased fibrinogen levels.

    METHOTREXATE may cause renal tubular injury.

    MITOMYCIN C may cause pulmonary toxicity.

    NITROGEN MUSTARD may cause myelosuppression and local tissue damage.

    NITROSUREAS (BCNU, CCNU) may cause myelosuppression, renal and pulmonary toxicity.

    TAXOL may cause hypersensitivity reaction, myelosuppression, cardiac toxicity and peripheral neuropathy.

    VINCRISTINE may cause neurotoxicity (autonomic neuropathy or encephalopathy), seizures and dilutional hyponatremia.

    VINBLASTINE may cause myelosuppression and is associated with local phlebitis.


    PROMINENT VASCULAR markings may be indicative of left to right shunt flow or interstitial lung disease such as pulmonary fibrosis.

    (see article under ADULT: ICU)


    Small PVC or silastic rubber catheters are placed in the second or third intercostal space of the mammillary line for pnuemothorax drainage or int the fifth to seventh space laterally for drainage of effusions and hemothoraces. Both 5 French and larger 8.5 French 15 cm pigtail catheters are available for placement by the Seldinger technique.

    Have the patient inspire maximally and hold his/her breath. Initially retract the chest tubes 0.5 to 1 inch prior to removing them smoothly and rapidly. Apply pressure with prepared dressings over chest tube insertion site when removing. Instruct patient to breathe normally. Most of the discomfort of chest tube removal relates to the initial movement of the tube. Removing the chest drain at END-INSPIRATION prevents the accidental entrance of air into the pleural space.


    Symptomatic CHF is clearly one of the most ominous findings in the patient presenting for surgery. In the Rotterdam Study of chronic disease in adults over the age of 55, only 60% of the people with LVEF of less 25% were symptomatic.

    CHF patients require extensive invasive monitoring in the intraoperative and postoperative period.

    normal to high HR
    sinus rhythm
    normal or increased preload
    decreased SVR
    increased inotropy


    CHF is defined as a syndrome of dyspnea and fatigue caused by LV dysfunction and activation of neurohumoral mechanisms that promote fluid retention. LV dysfunction is best described as either systolic or diastolic dysfunction and therapy will differ according to physiology. In the Rotterdam Study of chronic disease in adults over the age of 55, only 60% of the people with LVEF of less 25% were symptomatic. But conversely, approximately 30-50% of those with CHF have normal EF.

    FINDINGS include JVD, hepatomegaly, peripheral edema, S3 gallop, bibasilar rales, cardiomegaly and history of pulmonary edema.

    SYSTOLIC DYSFUNCTION (low EF secondary to inability to eject into a high pressured aorta) comprises 66% of those with CHF but 20% may not meet strict criteria for CHF (namely high LVEDP or high LAP read as PAWP). Prognosis is worse for CHF patients with systolic dysfunction.

    THERAPY is directed at improving performance with inotropes of little benefit to those with diastolic dysfunction. Symptomatic patients are treated with positive inotropes, diuretics, ACE inhibitors and vasodilators. Asymtomatic patients can be treated with ACE inhibitors alone.

    DIASTOLIC DYFUNCTION is defined as an inability to fill the LV with normal LA filling pressures. Prognosis is generally better than for these patients with diastolic dysfunction.

    THERAPY is focused on prevention of ischemia. Symptomatic patients are treated with ß-blockers and CCB. Asymptomatic patients are treated with antihypertensive regimens as the primary goal is to prevent the end organ damage of HTN.

    See separate entries for SYSTOLIC and DIASTOLIC DYSFUNCTION.


    CHIARI I MALFORMATION is characterized by herniation of the cerebellar tonsils through the foramen magnum into the cervical spinal canal. The cerebellar tonsils often are elongated and peglike. Mild caudal displacement and flattening or kinking of the medulla may be present. The vermis cerebelli and the fourth ventricle are normal or only minimally deformed. CMI is not directly associated with other congenital brain malformations. Myelomeningocele is a feature of Chiari II malformation.

    Symptoms may include suboccipital headaches, ocular symptoms (including retro-orbital pain, visual disturbances, photophobia, and diplopia), otoneurologic symptoms (including dizziness, vertigo, hearing disturbances, oscillopsia, nystagmus, and synkinesis), hindbrain compression symptoms (including weakness, paresthesia, ataxia, cranial nerve palsies, dysphagia, dysphasia, palpitations, syncope, apnea, and sudden death), SYRINGOMYELIA symptoms (including central cord syndrome, impaired sensation, impaired motor control, gait disturbance, torticollis, bowel or bladder symptoms, neuropathic joints, trophic phenomena and pain) and spinal cord dysfunction, which is present in as many as 94% of patients with syringomyelia and 66% without syringomyelia.

    The CHIARI II MALFORMATION is a more complex anomaly with skull, dural, brain, spinal and spinal cord manifestations. This disorder is almost invariably associated with myelomeningocele. Mortality rates are high.


    CH is useful for procedural sedation for children less than three at oral doses between 25-100 mg/kg with a maximum of 2 grams. Despite a wide margin of safety, CH may cause airway obstruction or repiratory depression in up to 6%. The drug is restricted in some countries secondary to theoretical carcinogenicity.


    Chlordiazepoxide or LIBRIUM is a benzodiazepine that exerts anxiolytic, sedative, appetite stimulating and weak analgesic effects. The medication may possess some peripheral anticholinergic activity. It has minimal depressant effects on ventilation and circulation in the absence of other CNS depressants.

    DOSING for premedication or sedation is at 5-10 mg (0.2 mg/kg) orally or 50-100 mg IM. For withdrawal symptoms, 50-100 mg may be given IM/IV or PO every 34 hours. Chlordiazepoxide is supplies in 5, 10 and 25 mg tablets.

    PHARMACOKINETICS Peak effects are achieved within five minutes and the duration of action ranges from 15-60 minutes for IV dosing and 2-6 hours following IM or PO dosing.


    Chloroprocaine (a modification of procaine) is a short duration amino ester LA with pKa of 8.9 prepared in solution with a pH of 2.5 to 4.0. It is characterized by rapid onset of action despite a high pKa.

    TOXICITY Due to its extremely low toxicity, a relatively high concentration is used. It has an extremely short plasma half-life because it is metabolized by cholinesterase and reports of CNS toxicity are extremely unusual. The TOXIC DOSE is thought to be in the range of 800-1000 mg or higher with epinephrine. It is thought to be the least toxic to the CNS and cardiovascular system of all agents in current use.

    The most relevant CLINICAL use is for epidural anesthesia. It may also used in peripheral blocks of short duration as well as in combination with long acting LA. With the newest formulation, it might be useful for short SAB but it is doubtful that this will ever be thoroughly studied for historical reasons.

    In OBSTETRICS, chloroprocaine is used in situations where epidural anesthesia must be rapidly converted to high level for cesarean or rapidly providing anesthesia to the perineum for application of forceps. There is limited or no transmission to the fetus.

    CONTROVERSY still exists with the use of chloroprocaine related to reports of persistent and serious neurological deficits associated with accidental SA injection. It should be noted that incremental dosing was almost invariably NOT utilized in the cases reported.

    It is most likely that the preservative and antioxidant, BISULFITE was responsible for this neurotoxic phenomenon and all preservatives have subsequently be removed. Problems have NOT been reported since the reformulation.

    SECOND CONTROVERSEY Epidural anesthesia with chloroprocaine has been reported to be associated with persistent severe lumbar muscle SPASM. This may be associated with the acid pH of chloroprocaine and the phenomenon is dose related (most commonly after 40 mL). The muscle spasm is NOT related to preservatives (bisulfite or methylparaben). Most authorities take this risk of muscle spasm which can present as opisthotonus as a relative contraindication to the use of chloroprocaine for outpatients at this time. Further investigation is pending but it is recommended that dosing limited to 25 mL may reduce the incidence of spasm to 5% or less.

    DISADVANTAGES One of the metabolites (4-amino 2-chloroprocaine) may impair subsequent action of bupivicaine in the epidural space. Epidural opioids are thought to be less effective following chloroprocaine for reasons that are not clear.


    Chlorpromazine is a phenothiazine tranquilizer with strong antiemetic, antiadrenergic, anticholinergic and sedative effects. The drug has weak antiserotonergic, antihistaminic and ganglionic blocking activity as well. The neuroleptic actions are most likely due to antagonism of dopamine as a synaptic neurotransmitter in the basal ganglia and limbic portions of the forebrain. Moderate extrapyramidal effects are evidence of interfernece with the normal actions of dopamine. The drug is useful as an antipsychotic, premedication, antiemetic and hiccough relieving therapy.

    DOSING for premedication is at 25-50 mg (0.5-1 mg/kg) orally or 12.5-25 mg (0.25-0.5 mg/kg) IM. The IV formulation should be given slowly at a rate of 1 mg per minute at a dose of 25-50 mg (0.25-0.5 mg per kg). The drug may be given every 6-8 hours for nausea or hiccoughs. Maximum IM dose for children is 40 mg/day for children less than 5 years of age and 75 mg/day for children 5-12 years of age.

    PHARMACOKINETICS Onset of action is rather slow at 30-60 minutes with the duration of action at 4-6 hours for PO dosing and 3-4 hours following IM dosing.

    The drug may suppress the laryngeal reflex with possible aspiration of vomitus. The drug may also lower the seizure threshold.

    Hypotension with any of the phenothiazines should NOT be treated with epinephrine as the phenothiazines cause a reversal of epinephrine’s vasopressor effects and a further lowering of BP. Drug induced hypotension should rather be treated with norepinephrine or phenylephrine.


    CHOLESTEOTOMA is keratinizing stratified squamous epithelium and accumulated desquamated epithelium within the middle ear or other pneumatomized portions of the temporal bone. They may be congenital or acquired as a complication or chronic middle ear inflammation. The condition presents with foul otorrhea, bleeding and conduction hearing loss secondary to destruction of the ossicular chain. It may be associated with otalgia, facial nerve paralysis, vertigo or intracranial complications.

    The routine use of FACIAL NERVE monitoring remains controversial. A survey of practicing otologists in 1990 showed that most experienced otologists do not believe that facial nerve monitoring is obligatory. Many experienced otologists only use it occasionally. Facial nerve monitoring requires experience and is unlikely to provide meaningful protection to an inexperienced operator.


    The physiology of the blue bloaters differs from that of COPD in that


    Patients with advanced disease develop intrapulmonary shunts, hypoxia, polycythemia and cor pulmonale.


    Cimetidine was the first commercially available drug to be used for peptic ulcer disease. It is an oral H2-receptor antagonist similar to famotidine, nizatidine and ranitidine. Cimetidine is a known inhibitor of many of the isoenzymes of the hepatic CYP450 enzyme system. Thus it exhibits many significant drug interactions with other medications.

    MECHANISM Cimetidine blocks the effects of histamine at the receptor located on the basolateral membrane of the parietal cell (designated the H2-receptor). The result is a reduction of both gastric volume and gastric acidity. Cimetidine decreases the amount of gastric acid released in response to other stimuli including food, caffeine, insulin, betazole and pentagastrin.

    Cimetidine does not reduce acid-output as dramatically as the proton-pump inhibiting medications (omeprazole). Cimetidine does not appear to alter gastric motility, gastric emptying, esophageal pressure or the secretion rate of the gallbladder or pancreas.

    DOSING Adults are given 800 mg PO at bedtime or 400 mg tiwce each day. IV doses are at 300 mg IV four times each day.

    INTERACTIONS Cimetidine can prolong opioid effects by decreasing hepatic blood flow and diminishing hepatic metabolism. Other drugs affected by concomitant cimetidine use include lidocaine, procaine and propranolol. Ranitidine can also reduce hepatic blood flow but binds less to the CYP450 system and has less impact on opioid metabolism than cimetidine.

    SIDE EFFECTS may include headache, cytopenias, bronchospasm, sinus tachycardia, bradycardia, AV block and premature ventricular contractions.


    DOSING for intubation at 0.2 mg per kg or 14 mg for average adult. This is four times the ED95 of 0.05 mg/kg. The PEDIATRIC intubating dose is 0.1-0.2 mg per kg. Provided in 2 mg per mL concentration hence following the 1 mL per 10 kg rule.

    INFUSIONS are administered at 1-3 mcg/kg/minute (less for use with potent inhalation agents).

    Devoid of the histamine releasing properties seen with atracurium, CISATRACURIUM also has slightly quicker onset (1.5-3 minutes) and similar duration of action (55-65 minutes). Cisatracurium has three times the potency of atracurium. Cisatracurium makes up 15% of the ten isomers of atracurium.

    In a 2001 study, cisatracurium is reported to be the least expensive NMB for brief pediatric procedures (1-2 hours) when NMB is indicated.

    METABOLISM is 20% organ dependent unlike atracurium (which is entirely non-organ dependent). In vitro studies demonstrate 80% metabolism by HOFFMAN degradation (a pH and temperature dependent process) to form LAUDANOSINE and one other metabolite. In CONTRAST to atracurium, nonspecific plasma esterases are NOT involved in metabolism.

    LAUDANOSINE (a product of atracurium and cisatracurium) can cause transient hypotension and with higher doses can lead to CNS excitation (twitching and seizures) in laboratory animals. Laudanosine levels with cisatracurium are five-fold LESS than with atracurium.


    Cousins MJ. Intrathecal and epidural administration of opioids. Anesthesiology 1984;61:276–310.

    White PF. Ketamine – its pharmacology and therapeutic uses. Anesthesiology 1982;56:119–36.

    Revill SI. The reliability of a linear analogue for evaluating pain. Anaesthesia 1976;31:1191–8.

    Gronert GA. Malignant hyperthermia. Anesthesiology 1980;53:395–423.

    Eger EI II. Minimum alveolar anesthetic concentration: a standard of anesthetic potency. Anesthesiology 1965;26:756–63.

    Watcha MF. Postoperative nausea and vomiting. Its etiology, treatment, and prevention. Anesthesiology 1992;77:162–84.

    Wang JK. Pain relief by intrathecally applied morphine in man. Anesthesiology 1979;50:149–51.

    Yaksh TL. Studies in the primate on the analgetic effects associated with intrathecal actions of opiates, alpha-adrenergic agonists and baclofen. Anesthesiology 1981;54:451–67.

    Mangano DT. Perioperative cardiac morbidity. Anesthesiology 1990;72:153–84.

    Yeager MP. Epidural anesthesia and analgesia in high-risk surgical patients. Anesthesiology 1987;66:729–36.

    Albright GA. Cardiac arrest following regional anesthesia with etidocaine or bupivacaine. Anesthesiology 1979;51:285–7.

    Cormack RS. Difficult tracheal intubation in obstetrics. Anaesthesia 1984;39:1105–11.

    Woolf CJ. Preemptive analgesia – treating postoperative pain by preventing the establishment of central sensitization. Anesth Analg 1993;77:362–79.

    Reves JG. Midazolam: pharmacology and uses. Anesthesiology 1985;62:310–24.

    Slogoff S, Keats AS. Does perioperative myocardial ischemia lead to postoperative myocardial infarction? Anesthesiology 1985;62:107–14.

    Bromage PR. Epidural narcotics for postoperative analgesia. Anesth Analg 1980;59:473–80.

    Froese AB. Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology 1974;41:242–55.

    Quasha AL. Determination and applications of MAC. Anesthesiology 1980;53:315–34.

    Melzack R. On the language of pain. Anesthesiology 1971;34:50–9.

    Maze M. Alpha-2 adrenoceptor agonists: defining the role in clinical anesthesia. Anesthesiology 1991;74:581–605.


    Cleft lip with or without cleft palate occurs in 1:1000 births. Isolated cleft palate occurs in 1:2500 births. Associated syndromes include fetal hydantoin, fetal trimethadione, Mohr syndrome, orofaciodigital syndrome, Robert’s syndrome, trisomy 18 and 4P deletion.

    Children with larger defects are less likely to have problems with airway obstruction. Large defects may make it possible for the tongue to prolapse into the nasopharynx.

    Oral RAE tubes are used to provide adequate surgical exposure. Dingman gags may be used to hold the mouth open while providing a groove to hold the ETT in place. Obstruction of the tube is possible and breath sounds and lung compliance should be continuously monitored. Blood loss can be significant for cleft palate repairs.

    Decadron (0.5-1 mg per kg) can be given to decrease post-operative swelling. Valley does not empirically utilize PONV drugs. Typical repairs may take from 60-120 minutes. Tongue sutures are usually placed to provide the ability to pull the tongue out and off of the palate following surgery.

    Postoperative obstruction may occur secondary to swelling of the hypopharynx (possibly related to gags), subglottic edema, flap edema, increased oral secretions, overlooked throat packing and posterior displacement of the tongue.


    Clonidine stimulates presynaptic alpha-2 receptors to inhibit cAMP production and inhibit further NE release. Central alpha-2 receptors in the locus ceruleus activate a descending inhibitory pathway to the spinal cord resulting in decreased sympathetic outflow. Additional receptors at the dorsal horn C fibers inhibit the transmission of nociceptive information. Clonidine is most often used for HTN but has numerous off label uses.

    CARDIAC RISK reduction for patients unable to take ß-blockers is afforded by 0.2 mg PO bid or TTS-2 patch (0.2 mg/24 hours) beginning on the evening prior to surgery.

    NEURAXIAL Small studies reveal that 150 mcg of intrathecal clonidine added to bupivicaine is more effective than epinephrine 0.2 mg in prolonging sensory AND motor blockade. Larger doses have been used in patients with cancer pain.

    Clonidine may be added to the single shot caudals in the pediatric population at a dosage of 1-5 mcg/kg or 1 mcg/kg in the outpatient. Clonidine may be added to continuous epidural infusions at total dosages between 0.15-0.25 mcg/kg/hour which generally translates to concentrations between 0.4-1.2 mcg per mL.

    Clonidine is not recommended for caudals in children less than 6 months of age due to 3 case reports of apnea in the PACU that may or may not be related to the use of clonidine.

    PERIPHERAL BLOCKS Clonidine may be added to peripheral nerve blocks (1 mcg/kg) and has been shown to prolong the period of analgesia.

    MISCELLANEOUS uses include preoperative anxiolysis at doses up to 5 mcg/kg PO and up to 1 mcg/kg IV. Patches for HTN in the pediatric patient should provide 5-20 mcg/kg/day.

    Clonidine at 150 mcg IV has been evaluated for treatment of postoperative SHIVERING in adults. It is as effective as meperidine 25 mg with a similar onset of action within 2-6 minutes. BP decreases by an average of only 10%.

    Dosing of clonidine at 1-3 mcg/kg IV after induction will attenuate the emergence DELERIUM that is common in pediatric patients maintained with sevoflurane and desflurane. Similar doses may also be useful for pain and anxiety in the PACU.

    Large doses of clonidine may produce significant hypotension, bradycardia and sedation. Some studies have demonstrated that larger epidural doses tend to produce a systemic vasoconstriction that overrides the central hypotensive effect. Overdose has occasionally been effectively treated with naloxone.

    Oral doses often prescribed for ADHD range between 0.1-0.3 mg per day divided into 3-4 doses. This is simiar to the occasionally administered premedication dose. Clonidine is reportedly helpful for ADHD patients with comorbid tic disorders or insomnia. It is also good for severe impulsivity, hyperactivity and aggression. It may stimulates appetite. It is especially helpful in younger children with ADHD symptoms asociated with prenatal insult or syndrome such as Fragile X. Three controlled trials have found benefits for patients with ADHD. Depression occurs in about 8% of users but usually resolves if the medication is discontinued; sedation can also be a problem. Recent investigations into possible interactions between clonidine and the stimulant drugs by the AMA, the FDA and others have concluded that the two drugs do not interact.


    PLAVIX is an inhibitor of platelet aggregation similar to TICLID which generally should be discontinued 5-7 days prior to surgery. See other data under ANTIPLATELET MEDS.


    Small airways lacking cartilaginous support depend on radial traction caused by the elastic recoil of surrounding tissue to keep them open. Patency of these airways, especially in basal areas, is highly dependent on lung volume. The volume at which these airways begin to close in dependent parts of the lung is called closing capacity. At lower lung volumes, alveoli in dependent areas continue to be perfused but are no longer ventilated. Intrapulmonary shunting of deoxgenated blood promotes hypoxemia.

    CC is usually measured using a tracer gas (xenon 133), which is inhaled near residual volume and then exhaled from total lung capacity.

    CC is normally well below FRC, but it rises steadily whith age. This increase is probably responsible for the normal age-related decline in arterial oxygen tension. At an average age of 44 years, closing capacity equals FRC in the supine position. By age 66, closing capacity equals or exceeds FRC in the upright position in most individuals. Unlike FRC, closing capacity is unaffected by posture.

    ClC = closing volume + RV


    The CLOSTRIDIUM TETANI neurotoxin, like those of C botulinum, is composed of a light chain, which is catalytic, and a heavy chain, which is necessary for toxin specificity and cell targeting.

    The toxin enters the nervous system primarily via the presynaptic terminals of lower motor neurons, where it can produce local failure of neuromuscular transmission. It then exploits the retrograde axonal transport system and is carried to the cell bodies of these neurons in the brain stem and spinal cord, where it expresses its major pathogenic action.

    Once the toxin enters the CNS, it diffuses to the terminals of inhibitory cells, including both local glycinergic interneurons and descending gamma-aminobutyric acid-secreting (GABA) neurons from the brain stem. The toxin degrades synaptobrevin, a protein required for docking of neurotransmitter vesicles with their release site on the presynaptic membrane. By preventing transmitter release from these cells, tetanospasmin leaves the motor neurons without inhibition. This produces muscular rigidity by raising the resting firing rate of motor neurons and also generates spasms by failing to limit reflex responses to afferent stimuli. Excitatory transmitter release in the spinal cord can also be impaired, but the toxin appears to have greater affinity for the inhibitory systems.

    The autonomic nervous system is affected as well and is predominantly manifested as a hypersympathetic state induced by failure to inhibit adrenal release of catecholamines.

    Toxin binding appears to be an irreversible event. At the neuromuscular junction, recovery depends on sprouting a new axon terminal. This is probably the case at other affected synapses as well.

    CLOSTRIDIUM BOTULINUM makes numerous extremely potent neurotoxins which are released when the organisms die and autolyse. Botulinum toxins act at the peripheral nerve endings, where they are bound, cleaving either synaptobrevin (as described for tetanus toxin) or synapse-associated proteins, called SNAP-25 and syntaxin.

    Toxin-infected neurons are unable to release acetylcholine at the neuromuscular junction and at the synaptic ganglia and parasympathetic motor end-plates of the autonomic nervous system, leading to DESCENDING paralysis from the cranial nerves down to the extremities.

    As with the tetani infection the synapse is apparently rendered permanently useless. Recovery of function requires sprouting of the presynaptic axon and subsequent formation of a new synapse.

    Botulinum toxin is transported within nerves in a manner analogous to tetanospasmin and can thereby gain access to the central nervous system. However, symptomatic central nervous system involvement is rare.

    Miscellaneous causes of coagulopathy that may preclude neuraxial techniques include:

    monoclonal gammopathy


    Aortic arch obstruction is divided into three types: (1) localized juxtaductal coarctation (by far, the most common), (2) hypoplasia of the aortic isthmus and (3) aortic arch interruption.

    JUXTADUCTAL coarctations usually occurs just distal to the left subclavian artery but may involve components of the aorta that are preductal, postductal or both. Closure of the aortic end of the ductus arteriosus (following pulmonary end closure) occurs several weeks or months after birth and usually occurs with a concomitant abrupt increase in the impedence at the coarctation.

    This lesion occurs 2-5 times more commonly in MALES than in females and there is a high degree of ASSOCIATION with gonadal dysgenesis (Turner’s syndrome) and bicuspid aortic valve. Other common associated anomalies include VSD and mitral stenosis or regurgitation.

    Severe obstruction in infancy is a prominent cause of LV failure and systemic hypoperfusion. Substantial left-to-right shunting across a patent foramen ovale and pulmonary venous hypertension secondary to heart failure cause pulmonary arterial hypertension. Because little or no aortic obstruction existed during fetal life, the collateral circulation in the newborn period is often poorly developed. In these infants, peripheral pulses characteristically are weak throughout the body until left ventricular function is improved with medical management. A significant pressure difference then develops between the arms and the legs, allowing detection of a pulse discrepancy.

    Most infants with early-onset heart failure respond poorly to medical management and balloon angioplasty, surgical excision of the coarctation or a subclavian flap angioplasty often is required. Some prefer an operation consisting of excision of the area of coarctation and extended end-to-end repair or end-to-side anastomosis with absorbable sutures to allow remodeling of the aorta over time.

    Aortic obstruction may develop slowly in infants in whom the posterolateral aortic shelf is not prominent at birth and in whom ductus arteriosus constriction is gradual. In these babies, compensatory myocardial hypertrophy and an extensive collateral circulation have time to develop. If the obstruction does not intensify and cardiac failure does not occur by age 6-9 months, circulatory compensation is likely until adult life.


    Three basic types of repair are used for correction of the coarctation and all are done through a left thoracotomy so that epidurals for POP are often very useful in the older patient.

    Cross-clamping of the aorta is obviously necessary and in older children partial CPB or a shunt may be used if the adequacy of collateral circulation is in question.

    ANESTHETIC preparation includes some provision for measuring blood pressure to the lower extremeties (usually with the use of a transport monitor) and preparation of nitroprusside and esmolol infusions for control of what is often a malignant hypertension in the postoperative period (lasting up to one week). Clonidine in the epidural infusion may be useful for control of this postoperative hypertension.

    There should be some allowance for hypertension (as high as 30% higher than baseline) of the upper circulation during cross-clamping.

    Dosing of methylprednisilone (controversial) and passive hypothermia (down to a goal of 34 degrees) may provide some degree of cord protection. The methylprednisilone is dosed at a 30 mg per kg IV loading dose and can be followed by 5.4 mg/kg/h for twenty-four hours. The incidence of paraplegia is between 0.14-0.4%.

    Patients older than six months may be most effectively managed by early extubation.


    Surgery is performed through a left thoracotomy and children older than six months may benefit from caudal epidural catheter placement and early extubation. Younger infants will typically remain on the ventilator for the first 12-24 hours after surgery and generally do not receive epidurals.

    ANESTHETIC requirements include preparation of phenylephrine, nitroprusside and esmolol infusions (at the standard concentration in a syringe pump).

    Other PREPARATIONS include: double transducer for CVP and arterial pressures, warming blanket on the bed but not turned on, transport monitor for the lower extremities, blood in the room at incision (transfusions are seldom required), albumin for fluid boluses, cefuroxime prophylaxis, mannitol, vecuronium, arterial line placed in the right radial, right internal jugular CVC and at least one peripheral IV.

    Standard INDUCTIONS are utilized and the patient is maintained with fentanyl (20-50 mcg/kg) and 0.5-0.8 MAC of isoflurane. Vecuronium is most often utilized for an early recovery and verification that spinal cord injury has not occured following the period of cross clamping.

    The CROSS CLAMP period is typically less than 30 minutes. The patient should be allowed to cool to 34 degrees but a warming blanket is placed on the bed for use as the clamp comes off and through emergence. Mannitol is often recommended at 0.5 g/kg prior to cross clamp but steroids are not routinely used for cord protection. A transport monitor should be used to monitor the lower extremity blood pressure and oximetry wave throughout the procedure. Shunting across the aorta is usually not performed in the infant despite a possible drop in lower extremity perfusion pressures during the cross clamp period.

    The upper extremity blood pressure may be permitted to rise by 25-30% over baseline pressures but will often fall dramatically after the clamp is removed requiring fluid boluses, phenylephrine infusions and rarely the brief reapplication of the aortic clamp.

    HTN is possible (as with older children and adults) but is usually treated easily with nitroprusside and esmolol to blunt any reflex tachycardia and tachyphylaxis. Hypertensive physiology may remain active for up to one week following the resection.


    Cocaine is a naturally occurring alkaloid and a topical anesthetic. The sympathetic vasoconstriction occurs secondary to a block in the uptake of NE at the adrenergic nerve endings. Small doses initially produce bradycardia and a decrease in BP by vagal stimulation but moderate doses will increase BP and HR.

    DOSING The LA is used for topical anesthesia and vasoconstriction. Cocaine is available in 1-4% solutions and is given topically at 1 mg/kg. Nasal instillation is provided at 1-2 mL per nostril (1-4% solution).

    PHARMACOKINETICS Onset of action is within one minute and peak effects occur within 2-5 minutes. The elimination half-life is between 30-90 minutes. Metabolites may be detected for up to 10 days (BJA 2006).


    Cocaine blocks the reuptake of NE and DA resulting in an exaggerated sympathetic stimulation.

    CLINICAL USE should be avoided in those patients taking guanethidine, reserpine, TCA or MAOI. The MAXIMUM dose of cocaine used in clinical practice is 200 mg for the adult or 3 mg/kg. 1.5 mg/kg is the preferrable maximum because this dose has been shown not to exert any significant sympathomimetic effect in combination with halothane.

    In some patients, doses as small as 0.4 mg/kg may cause HTN, VFIB, TdP and cardiac arrest. Prolonged QT (Na and K channel inhibition) is thought to cause the arrhythmias and SODIUM bicarbonate has been demonstrated to correct the problems.

    Although 1 gram is considered to be the usual LETHAL dose for an adult, considerable variation occurs and systemic reactions may appear with as little as 20 mg.

    Treatment of HTN episodes associated with toxicity should NOT include propranolol or other ß blockers as unopposed alpha stimulation has resulted in lethal hypertensive crises. PHENTOLAMINE is often cited as an agent of choice. NTG may be useful and studies related to the use of CCB are ongoing. Hydralazine use often results in an undesirable tachycardia.

    BENZODIAZEPINES have been shown to be most helpful in preventing the hyperthermia, acidosis, seizures, agitation and CV excitation of acute cocaine intoxication. Bicarbonate appears to have an important role in the setting of acute toxicity.

    LIDOCAINE can be safely used for ominous arrhythmias and the most common arrhythmias include sinus tachycardia, PVC, VT, VF and asystole. Lidocaine should not be utilized for the treatment of bupivicaine toxicity. BRETYLIUM (20 mg per kg IV) or AMIODARONE (150 mg) quickly reverses the cardiac depression and raises the threshold for VT secondary to LA toxicity.

    Patients with cocaine intoxication presenting with complaints of chest pain must be carefully managed because even young patients can sustain MI. Use of an alpha blocking agent (such as PHENTOLAMINE) reduces cocaine associated coronary vasoconstriction and myocardial ischemia. Chronic use of cocaine sensitizes the coronaries to catecholamine vasoconstriction.

    For GA, halothane should be avoided. Isoflurane has been associated with a dramatic increase in SVR, prolonged QTc and possible tendency to produce arrhythmias (BJA 2006 97:654).


    Typical code packs may contain the following items in addition to the routinely carried code medications.

    fast-track LMA with stylet
    fast-track ETT
    LMA number 4
    Eschmann or bougie nylon stylet
    needle cricothyroidotomy kit
    quantitative CO2 monitor
    airway exchange catheter

    The outside areas difficult airway box will have other items.

    jet ventilator tubing
    lighted stylet
    LMA sizes 3 and 5


    TYLENOL WITH CODEINE elixir contains 120 and 12 mg per 5 mL. Dosing for CODEINE in patients older than one year of age is at 0.5-1 mg/kg PO/SC/IM every 4-6 hours.

    3-6 years: 5 mL every 4-6 hour
    7-12 years: 10 mL every 4-6 hour

    ADULT DOSING is commonly initiated at 60 mg (1 mg/kg) given orally every 3-4 hours. Parenteral formulations are available but infrequently utilized.

    Tylenol #2 15 mg
    Tylenol #3 30 mg
    Tylenol #4 60 mg
    Tylenol elix 12 mg/5 mL

    ORAL codeine is approximately six times less potent that oral morphine.

    The Combitube is a double lumen tube with an esophageal lumen (closed at the distal end with perforations at the paharyngeal level) and a tracheal lumen open at the distal end. A large oropharyngeal latex balloon presses against the base of the tongue to seal the oral and nasal cavities. The smaller distal balloon will seal the esophagus or trachea depending on its position.

    When compared with the LMA, the Combitube provides better protection against aspiration and enables positive pressure ventilation with pressures exceeding 20 cmH2O.

    The primary INDICATION for the Combitube is as a backup device for airway management. It may be most useful for patients with visualization obscured by edema, blood, tissue damage or anatomic distortion. Uses in elective surgery include patients with known difficult airways and professional voice users concerned about vocal cord damage.

    The Combitube is available only in small (for patients 4-5.5 feet tall) and large (for those taller than 5.5 feet).

    The tube is inserted without laryngoscopy until the printed rings are aligned with the teeth. The distal balloon is filled with 5-15 mL of air while the proximal balloon requires 85-100 mL of air to seal the airway. With blind insertion, the tube is most commonly placed within the esophagus and ventilation can be maintained through the esophageal lumen (labelled lumen 1). If breath sounds are not present, then it is likely that the trachea has been intubated and ventilation is performed through the tracheal lumen (labelled lumen 2).

    In the prehospital setting, paramedics placed the Combitube without complications in 70% of those for which the Combitube was used primarily. In those patients which could not be intubated with standard laryngoscopy, the Combitube was placed with a success rate of just 60%.


    Congenital adrenal hyperplasia involves a functional defect in any of the five enzymatic steps required for cortisol synthesis but most commonly 21 (90-95% of cases) and 11-hydroxylase. This primary genetic defect transmitted as autosomal recessive impairs the ability of the adrenal cortex to synthesize cortisol causing increase feedback secretion of ACTH and adreno-cortical hyperplasia of the gland. Increase output of steroids proximal to the block (androgenic precursors) causes virilization in affected males and females. Its more severe form is associated with aldosterone deficiency and life-threatening salt wasting.

    Female pseudohermaphrodite due to virilizing CAH is the most frequent form of intersexuality found. The phenotypic picture varies from mild clitoral enlargement alone to complete masculinization of the urethral meatus at the tip of the penis. Prenatal diagnosis (southern blotting of DNA) is based on finding the disease gene on the short arm of chromosome 6. Likewise management in the mother (dexamethasone) is started empirically until the affected status is known by chorionic villus sampling. After birth management consists of cut-back or flap vaginoplasty with clitoral recession at 3-6 months of age. Children with high vaginal entry proximal to the urethra external sphincter can undergo early one-stage reconstruction at 8-12 months of age.

    Long term surgical results of female children show adequate sexual identification, reproduction, intellectual functioning and acceptable genitalia.


    Congenital lobar emphysema is an unusual lung bud anomaly characterized by massive air trapping in the lung parenchyma that nearly always occurs in infancy and affects males more commonly (2:1). Lobar over distension causes compression of adjacent lung tissue, mediastinal shift and decrease in venous return. When this occurs persistent progressive respiratory distress (dyspnea, tachypnea, wheezing, cough and cyanosis) develops requiring lobectomy.

    Asymptomatic CLE exists, more commonly beyond infancy and associated with an acute viral respiratory infection. Lobar hyperinflation, flat diaphragms and retrosternal air, mediastinal shift in simple films suggests the diagnosis. CT scan depicts the abnormal anatomy (lung herniation) and the morphology of the remaining lung. V/Q scans confirm the non-functioning nature of the affected lobe. Upper and middle right lobes are more commonly affected. Etiology centers in a combination of bronchial (flap/valve) obstruction with congenital cartilage dysplasia.

    Most common associated defect is cardiovascular (VSD, PDA). Symptomatic patients nearly always require lobectomy. Asymptomatic children do not benefit from surgical treatment but need close follow-up. Prenatally diagnosed cases need referral to surgery centers.


    Bacterial conjunctivitis is characterized by acute onset, minimal pain, occasional pruritus and sometimes exposure history. Staphylococcal and streptococcal species are the most common pathogens. Viral conjunctivitis is characterized by acute or subacute onset, minimal pain level, and often exposure history.

    Several studies demonstrate that acute conjunctivitis occurs with almost equal frequency between bacterial and viral causes. Viral conjunctivitis occurs more frequently in the summer and bacterial conjunctivitis occurs more often in the winter and spring. Mucopurulent conjunctivitis is caused by bacteria including (1) GPC: S epidermidis, S pyogenes and S pneumoniae, (2) GNC: Neisseria meningitidis and Moraxella lacunata and (3) GNR: genus Haemophilus and family Enterobacteriaceae.

    Treatment with antimicrobials and symptomatic therapy is recommended for all patients initially presenting with simple conjunctivitis. Numerous topical antimicrobial agents may be used, including topical sulfacetamide, erythromycin, gentamicin, ciprofloxacin or ofloxacin. Avoid neomycin solutions because 8-15% of patients have hypersensitivity reactions.


    Methylprednisolone, one 32-mg tablet, may be orally administered 12 and 2 hours before the study, or prednisone, one 50-mg tablet, may be orally administered 13 hours, 7 hours, and 1 hour before the study.

    If the patient had a previous moderate or severe reaction or one that included a respiratory component, an alternate study, such as sonography or MRI, should be considered. Otherwise, the following may be used: H1 antihistamines; diphenhydramine, one 50-mg tablet orally administered 1 hour before the study; H2-histamine receptor blockers, which is optional; cimetidine, 300 mg orally administered 1 hour before study; and/or ranitidine 50 mg orally administered 1 hour before the study.

    Most authorities restrict corticosteroid pretreatment to patients in whom previous idiosyncratic adverse reactions to ICM were moderate or severe. Usually, corticosteroids are well tolerated and cause no adverse effects when only a few doses are administered.

    Although the utility of H2-receptor blockers is questionable, these agents are well tolerated and might be of benefit, particularly because they are effective in the treatment of at least some allergic cutaneous reactions to agents other than ICM. However, H2 blockers should not be used without H1 blockers.

    The treatment of the nonidiosyncratic adverse reactions of nausea and vomiting is not considered a routine indication for corticosteroid premedication or the use of nonionic ICM.




    COPD is characterized by a destructive process of lung parnchyma resulting in a loss of elastic recoil. Obstruction can result in the formation of bullae with compression of normal lung tissue. COPD is the primary etiology of cor pulmonale.

    EVALUATION requires determining the extent of disease and the degree of reversible processes such as infection & bronchospasm. A SIMPLE DX may be made when the forced expiratory time is over SIX SECONDS which is the equivalent of an FEV1 less than one liter. CO2 retention occurs with FEV1:FVC ratios less than 0.35 and arterial CO2 over 50 mmHg is associated with an increased risk for postoperative complications.

    TLC over 7 liters
    FVC will be low
    FEV1 less than one liter
    RV over 33% of TLC

    The TOTAL CO2 on the electrolyte panel is equal to the bicarbonate plus dissolved CO2 (which adds about 2). A high number may indicate metabolic compensation for chronic hypercarbia.

    ANESTHESIA options are not limited but must take postoperative compromise into consideration.

    RA should not produce sensory block above T6 as this is associated with a decrease in ERV and limited ability to clear the airways with an effective cough.

    GA may be provided with any of the volatile agents. Isoflurane may better preserve HPV and decrease oxygen requirements. Nitrous oxide is not advisable for the patient with bullae or blebs which may expand and even rupture with the distension produced. GA may dry out the secretions of the airways.

    Large tidal volumes (10-15 mL/kg) with SLOW inspiratory time minimizes the likelihood of turbulent flow and maintains optimal VQ matching. The hazards of high airway pressures should be appreciated in the presence of pulmonary bullae. The use of large tidal volumes with slow inspiration should maintain oxygenation well without the deleterious CV effects of PEEP.

    If spontaneous ventilation is permitted, it should be recognized that the depression produced by the volatile agents will be greater as ventilation may be dependent on hypoxic drive.

    POSTOPERATIVE Vital capacity may be greatly decreased (up to 40%) for two weeks following upper abdominal or thoracic surgery. FRC does not decrease until about 16 hours after surgery suggesting that altered respiratory patterns are responsible. Any patient with a FEV1:FVC ratio less than 0.5 will likely require postoperative ventilation.


    Cor pulmonale is defined as an alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system. Pulmonary hypertension is the common link between lung dysfunction and the heart in cor pulmonale. Right-sided ventricular disease caused by a primary abnormality of the left side of the heart or congenital heart disease is not considered cor pulmonale, but cor pulmonale can develop secondary to a wide variety of cardiopulmonary disease processes. Although cor pulmonale commonly has a chronic and slowly progressive course, acute onset or worsening cor pulmonale with life-threatening complications can occur.

    Several different pathophysiologic mechanisms can lead to pulmonary hypertension and, subsequently, to cor pulmonale. These pathogenetic mechanisms include (1) pulmonary vasoconstriction due to alveolar hypoxia or blood acidemia; (2) anatomic compromise of the pulmonary vascular bed secondary to lung disorders, eg, emphysema, pulmonary thromboembolism, interstitial lung disease; (3) increased blood viscosity secondary to blood disorders such as polycythemia vera, sickle cell disease, macroglobulinemia; and (4) idiopathic primary pulmonary hypertension.


    Bulbar conjunctival injection is usually present. Visual acuity is usually normal, unless the abrasion lies within the central visual axis or is large (with the usual corneal endothelial folds and anterior chamber reaction associated with such abrasions).

    Routine use of topical antibiotics for corneal abrasions remains controversial. Many emergency physicians have stopped using these agents for minor injuries, although others continue treating corneal abrasions with broad-spectrum antibiotic ointments for infection prophylaxis and lubrication. Antibiotic use persists despite unproved efficacy and evidence that ointments may retard corneal epithelial healing. For large or dirty abrasions, many practitioners prescribe broad-spectrum antibiotic drops, such as trimethoprim/polymyxin B (Polytrim) or sulfacetamide sodium (Sulamyd) which are inexpensive and least likely to cause any complications. Alternatives are an aminoglycoside or a fluoroquinolone. Contact lens-associated abrasions warrant antibiotic treatment due to their propensity for developing infectious corneal ulcers (microbial keratitis). Coverage for gram-negative organisms (especially pseudomonads) is recommended with agents such as gentamicin (Garamycin), tobramycin (Tobrex), norfloxacin (Chibroxin) or ciprofloxacin (Ciloxan). Avoid antibiotics containing neomycin (Neosporin) because of the higher incidence of allergy to neomycin in the general population. Antibiotic drops are more comfortable than ointments but must be administered every 2-3 hours. Ointments, which retain their antibacterial effect longer, can be used less often (every 4-6 hours) but are more uncomfortable due to visual blurring.

    Some ophthalmologists are advocating that diclofenac (Voltaren) or ketorolac (Acular) drops and a disposable soft contact lens be used in addition to antibiotic drops. This therapy may prove to be an effective alternative to patching, permitting patient to maintain binocular vision during treatment. Compared to patching, the contact lens used with the NSAID may reduce pain.

    Minor abrasions should heal within 24-48 hours and do not require follow-up if completely asymptomatic at 48 hours. Large abrasions should be examined every 2 days until reepithelialization has occurred and the potential for infection no longer exists. Many ED physicians refer patients with large abrasions to an ophthalmologist for follow-up care.

    Advise eye rest (no reading or work that requires significant eye movement that might interfere with reepithelialization). Avoid light or wear sunglasses for comfort if significant photophobia exists. Cycloplegics may be required twice a day for large abrasions with significant photophobia or blepharospasm until healing is nearly complete.

    In the vast majority of patients, prognosis is excellent with full recovery including visual acuity. Some deep abrasions (involving the corneal stromal layer) within the central visual axis (central area of the cornea directly over the pupil) heal but leave a scar. In these instances, a permanent loss of visual acuity may occur.


    RCA: leads II, III & aVF
    LCX: leads I & aVL
    LAD: leads V3-V5

    The RCA courses in the right AV groove and provides nutrient branches to the right ventricular free wall, extending to the acute margin of the heart. The distal extent of the RCA varies and may extend posteriorly as far as the obtuse margin of the heart. In 90% of patients, the RCA supplies the posterior descending artery at the crux of the heart, which supplies the AV node and the posterior aspect of the interventricular septum. The first branch arising from the RCA is the conal or infundibular branch, which courses anteriorly to supply the muscular right ventricular outflow tract or infundibulum. The RCA supplies blood to the atria with a highly variable pattern of small branches. The sinus node artery arises from the proximal RCA in approximately 50% of patients.

    The LCA arises from the mid position of the left anterior sinus of Valsalva just above the level of the free margin of the aortic valve leaflet and generally below the sinotubular junction. The left coronary ostium is usually single, giving rise to a short, common LCA trunk that branches into the LAD and circumflex coronary arteries. The LAD courses in the anterior interventricular groove, giving rise to the anterior septal perforating branches as it extends toward the cardiac apex. Small branches may arise from the LAD and supply the anterior wall of the right ventricle. Diagonal branches arise from the LAD and course at downward angles to supply the anterolateral free wall of the left ventricle.

    The Cx courses along the left AV groove, around the obtuse margin and posteriorly toward the crux of the heart. Should the Cx reach the crux of the heart and supply the posterior descending artery, the left coronary system would be termed dominant. This occurs in approximately 10% of patients. Atrial branches may arise from the Cx and supply the sinus node in 40% of patients. Obtuse marginal branches arise from the Cx system to supply the posterolateral aspect of the LV. In an estimated 70% of patients, a coronary branch (termed ramus medianus, intermedius or intermediate branch) arises early off the LCA system to supply an area between diagonal branches from the LAD and obtuse branches from the Cx systems.

    The majority of the population have a right dominant system with RCA giving rise to posterior descending, LA branch, AV nodal branch and one or more posterior LV branches. In a left dominant system the RCA supplies only the RA and RV. Balanced systems exist in 7% of the population.

    The SA node is supplied by the RCA (55%) or the left circumflex (45%). Dominance is attributed to that coronary which ultimately supplies the SA node.

    CORONARY LESIONS do not reduce CBF until there is 85% REDUCTION in lumen DIAMETER though maximal vasodilation is blunted at 30-45% stenosis and is abolished at 88-93%. COLLATERAL vessels are only visible when dialated secondary to regional oxygen deprivation.

    MAJOR RISK is attributed to:

    50% stenosis in three vessels
    70% stenosis in the LAD with 50% stenosis in one other vessel, or
    50% stenosis in the left main

    A combination of proximal LAD and proximal left circumflex is also know as LEFT MAIN EQUIVALENT or LMEQ.

    Leads II, III, aVF are most useful for detecting ischemia in the distribution of the RCA (RA, RV, SA node, AV node and bundle of His). Leads I, aVL are most useful for lesions of the CIRCUMFLEX artery (lateral LV). Leads V3-V5 detect ischemia in the distribution of the LAD coronary (anterolateral aspects of the LV).

    The coronary SINUS courses through the left AV groove to drain into the RIGHT atrium.


    CORONARY LESIONS do not reduce CBF until there is 85% REDUCTION in lumen DIAMETER though maximal vasodilation is blunted at 30-45% stenosis and is abolished at 88-93%. COLLATERAL vessels are only visible when dialated secondary to regional oxygen deprivation.

    MAJOR RISK is attributed to:

    50% stenosis in three vessels
    70% stenosis in the LAD with 50% stenosis in one other vessel, or
    50% stenosis in the left main

    A combination of proximal LAD and proximal left circumflex is also

    Leads II, III, aVF are most useful for detecting ischemia in the distribution of the RCA (RA, RV, SA node, AV node and bundle of His). Leads I, aVL are most useful for lesions of the CIRCUMFLEX artery (lateral LV). Leads V3-V5 detect
    ischemia in the distribution of the LAD coronary (anterolateral aspects of the LV).


    BASAL production of CORTISOL is approximately 20 mg per day. FIFTEEN times the basal amount or 300 mg is produced under stress. STRESS DOSING is generally recommended for patients who have had 7-14 days of therapy over the past year. Usual regimens include hydrocortisone 100 mg IV tid for three doses with an optional taper over three days following surgery. Most other preparations have insufficient mineralocorticoid effects.

    PEDIATRIC STRESS DOSING is less often necessary as the HPA axis is thought to recover more rapidly after use of exogenous steroids. Hydrocortisone may be given as a single dose at 2 mg/kg or tapered over several days with therapy beginning at 2 mg/kg every six hours.

    G M EQ
    cortisol 1.0 1.0 20
    cortisone 0.8 0.8 25
    aldosterone 0.3 3K
    prednisone 4.0 0.8 5
    prednisilone 4.0 0.8 5
    methylpred 5.0 0.5 4
    fludrocort 10 125
    Decadron 30 0 0.7

    The table above reflects the relative potencies and equivalent doses in milligrams.

    SIDE EFFECTS include suppression of the hypothalamic-pituitary-adrenal axis, weight gain and skeletal muscle wasting. Other side effects of chronic corticosteroid therapy include osteopososis, peptic ulcer disease, skeletal muscle myopathy, CNS dysfunction, peripheral blood changes (increased hematocrit and increased number of circulating leukocytes), inhibition of normal growth (inhibition of DNA synthesis and cell division), electrolye and metabolic changes such as hyperglycemia, hypokalemia and increased sodium reabsorption with edema and weight gain. Increased susceptibility to bacterial or fungal infection also accompanies treatment with corticosteroids.

    COTE ET AL 1995

    The risk of post-recovery room apnea following GA is not less than 5% until (1) the 35 week preterm is older than 48 weeks PCA, and (2) the 32 week preterm is older than 50 weeks PCA. The risk of post-recovery room apnea is not less than 1% until (1) the 35 week preterm is older than 54 weeks, and (2) the 32 week preterm is older than 56 weeks PCA (Anes 1995 82:809).


    Warfarin sodium and other coumarin anticoagulants act by inhibiting the synthesis of vitamin K dependent clotting factors, which include Factors II, VII, IX and X and the anticoagulant proteins C and S. Half-lives of these clotting factors are as follows:

    factor II: 60 hours
    factor VII: 4-6 hours
    factor IX: 24 hours
    factor X: 48-72 hours
    protein C: 8 hours
    protein S: 30 hours

    The resultant in vivo effect is a sequential depression of Factors VII, IX, X and II activities. Vitamin K is an essential cofactor for the post ribosomal synthesis of the vitamin K dependent clotting factors. The vitamin promotes the biosynthesis of gamma-carboxyglutamic acid residues in the proteins which are essential for biological activity. Warfarin sodium is thought to interfere with clotting factor synthesis by inhibition of the regeneration of vitamin K1 epoxide. The degree of depression is dependent upon the dosage administered.

    Therapeutic doses of warfarin sodium decrease the total amount of the active form of each vitamin K dependent clotting factor made by the liver by approximately 30-50%.

    An anticoagulation effect generally occurs within 12-24 HOURS after drug administration though the INR may remain normal. PEAK effects may be delayed for up to 72-96 hours. The DURATION of action of a single dose of racemic warfarin sodium is 2-5 days.

    Anticoagulants have no direct effect on an established thrombus, nor do they reverse ischemic tissue damage. Once a thrombus has occurred, the goal of anticoagulant treatment is to prevent further extension of the formed clot and prevent secondary thromboembolic complications which may result in serious and possibly fatal sequelae.

    INDICATIONS Warfarin is indicated for the prophylaxis and treatment of venous thrombosis and its extension and pulmonary embolism (desired INR 2-3). It is indicated for the prophylaxis and treatment of the thromboembolic complications associated with atrial fibrillation (INR 1.4-3) and cardiac valve replacement (INR 2.5-3.5). It is also indicated to reduce the risk of death, recurrent myocardial infarction (INR 2.5-3.5), and thromboembolic events such as stroke or systemic embolization after myocardial infarction.

    ANESTHETIC management of patients anticoagulated perioperatively with warfarin is dependent on dosage and timing of initiation of therapy. The PT and INR of patients on chronic oral anticoagulation will require 3-5 days to normalize after discontinuation of the anticoagulant therapy. Vitamin K will reverse the effects of coumadin and low doses should be used if the patient is expected to resume coumadin therapy to prevent resistance. Vitamin K at 1 mg IV will reduce coagulopathy within 27 hours median.

    Theoretically, because the PT and INR reflect predominantly factor VII activity (factor VII has a 6-8 hour half-life), there may be an interval during which the PT and INR approach normal values, yet factor II and X levels are not adequate for normal hemostasis. It is nevertheless recommended that documentation of the patient’s normal coagulation status be achieved prior to implementation of neuraxial block.


    Typical prophylaxis consists of cefuroxime at 3 grams. SoluMedrol (controversial) is sometimes given prior to intiation of bypass.

    Heparin is dosed at 300 units per kg. Surgeons and perfusionists will want to know when the ACT level surpasses 200 and again at 400 for pump suckers and intiiation of bypass respectively. Recent studies reveal peak arterial ACT time at 30 seconds and venous at 60 seconds.

    Initiation of bypass causes a drop in systemic blood pressure as priming solution decreases the PVR and catecholamine concentrations are diluted. As hypothermia ensues, the blood viscosity increases again with a concomitant increase in PVR.

    Traditionally, pressures of 50 mmHg and flows of 2.2 L per m2 per minute are utilized since flows at this rate ensure near maximal oxygen uptake. Compare this with a normal cardiac index that ranges from 2.1 to 4.9. Most centers utilize non-pulsatile blood flow since there is no clear evidence for the benefit of pulsatile flow.


    DDX includes both physiological and mechanical causes. Among the most common causes is ventricular dysfunction:

    pre-existing dysfunction
    global ischemia
    reperfusion injury
    ischemia or infarction
    embolism from air or debris

    Abnormalities of cardiac rate or rhythm are another cause:

    conduction block or bradycardia
    supraventricular arrhythmias
    ventricular tachycardia
    lack of sinus rhythm

    This is especially true in conditions associated with decreased LV compliance (LVH seen in aortic stenosis).

    Mechanical problems may prevent adequate cardiac filling. This includes obstruction to blood inflow to the heart caused by the venous cannula, external compression of cardiac structures by retraction, high airway pressures or lung distention, unrecognized bleeding and surgically created abnormalities (restricted mitral valve opening following mitral valve reconstruction).

    There can also be ventricular outflow obstruction secondary to undiagnosed aortic stensois, malfunctioning of a prosthetic aortic valve, dynamic subaortic stenosis or aortic dissection.

    Metabolic abnormalities such as hyperkalemia, hypocalcemia and metabolic acidosis may impair cardiac function and prevent successful separation from CPB.

    Hypoxemia or hypercarbia with respiratory acidosis can also impair cardiac function.

    Profound vasodilatation can prevent successful weaning. In this circumstance ventricular function and cardiac index may be normal or supranormal, but the BP is too low to assure adequate tissue and organ perfusion. Vasodilatation may result from the liberation of vasoactive mediators, as part of the systemic inflammatory response to extracorporeal circulation, or from the direct and indirect effects of certain drugs (milrinone, ACEi, inhalational anesthetic agents).

    Before attempting separation from CPB electrolyte and acid-base abnormalities should be corrected. Abnormalities of HR and rhythm must also be corrected. If the heart rate is slow or if high grade A-V block exists epicardial pacing should be started. AV sequential pacing is the preferred modality to take advantage of atrial contraction in maintaining adequate preload.

    Vasopressors (NE, phenylephrine, vasopressin) can be used to improve blood pressure if CO is normal to high.

    After the correction of the metabolic abnormalities and HR and rhythm disturbances if ventricular function remains depressed inotropic support should be instituted. Inotropes can be divided into drugs whose principle mechanism of action is stimulation of cardiac beta-receptors (EPI, DA, DOB) and those that inhibit cardiac phosphodiesterase (amrinone and milrinone). The choice of inotropic agent is based on the direct effects and side-effects of the various agents and the clinical scenario. After a drug has been selected the dose should be titrated upwards until the desired improvement in ventricular function occurs, the upper range of dose is reached, or undesirable side-effects develop.

    When post-ischemia or reperfusion related dysfunction is the major cause of failure to wean from CPB full bypass support should be resumed. Stunned myocardium (myocardium that is reversibly dysfunctional related to ischemia) can recover with time. After bypass is resumed the ventricle should be fully decompressed and inotropic support discontinued to limit myocardial oxygen demand. If ventricular function remains inadequate to support separation from CPB, despite aggressive inotropic support and possibly a period of rest on CPB, mechanical support is needed.

    Alternatives for mechanical support include IABP counterpulsation and various ventricular assist devices. Additional therapy may include T4, methylene blue and ventricular assist devices.


    Neonates and infants who require extensive repair of complex congenital heart defects may have their repair using DHCA. The technique is also necessary for adults undergoing aortic arch surgery.

    The technique facilitates precise surgical repair under optimal conditions, free of blood or cannulas in the operative field, provides maximal organ protection and often resulting in shortened total CPB time. The scientific rationale for the use of deep hypothermic temperatures rests primarily on a temperature-mediated reduction of metabolism. Whole body and cerebral oxygen consumption during induced hypothermia decreases the metabolic rate for oxygen by a factor of 2-2.5 for every 10 degree reduction in temperature.

    The reduction in oxygen supply during deep hypothermic low-flow CPB is associated with preferential increases in vital organ perfusion and increased extraction of oxygen. Deep hypothermic low-flow CPB exerts a protective effect by reducing the metabolic rate for oxygen, promoting preferential organ perfusion and increasing tissue oxygen extraction.

    Extensive clinical experience using DHCA has shown that the safe circulatory arrest period may last 35-40 minutes. Beyond this duration, the incidence of permanent & transient neurologic sequelae may increase.

    During brain ischemia, excitatory amino acids such as glutamate and aspartate are released and are putative mediators of ischemic damage. Hypothermia has been shown to significantly decrease the release of EAA, suggesting another mechanism besides metabolism reduction for its protective effect. Membrane changes that transform a normal semiliquid to a semisolid form during hypothermia may act to prevent calcium influx during reperfusion and thereby account for additional protection noted in some experimental models.


    (J Cardiovascular Anesthesia 2004)

    Typical antibiotic prophylaxis consists of CEFUROXIME at 30 mg per kilogram. SOLUMEDROL (also at 30 mg per kg) is given prior to intiation of bypass.

    FENTANYL is usually given in bolus doses between 20 to 100 mcg per kg through the case – primarily prior to bypass. Limit fentanyl to about 20 mcg per kg if there are plans to extubate early.

    HEPARIN is dosed (as in adults) at 300 units per kg. Surgeons and perfusionists will want to know when the ACT level surpasses 200 and again at 400 for pump suckers and intiiation of bypass respectively.

    During the rewarming phase, it is often useful to incrementally bolus with PHENTOLAMINE to counteract vasoconstriction. In neonates, there may be some benefit to loading with MAGENESIUM sulfate (30 mg per kg) to reduce incidence of ventricular ectopy and JET (Am Heart Journal 2000).

    For early extubation, patients are often transitioned to propofol for transport.

    ACCESS Obtain two peripheral IV. A double lumen Cook CVP will be placed (5 cm for infants and children up to 8 years and 8 to 12 cm for older children). Arterial lines with 22-24 gauge catheters should also be set up.

    One of the peripherals should be with LR and the other with NS (for blood). Place dial-a-flow sets proximal to the double stop cocks and T-connectors.

    Connect the DISTAL CVP to a minidrip NS bag with a dial-a-flow and a gang of five.

    Triple transducers are needed for arterial line, PROXIMAL port of the CVC and a third for surgically placed RA, LA or PA lines.

    Children over 40 kgs may be set up as for adults – exception being that medications are still set up on the infusion pumps (see CV INFUSIONS – PEDIATRIC).




    OCULOMOTOR III exits in the middle of the cerebral peduncle and is compressed to result in a blown pupil.


    TRIGEMINAL V divides into three branches


    FACIAL VII divides into five branches



    VAGUS X is quite complex and composed of both afferent and efferent connections.

    ACCESSORY XI innervates the trapezius muscle.



    Craniosynostosis occurs at an incidence of 1:2000 with males more commonly affected. There is a positive family history in 39% of all cases. Autosomal dominant transmission is associated with Crouzon and Apert syndrome. Surgery usually takes place in infancy especially if multiple sutures are involved. Hydrocephalus occurs in 4-20% of all cases.

    SCAPHOCEPHALY is the most frequent form of craniosynostosis (50%) and affects the sagittal suture. The head appears narrow and elongated.

    PLAGIOCEPHALY (18%) involves a unilateral synostosis of the coronal suture and patients exhibit a flattening of the forehead, elevation of the orbit and distortion of the nasion on the affected side.

    TRIGONOCEPHALY (9%) occurs from synostosis of the metopic suture producing a triangular appearance of the forehead and hypertelorism.

    BRACHYCEPHALY (9%) involves both coronal sutures and can be associated with midface hypoplasia as with Apert or Crouzon syndrome.

    ANESTHETIC MANAGEMENT Airway management can be crucial in patients with associated craniofacial syndromes. Apert and Crouzon syndromes are associated with maxillary hypoplasia and a history of obstructive apnea. Endoscopic intubations can be required and nasal tubes are sometimes advantageous for optimal surgical exposure.

    Total BLOOD volume is limited in young infants to approximately 80 mL/kg. It is not uncommon to lose 25 to 50% of a patients blood volume within the first 30 minutes of surgery. Studies indicate blood losses of 25% with single strip craniectomy, 42% with metopic procedures, 65% with bicoronal and 85% with surgery for multiple suture involvement.

    Hypotensive anesthesia has not gained acceptance for craniosynostosis repair and hypotension can create negative pressure in the calvarial sinuses which may lead to an increase risk of venous air embolism. Nevertheless, it is prudent to limit crystalloid infusions to attenuate edema as long as satisfactory urine output is achieved and MAP is maintained above 60-65 mmHg.

    Coagulopathy can be suspected after significant blood replacement. Many recommend FFP administration if 30-35% of the blood volume is lost.

    Adequate IV ACCESS usually involves two 20 gauge peripherals for simple repairs. Central lines may be indicated for more complex repairs. Arterial blood pressure monitoring is almost always essential.

    The incidence of VAE during these repairs has been reported to be as low as 2-4%. Other recent investigations demonstrate incidence as high as 82%. The incidence of hypotension with VAE is greater in children (69%) than adults (36%). The value of monitoring and CVC for aspiration is controversial. It is generally possible to aspirate air in only 38% of the children with VAE.

    Dexamethasone and furosemide may be considered as cerebral edema is likely.

    For the majority of intracranial AVM, the general considerations are similar to those appropriate for bleeding aneurysm surgery – avoidance of acute HTN and the capability to manipulate BP accurately in the event of bleeding. Arterial access should almost always be started before induction and CVC should be placed for necessary CV infusions.

    A problem that is specific to AVM is the phenomenon known as perfusion pressure breakthrough or CEREBRAL DYSAUTOREGULATION. It is characterized by an often sudden engorgement and swelling of the brain, sometimes with a relentless cauliflower-like protrusion from the cranium. It tends to occur in the advanced stages of lengthy procedures on large AVM.

    The phenomenon is not entirely understood, but it has been attributed to the acute obliteration of the high-volume, low-resistance pathway that, for many years, has been stealing blood from the surrounding tissue. The result is the abrupt diversion of the AVM flow to the vasculature in adjacent and previously marginally perfused brain. It is presumed that these tissues have long been maximally vasodilated without the need ever to vasoconstrict and that they are incapable of doing so. Accordingly, the phenomenon is also referred to as autoregulation breakthrough or dysautoregulation.

    Induced hypotension is usually NOT utilized unless required for acute and extensive bleeding. Surgeons reason that the effects on the surrounding brain of devascularizing the AVM will be best appreciated if the devascularization occurs at normal pressures.

    If refractory brain swelling occurs, pressure may be lowered as part of an attempt to control the swelling, reasoning that blood flow through the involved area is pressure passive and will decrease as MAP declines. Hypocapnia, hypothermia and barbiturates may be synergistic with the value of hypotension which always should be used cautiously because of the associated ischemia risk.

    Intraoperative angiograms are commonly used for aneurysm surgery but should have little relevance to the provision of anesthesia. Access is typically through one of the femoral arteries through a catheter placed preoperatively and the catheter should be continuously flushed as any other arterial access.


    Induction for craniotomy must be tailored to the underlying brain pathology. Three basic techniques are described.

    TUMORS causing mass effects or symptoms of intracranial hypertension demand a control of ICP during induction. A small amount of STP and large doses of fentanyl (up to 10 mcg/kg in divided doses) can be given prior to vecuronium. Hyperventilation can also be helpful. Adjunct therapy includes IV lidocaine (1.5 mg/kg three minutes prior to intubation) and esmolol (0.5-1 mg/kg).

    ANEURYSMS demand tight control of BP as either HTN or hypotension can be detrimental. Patients with aneurysms can also have increased ICP but this is less common. A similar technique to the one above is useful with more attention paid to a tight control of BP.

    RAPID SEQUENCE inductions are often necessary but the use of SCh is generally contraindicated because of its propensity for raising ICP though increased CMRO. Priming doses of the nondepolarizers and larger doses than usual may be beneficial.

    MAINTENANCE anesthesia for craniotomy is usually performed with narcotic infusions and limiting the volatile agent to 0.5 MAC. Arterial CO2 should be kept low but hyperventilation should be reserved as a method of acutely lowering the ICP. Paralysis is usually warranted unless the surgery takes place near the brain stem. MANNITOL is ususally given at 0.5 g/kg with the commencement of drilling. Steroid infusions are typically requested (such as methyprednisilone at 125 mg/hr) and Dilantin loading may be necessary if requested by surgery.

    Arterial lines and large bore IV access are always required. Warming is often beneficial toward the end of the case.


    Preparation for surgery of the posterior fossa includes planning for maintenance of CPP and oxygenation, fascilitating brain relaxation, ensuring HD stability by appropriate monitoring, planning for rapid emergence and using techniques compatible with necessary physiologic monitoring. SPECIAL preparations that should be considered include the use of a multiorifice right atrial catheter, TEE or precordial Doppler for VAE, SSEP (for cervicomeduallary surgery, sitting postion and controlled hypotension), MEP and BAER.

    INDUCTION agents should be chosen based on the patient’s general physical condition. Nitrous is usually avoided during MAINTENANCE but always avoided when there is high risk of VAE, the patient is in the lateral or prone position or if deliberate hypotension is intended. Volatile agents must be at stable concentrations less than 1 MAC to allow optimal interpretation of evoked potentials. Muscle relaxation is avoided when MEP are monitored or surgery involves the brainstem. Relaxation is helpful when SSEP are monitored.

    Surgery near the cerebellopontine angle places the integrity of the FACIAL NERVE at a particular risk. Facial MEP recordings can be made with subdermal electrodes placed along the facial nerve. Potentials occur with stretch, compression or percussion of the nerve. Muscle relaxants must be avoided to obtain any tracing at all but the function of the cranial nerves is preserved in the presence of most anesthetic agents.

    EKG monitoring can be particularly useful during posterior fossa surgery and surgery involving the brainstem. Responses to various stimulations are as follows.

    TRIGEMINAL V stimulation results in a jaw jerk, hypertension and bradycardia (remember this as a Cushing response).

    FACIAL VII stimulation results in a facial twitch that can potentially be visually monitored in the sitting position.

    VAGUS X stimulation results in hypotension and bradycardia as expected.

    SPINAL ACCESSORY XI stimulation results in a shoulder jerk.

    PONS compression may result in ectopy, HTN or hypotension, tachycardia or bradycardia and gasping with irregular respirations.


    One formula useful for patients with stable creatinine as follows:


    which should be multiplied by 0.85 for females.

    Cricoid pressure as a maneuver to reduce the risk of aspiration of gastric contents during induction of general anesthesia has enjoyed considerable popularity since its introduction into clinical practice by Sellick in 1961. Work performed over the last two decades has refined our understanding of the physiology of this technique.

    FIRST, pressure must be applied to the cricoid cartilage, not the thyroid cartilage or other pharyngeal or laryngeal structures. The cricoid ring occludes the esophagus at the level of C5. Thyroid cartilage pressure may impair endotracheal intubation and because this structure is not complete posteriorly, effective compression of the esophagus does not occur.

    SECOND, sufficient pressure must be applied. Wraight measured the external force on the cricoid cartilage required to prevent saline from dripping down the esophagus in anesthetized subjects. They concluded that 44 N (about 10 POUNDS) was required in most subjects. In a companion study these investigators found that experienced anesthetists used forces ranging from 10-120 N.

    THIRD, the pressure must be applied in the midline. Forces sufficient to occlude the esophagus, when applied laterally, have been shown to displace the glottis and impair intubation.

    FOURTH, pressure must be applied before or concomitantly with the loss of consciousness. During intravenous induction of general anesthesia, upper esophageal pressure decreases before the patient loses consciousness, and it has been recommended, therefore, that cricoid pressure be applied during induction and then increased as the patient loses consciousness.

    The pressure gradient across the lower esophageal sphincter (LES-gastric pressure) is the “barrier pressure” resisting reflux. It has been convincingly demonstrated recently that application of cricoid pressure decreases lower esophageal sphincter (LES) tone and barrier pressure. Since moderate cricoid pressure is sometimes applied prior to the patient’s loss of consciousness and since this moderate force is sufficient to reduce LES tone, the authors concluded that cricoid pressure could actually increase the chance of regurgitation. The mechanism of this effect may be that pharyngeal stimulation relaxes the LES, as may occur during normal swallowing. Supporting this view is the observation that placement of an LMA causes decreased LES tone. No clinical outcome data supports the abandonment of cricoid pressure and further investigation will be required to determine how best to use the maneuver in patients with elevated gastric pressure.


    Cricothyrotomy is the treatment of choice for emergent surgical airway access when orotracheal intubation has failed in patients who can not be mask ventilated and are unable to maintain their own airway patency.

    PROCEDURE The thyroid and cricoid cartilages are identified and the larynx is stabilized between the thumb and index finger of the nondominant hand. The adult cricothyroid membrane measures 9 mm in height and 22 mm in width.

    Local anesthesia is rarely employed as the skin wheal can easily obscure the position of the membrane.

    A VERTICAL skin incision (risk free and usually avoiding local veins and the pyramidal lobe of the thyroid gland) of 3 cm is made over the space and the membrane is pierced with a number 11 scapel blade. The space is dilated with a hemostatic clamp or more quickly through a gentle 90 degree turn of the scapel blade.

    In the ideal situation, a number SIX lubricated tracheostomy tube can be inserted through the opening but the angulation is often prohibitive. In most patients, it should be possible to insert a conventional or reinforced 6.0 endotracheal tube. Several kits are also available that enable placement of temporary cricothyrotomy tubes with built in dilators and blades (Melker Emergency Set, NuTrake and QuickTrach).

    In the most URGENT circumstances, a 12-14 gauge catheter is placed over a needle through the cricothyroid membrane (18 gauge may be necessary for the pediatric patient). The catheter is directed caudally at a 45 degree angle, aspirating air with a 20 cc syringe to confirm placement before and after catheter advancement.

    PEDIATRICS Newborn cricothyrotomy may be performed with an 18 gauge angiocath. Infants require 16 gauge angiocaths and older children can usually be accessed as adults with a 14 gauge angiocath.

    Oxygenation and ventilation can be provided in various ways as described under TRANSTRACHEAL VENTILATION.

    COMPLICATIONS rates for nonemergent cricothyrotomy ranges from 6-8%. Emergent cricothyrotomy entails a complication risk as high as 40%. Problems include voice changes (the most common complication resulting from SLN damage), hemorrhage, aspiration, subcuaneous or mediastinal emphysema, pneumothorax (the most common pediatric complication) and esophageal puncture.


    The decreased incidence of complications with cricothyrotomy compared with that of tracheostomy is due at least partly to anatomy. Anatomic considerations make tracheostomy a relatively complicated and difficult procedure.

    Many delicate complex structures in the neck lie in close proximity to the trachea. Less encroachment on the MEDIASTINUM occurs with a cricothyrotomy than with a tracheostomy because the cricothyroid membrane is further away from the mediastinum and other critical structures. Early complications, including PTX, pneumomediastinum and mediastinal perforation occur less often with cricothyrotomy.

    Because the tracheal cartilage, unlike the cricoid and thyroid cartilage, is deficient posteriorly, the chance of damage to the posterior structures (ESOPHAGUS) lying immediately behind the airway is greater with a tracheostomy. The incidence of late complications, including fistulas, erosion of the innominate vessels, swallowing problems and voice disturbances is also less with cricothyrotomy.

    The position of the cricothyrotomy is farther away from the vascular THYROID and the incidence of bleeding is minimized.

    Cricothyrotomy is preferred over tracheostomy for definitive EMERGENCY management of the airway when intubation is impossible or contraindicated. Two notable exceptions include (1) children under 5 years of age (although some still would recommend needle cricothyrotomy with TTJV rather than tracheostomy) and (2) transection of the trachea with retraction of the distal trachea into the mediastinum.

    Young children tend to have very narrow slit-like cricothyroid membranes which are most often prohobitive of accepting anything larger than the edge of a scalpel blade.


    see Up to Date


    Armstrong David
    Arrieta Beverly
    Atkinson Luanne
    Barber Marlene
    Barnes Cynthia
    Barrett Rosemary
    Bateman Angie
    Block Jill
    Bombardier Brian
    Brown Anne
    Causey Michelle
    Chapman Terri
    DiNardo Stephen
    Fulmer Shannon
    Garrison Julie
    Gibson Sybil
    Glover Julie
    Gurney Paul
    Hackley Linda
    Harrington Anne
    Harrison Alecia
    Hazel Ellen
    Heckman Sue
    Hindman Joyce
    Howell James
    Hyman Susan
    Kager Cynthia
    Kemp Tamara
    Klibson Enna
    Koscal Tammy
    Kreis Joyce
    L’Heureux Catherine
    Lockwood Maria
    Lowe Javey
    Lowe Travis
    Mook Kevin
    Pope Karen
    Rapuzzi Don & Mary
    Rand Baxter
    Rector Jonathan
    Rowland Reba
    Sabin David
    Secrest Melody
    Shafer Susan
    Shedlick Ray & Jane
    Snakenburg Susan
    Spivey Donna & Jonathan
    Stone Gary
    Taylor Jodie
    Tilley Marilee
    Vega Edgar
    Ventura Estrella
    Weaver Michelle
    West Katie


    REFLEX SYMPATHETIC DYSTROPHY is one of three conditions described as the sympathetic-mediated pain syndromes. The other two are causalgia and sympathetic aggravated neuralgia (SAN).

    RSD refers to a condition in which autonomic dysfunction triggered by illness or injury plays a major role. CAUSAGIA is a specific term that refers to a syndrome of pain and autonomic nervous system dysfunction resulting from major nerve trunk injury. SAN refers to conditions in which pain arises from an injured peripheral nerve and is intensified by sympathetic stimulation but not primarily caused by sympathetic dysfunction. There can be considerable overlap between these syndromes.

    ETIOLOGY Approximately 90-95% of these cases occur after trauma. Other causes include iatrogenic causes of nerve damage (tight casts, venipuncture or IM injections), burns, infections, dental extractions or cerebral vascular disease.


    The ACUTE stage, which occurs days to months after the injury, is characterized by pain that is burning, aching and hyperesthetic with hyperpathia or allodynia to cold or mechanical stimulus. It can be accompanied by muscle spasm and edema. The pain is usually distal but can spread in a stocking glove distribution. Hands and feet are commonly the major sites of pain. The skin can be warm, dry and red but becomes cold and cyanotic. The patient will guard the use of the affected area. Treatment is MOST effective at this acute stage.

    The second or DYSTROPHIC STAGE occurs 3-6 months after the onset of initial symptoms. Pain continues as a burning and hyperesthetic sensation. The skin becomes cool, gray and cyanotic as the sympathetic hyperactivity becomes more marked. The edema becomes glazed. There is a decrease in hair and nail growth. Spontaneous burning pain may spread to involve the entire extremity. Muscle and joint wasting as well as bone demineralization occurs to a greater extent than would be expected secondary to disuse. Joints in the affected extremity become stiff and painful as a result of synovial edema, hyperplasia, fibrosis, and perivascular inflammation.

    The third or ATROPHIC stage occurs 6-12 months after the initial onset. The pain may be LESS severe. There begins to be irreversible atrophic changes. The limb is cool and the reduction of blood flow is marked. There are soft tissue and bony contractures which predominate as a cause of pain. Severe osteoporosis (Sudeck atrophy) may be seen on radiographs. This stage of RSD is resistant to many treatment modalities that are successful in earlier stages. Physical therapy has the greatest degree of success during this stage.

    REMEMBER the 4Ds for diagnosis: disproportionate pain, dystrophic changes, delay in recovery and dysfunction of the sympathetics.


    Treatment is based on the theory that if the pain cycle is broken, pain relief will endure. Treatment is aimed at interrupting the sympathetic discharge and breaking the pain cycle.

    A combination of pharmacologic treatment (NSAIDS and antidepressants) and selective sympathetic nerve blocks should be done initially. Early intervention is the key to successful treatment.

    Success rates of 90% or more have been reported. Patients treated with sympathetic blockade within 1 month of onset of symptoms had a success rate of 87% while if treated 6-12 months after onset of symptoms success rate falls to 50%. Blocks must be performed in series (usually 3-7) separated by one or two days.
    Physical therapy is helpful immediately after each block.

    The STELLATE (cervico-thoracic) SYMPATHETIC BLOCK is performed with 5-20 mL of 1.5% lidocaine or 0.25% bupivacaine. LUMBAR sympathetic block (LSB) can be done by blocking L2-3 ganglia via the posterior lateral approach with 5 mL of 1% lidocaine or 0.25% bupivacaine.

    Other techniques used but in general are less successful are IV regional blocks using 20-40 mL of 0.5% lidocaine with or without bretylium 1-2 mg/kg or guanethidine up to 40 mg (20 mg for arm and 40 mg for leg).

    Hydrocortisone 50-100 mg or prednisone 60 mg taper has also been used. Additional modalities that have been used with variable results are calcium channel blockers (nifedipine), anticonvulsants (Neurontin), oral steroids, phenoxybenzamine, topical capsaicin (depletes skin of substance P), transdermal nitroglycerin, TENS and dorsal column stimulators.

    Surgical and neurolytic sympathectomy have been tried with disappointing results. Pain typically returns in 6-12 months. Therapy for these patients should instead be directed toward extinguishing pain behavior, increasing strength and mobility and developing coping strategies.

    Burning pain is a term used to describe CAUSALGIA which is seen after a minority of injuries to peripheral nerves. High velocity projectiles, such as bullets, damaging major peripheral nerves constitute most causes of this disorder. Causalgias are most often seen in wartime.

    DIAGNOSIS Pain is usually burning in quality (89% incidence) and is often described as throbbing, aching, stabbing or crushing. Pain normally starts within 24 hours of injury (often accompanied by allodynia and hyperpathia). It is usually worse in the hands or feet even when the causative wound is more proximal.

    The pain may subside within six months or continue indefinitely.


    1) vasodilation (pink/warm) or
    2) vasoconstriction (clammy)
    3) dystrophic skin changes (hair loss, shiny, scaly, dry skin)
    4) excessive sweating or inability to sweat
    5) almost any sensory or emotional stimulus can exacerbate the symptoms
    6) major nerve trunk injury usually involved (brachial plexus, sciatic, median or others)
    7) pain relief must be seen by successful blockade of appropriate sympathetic trunk (diagnostic and therapeutic block)


    CRYOPRECIPITATE is prepared from FFP and contains:

    factor VIII
    factor XIII
    von Willebrand factor

    Cryoprecipitate is rich in factor VIII, with 5-13 units of factor VIII clotting activity per mL of solution.

    INDICATIONS for cryoprecipitate include hypofibrinogenemia, von Willebrand’s disease, hemophilia A (when factor VIII is unavailable) and preparation of fibrin glue. DOSAGE is one unit per 7-10 kg which raises the plasma fibrinogen by about 50 mg/dL in a patient without massive bleeding. Normal fibrinogen concentrations range between 200-400 mg/dL.




    The CUSHING REFLEX occurs in response to cerebral ISCHEMIA that is secondary to increased ICP from increased CSF production, decreased resorption or a mass effect. The initial reflex is a direct central nervous system sympathetic stimulation leading to increased heart rate, contractility and blood pressure in an effort to increase cerebral perfusion. This is followed by reflex bradycardia mediated by baroreceptors present within the carotid sinus and aortic arch as a result of the increased peripheral vascular tone.


    HYPERADRENOCORTICISM may reflect (1) overproduction of ACTH by the anterior pituitary (two-thirds of all cases) which is the definition of the Cushing DISEASE, (2) ectopic production of ACTH by malignant tumors (especially carcinoma of the lung, kidney and pancreas), (3) excess production of cortisol by a benign or malignant tumor of the adrenal cortex or (4) exogenous administration of cortisol or related drugs.

    DX is suggested by clinical findings.

    easy fatigue

    OSTEOPOROSIS reflects cortisol-induced loss of protein from bone. HIRSUITISM is present when hyperadenocorticism is secondary to excess secretion of ACTH reflecting the ability of this hormone to stimulate release of androgens as well as cortisol. Poor wound healing and increased susceptibility to bacterial and fungal INFECTIONS are also common.

    ANESTHESIA is rarely influenced by the presence of Cushings syndrome. Transpehnoidal microadenomectomy is the preferred treatment for the DISEASE while adrenalectomy is performed for the syndrome secondary to adrenal mass. Replacement therapy is often recommended as plasma cortisol levels will promptly fall after microadenomectomy or bilateral adrenalectomy. Transient diabetes insipidus and meningitis may occur after microadenomectomy. Patients are susceptible to volume overload and comcominant hyponatremia.


    The following is intended as guidelines for ADULT DOSING.

    nitroprusside 1-10 mcg/kg/min
    nitroglycerin up to 1 mcg/kg/min
    phentolamine 0.5-7 mcg/kg/min
    trimethaphan 0.3-6.0 mg/min
    esmolol 50-300 mcg/kg/min

    droperidol 2.5 mg (20/24 hrs)
    hydralazine 5 mg (40 mg/hour)

    dopamine 1-15 mcg/kg/min
    dobutamine 1-15 mcg/kg/min
    epinephrine 0.05 mcg/kg/min
    norepineph 1-8 mcg/min
    isoproterenol 0.1-0.2 mcg/kg/min
    phenylephrine up to 1 mcg/kg/min
    amrinone 0.75-1 mg/kg bolus…
    then 5-20 mcg/kg/min
    milrinone 50-75 mcg/bolus…
    then 0.4-0.8 mcg/kg/min

    SNP is commonly mixed as 100 mg (two vials) in 250 mL of D5W to a concentration of 400 mcg/mL. It is often started at 10-25 mcg/min.

    NTG is available as 50 mg in 250 mL or 200 mcg/mL. Often started at 10-25 mcg/min.

    EPINEPHRINE is commonly prepared with 4 mg in 250 mL for a concentration of 16 mcg/mL. It is bolused in doses of 2-50 mcg.

    PHENYLEPHRINE is prepared by adding 20 mg (two vials) to 250 mL NS to produce a concentration of 80 mcg/mL. Note that pediatric dosing during cardiac surgery may be quite higher.


    calcium Cl 0.25-1 g
    digoxin 1-1.5 mg bolus…
    then 0.125-0.5 mg
    glucagon 3-10 mg
    ouabain 0.3-0.5 mg


    epinephrine 0.05-1 mcg/kg/min
    dobutamine 1-10 mcg/kg/min
    dopamine 1-10 mcg/kg/min
    phenyleph 0.1-5 mcg/kg/min
    amrinone 1-4 mg/kg load, then
    3-10 mcg/kg/min
    milrinone 25-50 mcg/kg load,
    0.25-0.5 mcg/kg/min
    isoproterenol 0.05-2 mcg/kg/min
    calcium 5-20 mg/kg/hour

    nitroglycerin 0.5-10 mcg/kg/min
    phentolamine 0.5-1 mcg/kg/min
    nitroprusside 0.5-10 mcg/kg/min
    PGE1 0.05-0.15 mcg/kg/min

    lidocaine 1 mg/kg
    propranolol 10-100 mcg/kg
    labetalol 0.25 mg/kg
    esmolol 0.5 mg/kg load, then
    50-300 mcg/kg/min

    Use the following guidelines to prepare infusions. All but PGE1 are diluted to a total of 50 mL. More dilute infusions may be prepared for larger children.

    1) dobutamine, dopamine, nitroglycerin and amrinone: SIX times wt in kg = mg to add to 50 mL such that 1 mL/hr equals 2 mcg/kg/minute. Save additional amrinone for loading doses.
    2) phenylephrine and nitroprusside: THREE times wt in kg = mg to add to 50 mL such that 1 mL/hr equals 1 mcg/kg/minute.
    3) epinephrine and isoproterenol: 0.3 times wt in kg = mg to add to 50 mL such that 1 mL/hour equals 0.1 mcg/kg/minute
    4) prostin (prostaglandin E1): 75 times wt in kg = MCG to add to 25 mL such that 1 mL/hour equals 0.05 mcg/kg/minute. May dilute further for children over 6 kgs.
    5) milrinone: 1.5 times wt in kg = mg to add to 50 mL such that 1 mL/hr equals 0.5 mcg/kg/minute.


    a ß1 ß2 HR CO SVR
    epi 4 4 3 2 2 2
    NE 4 2 0 -1 -1 3
    eph 2 2 1 1 1 1
    DOB 0 2 1 1 3 0
    DA 2 2 1 2 3 1
    neo 4 0 0 -1 -1 3
    met 4 0 0 -1 -1 3
    isop 0 4 4 3 3 -2

    EPINEPHRINE is characterized by ß effects that predominate at lower dose (bronchodilation, increased CO). Alpha effects are seen at higher dosages resulting in an increase in SVR with decrease in stroke volume.

    NOREPINEPHRINE effects are characterized by predominant alpha effects at lower doses. NE has less inotropic effect and HR and CO may actually decrease.

    DOPAMINE is classically believed to stimulate DA at less than 4 mcg/kg/min with a transition to predominantly alpha effects at doses greater than 10. This does not hold true according to recent investigations.

    DOBUTAMINE increases myocardial contractility via CARDIAC ALPHA 1 and ß1 receptors. Dobutamine DILATES in the perphery as ß2 effects overshadow alpha effects. Most useful in low CO states with effects being similar to concomitant DA and SNP infusions. PVR decreases making dobutamine useful for right heart failure.

    EPHEDRINE releases NE from nerve terminals. Tachyphylaxis limits more than transient use.

    NONADRENERGIC SYMPATHOS inhibit phosphodiesterase-III (PDE-III) thereby increasing cyclic AMP to cause increase contractility and peripheral vasodilation:

    AMRINONE improves CI and EF while HR and MAP remain constant. Side effects include reversible hypotension, decreased platelets, increase LFTS, fever and GI side effects.

    MILRINONE is 20 times more potent than amrinone without the side effects


    V A PA CO
    nitric ox 0 0 +++ +/-
    NTG +++ + + +/-
    SNP +++ +++ +++ +/-
    phentol + +++ + +
    hydrala 0 +++ ? +
    amrinone + + + +
    prost E1 + +++ +++ +/-

    It is only NO that basically has no effect on the sytemic circulation. Most of the effect on cardiac output will depend on the net balance of effects on preload, afterload and myocardial oxygenation.

    Prostaglandin E1 almost always requires a left atrial infusion of norepinephrine to sustain systemic blood pressure.


    Considering the similarity between the right and left heart in children under 3 months old, what do you opine about the relevance of using CVP, assuming that we have an arterial line, for the control of blood loss in those patients?

    I have seen a CVP remain within the normal range up until the last few seconds when a child bled out – I don’t think it helps much in that sense – also if you over transfuse, it can stay fairly (high) normal as the liver will take up quite a bit of volume. My main reason for putting a central line in an infant in whom I am expecting large blood loss would be firstly to have secure venous access and secondly to enable me to give inotropes/calcium etc if required. Having put the line in, I would certainly monitor the pressure – although the absolute value might not be helpful, the trend might give you some guidance.

    I agree with both of you. In my experience finding the endpoint of transfusion (teratoma surgery) in babies in massive bloodloss is much more difficult than deciding to start it. In expected massive blood loss a CVL is helpful for the reasons David gave. Certainly the CVP is not the first guide to blood replacement. Another valueable indicator is the SpO2 which is falling when you are passing the endpoint in masive blood replacement, provided all other causes of hypoxemia are ruled out. This is one reason why I keep the FiO2 as low as possible in this kind of surgery. A slight decerase in SpO2 indicates beginning pulmonary congestion, which resolves quickly after decreasing the transfusion rate and distribution of the volume administered. Of course this is only one indicator of a complex clinical problem, but the smaller they are, and the harder they bleed, the more important it gets.


    The normal CVP tracing has three positive deflections (acv) and two negative deflections (xy). An accurate CVP is obtained by placing the transducer at only 5 cm lower than the surface of the chest. Placing the transducer at the midaxillary level will artificially raise the CVP by 7 cmH2O or 5 mmHg.

    The A WAVE is caused by contraction of the atrium against a competent tricuspid valve. The peak of the RA A wave follows the peak of the P wave by 80 msec. The peak of the LA A wave follows the P wave by 240 msec due to later depolarization of the left atrium. The peak of the A wave is the best estimate of ventricular EDP when compliance or distensibility are poor.

    LARGE A waves are caused by any condition that increases resistance to RA emptying such as tricuspid stenosis, pulmonary stenosis, pulmonary hypertension and right ventricular hypertrophy. This leaves the atrium overdistended when the tricuspid valve closes.

    CANNON A WAVES are giant A waves that occur when the right atrium contracts against a closed tricuspid valve. Cannon A waves occur in junctional beats (with retrograde atrial depolarization), complete heart block, ventricular dysrhythmias and tricuspid or mitral atresia.

    The C WAVE is caused by the bulging of the tricuspid valve into the atrium with the onset of ventricular contraction. The C wave follows the A wave at an interval equal to the PR interval and is best seen with prolongation of the PR interval.

    The X DESCENT comes as the atrium relaxes and the ventricle and tricuspid valve are displaced downward during ventricular systole. With TAMPONADE, the X usually remains visible while the Y descent is attenuated.

    The V WAVE occurs as blood passively accumulates in the IVC and right atrium. This occurs when the tricuspid and mitral valves are closed during ventricular systole. In the right heart, the V wave peaks near the end of the T wave while the left V wave occurs after the T wave.

    LARGE V WAVES may be produced by tricuspid or mitral regurgitation. It is commonly used to quantitate the degree of regurgitation. This is influenced by atrial compliance, ventricular systolic performance and impedence to ejection through the PA and aorta. V waves may disappear with afterload reduction. Other factors may produce large V waves such as L>R shunts through a VSD (that can double the venous return to the left heart), fluid overload and LV failure.

    DIFFERENTIATING the PAP trace from a PAWP may be difficult in the presence of large V waves and may lead to overadvancement of the PA line. The peak of the PA trace occurs 130 msec after the arterial upstroke while the peak of the V waves occur 350 msec after systemic arterial upstroke.

    The Y descent is the result of the tricuspid or mitral valve opening and the rapid emptying of the atrium into the ventricle.

    Other PEARLS of interest:

    1) v-a waves merge with tachycardia
    2) a-c waves merge with short PR
    3) AFIB results in a disappearance of the a wave and large c waves
    4) junctional rhythms or ventricular pacing results in cannon waves in early systole
    5) TR results in prominent c-v with a prominent y descent and obliterated x descent
    6) tricuspid stenosis results in accentuted a-waves
    7) RV infarcts result in high CVP, prominent a-v waves and steep x-y descents
    8) pericardial constriction results in PADP = PAOP = CVP as well as prominent x and y descents
    9) tamponade results in PADP = PAOP = CVP with prominent x descent but attenuated y descent
    0) 10 mmHg = 13 cmH2O indicates that mercury is thirteen times heavier than water


    Congenital cystic adenomatoid malformation is a lung bud lesion characterize by dysplasia of respiratory epithelium caused by overgrowth of distal bronchiolar tissue. Prenatally diagnosed CCAM prognosis depends on the size of the lung lesion and can cause: mediastinal shift, hypoplasia of normal lung tissue, polyhydramnios, and fetal hydrops (cardiovascular shunt).

    Classified in two types based on ultrasound findings: macrocystic (lobar, 5 mm or larger cysts, anechoic, favorable prognosis) and microcystic (diffuse, more solid, echogenic, lethal). CCAM occurs as an isolated (sporadic) event with a low rate of recurrence. Survival depends on histology. Hydrops is caused by vena caval obstruction, heart compression and mediastinal shift. The natural history is that some will decrease in size, while others disappear. Should be follow with serial sonograms.

    Prenatal management for impending fetal hydrops has consisted of thoraco-amniotic shunts (dislodge, migrate and occlude), and intra-uterine fetal resection (technically feasible, reverses hydrops, allows lung growth). Postnatal management consist of lobectomy.


    CF is the most common lethal disease inherited by the white population. CF is inherited as an AR trait. In the United States white population of Northern European origin, prevalence is 1:3K. In African Americans, prevalence is 1:15K. In Hispanics, prevalence is 1:9K. In Asian Americans, prevalence is 1:31K.

    CF is caused by defects in the gene for cystic fibrosis transmembrane conductance regulator (CFTR), which encodes for a protein that functions as a chloride channel and is regulated by cyclic adenosine monophosphate. These abnormalities result in viscid secretions in the respiratory tract, pancreas, gastrointestinal tract, sweat glands, and other exocrine tissues. Increased viscosity of these secretions makes them difficult to clear.

    More than 1300 CF mutations have been identified. In the commercially available CF gene sequencing method, the entire coding region, splice junction sites, and promoter region of the CFTR gene are amplified from genomic DNA by polymerase chain reaction (PCR) and the subjected to nucleotide sequence analysis on an automated capillary DNA sequencer. This test can detect more than 98% of disease-causing mutations. The detection rate is lower in African American, Hispanic, and Asian populations; therefore, failure to find 2 abnormal genes does not exclude the disease.

    Currently, the median age of survival is 36.8 years; the median age of survival is significantly higher in males than in females. Pulmonary involvement is progressive. Beginning as bronchitis, bronchiolitis, and, then, bronchiectasis, pulmonary involvement leads to cor pulmonale and end-stage lung disease. Hemoptysis and pneumothorax are complications. Sweat abnormalities may result in heat stroke and salt depletion, especially in infants. Mucocele and mucopyocele associated with chronic sinusitis and nasal polyps can cause erosion of the sinus wall, resulting in central nervous system complications from the space-occupying effect of mucopyocele or from associated complications. Portal hypertension occasionally causes death through esophageal varices.

    The clinical presentation, age at diagnosis, severity of symptoms, and rate of disease progression in the organs involved vary widely. Gastrointestinal tract complications result from pancreatic involvement (leading to insufficient pancreatic enzymes), pancreatic tissue damage (leading to diabetes mellitus in 8-12% of patients >25 y), and excessive administration of exogenous pancreatic enzymes (resulting in fibrosing colonopathy). Intestinal complications range from meconium ileus with associated complications during the neonatal period (12% of neonates with CF) to distal intestinal obstruction syndrome, rectal prolapse, peptic ulcer, and gastroesophageal reflux. Liver involvement may result in a fatty liver (30-60% of patients), focal biliary cirrhosis, multinodular biliary cirrhosis, and associated portal hypertension.

    The prevalence of cholecystitis and gallstones is higher in patients with CF than in other individuals. Delayed puberty and reduced fertility are other complications; most males are azoospermic because of agenesis of the vas deferens. Female fertility is probably only mildly impaired, and many successful pregnancies have been reported in women with CF.


    Cystic hygroma is an uncommon congenital lesion of the lymphatic system appearing as a multilocular fluid filled cavity most commonly in the back neck region, occasionally associated with extensive involvement of airway or vital structures. The etiology is intrauterine failure of lymphatics to communicate with the venous system. Prenatal diagnosis can be done during the first trimester of pregnancy as a huge neck tumor.

    DDx includes teratomas, encephalocele and hemangiomas. There is a strong correlation between the prenatal diagnosis and Turner’s syndrome (over 50%), structural defects (Noonan’s syndrome) & chromosomal anomalies (13, 18 and 21).

    Early diagnosis (prior to 30 weeks gestation) is commonly associated to those anomalies, non-immune hydrops and dismal outcome (fetal death). Spontaneous regression is less likely but can explain webbed neck of Turner and Noonan’s children. Prenatal diagnosis should be followed by cytogenetic analysis: chorionic villous sampling, amniocentesis, or nuchal fluid cell obtained from the CH itself to determine fetal karyotype and provide counseling of pregnancy.

    Infants with late diagnosis (after 30 weeks) should be delivered in tertiary center prepare to deal with dystocia and postnatal dyspnea of newborn. The airway should be secured before cord clamping in huge lesions.

    Intracystic injection of OK432 (lyophilized product of Streptococcus pyogenes) caused cystic (hygromas) lymphangiomas to become inflamed and led to subsequent cure of the lesion without side effects.


    Dantrolene is classified as a direct acting MUSCLE RELAXANT. Dantrolene has been shown to produce relaxation by affecting the contractile response of the skeletal muscle at a site beyond the myoneural junction, directly on the muscle itself. In skeletal muscle, dantrolene dissociates the excitation-contraction coupling, probably by interfering with the release of calcium from the sarcoplasmic reticulum. It is hypothesized that the addition of dantrolene to the triggered MH muscle cell reestablishes a normal level of ionized calcium in the myoplasm. Because dantrolene will decrease heat generated by skeletal muscle activity, it can cause a non-specific decrease in temperature and thus is not of any diagnostic value.

    DOSING Dantrolene is provided in 20 mg vials requiring 60 mL of PF water because of low solubility (vials also contain 3 grams of mannitol). Dantrolene should be administered by continuous rapid IV push beginning at a minimum dose of 1 mg/kg (most recommend 2.5 mg/kg) and continuing until symptoms subside or the maximum cumulative dose of 10 mg/kg has been reached. This is 35 vials for the 70 kg patient.

    When mannitol is used for prevention or treatment of late renal complications of MH, the 3 g of mannitol needed to dissolve each 20 mg vial of IV dantrolene should be taken into consideration. The maximum 35 vials would provide 100 grams of mannitol which is a substantial dose for most adults.

    The recommended PROPHYLACTIC dose of dantrolene IV is 2.5 mg/kg, starting approximately 1 hour before anticipated anesthesia and infused over approximately 1 hour. This dose should prevent or attenuate the development of MH provided that the usual precautions are followed.

    ORAL dantrolene is indicated preoperatively to prevent or attenuate the development of signs of MH in known or strongly suspect MH susceptible patients who require anesthesia for surgery. This use of either IV or oral prophylactic dantrolene is controversial and typically not administered.

    SIDE EFFECTS include a potential for hepatotoxicity such that dantrolene should not be used in conditions other than those recommended. Symptomatic hepatitis (fatal and non-fatal) has been reported at various dose levels of the drug.

    At the start of dantrolene therapy, it is desirable to obtain liver function studies for baseline. If abnormalities are confirmed, there is a clear possibility that the potential for dantrolene hepatotoxicity could be enhanced, although such a possibility has not yet been established.


    DOSING for hemophilia A, von Willebrand’s disease, cirrhotic and uremic bleeding disorders is at 0.3 mcg/kg IV (20 mcg max) over 30 minutes. It may be repeated every 12-24 hours though tachyphylaxis is possible. The drug is available at 4 mcg/mL and is diluted in 50 mL of NS.

    The INTRANASAL form is given at 300 mcg intranasally for patients over 50 kg (1 spray in each nostril) and 150 mcg intranasally if under 50 kg (single spray in 1 nostril).

    DIABETES INSIPIDUS requires only 1-2 mcg (0.5-1 mL) SC or IV given twice each day. DI may also be treated with intranasal DDAVP at 10-40 mcg (0.1-0.4 mL) once to three times daily or with oral DDAVP at 0.05-1.2 mg daily or divided into two to three doses.

    DDAVP or DESMOPRESSIN is the longer acting synthetic analogue of pituitary vasopressin. DDAVP possesses greater antidiuretic properties than vasopressin and is useful for central or neurogenic DI. Vasopressin can be used to treat central DI, is more titratable and is sometimes recommended by COPA if DI and hypotension are both problematic. DDAVP stimulates release of factor VIII, VWF, tissue plasminogen activator and prostacyclin leading to a overall decrease in bleeding time. The vasoconstriction produced by DDAVP is minimal.

    SIDE EFFECTS include a decrease in free water clearance, a decrease in serum sodium and osmalility, hypotension and thrombosis.


    Prompt evaluation is necessary because of the life-threatening occurences that may falsely present as delayed emergence including airway obstruction, hypoxia and hypercarbia.

    The differential diagnosis can be broken down into

    1) prolonged drug action
    2) metabolic encephalopathy
    3) neurologic injury

    PROLONGED DRUG ACTION may be secondary to overdosage, increased sensitivity, decreased binding, decreased metabolism or drug-drug interactions. Reversal medications such as naloxone, physostigmine and flumazenil may be useful.

    Central anticholinergic syndrome may be secondary to scopalamine, atropine, droperidol, haloperidol, meperidine, cocaine and procaine.

    METABOLIC ENCEPHALOPTHY may be secondary to preoperative or intraoperative factors.

    Hypoxemia, hypercarbia and acidosis should be ruled out first and may be secondary to a host of potential problems.

    Electrolyte disturbances affecting emergence include hyponatremia, hypermagnesemia and either hypercalcemia OR hypocalcemia. Hypokalemia may also produce generalized weakness.

    LOW Na, Ca or K
    HIGH Mg or Ca

    Glucose distrubances include hypoglycemia which could be induced by manipulation of pancreatic tumors or retroperitoneal carcinomas. Drugs that are associated with hypoglycemia include insulin, salicylates, sulfonamides, ethanol and propxyphene (Darvon). Hyperglycemia is associated with hyperosmolar nonketotic coma (a diagnosis with a 40-60% mortatlity rate).

    Hypothermia is associated with delayed emergence and prolonged neuromuscular block. Hyperthermia is not.

    Morphine and cimetidine have been associated with profound CNS depression in those patients with liver disease.

    Hypothyroidism is associated with decreased anesthetic requirements.

    NEUROLOGIC INJURIES (the third category) leading to delayed emergence include cerebral ischemia (secondary to positioning or deliberate hypotension), hemorrhage or cerebral embolic phenomenon (air or particulate matter after bypass).


    SIX etiologies:

    1) increased inspiratory FLOW
    2) increased TIDAL VOLUME or overdistension
    3) MACHINE problems: valve malfunction, inspiratory PEEP valve, flush valve engaged during inspiration, wrapper on CO2 absorbent
    4) increased PLEURAL pressure: coughing, effusion, ascites, abdominal insufflation, abdominal packing, retraction, restraints, head down position, tension PTX, MH and medications including narcotics or insufficient NMB
    5) increased RESISTANCE of the ETT: small caliber, kinks, secretions, herniated cuff
    6) increased RESISTANCE of patient AIRWAYS: bronchospasm, secretions, edema, stricture, endobronchial intubation

    The diagnoses requiring prompt attention include light anesthesia and coughing, tension PTX, endotracheal tube kinking and endobronchial intubation.

    The ICU BOOK comments on the value of evaluating the plateau pressure of the waveform. Those with no change in the plateau likely have increased peak pressures from airway obstruction (aspiration, bronchospasm, secretions, tube complications). Those with an increase in the plateau pressure likely have a decrease in compliance (abdominal distension, atelectasis, pneumothorax, pulmonary edema).



    light anesthesia
    patient anxiety
    prolonged tourniquet use
    clonidine, Aldomet, ß-blockers
    ephedrine with TCA or MAOI
    via alpha-adrenergic effect

    Although it is indisbutable that patients with preoperative hypertension will be more labile and may have an increased incidence of intraoperative and postoperative ischemia, it is unclear if there is much increase in morbidity or mortatlity in comparing these patients with others who are chronically hypertensive. The most recent guidelines by the American College of Cardiology and the Americal Heart Association does advise a delay for elective procedures in those presenting with preoperative SBP over 180 and DBP over 110 mmHg.


    fluid overload
    ischemia induced
    rate induced
    too fast with stenosis
    too slow with incompetence
    loss of atrial kick

    secondary to bleeding
    fluid shifts
    functional hypovolemia
    vasoplegia with ARB et al
    other SNS blockade

    ANESTHESIA relative OD
    ADDISON’S physiology

    pulmonary embolism
    tension pneumothorax
    air embolus
    cardiac tamponade


    The QUICK response for oral board situations involves acknowledgement of SIX principle etiologies – disturbances in viscosity, preload, afterload, contractility, rate and rhythm.



    1) inadequate oxygen supply – improperly filled tanks, empty reserve tanks, cracked flowmeter, flowmeter not turned up, system disconnection, large leaks, obstructed tube, malpositioned ETT
    2) inadequate alveolar ventilation – hypercarbia will lead to hypoxemia with alveolar carbon dioxide over 60 mmHg
    3) medullary chemoreceptor depression
    4) carotid body chemoreceptor depression


    1) partial shunt – secretions, atelectasis, pneumonia, pulmonary edema, bronchoconstriction, COPD, pneumothorax, compression or surgical packing, loss of normal HPV, diffusion impairment
    2) true shunt – arteriovenous fistulae, atrial septal defect, ventricular septal defect, [PATENT DUCTUS ARTERIOSUS]
    3) dead space from pulmonary embolus should not theoretically cause hypoxemia – nevertheless it is believed that pulmonary embolus incites a local release of mediators which secondarily cause bronchospasm and shunt


    1) decreased carrying capacity – anemia, CO poisoning, methemoglobin, hemoglobinopathies
    2) increased affinity for oxygen (which may cause tissue hypoxia without hypoxemia) – hypothermia, decreased 2,3-DPG, alkalosis, hypocarbia
    3)decreased cardiac output
    4) increased utilization or uptake – malignant hyperthermia, fever, hyperthyroidism, shivering

    One other type of hypoxia which does not fit in the above three categories is HYSTIOCYTIC HYPOXIA most commonly seen with cyanide toxicity. Oxygen delivery is adequate, but the cells are unable to utilize the oxygen.

    A practical and systematic approach to the patient may include quickly placing the patient on 100% oxygen and hand ventilating, then tracing the oxygen molecules from the source to the periphery where delivery is assessed. See also under [HYPOXIA – BASIC ETIOLOGY].


    hypokalemia or hypernatremia
    lithium (also enhances SCh)
    volatile agents
    local anesthetics
    neuropathy including post polio
    combination of NDMRs
    Eaton-Lambert syndrome

    It has been demonstrated (Anesthesiology 1990) that patients will recover to 100% twitch tension with or without neostigmine at the same time following NMB. Patients given neostigmine EARLY (before any twitch response which may be the equivalent of 10% recovery) will achieve 10% recovery more promptly but will achieve 90% recovery at the same time as those patients given reversal AFTER one twitch has recovered. According to this study with vecuronium, there is absolutely NO VALUE to repeating a dose of neostigmine if 70 mcg/kg is given initially. In other words, there is a limit or ceiling effect inherent to the use of neostigmine.


    It is useful to break the tachycardias into two groups – the primary tachycardias (from inherent pathology) and the secondary tachycardias (from some extrinsic stimulus to the heart).

    PRIMARY – abnormal wiring will often lead into supraventricular arryhthmias (atrial fribrillation, WPW) or ventricular arrhythmias (although this is more likely in the face of electrolyte disturbance, blood gas abberation or ischemia)

    SECONDARY – hypoxemia, hypercarbia, hypoglycemia, anemia, hypovolemia, tamponade, pneumothorax, PEEP, pain, pharamacologic causes, pheochromocytoma, carcinoid syndrome, thyrotoxicosis

    The other method of differentiation first distinguishes the stable from the unstable patient and secondarily the narrow complex tachycardia from those with wide QRS complexes (over 0.12 seconds or three small squares).

    SINUS TACHYCARDIA appears as a regular rhythm usually with P waves and with a rate between 100-160. It is not amenable to cardioversion.

    PREMATURE ATRIAL CONTRACTIONS appear as an irregular rhythm usually with a rate between 100-200, abnormal P wave morphology and variable PR intervals. PAC may lead to abberant conduction and wide complex tachycardia.

    JUNCTIONAL TACHYCARDIA presents with absent or abnormal P waves with normal QRS complexes and rates may be either slow or fast between 60-130 beats per minute. Inverted P waves may occur may occur during or after the QRS complex.

    PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA presents with regular rates between 150-250. P waves are often hidden but may possibly be seen retrograde in lead II or III.

    ATRIAL FLUTTER presents as a regular sawtooth appearance with atrial rates usually between 250-350. Both atrial flutter and fibrillation are best identified in leads V1, II, III and aVF.

    ATRIAL FIBRILLATION is a very irregular rhythm with atrial rates between 350-600 beats per minute and normal appearing (or occasionally prolonged) QRS complexes occurring at rates between 150-200. AF is considered controlled with rates below 100.

    MULTIFORM ATRIAL TACHYCARDIA results in atrial rates of 100-200 beats per minute with beat to beat variation in P wave morphology as well as PR and PP intervals. Most P waves will conduct to the ventricle. MAT is associated with COPD, CHF, valvular heart disease, diabetes, hypokalemia and drugs including digitalis, theophylline and beta agonists.

    presents with rates between 150-250 and QRS complexes measuring over 0.12 seconds. SVT with aberrant conduction may occasionally masquerade as ventricular tachycardia.


    VD or dead space is that portion of a breath that does not participate in gas exchange. TOTAL dead space is comprised of ANATOMIC deadspace (conducting airways) plus the ALVEOLAR dead space (ventilated but unperfused alveoli which can be created by embolic phenomena). ALVEOLAR dead space is otherwise known as PHYSIOLOGIC dead space although some references equate physiologic dead space with total dead space.

    DEAD SPACE accounts for 20-30% of total tidal volume in infancy through adulthood. In healthy awake individuals the contribution of pure alveolar deadspace (West zone ONE) is negligible. The bronchiolar constrictive reflex constricts airways to alveoli that are under perfused.

    Normal tidal volumes for adults are approximately 6 mL per kg and minute ventilation is about 80 mL per kg. Normal dead space calculates to about 2 mL per kg.

    The BOHR METHOD can estimate dead space in the intubated patient.

    Vd/Vt = (PaCO2 – PeCO2) / PaCO2

    Note that expired PCO2 (PeCO2) is an average PCO2 in an expired sample and NOT equivalent to the end-tidal PCO2.

    Factors that increase dead space include anything that increases PVR or alveolar pressure: PEEP or simple PPV, bronchodilation, decreased cardiac output, pulmonary embolus and excessive ventilator tubing.

    An increase in dead space results in HYPOXIA and HYPERCAPNIA according to the ICU Book. Hypercapnea ONLY appears once Vd rises above 50% of Vt which can occur with interface destruction (emphysema), heart failure, pulmonary embolism OR overdistension by PPV.

    The ANESTHESIA CIRCUIT increases total dead space (Vd/Vt) for two reasons.

    1) the apparatus simply increases the anatomic dead space. Inclusion of normal apparatus dead space increases the total Vd/Vt ratio from 33 to 46% in an intubated patient (there is conflicting information regarding this fact) and to about 64% in patients breathing through a conventional face mask.
    2) anesthesia circuits cause some rebreathing of expired gases, which is equivalent to dead space ventilation.


    Decompression illness (DCI) refers to the sequelae stemming from bubble formation due to a decrease in ambient pressure. Included in this term are the entities of decompression sickness (DCS), which is caused by supersaturation of inert gases causing tissue bubble formation and arterial gas embolism (AGE), which is caused by gas entry into the blood vessels during rapid decompression.

    In aviators, astronauts and divers, movement from higher to lower pressures causes significant effects. Supranormal pressures allow for body tissues to increase quantities of oxygen and nitrogen according to Henry’s law. With the resumption of normal or hypobaric pressures, these gases are eliminated at a rate proportional to the ambient pressure. However, if the movement to lower pressures occurs precipitously, the gas tension exceeds ambient pressure and bubble formation occurs. These bubbles can then block arteries, veins and lymphatic vessels, with the volume and location of these bubbles determining the outcome significance and severity.

    Basically there are four effects that are thought to play a role during recompression.

    1) reduction of gas bubble volume
    2) restoration of tissue structure and blood flow
    3) reabsorption of inert gas bubbles
    4) provision of oxygen delivery to the tissues

    While immediate therapy has been correlated with the best response, a delay in HBO therapy for DCI can still have favorable responses. As positive effects of HBO therapy have been observed up to 7 days following injury, some suggest that when symptoms exist, DCI treatment should be instituted even up to 10-14 days following decompression.

    Although oxygen alone is the current standard for HBO therapy, recent work with a helium and oxygen mixture (heliox) has demonstrated a faster resolution of bubbles. In addition, the application of heliox allows for higher therapeutic pressures to be utilized than with oxygen alone.

    Other therapeutic interventions that are being evaluated are the use of hemodilution and anticoagulation (to prevent hemoconcentration from slowing microcirculation) and the use of corticosteroids (to combat edema formation) and lidocaine (to possibly induce cerebral protection).


    Deep extubation may be useful in (1) patients at risk of bronchospasm or (2) to avoid bucking and valsalva upon emergence after delicate HEENT operations. The technique may be less useful in those patients at greater risk of bronchospasm as these patients often will pass through the symptomatic stage two with or without an ETT in place.

    The patient is brought to spontaneous ventilation with 100% oxygen and deep inhalational agent. Patients may benefit from extubation in the lateral position. Suctioning should confirm absence of gag reflex to confirm that anesthesia is beyond stage two. Nasal or oral airways may be inserted and left in place through emergence. It may also be useful to withold neuromuscular blockade reversal until immediately FOLLOWING extubation in an attempt to attenuate the risk of laryngospasm.


    1) GER (pregnancy, HH)
    2) full stomach (emergency cases)
    3) NG tube (controversial)
    4) difficult mask
    5) difficult intubation

    LMA REMOVAL during deep anesthesia is routinely performed by many clinicians. Most patients with elective LMA placements will have no contraindications to deep removal. The one exception may be the patient that is difficult to mask ventilate if mask ventilation is attempted prior to LMA placement.


    VF etiologies include ischemia, infarction, hypoxia, electrolyte imbalance, hypothermia and certain drugs. In the post bypass patient (and especially following CABG) coronary embolism, inadequate revascularization, hypothermia and inadequate myocardial protection may also contribute to fibrillation.

    The first maneuvers should be to optimize oxygenation and perfusion pressure, since these are essential for optimal myocardial function. Blood gas abnormalities (pH, K and Mg) should also be corrected.

    Surgeons generally defibrillate directly beginning with 5-10 joules. The energy level does not exceed 30 joules for direct defibrillation because higher levels may damage the myocardium. For refractory cases the patient may require amiodarone, LIDOCAINE, procainamide or bretylium (now off formulary) similar to any other patient with persistent fibrillation. Epinephrine and vasopressin (part of the ACLS persistent VF algorithm) are not usually recommended.

    Continued refractoriness strongly suggests coronary embolism, myocardial damage or inadequate repair.


    Defibrillation must be provided following confirmation of VF or PULSELESS VT. By the most recent recommendations (2006), MONOPHASIC defibrillation is provided in a SINGLE shock at 360 joules or 2-4 joules/kg in the pediatric patient. BIPHASIC defibrillators should provide 120 joules (rectilinear biphasic waveform) or 150-200 joules (biphasic truncated exponential waveform) in adults or 1-2 joules/kg in children. Shocks are repeated after 2 minutes of CPR.

    There should be no delay after two minutes of CPR, confirming the abscence of spontaneous circulation and the presence of VF/VT.

    Success has been reported after more than 12 shocks in patients that are not pharmacologically treated. If available, EPINEPHRINE or VASOPRESSIN should be provided after the initial three shocks. Of current survivors of VF arrest, 85% will respond to the first shock.

    Automatic external defibrillators provide computerized analysis of the underlying rhythm without an actual display for verification. They are appropriately used only for children over ONE year of age (2003). Various models may turn on once the gel pads are attached and automatically escalate the energy delivered over the first three shocks.


    Prompt evaluation is necessary because of the life-threatening occurences that may falsely present as delayed emergence including airway obstruction, hypoxia and hypercarbia.

    The DDX can be broken down into (1) prolonged drug action, (2) metabolic encephalopathy and (3) neurologic injury or preexisting CNS conditions.

    PROLONGED DRUG ACTION may be secondary to overdosage, increased sensitivity, decreased binding, decreased metabolism or drug-drug interactions. Reversal medications such as naloxone, physostigmine and flumazenil may be useful.

    Central anticholinergic syndrome may be secondary to scopalamine, atropine, droperidol, haloperidol, meperidine, cocaine and procaine.

    METABOLIC ENCEPHALOPTHY may be secondary to preoperative or intraoperative factors.

    Hypoxemia, hypercarbia and acidosis should be ruled out first and may be secondary to a host of potential problems.

    Electrolyte disturbances affecting emergence include hyponatremia, hypermagnesemia and either hypercalcemia OR hypocalcemia. Hypokalemia may also produce generalized weakness.

    Glucose distrubances include hypoglycemia which could be induced by manipulation of pancreatic tumors or retroperitoneal carcinomas. Drugs that are associated with hypoglycemia include insulin, salicylates, sufonamides, ethanol and propxyphene.

    Hyperglycemia is associated with hyperosmolar nonketotic coma (a diagnosis with a 40-60% mortality rate).

    Hypothermia is associated with delayed emergence and prolonged NM block. Hyperthermia is not.

    Morphine and cimetidine have been associated with profound CNS depression in those patients with liver disease.

    Hypothyroidism is associated with decreased anesthetic requirements.

    NEUROLOGIC INJURIES (the third category) leading to delayed emergence include cerebral ischemia (secondary to positioning or deliberate hypotension), hemorrhage or cerebral embolic phenomenon (air or particulate matter after bypass). Preexisting conditions may include malfunctioning VP shunts, undiagnosed brain tumors, thromboses or foramen magnum stenosis which can be exacerbated by hypercarbia, hypoxemia or hyperextension of the neck. Seizures are difficult to detect intraoperatively but may result in a postictal state that presents as delayed emergence.


    Hypotension is intentionally enhanced in modern anesthetic practice for one of four reasons.

    1) reduction of blood loss
    2) aneurysm surgery
    3) improved surgical visulaization
    4) improved cardiac performance

    Deliberate hypotension is commonly used for OMFS, spinal column fusions and craniotomies for intracranial aneurysm, AVM or a variety of vascular tumors. Goals include SBP to 80-90 mmHg, MAP to 50-65 mmHg or a 30% reduction from baseline.

    Methods include use of vasodilators or increased concentrations of volatile agent both with or without reverse Trendlenberg and PEEP (which may increase CVP and bleeding).

    Normovolemic hypotension can be produced by either a reduction in CO or a decrease in SVR. Drugs that have been used for induced hypotension include ganglionic blockers (trimethaphan, pentolinium), vasodilators (SNP, NTG, hydralazine, adenosine, prostaglandin E1), alpha-blockers (phentolamine, urapidil), beta-blockers (esmolol, propranalol), combination blockers (labetalol) and CCBs (verapamil, nicardipine).

    Lumbar epidural blocks with 20-25 mL of 0.75% levobupivicaine may be used for THA with infusions of epinephrine or phenylephrine to maintain MAP near 55 mmHg.

    It is common to begin hypotension with esmolol (up to 300 mcg/kg/min) and supplement with SNP as needed. The use of beta-blockade or a CCB (possibly prior to induction) may decrease the necessary SNP and decrease risk of toxicity.

    Attention must be given to the effects of hypotension on blood flow to various vascular beds including coronary, cerebral, spinal cord, renal and hepatic.

    Hypotension should be induced slowly to allow maximal dilation of the cerebral, coronary and renal vasculature. NORMOCAPNIA should be maintained because hypocapnia decreases CO, decreases coronary, cerebral and spinal cord flow, may alter drug action, decreases ionized calcium and potassium, shifts the dissociation curve to the left, may increase oxygen consumption and may inhibit HPV. Inspired oxygen should remain at 100%. Metabolic acidosis is NOT a feature of controlled hypotension.

    Tachyphylaxis is common with most any of the above described regimens and is usually seen concominantly with tachycardia (the key to preventing tachyphylaxis) and activation of the renin-angiotensin system. Tachyphylaxis is more common in the pediatric population.

    PEEP may be useful as it can quickly be added and taken away to titrate mean arterial pressures. Undesirable effects should be understood as PEEP tends to increase ICP, increase physiologic dead space, diminish urine flow and increase IVC pressure which may increase bleeding during vertebral surgery.

    It is useful to place the arterial transducer at the level of the auditory canal. One cm H2O translates to 0.7 mmHg of pressure (as mercury is 13 times the density of water).


    The TEETH are numbered from the top RIGHT of the patients mouth such that by examination the top incisors are numbered EIGHT and NINE and the bottom incisors are numbered TWENTY FIVE and TWENTY FOUR from the observers left to right.


    The corresponding nerve root for each area tested:

    C4 posterior shoulders
    C5 lateral upper arms
    C6 tip of the thumb
    C7 tip of the middle finger
    C8 tip of the pinky finger
    T1 medial lower arms
    T5 thorax, nipple level
    T10 thorax, umbilical level
    L2 upper part of the upper leg
    L3 lower medial upper leg
    L4 medial lower leg
    L5 lateral lower leg
    S1 sole of foot


    vapor pressure 664
    MAC adult 6.6
    MAC neonatal 9.2
    MAC infants 10
    B:G partition 0.42

    METABOLISM Desflurane undergoes less metabolism (0.02%) than any of the other volatile agents. Desflurane is the most likely to produce carbon monoxide (with low flow, dried out soda lime most specifically).

    CV During the maintenance of anesthesia, increasing concentrations of desflurane produces dose-dependent decreases in BP through decreased SVR.

    HR is typically not affected (beyond mild physiologic responses). Rapid increases in concentration (however) will trigger an increased sympathetic tone that will readjust to baseline after 5-8 minutes. This same effect is less pronounced, but present with isoflurane (both reactions are mediated by medullary responses to irritant airway receptors and are therefore not seen with sevoflurane and halothane).

    Deflurane is not considered to be dysrhythmogenic in the face of exogenous epinephrine unless doses exceed 7 mcg/mL (similar to isoflurane).

    PULMONARY effects are not unlike the effects of the other inhalational agents. Bronchospasm may be more common due to the agent pungency.

    CNS In patients with space occupying lesions, desflurane should be administered at 0.8 MAC or less, in conjunction with a barbiturate induction and hyperventilation (hypocapnia). Appropriate measures should be taken to maintain cerebral perfusion pressure. In one study of 10 patients receiving 1.1 MAC desflurane, CSF pressure increased 7 mmHg with final values of 11-26 mmHg above preadministration values. Under hypocapnic conditions (PaCO2 less than 27 mmHg), desflurane 1 and 1.5 MAC did not increase cerebral blood flow (CBF) in 9 patients undergoing craniotomies. CBF reactivity to increasing PaCO2 from 27 to 35 mm Hg was also maintained at 1.25 MAC.

    Electrical silence occurs at 1.5-2 MAC of desflurane.

    RENAL All agents decrease renal blood flow, GFR and UOP. These changes are not a result of ADH release but rather the effects of the volatiles on blood pressure and cardiac output.


    DOSING for PONV is between 0.2-1 mg/kg (maximum 10-25 mg) for pediatric patients. One study in tonsillectomy patients (AA 2007) demonstrates no greater efficacy (for ALL benefits) between 0.0625 and 1 mg/kg. The typical adult dose is 4 mg IV soon after induction. ANALGESIA is possible with doses of 0.2 mg/kg. Airway EDEMA is treated with doses of 0.5-1 mg/kg. Pediatric patients with CROUP are classically treated with 0.6 mg/kg either IM or PO.

    When methylprednisilone is used as an alternative for PONV prophylaxis…


    DOSING Typical doses for anesthetic adjunct and sedation include loading of 0.5-1 mcg/kg over 10 minutes followed by infusions ranging between 0.2-0.7 mcg/kg/hour for no longer than 24 hours. It has been studied for emergence delerium in the pediatric population at doses between 0.15-0.3 mcg/kg. It is provided in 2 mL vials with 100 mcgs per mL.

    Dexmedetomidine is a selective ALPHA-2 AGONIST with sedative, analgesic and mild amnestic properties. Alpha-1 activity is observed at high doses or after rapid infusions. The medication may be used as a premedication before thiopental induction (with effects comparable to the benzodiazepines), as an analgesic to reduce opioid requirements, for the treatment of shivering in the PACU or to blunt the cardiac stimulatory response prior to ketamine use.

    Many feel that the medication may be an ideal sedative for use in the ICU and may completely rewrite the taxonomy for such classifications of drugs. The hypnotic and anxiolytic responses to dexmedetomidine are attributed to the effects on the locus ceruleus nucleus.

    PHARMACOKINETICS The volume of distribution is over 100 liters. The half life is only six minutes and termination of effects can be expected after two hours.

    SIDE EFFECTS Common side effects include hypotension and nausea. Lower dose infusions usually do not cause cardiovascular side effects. More uncommon side effects include hypertension, bradycardia, atrial fibrillation and hypoxia coupled with pulmonary edema. Clonidine may reduce minute ventilation but does not clearly cause respiratory depression. Symptoms of overdose may include second-degree AV block, cardiac arrest and hypotension. Most symptoms resolve rapidly on discontinuation. Bradycardia usually responds to anticholinergic agents, including atropine or glycopyrrolate.


    100 mL of 10% Dextran 40 in 0.9% NaCl contains 10 grams of Dextran and sodium chloride 0.90 grams.

    100 mL of 10% Dextran 40 in 5% dextrose contains 10 grams of Dextran and hydrous dextrose 5 grams.

    CLINICAL PHARMACOLOGY Infusion of dextran increases the osmotic pressure, draws fluid into the vascular tree, results in an expansion of plasma volume slightly in excess of the volume infused and decreases from this maximum over the succeeding 24 hours.

    Dextran with dextrose is more osmotically active in increasing plasma volume (due to the greater number of molecules), although the volume effect has a shorter duration than Dextran 70 due to more rapid excretion of the smaller molecules. Maximum plasma volume expansion is reached approximately one hour post-infusion.

    Approximately 50% of the dextran with dextrose administered to a normovolemic patient is excreted in the urine within three hours and approximately 75% is excreted within 24 hours. The remaining 25% is partly hydrolyzed and excreted in the urine, partly excreted in the feces and partly oxidized.

    As adjunctive therapy in shock, 10% dextran with dextrose enhances blood flow, particularly in the microcirculation, by the mechanisms of increased blood volume, arterial pressure, cardiac output, capillary perfusion and reducing the tendency for sludging of blood that may accompany shock. Peripheral resistance and blood viscosity are also decreased.

    Dextran with dextrose is also utilized as a priming solution for extracorporeal circulation based on the properties of decreased destruction of erythrocytes and platelets, reduced intravascular hemagglutination and maintenance of electronegativity of erythrocytes and platelets.

    Sodium, the major cation of the extracellular fluid, functions primarily in the control of water distribution, fluid balance and osmotic pressure of body fluids. Sodium is also associated with chloride and bicarbonate in the regulation of acid-base equilibrium of body fluid.

    Chloride, the major extracellular anion, closely follows the metabolism of sodium and changes in the acid-base balance of the body are reflected by changes in the chloride concentration.

    Rarely, severe and occasionally fatal ANAPHYLACTOID reactions consisting of marked hypotension have been reported with the use of dextran. These reactions occurred in patients not previously exposed to dextran and early in the infusion period. It is strongly recommended, therefore, that patients not previously exposed to dextran be observed closely during the first minutes of the infusion period.

    The hematocrit should be determined after administration of dextran. Care should be taken to prevent a depression of hematocrit below 30% by volume. When large volumes of dextran are administered, plasma protein levels will be decreased.

    Excessive administration of potassium-free dextrose solutions may result in significant hypokalemia. Serum potassium levels should be maintained and potassium supplemented as required.

    DOSING Often used after revascularization procedures at 40 mL/hour. Dextran will not affect placement or discontinuation of epidural catheters (per Passanante) but hematomas have been described when Dextran 70 was administered immediately before or after neuraxial blockade.


    Dextromethorphan has recently demonstrated analgesic properties secondary to the drugs antagonism at the NMDA glutamate receptor.


    Hypernatremia secondary to nonosmotic urinary water loss is usually caused by (1) central or neurogenic DI characterized by impaired vasopressin secretion or (2) nephrogenic DI that results from resistance to the actions of vasopressin.

    The most common cause of central DI is destruction of the neurohypophysis as a result of trauma, neurosurgery, granulomatous disease, neoplasms, vascular accidents or infection. In many cases, CDI is idiopathic and may occasionally be hereditary. NDI may be either inherited or acquired. The latter can be further subdivided into disorders associated with renal medullary disease or with impaired vasopressin action. The causes of sporadic NDI are numerous and include drugs (especially lithium), hypercalcemia, hypokalemia and conditions that impair medullary hypertonicity (papillary necrosis or osmotic diuresis).

    DIAGNOSIS is generally made with serum sodium over 145 and urine osmolality that is unusually low for serum osmolality. The response to DDAVP will differentiate central from nephrogenic DI.

    THERAPY is by fluid and electrolyte replacement. Central DI may be treated with DDAVP given intranasally, IM or IV.
    Intraoperatively, patients on chronic therapy are most easily managed without DDAVP unless urine output is extreme with subsequent electrolyte disturbance.

    Nephrogenic DI may be treated by CHLORPROPAMIDE which potentiates the effects of ADH.


    MANAGEMENT primarily involves maintaining homeostasis by avoiding hypoglycemia and hyperglycemia (goal glucose between 90-110 mg/dL). Hyperglycemia is associated with hyperosmolarity, diuresis, electrolyte disturbances and impaired immunity. When time permits, the patient should be evaluated and treated for glucose imbalance, electrolyte disturbances and ketoacidosis. Indication of end-organ disease should also be sought. Decreased neck mobility and obesity should be considered in planning for intubation.

    Regular insulin (Humulin R) given IV is the best method for treating the hyperglycemic preoperative patient. Hyperglycemia most often reflects increases in cortisol, GH and NE, but inhalation agents will blunt the release of endogenous insulin in response to glucose.

    The RULE OF 1800 states that 1800 divided by a patient’s total daily insulin requirement will estimate the fall in blood glucose with one unit of insulin given SQ.

    If GLUCOSE is required, it may be bolused in doses of 15-25 mL of a 50% solution. FIFTEEN mL of D50 will typically increase blood glucose by 30 mg/dL in a 70 kg adult.

    A simple empiric METHOD for tight intraoperative control includes a glucose infusion at 1 mg/kg/min or 1.2 mL/kg/hour of D5LR or D5NS and regular insulin at 1-4 units per hour for 70 kg adult. Some texts argue against using lactated fluids as lactate is converted to glucose and may increase needs for insulin.

    EMERGENCY SURGERY Most common emergent procedures include appendectomy, incision and drainage procedures and LE amputations for infection. The stress, trauma or infection related to an emergency may increase insulin requirements and insulin resistance. As with elective procedures, three possibilities for extreme derangements should be considered.

    Metoclopramide is effective despite the presence of gastroparesis. If SUCCINYLCHOLINE is utilized, the patient with advanced DM and autonomic neuropathy should be pretreated with atropine or glycopyroolate to avoid BRADYCARDIA and possibly asystole.

    POSTOPERATIVE care for the patient with IDDM should ideally include a continuous insulin infusion to meet basal requirements in a titratable manner. SQ formulations include LISPRO (Humalog), regular insulin (Humulin R), NPH (Humulin N) and GLARGINE (Lantus).


    It is estimated that 2.4% of the general population suffers from DM. Diagnosis is defined by a fasting glucose over 126 mg/dL, random glucose over 200 or HgbA1c over 6.5%.

    Patients with NIDDM constitute 90% of all diabetics and are generally not prone to ketoacidosis. Patients with IDDM (primarily type I) are prone to ketoacidosis and may have coexisting autoimmune disorders (15%) such as hypothyroidism, Grave’s disease, Addison’s disease and myasthenia gravis. A third set of patients have diabetes secondary to other alterations including Cushing syndrome, pheochromocytoma & acromegaly.

    The most acute COMPLICATION of IDDM is ketoacidosis. Symptoms include polyuria, polydipsia, fatigue, nausea and vomiting developing over 1-2 days. Patients display anion gap acidosis with decreased bicarbonate.

    Late complications may be macroangiopathic (CAD, cerebrovascular and PVD), microangiopathic (retinopathy, nephropathy) and disorders of the nervous system (autonomic neuropathy and peripheral neuropathy).

    Perioperative morbidity is increased in patients with AUTONOMIC NEUROPATHY. Evidence of such includes orthostatic hypotension, resting tachycardia, absent beat-to-beat variability (vagal denervation), dysrhythmias (short QT being an ominous sign), silent ischemia, gastroparesis (20-30% of all diabetics) and hypoglycemic unawareness. Certain patients with IDDM (30-40%) also have limited joint mobility predominantly affecting the hands but possibly the atlanto-occipital joint.

    An occasional elderly patient with mild diabetes may present for emergency surgery in HYPEROSMOLAR NONKETOTIC COMA. These patients have enough endogenous insulin to prevent acidosis but may have glucose levels in excess of 1000 mg/dL and osmolarity over 300 mOsm (normal 285). They generally respond to 1-2 liters of NS over 2 hours if no CV contraindications exist. Slow insulin infusion or boluses are given taking care to not drop the glucose levels too quickly placing the patient at risk for cerebral edema.


    DKA is defined by hyperglycemia, ketonemia, ketonuria and metabolic acidosis with a pH less than 7.30 and bicarbonate less than 15 mEq/L. Patients with DKA usually present with a glucose levels between 300-500 mg/dL and moderate to severe dehydration or a 4-10 liter deficit in the adult. The ketoacids are created by the oxidation of mobilized fatty acids. The most effective test for diagnosing DKA is the…

    For adults, Barash recommends treatment with 10 units IV insulin followed by an infusion at (blood glucose/150) units per hour. In the child, insulin is infused at 0.1 unit/kg/hour. The goal for glucose correction is 80-100 mg/dL/hour.

    Isotonic fluids are given based on vital signs and UOP. KCl is added to fluids at 10-40 mEq/L when UOP exceeds 0.5 mL/hr. Pediatric patients should be replaced at rates not faster than 0.5 mEq/kg/hour.

    Dextrose is given (D5 at 100 mL/hr in the adult) once serum glucose falls below 250-300 mg/dL. Bicarbonate is recommended only if pH is below 7.1 though this is highly controversial. Hypophosphatemia may also require replacement though phosphate should be avoided if calcium is low or decreasing.

    Once acidosis and anion gap are corrected with bicarbonate over 16 mEq/L and the patient is tolerating oral feeds, SC insulin may be started with a normal requirement of 0.5-1 units/kg/day.

    Risk factors for CEREBRAL EDEMA include aggressive fluid replacement, rapid restoration of a normal glucose, elevated BUN, extreme acidosis, bicarbonate administration, rapid changes in sodium, younger age and initial diagnosis of DM.

    For every 100 mg/dL excess of glucose, the serum sodium will truely decrease by 1.6 mEq/dL.

    Assessing HgbA1c in a known diabetic as index of chronic hyperglycemia. Normal values are between 4.4 and 6.1%. The formula for estimating average glucose levels is


    Diaphragmatic hernia occurs in approximately 1:5000 births and is usually through the foramen of Bochdalek on the left side because the liver protects to some degree on the right. The incidence of left CDH is five times greater than that of right sided CDH. Herniation occurs because either the diaphragm fails to form completely before the gut returns to the abdomen from the yolk sac (9 weeks) or the gut returns to the abdominal compartment too early.

    The lung on the affected side is variably hypoplastic (more severe if the onset of the hernia is earlier in development) and the nonaffected side might also have some element of hypoplasia.

    Diagnosis of CDH may take place in utero or shortly after birth. The signs of hernia include cyanosis with respiratory distress, scaphoid abdomen, bowel sounds in the chest and lack of breath sounds on the affected side. Postnatal radiographic findings may be confused with lung cysts or congenital lobar emphysema.

    ASSOCIATED defects are common and include spina bifida, hydrocephalus, malrotation, esophageal atresia and patent ductus arteriosus.

    TREATMENT includes immediate tracheal intubation (either awake or with oxygen and halothane) and placement of a gastric tube for decompression. It is important to do everything possible to REDUCE PVR. This includes avoidance of hypoxemia and institution of hyperventilation to induce alkalosis. It is important to keep airway pressures as low as possible and to keep a high suspicion of pneumothorax during any episodes of sudden hypotension. Some recommend prophylactic placement of bilateral chest tubes to guard against this possibility. Others recommend high frequency ventilation when high and offensive airway pressures are unavoidable.

    REPAIR of the hernia is often delayed until cardiopulmonary function is optimized. This may require up to 24 hours in many centers. Anesthesia for repair of this problem usually consists of nondepolarizing muscle relaxant plus narcotics (often with fentanyl infusions at 20 mcg/kg/hour). Nitrous oxide is avoided because of possible distention of the abdominal contents. Mask ventilation with positive pressure is also avoided. Volatile agents may be used but according to some authors are best avoided before the chest is open because of potential depression of cardiac function.

    Several other agents have been advocated for reduction of PVR including PGE1, tolazoline and isoproterenol. ECMO has been used with some success as a bridge from fetal to extra-utero circulatory patterns and surgical repair may possibly take place on ECMO. Nitric oxide may provide a new and potentially useful way of reducing PVR and preventing persistent fetal circulation.

    It is important to note that the infant’s respiratory status will not be significantly improved following surgery and may indeed be worsened. It has been demonstrated that total thoracic compliance is markedly reduced following surgery leading to a frequent deterioration.


    Diastolic dysfunction is defined as an inability to fill the LV with normal LA pressures. Hypertrophic hearts with stiff ventricles caused by CAD are the major substrate for these patients with diastolic dysfunction and almost any patient with hypertrophy can be assumed to have some degree of diastolic dysfunction. Women may be more likely to develop diastolic (versus systolic) dysfunction.

    Prognosis is generally better than for those patients with systolic dysfunction (see separate listing).

    DIAGNOSIS Generally, an echocoardiogram indicating a normal or near-normal ejection fraction in the presence of clinically evident pulmonary venous hypertension and congestion is sufficient to SUGGEST the diagnosis of diastolic dysfunction. Other scenarios (such as sudden MR or AR) can also lead to CHF without sytolic or diastolic dysfunction. Actual diagnosis of diastolic dysfunction is difficult because of the contextual influences of HR, loading conditions and systolic function.

    THERAPY is focused on prevention of myocardial ischemia and differs from therapy for those with systolic dysfunction.

    SYMPTOMATIC patients may be treated with beta-blockers and calcium channel blockers though large scale studies are not available. Digitalis, under some circumstances, may in fact promote or worsen diastolic dysfunction. The congestive state in these patients is treated with salt restriction and carefully titrated diuretics to avoid excessive reduction in preload. The patient with diastolic dysfunction by definition has limited preload reserve.

    ASYMPTOMATIC patients are treated with antihypertensive regimens. While several types of therapy (ACE inhibitors > beta-blockade > diuretics > CCB) may diminish the degree of hypertrophy, the primary goal is to treat hypertension and the various sequelae that are secondary to hypertension itself.


    DOSING for premedication or sedation is between 2-10 mg (0.05-0.2 mg/kg) PO/IM/PR. Similar doses may be given by slow IV injection. Maximum daily dose is 30 mg.

    The INDUCTION dose is between 0.3-0.5 mg/kg.

    Anticonvulsant doses and doses for alcohol withdrawal range from 5-10 mg administered every 10-15 minutes.

    For STATUS EPILEPTICUS in children, give 0.1 mg/kg IV every 2 minutes to a maximum dose of 0.3 mg/kg or 10 mg per dose. Rectal dosing is at 0.5 mg/kg up to 20 mg. Diazepam should not be given as IM injection for status epilepticus.


    No general consensus exists on the definition of DIC. Disseminated intravascular coagulation is an acquired syndrome characterized by the activation of intravascular coagulation up to the point of intravascular fibrin formation. The process may be accompanied by concomitant secondary fibrinolysis and inhibited fibrinolysis. In essence, it is a systemic syndrome that simultaneously causes thrombosis and ongoing bleeding – this apparent dichotomy in effects complicates the choice of therapy.


    1) bacterial infections
    2) severe multisystem trauma
    3) solid and heme malignancies
    4) obstetric complications
    5) vascular disorders
    6) microangiopathic anemias

    Severe trauma can be associated with a number of DIC etiologies including the release of tissue materials (fat, bone, phospholipids and other emboli) into the circulation, hemolysis and endothelial damage. Each of these entities may accelerate coagulation activation. Patients with severe head trauma, which can lead to a large release of intracerebral tissue factors, have been identified as a group particularly at risk for aggressive coagulation activation and DIC.


    The following tests in combination are recommended.

    decreased platelet count
    PT (elevated in 50-75%)
    PTT (elevated in 50-60%)
    decreased antithrombin III
    FDP (elevated in 85-100%)

    A downward trend in the platelet count and the prolongation of global clotting times (PT/PTT) may reflect their consumption and depletion. These measures are sensitive but not specific signs. The addition of ANTITHROMBIN III is useful, as it specifically assesses the consumption of the most important inhibitor of thrombin.

    Fibrin degradation products (such as dimerized plasmin fragment D) may assist in differentiating DIC from other entities that cause low platelet counts and prolonged clotting times. FDP should be more than 10 mg/dL and D-dimer more than 0.5 mg/dL to make the diagnosis.

    One retrospective study of 82 ICU patients treated for DIC noted that the combination of increases D-dimer and decreased fibrinogen tests offered the highest diagnostic efficiency of 95% with sensitivity being 91% and specificity 94%. This was followed by (1) FDP alone with a sensitivity at 100% and specificity at 67%, (2) PT, PTT and FDP combination with a sensitivity at 91% and specificity at 71%, and (3) D-dimer with a sensitivity at 91% and specificity at 68%.

    The ULTIMATE DIAGNOSTIC PANEL is composed of D-dimer, FDP and antithrombin III be utilized for the following purposes: (1) D-dimer and FDP provides a rapid and specific diagnosis, (2) antithrombin III provides insight to the severity and prognosis, (3) FDP (rapid and less expensive than D-dimer) provides an adequate follow-up related to the progress of the condition once the DX is established.

    Fibrinogen levels, although frequently advocated, tend not to be helpful in diagnosing DIC as fibrinogen is an acute phase reactant and despite ongoing consumption, plasma levels of fibrinogen can remain normal for an extended period of time. The measurement of clotting factors other than fibrinogen are of little assistance in establishing the diagnosis of DIC, as their levels vary widely.


    The coagulation state of pregnancy has been described as low grade, well compensated, intravascular coagulation in which late complications can further activate the clotting system and lead to DIC.

    DIC is thought to occur in 10% of abruption patients rising to 30% in those with fetal demise. With PIH, abruption and demise the incidence is 83%. The risks of coagulation abnormalities in uncomplicated IUFD is approximately 3.2% (Can J Anes 1996).


    The treatment of DIC is controversial, in part due to the lack of clinical trials to support certain regimens and the variable and unpredictable course of the syndrome. The combination of widespread small vessel thrombotic deposition in the face of systemic consumptive bleeding does not lend towards one specific therapy. It is well established, however, that if the underlying disorder promoting the DIC, such as placental abruption or sepsis, can be identified and vigorously treated, supportive measures will usually stabilize the patient until resolution occurs.

    Plasma and platelet substitution therapy and low dose anticoagulant strategies are interventions that may assist in the management of DIC.

    The suggestion that blood component therapy may add fuel to the syndrome of DIC has never been verified in clinical or experimental trials. Similarly, the efficacy of plasma or platelets have not been demonstrated in controlled trials. Despite this, their use appears to be a rational therapeutic measure in patients with active bleeding or requiring invasive procedures, who have significant depletion of these elements.

    Most authors recommend that blood component therapy should not be given on the basis of laboratory results alone but rather the patient’s clinical condition.

    Although experimental evidence suggests that HEPARIN can partly inhibit coagulation during sepsis, there are no controlled clinical trials demonstrating a clinically important benefit with the use of heparin in patients with DIC. Until further work confirms the efficacy of heparin, some clinicians advocate that only low dose subcutaneous heparin should be administered to DIC patients for the prevention of venous thromboembolism.



    1) insertion of an LMA
    2) insertion of a Combitube
    3) mod nasal trumpet maneuver
    4) rigid ventilating bronchoscope
    5) institution of TTJV
    6) creation of a surgical airway

    Only the last three options are appropriate when difficulty is thought to be GLOTTIC (spasm, edema, tumor or abscess) or SUBGLOTTIC. Upper airway anomalies are more common etiologies of the CVCI situation.

    An optimal attempt at laryngoscopy should require no more than four attempts and can be defined as

    1) experienced laryngoscopist
    2) optimal sniffing position
    3) use of OELM
    4) one change in blade length or
    5) one change in blade type

    It should be understood that a best attempt at mask ventilation should be pursued prior to considering the CVCI options (each with inherent risks). The best attempt at mask ventilation requires two people with two or three (better) hands on the patient.

    The LMA can provide rescue ventilation in 94% of unanticipated CVCI cases and is likely to soon be a more integral part of the difficult airway algorithm.

    The ALGORITHM follows a somewhat less stressful path for the patient that can be ventilated by mask but can not be intubated by simple techniques. It should be remembered (nevertheless) that the patient that is initially easy to bag mask ventilate may become more difficult or impossible to mask ventilate after multiple failed attempts at laryngoscopy.


    Recommendations for stocking the difficult airway cart according to the Handbook of Difficult Airway Management are as follows.

    There is a matrix of risk benefit relationships that deserve careful analysis in the patient warranting RSI with an anticipated difficult airway. In general, one should risk the possibility of pulmonary aspiration over the more serious risk of failing to secure an airway.

    It has been stated by some authors that FOB intubations may be performed with less risk of aspiration if airway anesthesia is ommited from the procedure and patients are simply sedated. Patients without significant cardiac risk factors may tolerate this procedure well.

    A more optimal method of securing the airway may be with an AWAKE LOOK before administration of succinylcholine. Awake laryngoscopy should usually be performed with some light orapharyngeal anesthesia consisting of benzocaine spray or lidocaine ointment applied to a tongue depressor. Fentanyl, midazolam and even propofol can be carefully titrated to maintain cooperative spontaneous ventilation.

    If the awake LOOK should fail, then equipment for a FOB should be readily available.


    Three types of adverse respiratory events account for 75% of all closed claims: inadequate ventilation (38% of all closed claims), esophageal intubation (18%) and difficult intubation (17%). Three quarters of these events are estimated to be preventable. Approxmately 85% of these events will result in death or brain damage.

    FAILED INTUBATIONS occur in 0.05% (or 1:2230) of all surgical cases and 0.2% (or 1:500) of all obstetric cases (four times the overall incidence).

    Repeated use of conventional laryngoscopy often traumatizes the airway and may make even mask ventilation more difficult (a most common scenario amongst closed claims analyses). If there are not quick and atraumatic options for the patient that can be mask ventilated (better position, external laryngeal manipulation, new blade or another laryngoscopist) it is prudent to continue with mask anesthesia, awaken the patient or secure a surgical airway.

    DIFFICULT MASK AIRWAYS occur with a frequency of about 3-5% (100 times the incidence of failed intubations). Large studies have revealed risk factors (in decreasing order of importance) for difficult mask to include facial hair, BMI over 26 kg/m2, lack of teeth, age over 55 years and a history of snoring. Difficult intubations are four times as common in the difficult mask patient and impossible intubations are twelve times as common.


    Regional anesthesia versus GA may be acceptable in the patient with the recognized difficult airway if (1) surgery can be discontinued at any point without harm to the patient OR, (2) the patient and anesthesiologist are prepared for awake intubation and adequate access to the airway will exist during the operation AND (3) there are no contraindications for regional anesthesia.

    If surgery can be quickly terminated and if RA fails, then surgery can be cancelled, awake intubation can be performed or a second attempt at RA can be performed.


    Endotracheal intubation can be attempted with deep anesthesia and without muscle relaxants in certain situations.

    SUCCINYLCHOLINE may be useful when there is possibility of a difficult airway. Low dosing (0.5 to 0.75 mg/kg) provides optimal conditions within 75 seconds (versus 45 seconds) for a duration of 60 seconds. One disadvantage of succinylcholine is that there is often a period of time when poor ventilation will occur and transitioning to plan B may be more difficult. Second doses of succinylcholine (preceded by GLYCOPYRROLATE) may very rarely be indicated for circumstances of a good laryngoscopy grade when it is felt that incomplete paralysis interferred with successful intubation.

    NDMR The use of short-actinq non-depolarizers is rarely indicated in the recognized difficult airway but may be useful if there is certainty that the patient may be easily mask ventilated. One advantage may be an easier transition to plan B for failed optimal attempts at laryngoscopic intubation.




    Digoxin increases contractility by inhibiting NaK ATPase to increase intracellular sodium which subsequently exchanges through a separate channel with extracellular calcium. The principle CV effect of digitalis administered to patients with cardiac failure is a dose related increase in myocardial contractility that becomes significant with less than full digitalizing doses.

    CLINICAL The inotropic effect manifests as increased SV, decreased heart size and reduced LVEDP. Improved renal perfusion due to increased CO favors mobilization accounting for the diuresis that ensues after administration to patients in cardiac failure.

    Glycosides enhance VAGAL activity leading to delayed conduction through the AV node and decreases in HR. Toxic concentrations enhance sympathetic tone.

    The EKG EFFECTS of therapeutic plasma concentrations include (1) prolonged PR interval over 0.2
    (2) shortened QT interval because of more rapid ventricular repolarization, (3) ST-T segment depression (scaphoid or scooped out) due to decreased slope of phase 3 repolarization, (4) diminished amplitude or inversion of the T wave and (5) lowering of HR.

    ECG changes may persist for 20 days following discontinuation of digoxin.


    The narrow therapeutic window is 0.8-2.0 ng/mL and the half-life of the drug is 1.5 days.

    INTERACTIONS that increase digoxin levels include verapamil, quinidine, amiodarone, flecainide, erythromycin, succinylcholine, nondepolarizing muscle relaxants, potassium losing diuretics and tetracycline.

    HYPOKALEMIA, hypomagnesemia, HYPERCALCEMIA and hypoxemia enhance digoxin toxicity.

    DYSRHYTHMIAS include VTACH, VFIB, AV block, sinus bradycardia, junctional tachycardia and PVC (particularly bigeminy). VFIB is the most common cause of digitalis related death. Normal EKG findings consist of downward sloping ST segments. CNS symptoms include confusion, lethargy and visual changes described as yellow green halos, nausea and vomiting.

    TREATMENT is by GI decontamination followed by activated charcoal. Hemodialysis is NOT effective. Bradycardia may be treated with ATROPINE, isoproterenol and PACING. Ventricular arrhythmias should be treated with LIDOCAINE and PHENYTOIN is most often utilized for supraventricular arrhythmias. Avoid procainamide and quinidine as they may be proarrhythmic and slow AV conduction. CARDIOVERSION may be dangerous in severe toxicity. Hypomagnesemia and hypokalemia should be corrected.

    DIGIBIND (digoxin specific Fab antibody fragment) is indicated for life threatening arrhythmias refractory to conventional therapy.

    DOSAGE for adults and pediatric patients is calculated as:

    number of 40 mg vials=
    level (ng/mL) x weight (kg)/100

    Dissolve the digoxin immune Fab in 100-150 mL of NS and infuse IV over 15-30 minutes. Use a 0.22 micron in-line filter during infusion.

    Hypokalemia, CHF and anaphylaxis may occur. The complex is renally excreted. After administration, serum digoxin levels may be high and inaccurate because both free and bound digoxin is measured.

    Digoxin-like immunoreactive substances are present in young children up to the age of six years.


    Cardizem is a CCB which slows conduction through SA and AV nodes. It also dilates coronary and peripheral arterioles and reduces myocardial contractility.

    INDICATIONS include angina pectoris, temporary control of rapid ventricular rate during atrial fibrillation & flutter, multifocal atrial tachycardia and conversion of paroxysmal SVT to NSR. The CCB may occasionally be requested in vascular cases that are complicated by vasospasm.

    PO DOSING is at 30-60 mg every 6 hours. IV DOSING begins with an initial bolus at 0.25 mg/kg over 2 minutes – typically 20 mg. If response is inadequate after 15 minutes, a second larger bolus with 0.35 mg/kg over 2 minutes is given followed by a continuous infusion at 5-15 mg per hour (mix 125 mg in 100 mL of D5W).

    ADVERSE EFFECTS include bradycardia, heart block, impaired contractility and transient increase in liver function tests. Other adverse events include hypotension (less than verapamil), injection site reaction, flushing and arrhythmia.

    Diltiazem is CONTRAINDICATED in atrial fibrillation or flutter patients with WPW, short PR syndrome, sick sinus syndrome or second or third-degree AV block (without pacemaker).


    Diphenhydramine is indicated for acute hypersensitivity reactions and DYSTONIC reactions.

    DOSING is at 1-2 mg/kg IV or IM with a maximum dose of 50 mg. Antihistamine dosing for CHILDREN 2-6 years of age is 6.25 mg PO/IM/IV every 4-6 hours. Anaphylaxis doses for children is 1-1.25 mg/kg PO/IV/IM every 6-8 hours with a maximum of 300 mg per day.


    THIAZIDE diuretics, such as hydrochlorothiazide, act on distal convoluted tubule and inhibit Na+-Cl- symport. They can counteract the Na+ and H2O retention effect of hydralazine (direct vasodilator), and therefore are suitable for combined use. Thiazides are particularly useful for elderly patients, but not effective when kidney function is inadequate.
    Thiazides reduce blood K+ and Mg2+ levels, and induce hypokalemia and hyperuricemia. Thiazides retain Ca2+ and decrease urine Ca2+ content. Use carefully and monitor serum K level in patients with cardiac arrhythmias and when digitalis is in use.

    LOOP diuretics, such as fusosemide and bumetanide, are more powerful than thiazides. Often used for treatment of severe hypertension when direct vasodilators are administered and Na+ and H2O retention becomes a problem. They can be used in patients with poor renal function and those not respond to thiazides. Loop diuretics increase urine Ca2+ content.

    K-SPARING diuretics include triamterene, amiloride (both are Na+ channel inhibitors), and spironolactone (aldosterone antagonist). Used for treating hypertension in patients given digitalis. Also enhance the natriuretic effects of other diuretics (thiazides) and counteract the K+-depleting effect of these diuretics.


    Dobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the beta-receptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic and vasodilative effects. It does not cause the release of endogenous norepinephrine, as does dopamine. In animal studies, dobutamine produces less increase in heart rate and less decrease in peripheral vascular resistance for a given inotropic effect compared to isoproterenol.

    In patients with depressed cardiac function, both dobutamine and isoproterenol increase the cardiac output to a similar degree. With dobutamine, this increase is usually not accompanied by marked increases in heart rate (tachycardia is occasionally observed) but the stroke volume is usually increased. In contrast, isoproterenol increases the cardiac index primarily by increasing the heart rate while stroke volume changes little or declines.

    Facilitation of atrioventricular conduction has been observed in human electrophysiologic studies and in patients with atrial fibrillation.

    Systemic vascular resistance is usually decreased with administration of dobutamine. Occasionally, minimum vasoconstriction has been observed.

    The onset of action of dobutamine is within 1-2 minutes but as much as 10 minutes may be required to obtain the peak effect of a particular infusion rate. The plasma half-life of dobutamine in humans is 2 minutes. The principal routes of metabolism are methylation of the catechol and conjugation.

    DOSING The rate of infusion needed to increase cardiac output usually ranges from 2.5-15 mcg/kg/min. On rare occasions, infusion rates up to 40 mcg/kg/min have been required to obtain the desired effect.


    DA is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). It is a precursor to NE in the noradrenergic nerves and is an independent neurotransmitter in certain areas of the CNS (especially the nigrostriatal tract) and in a few peripheral sympathetic nerves.

    DA produces positive chronotropic and inotropic effects resulting in increased HR and contractility. This is accomplished both directly by action at the ß receptors and indirectly by causing release of NE from storage sites in sympathetic nerve endings.

    Onset of action occurs within five minutes of administration and with a plasma half-life of two minutes, the duration of action is less than ten minutes. If monoamine oxidase inhibitors are present, the duration may increase to one hour. The drug is widely distributed in the body but does not cross the blood-brain barrier to a significant extent.

    DOSING At LOW rates of infusion (0.5-2 mcg/kg/min) DA causes vasodilation that is presumed to be due to a specific agonist action on DA receptors (distinct from alpha and beta receptors) in the renal, mesenteric, coronary and intracerebral vascular beds. At these DA receptors, haloperidol is an antagonist. The vasodilation in these vascular beds is accompanied by increased GFR, RBF, sodium excretion and urine flow. Hypotension sometimes occurs. An increase in UOP produced by DA is usually not associated with a decrease in osmolality of the urine. The utility of renal dose DA is highly controversial (Chest 2003 123:1266-75).

    At INTERMEDIATE rates of infusion (2-10 mcg/kg/min), DA acts to stimulate the ß1 receptors, resulting in improved myocardial contractility, increased SA rate and enhanced impulse conduction in the heart. There is little, if any, stimulation of the ß2 receptors (peripheral vasodilation).

    DA causes less increase in myocardial oxygen consumption than isoproterenol and its use is not usually associated with a tachyarrhythmia. Clinical studies indicate that it usually increases systolic and pulse pressure with either no effect or a slight increase in diastolic pressure. Blood flow to the peripheral vascular beds may decrease while mesenteric flow increases due to increased CO. Total peripheral resistance (alpha effects) at low and intermediate doses is usually unchanged.

    At HIGHER rates of infusion (10-20 mcg/kg/min), there is some effect on alpha receptors, with consequent vasoconstrictor effects and a rise in BP. The vasoconstrictor effects are first seen in the skeletal muscle vascular beds, but with increasing doses, they are also evident in the renal and mesenteric vessels. At very high rates of infusion (above 20 mcg/kg/min), stimulation of alpha-adrenoceptors predominates and vasoconstriction may compromise the circulation of the limbs and override the dopaminergic effects of dopamine, reversing renal dilation and natruresis.

    Cardiac effects of DA are antagonized by beta-blocking agents such as propranolol and metoprolol. The peripheral vasoconstriction caused by high doses of DA is antagonized by alpha-blocking agents. DA induced renal and mesenteric vasodilation is not antagonized by either alpha or beta blocking agents.


    The double lumen ETT is used to isolate the ventilation of the right lung from the left lung. Because of the proximal takeoff of the RUL bronchus in relation to the carina, the left-sided DLETT is most commonly used.


    1) infection or hemorrhage
    2) bronchopleural fistula
    3) surgical of conducting airway
    4) giant unilateral bulla or cyst
    5) tracheobronchial tree disruption
    6) unilateral bronchopleural lavage
    7) therapy for proteinosis


    1) TAA repair
    2) pneumonectomy
    3) upper lobe resection


    1) full stomach (relative)
    2) patients with abnormal airways or lesions making placement difficult
    3) critical patients who would not tolerate being taken off PP or PEEP

    Patients with copious secretions are typically better served with UNIVENT tubes which more easily accomadate suctioning through larger catheters.

    DLETT are available in sizes ranging from 26-41 French and should accomadate pediatric patients as young as eight years of age. In younger children, conventional tubes may be used down the right or left main stem or Fogerty catheters (size 6-8) may be used through a conventional ETT with FOB guidance which is most easily inserted along the OUTSIDE of the ETT. See under elsewhere under [ENDOBRONCHIAL BLOCKER].

    SIZE recommendations

    age 6-8 3.5 UNI
    age 8-10 3.5 UNI 26 DLT
    age 11-12 4.5 UNI 26-28 DLT
    age 12-14 4.5 UNI 32 DLT
    age 14-16 6.0 UNI 35 DLT
    age 16-18 7.0 UNI 35 DLT

    The 37F DLT can be used for most adult females or any adult less than 5-4 while 39F tubes are used in adults up to 5-10 and 41F DLT can be used for most adult males taller than 5-10.

    The three commonly used ADULT sizes are typically inserted to 27, 29 and 31 cm respectively.

    136-164 cm 37 French at 27 cm
    165-179 cm 39 French at 29 cm
    180-194 cm 41 French at 31 cm

    See [ETT SIZE DETAILS] for other information on the double lumen endotracheal tubes.


    TRISOMY 21 occurs in approximately 1:600 live births and is more common in those patients born to parents of an advanced age.

    CARDIOPULMONARY Heart disease occurs in 50% of these patients. The most common lesions include VSD, AV canal, ASD and TOF. Most patients with Down syndrome have a high PVR and a propensity for early development of damage to the pulmonary vascular bed. This may relate to hypoxemia, the small oral and nasal cavity, mandibular hypoplasia, the large tongue or pharyngeal hypotonia. In addition, patients with Down syndrome may have abnormal lung parenchyma with a decreased number of alveoli and a decreased alveolar surface area.

    CERVICAL SPINE Approximately 20% of patients with Down have ligamentous laxity of the atlanto-axial joint that may allow C1-C2 subluxation and spinal cord injury. Preoperative cervical spine radiographs are probably unnecessary in the asymptomatic patient, but care should be taken to avoid cervical hyperextension, hyperflexion and excessive neck rotation. A concerning history may include history of neck pain or torticollis (rotary subluxation). Concerning physical findings may include weakness, unstable gait, hyperreflexia, clonus or Babinski sign.

    Many recommend screening with lateral cervical radiographs in the neutral, flexed and extended positions. The space between the posterior segment of the anterior arch of C1 and the anterior segment of the odontoid process of C2 should be measured. Measurements of less than 5 mm are normal, 5-7 mm indicates instability and greater than 7 mm is grossly abnormal. The cervical canal width should also be measured. The interpretation of these studies should be performed by a radiologist experienced in this area. Individuals with Down syndrome who have not been screened may need to be evaluated prior to surgical procedures, especially those involving manipulation of the neck. These children should be managed cautiously (Anes March 2005). From a letter by Litman (2006): There is no good evidence that radiographs, or even CT or MRI have any positive or negative predictive value regarding the risk of AA subluxation in Trisomy 21. The most prudent thing to do is screen for symptoms of spinal cord compression, and treat every Trisomy as if they are at risk ie, avoid extremes of neck motion in every direction and document.

    AIRWAY difficulties encountered in Trisomy 21 include congenital subglottic stenosis and OSA (75-80% incidence). A smaller than predicted ETT may be necessary because of the subglottic narrowing. A large protuberant tongue may predispose to obstruction during mask ventilation. Heavy sedation should be avoided because a proclivity for upper airway obstruction exists. Tracheal extubation should be done only with the patient awake. The likelihood of OSA necessitates postoperative monitoring for respiratory complications.

    OTHER abnormalities associated with Down syndrome include microcephaly, small nasopharynx, hypotonia and duodenal atresia. Mental retardation is always present but may vary from very mild to very severe.

    Steve Roodman published a case series in 2003 of 3 of 5 consecutive children with Down syndrome who developed profound BRADYCARDIA on induction with sevoflurane. Two children were treated with atropine alone and the third required epinephrine. Lawrence Borland published a paper in 2004 reporting on a retrospective audit of complications in children with Downs. One of his findings was that there was a 3.66% of severe bradycardia at induction (0.36% in controls). CHILDREN receive atropine at 10-20 mcg/kg IV (minimum 0.1 mg or 0.25 mL). IM and PO dosing is at 20 mcg/kg and many feel this is as important as pretreating for laryngoscopy.

    There has been some concern in the past regarding the use of SCh and ATROPINE in the patient with Down syndrome but further investigations have left most of these concerns unfounded.


    Doxapram HCl is a respiratory stimulant with action mediated through the peripheral carotid chemoreceptors. As the dose of doxopram is increased, the central respiratory centers in the medulla are stimulated with progressive stimulation of other parts of the brain and spinal cord. Opiate induced respiratory depression may be antagonized without antagonism of the analgesic effects. Doxapram may produce a pressor response due to release of catecholmaines and improved cardiac output.

    DOSING is by slow IV infusion at 0.5-1.5 mg/kg with a maximum of 4 mg/kg. Continuous infusions may be useful at 5 mg/minute.

    PHARMACOKINETICS Onset of action is within 20-40 seconds and peak effects occur within 1-2 minutes. The duration of action is between 5-12 minutes.

    Additive pressor effects may be seen in patients receiving sympathomimetics or MAO inhibitors. There is an increased risk of arrhythmias in patients receiving volatile anesthetics.


    Droperidol is a derivative of haloperidol (a butyrophenone), which is a fluorinated derivative of phenothiazines. It is used as an antiemetic, anxiolytic, sedative and as an adjunct to anesthesia. It is known to enhance the effects of other CNS depressants.

    Droperidol acts centrally at sites where DA, NE and serotonin act. It might occupy GABA receptors on the post-synaptic membrane which results in increased DA in the intersynaptic cleft thereby creating an imbalance between DA and acetylcholine. This results in alteration of normal CNS transmission of signals. In the chemoreceptor trigger zone, red astrocytes transport droperidol to the GABA receptors to exert its antiemetic effect. The drug has moderate ALPHA adrenergic blocking properties and was once used to control blood pressure during CPB cases.

    DOSAGE Premedication doses are between 2.5-10 mg IV/IM for adults and 100-160 mcg/kg IV-IM for children 2-12 years of age. Antiemetic effects are achieved with smaller doses of 0.625 mg IM/IV in adults and 75 mcg per kg in children. Some report antiemetic effects at doses as low as 250 mcg (0.1 mL).

    PHARMACOKINETICS Onset of action occurs within 5-8 minutes. It is often necessary to dose before emetogenic stimulation including manipulation of the extraoculars for strabismus surgery. Volume of distribution is 2 L/kg. Clearance rates are 14 mL/kg/min and elimination half-lifes are between 1.7-2.2 hours. The duration of action is between 3-6 hours but residual effects may persist beyond 24 hours.

    METABOLISM Biotransformation occurs in the liver forming 2 primary metabolites via N-dealkylation and conjugation with glucuronic acid. Elimination is through the liver and kidneys (10% unchanged).

    PHARMACODYNAMICS Droperidol produces CNS depression with marked tranquillity and indifference to surroundings as well as decreased anxiety. In dogs, there is potent cerebral vasoconstriction resulting in a 40% decrease in CBF without significant changes in CMRO2. SSEPs latency is increased while amplitude is decreased.

    There is virtually no effect on respiratory function when the drug is used alone.

    Vasodilation from moderate alpha blockade can decrease blood pressure with larger doses. There is little effect on contractility.

    The three SIDE EFFECTS that are of increasing concern (since late 2001) include extrapyramidal symptoms, dysphoria and arrhythmias secondary to prolonged QT segments. Risk factors include concomitant use of TCA and Flexeril. There may be a 20% incidence of major side effects with doses as low or greater than 1.25 mg.

    Extrapyramidal muscle movements (AKASTHESIA) may occur up to 12 hours after administration. This is self-limited and may be controlled with atropine or benztropine if desired. The extrapyramidal side effects may also be attenuated with benzodiazepine or diphenhydramine. Droperidol should not be used in Parkinson patients as it blocks DA receptors and can cause dystonic reactions.

    Patients may also experience DYSPHORIA if droperidol is given without a narcotic.

    Droperidol currently carries a warning about cases of SUDDEN DEATH at very high doses (greater than 25 mg) in patients at risk for cardiac arrhythmias. Recent research has shown QT prolongation within minutes after injection of a dose of droperidol at the upper end of the labeled dose range. Prolonged QT can cause a potentially fatal heart arrhythmia known as torsades de pointes.

    In the last year, there have been reports of TdP within or below the currently labeled dose range. There have been 25 deaths at 1.25 mg and one death at a dose of 0.625 mg.


    CYMBALTA is a NE and serotonin reuptake inhibitor that is indicated for painful peripheral diabetic neuropathy.

    Deep venous thromboses are so common in postoperative patients that without prophylaxis almost ONE PERCENT of all post surgical patients die of fatal PE. Because of this high mortality risk, prophylaxis against DVT is gaining widespread acceptance.

    PROPHYLAXIS For patients over 40 years old, those with malignancy having general surgery or any patients having thoracic, vascular, urologic or major gynecological surgery, low dose HEPARIN with or without compression stockings or external pneumatic compression is recommended.

    For orthopaedic patients (hip or tibial fractures, THA) low dose heparin is indicated although warfarin and LMWH have been shown to be equally effective. For TKR patients, external pneumatic compression, warfarin or low-dose heparin is recommended.

    For neurosurgery (craniotomy or laminectomy) patients, external pneumatic compression is recommended without heparin.

    Trauma patients or others at risk for bleeding, patients requiring long term immobilization and those determined to be at very high risk for DVT require placement of IVC filters by vascular radiology.


    Q waves on ECG
    history of angina
    history of ectopy requiring therapy
    insulin dependent diabetes
    age over 70 years


    These patients are SENSITIVE to BOTH depolarizing AND the nondepolarizing agents.

    ELS (myasthenic syndrome) is a rare disorder of NM transmission which is commonly associated with carcinoma of the lung (42-50% of all ELS cases) and should be suspected in all patients undergoing procedures who have suspected lung CA (primarily small cell carcinoma but ELS is also associated with squamous cell carcinoma). Interestingly, 35% of all patients with the lung cancer ELS association will present with symptoms of weakness prior to any primary pulmonary symptoms.

    Other ASSOCIATIONS include thyroiditis, vitamin B12 deficiency and primary autoimmune disorders.

    ELS can be confused with myasthenia gravis because of the limb-girdle weakness associated with both conditions. ELS differs from myasthenia gravis because it is NOT REVERSABLE with anticholinesterase drugs or corticosteroids and EXERCISE will IMPROVE strength rather than worsening weakness as with myasthenia gravis.

    The DIAGNOSIS is made only by antibody detection (Mayo clinic only) as EMG facilitation studies yield inconsistent results.

    ELS is secondary to the destruction of PRESYNAPTIC calcium channels at the motor end plate resulting in a decreased release of acetycholine when a nerve stimulus arrives at the myoneural junction.

    4-AMINOPYRIDINE is a drug which promotes calcium influx and calcium-dependent release of acetylcholine. In patients who are scheduled to have surgery, it is recommended to continue 4-aminopyridine administration right up until the time of surgery.

    Other TREATMENT modalities include excision of tumor, plasmapheresis, steroids, azathioprine and calcium chloride.


    The septal and posterior cusps of the tricuspid valve are largely derived from the right ventricle as it liberates a layer of muscle that skirts away from the cavity to become valve tissue. When this process occurs abnormally, the posterior and septal cusps of the tricuspid valve remain tethered to the muscle and adhere to the right ventricular surface – hence the diagnostic hallmark of Ebstein’s anomaly, apical displacement of the septal tricuspid leaflet.

    Functionally the valve is regurgitant because it is unable to appose its three leaflets during ventricular contraction. Valvular regurgitation and asynchronous, abnormal right ventricular function cause the dilatation and right heart failure observed in the more severe forms of the lesion. The wide spectrum of severity of the anomaly is based on the degree of tricuspid leaflet tethering and the relative proportion of ATRIALIZED and true right ventricle.

    The most common associated cardiac defect, a secundum ASD or patent foramen ovale, is reported in over 50% of patients. On physical examination, a clicking “sail sound” is heard as the second component of S1 when tricuspid valve closure becomes loud and delayed.

    ANESTHETIC concerns include the development of tachydysrhytmias and arterial hypoxemia due to increases in a right to left shunt (typically through the ASD or PFO).

    When patients of all ages are taken together, the predicted mortality is approximately 50% by the fourth or fifth decade. Surgical options include replacement or repair of the tricuspid valve and closure of the ASD. The feasibility of tricuspid valvuloplasty depends on the size and mobility of the anterior tricuspid leaflet, which is used to construct a unicuspid right-sided valve.

    Some patients with mild regurgitation may be initially treated by BT shunt followed by a Glenn procedure as a second stage (functionally unloading the volume from the right side of the heart).


    Echothiophate (Phospholine) is an organophosphate anticholinesterase used topically as a MIOTIC agent for the treatment of glaucoma. Its advantage over other topicals is its long duration of action.

    Remember that an increase in ACh is typically similar to an increase in parasympathetic tone. Similar anticholinesterase drugs are clinically useful in only a very few circumstances including paralysis reversal, myasthenia gravis therapy and treatment of some gut motility disorders.

    Echothiopate is noteworthy because (like neostigmine and pyridostigmine) it inactivates TRUE cholinesterase as well as PLASMA cholinesterase thereby prolonging the action of succinylcholine, mivacurium and ester local anesthetics. Activity levels fall to approximately 20% after several weeks of using the drops.


    ANESTHETIC CONCERNS for the patient that has survived ECMO relate primarily to placement of central access when necessary. ECMO requires sacrifice of the right internal jugular and most recommend that any CVC should be placed in either EJ or femoral veins.

    ACTH may result in Cushing syndrome and may be produced by small cell lung carcinoma, medullary thyroid carcinoma and thymoma.

    ADH may lead to water intoxication and may be produced by small cell lung carcinoma, pancreatic tumores and lymphoma.

    GONADOTROPIN produces gynecomastia and precocious puberty and may be produced by large cell lung carcinoma, ovarian tumors and adrenal tumors.

    MSH causing hyperpigmentation may be produced by small cell lung carcinoma.

    PARATHYROID hormone produces hyperparthyroidism (hypercalcemia and nephrolithiasis) and may be produced by renal cell carcinoma, squamous cell lung carcinoma, pancreatic tumors and ovarian tumors.

    TSH may produce hyperthyroidism and may be produced by chorioicarcinoma and embryonal testicular carcinoma.

    THYROCALCITONIN may produce hypocalcemia and may be produced by medullary thyroid carcinoma.

    INSULIN overproduction results in hypoglycemia and may be produced by retroperitoneal tumors.


    Edrophonium is an anticholinesterase drug with a different mechanism of action than neostigmine and pyridostigmine. Edrophonium forms a REVERSIBLE electrostatic attachment to the enzyme with a shorter duration of action than the other agents that are actually metabolized by acetylcholinesterase to irreversibly render the enzyme inactive.

    Edrophonium differs from the other inhibitors in that it has a QUICKER onset of action, LESS marked muscarinic side effects and LESS inhibition of plasma cholinesterase (hence it could be more useful for reversal of phase II block or blockade produced by MIVACURIUM). Edrophonium is LESS effective in patients with more profound neuromuscular block as the dose response curves are shifted further to the right.

    Edrophonium may be used to (1) antagonize the effects of the nondepolarizing drugs, (2) diagnose and assess therapy of myasthenia gravis versus cholinergic crisis and (3) evaluate the presence of phase II blockade produced by SCh. The phase II block may or may not respond to edrophonium but a small test dose is often appropriate.

    PHARMACOKINETICS The onset of action is within 1-2 minutes which is possibly a reflection of presynaptic action (promoting acetylcholine release) in addition to the binding with the acetylcholinesterase enzyme. While edrophonium was previously believed to be a drug with short duration of action, it is likely that edrophonium has effects lasting as long as neostigmine (54-60 minutes).

    DOSING for reversal is at 0.5 mg/kg but doses up to 1 mg/kg are useful for more profound block (greater than 90% twitch depression or no response to TOF stimulation). Atropine (which has a faster onset of action than glycopyrrolate) is given with edrophonium at doses between 7-15 mcg/kg.


    Most anesthetics produce a biphasic pattern on EEG with initial activation at low doses followed by dose dependent depression.

    VOLATILES Isoflurane is the only volatile that can produce an isoelectric pattern at 1-2 MAC. This is consistent with being the agent with the lowest critical blood flow (at 10 mL/100g/minute). Sevoflurane is similar to isoflurane. Desflurane and enflurane produce burst suppression but never produce an isoelectric pattern.


    EEG waves are classified according to frequency. In general, activation is represented by high frequency and low amplitude while depression is represented by low frequency and high amplitude.

    DELTA 0-3 Hz anesthesia
    THETA 4-7 Hz deep sleep
    ALPHA 8-13 Hz resting awake
    BETA > 13 Hz mentation


    Eisenmenger syndrome consists of pulmonary HTN and a right-to-left or a bidirectional shunt with peripheral cyanosis. Shunts may be ventricular, atrial or aortopulmonary and commonly present after shunt reversal in the end stages of PDA, VSD and ASD. It is common to the natural history of the disease to observe a calm before the storm once PVR has reached systemic levels and patients feel some relief from the effects of previously increased pulmonary blood flow and congestion.

    The prognosis is extremely poor with death before age 40 likely. It is not amenable to surgical correction. ANESTHETIC considerations include:

    1) avoid decreases in preload
    2) avoid decreases in SVR
    3) avoid increases in PVR by avoiding hypercarbia, acidosis, hypoxia, sympathetics, nitrous oxide and ketamine

    Patients are at extremely high risk for anesthesia, and usually require full invasive monitoring.


    Early repolarization is more common in males and is typically represented by taller T waves, a FISHHOOK appearance at the J points in V5-6 and ST segments less than 25% of the height of the T waves in V6. Bradycardia is also common in patients with early repolariztion. The primary DDX of pericarditis occurs in both sexes and is represented by less tall T waves, ST greater than 25% height of the T wave in V6 and tachycardia.


    peak T waves
    prolong PR
    flat P waves
    prolong QRS
    QRS merges with T wave

    ST depression
    PR/QRS prolonged
    flat T waves
    U waves in V2-3
    general decrease conduction
    increased ectopy
    greater risk for VFIB or AFIB

    shortened QT

    prolonged QT

    delayed interventricular conduction first-degree AVB
    prolonged QT interval
    complete heart block

    torsades de pointes
    prolonged PR
    wide QRS complexes
    prolonged QT intervals
    ST segment depression
    T wave inversions and tall T waves


    Normal INTERVALS include

    PR less than 200 msecs (5 blocks)
    QRS less than 120 msecs (3 blocks)
    QTc less than 440 msecs (11 blocks)

    Recall that each mm block represents 0.04 seconds and one large block represents 0.2 seconds. One small block in the vertical vector represent 0.1 mV and one large block represents 0.5 mV.

    For RATE DETERMINATION, remember the sequence of numbers


    correlating sequentially with one to six large squares between R waves.

    The VECTORS corresponding to the various limb leads are as follows

    lead I @ 0300 or 0 degrees
    lead II @ 0500 or 60 degrees
    lead AVF @ 0600 or 90 degrees
    lead III @ 0700 or 120 degrees
    lead AVR @ 1000 or -150 degrees
    lead AVL @ 0200 or -30 degrees


    LVH A left axis deviation beyond negative 15 degrees is often seen but voltage criteria are more useful. LVH is indicated by an R wave in V5 or V6 PLUS the S wave in V1 or V2 exceeding 35 mm (this and the AVL lead criterion are MOST important). Other criteria include:

    R wave in V5 over 26 mm
    R wave in V6 over 18 mm
    R wave in V6 larger than V5
    R wave in AVL over 13 mm
    R wave in AVF over 21 mm
    R wave in lead I over 14 mm

    RVH Right ventricular hypertrophy is indicated by a QRS axis over 100 degrees noted by a slightly negative complex in lead I. The normal progression on R waves throught the precordial leads is disrupted and may be reversed. Other features:

    the V1 R wave larger than S wave
    the V6 S wave larger than R wave


    The most notable abnormality is profound sinus bradycardia. Many leads may also show classic OSBORN WAVES or J WAVES seen at the junction of the QRS complex and the ST segment. The EKG must be interpreted within the clinical context: apparent elevations of the ST segment should not be misinterpreted as evidence of myocardial injury. Other ECG findings of hypothermia include atrial and ventricular dysrhythmias, as well as prolongation of the PR, QRS and QT intervals.


    SEPTAL infarction is indicated by Q waves in V1-2 with duration of at least 40 milliseconds (one mm) and at least 25% percent of the amplitude of the following R wave. While the QS pattern in V1-2 is usually associated with a septal infarct, it can occur with antomic changes due to lung disease, LVH, hypertrophic cardiomyopathy and with intraventricular conduction defects such as LAFB, LBBB and WPW.

    INFERIOR infarction (RCA) is indicated by Q waves in II, III and aVF. The DEPTH of the Q wave must be at least one-third the height of the R wave in the same complex.

    ANTERIOR infarction (LAD) may be represented by Mobitz type 2 block and LAFB (leftward axis). It may also be indicated by PRWP (lack of R wave in V3), or Q waves in V2-4.

    LATERAL infarction (LCx) usually involves changes in I, aVL and V5-6.

    POSTERIOR infarction (RCA) is indicated by reciprocal changes in anterior leads (such as large R waves in V1-2).


    TREADMILL testing has determined that 89% of significant ST depression can be detected in lead V5 (the right choice if only one lead can be displayed). The addition of an inferior lead (II, III or aVF) increases this sensitivity to 100% during EXERCISE TESTING.

    INTRAOPERATIVE ischemia is detected with a sensitivity of 80% using V5 and II while the combination of V4, V5 and II have a sensitivity of 96%. V4 and V5 alone have a sensitivity of 90%. V4 is at the fifth intercostal space and micclavicular line. V5 is at the same horizontal level as V4 and at the left anterior axillary line. The anterior axillary line is an imaginary vertical line along the anterior axillary fold or crease of armpit.

    IMPORTANT Leads II, III, aVF are most useful for detecting ischemia in the distribution of the RCA (areas supplied include RA, RV, SA node, AV node and bundle of His). Leads I, aVL are most useful for lesions of the CIRCUMFLEX coronary artery (lateral aspects of the LV). Leads V3-V5 detect ischemia in the distribution of the LAD (anterolateral aspects of the LV).

    Only with the use of an esophageal lead can ischemia of the RV and posterior LV be detected.

    Other indications of ischemia by EKG analysis include T wave abnormalities or inversions, new arrhythmias and new conduction abnormalities.

    T wave inversions (including pseudonormalization) can be seen with ischemia but it should be noted that changes in T wave morphology during surgery are extremely common and NOT clearly associated with untoward cardiac events. It may be more helpful to know whether or not T wave changes have accompanied prior episodes of angina pectoris in the individual patient.


    Most often secondary to anatomical lesion but etiologies include asynchrony, nonuniform refractory phase, changes in membrane responsiveness or a decrease in the magnitude of phase 4 of the transmembrane AP.

    1) QRS duration 120 msec (3 mm blocks) in complete LBBB
    2) broad notched R waves in lateral precordials V5-6 and usually I and aVL
    3) possible ST segment depression and T wave inversions in same leads
    4) small initial R waves in right precordials V1-2 followed by deep S waves
    5) absent septal Q waves in left leads

    LBBB usually appears in patients with underlying heart disease. The block may occasionally be intermittent and look somewhat like PVC on the rhythm strip. LBBB is associated with significantly reduced long-term survival, with 10-year survival rates as low as 50% reflecting the severity of the underlying cardiac disease.

    HEMIBLOCKS do not prolong the QRS complex. LEFT ANTERIOR HEMIBLOCK is associated with LAD (0 to -90 degrees), q waves in I and aVL and is fairly common in both normal and diseased hearts. The LEFT POSTERIOR HEMIBLOCK is associated with RAD (90 to 180 degrees), q waves in II, III and aVF, is ominous and seen only in diseased hearts. The LPFB implies compromise of L and R coronaries unlike the LAFB which has only one blood supply like RBB.

    A BIFASCICULAR block (RBBB plus block of ONE of the left fascicles) does not require prophylactic pacing but a RBBB plus posterior hemiblock is more likely to progress to complete block. A TRIFASCICULAR block (bifascicular plus prolonged PR interval) has a high possibility to progress to complete block and prophylactic pacing is usually warranted. The paradoxical combination of complete LBBB with right axis deviation has been reported as a marker of severe myocardial disease, especially dilated cardiomyopathy.

    The abnormal ventricular activation pattern of LBBB itself induces hemodynamic perturbations, including abnormal systolic function with dysfunctional contraction patterns, reduced EF and SV and abnormal diastolic function. Reversed splitting of the second heart sound and functional mitral regurgitation are common. Functional abnormalities in phasic coronary blood flow and reduced coronary flow reserve caused by delayed diastolic relaxation often result in septal or anteroseptal defects on exercise perfusion scintigraphy in the absence of coronary artery disease.

    Pharmacological STRESS TESTING with dobutamine or adenosine may be more specific than exercise scintigraphy in diagnosing left anterior descending coronary stenosis in the presence of LBBB.

    A major impact of LBBB lies in obscuring or simulating other ECG patterns. The diagnosis of LVH is complicated by the increased QRS amplitude and axis shifts intrinsic to LBBB. In addition, the very high prevalence of anatomical LVH in combination with LBBB makes defining criteria with high specificity difficult. The diagnosis of infarction may be obscured. The emergence of abnormal Q waves with infarction is dependent on a normal initial sequence of ventricular activation, which is absent with LBBB. In addition, ECG patterns of LBBB, including low R wave amplitude in the midprecordial leads and ST-T wave changes, can simulate anterior infarct patterns.

    A LBBB will mask EKG signs of hypertrophy, myocardial infarction and ischemia.


    INTRAOPERATIVE ischemia is detected with a sensitivity of 80% using V5 and II while the combination of V4, V5 and II have a sensitivity of 96%. V4 and V5 alone have a sensitivity of 90%. V4 is at the fifth intercostal space and mid-clavicular line. V5 is at the same horizontal level as V4 and at the left anterior axillary line. The anterior axillary line is an imaginary vertical line along the anterior axillary fold or crease of armpit.

    The P WAVE represents the depolarization of the atria. If P waves are absent and the QRS complex is irregular, AFIB is most likely. When P waves are absent in the presence of regular and narrow QRS complexes, this is commonly due to a AV nodal reentry pattern.

    In the presence of P waves, the rate should be between 60-100 beats per minute in adults. Rates in the 140-220 bpm range are usually atrial or AV nodal reentrant tachycardias and in the 260-320 bpm range most likely represent atrial flutter.

    Atrial depolarization occurs in a caudad and leftward orientation, producing upright P waves in the inferior limb leads (II, III, aVF) and a biphasic P wave in V1. The PR interval remains fairly constant, with a range of 0.12-0.2 seconds (3-5 blocks) in resting, healthy adults. The PR interval is measured from the beginning of the P wave to the onset of the QRS complex. Longer or shorter PR intervals suggest AV heart blockade or ventricular prexcitation, respectively. In addition, when the atria or ventricles have independent pacemaker foci, the P waves appear to march in and out of the QRS complex.

    BIPHASIC P waves can be normal in leads III, aVL and V1-3. When the M-shaped configuration is present and P waves are peaked in the inferior leads (II and aVF) with a normal PR interval, these alterations can suggest ATRIAL ENLARGEMENT or ectopic atrial depolarization.

    Inverted P waves after the QRS complex, again with a constant PR interval and observed in the inferior limb leads, can suggest retrograde atrial activation from a AV junctional or ventricular foci.

    Should dysrrhythmias occur, at least one of the following leads should be analyzed to maximize P waves: II, III, aVF or V1. Improvements in P wave tracings can be demonstrated via esophageal, transvenous or epicardial leads.

    Most recently, P wave signal averaged ECG have been advocated as an effective means of identifying and potentially predicting the risk of atrial dysrhythmias. Strip recordings or a 12 lead ECG should be evaluated should dysrrhythmias occur to assist in diagnosis and documentation.


    At birth the right ventricle is larger than the left. Changes in systemic vascular resistance result in the left ventricle increasing in size until it is larger than the right ventricle by age 1 month. By age 6 months, the ratio of the right ventricle to the left ventricle is similar to that of an adult. Right axis deviation, large precordial R waves, and upright T waves are therefore normal in the neonate. The T wave in lead V1 inverts by 7 days and typically remains inverted until at least age 7 years. Upright T waves in the right precordial leads (V1 to V3) between ages 7 days and 7 years are a potentially important abnormality and usually indicate right ventricular hypertrophy.


    Indications for preoperative EKG include known CAD or significant risk factors for CAD, hypertension and age over… A review of the resting 12-lead EKG is useful for evidence of

    1) myocardial ischemia
    2) prior MI
    3) conduction disturbances
    4) cardiomegaly
    5) electrolyte disturbances

    Prior MI, especially if subendocardial, may not be accompanied by persistent EKG changes. Premature ventricular beats may signal the likely intraoperative occurrence or presence of ischemia.


    Q waves normally appear within several hours of the onset of transmural infarction but in some patients may take several days to evolve. The ST segment usually has returned to baseline by the time Q waves appear and Q waves tend to persist for the lifetime of the patient.

    The DURATION of a pathologic Q wave must be greater than 0.04 seconds (some say 0.03). The DEPTH of the Q wave must be at least one-third the height of the R wave in the same complex.

    Small Q waves can be seen in the left lateral leads (I, AVL, V5 and V6) and occasionally in the inferior leads (especially II and III) in perfectly normal hearts. These Q waves are caused by the early left-to-right depolarization of the interventricular septum. Lead AVR should NEVER be used for Q wave evaluation as it normally has a very deep Q wave.

    NORMAL Q waves may be seen in 1-2-3-R-L-5-6.


    any Q wave in V1-V3
    Q wave over 20 mm in V4
    Q wave over 30 mm in V5
    Q wave over 30 mm in V6
    Q wave over 30 mm in I, II, aVF, aVL

    NON-Q WAVE INFARCTIONS have a lower initial mortality and a higher risk of later infarction than Q wave infarctions. These patients with non-Q wave infarctions should be treated more aggresively to prevent further cell death.

    Q WAVES are also occasionally demonstrated in the patient with hypertrophic cardiomyopathy.


    QRS widths often vary in different leads. The widest QRS measurement on the ECG is the correct one for measurement – usually leads I and V1. Normal durations fall between 0.07 and 0.11 seconds. The QRS complex should not be smaller than 6 mm in leads I, II and III nor should it be taller than 25-30 mm in the precordial leads.

    R wave progression is demonstrated in the precordial leads – the QRS starts off primarily negative (rS) in V1 and gradually becomes primarily positive (qRs) with the tallest R wave in V5 or V6. The transition from mostly negative to mostly positive normally occurs between V3 and V4. Normally the R wave in V6 is always less than the R wave in V5. Precordial R waves are very sensitive to lead placement and this must be considered in interpreting R wave progression.

    Poor R wave PROGRESSION (R waves do not usually dominate until V5-6) may represent infarction or injury of the anterior LV and carries almost as much significance as Q waves.

    Large R waves in leads V1-2 (as large as those in the next several leads) can reflect posterior infarction, lateral MI, RVH or septal hypertrophy. Consider RVH, posterior MI or WPW for tall R waves in the V1 lead. Low R waves in the right precordial leads is most likely due to LVH but also consider LAFB, COPD or MI. An R wave less than 2-3 mm in V3 is abnormal unless there is LVH. LVH causes loss of R height from V1-V3 without MI. Loss of R height between V1-2 or V2-3 in the absence of LVH suggests anterior MI.


    RBBB is a result of conduction delay in any portion of the right-sided intraventricular conduction system. The delay can occur in the main right bundle branch itself, in the bundle of His or in the distal right ventricular conduction system. The latter is the most common cause of RBBB after right ventriculotomy performed (as with correction of the tetralogy of Fallot).

    The relative fragility of the right bundle branch, as suggested by the development of RBBB after minor trauma produced by right ventricular catheterization, corresponds to the high prevalence of RBBB in the general population.


    1) QRS duration over 120 msec (3 mm blocks)
    2) broad notched R waves (RSR’) in right precordials V1-2
    3) ST segment changes and T wave inversions V1-2
    4) wide and deep S waves in left precordials V5-6, I and AVL

    RBBB is a common finding in the general population and many persons with it have no clinical evidence of structural heart disease. In this group without overt heart disease, the ECG finding has no prognostic significance.

    The new onset of RBBB does predict a higher rate of coronary artery disease, CHF and cardiovascular mortality. When cardiac disease is present, the coexistence of RBBB suggests advanced disease (as with more extensive multivessel disease) and reduced long-term survival in patients with ischemic heart disease.

    An apparently specific entity known as the BRUGADA SYNDROME has been described in which RBBB with persistent ST segment elevation in the right precordial leads is associated with susceptibility to ventricular tachyarrhythmias and sudden cardiac death.

    RBBB interferes with other ECG diagnoses, although to a lesser extent than LBBB does. The diagnosis of RVH is more difficult to make with RBBB because of the accentuated potentials in lead V1. RVH is suggested, although with limited accuracy, by the presence of an R wave in lead V1 that exceeds 1.5 mV and a rightward shift of the mean QRS axis. The usual criteria for LVH can be applied but have lower sensitivities than with normal conduction. The combination of left atrial abnormality or left axis deviation with RBBB also suggests underlying LVH.



    1) transmural ischemia (Q wave)
    2) Prinzmetal’s angina
    3) cardiac contusion
    4) pericarditis
    5) hyperkalemia
    6) hypothermia
    7) digoxin effects


    1) subendocardial ischemia
    2) LBBB
    3) pulmonary embolus
    4) CNS injuries
    5) hypokalemia
    6) digoxin effects

    Remember that autoregulatory properties of the subendocardium are exhausted before those of the subepicardium. The subendocardium of the LV is at greatest risk for ischemia secondary to increased requirements as well as restricted flow during systole when transmural pressures exceed 20 mmHg. It is thus more common to first observe ST DEPRESSION in the patient with myocardial ischemia.

    Transmural ischemia and ST ELEVATION is typically seen as a result of coronary thrombosis during acute infarction, epicardial artery spasm (Prinzmetal) or coronary artery embolism of air or particulate debris that can occure during cardiac surgery.


    1) SUBENDOCARDIAL: horizontal or downsloping ST segment depression at least 0.1 mV (1 mm) at 60 msec (1.5 mm) from J-point and persisting for one minute
    2) upsloping ST segment depression at least 0.2 mV at 80 msec from the J-point
    3) TRANSMURAL: ST segment elevation at least 0.1 mV (1 mm) in two or more limb leads or 0.2 mV in two or more precordial leads measured at the J-point

    ST segments can not be evaluated in the presence of BBB, paced rhythms, WPW, MVP, electrolyte disorders and digoxin therapy. ST segment changes are also less specific in patients with LVH.

    The severity of ST deviation can not be translated into severity of ischemia. Nevertheless, a larger shift can be a greater verification that ischemia is taking place.


    With severe hypertrophy, the myocardium can become so thickened that part of it (usually subendocardium) may not get the blood supply that it needs. Though uncomplicated hypertrophy affects only the QRS complex, subendocardial ischemia causes changes in the ST segment and the T wave.

    ST depression and T wave inversions that accompany hypertrophy are known as STRAIN. These changes are most obvious in those leads with large R waves so that RV strain is seen in V1 and V2 while LV strain is seen in leads I, AVL, V5 and V6.


    Repolarization is an active process requiring a great deal of energy. Subsequently, the T waves are susceptible to changes by many etiologies. T waves are typically directed in the same general direction as the QRS complex.

    ISCHEMIA causes T waves first to become tall and narrow and are referred to as hyperacute. Hours after an ongoing ischemic event, the waves become inverted. T wave inversion is a nonspecific finding and may be associated with BBB and ventricular hypertrophy.

    T waves of ischemia are usually inverted SYMETRICALLY. With preexisting inversions, ischemia may cause PSEUDONORMALIZATION of the T waves. ASYMETRIC inversions with gentle downslopes followed by rapid upstrokes may be secondary to nonischemic etiologies.

    PEDIATRIC T waves in the V1-2 leads are normally inverted AFTER four days of age through adolescence.

    ARVD arrhythmogenic RV dysplasia is often associayed with T wave inversions in V1-3.


    MICROSHOCK involves current delivered directly to the heart. A current of 50 MICROAMPS can cause ventricular fibrillation (depending on current density). 10 MICROAMPS is considered to be the limit of safety and the potential for leak is routinely evaluated during formal equipment checks.

    MACROSHOCK involves current delivered through the skin or tissue remote from the heart. Macroshock of 100 MILLIAMPS is required to cause heart fibrillation.

    6.0 Amps causes sustained myocardial contraction followed by normal rhythm. This current is usually associated with temporary respiratory paralysis if J >100 mA/cm.

    8-20 milliamps causes muscle contraction and 20 mA is considered to be the “let go” current level.

    1-2 milliamps causes pain and is considered to be the threshold for perception.

    The LIM is set to trigger an alarm at 2 or 5 milliamps, depending on the age and type of system. 5 mAmps is current standard. The LIM will not warn of microshock range leakage current, so equipment coming in direct contact with the heart (including the ECG monitor when placing a central venous catheter) should be pre-checked for leakage current during routine maintenance.

    10 microamps microshock safety
    50 microamps microshock VF
    1-2 milliamps pain sensation
    5 milliamps LIM alarm
    20 milliamps let-go current
    100 milliamps macroshock VF
    6 amperes sustains contraction


    ECT involves the application of current to the skin overlying one or both of the cerebral hemispheres. Induced SEIZURES should last longer than 25 seconds but should be terminated if lasting longer than 3 minutes. Caffeine is often administered to enhance seizure quality and occassionally to prevent post ECT headaches. The TONIC phase (20 seconds) is followed by the CLONIC phase (60 seconds) that is manifested by rhythmic muscle contractions. The seizure increases cerebral metabolic requirements which increases cerebral blood flow. Muscular contractions increase oxygen demand which subsequently increases cardiac output. Arrhythmias and ischemia are possible in susceptible patients.

    The CV RESPONSE to ECT involves an initial parasympathetic outflow that may result in bradycardia, heart block or brief asystole. This response is followed by a sympathetic outflow, which produces hypertension and tachycardia, usually lasting 5-10 minutes. The sympathetic response acompanies the generalized tonic clonic seizure.

    ANESTHETIC management is usually with methohexital at 0.5-1.0 mg/kg and succinylcholine 0.25-1 mg/kg. Methohexital (like any barbiturate) will raise the seizure threshold and shorten the duration of the seizure in a dose dependent fashion. Defasciculating agents are also useful but are not absolutely necessary.

    Other anesthetic agents have been used for ECT. Propofol is most commonly used in the absence of methohexital. Ketamine will prolong the induced seizure without the undesirable side effects seen in other circumstances. Induction with ketamine is slower and the emergence is prolonged as well. Etomidate causes pain on injection. Diazepam at 5-10 mg helps reduce emergence delirium in susceptible patients. The benzodiazepines will greatly prolong emergence when used as induction agents.

    The blood pressure cuff should be placed on the opposite arm of the IV and inflated prior to the administration of succinylcholine to allow for motor expression of the seizure. As an alternative, a blood pressure cuff on the lower extremity can be more easily managed by the psychiatric staff.

    Pretreatment with glycopyrrolate and/or esmolol is advocated by some centers.

    CONTRAINDICATIONS to ECT include space occupying lesions of the CNS, cerebral aneurysms, increased intracranial pressure, recent cerebrovascular accident, recent myocardial infarction and aortic aneurysm. ECT currents can interfere with permanent pacemaker activity and cardiology consulation is prudent in these patients.


    CALCIUM 8.5-10.5 mg/dL

    8-8.5 give 1 g gluconate over 1 hour
    7-8 give 2 g gluconate or 1 g Cl
    6-7 give 3 g gluconate or 1 g Cl

    MAGNESIUM 1.8-2.5 mg/dL

    1.5-1.9 give 1 g MgSO4 over 1 hour
    1.2-1.4 give 2 g MgSO4 over 2 hours
    0.8-1.1 give 3 g MgSO4 over 3 hours

    PHOSPHORUS 2.4-4.7 mg/dL

    1.5-2 give 15 mmol K-NaPO4 6 hours
    1.0-1.5 give 30 mmol K-NaPO4 6 hrs

    POTASSIUM less than 3.5 mEq/L

    3.8-4.1 give 20 mEq over 1 hour
    3.4-3.7 give 40 mEq over 2 hours
    2.8-3.3 give 60 mEq over 3 hours

    The dosages may be reduced by 50% for renal impairment or UOP less than 25 mL per hour.


    The incidence of ED varies between 2-54%. It is defined as a dissociated state of unconsciousness in which a child is incosolable, irritable, uncompromising and uncooperative. Characteristically children do not recognize or identify familiar objects or people.

    The incidence of ED is highest in children between 1-5 years of age. Episodes generally occur within three minutes of emergence, persist for 5-15 minutes and generally resolve without intervention.

    The cause of ED is unknown but there is an association with rapid emergence from the contemporary inhalation agents and inadequate pain control prior to emergence. Some studies have reduced the incidence with opioids, ketorolac or regional blocks while others have failed to influence the incidence.

    Elliot Krane states that ED is the result of “the ID waking up earlier than the EGO.”


    Hypoxia may occur upon awakening for a variety of reasons.

    1) hyperventilation (pain)
    2) hypoventilation
    3) decreased FRC from anesthesia
    4) weakness from muscle relaxants
    5) increased airway resistance
    6) pulmonary edema
    7) mucous plugging
    8) increased oxygen consumption
    9) decreased FIO2
    0) diffusion hypoxia

    Diffusion hypoxia is related to outpouring of large volumes of nitrous oxide by directly displacing oxygen or diluting alveolar CO2 with resultant decrease respiratory drive and ventilation.

    Various disease states may also lead to emergence desaturation:

    1) pulmonary embolism
    2) ARDS
    3) aspiration pneumonia
    4) bronchospasm
    5) non-cardiogenic edema


    Enalaprilat or VASOTEC IV is an ACE inhibitor that may be useful for postoperative HTN especially in patients on chronic ACE inhibitors. The drug is a good choice for prolonged effect in those with poor LV function, CHF or elevated SVR.

    DOSING is generally at 1.25 mg over five minutes and every six hours for those with normal renal function. Enalapril is the oral form of the drug which is dosed at 5-40 mg once or twice daily.


    Simple sore throats and hoarseness can occur in 20-50% of all patients following laryngoscopic intubation. This incidence differs little from the incidence of sore throat after LMA placement.

    Other potential COMPLICATIONS of laryngoscopy and intubation include recurrent laryngeal nerve damage (especially with high cuff pressures), hypoglossal or lingual nerve damage, vocal cord evulsion, desquamation of laryngeal and tracheal mucosa, airway wall edema or ulceration and tracheal perforation.

    Right mainstem intubations will seldom result in higher than usual airway pressures but will eventually result in atelectasis and hypoxemia from VQ mismatch (or shunt). Coughing and sympathetic responses are also possible with mainstem intubations.

    Commonly used ETTs incorporate high-volume low-pressure cuffs and pressure should be kept below 25 mmHg. Tracheal mucosa perfusion pressure is usually between 25-35 mmHg.

    A primary disadvantage of the DLETT is the incorporation of the low-volume high-pressure cuff along the bronchial lumen. There also may be a greater risk of trauma to the carina and surrounding structures.


    vapor pressure 175
    MAC in the adult 1.68
    blood:gas partition 1.9

    METABOLISM About 2% of the enflurane taken up through the alveoli is metabolized. Higher serum F levels are noted in patients treated with isoniazid and hydralazine and those that suffer from obesity.



    CNS Electrical silence does not occur with enflurane. The agent may produce fast frequency and high voltages on the EEG that are indistinguishable from seizure activity. This activity may be accompanied by tonic clonic twitching in the face and extremeties. Likelihood of this SEIZURE activilty is increased with over a 2 MAC concentration or hyperventilation to a PaCO2 of less than 30 mmHg.

    RENAL All volatile agents decrease renal blood flow, GFR and UOP. These changes are not a result of ADH release but rather the effects of the volatiles on blood pressure and cardiac output.


    Enoxaparin (Lovenox) is a LMWH which has antithrombotic properties. It is produced by depolymerization of standard heparin to fragments that are 33% the size of unfractionated heparin.

    Enoxaparin is characterized by a higher ratio of ANTI-FACTOR Xa to ANTI-FACTOR IIa activity (4:1 ratio) compared to unfractioned heparin (1:1 ratio). Less protein binding occurs with the LMWH preparation and responses are more predictable.

    DOSING for DVT prophylaxis following hip or knee replacement is at 30 mg SQ bid starting 12-24 hours postoperatively and continuing for 14 days. For DVT prophylaxis after abdominal surgery, dosing is at 40 mg SQ once a day starting 2 hours preoperatively and continuing for 12 days. For DVT prophylaxis during acute medical illness with restricted mobility, dosing is at 40 mg SQ each day for 14 days.

    For outpatient treatment of DVT without PE, dosing is at 1 mg/kg SQ bid. For inpatient treatment of DVT with or without PE, dosing is at 1 mg/kg SQ bid or 1.5 mg/kg SQ each day. Enoxaparin should be continued for over 5 days after warfarin is started and until INR is documented therapeutic.

    For unstable angina or NQWMI, high dosing is at 1 mg/kg SQ twice each day with aspirin (100-325 mg each day) for at least 2 days and until clinically stable.

    For recurrent thromboembolism, dosing is at 40 mg SQ each day.

    PHARMACOKINETICS Maximum anti-Factor Xa and antithrombin (anti-Factor IIa) activities occur 3-5 hours after SQ injection of enoxaparin. The volume of distribution of anti-Factor Xa activity is about 6 liters. Following IV dosing, the total body clearance of enoxaparin is 25 mL/minute. Elimination half-life based on anti-Factor Xa activity is about 4.5 hours after subcutaneous administration. Following a 40 mg dose significant anti-Factor Xa activity persists in plasma for about 12 hours.

    MONITORING of anti-Xa level is NOT recommended as it is not predictive of the risk of bleeding. These levels are occasionally monitored in children.

    LMWH is not fully neutralized by protamine.

    NEURAXIAL IMPLICATIONS Recent recommendations suggest that needle placement should be delayed at least 12 hours after the last standard LMWH dose. In patients receiving high doses at equal to or greater than 1 mg/kg/day, needle placement should probably be delayed for 24 hours.

    The first dose of LMWH should be delayed at least 2 hours following catheter removal from a nontraumatic placement.

    It is believed that traumatic needle or catheter placement may result in a significantly increased risk of hematoma formation if LMWH is administered. Recommendations suggest that initiation of LMWH should be delayed at least 24 HOURS post-operatively in this setting. Note that much controversy exists in the decision to employ LMWH therapy with the presence of an indwelling catheter. In this setting, an alternative method of thromboprophylaxis, such as external pneumatic compression is recommended.


    Ephedrine is primarily an indirect acting sympathomimetic which invokes release of the endogenous NE from the postganglionic nerve endings. Some direct stimulation also occurs.

    Indirect actions are characterized by alpha and beta-1 agonist effects because NE is a weak beta-2 agonist. In the presence of an intense beta blockade, ephedrine effects may be more equivalent to phenylephrine.

    Ephedrine, unlike epinephrine, does NOT cause hyperglycemia. Mydriasis accompanies the administration and CNS stimulation can occur in the conscious (less marked than with amphetamines).

    DOSING is according to response but the drug is usually given in increments of 5-10 mg. PEDIATRIC patients receive boluses at only 0.15 mg per kg.


    EB is a group of heriditary diseases of the skin that may also involve mucous membranes including the oropharynx and esophagus. EB is characterized by bullae formation due to separation within the epodermis followed by fluid accumulation. Bullae formation is initiated by lateral shearing forces.

    The spectrum of disease extends from the benign SIMPLEX variety to the more severe JUNCTIONAL and DYSTROPHIC varieties which usually result in death by the second decade. EB DYSTROPHICA may also manifest with severe scarring of the digits, constriction of the oral aperture (micorstomia) and esophageal strictures. Malnutrition, anemia, electrolyte derangements and hypoalbuminemia are common.

    ASSOCIATIONS with EB include porphyria, amyloidosis, multiple myeloma, diabetes meillitus and hypercoagulable states. Mitral valve prolapse may also accompany EB.

    ANESTHETIC concerns inlcude the potential need for stress corticosteroids. Trauma to the skin must be avoided by wrapping cotton gauze beneath blood pressure cuffs when necessary, wrapping IV catheters and arterial lines to secure them and nonadhesive pulse oximetry. The face may be lubricated with cortisol ointment to avoid trauma from the mask.

    Upper airway instrumentation must be minimized as the SQUAMOUS epithelium of the oropharynx is more susceptible to trauma than the COLUMNAR epithelium of the trachea. Laryngoscope blades must be generously lubricated and small orotracheal tubes should be chosen. Oral and nasal airways as well as oraopharyngeal suctioning should be avoided completely.

    There are no contraindications to the use of volatile agents or succinycholine. Regional anesthetics may be preferable when appropriate for patient care.


    Epidural hematomas (EDH) are blood clots that form between the inner table of the skull and the dura. Most EDH are caused by direct contact impact injury that causes a forceful deformity of the skull. Eighty percent are associated with skull fractures across the middle meningeal ARTERY or across a dural SINUS and are therefore located in the temporoparietal region. The high arterial pressure of the bleeding vessel dissects the dura away from the skull, permiting the formation of the hematoma. The incidence of skull fractures in children with EDH is lower than in adults because the elasticity of the skull during childhood permits it to spring back to its original position instead of breaking after a significant impact.

    An EDH is usually unilateral and up to 40% of patients have other intracranial lesions, usually subdural hematomas (SDH) or contusions. An EDH from arterial bleeding develops rapidly and at the time of detection, usually very little underlying brain tissue damage is noted.

    Because of their rapid formation, EDH from arterial bleeding are usually detected within hours after injury and often within 1 hour in children. EDH that develop from a dural sinus tear develop more slowly, and clinical manifestations may be delayed with resultant delays in detection. EDH are rare in the elderly, probably because of the close attachment of the dura to the periosteum of the inner table. They are also rare in children less than 2 years old.

    The classical PRESENTATION of the EDH is described as head trauma producing a decreased level of consciousness followed by a lucid interval. Often no return to a completely normal mental status occurs before a second episode of decreased consciousness takes place.

    The LUCID interval is not pathognomonic for an EDH and may occur in patients who sustain other expanding mass lesions. Only about 30% of patients with EDH present classically.

    Patients with an EDH will often complain of a severe headache, sleepiness, dizziness, nausea and vomiting. The development of signs and symptoms depends on how rapidly the EDH is expanding. A small EDH may remain asymptomatic but this is rare.

    Epidural bleeding is present in 0.5% of all head-injured patients and in about 1% of all head-injured patients who present in coma. If the patient is not comatose when the diagnosis is established, the mortality is nearly zero. If the patient is in coma, the mortality from EDH is about 20%.

    If rapidly detected and EVACUATED, the outcome is excellent. Predictors of mortality include the presenting mental status, the presence of other intracranial injury and patient age.


    Complications which occur with epidural placement and utilization include those described elsewhere under PULMONARY and CV EFFECTS as well as general complications listed under NEURAXIAL- COMPLICATIONS.

    Two other potential complications of the epidural placement include placement of a SA or IV catheter (both of which should be identified by traditional test dosing).

    The SA CATHETER can be removed or may be used as a continuous SA catheter for anesthesia.

    A TOTAL SPINAL (which may occur with epidural or SAB) must be managed efficiently. The total spinal presents abruptly with apnea, bradycardia, hypotension, flaccid paralysis, bilateral dilated and nonreactive pupils and a loss of consciousness. Patients are managed by rapid control of the airway, IV fluids, vasopressors and atropine. If a SA catheter is in place, some recommend to withdrawal twice the volume that was infused and replacement with preservative free normal saline. Outcome should be good if the management is performed correctly.

    The IV CATHETER (incidence 4-5% in the obstetric population)should generally be removed and replaced at another vertebral level. Recent studies indicate that only 30% of the catheters that are pulled out of an epidural vein will function in a completely normal manner. Physicians should also be more aware of the risks of epidural hematoma following traumatic placement of the epidural catheter.


    Hemodynamic effects are determined by the dermatomal level of sympathetic blockade. Blocks below T5 are seldom associated with marked hypotension because of compensatory vasoconstriction in unblocked segments. Blocks to higher levels not only further limit compensatory vasoconstriction but also affect the cardiac sympathetic nerves (the accelerators) that arise in the T1-4 segments. REMEMBER that the SNS arises from the thoracolumbar cord and fibers involved with arterial and venous tone arise from T5 through L1.

    Venous capacitance vessels affected by the sympathetic blockade result in a decreased venous return which may be more pronounced in the reverse Trendelenburg position. The decreased venous return obviously leads to a decreased cardiac output.

    Unopposed vagal stimulation can result in vaso-vagal stimulation, associated with profound bradycardia and even transient cardiac arrest.

    Sympathetic block at T6-L1 can also decrease the adrenal medullary response of catecholamine secretion which may further depress HR and cardiac output. If these fibers (T6-L1) are NOT blocked, then compensatory outflow may attenuate the vasodilation of the lower limbs (along with higher levels of vasoconstriction).

    Addition of EPINEPHRINE to the anesthetic solution may result in a MORE PROFOUND degree of hypotension. This is thought to be due to absorbed epinephrine stimulating ß2-adrenergic receptors in the peripheral vasculature, leading to more vasodilation and a fall in DBP. Otherwise stated, low serum concentrations of epinephrine have a predominant effect at the beta 2 receptors.

    Hypotension is most severe in hypovolemic patients because the compensatory vasoconstriction which is enabling them to maintain their BP is taken away with the sympathetic block accompanying the epidural.


    The disconnected catheter should be removed as soon as possible. One survey demonstrated that only 35% of all disconnected catheters are actually removed. When the distal end of a cut catheter is contaminated, bacteria may be cultured from the fluid 87 cm more proximal (Anes 1996 85:883).


    Duration of action for most agents is prolonged with administration of epinephrine. The effect is less pronounced (prehaps negligible) with bupivicaine. NOTE that spinal anesthesia with bupivicaine MAY be prolonged by adrenergic agents.

    no EPI EPI
    clorprocaine 46-60 60-90
    lidocaine 80-120 120-180
    mepivicaine 90-140 140-200
    ropivicaine 140-200 160-220
    etidocaine 120-200 150-225
    bupivicaine 165-225 180-240

    Numbers above correspond to minutes required for two dermatome REGRESSION of pinprick sensation (which is 35-50% of the time needed for complete regression).

    Generally 1-2 mL of anesthetic is required for each dermatomal level blocked. Elderly patients require lower LA concentration (due to normal demyelination of aging) and lower volumes (theoretically due to less leaking through osteophytic stenotic foramina).

    There is general consensus that a plateau effect occurs with epidural anesthetics so that once a certain quantity of anesthetic is injected, supplemental doses will not increase the block height but make the block more dense.

    With SPINAL anesthesia, there is an evident UNIFORM block of the sympathetics, motor and sensory elements (Barash states otherwise).

    The SEGMENTAL block of the EPIDURAL anesthetic (on the other hand) allows variable blockade of motor elements because of the higher minimum concentration of LA required to block the large motor nerves. In vivo, the sympathetics are blocked by the lowest concentrations followed by the fibers responsible for pain, touch and motor function.

    At high thoracic levels the ligamentum flavum may fail to fuse in the midline, and thus it should not be relied on as a tactile landmark during thoracic epidural needle placement.

    PAIN: bupivicaine 0.1% and morphine 40 mcg/mL [5-6 mL/hr thoracic or ~8 mL/hr lumbar]

    LABOR: bupivicaine 0.04%, fentanyl 1.7 mcg/mL, epinephrine 1:600K [bolus 15 mL; 15 mL/hr & PCA 5 ml q30 min]

    SECTION: lidocaine 2% 15-20 mL; chloroprocaine 3% 15-20 mL


    ADULT dosing for morphine ranges from 2-3 mg.

    PEDIATRIC dosing for single shot morphine is between 0.03 and 0.05 mg per kg in 3-10 mL NS. For continuous infusions, rates range from 3-8 mcg/kg/hour.

    SIDE EFFECTS include nausea, itching and respiratory depression at a greatest incidence occurring in a biphasic distribution.

    PRURITIS is the most common side effect generally occurring within a few hours of injection and possibly preceding analgesia. Pruritis is most likely induced by cephalad migration of the opioid in CSF and subsequent interaction with opioid receptors in the trigeminal nucleus. Treatment options include naloxone at no greater than 2 mcg/kg/hour, nalbuphine 3 mg IV bolus, propofol at 10 mg bolus followed by 30 mg over 24 hours, and ONDANSETRON. NSAIDS may also have a future role in prophylaxis (J Clin Anesth 2003).


    Continuous infusions for postoperative analgesia are often provided by lumbar, thoracic or caudal catheters. Most authorities will seldom use epidural analgesia in patients less than 6 months old though one paper (Paed Anaesth 1998) reported on 220 neonates (weight 0.9-5.8 kg) receiving epidurals for postoperative analgesia without unique consequences.

    The typical catheters are available in 20 gauge 100 cm lengths and may be inserted through a short 18 gauge angiocath into the caudal space or through an 8 cm 18-19 gauge Tuohy (as opposed to the 17 gauge provided in the adult packages) that is placed in the thoracic or lumbar region in the usual manner. The 23 gauge catheters that are provided in pediatric packages are often flimsy and prone to kinking. Loss of resistance techniques may be used for placing the lumbar and thoracic catheters. It has been recommended to avoid LOR with air due to occasional reports of venous air embolism.

    DISTANCE to the epidural space may be as shallow as 3 mm in the neonate. Formulas are available but some authors state that there is a poor correlation with the weight of the patient. One commonly used formula to estimate depth in mm:

    10 + (age in years times two)

    MORPHINE dosing for single shot is between 0.03-0.05 mg per kg in 3-10 mL NS (or bupivicaine). For continuous infusions, rates range from 3-8 mcg/kg/hour.

    BUPIVICAINE is often infused at a concentrations of 0.1-0.125%. MAXIMUM rates for infants are at 0.25 mg/kg/hour (48 hours maximum) and for older patients at 0.5 mg/kg/hour. Infants may be at increased risk for toxicity because of lower levels of alpha acid glycoprotein, lower bicarbonate reserves and possibly diminished clearance. Interestingly, AAP do rise in postoperative patients and approach adult levels by postoperative day four.

    FENTANYL can be bolused at 0.5-1.0 mcg/kg and infused at up to 1.0 mcg/kg/hour. As with adults, fentanyl boluses may be useful for break through pain.

    CLONIDINE may be added to continuous epidural infusions at total dosages between 0.15-0.25 mcg/kg/hour which generally translates to concentrations between 0.4-1.2 mcg per mL.

    NUBAIN may be useful for perceivable itching at 0.1 mg/kg.

    NARCAN infusions are dosed between 4-8 mcg/kg/minute.


    Respiratory effects of epidural blockade are minimal. With a sensory level of T3 and an associated motor level of T8, there is no significant change in either vital capacity (VC) or functional residual capacity (FRC). There is also no impairment of ability to cough.

    In patients with severe pain, epidural blockade probably improves VC and FRC as well as PaO2, which may result in improved gas exchange and more effective coughing.

    Potential PROBLEMS

    1) potential for PHRENIC nerve palsy (C3-5) is low except with intentional cervical epidurals
    2) respiratory ARREST is usually not related to sensory or motor blockade or depressant effect of local anesthetic. The most common cause is extensive sympathetic block with reduced cardiac output and resultant ischemia to the CNS medullary centers.
    3) epidurals with narcotic infusions may cause respiratory DEPRESSION through a direct effect of the narcotic at the respiratory center


    Test doses are recommended before initial and subsequent dosing of an epidural catheter to rule out IV and subarrachnoid injections. The most commonly recommended initial test dose utilizes 3 mL of 1.5% lidocaine with 1:200K epinephrine (15 mcg total).

    INTRAVENOUS 15 mcg of epinephrine given IV should increase the HR by 20 bpm within 45 seconds but effects may last for only 15 seconds. Tachycardiac responses to epinephrine are LESS reliable in the pediatric AND elderly populations and especially in those that are heavily sedated or under GA.

    Other indicators of IV epinephrine include HTN (SBP increased by 15 mmHg), T wave DEPRESSION, circumoral pallor, palpitations and tremulousness (in awake patients).

    One recent study (Anest Analg 2001 93:1332) demonstrated that T wave DEPRESSION (by 25% in lead II) or HTN (SBP increase by 15 mmHg) are the most sensitive and specific indicators in awake AND anesthetized elderly patients with IV epinephrine at 15 mcg.

    In contrast to this epinephrine response, the T WAVE ELEVATION seen in the PEDIATRIC age group is thought to result from the combined effects of LA and epinephrine. These effects can be demonstrated in any of the limb or precordial leads and are not independently related to adrenergic response to epinephrine.

    Other methods that are occasionally used to detect IV injections include isoproterenol, ephedrine, fentanyl (in the alert and nonsedated patient) and air. Large doses (capable of producing total spinals) of LA are required before systemic symptoms are noted.

    INTRATHECAL The effects of SA injection may not be apparent for 3-5 minutes and are obviously secondary to effects of the LA and not the adrenergic agents. Patients may experience a sudden reduction in pain, warmth, weakness or dysthesias of the lower extremities. Total spinals are rare when proper test doses are administered along with each bolus dose.


    The patient should not be hypersensitive to radiographic contrast. Approximately 0.5 mL of Iohexol (Omnipaque) 180 or 240 is required – the catheter dwell is typically 0.25 mL. Do not use either the 140 or 350 preparation. Patients should be observed for at least thirty minutes following injection.


    Epinephrine is a sympathomimetic that is naturally secreted from the adrenal medulla. It activates an adrenergic receptive mechanism on effector cells and imitates all actions of the sympathetic nervous system except those on the arteries of the face and sweat glands.

    Epinephrine acts on both alpha and beta receptors and is the most potent ALPHA receptor activator being 2-10 times more active than norepinephrine. At very low serum concentrations (as seen with epidural solutions containing epinephrine) there is predominant effect at the ß2 receptors leading to vasodilation and a decrease in the MAP.

    CODE DOSES are utilized for (1) arrest: VF, pulseless VT and PEA,
    (2) bradycardia after atropine, DA and possibly TCP, (3) severe hypotension and (4) anaphylaxis

    CODE DOSES begin at 1 mg (10 mL of the commonly available 1:10,000 concentration) for adults and 10 mcg/kg for pediatric patients. HIGH doses may be given to children AND adults up to 0.2 mg/kg but are not recommended by the latest ACLS protocols. ETT doses for adults begin at 2-3 mg and 100 mcg/kg for the pediatric patient.

    Neonatal resuscitation doses (asystole and persistent bradycardia) are also given at 100 mcg/kg per ETT (commonly 0.1 mL per kg of the 1:1000 concentration).

    DOSING for INFUSIONS usually range from 0.01-1.0 mcg/kg/minute with incremental bolus doses between 1-10 mcg/kg. INFUSIONS for adults may be prepared by adding 30 mg to 250 mL of NS or D5 (120 mcg per mL) and infusing at a rate of 100 mL per hour.

    beta effects 0.01-0.03
    beta over alpha 0.03-0.15
    alpha and beta 0.15-0.5

    PEDIATRIC infusions are started at the high end of 1 mcg/kg/minute and are prepared by adding 0.3 mg/kg to 50 mL NS such that 1 mL/hour is the equivalent of 0.1 mcg/kg/minute.

    The normal INTRINSIC SECRETION is equivalent to 0.2 mcg/kg/minute (or roughly 1 mg every seventy minutes in the average adult).

    When added to LOCAL ANESTHETICS, the total dose should be limited to 10 mcg/kg for the pediatric patient and 200-250 mcg in the adult patient. These limits probably do not apply to the injectate utilized during tumescent liposuction.


    Miscellaneous uses for epineprine include treatment for croup and severe asthma.

    LARYNGEAL EDEMA is treated with 1 mL of 2.25% RACEMIC EPINEPHRINE (or 5 mL of 1:10,000 L-epinephrine) diluted in 3 mL NS and nebulized not more often than every 30 minutes and preferably every 2-6 hours.

    PEDIATRIC patients less than 20 kg are treated with 0.25 mL of 2.25% RE diluted in NS (or 2 mL of L-epinephrine) every 2-6 hours. Patients at 20-40 kg may be treated with 0.5 mL of 2.25% RE in NS.

    BRONCHOSPASM & ANAPHYLAXIS in adults may be treated by 0.1-0.3 mg of 1:1000 solution SC. The PEDIATRIC patient may receive 0.01 mL/kg (up to 0.5 mL) of 1:1,000 solution SC repeated every 15 minutes as necessary. The sustained release form (1:200 solution) may be given in doses up to 0.15 mL SC and repeated every 8-12 hours as needed.


    Epoprostenol (also known as prostacyclin, PGl2 and PGX) is a metabolite of arachidonic acid and a naturally occurring prostaglandin produced by the intima of blood vessels.

    Epoprostenol has two major pharmacological actions: (1) direct vasodilation of pulmonary and systemic arterial vascular beds, and (2) potent inhibition of platelet aggregation at higher doses.

    At low doses, vagally mediated bradycardia often occurs, but at higher doses, epoprostenol causes reflex tachycardia in response to direct vasodilation and hypotension. No major effects on cardiac conduction have been observed.

    Additional pharmacologic effects of epoprostenol in animals include bronchodilation, inhibition of gastric acid secretion and decreased gastric emptying. Side effects may include thrombocytopenia, rebound pulmonary HTN and pulmonary edema.

    Many of the actions of epoprostenol are exerted via the stimulation of adenylate cyclase, which leads to increased intracellular levels of cAMP. A sequential stimulation of adenylate cyclase, followed by activation of phosphodiesterase, has been described in human platelets. Elevated cAMP levels regulate intracellular calcium concentrations by stimulating calcium removal and this platelet aggregation is ultimately inhibited by the reduction of cytoplasmic calcium, upon which platelet shape change, aggregation and the release reaction depend.

    Effects on platelets have been found to disappear within 2 hours of discontinuing the infusion and hemodynamic changes due to epoprostenol to return to baseline within 10 minutes of termination of 60 minute infusions at 1-16 ng/kg/min. Higher doses of epoprostenol sodium (20-30 ng/kg/min) disperse circulating platelet aggregates and increase by up to two fold the cutaneous bleeding time. Epoprostenol may be useful for pretreating the patient with HIT requiring heparin for emergency bypass surgery. Epoprostenol potentiates the anticoagulant activty of heparin by approximately 50%, possibly reducing the release of heparin neutralising factor.

    The half-life for this process in man is expected to be no more than 6 minutes, and may be as short as 2-3 minutes, as estimated from in vitro rates of degradation of epoprostenol in human whole blood. Extensive clearance by the liver has been demonstrated, with approximately 80% being removed in a single pass. Urinary excretion of the metabolites of epoprostenol accounts for between 40-90% of the administered dose, with biliary excretion accounting for the remainder. Urinary excretion is greater than 95% complete within 25 hours of dosing.


    EPO takes 1-3 weeks for preoperative effectiveness but may be the equivalent of producing one unit of blood each week. Risks from volume expansion include hypertension, thrombophyllic states and potential for CHF.


    The ESCHMANN introducer, also known as a gum elastic bougie is a 60 cm long, 15 French stylet that is angled at 40 degrees approximately 3.5 cm from the distal end and is made from a woven polyester base. 10 Fr sizes are available for the pediatric population.

    The ESCHMANN introducer may be used in place of a stylet or it may be inserted as an introducer to a railroaded ETT.

    The ESCHMANN is useful for the anterior larynx when only the epiglottis is visualized. Correct placement is indicated as the tip clicks along the anterior tracheal cartilages.


    When performed by a skilled experienced clinician within an appropriate setting and with carefully selected patients, the chance of significant complication from ESIs is small and remote. Similar to the regional analgesia procedures, theoretical risks of ESIs include inducing bleeding and infection. Common risks of epidural injection are backache, postural puncture headache (0.5%-1% for lumbar interlaminar and 0.6% for caudal epidural injections), nausea, vomiting, dizziness, and vasovagal reaction. Epidural hematoma occurs in 0.02%-0.01% of performed procedures. Nerve root injury and meningitis also have been reported. Risks of injected steroids in at-risk patients (eg, those with ulcers or diabetes, history of tuberculosis, acquired immunodeficiency syndrome [AIDS], bacterial infections, psychiatric disorders) are not known at the present time. Mild hypothalamic-pituitary-adrenal (HPA) axis suppression has been reported from 1-3 months after receiving a total of 3 epidural injections (once weekly) with 80 mg of Aristocort in 7 mL of 1% Lidocaine.


    Studies have indicated that ESI is most effective in the presence of acute nerve root inflammation. Clinical manifestations of nerve root inflammation include some or all of the following: radicular pain, dermatomal hypesthesia, weakness of muscle groups innervated by the involved nerve roots, diminished deep tendon reflexes and positive straight leg-raising tests. ESIs can provide both diagnostic and therapeutic benefits. Diagnostically, ESI may help identify the region and spinal column of potential pain generation through pain relief after LA injection to the site of presumed anatomic pathology. If the patient receives several weeks or more of pain relief, then it may be reasonable to assume that an element of inflammation was involved in his or her pathophysiology. This last element of diagnostic information also is the therapeutic element. Since prolonged pain relief is presumed to be due to a reduction in an inflammatory process, it is also reasonable to assume that during the prolonged pain relief, the afflicted nerve roots are also relatively protected from the deleterious effects of inflammation.

    Approximately 60-75% of patients receive some relief after ESI. Benefits include relief of radicular pain and LBP (generally relieving leg pain more than back pain), improved quality of life, reduced analgesic consumption, improved maintenance of work status and obviating need for hospitalization and surgery in many patients. Most patients take several days to respond to ESI. This is generally due to the delayed effects of the corticosteroid.

    The commonly used compounds with prominent glucocorticoid action include betamethasone sodium phosphate and betamethasone acetate (Celestone Soluspan), methylprednisolone acetate (Depo-Medrol) and triamcinolone hexacetonide (Aristospan). Each milliliter of Celestone Soluspan contains 3 mg of highly soluble betamethasone sodium and 3 mg of the relatively insoluble acetate salt. Thus, Celestone Soluspan provides both rapid onset and extended anti-inflammatory activity. Depo-Medrol and Aristospan, being relatively insoluble, provide a sustained anti-inflammatory effect. Depo-Medrol contains benzyl alcohol, which is potentially toxic when administered locally to neural tissue and may increase the risk of arachnoiditis or meningitis. Many physicians prefer to use only steroids without such preservatives.

    The response of ESI is related to the underlying pathophysiology. In general, acute radicular pain from lumbar disc herniation responds more favorably than the radicular pain from lumbar spinal stenosis. The patients with radicular pain after lumbar spine surgery frequently received less benefit from ESI unless the radicular pain is from a recurrent HNP. In general, patients who have had symptoms fewer than 3 months have response rates of 90%. When patients have radiculopathy symptoms for fewer than 6 months, response decreases to approximately 70%. Response decreases to 50% in patients who have had symptoms for over a year. Patients with shorter duration of symptoms also have more sustained relief than those with chronic pain. Patients with chronic back pain have better response if they develop an acute radiculopathy.


    Several indications for ESI have been reported in the literature. Although the primary indication is radicular pain associated with a herniated nucleus pulposus, a variety of indications have been reported.

    LUMBAR ESI may be indicated for lumbar radicular pain associated with any of the following conditions: (1) lumbosacral disc herniation, (2) spinal stenosis with radicular pain (central canal stenosis, foraminal and lateral recess stenosis), (3) compression fracture of lumbar spine with radicular pain, (4) facet or nerve root cyst with radicular pain.

    CERVICAL ESI have been used to treat the following conditions: (1) pain associated with acute disc herniation and radiculopathy, (2) postlaminectomy cervical pain, (3) cervical strain syndromes with associated myofascial pain, (4) postherpetic neuralgia.

    THORACIC ESI have been reported within the medical literature as treatment pain associated with the following conditions: (1) acute thoracic disc pathology, (2) thoracic radicular pain secondary to disc herniations, (3) postherpetic neuralgia, (4) trauma, (5) diabetic neuropathy, (6) degenerative scoliosis, (7) idiopathic thoracic neuralgia, (8) thoracic compression fracture.

    Absolute CONTRAINDICATIONS for ESI include the following: (1) systemic infection or local infection at the site of planned injection, (2) bleeding disorder or anticoagulation, (3) history of significant allergic reactions to injected solutions (contrast, anesthetic, corticosteroid), (4) central canal stenosis at the site of planned injection. It is acceptable to enter through the adjacent foramen or via an interlaminar approach 2 segments below.


    Cervical, thoracic, and lumbar epidural injections can be approached through translaminar and transforaminal injections. Lumbar epidural injection can be performed using 3 approaches. Translaminar epidural injection refers to injection into the interlaminar space of the spine. Hence, many spine specialists refer to translaminar injection as interlaminar injection. The interlaminar epidural injection can be performed through paramedian or midline approaches. The epidural needle penetrates skin, SQ tissue, paraspinal muscles (paramedian approach) or interspinous ligament (midline approach) and ligamentum flavum. Transforaminal approach is performed by placing the needle in the neuroforamen ventral to the nerve root. The needle is directed in an oblique approach until the tip of the needle touches the posterior lateral portion of the vertebral body, located superior to the intervertebral foramen just under the pedicle. Caudal lumbar epidural injections may be performed by inserting a needle through the sacral hiatus into epidural space at the sacral canal.

    The interval between the injections varies with the steroid preparations used. Since injected methylprednisolone was reported to remain in situ for approximately 2 weeks, the clinician should expect to wait 2 weeks after the injection to assess the patient’s response and to administer a repeat injection. This 2-week interval may be shortened if using a different steroid (short-acting steroid).

    Clinicians and patients often must consider the number of ESIs that should be performed. Studies have demonstrated that patients who did not respond to an initial injection did still show improvement after 1-2 more epidural steroid injections. Further studies have suggested that the total dose for methylprednisolone is approximately 3 mg/kg of body weight to prevent the excessive salt and water retention. In general, up to 3-4 epidural injections may be performed if clinically indicated. Some clinicians schedule a series of 3 ESIs and proceed with these regardless of the clinical response to the first 1 or 2 injections. However, there are no medical outcome studies to clearly support such a regiment.

    The volume of the injection is dictated mainly by the approach used. In cervical and thoracic epidural injections, a total of 3-5 mL may be used for ESI using the interlaminar approach. However, in transforaminal ESI, clinicians generally use a total volume of only about 1.5-2 mL. The volume used for lumbar ESI is slightly greater, generally using 6-10 mL for interlaminar ESI, up to 20 mL for caudal ESI, and 3-4 mL for transforaminal ESI. For interlaminar ESI, typical corticosteroid doses are 12-18 mg for Celestone and 80-120 mg for methylprednisolone. Half of these steroid doses are generally used when performing transforaminal ESI. The epidural steroid is injected in a diluent, such as lidocaine (1-2%) and/or NS.


    ESMOLOL (Brevibloc) is a ß1 selective receptor blocking agent with rapid onset, very short duration of action and no significant intrinsic sympathomimetic or membrane stabilizing activity at therapeutic dosages. Its elimination half-life after IV infusion is approximately NINE MINUTES. Esmolol inhibits the ß1 receptors located chiefly in cardiac muscle, but at HIGHER doses esmolol does begin to inhibit ß2 receptors located chiefly in the bronchial and vascular musculature.

    METABOLISM Esmolol is rapidly metabolized by hydrolysis of the ester linkage, chiefly by the RBC ESTERASES and NOT by plasma cholinesterases or red cell membrane acetylcholinesterase. Total body clearance in man is found to be about 20 L/kg/hr, which is greater than cardiac output and thus the metabolism of esmolol is not limited by the rate of blood flow to metabolizing tissues such as the liver or affected by hepatic or renal blood flow. Esmolol has a rapid distribution half-life of about 2 minutes and an elimination half-life of about 9 minutes.

    CLINICAL USE Esmolol is indicated for the rapid control of ventricular rate in patients with atrial fibrillation or atrial flutter in perioperative, postoperative or other emergent circumstances where short term control of ventricular rate with a short-acting agent is desirable. Esmolol is indicated for the treatment of tachycardia and hypertension that occur during induction and tracheal intubation, during surgery, on emergence from anesthesia and in the postoperative period.

    It is also useful for DELIBERATE HYPOTENSION either independently or in conjunction with nitroprusside or a volatile agent to prevent reflexive tachycardia.

    DOSING Esmolol may be bolused in doses of 5-10 mg. Infusions may be prepared with almost any fluid to the concentration of 10 mg per mL (2.5 grams or 2500 mg per 250 mL diluent).

    A loading dose of 500 mcg/kg/min (0.5 mg/kg/min) over one minute is followed by a maintenance infusion of 50 mcg/kg/min (0.05 mg/kg/min). As the desired heart rate or endpoint is approached, the loading infusion may be omitted and the maintenance infusion titrated to a maximum of 300 mcg/kg/min (0.3 mg/kg/min) or downward as appropriate. Maintenance dosages above 200 mcg/kg/min (0.2 mg/kg/min) have not been shown to have significantly increased benefits.

    Abrupt cessation of esmolol in patients has not been reported to produce the withdrawal effects which may occur with abrupt withdrawal of other beta-blockers following chronic use in coronary artery disease patients. Caution should still be used in abruptly discontinuing infusions of esmolol in CAD patients.


    Although the esophageal stethoscope has been used for many years, the effect of the depth of placement on the quality of the sounds obtained has never been investigated. The amplitude and frequency characteristics of the first and second heart sound and of inspiratory and expiratory breath sounds were determined at various stethoscope depths (from the distal tip) in 17 healthy anesthetized adults.

    The amplitude for each type of sound varied markedly with depth. Maximal amplitude for S1 was at 34 cm, for S2 at 27 cm, for inspiratory breath sound at 28 cm and for expiratory breath sound at 26 cm. There was a positive linear correlation between the depth of maximal amplitude of these sounds and patient height. Peak frequency, in general, did not change with depth. We conclude that investigators should measure and document depth when performing studies involving the esophageal stethoscope.

    Implications: A depth of 28-32 cm is recommended for clinical use. S1, S2 and inspiratory and expiratory sounds have a high amplitude in that range (Anes Analg 1998 86:1276-9).


    Carbon dioxide is constantly being added to the alveolar gas from the pulmonary blood and removed from it by alveolar ventilation. The concentration of CO2 is equal to the alveolar CO2.

    Dry barometric pressure is not much of a factor. Normal variations at sea level are unlikely to influence PCO2 by more than 2 mmHg.

    MEAN INSPIRED CO2 Decreasing the amount of rebreathing will decrease ETCO2, assuming ventilation remains unchanged. Decreasing apparatus deadspace, as wlth changing from mask to ETT, will decrease rebreathing.

    CO2 OUTPPUT Output is more important in determining alveolar PCO2 than production. Output equals production only in a steady state. A decrease in cardiac output decreases alveolar PCO2. Causes of decreased production include hypothermia, deep anesthesia (thus reducing catecholamine release), muscle relaxation (thus inhibiting shivering) and hypotension.

    ALVEOLAR VENTILATION is the most important factor influencing alveolar CO2. Increases in respiratory frequency or rate will decrease ETCO2. An elevated fresh gas flow can artificially lower ETCO2 by dilution.

    CONCENTRATION EFFECT Alveolar CO2 may be temporarily influenced by net transfer of soluble inert gases across the alveolar/capillary membrane (such as nitrous oxide at the start of a case). Uptake of the inert gas increases the concentration of CO2 in the alveolar gas. The converse occurs during elimination, resulting in a transient reduction of ETCO2.

    DEAD SPACE Lung units which are ventilated but not perfused will contribute a significant amount of CO2-free gas to the end-expiratory gas, thus lowering ETCO2.

    SHUNTING Shunt has little impact on CO2 transport, in contrast to O2. Only in exceptional patients with shunts greater than 30% will the ETCO2 change by more than 2mmHg.


    The normal PACO2-ETCO2 gradient in patients without significant pulmonary disease is 3-5 mmHg.

    There are THREE major factors that may cause the PACO2-ETCO2 gradient to INCREASE.

    1) PaCO2 < > PACO2. Both increases and decreases in V/Q increase the difference between PACO2-ETCO2. As V/Q approaches 0 (as with endobronchial intubation), the blood from areas that are perfused but not ventilated mixes with O2 rich blood raising PaCO2 in spite of a normal or low ETCO2. As V/Q approaches infinity (as with pulmonary embolism), the gas from the non-perfused areas maintains a PACO2 of zero which mixes with gas from the perfused lung thus lowering the ETCO2.

    2) PACO2 > true ETCO2. This happens when undiluted alveolar gas is not delivered to the upper airway. Examples are when the patient is breathing erratically or not exhaling completely (COPD or bronchospasm) or when the respiratory rate is rapid (high-frequency ventilation as with children and infants). Factors that contribute to this are a low ratio of tidal volume to equipment dead space, rapid rate and rate of sampling higher than expiratory flow rate. Studies show that PACO2-true ETCO2 gradient does not increase significantly in patients over 12 kg but can increase in patients less than 12 kg.

    3) true ETCO2 > measured ETCO2. This is caused by problems with the capnograph itself as with sampling catheter leaks, calibration errors or slow instrument response time. This can also happen with cuff leaks or in children with uncuffed tubes.

    REVERSE gradient such that PACO2 is less than ETCO2. There are a number of arcane explanations for this but the best is equipment error.


    Ethycrynic acid is a diuretic useful for treatment of hypertensio, increased intracranial pressure, edema associated with CHF, hepatic cirrhosis and nephrotic syndrome.

    DOSING is between 0.5-1 mg/kg by slow IV injection. Oral doses range between 50-200 mg/day.


    Etidocaine is an amino amide with a pKa of 7.7 and a pH of 4.5 and virtually identical clinical profile to bupivacaine. The toxic dosis though to be in the 300-400 mg range with the higher doses being tolerable with epinephrine.

    Etidocaine is ideally suited for infiltration anesthesia at 0.5%, peripheral nerve block at 0.5-1% with duration between 3-12 hours and epidural anesthesia at 1-1.5% providing 3-5 hours of anesthesia. Profound motor block is sometimes associated with a limited sensory block and this may make the agent less ideally suited for epidural anesthesia when compared to bupivacaine with the similar toxicity profile.


    It has been appreciated for some 15 years that etomidate infusions in critically ill patients suppress adrenocortical output. The mechanism appears to be inhibition of 11-ß hydroxylase, which catalyzes a rate-limiting step in the production of cortisol from cholesterol in the adrenal cortex. Stimulation of the adrenal cortex with exogenous ACTH does not lead to the normal increase in cortisol seen in untreated patients. Etomidate also impairs formation of aldosterone.

    Accumulation of 11-deoxycortisol and 11-deoxycorticosterone, precursors of cortisol and ACTH, respectively, which have mineralocorticoid effects, appears to compensate for the lack of aldosterone and electrolyte abnormalities are typically not seen.

    Recent evidence suggests that even single doses of etomidate interfere with cortisol and aldosterone production for 6-24 hours. While this is almost certainly not clinically significant in most cases, many suggest caution in critically ill postoperative patients who have received etomidate. Some authors suggest that prolonged infusions of etomidate in ICU settings have contributed to patient mortality.

    Most other induction agents are also associated with decreased cortisol following anesthesia induction for minor surgery, with the exception of methohexital, which has been associated with an increase in this hormone.

    In contrast to etomidate, these other induction drugs do not inhibit the response to exogenous ACTH. This may be due to the ability of these drugs to block some of the stress-induced increase in cortisol caused by surgical trauma, rather than a direct effect on cortisol synthesis. Support for this idea comes from another investigation, which found increases in cortisol during operation following either thiopental or midazolam induction during major surgery.


    DOSAGE Given for induction at 0.1-0.4 mg/kg or approximately 10 mL or 20 mg per 80 kg in moderate dosing. A continuous infusion may be given at 5-20 mcg/kg/min. The drug is supplied as a concentration of 2 mg/mL.

    A carboxylated imidazole often used for induction in patients that are hemodynamically unstable. The drug is water-soluble at acidic pH but lipid-soluble at physiologic pH.

    PHARMACOKINETICS Clearance of 10-20 mL/kg/min. The half-life is reported between 2-5 hours. The Vd is between 2.2 – 4.5 L/kg and 76% is bound to albumin. Etomidate undergoes hepatic metabolism via hydrolysis (extraction ratio 0.9).

    PHARMACODYNAMICS Etomidate decreases CBF through cerebral vasoconstriction and decreases CMRO by 35-45%. It increases amplitude and latency of SSEP.

    It is useful in that it causes minimal change in HR, SVR and CO. Nevertheless MAP may decline by 15%. There is no apparent change in renal blood flow.

    Occasional transient apnea may occur. Etomidate decreases tidal volume and increases respiratory rate similar to the volatile agents.

    It is known to inhibit subcortical areas leading to MYOCLONUS (33% incidence) and hiccoughs. Propofol and thiopental may also cause myoclonus but in decreasing order of incidence.

    One notorious side effect is an inhibition of 11-ß-hydroxylase activity for 4-8 hours subsequently decreasing cortisol and aldosterone levels but this is probably not important in humans with short term dosing and no clinic complications have been reported following single induction doses. See ETOMIDATE – ADRENAL.

    Etomidate does NOT blunt the sympathetic effect of laryngoscopy unless it is used with an opioid. Like propofol, it may be painful on injection secondary to its propylene glycol prepartion. The propylene glycol is also associated with acute renal failure during prolonged infusions Etomidate is also EMETOGENIC and this may be the single most serious side effect of administration.



    Doses are increased by 2-2.5 times.


    2.5 3.6 4.9 120
    3.0 4.3 7.1 140
    3.5 4.9 9.6 160
    4.0 5.6 12.6 180
    4.5 6.2 15.9 200
    5.0 6.9 19.6 220
    5.5 7.5 23.7 250
    6.0 8.2 28.3 260
    6.5 8.9 33.2 260
    7.0 9.5 38.5 260


    TL BL OD
    26F xx xx xx
    28F 4.5 4.5 9.8
    32F xx xx xx
    35F 6.0 6.0 12.1
    37F 6.5 6.5 13.2
    39F 7.0 7.0 14.3
    41F 7.4 7.4 15.4


    ID OD
    3.5 8.0 eq to 6.0 ETT
    4.5 9.0 eq to 6.5 ETT
    6.0 11
    6.5 11.5
    7.0 12.0
    7.5 12.5
    8.0 13.5
    8.5 14.0
    9.0 14.0


    Brain stem auditory evoked potentials are electrical signals generated by depolarizations in structures along the conductive pathway from the ear to the auditory cortex. Signals are produced by clicks in the ear being monitored while white noise delivered to the contralateral ear eliminates the interference possible through bone conduction.

    BAER signals (like facial nerve signals) are robust and are very resistant to the depressant effects of anesthetic agents (unlike SSEP). BAER therefore provides a means of assessing the intraoperative function of both the eighth (acoustic) cranial nerve and the brain stem.

    This type of monitoring is used extensively during resection of acoustic nerve tumors, microvascular decompression of the cranial nerves and other lesions of the medulla or brain stem.


    Motor evoked potentials can be recorded from (1) muscle after stimulation of either the anterior spinal cord or the motor cortex with electrical or magnetic stimuli or (2) epidural spaces from cortical stimulation. These potentials allow assessment of the function of the motor pathways from stimulation site to the periphery.

    Cortical MEP have been used clinically to monitor patients with cervical cord lesions, Chiari malformations and medullary tumors.

    MEP are generally limited due to lack of technical familiarity and by their sensitivity to depression by most anesthetic agents and muscle relaxants. Cortical MEP signals monitored from the epidural space are influenced by anesthetics in a manner similar to the SSEP. More peripheral monitoring (of the peripheral nerves or actual muscle fiber) are VERY sensitive to the effects of volatiles (at 0.2 MAC concentrations), thiopental and midazolam.


    All anesthetic agents except muscle relaxants can affect SSEP to varying degrees. Nevertheless, excellent results can be obtained if anesthetic depth is STABLE and adequate monitoring can take place even with the use of 50% nitrous oxide.

    An increase in latency (slower conduction), a decrease in amplitude or a complete loss of an evoked potential should be considered indicative of surgical injury or ischemia until proven otherwise. Consensus opinion appears to be that an increase in latency of 10-15% and a decrease in amplitude of greater than 50% should be cause for serious concern.

    halothane – +
    enflurane – +
    isoflurane – +
    nitrous – 0
    barbiturate – +
    etomidate + 0
    ketamine + 0
    midazolam – 0
    opioids 0 0
    propofol 0 +

    In general, volatile agents kept below 0.5 MAC will not interfere with evoked potential monitoring but nitrous oxide should be avoided. At higher concentrations, decreases in amplitutude are greater than observed increases in latency.

    Opioid infusions are helpful in these settings and neuromuscular blocker (if permissable) may make evoked potential monitoring somewhat easier.

    OTHER FACTORS A decrease in MAP below levels of cerebral autoregulation produces a decrease in amplitude with no change in latency. HYPOTHERMIA will produce an increase in latency and a decrease in amplitude. Changes in OXYGEN delivery to neural tissues will also alter SSEP. Isovolumic HEMODILUTION at hematocrits below 15% and hypoxemia have alse been shown to alter SSEPs.


    Visual evoked potentials are produced by light stimulation to the eyes. The responses appear to be generated bilaterally in the visual cortex which is supplied by the posterior cerebral artery.

    VEP monitoring has been used for craniofacial surgery as well as pituitary surgery when tumor tissue may not be well differentiated from normal optic nerve.

    Intraoperative application is limited because flash stimulation may not actually monitor the fields of vision and the large bulky gogles required pose technical problems. Studies have revealed that intraoperative variations in the signals achieved do not always correlate with clinical outcome.

    Influences on recordings are similar to those influences on other SSEP. Volatile agents should be limited to less than 0.5 MAC. Opioid analgesia and the use of etomidate may be desirable.


    The EXIT procedure stands for the ex utero intrapartum technique procedure. It is a technique which allows for the continuance of fetoplacental circulation during cesarean section – accomplished by initially delivering the infant head and shoulders, while leaving the placenta in place so that there is intact uteroplacental blood flow. The umbilical cord is clamped after the infant airway is secured. The infant is then fully delivered.

    The importance of the establishment of an airway is paramount to successful neonatal care. Ultrasound now enables clinicians to diagnose potentially compromised airways in utero. Head and neck masses traditionally lead to high mortality owing to their effects on airway patency and securement. There are case reports of infants with large neck masses who were intubated with intact uteroplacental circulation.

    The EXIT procedure has been used to secure the airway in infants suffering from cystic hygroma, cervical or oropharyngeal teratomas and hemangiomas.

    Two cases are described of fetal tracheal intubation with intact uteroplacental circulation. One patient was a 36 week fetus with a 8 by10 cm neck mass. A cesarean section was performed under GA. After the head was delivered through the incision the child was intubated with some difficulty. The authors note that during the intubation the fetal heart rate was 110 beats per minute and a pulse oximeter probe on the earlobe showed saturation readings between 78-82%. Apgar scores were 3-5-8 at 1-5-10 minutes respectively. Umbilical vein blood gas was 7.40-45-39.

    The other child described was a 30 week fetus noteworthy for a large pharyngeal mass. Under GA, a hysterotomy was performed and the fetal head was delivered. A 10 by 10 cm epignathus teratoma was present. The child was intubated with much difficulty in about five minutes. Again, intact uteroplacental circulation was maintained during intubation. The authors report fetal heart rate of 100-120 beats per minute during the intubation period. Apgar scores were 2-4 at 1-5 minutes respectively. After volume resuscitation was begun, initial post-ductal arterial blood gas analysis showed a pH of 7.36-39-136.

    Schulman and colleagues discuss their preference for maternal general endotracheal anesthesia with halothane noting that this offered them uterine relaxation and tocolysis. They also note that halothane crosses the placenta and provided them with fetal anesthesia that had the benefit of providing fetal immobility during tracheal intubation but possibly the negative effect of neonatal depression. They also note that regional anesthesia could have provided adequate maternal anesthesia, but felt that it would not offer adequate uterine relaxation, possibly leading to premature separation of the placenta. Additionally, maternal regional anesthesia would not have provided fetal skeletal muscle relaxation. Shih employed maternal deep inhalational GA (2-3% isoflurane) to provide profound uterine relaxation in an effort to maintain uteroplacental blood flow. They note that 60 minutes of fetoplacental circulation may be obtained with deep inhalational anesthesia, while significant fetoplacental circulation may only be present for 5 minutes in unanesthetized patients.

    Interestingly, Shih employed angiotensin II to treat maternal hypotension based on studies in prepregnant animals suggesting that angiotensin II causes less vasoconstriction of uterine vessels than other systemic vessels and the incidence of fetal acidemia is not increased when angiotensin II is used to control maternal hypotension. Additionally, angiotensin II does not cross the placenta.


    The more appropriate name for this device is the PRESSURE SENSOR SHUTOFF VALVE. It is designed to help prevent delivery of hypoxic gas mixtures from the anesthesia machine due to failure of oxygen supply.

    The valve shuts off all OTHER gases when the PRESSURE in the oxygen delivery line is less than 20-30 psi.

    The device will prevent the administration of a hypoxic mixture from either an oxygen pipeline cut off or an exhausted cylinder. As long as oxygen pressure remains greater than 20-30 psi all the other gas lines will remain open.

    A hypoxic mixture can still be delivered if the pipeline or cylinder contains the wrong gas or if the proportioning device fails. Recall Freids presentation on the hypoxic patient in Japan secondary to supply tank being filled with argon. This problem could be resolved by oxygenation by opening the emergency E cylinders and DISCONNECTING the wall oxygen supply.


    FPP is categorized as a myopathy. The periodic paralysis myopathies come in three forms based on baseline potassium concentrations: hypokalemic (most common), normokalemic and hyperkalemic.

    Genetic research indicates that periodic paralyses are caused by mutations in the genes that control development of sodium or calcium ion channels in the muscle membrane. DNA testing is available but unreliable for absolute diagnosis.

    HYPOKALEMIC FPP is an inherited autosomal dominent disease. Attacks usually begin in the first or second decade and occur in both sexes. Attacks start out infrequently but may ultimately occur daily. Attacks last from minutes to days.

    The attacks are characterized by proximal weakness of the arms and legs (especially hips and shoulders) followed by distal weakness, usually sparing smooth and cardiac muscle. Occasional bulbar or respiratory weakness can be fatal. Reflexes are decreased or absent. Patients can lose sensation in paralyzed limbs but are alert during attacks.

    Usually there is a fall in serum potassium during the attack. During this time there may be urinary retention of sodium, potassium, chloride and water.

    Attacks resolve suddenly with full recovery of muscle function, but with repeated attacks permanent paralysis may occur. Patients can have a positive Babinski’s reflex.

    Concurrent problems during an attack may include cardiac arrhythmias due to hypokalemia. Airway protection must be considered if bulbar and respiratory weakness occurs.

    Prevention is with acetozolamide and avoidance of triggering situations. Attacks may be triggered by ingestion of a high carbohydrate meal, with rest after exercise, by infusions of glucose/insulin, stress and hypothermia. Treatment includes potassium infusion and treatment of cardiac arrhythmias.

    The HYPERKALEMIC form of FFP is much rarer than the hypokalemic form. It seems to be associated with a mutation of the sodium channel in muscle membranes. Prevention is also with acetozolamide and avoidance of triggering situations. Triggers may be exercise, potassium infusions, metabolic acidosis and hypothermia. Treatment is directed toward protection of the heart from high potassium levels (calcium) and reduction of serum potassium levels.

    The ANESTHETIC management of patients with periodic paralysis first involves knowing the patient’s history and their particular disease characteristics. The concurrent diseases must be ruled out (such as Andersen’s disease with long QT syndrome). The primary goal of the anesthetic is to avoid events (perioperatively) that are known to precipitate muscle weakness. Electrolytes should be normalized, hypothermia should be avoided and frequent monitoring of the serum potassium level is indicated. The ECG should be constantly monitored for signs of arrthymias.

    These patients can be considered at RISK FOR MH, thus avoidance of MH triggers is indicated. Use of nondepolarizing muscle relaxants is thought to be acceptable, although abnormal sensitivity to these agents may be encountered and adequate muscle strength must be assured prior to extubation.


    Famotidine or PEPCID

    Patients wit CrCl less than 50 mL/min should receive 20 mg daily.


    Fat embolism syndrome is a multisystem disorder affecting primarily the pulmonary and cerebral organs. The onset is typically gradual with hypoxemia, confusion, fever and a petechial rash developing 12-36 hours following trauma.

    MAJOR criteria

    1) petechial rash
    2) respiratory: tachypnea, dyspnea, bilateral inspiratory crepitus, bilateral diffuse patchy shadowing
    3) neurological: confusion, drowsiness, coma

    MINOR criteria

    1) tachycardia
    2) fever over 39.4
    3) jaundice
    4) renal changes: anuria or oliguria
    5) thrombocytopenia to less than 50% of admission value, sudden decrease in hemoglobin at least 20% less than admission value, ESR over 71 and fat macroglobulemia on peripheral blood smears

    The presence of any one major plus four minor criteria in addition to macroglobulemia was felt by one study to constitute the diagnosis of FES. Although criticized, as fat droplets may be found in blood of healthy volunteers, these criteria are reasonably reliable. The petechial rash, found on the conjunctiva, oral mucous membranes and skin folds of the neck and axilla is felt to be almost pathognomic of FES. This unusual distribution is thought to be secondary to fat droplets accumulating in the arch of the aorta prior to embolization to non-dependent skin via the subclavian and carotid vessels.

    A number of investigations have been used to help diagnose FES, none being 100% specific. Arterial blood gases will show a low pO2 and pCO2 (respiratory alkalosis) secondary to shunt and hyperventilation. Thrombocytopenia and low hemoglobin are frequent findings and probably reflective of a low grade DIC. Blood and urine specimens may show fat globules, although again this is a nonspecific finding. There may be hypocalcemia due to saponification of the circulating unbound free fatty acids.

    The classical CXR will show a snow storm appearance or later an ARDS like picture. ECG may show right heart strain. Some use a pulmonary artery catheter to show raised PA pressures and also to sample PA blood for fat. Others advocate doing bronchoalveolar lavage looking for macrophages, which as they are lung scavenges, might contain fat. Some centers suggest brain CT or MRI looking for cerebral edema. TEE has also been used to successfully show embolic phenomena during intramedullary procedures.

    By far the most important treatment is PREVENTION, which involves early immobilization. The risk is reduced by operative correction rather than conservative therapy (traction). Retrospective studies have shown that if operated on within 24 hours, the incidence of ARDS is 17% but rises to 75% if surgery is delayed.

    The prognosis in patients who develop FES is good. Mortality is estimated between 5-15% and most patients will make a full recovery. Most of the long term morbidity is associated with cerebral complications, especially focal neurological deficits.


    The FEMORAL NERVE BLOCK is an alternative to the lumbar plexus block for the patient in the supine position. The technique aims at injecting LA just below the fascia iliaca under which run all the nerves emerging from the lumbar plexus.

    TECHNIQUE Several methods have been described – nerve stimulator, paresthesia, double click, arterial pulsation or infiltration. The DOPPLER may be used to better identify the artery.

    Attempts to block the femoral frequently require multiple attempts and inconsistent success rates. Some have suggested that performing the block with a stimulator at the level of the inguinal skin CREASE has given some invetigators more consistent results.

    A 2 inch short bevel insulated needle attached to nerve stimulator is inserted adjacent to the LATERAL border of the femoral artery at the level of INGUINAL CREASE, a skin fold 3-6 cm BELOW and parallel to the inguinal ligament. Two resistances followed by a loss of resistance are sought. The first one occurs as the tip of the needle crosses the fascia lata and the second one occurs as the fascia iliaca is pierced.

    The needle is slowly advanced cephalad at an angle 60 degrees to the horizontal plane while seeking a QUADRICEPS muscle twitch. If a quadriceps muscle twitch is not obtained, the needle is withdrawn and redirected 10 degrees laterally. If this maneuver does not elicit a quadericeps muscle twitch, the subsequent needle insertions should be placed at increments of 5 mm lateral to the previous insertion sites.

    When the initial response is a sartorius muscle twitch, the quadriceps twitch is sought by incrementally redirecting the needle laterally and advancing the needle several mm beyond the point at which the sartorius muscle twitch was induced. After injecting 30 mL of LA the onset of blockade is expected within 3-5 minutes.

    The block is documented by loss of sensation in the anteriomedial thigh and saphenous nerve distribution as well as the presence of quadriceps muscle relaxation.

    MEDICATIONS Lidocaine 1% provides 2-2.5 hours of anesthesia (maximum 30 mL or 300 mg). Mepivicaine 1.5% with epinephrine provides 2-3 hours of anesthesia (33 mL or 500 mg maximum). Bupivicaine 0.5% provides 3-8 hours of anesthesia (35 mL maximum).

    DISADVANTAGES The femoral and lateral cutaneous nerves are almost always blocked. The obturator nerve is blocked in more than 75% of all patients but is MORE consistently blocked than it is with the lumbar plexus approach. The innervation of the obturator is highly variable between individuals.

    The FASCIA ILIACA BLOCK is a block similar to the FEMORAL nerve block that relies on anatomical landmarks and not on the use of the stimulator. It is most appropriate for blockade of the femoral and LFC nerves. The block is purportedly underutilized for postoperative analgesia following operations at the knee.


    DOSING for HTN is at 0.1 mcg/kg/min which may be titrated every 15 minutes to up to 1.6 mcg/kg/min (mix 10 mg in 250 ml D5W for 40 mcg/mL). This is now the drug of choice for hypertensive crisis as it does not increase CBF. Low doses up to 0.05 may serve as renal protective doses protecting the kidneys in acute anemic hypovolemia, during routine radiocontrast procedures and cardiovascular procedures (J Card Vasc Anest 2007 and 2003).

    Fenoldopam is a selective DA-1 agonist with predictable pharmacokinetics useful for treatment of severe HTN, postoperative HTN and controlled hypotension.

    The DA-1 receptors are located postsynaptically and mediate vasodilation of renal, mesenteric, coronary and cerebral blood vessels. Activation of these receptors is mediated by adenylate cyclase.

    Fenoldopam produces dose-related increases in renal plasma flow and decreases in renal vascular resistance. The drug also produces diuresis, natriuresis and kaliuresis without significantly affecting the GFR. Fenoldopam is equipotent with SNP in lowering SBP and DBP in patients with severe HTN. Unlike SNP, fenoldopam will improve renal blood flow and creatinine clearance.

    At higher concentrations, fenoldopam produces moderate antagonism at the ALPHA-2 receptors but is void of the potential adverse effects of DOPAMINE including the DA-2 and ALPHA-1 effects which diminish RBF, GFR and sodium excretion.

    The drug is intended for short term use of less than 48 hours and may be tapered or abruptly discontinued without consequence of rebound hypertension.

    PHARMACOKINETICS Onset of action takes place between 30-60 seconds after administration. Peak effects are achieved withing 1-2 minutes. The duration of action is between 1-15 minutes.

    SIDE EFFECTS include hypotension and dose dependent tachycardia. Hypokalemia to values below 3.0 mEq/L have been observed after infusions lasting less than six hours. The preparation does contain sodium metabisulfite which may cause allergic and anaphylactic reactions.

    The cost for infusions at 1-1.6 mcg/kg/minute may be over 1000 dollars per day.


    Fentanyl citrate is a narcotic analgesic that is about 100 TIMES more potent than morphine. A dose of 100 mcg is approximately equivalent in analgesic activity to 10 mg of morphine (or 75 mg of meperidine).

    Fentanyl preserves CARDIAC stability and blunts stress-related hormonal changes at higher doses.

    Alterations in respiratory rate and alveolar ventilation, associated with all narcotic analgesics, may outlast analgesic effects. As the dose of narcotic is increased, the decrease in pulmonary exchange becomes greater. Large doses will produce apnea by central depression or by muscle rigidity.

    Fentanyl appears to have LESS EMETOGENIC activity than either morphine or meperidine.

    Recent assays in man show no clinically significant HISTAMINE release with large dosages up to 50 mcg/kg.

    DOSING is highly variable with patients tolerating small doses up to 5 mcg per kg for conscious sedation and up to 150 mcg per kg providing total ansethesia for patients that are particularly vulnerable to other anesthetic agents.

    NASAL fentanyl (2 mcg per kg) may be useful for brief pediatric procedures without IV access such as PE tubes and nasolacrimal probes.

    The PHARMACOKINETICS of fentanyl can be described best as a three compartment model, with a distribution time of 1.7 minutes, redistribution of 13 minutes and a terminal elimination half-life of 219 minutes.

    The volume of distribution for fentanyl is fairly large at 4 L/kg indicative of the high lipid solubility. Obese patients are therefore dosed by total body weight.

    Fentanyl plasma protein binding capacity increases with increasing ionization of the drug. Alterations in pH may affect its distribution between plasma and the central nervous system. It accumulates in skeletal muscle and fat and is released slowly into the blood.

    Fentanyl, which is primarily transformed in the liver, demonstrates a high first pass clearance and releases approximately 75% of an IV dose in urine, mostly as metabolites with less than 10% representing the unchanged drug. Approximately 9% of the dose is recovered in the feces, primarily as metabolites.

    The onset of action of fentanyl is almost immediate when the drug is given IV though the maximal analgesic and respiratory depressant effect may not be noted for several minutes. The usual duration of action of the analgesic effect is 30-60 minutes after a single intravenous dose of up to 100 mcg.

    Following IM administration, the onset of action is between 7-8 minutes and the duration of action is between 1-2 hours.

    The most common serious ADVERSE REACTIONS reported to occur with fentanyl are respiratory depression, apnea, rigidity and bradycardia. If these remain untreated, respiratory arrest, circulatory depression or cardiac arrest could occur. Other adverse reactions that have been reported are hypertension, hypotension, dizziness, blurred vision, nausea, emesis, laryngospasm and diaphoresis.


    DURAGESIC patches are available in dosages ranging from 25 to 100 mcg per hour. The patches are intended to provide 72 hours of analgesia but effects will last much longer.

    DOSING Conversion tables are available through package inserts and do not follow a liner progression. The 25 mcg patch is equivalent to 45-135 mg of ORAL morphine each day. The 100 mcg patch is equivalent to 315-404 mg of ORAL morphine each day.

    Conversions from IV morphine based on 24 hour doses:

    8-22 mg/day 25 mcg/hour
    22-37 mg/day 50 mcg/hour
    38-52 mg/day 75 mcg/hour
    53-67 mg/day 100 mcg/hour
    68-82 mg/day 125 mcg/hour
    83-96 mg/day 150 mcg/hour
    98-112 mg/day 175 mcg/hour
    113-127 mg/day 200 mcg/hour

    Titration should not be performed before the first three days of therapy and thereafter not more often than every six days. It may take up to six days after increasing the dose to reach equilibrium with the new dosing regimen. With DISCONTINUATION, it will take over 17 hours for the fentanyl serum concentration to fall by 50%.

    The concomitant use with potent cytochrome P4503A4 inhibitors (ritonavir, ketoconazole, itraconazole, troleandomycin, clarithromycin, nelfinavir and nefazodone) may result in an increase in fentanyl plasma concentrations, which could increase or prolong adverse drug effects and may cause potentially fatal respiratory depression.


    FHR can be documented preoperatively and postoperatively for all fetuses after the age of 10-12 weeks.

    NORMAL PATTERN fetal rhythms are characterized by a heart rate of 120-160 beats per minute, beat to beat variability with long-term variability band width between 6-25 beats per minute. There are no decelerative periodic changes but there may be periodic accelerations. An absence of beat to beat variability may occur in prematurity and sleep, but can also indicate drug effect, hypoxia and neurologic damage.

    EARLY decelerations are noted by the onset, nadir and recovery of the fetal heart rate to baseline COINCIDING with the onset, peak and end of the uterine contraction. These are usually attributed to compression of the fetal head and VAGAL stimulation, although the stimulus causing early deceleration may be more ominous.

    LATE decelerations are smooth in configuration and are the mirror image of contraction. Their onset, nadir and recovery are delayed by 10-30 seconds after onset, apex and resolution of the contraction. They are likely to be the consequence of uteroplacental INSUFFICIENCY which may be due to maternal hypotension or hypertension. They do not necessitate immediate delivery.

    VARIABLE decelerations are characterized by the appearance of the dip which is variable in duration, profundity and shape from contraction to contraction and they are usually abrupt in onset and cessation. Variable decelerations may be the consequence of CORD compression and may be predictive of fetal acidosis.

    EARLY… vagal response
    LATE… insufficiency
    VARIABLE… cord compression


    ADULT HGB is composed of four polypeptide chains – two alpha chains and two beta chains. Each globin molecule will carry one hematoporphyrin ring that can subsequently carry one oxygen molecule. This molecule enables the transport of 20 mL of oxygen per dL of blood. The P50 (PaO2 at which hemoglobin is 50% saturated) is 26.7 mmHg.

    FETAL HGB is composed of four polypeptide chains – two alpha chains and two GAMMA chains. At birth fetal hemoglobin comprises 53-95% of total hemoglobin and by age SIX MONTHS this drops to 5%. The P50 of fetal hemoglobin is 19 mmHg which allows fetal Hb to bind O2 with more avidity – a leftward shift of the oxyhemoglobin dissociation curve.

    MATERNAL-FETAL Despite low oxygen tension in the fetal blood, the tissue receives adequate oxygenation for three reasons.

    1) presence of fetal hemoglobin
    2) hemoglobin concentration is 50% greater in the baby
    3) the BOHR EFFECT

    Blood entering the placenta on the fetal side has a high concentration of CO2. This equilibrates with maternal blood rapidly. As maternal blood takes up more CO2 it gives up more O2 and as the fetus gives up more CO2, the hemoglobin binds more O2. This favors the transport of O2 from mother to fetus.

    SICKLE CELL DISEASE Since fetal Hb is composed of gamma chains, it is not affected by the genetic alteration that affects the beta chains of sickle cell disease. Increased levels of fetal Hb inhibit polymerization of S Hb and reduce the incidence of sickling events.


    LF-P 2.2 3.0
    LF-DP 3.1 4.0
    3.5 4.5
    LF-2 4.0 5.0

    The Olympus LF-P (ultrathin bronchoscope) is a 2.2 mm OD bronchoscope (without a suction port) that is compatible with endotracheal tubes as small as 3.0 mm ID and double lumen tubes as small as 28 French. The LF-P may also be used in the pediatric sized Univent tubes (3.5 and 4.5 ID). The working length of the LF-P is 60 cm.

    The Olympus LF-DP is a self-powered 3.1 mm OD bronchoscope with a 1.2 mm suction port that is compatible with endotracheal tubes as small as 4.0 mm ID and double lumen tubes as small as 32 French. The working length of the LF-DP is 60 cm.

    The 3.5 mm OD bronchoscope may be used in endotracheal tubes as small as 4.5 mm ID.

    The Olympus LF-2 is a 4.0 mm OD bronchoscope with a 1.5 mm suction lumen that may be used in endotracheal tubes 5.0 ID or larger, 37 French or larger double lumen tubes and all of the adult sized Univent tubes (greater than 4.5 ID). The working length of the LF-2 is 60 cm.

    The depth of field for most of the Olympus bronchoscopes ranges from 3-50 mm.


    For ADULTS, the use of a 5 mm OD bronchoscope with a 2 mm suction channel is ideal for tracheal intubation. PEDIATRIC patients may be intubated with 3.5 mm bronchoscope (4.5 ETT) or a 2.2 mm bronchoscope (3.0 ETT). There is also an Olympus 3.1 mm self powered unit with a suction port that can be used with a 4.0 ETT.

    ORAL fiberoptic intubations may be performed with lidocaine ointment on tongue depressors followed by viscous lidocaine pledgets on Jackson laryngeal forceps (or renovascular pedicle forceps) placed in the piriform sinuses (3-5 minutes each side) to block superior laryngeals. Lidocaine 4% is applied to the lower airway by tube nebulizer and tongue depressor (alternatively through the fiberoptic scope) while the patient is panting. Ovassapian (slide out) or Berman (breakaway) airways are placed and cords should be visible at a total depth of 10 cm. Generous fentanyl and light Versed are required. Glycopyrrolate (up to 0.3 mg for the adult) is optimally given in the holding area.

    NASAL intubations are done more commonly as the FOB is more likely to remain midline and the gag reflex is not as easily triggered.

    Patients are pretreated with glycopyrrolate and often a 4% lidocaine neb in the holding area. The nose may be prepped initially with Otrivin drops or phenylephrine and lidocaine. Incrementally sized nasal trumpets coated with lidocaine jelly are inserted. The lower airway may be anesthesized by transtracheal lidocaine, lidocaine through the fiberoptic scope or Hurricaine (benzocaine) spray through the mouth with the patient panting.

    The fiberoptic scope is then passed through an ETT and the vocal cords are visualized. A jaw thrust may occassionally be useful. The patient can be given an IV induction agent as soon as the tube is secured.

    To provide more time with nasal or oral FOB intubations, it is often possible to provide limited airway control with a nasopharyngeal airway mounted with an ETT adaptor and connected to the anesthesia circuit (see information under MODIFIED NASAL TRUMPET MAENEUVER). Oxygen may also be blown by or administered through the suction port.

    Two other uses of the FOB include intubation through an LMA and FOB intubation over a retrograde guide wire which does not consistently allow easy passage of the ETT.

    See also AIRWAY ANESTHESIA for more details regarding specific and useful nerve blocks.


    According to the latest ACLS protocols, the fibrinolytic agents, along with percutaneous coronary intervention, are a CLASS I intervention for the patient presenting with ST segment ELEVATION or new onset BBB that is less than 75 years of age with symptoms persisting for less than 12 hours. PCI (stenting or angioplasty) is the treatment of choice for those with cardiogenic shock or those with contraindications to fibrinolysis.

    Other patients that may benefit from FIBRINOLYTICS include those with posterior infarctions (ST depression in V1-4) and those with hyperacute T waves. Older patients may benefit from fibrinolytic therapy but are at a greater risk for intracranial hemorrhage.

    ALTEPLASE (tissue plasminogen activator) combined with heparin is currently the most effective therapy for early coronary reperfusion. This benefit is achieved with a small but definite increase in the risk of intracranial hemorrhage.

    Alteplase is bolused at 15 mg IV and followed by infusions for 90 minutes. Concomitant heparin is bolused at 60 units per kg (maximum 4000 units) and then infused at 12 units per kg (maximum 1000 units per hour). PTT should be maintained at 50-70 seconds.

    STREPTOKINASE is the agent of choice for those with a greater relative risk of hemorrhage. Prior exposure within 5 days to 2 years is a contraindication to administration due to high prevalence of neutralizing antibodies and risk for anaphylaxis.

    RETEPLASE may be an equivalent therapy to tPA and is given as two bolus doses without the need for infusion.


    SUCCESS Evidence of succesful reperfusion is by pain relief, reperfusion dysrhythmias, large increases in CPK and improvement in ECG findings. Ominous findings include recurrent pain, ventricular dysrhythmias after 48 hours and CHF.


    Fibromyalgia is a common cause of chronic musculoskeletal pain. It is one of a group of soft tissue pain disorders that affect muscles and soft tissues such as tendons and ligaments. None of these conditions is associated with tissue inflammation and the etiology of the pain is not known.

    Fibromyalgia is 10 times more common in females. The prevalence of this disorder in the community increases with age from two percent at age 20 to eight percent at age 70. Most patients present between the ages of 30 and 55. In approximately one-half of cases, the symptoms appear to begin after a specific event, most often some form of physical or emotional trauma or a flu-like illness.

    The cardinal manifestation of fibromyalgia is diffuse musculoskeletal pain. Although the pain may initially be localized, often in the neck and shoulders, it eventually involves many muscle groups. Patients typically complain of axial pain in the neck, middle and lower back, and pain in the chest wall, arms and legs. The pain is chronic and persistent, although it usually varies in intensity. Patients often have difficulty distinguishing joint and muscle pain and also may report a sensation of swelling – however, the joints do not appear swollen or inflamed on examination. Pain is often aggravated by exertion, stress, lack of sleep and weather changes. Sensations of numbness, tingling, burning, or a crawling sensation are often described.

    Patients also may have a variety of poorly understood pain symptoms, including abdominal and chest wall pain and symptoms suggestive of irritable bowel syndrome, pelvic pain and bladder symptoms of frequency and urgency suggestive of the female urethral syndrome or interstitial cystitis.

    Fatigue is present in more than 90 percent of cases and is occasionally the chief complaint. Most patients report light sleep and feeling unrefreshed in the morning, while others report symptoms suggestive of pathologic sleep disturbances such as sleep apnea or nocturnal myoclonus. In addition, light-headedness, dizziness, and feeling faint are common symptoms. Both mood disturbances (depression, anxiety, and heightened somatic concern) and cognitive disturbances (such as short term memory loss) and headaches (either muscular or migraine-type) are also frequent complaints.

    Additional symptoms and clinical manifestations may include complaints of ocular dryness, multiple chemical sensitivity and allergic symptoms, dysphagia, dizziness, palpitations, dyspnea, vulvodynia, dysmenorrhea, nondermatomal paresthesias, osteoporosis, weight fluctuations, night sweats, dysphagia, dysgeusia, glosodynia and weakness.

    The only helpful finding on examination is excessive muscle tenderness. This excess tenderness is best determined by palpation of predefined muscle and tendon insertions, termed tender points. These tender points are usually bilateral and symmetrically tender. However, patients with fibromyalgia are more tender than healthy controls at any musculoskeletal site. Aside from this finding, the musculoskeletal examination is unremarkable and there is no evidence to indicate a systemic connective tissue or neurologic disease, unless the patient has an associated illness.



    Flecainide is a fluorinated analogue of procainamide and a class 1C antiarrhythmic. It produces a dose-related decrease in intracardiac conduction in all parts of the heart with the greatest effects on the His-Purkinje system. This results in QRS complex widening and prolonged QT intervals. Pacing thresholds are increased by flecainide. Although it does not usually alter HR, it usually exerts a moderate negative inotropic effect and reduces EF. Flecainide is utilized only for life-threatening ventricular arrhythmias such as sustained ventricular tachycardia.

    DOSING is at 100-200 mg PO every 12 hours. The IV form is not available for general use in the US.

    PHARMACOKINETICS Peak effects occur within 2-4 hours and the duration of action is between 12-27 hours.

    Additive negative inotropic effects occur with ß-blockers and calcium channel blockers.


    The total WATER content of the body varies depending on age and sex of the patient. In babies, the proportion of body water is about 75%. In a young male the proportion is at 64% (female 53%) and in an elderly male the proportion is at 53% (females 46%).

    With an AVERAGE total water content of 60%, the various fluid compartments break down as follows.

    60% intracellular (35% weight)
    40% extracellular (25% weight)

    The EXTRACELLULAR water subsequently breaks down as follows.

    interstitial (19% body weight)
    plasma (4.5% body weight)
    transcellular (1.5% body weight)

    The transcellular water is comprised of fluid of the CSF and that of the intestinal tract.


    Speed that a LITER may be infused in minutes:

    gauge gravity pressure
    18 30 6.5
    16 18 5
    14 9 3.5
    12 5.5 2.5

    For CENTRAL VENOUS LINES the flow rates for the double lumen are at 1500 mL/hr (18 gauge) and 5000 mL/hr (14 gauge). For the triple lumen catheters the flow rates are at 3100 mL/hr (16 gauge) and 1500 mL/hr (two 18 gauge lumens). Total combined flow rates are similar at 6200 mL/hour for the triple and 6500 mL/hr for doubles lumen CVC.

    The DISTRIBUTIONS of various fluids should be considered. D5W has a distribution of TBW (60% body weight or 42 L in an average man). LR has a distribution of the extracellular water (25% body weight or 14 L in an average man). Albumin and hetastarch have a distribution equal to that of plasma (4% body weight or 3.1 L in an average man) .


    Various methods of resuscitation have been evaluated in a variety of clinical conditions. Much controversy remains even 35 years after the first descriptions of resuscitation with colloid and hetastarch.

    The DISTRIBUTIONS of various fluids should be considered. D5W has a distibution of TBW (60% or 42 liters in an average man). LR has a distibution of the extracellular water (25% or 14 liters in man). Albumin and hetastarch have a distribution equal to that of plasma (4.5% or 3.1 liters in an average sized man).

    PLASMA VOLUME EXPANSION of the various fluids is calculated by multiplying volume infused by plasma volume and dividing by the volume of distribution for the particular fluid.

    PVE = (VOL) PV / Vd

    CRYSTALLOID solutions with a volume of distribution equal to ECW or fourteen liters have a PVE of 21%. LR actually has a PVE of 50-60% for the initial twenty minutes after infusion.

    DEXTROSE has a volume of distribution equal to TBW or 42 liters and a PVE of 7%.



    HETASTARCH has a PVE of 38% meaning that 38% will remain intravascular, 23% diffuses into the interstitium and the remainder is renally excreted.


    Flumazenil (ROMAZICON) is a potent inhibitor of the benzodiazepines with little or no agonist activity. It competitively inhibits the activity at the benzodiazepine recognition site on the GABA receptor complex. It reverses sedation, respiratory depression, amnesia and the psychomotor effects of the the benzodiazepines.

    DOSING is between 8-20 mcg/kg for adults (typically 0.2 mg IV up to 1 mg maximum or 3 mg for a benzodiazepine overdose). PEDIATRIC dosing is similarly between 10-20 mcg/kg with a maximum dose of 0.2 mg. Infusions may be continued at 0.5-1 mcg/kg/minute with a maximum of 1-3 mg in any given hour.

    PHARMACOKINETICS Peak effects occur within 2-10 minutes and the duration of action is between 45-90 minutes which varies depending on plasma benzodiazepines.

    In an provocative case report, it has been suggested that CCB toxicity may also be treated with benzodiazepine antagonists. Noting that myocardial benzodiazepine receptor ligands exist and appear to affect calcium-channel activity (consistent with a report of a benzodiazepine overdose resulting in first degree AV block) the authors suggested that FLUMAZENIL may be a useful adjunct in the management of CCB toxicity.

    Flumazenil may also be useful in treating the patient with severe hepatic encephalopathy.

    The reversal of benzodiazepine effects may be associated with the onset of seizures in certain high risk populations. Risk factors may include major drug withdrawal, recent therapy with repeated doses of parenteral benzodiazepines or concurrent tricyclic antidepressant poisoning. Seizures associated with flumazenil should be treated with benzodiazepines, phenytoin or barbiturates.


    The FONTAN procedure was initially developed in 1968 for patients with tricuspid atresia but is now utilized for patients with a variety of congenital heart defects where MIXING of systemic and pulmonary venous blood occurs. This includes patients with a single ventricle (hypoplastic left heart) and those with pulmonary atresia with an intact ventricular septum.

    The original operation included a Glenn shunt which drained the SVC directly into the distal right pulmonary artery. The proximal end of the right PA was joined to the right atrial appendage by an aortic valve homograft and a pulmonary valve homograft was placed at the IVC-RA junction. The main PA was ligated and the ASD was closed. Later modifications eliminated the Glenn shunt and homograft valve placements.

    ESSENTIALS The FONTAN serves to route all systemic venous return directly to the lungs with pulmonary venous return to the LA or atrial confluence and then to a single ventricle and through the aorta. The IVC blood flow is directed to the SVC through a tube graft within the RA. The SVC is anastomosed to the right and left pulmonary arteries.

    Due to the low driving pressures (RA) available for pulmonary blood flow, the presence of low pulmonary blood vascular resistance and unobstructed anastomoses are critical.

    Contemporary contraindications include only severe pulmonary HTN. Traditional Fontan CRITERIA included:

    1) age 4-15 years
    2) mean PAP less than 20 mmHg
    3) PVR less than 4 Woods units/m2
    4) normal sinus rhythm
    5) LV ejection fraction over 0.60
    6) PA:Ao diameter ratio over 0.75
    7) normal systemic venous drainage
    8) absence of MV dysfunction
    9) no PA distortion from prior shunts

    Systemic to pulmonary shunting is universally present prior to the Fontan procedure with the exception of those patients who have undergone a Glenn procedure.

    ANESTHETIC requirements include preparation of dobutamine, phenylephrine, NTG and nitroprusside infusions as well as planning for early extubation to encourage pulmonary flow.


    The pediatric patient with a suspected foreign body aspiration may be managed either with deep anesthesia and spontaneous ventilation or lighter anesthesia with controlled ventilation and paralysis. There are advantages and disadvantages to both methods.

    Proponents of the SPONTANEOUSLY breating technique argue that the use of controlled ventilaiton requires unusually high airway pressures that will often lead to VQ inequalities and possible air trapping (that can lead to hypotension). The spontaneously breathing may still ventilate through entrainment after the telescope is inserted through the proximal end of the rigid bronchoscope.

    For the CONTROLLED ventilation technique, it is useful to use fast acting induction agents which will lessen the chance of gastric regurgitation. Propofol infusions (with or without remifentanil) and short acting paralytics (such as mivacron) are useful. At the conclusion of the case, the patient may be intubated with a conventional ETT and the usual extubation criteria may be implored.


    Cross matching is not required for FFP transfusions though type specific transfusions are required. The universal donor for FFP is type AB.

    NIH INDICATIONS for FFP therapy

    1) isolated deficiency replacement
    2) reversal of warfarin effects
    3) massive blood transfusion
    4) antithrombin III deficiency
    5) certain immunodeficiencies

    Recall that massive blood cell transfusion (greater than one blood volume over several hours) is more likely to result in thrombocytopenia and FFP therapy should be reserved specifically for suspected coagulation factor deficiency.

    In the blood the normal fibrinogen level is between 150-250 mg/dL which is equivalent to 18 grams in TBV or 1300 mg per unit of blood. One unit of FFP (usually 200 mL) contains 500 mg of fibrinogen (at a normal concentration of 250 mg/dL).

    Thus one unit of FFP contains 38% of the fibrinogen of one unit of whole blood. To replace an entire fibrinogen load (to 150 mg/dL) one would need to transfuse 14 units of FFP. To replace that which is actually lost during a surgical procedure whould require 3-5 units of FFP for every liter of blood lost. COUMADIN can generally be reversed with 2-3 units of FFP.

    FFP contains more CITRATE than packed RBC so calcium should be monitored and patients may become acutely hypotensive during transfusion.

    FFP is good for 24 hours after thawing. The blood bank recommends administering FFP with the standard 170-260 micron transfusion filter to decrease the presence of microaggregates.

    FFP carries the same risk for HIV and HCV as other blood products. FFP does not require irradiation to avoid graft versus host disease and FFP does not transmit CMV.

    CRYOPRECIPITATE is prepared from FFP and contains factors VIII, XIII, fibrinogen, vWF and fibronectin. Cryoprecipitate is rich in factor VIII, with 5-13 units of factor VIII clotting activity per mL of solution.

    INDICATIONS for cryoprecipitate include hypofibrinogenemia, von Willebrand’s disease, hemophilia A (when factor VIII is unavailable), uremic coagulopathy and preparation of fibrin glue. DOSAGE is one unit per 7-10 kg which raises the plasma fibrinogen by about 50 mg/dL in a patient without massive bleeding.


    DOSING generally escalates to a maximum of 1 mg/kg IV every six hours. Continuous infusions are thought to be not as effective as bolus dosing, but may be utilized when patients are intolerant of hemodynamic swings that may be secondary to inermittent diuresis.

    Furosemide is a LOOP diuretic used in the management of edema associated with CHF, cirrhosis, hyperchloremic acidosis and renal disease including nephrotic syndrome. The exact mechanism of action is unclear but the drug appears to primarily inhibit is reabsorption of sodium and chloride in the ascending loop of Henle. These effects increase the urinary excretion of sodium, chloride and water resulting in a profound diuresis. Furosemide also increases the excretion of potassium, hydrogen, calcium, magnesium, bicarbonate, ammonium and phosphate.

    Initially, diuretics lower BP by causing hypovolemia (decreased plasma and extracellular fluid), a temporary increase in GFR and a decreased CO. CO eventually returns to normal, but peripheral resistance is reduced resulting in a lower BP. Excessive fluid loss and dehydration may result in hypovolemia and electrolyte imbalance (hypokalemia, hyponatremia and hypocalcemia). Concomitant use of other agents that increase cardiac irritability (such as epinephrine or halogenated inhalation agents) may also increase the risk of perioperative dysrhythmias. If a surgical patient is currently using the diuretic, one might expect an enhanced effect of vasodilators and beta-blockers which is most likely secondary to the decreased circulating volume.

    Furosemide has unique abilities to decrease pulmonary venous constriction secondary to prostaglandin release from the kidney. Patients with pulmonary edema may show signs of clinical improvement prior to evidence of diuresis.

    Experimental data suggests that the naturetics may improve renal function by (1) decreasing active transport and reducing renal oxygen demand and (2) increasing the clearance of necrotic cellular debris thus reducing tubular obstruction. These data appear theoretical in terms of actual improvement in renal function. However, patients who convert from oliguric to nonoliguric states do have a decrease in overall severity of renal failure and a decrease in mortality.


    Glucose-6 phosphate dehydrogenase deficiency is the most common of the inherited erythrocyte enzyme deficiencies. Approximately 1-8% of American blacks males are affected. Asian and mediterranean populations are also susceptible.

    G6PD is one enzyme that is essential to the HMP shunt which produces NADP, the major reducing compound of the erythrocyte. Without NADP the red blood cell is susceptible to damage by OXIDATION. A deficiency of G6PD results in decreased levels of reduced glutathione when the RBC is exposed to oxidant chemicals. This increases the rigidity of the RBC membrane and accentuates CLEARANCE of these stiff cells from the circulation. In severe forms of G6PD deficiency, oxidation produces denaturation of globin chains and causes intravascular HEMOLYSIS.

    There are a number of DRUGS that accentuate the oxidative destruction of erythrocytes including analgesics, antibiotics, sulfonamides and antimalarials.

    aspirin (in high doses)
    LIDOCAINE (controversial)
    quinine and quinidine
    methylene blue

    Affected patients are unable to reduce methemoglobin produced by sodium nitrate and therefore sodium NITROPRUSSIDE and PRILOCAINE should not be administered to these patients.


    The precise mechanisms for anlgesia of gabapentin or NEURONTIN are unclear. DOSING generally begins at 300 mg QHS and may be titrated upwards to 600 mg TID. For the elderly or patients with CRI, it is wise to begin therapy at 100 mg QHS and increase to a maximum of 100 mg TID. No adjustment is necessary for hepatic insufficiency.

    The primary ADVERSE EFFECTS include somnolence, dizziness, ataxia, fatigue and impaired concentration.

    Neurontin is approved for control of postherpetic neuralgia but may also benefit patients with diabetic neuropathy, cancer pain, multiple sclerosis, phantom limb pain, Guillain Barre syndrome and post-mastectomy pain.

    A four to six week trial is typically required to adequately assess the analgesic efficacy of any of the anticonvulsant therapies.


    Ganglionic blocking drugs (such as pentolinium and trimethaphan) compete with acetylcholine for the NICOTINIC receptors on the postjunctional membrane at the autonomic ganglia. As most organs are reciprocally innervated by sympathetic and parasympathetic nerves, the overall effect of autonomic blockade depends on the predominance of one or the other sytem at the end organ.

    The arteriole and venules of the skin and splanchnic viscera have predominantly SYMPATHETIC vasoconstrictor innervation, so ganglionic blockade produces sympathetic block with peripheral dilation, increased capacitance and hypotension.

    In contrast, the iris, ciliary muscle, GI tract, urinary bladder and sweat glands are all under predominantly PARASYMPATHETIC control. Ganglionic blockade thus produces mydriasis, cycloplegia, constipation, urinary retention and abolition of sweating.

    Because of these parasympathetic blocking side effects, ganglionic blocking agents are no longer routinely used for treatment of hypertension.

    Nevertheless, TRIMETHOPHAN may still be useful for hypertensive encephalopathy because it does not increase CBF and does not often result in excessive tachycardia. Continuous infusions (at 10-200 mcg/kg/minute) may be used for deliberate hypotension.


    oxygen 2000 625
    nitrous 750 1600
    air 1800 625

    OXYGEN is stored as a gas in the OR because the critical temperature at which O2 exists as a liquid (minus 120 Celsius) is far below room temperature.

    Oxygen behaves as an ideal gas and it obeys the ideal gas law.

    PV = m / MRT

    where V = volume, m = mass, M = molecular weight and R = universal gas constant. Manipulations of this equation lead us to other commonly regarded gas laws.

    For any isothermal process (temperature constant) the product PV is constant. The is BOYLE’S law and one may remember that the boiling temperature is usually a constant.

    For an isobaric process (pressure constant) the ratio V/T is constant. This is CHARLES law and one may remember that Charles never travelled to different altitudes.

    At room temperature, a full OXYGEN cylinder is at 2000 psi and contains 625 L of gas. When half empty and at 1000 psi of pressure, it contains 312 L of gas.

    Oxygen is stored and shipped for hospital supply in liquid form in large tanks at 5-10 atm of pressure and minus 150 degrees Celsius. It is later vaporized for use throughout the hospital.

    NITROUS OXIDE is a vapor at room temperature (20 C), but can be liquefied by a pressure of 51 atm or 750 psi. As N2O is removed from the tank, more N2O is vaporized, maintaining the liquid/vapor equilibrium and keeping the pressure at 51 atm or 750 psi until all of the liquid is vaporized.

    Because the density of N2O vapor at 51 atm and 20 degrees is less than one fourth the density of liquid N2O, the tank is actually less than 25% full (with less than 400 L) just before the tank pressure begins to fall. Big Blue states that 215 LITERS remain when the pressure begins to fall.

    E TANKS have an internal physical volume of approximately 5 liters. At a tank pressure just below 51 atm (roughly 50 atm), the volume of gas in the tank would be 250 liters (5 times 50) if nitrous behaved as an ideal gas. The fraction of a full tank present at that time would be approximately 250/1590 or 0.16. However, it is greater than this because nitrous behaves as an ideal gas only at much lower pressures.

    CRITICAL TEMPERATURE Tc is the highest temperature at which a substance can be liquefied by ANY given amount of pressure.

    N2O Tc + 36 degrees C
    Air Tc -141 degrees C
    O2 Tc -119 degrees C
    CO2 Tc + 31 degrees C

    CONVERSIONS 1 atmosphere is the barometric pressure at sea level. One atmosphere is equivalent to 760 mmHg, 1033 cmH2O, 14.7 psi and 101.3 kPa.


    Gastroschisis results from occlusion of the omphalomesenteric artery during gestation and involves herniation of the viscera through the lateral abdominal wall defect. Gastroschisis occurs in 1 in 15,000 births, and is associated with a low incidence of other anomalies. Intestinal atresia, however, is higher in neonates with gastroschisis, compared with omphaloceles.

    Closure may be associated with increased abdominal pressures and the expected sequlae. Patients may be monitored by bladder pressures and periodic blood gas analysis may be helpful in ruling out acidosis.

    Paradoxically, there have been some reports of systemic hypertension after closure theoretically secondary to renal artery compression.


    GER is caused by regurgitation of acidic gastric contents into the esophagus and possibly the pharynx producing retrosternal discomfort. One-third of healthy adults report symptoms of GER at least once a month. The more concerning history may include reports of food regurgitated to the mouth or waking at night with a sour taste in the mouth.

    The underlying defect is a decrease in the resting tone of the LES at the terminal 1-3 cm of the esophagus (13 mmHg versus 29 mmHg in normal patients) but some authors point out that the essential physiology is that of an increased barrier gradient.

    The LES is innervated by vagal and sympathetic nerves. It typically increases in tone in response to an increase in intragastric pressure. Decreased tone is seen with obesity (controversial), pregnancy and occasionally with hiatal hernia (although these patients may have normal tone).

    Basic therapy for GER consists of oral antacids and avoidance of substances that reduce tone at the LES (fat, chocolate, alcohol and nicotine). Nissen fundoplication or Roux-en-Y duodenal diversion is reserved for those with the most severe symptomatology.

    Routine avoidance of anticholinergics or the preoperative use of metoclopramide or H2 blockers can NOT be substantiated by clinical evidence (LES – DRUG EFFECTS). Succinylcholine will increase pressure of the LES but fasciculations leave the actual barrier pressure unchanged.

    RSI is recommended for most cases of severe GER. A properly performed RSI includes placing the patient in the head up position and cricoid pressure as the patient is induced. Active regurgitation is obviously not possible with paralysis and gentle breaths can always be considered with cricoid pressure in place.

    The overall incidence of ASPIRATION during GA is similar for adults and the pediatric population (about 3.5 cases per 10K anesthetics).

    Some studies have documented that there is no correlation between reflux and BMI, smoking, duration of fasting, alcohol consumption and either gastric fluid volume or pH. One study has reported that in otherwise healthy, fasted, obese patients (BMI over 30), there was actually a lower incidence of combined high-volume, low-pH stomach contents when compared with lean patients.


    The literature supports the use of ERYTHROMYCIN as a prokinetic agent. Many children with GER are adequately controlled with acid suppression alone; however, if use of a prokinetic agent is warranted, erythromycin in combination with acid suppression should be considered. Given the lack of prospective controlled studies demonstrating metoclopramide’s efficacy and safety in the treatment of GER in children, metoclopramide should not be considered a treatment option (Annals of Pharmacotherapy 2005 39:706).

    Domperidone is a dopamine-receptor blocking agent that produces an anti-emetic effect. Domperidone does not cross the blood-brain barrier to any appreciable degree and so exerts relatively little effect on cerebral dopaminergic receptors. The drug is not yet available in the US.

    For unclear reasons, the incidence of GERD is going up in adult and pediatric populations (after the toddler years) that is not only secondary to public awareness. There is a new entity known as allergic esophagitis that may be adding to the incidence – this variety is VERY resistant to conventional treatments with H2 blockers or PPIs and they actually treat it with swallowed Flovent. Per Litchman: the yield for doing an EGD looking for erosive disease or testing for H Pylori will be extremely LOW – but naturally they are always happy to do the tests. They do about 300 pediatric EGD procedures a year and see about one case of erosive disease each month. They are seeing some H Pylori in the migrant and poor populations but the incidence in other pediatric populations is extremely low. They get a lot of false positive results with the blood tests at UNC though the literature apparently reports a lot of false negative results. The best test is the H Pylori breath test that they do in the peds GI suite which involves drinking something and breathing into a bag.


    Maalox 15-30 mL

    The GLENN procedure was developed in 1958 to create a more physiologic circulation for cyanotic patients with tricuspid atresia by providing more pulmonary blood flow without adding to the volume load of the systemic ventricle as occurred with systemic to pulmonary shunts.

    ESSENTIALS The GLENN SHUNT is an end-to-side anastomosis of the distal end of the divided right PA to the SVC with division of the SVC-RA junction and proximal right PA. It is sometimes referred to as a partial Fontan or a hemi-Fontan procedure.

    Following the Glenn procedure, the patient will remain cyanotic as IVC blood continues into the RA and is mixed into the systemic circulation.

    During the pioneering years of the procedure, deterioration was often noted to occur five years following the Glenn procedure secondary to an increase in PVR and the development of collateral IVC circulation. Today, the Glenn procedure is occasionally used as an interim palliation for high risk Fontan procedure candidates.

    POSTOPERATIVE care includes early extubation, maintaining CVP (equivalent of PAP) at 20 and LAP at 10 mmHg.


    Glucagon is a polypeptide produced by the alpha cells of the pancreas. It acts to convert liver glycogen to glucose. It produces smooth muscle relaxation of the common bile duct, stomach, duodenum, small intestine and colon. In the heart, it enhances formation of cyclic AMP but, unlike the catecholamines, it may enhance contractility even in the presence of beta blockade.

    Glucagon is recommended in the treatment of severe beta-blocker or calcium channel blocker overdose. The resulting inotropic action results from direct adenylate cyclase stimulation. Glucagon may also be useful in the treatment of hypoglycemia and biliary tract spasm.

    DOSING Glucagon is administered in doses of 1-2 mg but when given in high doses, should be mixed with sterile water rather than the phenol diluent which is often packaged with the drug. Infusions may be administered at up to 10 mg/hour.

    PEDIATRIC dosing is at 0.02-0.04 mg/kg IV with a maximum of 1 mg.


    The balance of serum glucose levels is controlled to some degree by the autonomic nervous system and these mechanisms are important for understanding various effects of medications with autonomic activity.

    PARASYMPATHETIC stimulation activates glycogenesis in the liver.

    Sympathetic ALPHA stimulation will inhibit insulin secretion leading to HYPERGLYCEMIA. This is the mechanism by which the patient with pheochromocytoma becomes hyperglycemic.

    BETA-2 stimulation will activate insulin secretion, activate lipolysis and gluconeogensis.

    Nonspecific beta-blockers (such as propranolol) will antagonize the hyperglycemic response to stress while specific BETA-1 blockers will not affect glucose control to the same degree.


    PEDIATRICS Normal glucose REQUIREMENTS for a child are around 300 mg/kg/hour or 5 mg/kg/min. These requirements may be substantially higher in the neonate.

    As a general RULE, those infants that are either preterm or younger than 3 months of age may receive maintenance glucose infusions concentrated to at least a 2.5% concentration (prepared by adding 1 ampule of D50 or 25 grams of glucose to 1 liter of fluid). For better control, D50 may be added to each 50 mL aliquot in the buratrol such that the addition of 2.5 mL produces a 2.5% solution and so forth.

    2.5 mL = 1250 mg

    Infants between the ages of 3-6 months may require glucose but are best managed by first documenting a capillary glucose level.

    RISK factors for HYPOGLYCEMIA

    1) chronic illness or sepsis
    2) low weight
    3) prolonged fasting
    4) term neonates
    5) preterm infants
    6) infants of diabetic mother
    7) erythroblatosis fetalis
    8) liver dysfunction
    9) total parenteral nutrition

    ADULTS As a rule of thumb, 7.5 grams of dextrose (15 mL of D50 solution) will increase blood glucose by 30 mg/dL in a 70 kg adult.

    GLUCOSE infusions should be avoided in those at risk for cerebral ischemia including children for craniotomy or cardiac bypass procedures.


    These drugs inhibit the integrin glycoprotein IIb/IIIA receptor in the membrane of platelets thus inhibiting platelet aggregation. They are indicated for acute coronary syndromes with ST DEPRESSION (ST elevation is treated with fibrinolyis or PCI).

    ABCIXIMAB (Reopro) is approved for patients with non-Q wave MI or unstable angina with planned percutaneous coronary intervention (PCI) planned within 24 hours. Platelet function recovers in 48 hours after discontinuation.

    EPTIFIBATIDE (Integrelin) and TIROFIBAN (Aggrastat) are approved for non-Q wave MI, unstable angina managed medically and unstable patients undergiong PCI. Platelet function recovers in 4-8 hours after discontinuation.

    General CONTRAINDICATIONS include internal bleeding, coagulopathy, history of intracranial hemorrhage, surgical procedure within one month, platelet count less than 150K or concomitant use of another glycoprotein inhibitor.

    SUCCESS Evidence of succesful reperfusion is by pain relief, reperfusion dysrhythmias, large increases in CPK and improvement in ECG findings. Ominous findings include recurrent pain, ventricular dysrhythmias after 48 hours and CHF.


    DOSING of glycopyrrolate as an ANTISIALAGOGUE is at 5 mcg/kg IV (0.3-0.6 mg for the average adult).

    For OCR prophylaxis, the pediatric patient is given 5-10 mcg/kg IV. Oral dosing is at 0.04-0.1 mg/kg not more often than every six hours.

    For BRADYCARDIA, glycopyrrolate is given at 5-10 mcg/kg every 2-3 minutes.

    For REVERSAL when given with an anticholinesterase (neostigmine) it is dosed at 10 mcg/kg.

    PHARMACOKINETICS Onset of action is within 2-3 minutes (slower than atropine) and duration of action is from 30-60 minutes (same as atropine).

    Glycopyrrolate is twice as potent as atropine in its antisialagogue effects but less potent than scopolamine. It is useful when a lack of sedation is desired.

    GOLDMAN ET AL 1977

    Multifactorial index of CARDIAC RISK in noncardiac surgical procedures. (NEJM 1977)

    To determine which preoperative risk factors might affect the development of cardiac complications after major noncardiac operations, Goldman prospectively studied 1001 patients over 40 years of age. By multivariate discriminant analysis, NINE independent significant correlates of life-threatening and fatal cardiac complications were identified.

    1) preoperative third heart sound or jugular venous distention
    2) myocardial infarction in the preceding six months
    3) more than five premature ventricular contractions per minute documented at any time before operation
    4) rhythm other than sinus or presence of premature atrial contractions on preoperative EKG
    5) age over 70 years
    6) intraperitoneal, intrathoracic or aortic operation
    7) emergency operation
    8) important valvular aortic stenosis
    9) poor general medical condition

    Patients could be separated into four classes of significantly different risk. Ten of the 19 postoperative cardiac fatalities occurred in the 18 patients at highest risk.

    If validated by prospective application, it is believed that the multifactorial index may allow preoperative estimation of cardiac risk independent of direct surgical risk.


    allograft = homograft
    xenograft = heterograft


    The GBS is an idiopathic acute inflammatory demyelinating polyneuropathy characterized by progressive muscle weakness and areflexia, with spontaneous remission being the rule. It has an annual incidence of 2 cases per 100,000 and occurs at all ages and in both sexes. With the marked decline in the incidence of polio, the GBS is now the most common cause of acute flaccid paralysis in healthy people.

    Peripheral nerve demyelination in GBS is believed to be immunologically mediated. A variety of clinical and experimental data have implicated both humoral factors and cell-mediated immune phenomena which damage myelin or the myelin-producing Schwann cells.

    Approximately 66% give a history of an antecedent URI or GI infection. GBS has been reported to follow vaccinations, epidural anesthesia and thrombolytic agents and has been associated with some systemic processes, such as Hodgkin’s disease, SLE, sarcoidosis, and infection with Campylobacter, Lyme disease, H influenzae, EBV, CMV, HSV, mycoplasma and recently acquired HIV infection. One study examined 308 patients for serologic evidence of infection with 16 agents and found that evidence of recent infection with Campylobacter, CMV, and EBV was significantly more frequent in the GB group.

    66% develop the neurologic symptoms 2-4 weeks after what appears to be a benign respiratory or GI infection. The initial symptoms are fine paresthesias in the toes and fingertips, followed by LE weakness that may ascend over hours to days to involve the arms, cranial nerves and (in severe cases) the muscles of respiration. Early in the course, patients frequently complain of aching or sciatica lower back or leg pain. Patients are hyporeflexic and there is an absence of pathologic reflexes such as the Babinski sign (the positive upgoing plantar reflex). At some point during their illness, up to 25% of patients require mechanical ventilation.

    More than 90% of patients reach the nadir of their function within 2-4 weeks (average 12 days), with return of function occurring slowly over weeks to months. A chronic (extending beyond two months), slowly progressive or relapsing inflammatory demyelinating polyneuropathy is generally considered a distinct entity from acute GBS.

    The main modalities of therapy for GBS include plasmapheresis and administration of intravenous immune globulin. Even before initiating specific therapy, common problems are when and whether to admit to the ICU and when to consider mechanical ventilation. Hyperkalemia with SUCCINYLCHOLINE has been reported.

    Corticosteroids, once the mainstay of therapy for GBS, have not been shown to be beneficial and no longer have a role. Interferon-ß has been reported to be beneficial in individual cases, but its safety and efficacy have not been established in clinical trials.

    Autonomic dysfunction is a well-recognized feature of this disease and is a significant source of mortality. Consequently, close monitoring of BP, fluid status and cardiac rhythm are essential to the management of these patients. Care must also be taken when vasoactive or sedative drugs are used, since the dysautonomia may exaggerate the hypotensive responses to these drugs.

    The majority of patients with GBS either recover completely (15%) or are left with only minor deficits (distal numbness or foot-drop) that do not interfere with activities of daily life (65%). However, 5-10% of patients will suffer permanent disabling weakness, imbalance, or sensory loss, and 3-8% percent of patients die despite intensive care. Causes of death include acute RDS, sepsis, PE and unexplained cardiac arrest.




    ABDOMINAL HYSTERECTOMY may be performed under GA, CSE, CSA or epidural anesthesia.


    TUBAL LIGATION Less invasive hysteroscopic methods for tubal ligation may be performed at eight weeks post conception with MAC and moderate sedation. Tradiotional BTL through an abdominal incision may be performed with 5% lidocaine SAB at 1.5 mL or 75 mg for one hour or less of operative time.


    The HP equation also known simply as the Poiseuille equation describes laminar flow through a tube for gas and liquid substances. It relates flow rate as proportional to pressure gradient and radius to the fourth power and inversely proportional to viscosity. Hence, radius is more important than tube length and viscosity is more important than density in determining whether flow will be laminar versus turbulent.

    REYNOLD’S NUMBER is a dimensionless parameter derived from an equation involving density, velocity, radius and viscosity. A value over 2000 is an indication of turbulent flow.


    Haloperidol is an antipsychotic that blocks postsynaptic DA receptors but also has anticholinergic and alpha blocking properties.

    DOSING for ICU sedation or persistent singultus (hiccoughs) in the adult is at 2-10 mg IV every 2-4 hours. IDEALLY, it should be dosed at 0.5-1 mg IV every 10 minutes until effect is achieved. The pediatric patient may receive 0.025-0.05 mg/kg IV or PO every 4-6 hours.

    SIDE EFFECTS Haloperidol has less potential than chlorpromazine (Thorazine) for causing hypotension but may cause prolongation of the QT interval. The incidence of dysrhythmias in the ICU is said to be approximately 0.4% though the drug should be avoided in the patient with prolonged QT or history of torsades des pointes. Haldol may cause EPS including dystonia and akathisia but the incidence is lower following IV versus PO or IM administration.


    Characteristics are as follows.

    vapor pressure 243
    MAC adult 0.74
    MAC neonatal 0.87
    blood:gas partition 2.4

    Halothane is the only agent commonly used that is an ETHANE derivative (as opposed to ether derivatives noted by the C-O-C linkage).

    METABOLISM Halothane undergoes significant metabolism (20-46%) through oxidative and reductive pathways. The oxidative metabolites are not toxic, but the REDUCTIVE metabolites may produce hepatotoxicity. Reductive metabolism occurs during inadequate oxygen delivery to the liver and stimulation of the P450 enzymes by various drugs or chemicals.

    CARDIOVASCULAR Halothane has been associated with several cardiac dysrrhythmias. Studies have demonstrated a strong association between halothane and ventricular arrhythmias, especially ventricular tachycardia.

    Halothane administration has also been associated with prolongation of the QT interval, which poses a risk of ventricular tachycardia and torsades de pointes. The recent prescribing information for halothane cautions its use in patients with existing QT prolongation or in patients receiving other drugs known to prolong the QT interval.

    Halothane is the most dysrhythmogenic due to slowing at His-Purkinje (most others slow only at AV node). Exogenous epinephrine at doses greater than 1.5 mcg/kg should be avoided.

    Halothane can be considered the BEST agent for AS, IHSS and TOF. It behaves like verapamil (most other agents behave like nifedipine). It does not increase HR because the baroreceptor reflex is inhibited.

    There is an increase in cutaneous blood flow but no effect with muscle blood flow (as common with other agents). There is no net decrease in SVR.


    CNS Burst suppression occurs only at very high concentration near 3.5 MAC.

    Halothane increases CBF more than other agents with a 200% increase at 1.1 MAC. This effect will diminish to predrug level within four hours. It is least protective in that critical CBF to prevent ischemia is at 18-20 mL/100g/min.

    RENAL All agents decrease renal blood flow, GFR and UOP. These changes are not a result of ADH release but rather the effects of the vloatiles on blood pressure and coardiac output.


    Extrinsic mechanisms, which can be either neurally or hormonally triggered, elicit many of the cardiovascular responses most familiar to anesthesiologists. Sympathetic stimulation (whether from hypoxemia, hypercarbia, hyperpyrexia, hypotension or inadequate depth of anesthesia) frequently causes an increase in HR. Likewise, parasympathetic stimulation from visceral manipulation may produce vagal-mediated bradycardia. The denervated patient is unable to mediate these responses and requires a high level of clinical vigilance from the anesthesiologist.

    The denervated heart responds to stress by increasing cardiac output via the Frank-Starling mechanism. During anesthesia the denervated heart may not be able to maintain adequate cardiac output in the face of vasodilation and surgical blood loss and must rely on circulating catecholamines and optimum loading conditions to maximize ventricular performance.

    When HYPOTENSION occurs, it must be kept in mind that the INDIRECT ACTING vasoconstrictors and cardioactive drugs are NOT EFFECTIVE. Preferred agents include phenylephrine, norepinephrine or epinephrine keeping in mind that these agents may produce an exaggerated cardiovascular response.

    The management of intraoperative HYPERTENSION is similar for both innervated and denervated patients. Commonly used intravenous antihypertensive (nitroprusside and nitroglycerin) are effective. Their hypotensive effects may be magnified following cardiac transplantation.

    CYCLOSPORINE relatated hypertension may cause a vasoconstrictive state whereby the effective intravascular volume is chronically reduced. As a result, vasodilator therapy may cause a precipitous fall in blood pressure. Alternatively, beta-blockers can also be used, but due to frequent and variable changes in loading conditions during surgery, long-acting beta-blockers should be used with caution.

    Most neuromuscular blocking agents can be used safely after cardiac transplantation. When SUCCINYLCHOLINE is necessary, these patients must be pretreated with atropine or glycopyrrolate to prevent bradycardia and possibly asystole that occurs secondary to the proliferation of non-vagal related muscarinic receptors. In the presence of hepatic or renal insufficiency (perhaps secondary to cyclosporine toxicity), avoidance or judicious use of agents that require these organs for clearance is suggested.

    Anticholinesterases normally act indirectly on the myocardium and should have no HR effects on the denervated heart. According to recent data, however, neostigmine CAN induce bradycardia via a direct activation of cholinergic receptors on cardiac ganglionic cells, causing release of acetylcholine from their nerve terminals. Anticholinergic agents may be given to counteract only the systemic muscarinic effects of acetylcholinesterase inhibition (salivation, intestinal secretions) and will not blunt the possibility of bradycardia with neostigmine.


    During donor heart harvesting, sympathetic postganglionic, parasympathetic preganglionic & both sympathetic & parasympathetic afferent nerves are transected. Preganglionic parasympathetic de-efferentation increases resting baseline HR of the donor heart, primarily because of loss of vagal input causing increased SA and AV nodal automaticity. In contrast, the remnant recipient atria remains under intact vagal effects.

    Deafferentation affects many of the important cardiac reflexes as well as vital sensory input, such as pain during myocardial ischemia and infarction.

    In the absence of disease, predominantly rejection and CAD, the transplanted heart has preserved or mildly depressed resting contractility and SV. Normal contractility appears to be an intrinsic property of the heart and is independent of autonomic neural control.

    During exercise, the denervated heart must rely on circulating levels of catecholamines and the Frank-Starling mechanism to maintain adequate cardiac output. Whereas normal hearts respond to increased aerobic demands by increasing HR (as SV remains virtually unchanged), the denervated heart is preload-
    dependent and responds initially to demands by increasing SV through preload augmentation.

    Adrenal secretion of catecholamines in response to stress or exercise can markedly improve ventricular performance, BUT compared with healthy control hearts, the cardiac transplant patient exhibits reductions in maximal exercise capacity, peak cardiac output and maximum oxygen uptake.

    The question of whether or not reinnervation occurs in humans after cardiac transplantation remains unanswered. Evidence for parasympathetic reinnervation can occur after 2-6 months whereas sympathetic reinnervation is delayed for 1 or more years.

    DRUGS whose cardiovascular actions are dependent on the autonomic nervous system (ATROPINE, edrophonium, HYDRALAZINE, pancuronium) have no effects in the denervated heart. Similarly, sympathomimetic drugs that act indirectly (EPHEDRINE) by releasing neuronal NE have a blunted effect on transplanted hearts.

    Nonadrenergic inotropes, including the PHOSPHODIESTERASE INHIBITORS (milrinone, amrinone, aminophylline, and glucagon), continue to be effective in the denervated heart. Because deafferentation and deefferentation interrupt the normal autonomic compensatory responses, hypotension or reduction in preload consequent to amrinone or milrinone therapy may be significant.

    Cardiac glycosides, such as DIGOXIN, maintain their direct effects on the denervated heart (inotropy). Nevertheless, the indirect actions on the AV node, which are mediated by the vagus nerve, are absent.

    BETA-BLOCKERS can be used safely in the posttransplant patient. At rest or with minimal exercise, both the HR and the BP responses to ß blockade are identical to normal controls. At submaximal exercise, however, these agents produce a greater negative chronotropic effect on the denervated heart.

    Anticholinesterases normally act indirectly on the myocardium and should have no HR effects on the denervated heart. According to recent data, however, NEOSTIGMINE can induce bradycardia via a direct activation of cholinergic receptors on cardiac ganglionic cells, causing release of acetylcholine from their nerve terminals.


    With turbulent states, the density (rather than the viscosity) of gases becomes important and HELIOX, a blend of helium and oxygen has been utilized successfully to reduce airway resistance, peak airway pressures and PaC02 levels when administered to spontaneously and mechanically ventilated patients.

    The mixture, containing 60-80% helium and 20-40% oxygen is less dense than air and therefore provides less turbulent flow. Although HELIOX is an option should oxygenation in an asthmatic become a problem, it can be cumbersome to attach to a circuit and attachments should be considered in advance. Moreover, the improvement in oxygenation due to decreased turbulence is small and oxygenation may not be improved relative to use of 100% oxygen.


    HELLP develops in approximately 10-20% of all women with preeclampsia. The majority of cases are diagnosed between 22-36 weeks gestation. HELLP syndrome probably represents a severe form of preeclampsia but this remains controversial. As many as 15-20% of patients do not have antecedent HTN or proteinuria.

    The DIAGNOSIS of HELLP syndrome is based upon characteristic laboratory findings in patients of appropriate gestational age. Imaging tests (CT or MRI) are useful when complications such as hepatic infarction, hematoma or rupture are suspected. The diagnosis is generally established by the presence of preeclampsia and the following criteria:

    microangiopathic hemolytic anemia
    platelet count less than 100,000
    serum LD over 600 IU/L
    total bilirubin over 1.2 mg/dL
    serum AST over 70 IU/L

    Signs of DIC occur in 20% of these patients such that platelet counts, PT (elevated in 50-75%), PTT (elevated in 50-60%) and FDP or fibrin degradation products (elevated in 85-100%) should be assessed when possible.

    Although patients may have no symptoms, most complain of abdominal pain and tenderness. Pain is located in the midepigastrium, RUQ or below the sternum. Many patients also have nausea, vomiting and malaise which may be confused with viral hepatitis, particularly if the serum AST and LDH are markedly elevated. Jaundice is evident in less than 5%.

    Other signs and symptoms may also be present including pulmonary edema 6%, ascites 8% and ARF usually occurring in the setting of DIC.

    Hepatic imaging often reveals the complications of HELLP. Abnormal imaging findings are found in 45%. The most common findings were subcapsular hematoma and intraparenchymal hemorrhage.

    Biopsy is rarely necessary to establish the diagnosis and may be hazardous to perform because of coagulopathy. When it has been performed, it typically shows periportal hemorrhage and fibrin deposition. Macrovesicular fat may be present in modest quantities and is distributed throughout the liver lobule. There is little correlation between the histologic findings and clinical presentation.

    DDX HELLP syndrome may occasionally be confused with other diseases complicating pregnancy including acute fatty liver of pregnancy, GE, hepatitis, appendicitis, GB disease, idiopathic thrombocytopenic purpura, hemolytic-uremic syndrome or thrombotic thrombocytopenic purpura. Marked elevations in serum aminotransferases are not typical of HELLP and when they occur, they may indicate hepatic infarction or subcapsular hematoma rather than viral hepatitis.



    Indications for DIALYSIS include uremic pericarditis, severe hyperkalemia, pulmonary edema, persistent severe metabolic acidosis (pH less than 7.2) and symptomatic uremia. Symptoms of uremia include anorexia, hiccoughs, nausea and vomiting, encephalopathy and glove and stocking neuropathy. Dialyzable drugs include theophylline, various alcohols, lithium and salicylates (useful for electrolyte disturbances).

    HUS is characterized by acute renal failure, microangiopathic hemolytic anemia, fever, and thrombocytopenia. Diarrhea and upper respiratory infection are the most common precipitating factors. HUS is one of the most common causes of acute renal failure in children.

    In children, HUS often follows a prodromal infectious disease, usually diarrhea (90%), less often an upper respiratory infection (10%). Use of antimotility drugs may increase the risk of developing HUS. The most commonly associated diarrheal illnesses include those due to the pathogens Escherichia coli serotype 0157:H7 and Shigella, Salmonella, Yersinia, and Campylobacter species. The Shiga and Shigalike toxins, produced by some strains of Shigella dysenteriae and E coli 0157:H7, respectively, have been associated with approximately 70% of cases of HUS in children. Because of the cytotoxic activity of these toxins on Vero cells, they are referred to as verotoxins. HUS also is associated with viruses, including varicella, echovirus, and coxsackie A and B, as well as other infections such as Streptococcus pneumoniae. HUS has also been associated with AIDS, cancer, and the administration of chemotherapeutic agents. Mitomycin C is the most common chemotherapeutic agent associated with HUS. Malignancies found in conjunction with HUS include prostatic, gastric, and pancreatic malignancies. Some have suggested that HUS is mediated by immune complexes. Some cases of HUS are familial, which may reflect a genetic or human leukocyte antigen (HLA)-type predisposition.

    HUS and thrombotic thrombocytopenic purpura represent different ends of what is probably the same disease continuum. Endothelial cell injury appears to be the primary event in the pathogenesis of these disorders. The endothelial damage triggers a cascade of events that result in microvascular lesions with platelet-fibrin hyaline microthrombi that occlude arterioles and capillaries. The platelet aggregation results in a consumptive thrombocytopenia. The epithelial damage may result from toxins released by bacteria or viruses. In TTP, the hyaline microthrombi occur throughout the microcirculation, and microvascular thromboses may be found in the brain, skin, intestines, skeletal muscle, pancreas, spleen, adrenals, and heart. On the other hand, in HUS, they essentially are confined to the kidneys. Many of the infectious agents and drugs implicated in HUS/TTP are toxic to the vascular endothelium.

    Although the vascular lesions are identical in HUS and TTP, involvement of the CNS predominates in TTP. Renal involvement is the defining feature of HUS. On gross examination, the kidneys are swollen and pale; many fleabite hemorrhages are on the surface. In HUS and TTP, the platelet and fibrin microthrombi within the renal microvasculature are accompanied by thrombocytopenia and a microangiopathic hemolytic anemia. Vasculitis is usually absent.

    The mortality rate is 5-15%. Younger children who present in the summer with the typical diarrheal prodrome tend to do better than older children who develop HUS during the colder months of the year. Adults with HUS generally have a poorer prognosis than children. In one study, 14% of adults with HUS died. Cancer and chemotherapy associated HUS are associated with a poor prognosis, despite therapy. With supportive care, approximately 85% of patients recover and regain normal renal function.


    HEMOPHILIA A is an X-linked recessive disorder of males due to a defective or deficient factor VIII:C molecule. The incidence is 1:10K. A useful screening test is the PTT which is prolonged in all but those with mild disease.

    Spontaneous hemorrhage occurs with levels below 3%. Hemarthrosis and deep skeletal muscle hemorrhage occurs with levels less than 10-15%. OVER 30% ACTIVITY is required prior to major surgery but many recommend full correction to 100% activity levels.

    Preoperative preparation requires establishing a factor VIII plasma concentration that will ensure hemostasis. Calculation of replacement therapy is based on the convention that 100% of a procogulant translates to 1 unit of procoagulant per milliliter of plasma and the the plasma volume is 40 mL per kg. A 50 kg patient with 1% activity requires 2000 units to achieve 100% activity. The half-life of factor VIII is generally 10-12 hours and factor is given at the half-time interval.

    Factor VIII:C can be administered as cryoprecipitate or as heat-treated lyopholized concentrate. About 10% of hemophiliacs acquire an antibody to factor VIII and hence do not achieve the anticipated factor VIII plasma concentration.

    DDAVP is the synthetic analogue of ADH and can be administered in the treatment of traumatic hemorrhage in mild to moderate hemophiliacs and even in preparing such patients for minor surgery.

    HEMOPHILIA B (Christmas Disease) is an X-linked disorder caused by a defective or deficient factor IX molecule.

    Pateints should receive replacement factor to achieve activity levels of 30% prior to surgery. The dosing interval for factor IX concentrate is based on an elimination half-time of 24 hours. FFP is no longer considered the treatment of choice for these patients.

    HEMOPHILIA C is an AR deficiency of factor XI. PTT values may be elevated. Concentrates are not available in the US and patients often require preoperative treatment with FFP. The half-life of factor XI is 80 hours.



    The duration of heparin action depends on body temperature and the dose administered. IV doses of 100, 200 and 400 units/kg have elimination half-times of 56, 96 and 152 minutes. These durations are prolonged by reductions in body temperature below 37 degrees C. The duration of action of heparin is also prolonged in the presence of hepatic and renal dysfunction. Conversely, patients with PE require larger doses because of more rapid clearance of the drug. The mechanism of this phenomena is unclear.

    Digitalis, tetracyclines, nicotine or antihistamines may partially counteract the anticoagulant action of heparin sodium. NTG administration may also increase the amount of required heparin.


    Heparin inhibits reactions that lead to the clotting of blood and the formation of fibrin clots both in vitro and vivo. Heparin acts at multiple sites in the normal coagulation system. Small amounts of heparin in combination with ANTITHROMBIN III (heparin cofactor) can inhibit thrombosis by inactivating activated Factors X, XII, XI and IX and inhibiting the conversion of prothrombin to thrombin. Once active thrombosis has developed, larger amounts of heparin can inhibit further coagulation by inactivating thrombin and preventing the conversion of FIBRINOGEN to FIBRIN. Heparin also prevents the formation of a stable fibrin clot by inhibiting the activation of the fibrin stabilizing factor.

    Bleeding time is usually unaffected by heparin. Clotting time is prolonged by full therapeutic doses of heparin but in most cases, it is not measurably affected by low doses of heparin.

    PHARMACOKINETICS Peak plasma levels of heparin are achieved 2-4 hours following SQ administration, although there are considerable individual variations. Loglinear plots of heparin plasma concentrations with time for a wide range of dose levels are linear which suggests the absence of zero order processes. The liver and the RES are the site of transformation. The absence of a relationship between anticoagulant half-life and concentration half-life may reflect factors such as protein binding of heparin.

    Heparin does not have fibrinolytic activity and therefore, it will not lyse existing clots.

    DOSAGE Heparin should be given by intermittent IV injection, IV infusion or deep SC (intrafat) injection. The IM route of administration should be AVOIDED because of the frequent occurrence of hematoma.

    A UNIT of heparin is that which will prevent 1 mL of citrated sheep blood from clotting for one hour after the addition of calcium chloride.

    When heparin is given by continuous infusion, the coagulation time should be determined approximately every 4 hours in the early stages of treatment. When the drug is administered intermittently, tests should be performed before each injection during the early stages of treatment.

    Dosage is adequate when the PTT is 1.5-2 times normal. GOALS for DVT and PE are PTT between 56-87 seconds. GOALS for ACS and ischemic stroke are PTT between 50-70 seconds.

    Periodic platelet counts, HCT and tests for occult blood in stool are recommended during the entire course of heparin therapy.

    Patients undergoing CBP should receive an initial dose of not less than 150 units (preferably 300) of heparin per kilogram. A dose of 300 units per kilogram is used for procedures estimated to last less than sixty minutes while 400 units per kilogram is utilized for longer procedures.

    FFP as a soure of antithrombin III may be required if over 600 units per kg is required to elevate the ACT. The DDX for heparin resistance also includes thrombocytosis and sepsis.


    Mild thrombocytopenia occurs in 30-40% of patients treated with heparin and for the most part is clinically insignificant. Mild cases are caused by heparin induced platelet aggregation.

    In 0.6-6% of patients treated with heparin (of any form) for over five days, a severe TCP develops. HIT should be suspected when platelet counts decrease by 50% or thrombosis occurs 5-14 days after initiation og heparin. Rapid onset HIT is possible in those exposed to heparin within the preceeding three months. It is suspected when hypotension, pulmonary HTN or tachycardia occurs after heparin bolus. Lower platelet counts make the DX more likely (AA September 2007).

    The condition is secondary to formation of platelet antibodies which are heparin dependent for function. An aggregation of platelet-antibody complexes cause venous thromboses and deplete the blood of functional platelets.

    Aggregated platelets release a factor which binds and inhibits heparin and as a result, patients are likely to be resistant to heparin anticoagulation. Contributing to this phenomenon is depletion of antithrombin III, which heparin requires as a sort of cofactor in order to execute its anticoagulant effect.

    The only effective treatment for HIT is to stop exposure to heparin. As long as the immune system is exposed to the antigen, it will continue to produce antibodies. Even the small amount of exposure which results from heparinized lines may stimulate antibody formation. TCP may take several days to resolve. Antibodies usually do not persist for more than 80 DAYS. Platelet transfusion is not indicated or recommended.

    For patients with history of HIT, heparin administration may be preceded with platelet inhibitors such as the synthetic PGI2 analogue EPOPROSTENOL, ASA or dipyridamole. in order to prevent AGGREGATION and therefore consumption.

    For patients with ANTIBODIES present alternatives to heparin include LEPIRUDIN, DANAPAROID, ARGATROBAN and bivalirudin (enzymatically metabolized).

    The HAT test is used as a diagnostic tool for HIT.


    Reversible changes in liver function are common in the postoperative period and it is sometimes difficult to differentiate surgical and anesthetic causes. Decreased hepatic blood flow (with GA and RA) and global stresses placed on the body will generally produce mild impairment in function (50% incidence).

    Jaundice indicates a serum bilirubin exceeding 4 mg/dL and a more serious derangement can be assumed. Jaundice is seen in up to 20% of patients after major surgery and etiologies should be sought. Specific causes are seldom identified and liver function often normalizes quickly. A useful classification scheme of postoperative jaundice:

    1) overproduction of bilirubin: hemolytic anemia, hemolysis after transfusion, resorption of hematoma
    2) hepatocellular damage: intrahepatic cholestasis, circulatory failure, halothane, methoxyflurane, other drug-induced (isoniazid, dilantin, sulfonamides), preexisting liver disease
    3) extrahepatic obstruction: common duct stone, bile duct injury, postoperative pancreatitis
    4) miscellaneous: cholecystitis, Gilbert syndrome

    Presence of bilirubin in the URINE indicates an abundance of CONJUGATED bilirubin. Predominantly conjugated hyperbilirubinemic patients (with a fraction over 50%) are divided into the impaired hepatic excretion group (intrahepatic defects) and those with extrahepatic biliary obstruction. Those with intrahepatic defects include rare familial disorders and acquired disorders (viral or drug induced hepatitis or cholestasis or sepsis).

    Patients with predominantly UNCONJUGATED bilirubin include those with overproduction (hemolysis), decreased uptake (prolonged fasting, sepsis) and decreased conjugation (Gilberts, neonatal jaundice, drug induced transferase deficiency and hepatocellular disease).

    Aminotransferases may be increased in nearly all types of liver disorders but are primarily increased in patients with extensive hepatocellular damage of viral, drug or hypoperfusion etiologies. Elevations may be seen following periods of hypotension while neurologic and cardiac systems are preserved.

    Alkaline phosphatase may also be increased in most any type of liver dysfunction, but is exceedingly high (3-10 times normal) in cases of extrahepatic obstruction.

    An increase in GGT may correlate with elevated alkaline phosphatase in biliary tract diseases, but in general is an extremely non-specific test. An elevation of LDH is generally not specific.

    Evaluation of the serum proteins and coagulation cascade is generally of little value in the diagnosis of liver dysfunction. Albumin is usually low and PT is increased in patients with parenchymal versus obstructive disorders. PT increases are usually seen before a fall in albumin reflecting the shorter half-lives of the proteins. When PT is increased in a patient with obstructive disease, it is usually correctable with vitamin K administration.

    Numerous studies have supported the existence of halothane (1: 35K) and enflurane (1:800K) hepatitis. Isoflurane and nitrous oxide are not hepatotoxic agents though isoflurane and sevoflurane may cause transient elevations in bilirubin and transaminases.

    Ketamine may cause transient increases in LFT while etomidate, propofol, thiopental, midazolam and the opioids have not in the absence of intraoperative alterations in blood pressure and hepatic perfusion.


    The anesthesiologist should assess the usual preoperative areas with particular attention to CNS, CV system, GI complaints, renal function and coagulipathy.

    CNS Encephalopathy is found in association with severe acute or chronic liver disease and clinical findings may include dulling of the intellect, personality changes, incoordination, dysarthria, asterixis and increased tone with hyperreflexia. Encephalopathy can indicate progressively worsening disease and increased portal shunting. Precipitating factors include infection, GI bleed, constipation or dietary excess of protein.

    CV Patients with liver disease often have a hyperdynamic circulation characterized by an increased CO. This increase in CO may reflect increased intravascular fluid volume secondary to activation of the renin angiotensin system, decreased viscosity of the blood secondary to anemia and generalized arteriolar vasodilatation. Pulmonary HTN is occasionally observed suggestive of vasoactive substances that bypass normal hepatic degradation. Patients with alcoholic disease may also have a cardiomyopathy with associated CHF.

    GI Portal HTN is manifested in part by HSM and ascites. Ascites generally implies a grave prognosis. Therapy and amelioration of ascites probably puts patients at lower risk. Esophageal varices secondary to portal HTN may cause chronic bleeding or severe hemorrhage requiring massive transfusion, balloon tamponade or sclerotherapy.

    RENAL Failure may develop secondary to hepatorenal syndrome associated with oliguria & lack of sodium excretion. Predisposing factors for the development of HRS include infection with endotoxin release and high bilirubin. The renin-angiotensin system is activated in patients with liver disease and causes sodium and water retention which contributes to the ascites mentioned above.

    Hyponatremia can be misleading as total body sodium stores are usually greater than normal in patients with liver disease.

    PULMONARY Patients with liver disease often have true pulmonary shunts and frequently have VQ mismatches which contribute to hypoxemia. They also can have a low PCO2. Mechanical infringement secondary to ascites also impairs function. Many cirrhotics also are heavy smokers and must be evaluated for COPD.

    METABOLIC Metabolic & respiratory alkalosis can be present in patients with liver disease. Alkalosis leads to development of hypokalemia. Fasting glucose may be elevated in the moderately severe cirrhotic due to insulin resistance and those with severe liver disease may have persistent hypoglycemia.

    CLOTTING Coagulopathies are extremely common due to decreased synthesis of coagulation factors, shortened circulating half-life of coagulation products, production of abnormal products, decreased platelet count and impaired platelet function. All factors, with the exception of VIII, are produced by the liver.

    LAB Useful lab values to assess preoperative function include bilirubin, albumin (half-life of three weeks), PT and INR, transaminases, creatinine clearance, hematocrit and hemoglobin, platelets, glucose, electrolytes, ABG and hepatitis panel.

    Elective surgery for patients with ACUTE viral hepatitis should be delayed as the risk of perioperative mortality approaches 10%.


    Hepatic encephalopathy is a reversible neuropsychiatric syndrome seen in association with severe acute or chronic liver disease. Clinical features may be subtle at first, including changes in personality and dulling of the intellect. Later, progressive neurologic disturbances including incoordination, dysarthria, a flapping tremor and increased tone with hyperreflexia may supervene.

    The development of hepatic encephalopathy may merely reflect a gradual worsening of the liver disease with worsening of portal systemic shunting. On the other hand, encephalopathy is often precipitated by infection, GI hemorrhage, hypokalemia, alkalosis, azotemia and constipation or dietary excess of protein. Iatrogenic factors precipitating encephalopathy include injudicious use of sedatives (especially benzodiazepines), opiates and diuretics.

    TREATMENT for encephalopathy focuses on reversal of precipitating factors. Lactulose and neomycin are often used to limit bacterial production of toxins that cannot be cleared by the dysfunctional liver. FLUMAZENIL, the benzodiazepine receptor antagonist, has been shown to reverse the coma in selected patients over a prolonged period.

    The EEG in hepatic encephalopathy typically shows bilateral slow waves that are synchronous and symmetric (delta wave activity) and are superimposed on the normal alpha rhythm. This pattern is also seen in several other metabolic encephalopathies and is therefore not pathognomonic. Blood AMMONIA concentration is generally higher on average in patients with hepatic encephalopathy than in patients with chronic liver disease without encephalopathy but this test is not specific or diagnostic.


    CAYENNE is also known as chili pepper and paprika. Used externaly for muscle spasm or soreness and internally for GI tract disorders. External use causes potential for skin ulcerations & blistering with over 2 days use. Internal overdose may cause severe hypothermia.

    ECHINACEA for common colds, wounds and burns, UTI and URI. May cause hepatotoxicity, especially when used with other hepatotoxic drugs. May increase phenytoin and phenobarbital concentrations. May see decreased effectiveness of corticosteroids. Recomended to discontinue as soon as possible.

    EPHEDRA uses include OTC diet aids, bacteriostasis and anittussive. Arrhythmias with digoxin or halothane, enhanced sympathomimetic effects with guanethidine and MAO inhibitors. HTN with oxytocin. Discontinue at least 24 hours prior to surgery.

    FEVERFEW is used for migraine prophylaxis & antipyresis. Side effects and interactions include platelet inhibition & increased bleeding (should avoid use in patients on warfarin or other anticoagulants). Rebound headache with sudden cessation. 5-15% incidence of aphthous ulcers or GI tract irritation. Discontinue 14 days prior to surgery.

    GARLIC uses include lipid lowering and blood pressure control. Garlic also has antiplatelet, antioxidant and antithrombolytic properties. Side effects and interactions include possible potentiation of warfarin. Garlic will increase INR. Discontinue 7 days prior to surgery.

    GINGER uses include antinausea & antispasmodic. Side effects and interactions include potent inhibition of thromboxane synthetase which may increase bleeding time. Discontinue 14 days prior to surgery.

    GINGKO uses include circulatory stimulant and enhancement of mental capacity. May enhance bleeding in patients on anticoagulant or antithrombolytic therapy. Discontinue at least 36 hours prior to surgery.

    GINSENG used as adaptogenic, increased energy level and antioxidant. Side effects include ginseng abuse syndrome (with over 15 g per day – symptoms of the syndrome include sleepiness, hypertonia and edema). Should avoid use with other stimulants which could cause tachycardia or hypertension. Discontinue 7 days prior to surgery.

    GOLDENSEAL is used for diuresis, inflammatioa, laxative and hemostasis. Goldenseal functions as oxytocic and an aquaretic not a diuretic (no sodium excreted, just free water). The drug may worsen edema and hypertension. Overdose may cause paralysis (amount not known).

    KAVA KAVA is used for anxiety. Potentiates barbiturates and benzodiazepines and can potentiate ethanol effects. Discontinue 24 hours prior to surgery.

    LICORICE is used for gastric & duodenal ulcers, gastritis, cough and bronchitis. Glycyrrhizic acid in licorice may cause high blood pressure, hypokalemia & edema. Contraindicated in many chronic liver conditions, renal insufficiency, hypertonia, and hypokalemia. Discontinue 14 days prior to surgery.

    SAW PALMETTO is used for BPH, as an antiandrogenic and antiexudative mediacation. May see additive effects with other hormone therapies such as birth control pills or estrogen therapy.

    ST JOHN’S WORT is commonly used for depression and anxiety. May be a photosensitizing agent, possible interaction with MAO inhibitors (not proven), may prolong effects of anesthesia. Discontinue 5 days prior to surgery.

    VALERIAN is commonly used as a mild sedative and mild anxiolytic. Will likely potentiate barbiturate effect, may decrease symptoms of benzodiazepine withdrawal (secondary to benzodiazepine effects at different receptors).

    VITAMIN E may increase bleeding by antagonism of the vitamin K dependent coagulation factors and platelet aggregation.


    Hering and Breuer noted in 1868 that animals, who were slightly anesthetized and spontaneously breathing, would cease or decrease ventilatory effort during sustained lung distention. As this reflex is mediated by the vagus nerve, it can be blocked by bilateral vagotomy. The reflex is very prominent in lower order mammals such that even 5 cm H2O CPAP will induce apnea.

    In human the reflex is very WEAK and humans can continue to breathe spontaneously even with application of CPAP in excess of 40 cm H2O. The reflex is associated with inhibition of inspiratory muscles function.

    A second component or co-reflex of the Hering-Breuer reflex known as the DEFLATION REFLEX, produces increased ventilatory muscle activity in the face of sustained lung deflation. This reflex is even less significant in humans.


    Hetastarch (Hespan) is a mixture of synthetic polysaccharides with a mean molecular weight of 450,000. There is minimal risk of disease transmission because it is not a biologic product.

    It is eliminated from the body by several mechanisms, depending on molecular weight. Small fragments (less than 50,000 molecular weight) are actually excreted in the urine creating a mild diuretic effect. The larger fragments are metabolized by alpha-amylases at several sites with subsequent excretion in bile and urine.

    Due to its complex pattern of metabolism and excretion, the elimination HALF-LIFE during the first week averages about 13 DAYS with progressively longer terminal elimination times as time after administration increases. One study demonstrated 38% remaining in the intravascular space after 24 hours, 23% diffusing into the interstitium and the remainder renally excreted.

    The usual maximum daily dose is 20 mL/kg IV. Doses greater than this may cause dilutional coagulopathy.

    There is confusion about how hetastarch leads to coagulopathy by mechanisms more complicated than simple dilution. Hetastarch may BIND to FVIII and or fibrinogen and some studies have indicated a binding and deactivation of platelets.


    Hexadimethrine is the only known alternative to protamine for reversing the effects of heparin. The use of hexadimethrine may result in hypotension, decreased cardiac output and increases in PVR that is more pronounced than those same effects secondary to protamine.

    The drug may be used in patients with known sensitivity to protamine but in many circumstances the effects of heparin are simply allowed to resolve without reversal. The drug is not available in the US.


    HEXTEND is a mixture of the synthetic polysaccharides (identical to Hespan) combined in a solution with the electrolyte composition similar yet not identical to LR.

    Manufacturers report that up to three liters may be safely used without affecting hemostasis. This is in contrast to the usual maximum daily dose of 20 mL/kg IV for HESPAN. The differences in the two products have yet to be clearly explained but may be related to the small amounts of calcium that are present in HEXTEND. The solution has a plasma volume expansion of 38% meaning that 38% will remain intravascular, 23% diffuses into the interstitium and the remainder is renally excreted. This is in contrast to the 21% plasma volume expansion of NS and LR.

    LR contains 3 mEq/L of calcium while the plasma itself has an average of 5 mEq/L. LR contains only 109 mEq/L of chloride while HEXTEND contains 124 mEq/L of chloride.


    High frequency jet ventilation differs from conventional positive pressure ventilation in that a smaller tidal volume and more rapid rates are used. Tidal volumes are usually similar to dead space (usually 3-4 mL per kg) and rates are between 60-150 breaths per minute. HFJV (in contrast to HFOV) has no utility in the intensive care setting except in the patient with persistent bronchopleural fistula.

    Gas transport depends more on molecular diffusion, high-velocity flow and coaxial gas flow in the airways with gas in the center moving distally and that in the periphery moving proximally. With HFV, the distribution of ventilation depends more on resistance and compliance becomes less important.

    High frequency jet ventilation (HFJV) uses the pulse of a small jet of fresh gas introduced from a high-pressure source (50 psi which is most easily provided through a wall source) into the airway through one of several routes.

    1) small catheter by transtracheal ventilation
    2) tube exchanger with an adaptor
    3) additional lumen within an ETT
    4) bronchial blocker lumen of a Univent tube

    The jet ventilation is often provided by free standing jet ventilator units (with frequency set by dial) or hand held devices that require manual manipulation of the air jet handle at the desired respiratory rate. Most jet injectors provide a fresh oxygen jet which entrains gas from an injection cannula side port reservoir resulting in a variable oxygen concentration.

    Using high fresh gas flows from an anesthesia circuit (the fresh gas outlet) is a suboptimal alternative with the beneficial possibility of adding inhaled anesthetics to the oxygen mixtures. The fresh gas outlet may often provide pressures as low as 10 psi.

    The only current FDA approved use for HFJV outside the operating room is ventilation of patients with bronchopleural fistulae. HFJV has no apparent benefit in ARDS.

    OSCILLATORS are distinctly different in that the oscillators will actively PULL gas out of the system during expiration – effectively preventing the hyperinflation that can occur with HFJV. Respiratory rates are much higher with oscillation when compared to high frequency jet ventialtion and measured in Hz (typical rates ranging from 10-15 Hz). [HIGH FREQUENCY OSCILLATION] is useful in the intensive care setting.


    AMBI SCREWS may generally be done with SA isobaric bupivicaine (0.5-0.7%) commonly at 10-12 mg with or without morphine. Isobaric formulations allow injured extemeties to be placed in the non-dependent position but ketamine or fentanyl may be required. Isobaric solutions are also generally recommended when LOW spinal levels are all that is required. The more fragile elderly patient may benefit from the use of a CSA allowing incremental dosing of the isobaric bupivicaine generally at doses of 5-8 mg. Lumbar and sciatic blocks are also an option.

    TOTAL HIP ARTHROPLASTY can be performed with tetracaine or bupivicaine (12-20 mg) SAB. Motor blocks will be more profound with tetracaine but that bupivicaine provides fewer problems with break through pain. HYPOBARIC solutions may be preferable to isobaric solutions by allowing for prolonged unilateral blocks without increase in hemodynamic disturbance (AA 2003 97:589). In the more fragile patient, the use of CSA might provide the most ideal anesthetic.

    REPEAT THA will often require more time and is most often performed with CSA or CSE techniques.


    Hirschsprung’s is the congenital absence of parasympathetic innervation of the distal intestine. The colon proximal to the aganglionic segment becomes distended and its wall markedly thickened because of muscle hypertrophy. Occurs at an incidence of 1:1500 live births with a 4:1 male predominance. Only 4% of those affected are premature.

    Symptoms usually begin at birth, frequently with delayed passage of meconium. Any newborn who fails to pass meconium in the first 24-48 hours of life should be evaluated for possible Hirschsprung’s disease. In some infants, the presentation is that of complete intestinal obstruction. Others have relatively few symptoms until several weeks of age, when the classic symptom of constipation has its onset. Diarrhea is not uncommon but differs from the usual infantile diarrhea in that it is associated with abdominal distension. Occasionally the patient will go many years with mild constipation and diagnosis will be delayed.

    The initial treatment requires performing a leveling colostomy in the most distal colon with ganglion cells present. This requires exploration with multiple seromuscular biopsies of the colon wall to determine the exact extend of the aganglionosis. The colostomy is placed above the transition zone. Placement of the colostomy in an area of aganglionosis will lead to persistent obstruction. Once the child has reached an adequate size and age (4-12 months), a formal pull-through procedure is done.

    Surgery is performed in the supine postion and may involve rather large surgical incisions and consequent fluid shifts. One shot caudals or lumbar epidurals may be useful.


    H1 H2
    chronotropic +
    inotropic +
    coronary vasodilator + +
    increase PR +
    vent irritability +
    potentiate VF + +
    shift in pacemaker +
    decrease SVR + +
    incr permeability +
    bronchoconstrict +
    bronchodilate +
    pulm vasoconstrict +
    pulm vasodilation +
    H1 H2

    Somewhat important to remember is the conflicting action within the respiratory system. H1 ACTION results in bronchoconstriction and pulmonary vasodilation. H2 ACTION results in bronchodilation and pulmonary vasoconstriction.

    The dominant effects are nevertheless bronchoconstriction, pulmonary vasoconstriction and systemic vasodilation – effects quite similar to those of HYPOXIA.

    PROPHYLAXIS for anaphylaxis may include an H1 blocker such as diphenhydramine (0.5-1 mg/kg PO/IV/IM) that would block bronchocontriction AND an H2 blocker such as ranitidine that would block pulmonary vasoconstriction but could (if given alone) potentiate bronchoconstriction.

    Effective prophylaxis for patients previously responding to CONTRAST media should include 50 mg of prednisone given every six hours for one day with the last dose given one hour prior to the study. Diphenhydramine 50 mg IM is also given one hour prior to study. This regimen is very effective although 5% of patients may still experience mild allergic reactions.

    Histamine RELEASE caused by various medications is more likely to lead to flushing, systemic vasodilation and hypotension though bronchospasm may occasionally occur. Most often, subsequent dosing of the offending agent does not produce the same degree of histamine release.


    Histiocytosis encompasses a group of diverse disorders that have in common, as a primary event, the accumulation and infiltration of monocytes, macrophages, and dendritic cells in the affected tissues. Such a description excludes diseases in which infiltration of these cells is in response to a primary pathology. The spectrum of clinical presentation in this group of disorders varies greatly, ranging from mild to life threatening.

    LCH can be local and asymptomatic (isolated bone lesions) or it can involve multiple organs and systems with significant symptomatology and consequences.

    Bone involvement is observed in 78% of cases and often includes the skull 49%, innominate bone 23%, femur 17%, orbit 11%, and ribs 8%. The lesions can be singular or multiple. Asymptomatic or painful involvement of vertebrae can occur and result in collapse. Long bone involvement can induce fractures. Extension to the adjacent tissues can produce symptomatology, which may be unrelated to the bone involvement.

    Diabetes insipidus and delayed puberty are observed in as many as 50% of patients. Hypothalamic disease also may result in growth hormone deficiency and short stature.

    Maxillary, mandibular, and gingival disease may cause loss of teeth, hemorrhagic gum and mucosal ulceration and bleeding. Erosion of gingiva may give the appearance of premature eruption of the teeth in young children.

    Cutaneous LCH is observed in up to 50% of patients with LCH. Rash is a common presentation, and skin lesions may be the only site of the disease or a part of systemic involvement. Skin infiltrates have a predilection for the midline of the trunk and the peripheral and flexural areas of skin. Skin infiltrates can be maculoerythematous, petechial xanthomatous, nodular papular or nodular in appearance. Bronzing of the skin can occur.

    Scalp disease frequently presents as scaly erythematous patches, which may become petechial and eroded with serous crust. The lesions often are not pruritic, but tenderness and alopecia can occur. In infants, a nodular form of the disease marked by eruption of lesions mimicking varicella has been reported.

    Pulmonary involvement is observed in 20-40% of patients and may result in respiratory symptoms, such as cough, tachypnea, dyspnea, and pneumothorax. A male predominance exists. Pulmonary function test results may be abnormal. Diffuse cystic changes, nodular infiltrate, pleural effusion, and pneumothorax are known to occur. Imaging studies may reveal the existence of cyst and micronodular infiltrates. Pulmonary function tests may reveal restrictive lung disease with decreased pulmonary volume.

    GI bleeding may be the presenting sign with GI involvement. Appropriate imaging studies, endoscopy and biopsy may be helpful to confirm the diagnosis. Liver involvement is characterized by elevated transaminases and, less commonly, increased bilirubin. Hematologic changes may be cause may be caused by marrow involvement or enlargement of the spleen.

    Lymph node enlargement has been observed in approximately 30% of patients. Rarely, the nodes are symptomatic but, if massive in volume, may result in obstruction of, or damage to, the surrounding organs and tissues. Suppuration and chronic drainage may occur. Enlargement of the lymph nodes surrounding the respiratory tract may result in pulmonary-related symptoms, such as cough, dyspnea or cyanosis.

    Infiltration of various areas of the brain gives rise to corresponding signs and symptoms, including cerebellar dysfunction and loss of coordination. Most commonly, disruption of hypothalamic and pituitary function are observed. These include symptoms secondary to DI and, to a much lesser extent, GH deficiency and hypopituitarism. Other symptoms, such as seizures and those related to increased intracranial pressure, depend on the site and volume of the space-occupying lesion.


    Consideration to the various medications used for the treatment of HIV infection should be considered.

    With respect to RA, the involvement of the neurologic and hematologic systems are of particular concern.

    Zidovudine (a thymidine analog which interferes with the replication of HIV), dideoxyinosine (ddI) and dideoxycytidine (ddC) are commonly associated with lower extremity symptoms. While ZDV is mostly associated with myalgia and proximal muscle weakness, ddI and ddC often present with a neuropathic, burning type of pain in the legs and feet. Currently no reports have evaluated the effect of regional techniques on the outcome of these pathologies. In terms of hematologic effects, ZDV and trimethoprim-sulfamethoxazole can cause anemia, neutropenia and thrombocytopenia, most likely through bone marrow suppression. Gancyclovir (indicated for CMV) can cause thrombocytopenia.

    The nephrotoxicity of Foscarnet (a drug used for CMV retinitis) and pentamidine (an aerosolized drug for pneumocystis carinii pneumonia prophylaxis) may require additional attention to fluid and drug management. The hepatic toxicity caused by TMP-SMX (also used for pneumocystis prophylaxis) may have implications on drug metabolism and clearance. Long-term toxic reactions to ZDV include increased relationships with malignancy, chromosomal breaks and CHF.

    Similar to the effects from the aggressive agents used for chemotherapy, the medications used to control HIV and its associated diseases can have dramatic and unintended side effects. In particular, the suppression of hematologic lines and the lower extremity neurologic effects may require a risk benefit analysis prior to the provision of anesthetic and particularly RA techniques.



    The major neuropathologic features of the most severe cases of holoprosencephaly include a single sphered cerebral structure with a common ventricle, a membranous roof over the third ventricle that is often distended into a large cyst posteriorly, an absence of olfactory tracts, and bulbs, and hypoplasia of the optic nerves or the presence of only a single optic nerve. The corpus collosum is usually absent. The malformation of the forebrain may be so severe that there is a marked disturbance of formation of both telencephalon and diencephalon.

    Incidence is around 113K births. The incidence is about 50-fold greater in aborted human embryos, indicating that most cases are eliminated prenatally.

    The facial anomaly in the most severe cases is represented by a single median eye or even no eyes at all and a rudimentary nasal structure often located above the midline orbit. Less severe deformities include: moderate ocular hypotelorism, a flat nose, and median cleft lip and palate, often with an absent philtrum and similar features with bilateral cleft lip and palate.

    Abnormalities of other organ systems occur in about 75% of cases and consist primarily of disturbances of cardiac, skeletal, genitourinary and gastrointestinal development.

    The neurologic features in the most severe cases are obvious from the neonatal period. Infants exhibit frequent apneic spells, seizures, stimulus-sensitive tonic spasms, poikilothermia, total failure of neurologic development and death.

    Endocrine abnormalities may include hypopituitarism, ACTH adrenal axis failure and diabetes insipidus.

    Most affected patients die before six months of age. Mildly affected patients may live to adulthood.


    HTLV-I is the etiologic agent for acute T cell leukemia (ATL) and HTLV associated myelopathy (HAM). In ATL, a proliferative disorder of T cells is observed, characterized by skin lesions, lymphadenopathy, hepatosplenomegaly, lytic bone lesions and hypercalcemia. HAM, also called tropical spastic paresis, is a chronic progressive demyelinating disease that affects the spinal cord and white matter of the CNS, causing weakness and spasticity predominately in the lower limbs. Major pathological findings include inflammatory perivascular and parenchymal infiltration with degeneration, leading some to speculate that an immunologic mechanism is involved in the development of HAM. Ocular complications are observed in both HAM and ATL.

    Patients with HAM may present with peripheral neuropathy. ATL has the following 4 distinct types and characteristics: (1) smoldering ATL: 5% or more abnormal T cells with total lymphocyte count within the reference range, malignant cells with monoclonal proviral integration, skin lesions, occasional pulmonary involvement, no hypercalcemia, lymphadenopathy, or other visceral involvement, serum LD may be elevated, (2)
    chronic ATL: absolute lymphocytosis over 4.0, T-cell lymphocytosis over 3.5, serum LD may be twice the reference range,
    possible lymphadenopathy, hepatomegaly, splenomegaly, skin, or pulmonary involvement, no hypercalcemia, ascites or pleural effusion, no CNS, bone or GI involvement, (3) lymphomatous ATL: lymphadenopathy in the absence of lymphocytosis, histological evidence of lymph node involvement required, and (4) acute ATL: short and aggressive clinical prodrome, hypercalcemia, skin lesions, pulmonary involvement and lymphocytosis.

    Patients with ATL are immunocompromised, which leads to opportunistic infections, including the following: pneumocystis carinii pneumonia, cryptococcal meningitis, fungal infections, viral infections (CMV, herpes zoster, HSV), strongyloides stercoralis. Coinfection with HIV may alter the progression of either disease and complicate treatment.

    Infection with HTLV-I or HTLV-II is lifelong and patients are usually asymptomatic.

    ATL often does not proceed to advanced stages. If it does, patients with smoldering ATL live an average of 2 years, while those with acute ATL live an average of 6 months. Chemotherapy or interferon plus antiretrovirals can cause complete remission in a significant proportion of cases.
    HAM may respond to treatment. If it does not, prognosis is poor. Within 10 years, many patients are bedridden or unable to walk unassisted.


    Dry gas supplied by the gas machine may cause clinically significant desiccation of mucus and an impaired mucociliary elevator. This may contribute to retention of secretions, blocking of conducting airways, atelectasis, bacterial colonization and pneumonia.

    ABSOLUTE humidity is the maximum mass of water vapor which can be carried by a given volume of air (mg/L). This quantity is strongly determined by temperature (warm air can carry much more moisture).

    RELATIVE humidity is the amount present in a sample, as compared to the absolute humidity possible at the sample temperature (expressed as a percentage).

    Active heater humidifier units function by directing inspiratory respiratory gases over or through a heated water bath, where the gas becomes warmed and humidified. These devices are useful for aiding in the maintenance of thermal equilibrium and for avoiding the drying and inspissation of respiratory secretions which could lead to ciliary dysfunction.

    Because these units add a number of additional circuit connections, the chance of a circuit leak or disconnect is increased. Additionally, if the gas is heated too aggressively, thermal lung injury may result. Because the warm moist environment of the heated bath provides a good culture medium for bacteria, the chance of respiratory infection is present if these devices are not thoroughly cleaned and disinfected between uses.

    An often overlooked problem is that with high gas flows, over a period of time, large amounts of fluid may be delivered to the patient via absorption through the respiratory tract. While this rarely creates a problem in the adult, it can cause severe hypervolemia and pulmonary edema in small neonates and infants.


    Midazolam and glycopyrrolate premedication is often useful.


    The phthalazine derivative lowers BP almost exclusively by a direct relaxant effect on ARTERIOLAR smooth muscle. The vasodilation probably reflects hydralazine interference with calcium transport in vascular smooth muscle. Decreases in BP is usually accompanied by tachycardia which is only partially explained by reflex mechanisms.

    DOSING is between 2-40 mg or 0.1-0.2 mg/kg IV or IM. PO dosing is between 10-100 mg QID. Higher doses are required in rapid acetylators.

    PK Onset of action is within 5-20 minutes following IV administration. Peak effects occur within 10-80 minutes and the duration of action is between 2-4 hours.

    PHARMACODYNAMICS The drug maintains or increases renal, uterine and cerebral blood flow. It also increases plasma renin activity.


    Nonobstructive or COMMUNICATING hydrocephalus is due to overproduction of abnormal absorption of cerbrospinal fluid.

    OBSTRUCTIVE hydrocephalus may be due to congenital, neoplastic, post-traumatic or postinflammatory lesions. Congenital causes of obstruction include (1) Arnold-Chiari malformation in which the basilar SA pathways are underdeveloped, (2) aqueductal stenosis between the third and fourth ventricles, and (3) Dandy-Walker syndrome with occlusion at the outlet of the fourth ventricle by a congenital membrane. Ventricular dilation commonly follows periventricular and intraventricular hemorrhage that most often occurs in preterm infants.

    Hydrocephalus due to Arnold-Chiari malformation or aqueductal stenosis can lead to medullary and lower cranial nerve dysfunction resulting in swallowing abnormalities, stridor and atrophy of the tongue.


    HYDROCODONE or VICODIN is available in formulations of 2.5 to 10 mg with 500 mg of acetaminophen. Approximately 7.5 mg of PO hydrocodone is equianalgesic to 60 mg of PO morphine – similar to the conversions for hydromorphone. NORCO is available without acetaminophen.

    LORTAB ELIXIR contains 500 mg of acetaminophen and 7.5 of hydrocodone per 15 mL. Pediatric dosing is at 0.1-0.2 mg/kg every 6-8 hours. The maximum for children less than 2 years of age is 1.25 mg or 2.5 mL. The maximum for children 2-12 years of age is 5 mg or 10 mL. The maximum for children over 12 is 10 mg or 20 mL and many of these children may be given the tablet form.

    SHORTCUT Two millileters or 1 mg for every 10 kg of weight.


    Hydromorphone or DILAUDID is an opiate agonist that is a hydrogenated ketone of morphine. Hydromorphone is 5-7 TIMES more potent than morphine meaning that 1.5-2 mg of hydromorphone is equivalent to 10 mg of morphine. Hydromorphone has a SHORTER duration of action and causes less sedation, nausea and vomiting than morphine.

    DOSING is typically between 0.5-2 mg (0.015 mg/kg for pediatric patients) by slow IV injection every 3-4 hours. Continuous infusions may be given at 0.3 mg/hour (0.006 mg/kg/hour for pediatric patients). PO dosing is between 2-4 mg (0.04-0.08 mg/kg for pediatric patients) every 3-6 hours as the enteral form is usually half as potent as the IV formulation. Tablets are available in 2, 4 and 8 mg.

    PCA DOSING is typically initiated with a loading dose (1-2 mg for adults) followed by optional bolus INFUSIONS at 0.2-0.4 mg/hour (2-10 mcg/kg/hr) with BOLUS dosing at 0.1-0.5 mg (2-10 mcg/kg) every 10-20 minutes. One hour limits may be set at 1 mg with four hour limits at 2.5 mg for most adults.

    PALLADONE is a long acting hydromorphone formulation that provides 24 hours of sustained serum levels.

    SPINAL dosing is at 0.1-0.2 mg (2-4 mcg/kg). Epidural boluses are at 1-2 mg (20-40 mcg/kg) while infusion dosing ranges between 0.15-0.3 mg/hour (2-3.5 mcg/kg/hour).

    PHARMACOKINETICS Peak effects are achieved within 5-20 minutes and the duration of action is 2-4 hours with IV dosing, 4-6 hours IM/PO and 1-16 hours following epidural administration.

    The lipophilicity of hydromorphone is…


    HBO techniques are ideal adjunctive therapies for any injury which creates significant tissue hypoxia. Included in such injuries are medical emergencies in which gas bubbles are released in tissues (decompression illness and intravascular entrainment of a gas) or where a recurrent cycle of ischemia and edema prevent tissue healing (crush injuries, compartment syndromes or peripheral ischemia).

    The use of HBO therapies has grown tremendously, with new and interesting applications being found. Sunami et al noted that the ischemic cerebral infarct size was reduced in rats when hyperbaric oxygen therapy was applied.

    As these treatments are used in some of the most critically ill patients, the services of an anesthesiologist are often required.

    The goals and benefits of HBO therapy encompass five basic elements.

    1) hyperoxygenation
    2) vasoconstriction
    3) improvement of cellular function
    4) inhibition of infection
    5) prevention of reperfusion injury

    HENRY’S LAW states that at a constant temperature, the amount of gas dissolved in a liquid or tissue is proportional to the partial pressure of the gas in contact with the liquid or tissue. With that application of pressure (between 2-3 atmospheres), the amount of oxygen transported in the plasma alone can meet the total metabolic needs of the body. Thus, red cells are no longer necessary for the transport of oxygen. Moreover, this allows oxygen to be transported into areas of the microcirculation where red cell flow is obstructed. With the high oxygen diffusion gradient which is generated with in the hyperbaric chamber, tissue levels of oxygen increase dramatically, and this counteracts tissue hypoxia and edema.

    The vasoconstriction which occurs as a protective reaction to hyperoxia is beneficial in that it reduces blood flow which ultimately limits fluid extravasation and edema formation. This reduction in edema formation ultimately limits the collapse of capillaries, improves microcirculation blood flow, and increases oxygenation.

    More recently, and in apparent contradiction to this effect, Thomas et al demonstrated that the sympathectomy produced by an axillary brachial plexus blockade improved tissue oxygenation. The authors hypothesized that a sympathectomy presumably improves oxygen delivery by preventing the vasoconstriction of hyperoxia. Further work will need to find an explanation for these dichotomous results during HBO therapy.

    As neutrophils utilize oxidative mechanisms to kill bacteria, raising oxygen tension improves their abilities against both anaerobic and aerobic organisms. Two organisms, Clostridia and Bacteroides (both anaerobes) are specifically inhibited under high oxygen conditions. Of further benefit, the delivery of oxygen via hyperbaric conditions increases the tissue tensions to the infected areas more rapidly than to the surrounding healthy tissue. Korhonen et al, in studying the effects of such therapies in the treatment of patients with necrotizing fasciitis, speculated that this oxygen tension enhancement in infected areas was the result of improved microcirculation or decreased oxygen utilization. Further investigation will hopefully elucidate the benefits and etiology of this observation.

    It appears as the effects of HBO and antibiotics are additive in treating infections. In a study utilizing rats as a model of chronic osteomyelitis, Mendel et al noted that although antibiotics alone were more effective in treating infections than HBO therapy alone, when used together, a significantly greater number of Staph aureus colonies were killed.


    Normal total calcium values range from 8-10.2 mg/dL and ionized calcium ranges from 4-4.6 mg/dL or 1-1.3 mmol/L. Calcium is essential for bone formation and neuromuscular function. 99% of body calcium is in bone and the remaining 1% is in the ECF. Nearly 50% of serum calcium is ionized (free), whereas the remainder is complexed, primarily to albumin. Changes in albumin alter total calcium concentration without affecting the clinically relevant ionized calciums. If serum albumin is abnormal, clinical decisions should be based on ionized calcium levels.

    ANESTHETIC primary concerns include HTN, QT shortening, volume depletion and renal dysfunction. Depression of intraventricular conduction, PVC and VFIB are possible. Management should involve maintenance of hydration and urine output. The EKG is useful to detect conduction defects with prolonged PR, short QT intervals and widening of the QRS complex. Patients who have muscle weakness should receive decreased doses of nondepolarizing muscle relaxants.

    Hypercalcemia is most commonly diagnosed in asymptomatic patients, whereas previously, clinical features were the earliest manifestation.

    SYMPTOMS Hypercalcemia can produce any of a number of symptoms, the most prominent involving the renal, skeletal, neuromuscular and GI systems – anorexia, vomiting, constipation, polyuria, polydipsia, lethargy, confusion, formation of renal calculi, pancreatitis, bone pain and psychiatric abnormalities. Free intracellular calcium initiates and regulates muscle contraction, release of neurotransmitters, secretion of hormones, enzyme action and energy metabolism.

    Nephrolithiasis occurs in 60-70% of patients with hyperparathyroidism. Sustained hypercalcemia can result in tubular and glomerular disorders, including proximal (type II) renal tubular acidosis. Polyuria and polydipsia are common complaints.

    DIFFERENTIAL More than 90% of all cases are due to primary hyperparathyroidism or malignancy. Other causes of hypercalcemia are uncommon (sarcoidosis, vitamin D toxicity, hyperthyroidism, lithium, milk alkali syndrome and immobilization) and are usually clinically evident. Thiazide diuretics cause persistent hypercalcemia in patients with increased bone turnover (mild primary hyperparathyroidism). Familial hypocalciuric hypercalcemia is a rare, autosomal dominant disorder characterized by asymptomatic hypercalcemia from childhood and a family history of hypercalcemia.

    THERAPY essentially involves diuresis and administration of normal saline to dilute plasma calcium. These primary treatments are also useful because sodium inhibits the renal reabsorption of calcium. Additional therapies include bisphosphonates, calcitonin, ambulation and treatment of the underlying condition. Certain conditions, including numerous cancer-related hypercalcemias, can be treated with calcium-lowering agents such as mithramycin and glucocorticoids.


    CARDIOVASCULAR Hypercapnia appears to cause direct depression of both the cardiac muscle and vascular smooth muscle tone BUT simultaneously results in stimulation of the sympathetic adrenal system which generally compensates for the primary cardiovascular depression.

    Even in patients under halothane anesthesia, plasma catecholamine levels may increase in the presence of hypercapnia. Thus, hypercapnia, like hypoxemia, may cause increased myocardial O2 demand (tachycardia, EARLY hypertension) and decreased myocardial O2 supply (tachycardia, LATE hypotension.)

    Hypercapnia is a potent pulmonary vasoconstrictor even after inhalation of 3% isoflurane for 5 minutes. It is ONLY in the lungs that carbon dioxide causes DIRECT vasoconstriction.

    Hypercapnia during GA (especially with halothane) may result in ventricular arrhythmias. This was commonly seen in the spontaneously breathing patient under halothane anesthesia.

    RESPIRATORY The maximum stimulant respiratory effect is attained by a PaCO2 of about 100 mmHg. With higher PaCO2, stimulation is reduced and at very high levels respiration is depressed and later ceases alltogether.

    Anesthetic agents tend to decrease the slope of the PCO2-ventilation response curve. Opioids will decrease the slope AND shift it to the right. Doxapram will shift the curve to the left and once was used as a respiratory stimulant.

    In patients with ventilatory failure, CO2 NARCOSIS occurs when the PaCO2 rises above 90-120 mmHg.

    Alveolar hypercapnia (generally over 60 mmHg) displaces alveolar O2 thus resulting in hypoxemia. This is the primary failure during apneic oxygenation with a patent airway.

    The medullary chemoreceptors are actually responsive only to hydrogen ion and indirectly to CO2.

    Hypercapnia and acidosis shifts the oxyhemoglobin curve to the right (the BOHR effect), facilitating tissue oxygenation. It is for this reason that the patient with metabolic acidosis should not be mechanically hyperventilated for compensation.

    CNS Carbon dioxide concentrations of 30% (PaCO2 over 200 mmHg) is sufficient for the production of anesthesia BUT at this concentration the hypercapnia is associated with total and reversible flattening of the EEG. Much lower levels of hypercarbia will often result in seizures.

    Cerebral blood flow varies directly with PaCO2. CBF INCREASES 1-2 mL/100g/min (or 2-4%) for each 1 mmHg increase in PaCO2. Therefore, hypercapnia could result in increased intracranial pressure in the presence of a space-occupying lesion, intracerebral bleed or trauma.

    ELECTROLYTES Hypercapnia is accompanied by a leakage of potassium from the cells into the plasma. Because plasma potassium levels take an appreciable time to return to normal, repeated bouts of hypercapnia at short intervals result in a stepwise rise in plasma POTASSIUM.

    REMEMBER that hypercarbia decreases pulmonary flow but increases coronary and cerebral blood flow.


    This NON-ANION GAP acidosis associated with normal saline infusions (high chloride load) was once referred to as dilutional acidosis and is often seen following major operations such as hepatobiliary or pancreatic surgery or spinal fusions. The acidosis has also been observed in routine fluid resuscitations for dehydration and ketoacidosis.

    Studies demonstrate large saline infusions lead to decreases in serum bicarbonate, decreases in serum proteins, decreases in anion gaps and increases in chloride concentrations. The ANION GAP is most useful for differentiating anion gap acidoses (ketoacidosis, lactic acidosis, uremic acidosis) from the non-anion gap acidosis as seen with hyperchlormia.

    Previous explanations in support of the dilutional acidosis were based on the possibility that hypervolemia and increased renal perfusion led to inability of the proximal tubules to handle HCO3 subsequently leading to bicarbonaturia.

    STEWART’S three major influences of pH include (1) pCO2, (2) nonvolatile weak plasma acids albumin and inorganic phosphates, and (3) the STRONG ION DIFFERENCE. The SID is the difference between strong cations (sodium and potassium) and strong anions (chloride and lactate). A normal SID is about 40 and a decrease in the SID leads to acidosis while an increase in the SID leads to alkalosis. Bicarbonate concentration is a dependent variable according to contemporary theory.

    Anesthesiologists commonly interpret acidosis to represent hypovolemia, tissue hypoperfusion and lactic acidosis. The practice of chasing acidosis with fluids may actually worsen the condition. Metabolic acidosis may impair cardiovascular function leading to hemodynamic instability.

    Mild symptoms of metabolic acidosis may be seen in normal patients given 50 mL/kg of NS. Early symptoms include confusion, headache, nausea and abdominal pain. Hyperchloremia alone may produce vasoconstriction, decreased renal blood flow, GFR and urine output.

    Prevention is more effective than treatment though furosemide may be considered in some cases for its chlorouretic effects.



    ANTIPHOSPHOLIPID is common amongst patients with PVD.

    ANTITHROMBIN III DEFICIENCY is best assessed by activity level. Heparin itself may decrease AT3 levels.



    LUPUS ANTICOAGULANTS may predispose to thrombosis and ironically increase PTT. The PTT mix may partially but not fully correct as with factor deficiencies.


    PROTEIN C DEFICIENCY is best assessed by activity level. Heparin and coumadin may depress activity levels.

    PROTEIN S DEFICIENCY is best assessed by antigen level.




    EFFECTS of hyperglycemia include: (1) delayed gastric emptying, (2) DIURESIS and hypokalemia, (3) HYPOPHOSPHATEMIA, (4) delayed wound healing, (5) impaired WBC function, (6) exacerbation of ISCHEMIC damage to the brain, spinal cord and kidneys, (7) cognitive dysfunction and dramatically increased MORTALITY after CABG and (8) greater incidence of postoperative PE.

    For every 100 mg/dL excess of glucose, the serum sodium will decrease by approximately 1.6 mEq/dL. This is not the pseudohyponatremia that is seen with high triglyceride levels.


    Indications for TX include prolonged PR intervals with eventual loss of the P wave, prolonged QRS complex, ST segment elevation and peaking of the T waves. The rhythm may degenerate into sinusoidal patterns, VT or VFIB. Conduction changes usually take place with potassium greater than 6.5 mEq/L but may develop earlier if levels increase abruptly.

    ANESTHESIA Most recommend an upper limit of 5.6 mEq/L prior to elective surgery. Urgent need for SCh or blood transfusion could otherwise push K to dangerous concentrations. In the presence of hyperkalemia, it is wise to AVOID HYPERCARBIA and LIDOCAINE injection. Cardiac depressant effects of LIDOCAINE are markedly increased in the presence of hyperkalemia.

    ETILOGIES include spurious findings (hemolysis, thrombocytosis or leukocytosis) but more importantly

    (1) REDISTRIBUTION from acidosis including ketoacidosis, ß blockade, SCh, ACEI, NSAIDS, prolonged fasting over 16 hours, CYA, THAM, TMP-SMX, pentamidine, familial periodic paralysis or digoxin toxicity, (2) INCREASED INTAKE from IV or PO administration, rhabdomyolysis, tumor lysis, transfused organs & stored blood transfusions, (3) IMPAIRED RENAL FUNCTION indicated by GFR less than 20 mL/min, aldosterone deficiency or tubular hyperkalemia

    TX includes calcium chloride (7-14 mg/kg or 1000 mg over three minutes), sodium bicarbonate (0.5-1 mEq/kg or one 50 mEq ampule), Kayexelate (50 grams PR) and glucose with insulin [one 50 mL amp of D50 (or 25 grams) with 10-15 units of regular insulin IV]. Do not give bicarbonate after calcium chloride. Nebulized ALBUTEROL may also be used for quick effect.

    Calcium CHLORIDE will restore contractility within 1-2 minutes though effects may last for only 15-20 minutes. Calcium GLUCONATE (although less potent and dosed at 10-50 mg/kg) has been advocated by some as this preparation induces more potassium secretion by the renal tubules. Bicarbonate peak effects occur within 5 minutes and the effects of insulin are not maximized (lowering potassium by 1.5-2.5 mEq/L) until 30 minutes after administration.

    It is important to NOT use CALCIUM in TX of hyperkalemia secondary to DIGITALIS toxicity as acute hypercalcemia may precipitate or exacerbate digitalis toxicity.


    Serum magnesium has a normal range of 1.6-2.2 mg/dL or 0.8-1.2 mmol/L. Magnesium homeostasis is regulated by renal and GI mechanisms. Hypermagnesemia is usually iatrogenic and is frequently seen in conjunction with renal insufficiency.


    1) renal insufficiency with creatinine clearance less than 30 mL/minute
    2) nonrenal etiology with excessive use of magnesium cathartics worsened with renal failure or simple iatrogenic overtreatment
    3) less common causes of mild elevation include hyperparathyroidism, Addison’s disease, hypocalciuric hypercalcemia and lithium therapy

    Hypermagnesemia is commonly caused by overzealous replacement of magnesium, inadequate adjustment of magnesium dosage for renal insufficiency and overuse of magnesium-containing cathartics.


    1) CV symptoms of hypermagnesemia with serum levels close to 10 mEq/L include delayed interventricular conduction, first-degree heart block and prolongation of the QT interval. Hypotension can be seen with levels as low as 3 mEq/L. Low grade heart block progressing to complete heart block and asystole occurs at levels greater than 12.5 mEq/L.
    2) NEUROMUSCULAR symptoms include hyporeflexia at a magnesium level over 4 mEq/L or 2 mMol/L. An early sign of magnesium toxicity is diminution of deep tendon reflexes caused by neuromuscular blockade. Somnolence and coma occur at levels over 13 mEq/L or 6.5 mMol/L.
    3) RESPIRATORY depression occurs secondary to respiratory muscle paralysis.

    Hypermagnesemia should always be considered when these symptoms occur in patients with RENAL failure, in those receiving therapeutic magnesium and in laxative abuse.


    1) moderate hypermagnesemia (asymptomatic and CV STABLE patients) can be managed by simple elimination of intake and maintenance of renal magnesium clearance.
    2) SEVERE hypermagnesemia is treated with furosemide 20-40 mg IV. Saline diuresis should be initiated with 0.9% saline and infused to replace urine loss.
    3) with ECG abnormalities (peaked T waves, loss of P waves, or widened QRS complexes) or if respiratory depression is present, IV calcium gluconate should be given as 1-3 ampules (10% solution, 1 gm per 10 mL amp) added to saline infusate. Calcium gluconate can be infused to reverse acute CV toxicity or respiratory failure as 15 mg/kg over a four hour period.
    4) parenteral INSULIN and GLUCOSE can be given to shift magnesium into cells.

    DIALYSIS is necessary for patients with severe hypermagnesemia after stabilization of the ECG findings.


    DDX HYPOVOLEMIC hypernatremia is secondary to extrarenal losses (diarrhea, vomiting, fistulas, significant burns), renal losses (osmotic diuretics, diuretics, postobstructive diuresis, intrinsic renal disease) or adipsic hypernatremia is secondary to decreased thirst. This can be behavioral or rarely, secondary to damage to the hypothalamic thirst centers.

    HYPERVOLEMIC hypernatremia is secondary to hypertonic saline, sodium bicarbonate administration, accidental salt ingestion (infant formula error) or mineralocorticoid excess (Cushing syndrome).

    EUVOLEMIC hypernatremia is secondary to extrarenal losses (increased insensible loss as with hyperventilation), renal losses (central DI, nephrogenic DI). These patients appear euvolemic because most of the free water loss is from intracellular and interstitial spaces, with less than 10% occurring from the intravascular space. Typically, symptoms result if serum sodium is more than 160-170 mEq/L.

    CENTRAL DI DDX: head trauma, suprasellar or intrasellar tumors, granulomas (sarcoidosis, Wegener granulomatosis, TB, syphilis), histocytosis (eosinophilic granuloma), infectious (encephalitis, meningitis, Guillain-Barré syndrome), vascular (cerebral aneurysm, thrombosis, hemorrhage, Sheehan syndrome), congenital and transient DI of pregnancy.

    NEPHROGENIC DI (deficient renal response to ADH) DDX: advanced renal disease (interstitial disease), electrolyte disturbances (hypokalemia, hypercalcemia), systemic diseases (sickle cell disease, Sjögren syndrome, amyloidosis, Fanconi syndrome, sarcoidosis, renal tubular acidosis, light chain nephropathy), dietary disturbances (excessive water intake, decreased salt intake, decreased protein intake), drugs (lithium, demeclocycline, colchicine, vinblastine, amphotericin B, gentamicin, furosemide, angiographic dyes and osmotic diuretics).

    Miscellaneous causes include postobstructive diuresis, diuretic phase of ARF, osmotic diuresis and paroxysmal HTN.

    When hyponatremia is discovered in a patient, order urine osmolality and sodium levels. Check serum glucose level to ensure that osmotic diuresis has not occurred.
    Hypernatremia should not be corrected at a rate greater than 1 mEq/L per hour. Using isotonic sodium chloride solution, stabilize hypovolemic patients who have unstable vital signs before correcting free water deficits because hypotonic fluids quickly leave the intravascular space and do not help to correct hemodynamics. Once stabilization has occurred, free water deficits can be replaced either orally or IV.

    Euvolemic patients can be treated with hypotonic fluids, either orally or intravenously (D5W, quarter or half isotonic NS solution) to correct free fluid deficits.

    Hypervolemic patients require removal of excess sodium, which can be accomplished by a combination of diuretics and D5W infusion. Patients with ARF may require dialysis.


    Primary hyperparathyroidism most commonly begins in the third to fifth decades of life and occurs two to three times more frequently in women than in men. Primary hyperparathyroidism usually results from enlargement of a single gland, commonly an adenoma and very rarely a carcinoma. Hypercalcemia almost always occurs.

    Many of the prominent symptoms of hyperparathyroidism are a result of the hypercalcemia that accompanies it. Regardless of the cause, hypercalcemia can produce any of a number of symptoms, the most prominent involving the renal, skeletal, neuromuscular and GI systems – anorexia, vomiting, constipation, polyuria, polydipsia, lethargy, confusion, formation of renal calculi, pancreatitis, bone pain and psychiatric abnormalities. Free intracellular calcium initiates and regulates muscle contraction, release of neurotransmitters, secretion of hormones, enzyme action and energy metabolism.

    Nephrolithiasis occurs in 60-70 percent of patients with hyperparathyroidism. Sustained hypercalcemia can result in tubular and glomerular disorders, including proximal (type II) renal tubular acidosis. Polyuria and polydipsia are common complaints.

    Skeletal disorders related to hyperparathyroidism are osteitis fibrosa cystica and simple diffuse osteopenia. The rate of bone turnover is five times higher for patients with hyperparathyroidism than for normal controls. Patients may have a history of frequent fractures or complain of bone pain, the latter especially in the anterior margin of the tibia.

    Because free intracellular calcium initiates or regulates muscle contraction, neurotransmitter release, hormone secretion, enzyme action, and energy metabolism, abnormalities in these end organs are often symptoms of hyperparathyroidism. Patients may experience profound muscle weakness, especially in proximal muscle groups, as well as muscle atrophy. Depression, psychomotor retardation, and memory impairment may occur. Lethargy and confusion are frequent complaints.

    In emergency situations, vigorous expansion of intravascular volume usually reduces serum calcium to a safe level (less than 14 mg/dL). Administration of furosemide is also often helpful in these situations. Phosphate should be given to correct hypophosphatemia, which decreases calcium uptake into bone, increases calcium and stimulates breakdown of bone. Hydration and diuresis, accompanied by phosphate repletion, suffice in the management of most hypercalcemic patients. If additional intervention is needed, glucocorticoids, mithramycin, or calcitonin may be given. Corticosteroids inhibit further gastrointestinal absorption of calcium. Mithramycin lowers calcium levels by approximately 2 mg/dL in 36-48 hours through its effect on osteoclasts. Its toxic effects include thrombocytopenia, decreased levels of clotting factors, hepatotoxicity, azotemia, proteinuria, hypocalcemia, hypophosphatemia, and hypokalemia. Most of these side effects can be reversed simply by discontinuation of the drug. Consultation with an endocrinologist or oncologist is advisable before mithramycin is given, because it has a narrow therapeutic-to-toxic ratio.

    Calcitonin lowers serum calcium levels through direct inhibition of bone resorption. It can decrease serum calcium levels within minutes after its intravenous administration. Calcitonin is less effective than phosphate or mithramycin, however, for patients with hypercalcemia caused by hyperparathyroidism. Side effects include urticaria and nausea.

    It is especially important to know whether hypercalcemia has been chronic, because serious cardiac, renal, or CNS abnormalities may have resulted.


    SYMPTOMS include hypotension, bradycardia, arrhythmias, bronchospasm, apnea, laryngeal spasm, tetany, seizures, weakness, psychosis and confusion.


    1) exogenous phosphate from enemas, laxatives, diphosphonates, vitamin D excess
    2) endocrine disturbances including hypoparathyroidism (hypocalcemia will cause hyperphosphatemia), acromegaly and PTH resistance
    3) excess phosphate production from rhabdomyolysis, sepsis, fulminant hepatic failure, severe hypothermia, hemolysis, acidosis, renal failure, chemotherapy and tumor lysis syndrome.

    LABS to obtain include chemistries calcium, parathyroid hormone, 24 hour urine phosphate and creatinine.

    THERAPY includes correction of hypocalcemia, restriction of dietary phosphate and saline diuresis.

    MODERATE hyperphosphatemia

    1) aluminum hydroxide (Amphojel)
    2) aluminum carbonate (Basaljel)
    3) calcium carbonate (Oscal)

    Aluminum agents will bind to intestinal phosphate and decreases absorption. Keep calcium-phosphate product at less than 70 and start calcium only if phosphate is less than 5.5.

    SEVERE hyperphosphatemia

    1) volume expansion with NS 1 L over if the patient is not azotemic
    2) dialysis is recommended for patients with renal failure


    light anesthesia
    patient anxiety
    prolonged tourniquet use
    essential HTN
    renovascular disease
    autonomic hyperreflexia
    indigo carmine dye
    clonidine, Aldomet, ß-blockers
    TCA or MAOI with ephedrine


    labetalol gtts
    esmolol gtts


    ACE INHIBITORS are effective and well-tolerated. They are less effective in African Americans unless combined with thiazide diuretics. They do not effect lipids or glucose toloerance. They reduce mortality in those with CAD, prolong survival in those with CHF and preserve renal function in those with diabetes. They are superior to CCB in preventing progression to renal failure in AA with hypertensive nephropathy. They are associated with postoperative renal dysfunction.

    ANGIOTENSIN II RECEPTOR ANTAGONISTS (losartan or Cozaar, irbesartan) are effective in lowering BP without causing cough.

    ß-BLOCKERS are effective but (like ACE inhibitors) may be less effective in African Americans. ß-blockers alone may be less effective than diuretic alone for treatment of the elderly (see ß-blockers under separate listing).

    DIURETICS have been shown to decrease mortality in those with HTN. Thiazides reduce the incidence of stroke and CV events in elderly with isolated systolic HTN. Loop diuretics are more effective in patients with renal insufficiency.

    CALCIUM CHANNEL BLOCKERS cause vasodilation and the cardiac response is variable. Verapamil and diltiazem may slow HR and can affect AV conduction and should therefore be used with caution in patients on beta-blockers.

    CENTRAL ALPHA-ADRENERGIC AGONISTS (clonidine, methyldopa) do not inhibit reflex responses as completely as sympatholytic drugs that act peripherally. They frequently cause sedation, dry mouth and depression.

    ALPHA-ADRENERGIC BLOCKERS (prazosin, terazosin) cause less tachycardia than vasodilators but more frequent postural hypotension. There use is associated with an increased incidence of CHF when compared to diuretics. These drugs may provide symptomatic relief for prostatism in men, but may cause stress incontinence in women.

    DIRECT VASODILATORS frequently produce reflex tachycardia but rarely cause orthostatic hypotension. They should be given with a beta-blocker or a centrally-acting drug to minimize a reflex increase in HR and a loop diuretic to avoid sodium and water retention. Hydralzine (over 200 mg) is associated with a lupus-like reaction. Minoxidil should be reserved for refractory cases secondary to hirsuitism and fluid retention.

    PERIPHERAL ADRENERGIC NEURON ANTAGONISTS (reserpine) can cause depression. Guanadrel decreased CO and may lower SBP more than DBP – postural and exertional hypotension occur commonly and is aggravated by heat and alcohol.

    The best tolerated drugs are the diuretics and angiotensin II receptor antagonists. ß-blockers, ACE-I and CCB generally have mild adverse effects. Many believe that CCB should be reserved for those that can not tolerate or do not respond to other agents. From the Medical Letter March 2001.


    Approximately 20% of all Americans are hypertensive as defined by the JNC as pressures greater than 140/90 mmHg. Only 20% of these patients are well controlled.

    Less than 10% of all hypertensive patients have secondary HTN requiring thorough evaluation. Risk factors include resistance to treatment and development at either an early or late age.

    ANESTHESIA Patients that are particularly labile, have pressures over 180/110 mmHg and those with suspected cerebral, renal or coronary disease require thorough evaluation prior to elective surgery.

    The 1979 study by Goldman revealed increased risk for lability, arrhythmia, MI, CHF and renal failure in those presenting for elective noncardiac surgery with DBP over 110 mmHg. One older study (1970) in England demonstrated greater risk for CHF, MI and death if elective surgery proceded with a DBP over 110 mmHg.

    Nevertheless, neither esmolol nor labetalol were available at the time of these studies and perioperative hypertension is simply easier to treat in the twenty first century.

    Although it is indisbutable that patients with preoperative hypertension will be more labile and may have an increased incidence of intraoperative and postoperative ischemia, it is unclear if there is much increase in morbidity or mortatlity in comparing these patients with others who are chronically hypertensive. The most recent guidelines by the American College of Cardiology and the AHA does advise a delay for elective procedures in those presenting with preoperative SBP over 180 and DBP over 110 mmHg.

    Also of interest is the 2002 JAMA editorial by Fleisher on preoperative evaluation of the patient with hypertension.


    A HYPERTENSIVE CRISIS is defined by a diastolic pressure over 130 mmHg. Possible etiologies include

    chronic essential HTN
    renovascular HTN
    sudden withdrawal of HTN therapy
    cocaine, LSD, amphetamine, TCA
    head injury
    Guillain Barre syndrome
    spinal cord injury
    collagen vascular disease
    thoracic aorta dissection

    FENOLDOPAM dosing for HTN is at 0.1-0.17 mcg/kg/min and may be titrated every 15 minutes to up to 1.6 mcg/kg/min (mix 10 mg in 250 ml D5W for 40 mcg/mL). This is now the drug of choice for hypertensive crisis as it does not increase CBF. Onset is within 5-15 minites and duration of action is 1-4 hours.

    LABETALOL (Normodyne, Trandate) also may be useful at 20-80 mg IV bolus, repeated as needed (maximum 300 mg) or 2 mg/min IV infusion. The onset of action is within 2-10 minutes and duration of action is 2-4 hours.

    HYDRALAZINE (Apresoline) at 10-20 mg IV or IM bolus may be repeated every 4-6 hours as needed (maximum 40 mg). The onset of action is within 10-20 minutes and duration of action is 3-8 hours.

    NITROPRUSSIDE is used most often because its onset of action is nearly instantaneous and its dose can be carefully adjusted for a smooth reduction in blood pressure. However, nitroprusside tends to cause cyanide or thiocyanate toxicity when it is given for more than a few days, particularly in patients with renal or hepatic insufficiency. Nitroprusside also has the potential to increase intracranial pressure, which may limit its usefulness in patients with possible or known central nervous system complications. FENOLDOPAM (Corlopam) is approved by the FDA for treatment of hypertensive crisis. This selective dopamine receptor agonist causes peripheral vasodilatation by stimulating DA-1 receptors. It increases renal blood flow and GFR rate, which often improves renal function in patients who present with renal insufficiency. Fenoldopam has a few minor side effects, such as HA, dizziness and flushing, but it tends to increase intraocular pressure and thus should be used with caution in patients with glaucoma. Patients should be closely monitored for dose-related tachycardia, which tends to diminish over time. Fenoldopam may also cause significant HYPOKALEMIA. The efficacy of fenoldopam appears to be similar to that of nitroprusside in treatment of severe hypertension.

    Hypertensive emergencies can be treated with IV vasodilators, such as diazoxide (Hyperstat), which is rarely used, hydralazine (Apresoline), enalapril (Vasotec) and nicardipine (Cardene). IV adrenergic inhibitors, such as phentolamine (Regitine), esmolol (Brevibloc) and labetalol can also be effective. Drug selection data are limited and solid guidelines are not yet available because outcomes with specific agents have not been compared. Currently, drug selection is primarily determined by rapidity of action, ease of administration and the potential for side effects.


    The DDX includes (1) inflammation usually related to infection and possibly sepsis through the endogenous pyrogens interleukin-1 and TNF-alpha, (2) MALIGNANT HYPERTHERMIA, (3) hypermetabolic states including thyrotoxicosis and pheochromocytoma, (4) injury to the hypothalamic regulatory center from anoxia, edema, trauma or tumor, (5) fat emboli syndrome concominantly with hypoxemia, tachypnea, confusion, petichiae, (6) neuroleptic malignant syndrome, (7) sympathomimietics including MAO inhibitors, MDMA or ECSTASY, amphetamines, cocaine and TCA leading to hypermetabolic states, and (8) anticholinergics agents which may promote unopposed sympathetic vasoconstriction and suppress sweating.

    The EFFECTS of hyperthermia are numerous.

    Patients under GA will usually not sweat until core temperature is above 39 degrees.


    Major causes inckude GRAVES disease (70-80%), toxic thyroid adenoma and toxic multinodular goiter. SIGNS & SYMPTOMS include goiter, tachycardia, anxiety, tremor, heat intoloerance, fatigue, weight loss, eye signs, weakness and AFIB.

    Routine THERAPY includes the antithyroid mediactions (PTU or propylthiouracil, Tapazole or methimazole and propranalol), subtotal thyroidectomy and radioactive iodine which is the treatment of choice for those older than 40.

    PTU generally takes one week before clinical response is seen but six weeks before most patients are actually euthyroid. The action of methimazole is similar to that of PTU but the drug is at least 10 times as potent. Methimazole may be less consistent in action.

    The THYROID STORM may occur in the operative or early postoperative period. Manifestations include hyperthermia, tachycardia, CHF, dehydration and shock. Treatment includes cooled NS administration and continuous ESMOLOL infusions which prohibits peripheral T4 to T3 conversion. When hypotension is persistent, CORTISOL 100-200 mg IV may be considered.

    ANESTHETIC MANAGEMENT of those with hyperthyroidism includes postponement of elective surgery until the patient is euthyroid, avoiding anticholinergics drugs with premedication and evaluating upper airway for goiterous obstruction.

    Patients may be induced with STP and neuromuscular blockers that are preferably void of CV effects. HTN may be exaggerated in response to indirect acting vasopressors.

    The postoperative period following thyroidectomy may be complicated by airway compromise secondary to recurrent laryngeal nerve damage (incidence only 1:30K), obstruction by tracheomalacia or hematoma and laryngospasm secondary to hypocalcemia. CALCIUM levels may fall to symptomatic levels as quickly as 18 HOURS postoperatively but typically will not reach their nadir until 2-3 days postoperatively.


    When corrective therapy for hyponatremia requires the use of isotonic or hypertonic saline, replacement may be guided by calculation of the sodium deficit. Normal TBW (in liters) is 60% of the lean body weight in men and 50% of the lean body weight in women. Sodium DEFICIT (in mEq) is calculated:

    TBW (130 – current plasma Na)

    Sodium chloride 3% contains 513 mEq of sodium per liter (or 3.3 times the concentration of isotonic saline). Infusions should be limited by raising the plasma sodium NO FASTER THAN 0.5 mEq per liter per hour.

    A deficit of 10 mEq per liter should be corrected over twenty hours and the proper amount of sodium should be infused over this time period.

    Hypertonic saline solutions have been used for decades for the treatment of symptomatic hyponatremia. In recent years there has been enthusiasm for treating victims of acute volume depletion (usually hemorrhagic shock or burns). The solution most commonly used in this setting is 7.5% SALINE versus 3%, which is very hypertonic at 2400 mOsm/L. The usual dose for initial resuscitation is 4 mL/kg given as a rapid infusion or bolus. Some authors have found that 7.5% NaCl plus dextran 70 solutions are even more effective in restoring plasma volume.

    In laboratory and clinical investigations, HS expands plasma volume effectively and rapidly. In emergency room patients given 250 mL of 7.5% NaCl with or without 6% dextran 70, estimated plasma volume increased 25%, compared to 8% when isotonic saline was given. MAP was higher in those receiving hypertonic solutions and less total fluid and blood was required to stabilize vital signs in these groups. Similar improvements have been noted in septic patients who presumably have functional hypovolemia. The volume expansion that occurs with HS is thought to be due to movement of fluid from the intracellular to the extracellular compartment, since sodium is primarily an extracellular ion. This is in contrast to the effect of colloids, which may draw in water from the interstitial space to the intravascular space.


    Normal total calcium values range from 8-10 mg/dL and ionized calcium ranges from 4-4.6 mg/dL or 1-1.3 mmol/L.

    Plasma calcium is present in three forms: 50% is bound to proteins (80% albumin), 10% is chelated to anions (sulfates and phosphates) and the remainder is in the free form. The ionized fraction of calcium is the active form which is not affected by hypoalbuminemia.

    Acidosis decreases the binding of calcium to albumin thus increasing the level of ionized calcium. Alkalosis has the opposite effect (remember this condition in the hyperventilating patient).

    DDX for ionized hypocalcemia includes alkalosis, transfusion, CPB, medications (aminoglycosides, cimetidine, heparin, theophylline), fat embolism, magnesium depletion, pancreatitis, renal insufficiency and sepsis.

    Magnesium depletion promotes hypocalcemia by inhibiting parathormone secretion and reducing end-organ responsiveness to parathormone. Calcium is usually restored by magnesium replacement.

    PRESENTATION is related to enhanced cardiac and neuromuscular exitability and reduced contractile force in cardiac and smooth muscle. Neuromuscular symptoms include perioral numbness hyperreflexia, seizures and tetany. Chvostek’s sign (facial) is nonspecific (present in 25% of normal adults) and Trousseau’s sign (carpopedal spasm with an occlusive BP cuff) is insensitive (absent in 30%).

    CV effects include hypotension, decreased cardiac output and ventricular ectopy.

    THERAPY is directed at the underlying etilogy and calcium replacement. Calcium chloride has three times the elemental calcium contained in the gluconate formulation. Bolus doses should be followed by infusion of 1-2 mg elemental calcium per kg per hour.

    CALCIUM CHLORIDE 10% contains 27 mg (1.36 mEq) of elemental calcium per mL and is bolused in increments of 5-10 mL. Infusions range from 2-6 mL per hour for a 70 kg adult which extrapolates to 3-10 mg/kg/hour.

    CALCIUM GLUCONATE 10% contains 9 mg (0.46 mEq) of elemental calcium per mL and is bolused in increments of 22 mL (possibly in 100 mL of NS).


    HYPOCARBIA decreases CO, decreases coronary, cerebral and spinal cord flow, may alter drug action (by altering serum pH), decreases ionized CALCIUM and POTASSIUM, increases the incidence of JUNCTIONAL rhythms, shifts the oxygen dissociation curve to the left (increasing oxygen affinity), may increase oxygen consumption and may inhibit HPV.

    Hypocarbia through alkalosis at the medullary chemoreceptors will decrease ventilatory effort.

    It is unique to the coronary and cerebral blood flow to DECREASE with hyperventilation and hypocarbia. This may be beneficial to the head trauma patient but detrimental to the patient with myocardial ischemia that is hyperventilating. Contrast this with metabolic alkalosis which may increase cerebral flow secondary to responsive hypercapnia.

    There is inhibition of HPV in the pulmonary beds (thus vasodilation) and in general there is a DECREASE in SYMPATHETIC tone.


    Alkalosis secondary to hypochloremia is commonly secondary to renal and GI losses. Hypocloremia may also be secondary to compensation for chronic hypercapnia, lactic acidosis and DKA.



    Consequences of hypoglycemia primarily relate to neurologic injury. The absolute value associated with injury is not clear. Hypoglycemia is defined as less than 50 mg/dL in infants and older children and 40 mg/dL in premature and term neonates.

    BG between 40 and 80 or a rapid rate of fall may result in confusion, ataxia, dizziness, lethargy, weakness, HA and focal deficits. BG between 30-40 may result in LOC and seizure but levels this low usually must be sustained for 20-30 minutes.

    TREATMENT for both the adult and the pediatric patient is dextrose 0.5-1 g/kg IV. Maintenance requirements for the pediatric patient range from 8-14 mg/kg/minute. An ampule of D50 contains 50 mL or 25 grams of dextrose. A 1000 mL of D5 contains 50 grams of dextrose.


    REDISTRIBUTION from the intracellular shift of potassium by insulin, ß2 agonist drugs, catecholamine release, hypothermia, thyrotoxic periodic paralysis and ALKALOSIS.

    NON-RENAL (1) GI loss through diarrhea, laxative abuse, villous adenoma, biliary drainage, enteric fistula, clay ingestion, resin ingestion or NG suction, (2) sweating, prolonged low intake, HD and peritoneal dialysis

    RENAL LOSS divided into HTN and NORMOTENSIVE categories

    HYPERTENSIVE (1) high renin: malignant HTN, renal artery stenosis, renin-producing tumors, (2) low renin and high aldosterone: primary hyperaldosteronism (adenoma or hyperplasia), (3) low renin and low aldosterone: CAH (11 or 17-OHase deficiency), Cushings syndrome or disease, exogenous mineralocorticoids (Florinef, licorice, chewing tobacco), Liddle’s syndrome

    NORMOTENSIVE (1) metabolic acidosis: RTA type I or II, (2) metabolic alkalosis and urine chloride less than 10 mEq/day with vomiting, (3) metabolic alkalosis and urine chloride greater than 10 mEq/day with Bartter’s syndrome, diuretics, magnesium depletion, normotensive hyperaldosteronism

    DRUGS associated with potassium loss include amphotericin B, ticarcillin, piperacillin and loop diuretics.

    EVALUATION 24-hour potassium excretion should be measured. If over 20 mEq per day, then excessive urinary K loss is the cause. If less than 20 mEq per day, low K intake or non-renal K loss is the cause.

    In patients with excess renal loss and HTN, plasma renin and aldosterone should be measured to differentiate adrenal from nonadrenal causes of hyperaldosteronism. If HTN is absent and patient is acidotic, RTA should be considered. If HTN is absent and serum pH is normal to alkalotic, a high urine chloride (over 10 mEq/d) suggests hypokalemia secondary to diuretics or Bartter’s syndrome. A low urine chloride (less than 10 mEq/d) suggests vomiting as the etiology.


    HYPOKALEMIA is defined by a serum concentration less than 3.5 mEq/L. Almost 98% of total body K is intracellular and each 1 mEq/L decrease may reflect a total body deficit of 200-400 mEq. If serum concentration is over 2.6 mEq/L, there are no EKG changes and the patient is not on digitalis, then surgery may proceed. Patients may be more susceptible to ventricular dysrhythmias and postoperative AFIB or flutter. Hypokalemia also may be associated with perioperative weakness and HTN. HYPOCARBIA should be avoided in the presence of hypokalemia.

    Replace with KCl is used unless hypophosphatemia is present, where potassium phosphate is indicated. The maximal rate of K replacement is 30 mEq/hour or 0.5 mEq/kg/hour. The concentration of IV fluids should be 80 mEq/L or less if given via a peripheral vein. Constant EKG monitoring is mandatory.

    Common ETIOLOGIES include REDISTRIBUTION from the intracellular shift of potassium by insulin, ß2 agonists, catecholamine release, hypothermia, thyrotoxic periodic paralysis and ALKALOSIS.

    DRUGS associated with K loss include amphotericin, ticarcillin, piperacillin and loop diuretics.

    CARDIAC EFFECTS EKG effects include depressed ST, decreased T wave amplitude, U waves (best in V2-3) and a prolonged QT-U interval. Patients are more susceptible to digitalis toxicity. Patients may have orthostatic hypotension and impaired contractility.

    MUSCULOSKELETAL: WEAKNESS, hyporeflexia, restless legs and cramping can lead to paralysis. In severe cases, respiratory paralysis may occur. GI SXS: NV, constipation and ileus. RENAL: polyuria and concentrating defects.


    Normal magnesium levels are between 1.6-2.2 mg/dL. Most common etiologies of low Mg include malignancy, COPD and alcoholism.

    DECREASED INTAKE with protein calorie malnutrition, prolonged IV fluid and catabolic illness are common causes.

    GI LOSSES may result from prolonged NG suction, laxative abuse, pancreatitis, extensive small bowel resection, short bowel syndromes, biliary and bowel fistulas, enteropathies, cholestatic liver disease and malabsorption syndromes.

    RENAL LOSSES may occur secondary to RTA, GN, AIN or ATN. Renal loss may also be secondary to hyperthyroidism, hypercalcemia and hypophosphatemia. Agents that enhance magnesium renal excretion include alcohol, loop and thiazide diuretics, amphotericin B, aminoglycosides, cisplatin, pentamidine and colony stimulating factor therapy.

    ALTERATIONS in DISTRIBUTION include redistribution of circulating magnesium which occurs by intracellular shifts, sequestration, hungry bone syndrome or by acute administration of glucose, insulin or amino acids. Magnesium depletion occurs during severe pancreatitis, large quantities of IV fluids and pancreatitis-induced sequestration of magnesium.

    CARDIOVASCULAR manifestations include ventricular tachycardia (torsades de pointes), ventricular fibrillation, atrial fibrillation, multifocal atrial tachycardia, ventricular ectopic beats, hypertension, enhancement of digoxin-induced dysrhythmias and cardiomyopathies. Prolonged
    PR and QT intervals, ST segment depression, T wave inversions, wide QRS complexes and tall T waves may also occur.

    NEUROMUSCULAR findings (similar to those of hypocalcemia) may include positive Chvosteks and Trousseaus signs, tremors, myoclonic jerks, stridor, weakness, seizures and eventually coma.

    Concomitant ELECTROLYTE abnormalities of sodium, potassium, calcium or phosphate are common.

    EVALUATE when magnesium is less than 1.6 mg/dL (0.7-0.8 mMol/L). When secondary to renal loss, magnesium excretion exceeds 24 mg/day. Low urinary magnesium excretion (less than1 mMol/day) suggests magnesium deficiency due to decreased intake, nonrenal losses or redistribution of magnesium.

    ASYMTOMATIC deficiency may be treated through balanced diet, with oral magnesium supplements (0.36-0.46 mEq/kg/day) or 16-30 mEq/day in a TPN formulation. Magnesium oxide is better absorbed and less likely to cause diarrhea than magnesium sulfate.

    Magnesium oxide preparations include Mag-Ox 400 (240 mg elemental magnesium per 400 mg tablet), Uro-Mag (84 mg elemental magnesium per 400 mg tablet) and magnesium chloride (Slo-Mag) 64 mg/tab, 1-2 tabs bid.

    SYMPTOMATIC deficiency requires IV magnesium repletion with EKG and respiratory monitoring. Magnesium sulfate 1-6 gm of in 500 mL of D5W can be infused at 1 gm/hr. An additional 6-9 gm of MgSO4 should be provided as intermittent bolus therapy or by continuous infusion over the next 24 hours. Parenteral MgSO4 (4 mMol per gram) is more frequently used than Mg chloride.

    SEVERE magnesium deficiency may require additional therapy over a number of days because of slow repletion of cellular magnesium stores.

    Polymorphic VT or TDP is characterized by polymorphic VT with long QT intervals. Treatment consists of MgSO4 at 2-4 gm IV over 5-10 minutes followed by 8-12 gm infused over 24 hours. Pediatric patients should receive 50 mg/kg.


    iatrogenic fluid overload
    iatrogenic diuresis
    congestive heart failure
    renal or liver disease
    adrenal insufficiency
    cerebral salt wasting

    For every 100 mg/dL excess of glucose, the serum sodium will appear to decrease by 1.6 mEq/dL. This is not the pseudohyponatremia that is seen with high triglyceride levels.

    Most deficits should not be corrected more than 1-2 mEq/L/hour to prevent central pontine myelinolysis. Acute changes as with TURP syndrome may be treated more aggressively.

    See Unbound Medicine article on Palm for complete details.


    SYMPTOMS include CHF, weakness, tremor, ataxia, seizures, coma, respiratory failure, delayed weaning from ventilator, hemolysis and rhabdomyolysis.

    DDX includes (1) increased URINARY excretion by hyperparathyroidism, renal tubular defects or diuretics
    (2) decrease in GI absorption by malnutrition, malabsorption, phosphate binding minerals (aluminum antacids), (3) abnormal vitamin D metabolism or deficiency, familial hypophosphatemia or tumor associated hypercalcemia and (4) intracellular SHIFTS of phosphate with DKA, respiratory alkalosis, alcohol withdrawal and recovery from starvation.

    LABS to obtain include chemistries, LDH, albumin, PTH, urine electrolytes and 24 hour phosphate and creatinine excretion.

    DIAGNOSTIC APPROACH by 24 hr urine excretion: (1) if 24 hour urine phosphate is less than 100 mg/day, causes include GI losses (emesis, diarrhea, NG suction, phosphate binders), vitamin D deficit, refeeding, recovery from burns, alkalosis, alcoholism and DKA
    (2) if 24 hour urine phosphate is over 100 mg/day, causes include renal loss, hyperparathyroidism, hypomagnesemia, hypokalemia, acidosis, diuresis, renal tubular defects and vitamin D deficiency

    TX for PO4 1.3-2.4 mg/dL

    1) Na or KPO4 10 mmols IV over four hours
    2) Nutra-Phos 2 capsules PO bid-tid (250 mg elemental phosphorus per tab, 7 mEq Na and 7 mEq K per tab)
    3) Phospho-Soda (129 mg P, 4.8 mEq Na/mL) 5 mL PO bid-tid

    TX for PO4 less than 1.3 mg/dL

    1) Na or KPO4 20 mmols IV over six hours
    2) add KPO4 to IVF in place of KCl (max 80 mEq/L infused at 100-150 mL/h). Max IV dose 7.5 mg PO4 per kg over 6-8 hours or 2.5-5 mg elemental phosphorus/kg IV over 6-8 hours.

    KPO4 and NaPO4 contain 3 mM or 93 mg phosphate per mL and 4 mEq Na or K per mL. Creatinine should be less than 2 mg/dL prior to phosphorus replacement. Doses should be reduced by 25-50% if hypercalcemia is present.

    fluid overload
    ischemia induced
    rate induced
    too fast with stenosis
    too slow with incompetence
    loss of atrial kick

    secondary to bleeding
    fluid shifts
    functional hypovolemia
    vasoplegia with ARB et al
    regional blockade or SNS blockade

    ANESTHESIA overdose
    ADDISONS physiology

    pulmonary embolism
    tension pneumothorax
    venous air embolus
    cardiac tamponade
    hypertrophic cardiomyopathy


    A reasonable response to hypotension in the OR may include simultaneously turning down any volatile agent while increasing oxygen concentration, bolusing a vasopressor, cycling the BP cuff while palpating for a pulse and verifying the position of the transducer if an intraarterial catheter is in place.



    Deliberate hypothermia is used to protect against tissue ischemia. It is usually utilized during cardiac and neurosurgery but is also useful for optimal recovery following arrest. GA itself decreases the thermoregulatory threshold by approximately 2.5 degrees.

    METABOLISM Whole body metabolic rate is decreased by approximately 8% per degree Celsius, which equates to about half the normal rate at 28 degrees. Oxygen demand is concurrently diminished along with O2 consumption, which permits aerobic metabolism to continue and toxic waste production of lactate and superoxide radicals to decline.

    CNS An autoregulatory increase in cerebrovascular resistance occurs with hypothermia which decreases CBF. The decrease in CBF is proportional to the decline in metabolic rate such that the arteriovenous PO2 difference remains constant and venous lactate is not increased.

    At around 33 degrees, cerebral function declines with LOC at 28 degrees. Near temperatures of 26 degrees, nerve conduction decreases with an increase in peripheral muscle tone. EEG slowing occurs and becomes flat at 20 degrees. MAC is decreased and emergences are prolonged by hypothermia.

    At central temperatures above 33 degrees, SSEPS and auditory evoked potentials are not significantly affected. As temperature declines, increased latency occurs in SSEPS.

    CV Decreases in HR, CO and BP occur with hypothermia but initial responses may be limited to an actual increase in SVR. Contractility is increased and SV is maintained. EKG changes include sinus bradycardia, widened QRS and prolonged PR interval. Many leads may show classic OSBORN WAVES or J WAVES seen at the junction of the QRS complex and the ST segment. Below 28 degrees, ventricular irritability increases. Fibrillation usually happens between 25-30 degrees.

    RESPIRATORY The ventilatory CO2 response is minimally affected by hypothermia. At temperatures less than 33 degrees, hypoxic drive is depressed. PVR is typically increased in a similar fashion as SVR.

    RENAL Renal vascular resistance is increased by hypothermia thereby decreasing renal blood flow. Normal urinary volume is maintained by inhibition of tubular reabsorption of Na and K, causing cold diuresis.

    HEPATIC Decreased hepatic blood flow decreases the metabolism of some drugs.

    OXYGEN The oxyhemoglobin dissociation curve is shifted LEFT with hypothermia. This decreases tissue oxygen availability because the AFFINITY of oxygen for hemoglobin is INCREASED approximately 5.7% per degree Celsius. Decreases in metabolic rate offset the increases in oxygen affinity.

    VISCOSITY & COAGULATION Changes in viscosity and coagulation are minimal at temperatures above 33 degrees. Lower temperatures can result in impaired coagulation and increased viscosity.


    Hypothyroidism affects two out of every thousand women. It affects about 6-10% of women over the age of 65 and about 2-3% of men. The most common cause is HASHIMOTO’S thyroiditis, a chronic autoimmune destruction of the thyroid. Other causes of hypothyroidism include radioactive iodine, thyroidectomy, thioamide drugs and iodine ingestion. Transient hypothyroidism can occur in patients with acute thyroiditis.

    Elective surgery should be deferred in the patient with symptomatic hypothyroidism. There is little evidence to delay elective surgery in subclinical hypothyroidism. There is no increase in morbidity in patients with mild-moderate hypothyroidism.

    PREOPERATIVE Opioids may have exaggerated effect. Consider cortisol because decreased adrenal function may accompany hypothyroidism.

    INDUCTION Ketamine is often the induction of choice but low dose thiopental has been used as well. Nitrous oxide alone might produce unresponsiveness in the severely hypothyroid. Keep in mind that there may be an exaggerated muscle relaxant effect at induction. Pancuronium is a mild CV stimulant which may be useful.

    MAINTENANCE Thyroid dysfunction is NOT listed as an influence of MAC. Experts usually recommend nitrous oxide plus opioid, benzodiazipine or ketamine. Volatiles may cause excessive myocardial depression in severely hypothyroid patients. MAC requirements are not actually decreased but a decreased cardiac output will accelerates anesthetizing brain levels of volatile anesthetics. There is diminished CO2 production and decreased minute ventilation is required during controlled ventilation.

    These patients are susceptible to hypothermia and CHF therefore an arterial line and CVP should be considered along with measures to maintain body temperatures. They have a decreased clearance of free water and therefore are susceptible to hyponatremia.

    The treatment of hypotension may be particularly difficult because fluids and peripheral vasoconstrictors may lead to CHF and positive inotropes can result in dysrhythmias. A small dose of ephedrine is the usual first choice though PDEI and glucagon should be considered. Consider adrenal insufficiency for refractory hypotension.

    REGIONAL anesthesia may be an appropriate choice for many surgical cases. Metabolism of amide local anesthetics may be slowed therefore the hypothyroid patient may be more susceptible to toxicity.

    MYXEDEMA coma is a severe form of hypothyroidism with stupor, hypoventilation, hypothermia, hypotension and hyponatremia. This is a medical emergency with high mortality requiring aggressive therapy.

    There are theoretical advantages for TREATING the myxedema patient with a combination of T3 and T4. LIOTHYRONINE (synthetic T3) has a faster onset of action but also a higher risk of complications. LEVOTHYROXINE (synthetic T4) is the prohormone of T3 and is the standard therapy for chronic hypothyroidism. Inotropic and chronotropic effects will increase myocardial oxygen demand and ischemia may occur.


    Patients under general anesthesia may have a reduced tidal volume for a number of reasons.

    1) rapid shallow breathing secondary to moderate anesthetic depth in the spontaneously breathing patient
    2) airway resistance increased secondary to reduced lung volume, airway obstruction or endotracheal tube compromise
    3) lung compliance may be decreased
    4) surgical posture may interfere with diaphragmatic and chest wall movement

    Hypoventilation results in hypercapnia. Physiologic consequences of hypercapnia occur not only as a result of the direct effects of increased CO2 but also through the resulting decrease in pH.

    DIRECT cardiovascular effects of hypercapnia are vasodilatation and decreased myocardial contractility.

    Neurologically, carbon dioxide is considered to be a generalized depressant of the CNS. Its use in concentrations needed for anesthesia (about 30% or pCO2 at 210 mmHg) is known to cause seizures. Hypercapnia is associated with stimulation of the autonomic nervous system yielding increases in plasma epinephrine and norepinephrine levels such that INITIAL manifestations include tachycardia and hypertension.

    Hypercapnia also produces increased serum potassium levels. Acidosis also causes the oxyhemoglobin curve to shift to the RIGHT – decreasing oxygen affinity by what it known as the BOHR effect.


    See also the entry on HYPOXIA – DIFFERENTIAL which is more directly related to the anesthesized patient. Oxygen tension is measured by the CLARK electrode (the Severinghaus electrode measures CO2).

    The THREE CORE causes of hypoxia are hypoventilation, pulmonary disorder (V/Q mismatch) and DO2/VO2 imbalance (delivery to uptake imbalance).

    FIRST STEP (of two) evaluation includes determination of the A-a GRADIENT where a normal gradient indicates alveolar hypoventilation (drug or neuromuscular) and an increased gradient may be secondary to either V/Q abnormality or systemic DO2/VO2 imbalance. The inspiratory force may be useful in evaluating the hypoventilating patient as those with central hypoventilation will have normal inspiratory force.

    SECOND STEP (for those with an increased gradient) requires measurement of MVO2 (mixed venous) to differentiate patients with V/Q abnormality (normal MVO2) and those with delivery uptake imbalance (low but possibly normal MVO2) which may be secondary to anemia, cardiac failure, hypermetabolism.

    It is important to understand that in the normal lung, a decrease in venous PO2 has very little effect on arterial PO2. In the diseased lung with high shunt fraction (edema or pneumonia), the MVO2 is an important consideration in the evaluation of hypoxemia.


    The essential feature of hypoxia is the cessation of oxidative phosphorylation. Anaerobic pathways, especially the glycolytic pathway, come into play, producing hydrogen and lactate ions. These ions accumulate in the circulation. This anaerobic metabolism produces only 5% as much ATP per mole of glucose compared with the aerobic route and therefore, the ATP:ADP ratio falls.

    The effects of hypoxia on the cardiovascular system are either REFLEX-mediated (neuronal and humoral) or via DIRECT action.

    REFLEX effects occur first, producing excitatory and vasoconstrictive effects. Neurogenic reflexes originate from carotid and aortic chemoreceptors along with cerebral stimulation. The humoral reflex effects result from catecholamine and renin-angiotensin release. The DIRECT effects are inhibitory and vasodilatory and occur late.

    MILD hypoxia (saturation over 80%) causes catecholamine release with consequential increased heart rate, cardiac output and myocardial contractility. Systemic vascular resistance only changes slightly. Mild hypoxia in those that are beta blocked may result only in increased systemic vascular resistance and thus decreased cardiac output.

    With MODERATE hypoxemia (60-80%) systemic vascular resistance and blood pressure decreases but heart rate may continue to be high secondary to hypotension induced baroreceptor stimulation.

    In SEVERE hypoxia (saturation less than 60%) local depressant effects predominate, resulting in decreased blood pressure and heart rate which results in shock and ultimately ventricular fibrillation or asystole. These reflex responses may be suppressed in the well-anesthetized patients. Therefore only the direct effects of moderate to severe hypoxia may be present during anesthesia.

    PAP is increased with hypoxia secondary to HPV. The pulmonary distribution of blood flow becomes more homogeneous.

    Hypoxia displaces the oxyhemoglobin dissociation curve to the right which increases oxygen tension in the tissues. Increased 2,3-DPG and acidosis also have this effect.

    Chronic hypoxia also leads to polycythemia, which will ultimately improve O2 delivery.



    1) inadequate oxygen supply: improperly filled tanks, empty reserve tanks, cracked flowmeter, flowmeter down, system disconnection, large leaks, obstructed tube, malpositioned ETT
    2) inadequate alveolar ventilation: hypercarbia will lead to hypoxemia with PACO2 over 60 mmHg
    3) medullary chemoreceptor depression
    4) carotid body chemoreceptor depression


    1) partial shunt: secretions, atelectasis, pneumonia, pulmonary edema, bronchoconstriction, COPD, pneumothorax, compression or surgical packing, loss of normal HPV, diffusion impairment
    2) true shunt: AV fistulae, atrial septal defect, ventricular septal defect, patent ductus arteriosus (see elsewhere)
    3) dead space from pulmonary embolus should not theoretically cause hypoxemia – nevertheless it is believed that pulmonary embolus incites a local release of mediators which secondarily cause bronchospasm and shunt


    1) decreased carrying capacity: anemia, CO poisoning, methemoglobin, hemoglobinopathies
    2) increased affinity for oxygen (which may cause tissue hypoxia without hypoxemia): hypothermia, decreased 2,3-DPG, alkalosis, hypocarbia
    3) decreased cardiac output
    4) increased utilization or uptake: MH, fever, hyperthyroidism and shivering

    One other type of hypoxia which does not fit in the above three categories is HYSTIOCYTIC HYPOXIA most commonly seen with cyanide toxicity. Oxygen delivery is adequate, but the cells are unable to utilize the oxygen.

    A practical and systematic approach to the patient may include quickly placing the patient on 100% oxygen and hand ventilating, then tracing the oxygen molecules from the source to the periphery where delivery is assessed.


    Chemoreceptors located centrally and peripherally in the CAROTID and AORTIC BODIES are of major importance in the reflex control of respiration. The nerve supply to the CAROTID BODIES is the sinus nerve of Hering which is a branch of the glossopharyngeal nerve (IX). The AORTIC BODIES are innervated by the vagus (X). The medulla and pons contain the brainstem centers responsible for control of respiration and sectioning the brainstem above the pons will not alter respiratory rhythm or the integrated response to hypoxia, hypercarbia or acidosis.

    The medullary reticular formation contains two distinct centers for respiratory control: the dorsal respiratory group (DRG) responsible for the intrinsic respiratory rhythm and inspiratory control and the ventral respiratory group (VRG) which controls both inspiration and expiration. The lower pons contains the apneustic center which is capable of prolonging the inspiratory phase of respiration which will increase tidal volume and decrease respiratory rate. The upper pons contains the pneumotaxic center which switches off inspiration at appropriate times to control the inspiratory volume.

    While peripheral and central chemoreceptors respond to changes in PCO2, it is only the peripheral chemoreceptors in the carotid bodies that respond to hypoxemia. The triggering of these chemoreceptors to hypoxia does not begin to have significant clinical effect until PO2 has fallen to a level of 50 mmHg (although studies indicate that the receptors are firing even at normal sea level PO2 and in normal individuals the “hypoxic” drive is thought to account for 10% of minute ventilation). Unlike the ventilatory drive to hypercarbia, the hypoxic drive occurs in a curvilinear relationship and is much more reactive to small changes at the lower range of PO2. It is also important to note that a depression of ventilation is noted at the extreme levels of hypoxia and this is thought to be secondary to hypoxia of the respiratory neurons in the brain.

    Denervation of the carotid bodies (as possible after bilateral CEA) will ABOLISH the ventilatory response to hypoxia. The response to hypoxia is enhanced (shifting the curve) in the face of hypercarbia (acting primarily through pH at the central chemoreceptors) and acidosis (as acidemia and hypoxia act synergistically at the peripheral chemoreceptors).

    While inhalational anesthesia is capable of abolishing the physiologic responses to hypercarbia and hypoxia, the depression of the hypoxic response is potentially more harmful. Unlike the response to hypercarbia, the hypoxic drive is blunted at subanesthetic doses (0.1 MAC) and abolished at 1 MAC.


    HPV is a local response of PA smooth muscle to a decreased regional ALVEOLAR oxygen tension (generally less than 70 mmHg). It acts to maintain a normal V/Q ratio but is significant only when there is a normally ventilated portion of the lung to perfuse (as with one lung ventilation).

    Although the IV anesthetics do not inhibit HPV, the volatile anesthetics and potent vasodilators do. Important INHIBITORS include:

    2) nitroglycerin
    3) nitroprusside
    5) calcium channel blockers
    6) many beta agonists
    7) PGE
    8) PGI2 (prostacyclin)
    0) volatile agents

    Inhaled nitric oxide and aerosolozed Prostin can also inhibit HPV.

    It is worthwhile to note that it is ONLY in the lung that CO2 or hypercarbia DIRECTLY leads to vasoconstriction. Through most of the systemic vasculature, some degree of vasoconstriction can be seen secondary to increased sympathetic tone. In the cerebral and coronary vasculature, hypercarbia or acidosis leads to vasodilation and increased flow (by the natural and direct effect of CO2).
    Some references state that in actuality, HPV is enhanced by metabolic acidosis but is not enhanced by respiratory acidosis.

    One class of drugs that can ENHANCE HPV are the NSAIDS that inhibit the cyclooxygenase pathway and block prostaglandin formation.


    Ibutilide is a class III antiarrhythmic for treatment of supraventricular arrythmias including atrial fibrillation and flutter. It is most effective for the conversion of atrial fibrillation or flutter of relatively brief duration.

    DOSING is at 1 mg over 10 minutes. A second dose may be administered at the same rate 10 minutes later. For adults less than 60 kg, the dose is at 0.01 mg per kg.

    SIDE EFFECTS Ventricular arrhythmias may develop in 2-5% of all patients treated (polymorphic VT or TDP). QT intervals should be less than 0.4 seconds prior to therapy, magnesium should be between 1.8 and 4.0 mg/dL and potassium should be between 4.0 and 5.5. Patients also should not have received any drugs that prolong the QT interval within 48 hours prior to therapy. Patients with impaired LV function are at highest risk.


    Intracranial pressure is normally 5-15 mmHg and reflects the volume of brain, CSF and the blood within the cranial vault. Increased ICP reduces cerebral perfusion pressure and may produce cerebral ischemia and ultimately brain herniation. The goal in the treatment of ICP is to improve intracranial compliance or reduce the ICP.

    DIURETICS Osmotic diuretics (mannitol 0.5-1.5 mg/kg) increase plasma osmolality and draw water from the intracellular and interstitial spaces into the vasculature. This decreases intracranial volume, lowers ICP and improves intracranial compliance. The osmotic diuretics are only effective in regions where the blood brain barrier is intact. Mannitol initially increases intravascular volume and may precipitate congestive heart failure in susceptible patients.

    Loop diuretics (furosemide, ethacrinic acid) lower ICP by dehydration effect and by decreasing CSF production. They do not increase intravascular volume and are thus safer in patients with cardiac dysfunction.

    STEROIDS reduce edema associated with tumors (vasogenic edema). Because their effects occur slowly (over 12 hours), steroids are not useful for treating acute elevations in ICP.

    BARBITURATES are potent cerebral vasoconstrictors and may be used to decrease ICP in patients resistant to other modes of therapy. See other information under BARBITURATE COMA.

    Metoclopramide IV has been associated with increased ICP in patients with head injuries.


    This block provides excellent analgesia for groin operations including hernia repairs, hydrocelectomy and orchiopexy. One study (Langer 1987) has also demonstrated a benefit as preemptive analgesia with children receiving the block after induction requiring less pain relief 48 hours after surgery.

    ANATOMY The inguinal area is supplied by three nerves: the iliohypogastric, the ilioinguinal and (to some degree) the genital branch of the genitofemoral nerve.

    TECHNIQUE The nerves can be blocked by a simple infiltration of the abdominal wall in the area medial to the anteriorsuperior iliac spine. A 25 gauge needle is used to puncture the skin just medial and inferior to the ASIS just above the inguinal ligament. Three pops are felt through the skin, external and internal obliques. Several fan shape injections are made as the needle is withdrawn and a subcutaneous wheal will improve the success rate.

    Bupivicaine (0.25-0.5%) with or without epinephrine (1:200,000) can be used in volumes up to 10 mL. The maximum dose of bupivicaine in children with or without epinephrine is 3 mg per kg.


    Imperforate anus may be part of the VACTERL association. ANESTHETIC management includes rapid sequence intubation or awake intubation for the patient with a predicted difficult airway. Patients may be volume depleted secondary to held enteral feeds and hyperosmolar constrast for radiographic surveys.

    ADD information from SMITHS.



    Provided in 5 mL ampules of indigotindisufonate sodium in water.

    Excreted largely by the kidneys where it retains its blue color. Elimination begins soon after injection usually apearing in the urine within ten minutes of administration. The biological half-life is 4-5 minutes. Larger quantities can be used IM.

    The chief application of indigo carmine is in localizing ureteral orifices during cystoscopy and ureteral catheterization.

    SIDE EFFECTS Occasional idosyncratic reactions may occur. A mild PRESSOR effect can be seen in some patients. No toxic effects have been documented with overdose.

    Indigo carmine should be protected from light for storage.



    1) lower solubility
    2) greater VA
    3) lower CO (most influential with soluble agents)
    4) smaller FRC (correlating with 2)


    1) greater solubility
    2) decreased VA (as with endobronchial intubation)
    3) higher CO (more influential with the soluble agents)
    4) lower barometric pressure
    5) R>L shunt (greater influence with insoluble agents – note that L>R has no influence)
    6) increase FRC

    NOTE how these factors are related to the factors associated with achievement of PA pressures and the FA/FI curves. The confusion with this topic revolves around the simple truth that the more soluble agents (halothane and isoflurane) are taken up more quickly by the sytemic circulation but are slower to achieve adequate alveolar concentrations and are slower to induce anesthesia.

    There are SIX FACTORS that determine the PA pressure – three of which determine INPUT and three which describe UPTAKE. Another way to conceptualize this is as three influences of uptake into the alveoli and three influences of uptake from alveoli to the arterial blood.

    1) PI which is the inspired partial pressure (not concentration)
    2) VA – alveolar ventilation
    3) properties of the anesthetic breathing system (volume, gas flow, plastic solubility)
    4) solubility
    5) cardiac output
    6) alveolar-to-venous partial pressure difference


    Infants have a larger tongue relative to adults. This increases the risk of airway obstruction during induction and laryngoscopy. Infants have angled vocal cords and difficulties may arise when trying to blindly pass an ET tube. The anterior commissure may prevent the ET tube from entering the trachea.

    The larynx of an infant is funnel-shaped and narrowest at the level of the cricoid cartilage. In the adult it most narrow at the level of the glottis. An ETT that passes through the vocal cords in an infant may be impeded in the subglottic region because of this anatomic difference.

    The uncuffed ETT is generally used in pediatric patients less than 8-10 years of age but cuffed tubes may be used successfully in younger children with careful attention to the pressure of the cuff. There is concern that infants may be prone to tracheal mucosal ischemia with a cuffed tube secondary to lower mucosal perfusion pressures.

    It is advantageous to use the largest ETT available (in an infant) as resistance to flow in a ETT varies inversely to the radius to the fourth power.

    The infant epiglottis is typically short, stubby and will often hang over the larynx.

    The infant airway is located more superior and anterior than in the adult. The GLOTTIS is at the C3-4 level versus the C5-6 level in the adult. A straight blade may be more useful for visualizing the vocal cords in this setting.


    Dermatomyositis and polymyositis are inflammatory myopathies that share many clinical manifestations but have distinctive pathogenetic and clinical differences. Both DM and PM present clinically with symmetric, proximal muscle weakness, usually of insidious onset. Dysphagia or regurgitation of swallowed food with possible aspiration may occur secondary to involvement of striated esophageal muscle. Both myopathies may be associated with malignancy, but the incidence is higher in DM. Two classic skin manifestations are seen in DM: (1) the Gottron sign, an erythematous, symmetric, nonscaling rash over the extensor surfaces of the MCP and IP joints, elbows and knees, and (2) heliotrope rash, a reddish-violaceous erythema of the upper eyelids. Pathogenetically, DM is associated with immune complex deposition in the vessels, whereas PM appears to result from T-cell–mediated cytotoxicity.

    A clinical diagnosis is supported by an increase in muscle enzymes (CPK, phosphokinase, aldolase, LD, AST and ALT) and an EMG showing increased membrane irritability. A muscle biopsy specimen obtained usually from a clinically weak muscle demonstrates muscle fiber necrosis, degeneration, and regeneration and an inflammatory cell infiltrate that is perifascicular or perivascular in DM and intrafascicular in PM.

    Other possible causes that can cause muscle weakness – such as amyotrophic lateral sclerosis, myasthenia gravis, muscular dystrophies, endocrine diseases, drugs such as lipid-lowering agents, AZT, colchicine and viral infections such as influenza, mononucleosis, rickettsia, HIV and parasites – need to be excluded.

    Corticosteroids are the mainstay of therapy in inflammatory myopathies. The response to corticosteroids, assessed by the improvement in muscle strength and normalization of muscle enzymes, is evaluated at 3 months. Failure to improve or an incomplete response justifies the use of the immunosuppressive drugs such as azathioprine and/or methotrexate.


    The INFRACLAVICULAR block is useful as an alternative to the axillary block for surgery of the elbow and distal.

    TECHNIQUES described in the literature: the classic coracoid, infraclavicular fossa and the Raj approach.

    CORACOID TECHNIQUE The arm may lie in any position (as with SCB) and the neck may be in a neutral position. A point is marked on the chest wall 2 cm MEDIAL and 2 cm INFERIOR from the LATERAL ASPECT of the CORACOID process (which is generally most prominent). From this point a 10 cm insulated needle is passed directly posterior. Electrical stimulation usually results in pectoralis muscle contraction at a depth of 1-3 cm with plexus stimulation at a depth of 3-7 cm.

    The stimulation of the CORDS (cephalad to caudad) is demonstrated:

    LATERAL CORD terminates at musculocutaneous and MEDIAN and often illicits PRONATION. MEDIAN: pronation, wrist flexion, finger and thumb flexion, opposition of thumb and little finger and lateral palmar sensory.

    POSTERIOR CORD terminates at RADIAL illiciting WRIST EXTENSION. RADIAL: wrist extension, finger and thumb extension, thumb abduction.

    MEDIAL CORD terminates primarily in ULNAR with some contributions to median and often illicits WRIST FLEXION. ULNAR: wrist flexion, finger abduction and adduction, thumb flexion, thumb adduction, palmar and dorsal fourth and fifth sensory.

    The MUSCULOCUTANEOUS contraction is first encountered as this nerve leaves the SUPERIOR aspect of the brachial plexus at this point. SUPRASCAPULAR or AXILLARY nerve stimulation may also be encountered high in the plexus, resulting in shoulder motor response and referred arm movement. Both of these responses seem to yield lower rates of successful blockade than stimulated hand movement. If either of these unsolicited responses are encountered, the needle should be directed slightly INFERIORLY until hand movement is obtained. If no stimulation is encountered with the initial perpendicular positioning of the needle, progressive caudad redirection will often result in the appropriate response.

    MEDICATIONS Mepivicaine or lidocaine 1.5% with epinephrine provides 2-3 hours of anesthesia (33 mL maximum) and levobupivicaine 0.5% provides 3-8 hours of anesthesia (35 mL maximum).

    Unlike the SCB, a needle redirected within this parasagittal plane is unlikely to contact lung as the plane lies lateral to the ribcage. Medial misdirection may nevertheless cause PNEUMOTHORAX (case report A&A July 2007). Redirection too lateral often results in blockade similar in character to axillary block but often with a prolonged latency.

    DISADVANTAGES of the ICB: (1) greater likelihood of sparing the ULNAR nerve – similar to the interscalene but unlike the axillary and supraclavicular blocks, (2) small risk of PNEUMOTHORAX which is negligible with axillary block, and (3) risk of HEMATOMA and difficulty with compression also which is negligible with axillary block.



    Inguinal hernia repair is the most frequent general surgical procedure performed by pediatric surgeons. Males are affected more than females and the incidence is highest in the first year of life. Right sided hernias (60%) are more common than left (30%) and bilateral hernias (10%).

    ANESTHESIA Children with incarcerated hernias and indication of bowel obstruction must be induced by rapid sequence though some would argue that without active vomiting that mask inductions are acceptable.

    Caudal epidural or ilioinguinal iliohypogastric nerve blocks can provide postoperative analgesia as well as diminishing the intraoperative anesthetic requirements. Local infiltration of the surgical site is also an option but is probably used less often.

    PREMATURE infants have a particularly high incidence of inguinal hernia and may be managed through the entire surgical procedure by spinal or caudal epidural. In infants beyond the vulnerable period (52-60 weeks post-conception) and not on apnea monitors or methylxanthine, the advantage of a completely regional technique is attenuated.

    Many use regional for those less than 2.5 kg and GA for larger infants. If the surgeon feels that the repair may be more technically challenging, he or she may be more uncomfortable with the time constraints of a regional technique.

    SPINAL Hyperbaric TETRACAINE (0.5% with 10% dextrose) can be used at a dose between 0.4-1.5 mg per kg with 20-40 mcg of epinephrine. Hyperbaric BUPIVICAINE (0.5% with 7.5% dextrose) can be used at a dose of 0.8 mg per kg also with 20-40 mcg of epinephrine. The epinephrine may prolong anesthesia by 35%. T6 levels are required. One study demonstrated 90 minutes of surgical time with 0.4 mg/kg of tetracaine with epinephrine and 60 minutes without epinephrine.

    One inch 25 gauge neonatal spinal needles with stylets are most often used. EMLA cream may be applied up to two hours before the procedure. IV catheters may be placed in the LE after the block but many recommend placement before spinal anethetic so that surgical time is optimized.

    EPIDURAL Bupivicaine by caudal injection may be used when spinals are difficult to place or as a safer alternative to SAB. Alternatively, they may also be useful following surgery with SAB for postoperative pain management. For surgical caudal blocks, most recommend 0.375% levobupivicaine at 1 mL/kg. This dosing exceeds the normal limits of safety but has demonstrated safety in animal and human pharmacokinetic models.


    General PRINCIPLES of inhaled anesthetics – the brain anesthetic concentration determines level of anesthesia. The partial pressure of an inhaled anesthetic in the alveoli (PA) is in equilibrium with the partial pressure of the arterial blood (Pa) and the brain (Pbr).

    PA (therefore Pbr) of an inhaled anesthetic is determined by delivery into the alveoli minus the uptake from the alveoli into the arterial blood.

    In the infant, ANESTHETIC DELIVERY to lungs is INCREASED secondary to increased minute ventilation and a smaller FRC ratio. This is accompanied by an increased metabolic rate marked by an increased O2 consumption (2-3 times that of adults).

    DELIVERY and three factors:

    1) inspired partial pressure (PI)
    2) alveolar ventilation (VA)
    3) characteristics of the system

    UPTAKE and three factors:

    1) solubility of the volatile
    2) cardiac output
    3) alveolar to venous difference

    With all other variables held constant, an increased CO results in more rapid uptake of anesthetic causing the rate of rise in the PA to slow and thus induction is slowed. HOWEVER, if both ventilation and CO increase, the rate at which tissue equilibration occurs is accelerated. This increases the narrowing of (A-vD) which reduces the impact of the increase in CO on uptake. Therefore, an increase in ventilation and cardiac output will accelerate the rate of rise of PA (also seen as a steep FA/FI curve).

    Age-related differences in blood-gas partition coefficients (decreased solubility in infants) may also decrease uptake thereby promoting a more rapid rise in PA and a more rapid induction.

    The A-v difference reflects tissue uptake. Vessel rich organs include the brain, heart, liver and kidneys. These tissues equilibrate rapidly with the alveoli. Infants have a greater proportional distribution of CO to these groups than adults which also contributes to a more rapid rate of induction.

    RISKS of inhalation induction include: upper airway obstruction, laryngospasm, bradycardia or hypotension as a consequence of hypoxia and a potential increased risk of vomiting and aspiration.


    INSULIN is a hormone secreted by the beta cells of the islets of Langerhans and is composed of two chains of amino acids connected by disulfide linkages. In the liver, insulin enhances the phosporylation of glucose to glucose-6-phosphate which is converted to glycogen or further metabolized. Insulin stimulates protein synthesis and lipogenesis and inhibits lipolyiss and release of free fatty acids from adipose cells. Insulin promotes the intracellular shift of potassium and magnesium.

    REGULAR insulin (trade names Humulin R and Novolin R) has a SC half-life of 1.5 hours half-life and an IV half-life of 52 minutes.

    GLARGINE insulin (trade name LANTUS) provides BASAL insulin without peaks. It is ONLY for SC use and clinical effects are evident for 24 hours. Patients scheduled for surgery may receive normal glargine doses or reduce the dose by 50%.

    NPH insulin (trade names Humulin N and Novolin N) has clinical efficacy for 14 hours and must be given bid to approximate the effects of LANTUS.

    LISPRO insulin (trade name Novolog or Humalog) is a rapid acting insulin analog with a SC half-life of 1 hour and a IV half-life of 26 minutes. Lispro is most useful in reducing postprandial hyperglycemia and nighttime hypoglycemia. It is commonly used in insulin PUMPS. There is no advantage to this preparation over regular insulin if given IV except possibly a shorter half-life.

    The RULE OF 1800 states that 1800 divided by a patient’s total daily insulin requirement will estimate the fall in blood glucose with one unit of insulin SQ. One unit may decrease glucose by 25-30 in a 70 kg patient.

    Hypoglycemic action is POTENTIATED by concomitant administration of alcohol, anabolic steroids, fenfluramine, MAOI, guanethidine, salicylates, penylbutazone, sulfinpyrazone, sulfonylureas and tetracycline.

    PREOPERATIVE management has been recently reviewed (Archives IM 1999). For short procedures in the early morning, it is recommended to delay the morning dose of insulin until after the procedure. For those unable to eat breakfast but likely to eat lunch, two-thirds of a single dose of regular insulin or one-half of the morning dose of NPH insulin for those typically receiving twice daily doses of intermediate acting insulin.

    Patients unable to eat lunch should take one-third to one-half of their total morning doses (regular and intermediate acting). Patients having surgery later in the day may require glucose infusions at 5-10 grams per hour often provided as 100-200 mL/hr or 2-4 mL/kg/hour of D5LR.

    Insulin euglycemia may be one useful therapy for the patient with calcium channel blocker or beta blocker toxicity.


    One equation for INFUSIONS: insulin in units per hour is equal to plasma glucose divided by 150.

    see SS crib sheet from DHR


    The intercostal block is most commonly used in lieu of neuraxial block when coagulopathy or other contraindication exists. In very rare circumstances intercostal blocks may be accompanied by celiac plexus or stellate ganglion block for abdominal or thoracic surgery.

    The intercostal nerves are the primary rami of T1 through T11. T1 also contributes to the brachial plexus while T2-3 provide fibers to the formation of the intercostobrachial nerve. Each intercostal has four branches.

    1) gray ramus communicans which passes anteriorly to the sympathetic qanglion
    2) posterior cutaneous branch
    3) lateral cutaneous branch arisinq just anterior to the midaxillary line
    4) anterior cutaneous branch which is the termination of the nerve

    TECHNIQUE Patients are most easily blocked in the prone position. A line may be drawn through the spinous processes with parallel lines over the posterior angles of the ribs (about 5-8 cm lateral). Lidocaine wheals are placed and a 22 gauge regional needle is inserted to the rib and then walked off inferiorly about 3-5 mm where 3-5 mL of local anesthetic is injected.

    The incidence of pneumothorax (most of which are asymptomatic) is less than 1% in multiple series. Nevertheless, it is prudent to carefully observe patients for at least 30 minutes following placement of the intercostal block.


    ISB may be used for surgery of the clavicle, shoulder and upper arm. Paravertebral or intercostal blocks are often necessary for more extensive surgery.

    This block preferentially reaches the caudad part of the cervical plexus (C3-4) as well as superior & middle trunks of the brachial plexus (C5-7). It less often blocks the inferior trunk from which the median and ulnar nerves originate. A 20-50% FAILURE rate for blocking the ULNAR nerve makes this block inappropriate for surgery of the hand. Overall failure rate may be as high as 8%.

    TECHNIQUE The patient is positioned with the back of the bed at 45 degrees and pillows removed, the ipsilateral arm at the side and directed downward. The head is turned 30 degrees contralaterally. At the level of the CRICOID or C6, the groove between the anterior and middle scalene muscle is appreciated approximately 2 cm posterior to the posterior margin of the SCM. A deep inspiration or head lift against resistance may make this anatomy more easy to appreciate. A 2 inch stimulator needle is directed in a slightly posterior and slightly CAUDAL direction – as if it would exit the posterior neck at the midline level of C7 or T1. No more than 1-1.5 cm depth is required to reach the plexus.

    Any response of the hand, arm or anterior shoulder with stimulation below 0.5 mA is appropriate for shoulder surgery. Diaphragmatic contracture or hiccough results from phrenic nerve stimulation too medial or ANTERIOR on the belly of the anterior scalene, whereas trapezius muscle stimulation indicates placement too POSTERIOR. Do not accept chest wall movement as the long thoracic nerve (C5-7) has already divided from the brachial plexus and courses behind it.

    For some procedures, anterior insertion of the arthroscope or extension of the skin excision may encroach on dermatomes not innervated by the brachial plexus (INTERCOSTOBRACHIAL T2) and a band of SQ infiltration at the anerior axilla and lateral chest wall may be required (following the anterior band of a tank top). This adjunct is most commonly performed with the axillary block for UE tourniquet pain.

    MEDICATIONS Mepivicaine or lidocaine 1.5% with epinephrine can provide 2-3 hours of anesthesia (33 mL maximum). Levobupivicaine or ropivicaine 0.5% can provide 3-8 hours of anesthesia (35 mL maximum). In COMBINATION 20 mL of 2% mepivicaine can be used with 20 mL of 0.5% ropivicaine to provide 400 mg mepivicaine (700 mg maximum with epinephrine) and 100 mg of ropivicaine (200-300 mg maximum with epinephrine).

    COMPLICATIONS include PTX, spinal or epidural injection, vertebral artery injection and possible neuritis. PHRENIC nerve block is extremely common (up to 100%) and recurrent laryngeal nerve block (30-50% incidence) may lead to hoarseness. Phrenic nerve blocks may be somewhat attenuated by cephalad pressure during injections to promote caudal spread. Stellate ganglion blocks (HORNER’s syndrome) are possible but require no intervention. Rarely, severe bronchspasm may accompany this sympathetic block. This block should be avoided in those with severe respiratory disease.


    Major INDICATIONS for IABP include cardiac failure after CPB (3-5% of all CPB patients), preoperative stabilization for refractory angina pectoris or severe LV dysfunction and complications of MI that are refractory to pharmacologic therapy.

    Specific indications following CPB include repeated inability to separate from bypass, hypotension (SBP less than 80) with CI less than 2.0, LAP over 20 mmHg and high PVR greater than 2500 despite adequate inotropic and vasodilator therapy. Only 50-80% of these patients will eventually leave the hospital.

    Perioperative conditions that may require IABP include acute mitral insufficiency, ventricular septal rupture, ventricular aneurysms, refractory cardiogenic shock and complicated or failed PTCA.

    The PHYSIOLOGY of the IABP provides diastolic augmentation of BP and successive afterload reduction. Myocardial oxygen supply is enhanced and oxygen demand is reduced. Ischemia is reduced, CO is augmented by 20-50% and urinary output is increased. DBP and CPP are increased while SBP is only slightly decreased resulting in an increase in MAP.

    The increased DBP forces blood back through the coronaries while the ventricle is relaxed. The systolic deflation produces a pressure sink or vascular void of approximately 40 mL in the aortic root. Normal SV is approximately 70 mL.

    Myocardial oxygen consumption is determined by HR, preload, afterload and contactility. Systolic wall tension uses approximately 30% of myocardial oxygen demand. Wall tension is influenced by ventricular pressure, afterload, end-diastolic volume and myocardial wall thickness.

    CONTRAINDICATIONS include severe aortic insufficiency (which is enhanced by the IABP) and thoracic or abdominal aneurysms.

    The balloon is placed through the femoral artery at 3 cm below the left subclavian to just above the renal artery branching. Placement and timing of the balloon are critical.

    The usual sequence of WEANING from the IABP includes: early extubation, discontinued inotropes, weaning of vasodilators and finally a step-wise weaning of the balloon inflation to a cadence of one-to-four.

    Possible COMPLICATIONS include aortic dissection, renal artery occlusion, splenic infarction, mesenteric infarction and spinal cord infarction.


    Involvement in the care of the head trauma patient begins immediately on arrival to the trauma unit.

    In the asymptomatic patient, there is rarely a need for any specific therapy to reduce ICP. Pathology will determine whether any specific TX is required. In the unconscious patient, lowering ICP is a primary goal of all early therapy.

    MEASURES to reduce ICP include (1) head up tilt (15-20 degrees) with the head midline to open jugulars, (2) relative restriction of fluids with hypertonic solutions being useful, (3) maintenance of a normal BP and (4) mild hyperventilation

    HYPERVENTILATION is one of the most rapidly effective therapies. The normocapnic CBF decreases by half at a PaCO2 of 20 mmHg. This is equivalent to a 2-4% change for every 1 mmHg change in pCO2. CBF will double with an PaCO2 at 80 mmHg. Hyperventilation is effective for a maximum of 24-36 hours. As the pH of the CSF will then readjust to return CBF to normal.

    Other measures include (5) mannitol 0.5-1 grams/kg given over 3-5 minutes is effective within minutes – more rapid administration in an anesthetized patient may increase arterial pressure, which in turn may increase ICP, (6) steroids have no clear value, (7) barbiturates are reserved for situations in which other measures have failed – close monitoring of ICP, arterial and CVP is recommended, (8) hypothermia to 32 degrees is associated with a 40-50% decrease in CMRO and a concomitant reduction in CBF, CBV and ICP – a one degree Celsius change shifts the CBF by approximately 5-7%, (9) ventriculostomies into the anterior horn of the lateral ventricle for monitoring and CSF drainage are usually placed in patients presenting with GCS of less than 8 – adults usually produce 600 mL of CSF daily

    Within physiologic limits, the arterial oxygen tension has little effect on CBF. Nevertheless, extreme hypoxemia will dramatically increase CBF (doubles CBF at a pO2 of 30).

    Treating HTN in the patient with intracranial HTN is challenging. Options to consider include nicardipine, labetalol and esmolol infusions.


    CONGENITAL: (1) dermoid – often cystic; may contain sebaceous waxy material, hair.
    (2) teratomas – greater amount & variety of structures easily on X-ray and tend to lie in midline.

    MESODERMAL: meningioma – tumor is encapsulaled; easily separated from nervous tissue – benign and removable if not too large.

    ECTODERMAL GLIOMAS (1) glioblastoma mutiforme – infiltrative; rapid-growing; occurs: most frequently in mid-aged; apt to involve both cerebral hemispheres via the corpus callosum; Average Survival: 1 year. (2) medulloblastoma – rapidly growing tumor of the vermis of the cerebellum. Occurs usually in children; characteristically metastasizes to the surfaces of the remaining CNS via subarachnoid spaces; Average Survival, with X-rad, 15 months. (3) astrocytoma – usually occurs in cerebrum of adults and cerebellum of children (but may be in adult cerebellum). Slow growing; may become cystic; star-shaped cells when under microscope; Average Survival: 6 years. May give rise to Glioblastoma multiforme within it. (4) oligodendroglioma – slow growing; solid; calcified — usually found in cerebral hemispheres of adults. Average Survival: 5 years. (5) astroblastoma – a rare glioma which occur in the cerebral hemispheres of middle-aged adults. DDx – it and Glioblastoma multiforme by microscopic nvestigation. Average Survival: 3 years. (6) spongioblastomas – occur predominantly near the optic chiasm of children and in the pons; may give appearance of “hyperlrophy” of the pons. Ave. Survival: 1 year. (7) ependymomas – occur chiefly in children; slow growing; apt to calcify; arise in or near ventricle walls; more common in the fourth ventricle than elsewhere; Average Survival: short. (4th – one going vertically cerebellum & 3rd ventricle – below Aqueduct of Sylvius.)

    PITUITUARY TUMORS: chromophobe – relatively common in anterior pituitary gland of adults;compression of adjacent optic chiasm and hypothalamus is common

    METASTATIC Most common source of metastalic tumors in the brain: bronchogenic carcinoma but also carcinoma of breast, thyroid and GI tract. 10-25% of all brain tumors are actually metastatic.



    INDICATIONS for arterial lines

    1) expectation of large or sudden hemodynamic changes
    2) need for continuous, accurate beat-to-beat BP measurement
    3) need for frequent blood sampling.

    Intra-arterial pressure monitoring provides unsurpassed reliability and accuracy, especially at the extremes of BP. An accuracy within 5 mmHg can be expected throughout the measurement range.

    Measured systolic pressures tend to increase and diastolic pressures tend to decrease as the location of catheter becomes more peripheral (this is reflected as a more dynamic and wider pulse pressure in the periphery). Vascular disease and vasoconstriction predictably decrease both systolic and diastolic measurements. In these settings femoral invasive or brachial non-invasive techniques are more accurate than radial catheters.

    The pressure waveform can be very useful in quantitatively inferring the patient’s inotropic and volume status. A crisp upstroke implies a more hyperdynamic situation and a broad peak or a plateau implies adequate diastolic filling and venous volume.

    Marked variation of BP with ventilation is often a sign of hypovolemia or tamponade. A marked decrease in pulse pressure with a normal mean usually indicates a failing catheter, faulty flush system or severe vasoconstriction.

    Many different techniques have been for cannulation. There is little to suggest that any technique is consistently better or safer than another. A well-trained clinician should expect a success rate of 90% on the first attempt in a healthy patient with normal anatomy. Severe hypotension, vascular disease or previous cannulation can make cannulation difficult or impossible.

    Potential complications include symptomatic or asymptomatic arterial thrombosis. The ratio of the cannula diameter to the vessel diameter is the single most important factor predisposing to thrombosis. Other complications include infection, accidental injection of intravenous drugs, nerve trauma and exsanguination from accidental disconnection.

    There is no evidence that shape, size, material and duration of cannulation are important predictors of complications. There is no evidence that one cannulation site is safer than another. In addition, there is no evidence that the Allen’s test is of any value in predicting morbidity.


    Anesthetic preconditioning and postconditioning have been demonstrated with all of the commonly used volatile agents and is mediated by activation of K ATP channels. There is some evidence that desflurane may be more effective than isoflurane which is better than sevoflurane. The protective effects may be blocked by use of the sulfonylurea agents such as glyburide.

    Ischemic conditioning by transient occlusions is also mediated by activation of the K ATP channels.


    ISOFLURANE is a stereoisomer of enflurane with remarkably different properties. Only 0.2% of the agent is metabolized (more metabolism than desflurane but less than that of sevoflurane).

    vapor pressure 238
    MAC adult 1.15
    MAC neonatal 1.6
    MAC infants 1.87
    blood:gas partition 1.4

    CARDIOVASCULAR Forane markedly increases muscle blood flow and MAP will fall by 50% at 2 MAC. Forane may be the best agent for AI as CO is maintained but SVR and afterload does decrease.

    Coronary steal syndrome has only been clearly demonstrated in animal models. There are, nevertheless, at least two case reports of introperative ischemic changes that were reversed once isoflurane was substituted with halothane. 25% of the CAD population is considered to have steal prone anatomy (based on large catheterization review studies).

    Forane may be dysrhythmic with over 4.5 mcg/kg of exogenous epinephrine (three times the dose required with halothane).

    PULMONARY Forane is a good choice for lung disease and for one-lung anesthesia. There is LESS inhibition of HPV which ultimately results in less transpulmonary shunting and better oxygenation.

    In the spontaneously breathing patient, tachypnea will plateau over 1 MAC. Respiratory depression (and response to hypercarbia) is greater with isoflurane than any of the other volatile agents.

    CNS Cerebral oxygen requirements begin to fall at 0.4 MAC and this is also the point at which amnesia is likely to occur. Burst suppression occurs at 1.5 MAC and electrical silence predominates at concentrations of 2 MAC.

    Forane is associated with the lowest CBF to prevent ischemia at 10 mL/100g/min. This is referred to as the critical blood flow point. Forane is probably the most potent enhancer of NMB and can accelerate a phase I to a phase II block.

    RENAL All agents decrease renal blood flow, GFR and UOP. These changes are not a result of ADH release but rather the effects of the volatiles on blood pressure and cardiac output.


    Isoproterenol is a synthetic sympathomimetic amine that is structurally related to epinephrine but acts almost exclusively on the ß receptors.

    Isoproterenol acts primarily on the heart and on smooth muscle of bronchi, skeletal muscle vasculature and alimentary tract. The positive inotropic and chronotropic actions of the drug result in an increase in minute blood flow. There is an increase in heart rate, an approximately unchanged stroke volume and an increase in ejection velocity. The rate of discharge of cardiac pacemakers is increased with isoproterenol.

    Venous return to the heart is increased through a decreased compliance of the venous bed. SVR and PVR are decreased and there is an increase in coronary and renal blood flow. SBP may increase and DBP may decrease. MAP is usually unchanged or reduced. The peripheral and coronary vasodilating effects of the drug may aid tissue perfusion.

    Isoproterenol relaxes most smooth muscle with the most pronounced effect being on bronchial and GI smooth muscle. It produces marked relaxation in the smaller bronchi and may even dilate the trachea and main bronchi past the resting diameter.

    Isoproterenol is metabolized primarily in the liver by COMT. The duration of action of isoproterenol may be longer than epinephrine but is still very brief.

    INDICATIONS include refractory bradycardia, bradycardia in heart transplant patients, carotid sinus hypersensitivity, CHF, shock with severe aortic regurgitation, pulmonary hypertension, refractory torsades de pointes, beta blocker overdose and status asthmaticus.

    DOSING Dilute 10 ml (2 mg) in 500 mL of 5% DEXTROSE for a concentration of 4 mcg per mL. The initial dose is usually 0.5-5 mcg per minute or up to 1.25 mL of diluted solution per minute. Rates over 30 mcg per minute have been used in advanced stages of shock. PEDIATRIC infusions range between dosages of 0.05-0.2 mcg/kg/minute.

    The rate of infusion should be adjusted on the basis of heart rate, central venous pressure, systemic blood pressure and urine flow. If the heart rate exceeds 110 beats per minute, it may be advisable to decrease or temporarily discontinue the infusion.

    For status ASTHMATICUS, 1 mL of the undiluted medication (0.2 mg) can be given SQ or IM.


    Isosulfan blue or LYMPHOZURAN

    JET is a narrow complex junctional or high fascicular tachycardia with a rate faster than (or equeal to) the atrial rate. Rates less than 170 may be fairly well tolerated while faster rates are not. There is often a small amplitude superioirly vectored P wave with a short PR interval reflecting retrograde capture of the atrium from the pacemaker. Although JET is usually a regular complex tachycardia, it may be present as wide complex tachycardia when there is an existing or rate-related BBB. JET may be irregular in cases where there is no retrograde propagation of the impulse into the atrium resulting in AV asynchrony (Ann Thor Surg 2002 74:1607).

    ASSOCIATIONS JET usually follows extensive manipulation of the atrial and junctional tissue such as venous switch procedures (Mustard and Senning for transposition), the Fontan operation (particularly lateral tunnel modification) and more rarely resection of atrial septum as in the Norwood operation for hypoplastic left heart syndrome. The accelerated junctional rhythm is poorly tolerated in the patient with single ventricle physiology. Incidence reports vary from 1-20%.

    THERAPY Definitive therapy is not yet established. The goal of therapy is to slow the junctional rhythm sufficiently so that atrial pacing with intact AV conduction will produce AV synchrony at sufficiently slow rates and improve the hemodynamic state. Electrolytes must be optimized with ICa at 5.0 and magnesium at 2.

    1) MAGNESIUM loading at 30 mg/kg as the patient comes off bypass is often used as prophylaxis and may be given on pump (small risk of hypermagnesemia is weakness)
    2) cardioversion (overdrive pacing or transthoracic cardioversion) may be effective ONLY if intrinsic JET rates are less than 160 bpm
    3) AMIODARONE may be useful in refractory unstable patients in increments of 1 mg/kg up to a maximum of 5 mg/kg and possibly followed by infusions at 10-15 mg/kg/day for 2-3 days (Pediatric Cardiology 2002)
    4) central HYPOTHERMIA (to 35 degrees by esophageal monitor) in conjunction with PROCAINAMIDE is currently the most widely used strategy – procainamide is loaded at 10-15 mg/kg and followed by a continuous infusion

    Lidocaine, verapamil and adenosine work only transiently if at all. Because verapamil is a negative inotrope, it is contraindicated in these hemodynamically unstable patients.

    Beta blockers, such as continuous esmolol, may slow the junctional rate but at the cost of myocardial depression and decreased blood pressure. Digoxin has been reported to be effective (80% effectiveness in one single study) though it is unclear whether the observed improvement is simply a result of the usual subsiding of the tachycardia as the edema and inflammation recede. Procainamide, dilantin and propaferone (not available in IV form) have been used with success as well.


    JRA is one of the most common rheumatic diseases of children and a major cause of chronic disability. It is characterized by an idiopathic synovitis of the peripheral joints, associated with soft tissue swelling and effusion. In the ACR classification criteria, JRA is regarded not as a single disease but a category of diseases with three principal types of onset:

    1) oligoarthritis – pauciarticular
    2) polyarthritis
    3) systemic-onset disease

    Initial symptoms often include morning stiffness and gelling, ease of fatigue particularly after school in the early afternoon, joint pain later in the day, and joint swelling. The involved joint is often warm, lacks full range of motion, and is occasionally painful on motion but usually not erythematous.

    Oligoarthritis (pauciarticular disease) predominantly affects the joints of the lower extremities, such as the knees and ankles. Involvement of upper extremity large joints, while seen, is not characteristic of this type of onset. Involvement of the hip is almost never a presenting sign of JRA. However, hip disease may occur later, particularly in polyarticular JRA, and is often the first sign of a deteriorating functional course.

    Polyarthritis (polyarticular disease) is generally characterized by involvement of both large and small joints. As many as 20-40 separate joints are often affected, although inflammation of only five or more joints is required as a criterion for classification of this type of onset or course. Polyarticular disease often resembles the usual presentation of adult rheumatoid arthritis. Rheumatoid nodules found on extensor surfaces of elbows and over the Achilles tendon are associated with a more severe course. Micrognathia reflects chronic temporomandibular joint involvement. Cervical spine involvement of the apophyseal joints occurs frequently, with risk of atlantoaxial subluxation.

    Systemic-onset disease is characterized by a quotidian fever with daily temperature spikes to at least 39 for a minimum of 2 weeks. Each febrile episode is often accompanied by a characteristic faint erythematous macular rash; lesions may be linear or circular, from 2 to 5 mm in size, distributed most commonly over the trunk and proximal extremities. In addition to arthritis, patients with systemic-onset disease often have prominent visceral involvement including hepatosplenomegaly, lymphadenopathy, and serositis, such as a pericardial effusion.


    DOSING The induction dose is 1-2.5 mg/kg IV or 2-5 mg/kg IM. Unconsciousness is provided for 10-15 minutes though analgesic effects may continue into the postoperative period. Dosing for ANALGESIA in the PACU is at 0.1-0.5 mg/kg. CNS effects can be seen at the higher dose but are attenuated by benzodiazepines.

    PO DOSING for children or patients with retardation is at 2-4 mg/kg. Because much of the drug is metabolised to norketamine in the first pass of the liver better analgesia with fewer psychological problems may be observed.

    Opioid SPARING effects may be seen with low dose simple infusions at 150 mcg/kg/hr especially if loaded by 150-250 mcg/kg (Eur J Pain 2006). LIMIT total dose to 1 gram.

    BRONCHOSPASM may be treated with 1-2.5 mg/kg/hour.

    SEDATION may be provided with 0.5-1 mg/kg and the drug may be given as an infusion with propofol at 1 mg per mL (of propofol). Recent study (AA 2001 92:1465) demonstrated significant benefit without increase in adverse events with propofol-ketamine MAC.

    NEURAXIAL Epidural or caudal dosing is at 0.5 mg/kg.

    KETAMINE may be useful for induction in select circumstances including pericardial tamponade with a full stomach, symptomatic hypothyroidism, severe CHF and acutely hypovolemic patients (such as the patient with postpartum hemorrhage). It still should be used cautiously in patients that are catecholamine depleted or in those with a high preexisting sympathetic tone.

    PHARMACOKINETICS Clearance ranges between 16-18 mL/kg/min. The half-life is reported to be between 1-2 hours. The Vd for ketamine is 2.5-3.5 L/kg. The drug is metabolized in the liver with an extraction ratio of 1 and excreted by the kidney. The primary metabolite, norketamine, is less potent but may contribute to overall analgesic properties.

    Ketamine is available in the US as a mixture of the R and S isomers. The S isomer available in some countries, is a more potent analgesic and produces fewer PCP-like side effects than the R isomer.

    PHARMACODYNAMICS Ketamine produces dissociation between thalamocortical and limbic systems. It depresses function in cortex and thalamus while simultaneously activating activity of the limbic system. The drug ANTAGONIZES activity at the NMDA receptors and may stimulate spinal opioid receptors. The NMDA receptors of the spinal cord are thought to be involved with central sensitization and wind-up phenomenon.

    Recent studies have compared magnesium (30 mg/kg and also a NMDA antagonist) with ketamine for preemptive pain management.

    Other effects include salivation, tachypnea, bronchodilation, tachycardia, increased CO, increased MAP and increased PAP. Ketamine increases central sympathetic outflow and prevents the reuptake of NE into the sympathetic nerve endings. It is nevertheless an intrinsic cardiac depressant and in those with a preexisting high sympathetic tone (CHF and cardiac tamponade) a fall in MAP can be expected.

    Ketamine will increase CBF and ICP. It will induce nystagmus and may cause myoclonus. It will decrease auditory and visual evoked potentials but will increase the amplitude of SSEP (no change in latency).


    Ketorolac is a NSAID agent that also possesses antipyretic and analgesic properties. It is chemically related to indomethacin and tolmetin. Ketorolac is indicated for the short-term relief of pain. The onset and efficacy of analgesia after systemic administration are claimed to be comparable to that of morphine, but ketorolac causes less drowsiness, nausea and vomiting.

    The antiinflammatory effects of ketorolac may result from the peripheral inhibition of prostaglandin synthesis through inhibition of the enzyme cyclooxygenase. Prostaglandins sensitize pain receptors and their inhibition is believed to be responsible for the analgesic effects of ketorolac. Most NSAIDs do not alter the pain threshold or affect existing prostaglandins, so the analgesic action is most likely peripheral. Antipyresis may occur through peripheral dilation caused by a central action on the hypothalamus. This results in an increased cutaneous blood flow and subsequent heat loss. Decreased gastric mucosal cytoprotection, impairment of renal function and inhibition of platelet aggregation also may result from prostaglandin inhibition. Ketorolac may exhibit weak anticholinergic and alpha-adrenergic blocking activity.

    DOSING Adult dosing is 15-30 mg IV or IM every six hours for no more than FIVE DAYS. Smaller adults and those with renal impairment should receive no more than 60 mg each day. Pedaitric dosing is at 0.5 mg per kg but has been given at doses up to 1 mg per kg (AA 2002).

    ADVERSE EFFECTS include abdominal pain, nausea, headache and dizziness. Severe GI reactions occur in fewer than 1% of patients and include gastritis, peptic ulcer, GI bleeding and GI perforation.

    Postoperative bleeding also has been reported. In December 1993, French authorities suspended use of parenteral ketorolac due to this adverse reaction. GI bleeding or erosive gastritis can be minor or life-threatening and may result from a combination of direct irritant action on the stomach mucosa and a prolonged bleeding time, due to changes in platelet aggregation. Occult GI bleeding occurs in many patients and is not necessarily correlated with GI distress.

    Nephrotoxicity associated with ketorolac includes renal insufficiency, acute renal failure (unspecified), and nephritis (less than 1%). Impairment of renal function may result from inhibition of renal prostaglandin synthesis. Transient azotemia and serum creatinine have been reported in 2-3% of patients receiving long-term oral therapy. NSAIDs are assoicated with renal adverse effects including renal papillary necrosis, nephrotic syndrome, hematuria, proteinuria, and interstitial nephritis. The incidence of these reactions are low, but can be serious.

    Elevated hepatic enzymes occur in up to 15% of patients receiving systemic NSAIDs. Elevations greater than three times the upper limit of normal have occurred in fewer than 1% of patients receiving ketorolac. Liver-function abnormalities or clinical hepatotoxicity have been reported in fewer than 1% of patients. Ketorolac should be discontinued if elevated liver-function tests persist or worsen, or if signs or symptoms of hepatic disease develop.

    Peripheral edema has been reported in 3-9% of patients receiving ketorolac. Ketorolac should be used cautiously in patients with congestive heart failure or other diseases that predispose to fluid retention.


    ARTHROSCOPY can be performed with (1) local infiltration and IV sedation, (2) by GA or (3) by SAB. Regional blocks for arthroscopy are generally inappropriate althouqh femoral nerve block may be easily performed postoperatively for those with extraordinary pain.

    OPEN procedures of the knee require anesthesia of the LFC, femoral, obturator (often by lumbar plexus block) and sciatic nerves. GA and neuraxial anesthesia are also appropriate but are less desirable because of the superior postoperative pain control achieved with peripheral blocks. It should be noted that SCIATIC nerve injury is common after knee surgery. EMG studies reveal an incidence of 30% with only half fully recovering after 5 years (Clin Orth Relat Res 1990 261:233).

    Anesthesia extending from S2 to T12 is adequate for knee surgery. A sensory level to T8 is required if a tourniquet is used through the procedure. A recently study (AA 2001) has compared the use of low dose SAB with local infiltration and concluded that both techniques are comparable in overall satisfaction and time requirements. The SAB described consisted of 20 mg of lidocaine and 20 mcg fentanyl in 4% dextrose solution. ISOBARIC lidocaine is most commonly used for such procedures at doses between 40-50 mg. Bupivicaine 0.75% at 15 mg may be used as an alternative to lidocaine.

    Complex arthroscopy or MENISCUSECTOMY may require GA or spinal anesthesia. Many orthopedists prefer to perform arthroscopy with GA because of the relaxing effects that improve the ability to manipulate and examine the knee.

    Total knee REPLACEMENTS may be performed under spinal anesthesia with isobaric or hyperbaric bupivicaine (12-15 mg) with epinephrine washes or tetracaine.


    Raising the pH of local anesthetics increases the non-ionized free base. Remember bases ionize in acid. This theoretically increases the rate of diffusion across the lipophilic nerve sheath as it is the non-ionized form of the drug that traverses the sheath. Subsequently, the onset and spread of the block are more rapid. Note that local tissue acidosis as produced by infection is associated with poor quality of local anesthesia.

    Epinephrine is unstable at alkaline pH and LA that is manufactured with epinephrine is slightly acidic.

    Limitations of NaHCO3 supplementation (added to 10 mL of LA) to prevent precipitation.

    0.25 – 1mL 2% LIDOCAINE
    0.05mL 0.5% BUPIVICAINE


    True allergic reactions to LA probably account for less than 1% of all adverse LA reactions. All four types of hypersensitivity reactions have been demonstrated but type 4 reactions (which are cell-mediated delayed reactions) account for 80% of all LA allergic reactions.

    ESTER AGENT reactions are most commonly associated with the metabolism of the ester agents to para-amino-benzoic acid (PABA) by plasma cholinesterase. These allergies have been linked to the presence of similar aromatic molecules used as preservatives in food, pharmaceutical and cosmetic products, thereby priming the immune system for allergic reaction.

    True allergic reactions to the AMIDE AGENTS are rare. Some allergies to LIDOCAINE have been reported but are most likely related to METHYLPARABEN which is often added as a preservative to multidose vials of both amides AND esters. Methylparaben is metabolized to PABA.

    There is no cross-reactivity between esters and amides provided that they are preservative free.

    There also exists a phenomenon known as DENTIST ALLERGY. Shortly after LA injection, the patient becomes flushed, experiences palpitations and may have considerable HYPERTENSION and tachycardia.

    Lack of familiarity with these symptoms leads to the conclusion that the patient is having an allergic reaction . The explanation is more likely related to the unique anatomy of the oral cavity, the highly compact space of injection with the high degree of vascularity associated with the high probability for pressurized IV injection of these agents.

    Because the concentration and volume of the LA is low, the toxicity experienced is most likely related to adrenergic effects of exogenously applied epinephrine, as opposed to true allergy which is more typically associated with histamine mediated tachycardia and HYPOTENSION.

    Disproving one of these allergic phenomenon require a combination of a knowledge of the true extremely low incidence of allergy to amides, as well as skin testing.


    The CV system is much more resistant to the toxic effects of LA than the CNS. In general, 3-4 TIMES higher serum concentrations are required for CV toxicity as opposed to CNS toxicity. Bupivicaine only requires TWICE the CNS toxic concentrations to produce CV effects. It is the LEVO enantiomer that is the safer form of all the LA.

    All LA, with the exception of cocaine and ropivicaine, are direct relaxants of smooth muscle which makes them VASODILATORS.

    At low serum levels, the sole effect of CV toxicity may be a slowing of repolarization or a loss of automaticity. At higher levels, LA have direct myocardial DEPRESSANT actions (blocking Na channels during systole) and these are agent specific depending on how quickly the drug dissociates. EKG CHANGES (particularly with bupivicaine) may include:

    prolonged PR interval
    prolonged QRS complex
    sinus tachycardia
    ventricular tachycardia
    frequent PVC
    variable AV block
    ST segment changes

    Lidocaine cardiotoxicity is most often limited to simple sinus tachycardia and ST segment changes.

    Specific CV depression with highly lipid soluble agents such as BUPIVICAINE and etidocaine is not only associated with their increased lipid solubility, but the specific binding of these agents to cardiac conduction system which magnifies their cardiac toxicity. Bupivicaine, secondary to its slow-on and slow-off binding to the cardioreceptors, is capable of disrupting both the systolic AND diastolic function of the cardiac cycle.

    Other factors which magnify LA toxicity include hypoxia, hypercarbia and tissue acidosis. Both metabolic and respiratory acidosis greatly magnify LA toxicity by causing ion trapping. Problems are often magnified during PREGNANCY secondary to the increase of plasma levels of progesterone. Concominant use of medications that inhibit myocardial impulses (ß-blockers, digitalis and CCB) may also lower the threshold for cardiotoxicity.

    AMIODARONE (5 mg/kg or 150 mg) or BRETYLIUM (20 mg/kg and unavsilable in the US) quickly reverses the cardiodepression and raises the threshold for VT secondary to LA. Lidocaine and phenytoin are not useful. Insulin and glucose infusions or LIPID infusions may be useful for refractory bupivicaine toxicity.

    Other supportive measures including VASOPRESSIN (40 units), epinephrine (1-15 mcg/kg) and CPR may be required though epinephrine is known to potentiate bupivicaine toxicity.

    LIPID infusion reduces bupivacaine-associated cardiotoxicity. Partition experiments suggest that the primary benefit of lipid infusion results from a lipid sink effect. The 20% intralipid is administered as a 100 mL bolus followed by 400 mL given over the subsequent fifteen minutes.


    ESTERS Chloroprocaine is the least cardiotoxic and fastest acting local anesthetic available in the US. It is one of the safest agents for use in obstetrics. Chloroprocaine breaks down very rapidly in the presence of normal pseudocholinesterase and it is unlikely to reach the fetus in appreciable amounts.

    AMIDES These drugs are all broken down in the liver and their half-lives are long. They have relatively low molecular weights and high lipid solubilities permitting greater permability through the placenta.

    The ease of placental transfer is also determined by a high proportion of NON-IONIZED drug and this in turn is favored by a low dissociation constant (LOW pKa) and high lipid solubility. The five amide agents can be ranked in order of pKa and diffusibility as follows.

    mepivacaine (pKa 7.65) >
    etidocaine (pKa 7.76) >
    lidocaine (pKa 7.85) >
    ropivacaine (pKa 8.1)>
    bupivacaine (pKa 8.16)

    From this scale it can be seen that mepivacaine is likely to show the greatest degree of placental transfer and bupivacaine will demonstrate the least.


    Local anesthetics consist of an aromatic ring and a carbon chain tertiary amine. These two groups are joined by either an ester or an amide link. The tertiary amine is a base (proton acceptor).

    Local anesthetics first diffuse through the cell wall of the neuron where they are protonated by the higher concentration of hydrogen ions. The LA then enters the sodium channel (from the intracellular position) and binds to the transmembrane pores. LA binds only with the sodium channel in its open (activated) or inactive state – they do not bind to the resting channel. This characteristic explains what is known as the frequency dependent blockade.

    LIPID SOLUBILITY The more lipid soluble agents penetrate the nerve membrane more easily and have a greater intrinsic POTENCY. There is a direct correlation between the lipid:water partition coefficient and the minimum concentration required for blockade. This coefficient is highest for bupivicaine, followed by etidocaine, ropivicaine, tetracaine and then lidocaine.

    PROTEIN BINDING The duration of action depends on binding to the protein components of the nerve membrane. Local anesthetics also bind to two principal sites in the plasma: alpha-glycoprotein and albumin.

    pKa Agents with lower pKa values (such as lidocaine 7.9) act more quickly than agents with higher pKa values (bupicaine at 8.1). It is the more lipid-soluble uncharged free base form of the local anesthetic that diffuses through the cell membrane to take effect. Remember that bases ionize in acid so that the more basic molecules (such as bupivicaine) will be more ionized (and less penetrating) at a physiologic pH.

    IMPORTANT CLARIFICATION It is the unionized form that is required to cross the lipid membrane but the ionized form that is the ACTIVE form. This concept directly relates to the theoretically dangerous phenomenon of ion trapping – anesthetics will ionize in the acidic environment of the newborn and be trapped from crossing back across the placental barrier.

    POTENCY lipid solubility
    DURATION protein binding
    ONSET pKa



    kg PLN EPI
    tetracaine 1.5 100 200
    bupivicaine 2 175 225
    cocaine 3
    ropivicaine 4 200 300
    etidocaine 3-4 300 400
    lidocaine 7 300 500
    mepivicaine 7 300 500
    procaine 14 400 600
    prilocaine >6 600 600
    chloroprocaine 20 800 999

    More easily stated, the maximum dosage of BUPIVICAINE 0.5% will be 35 mL without epinephrine and 45 mL with epinephrine. More commonly used maximum for BUPIVICAINE 0.25% WITH EPINEPHRINE IS ONE MILLILITER PER KILOGRAM.

    The maximum dosage of LIDOCAINE 1% will be 30 mL without epinephrine and 50 mL with epinephrine.

    The maximum dose of EPINEPHRINE as a LA additive is 10 mcg/kg for the pediatric patient and 200-250 mcg in the adult patient. This equates to roughly 40-50 mL of a 1:200K solution in the adult. Epinephrine should be limited to 3-4 mcg/kg every 20 minutes in the presence of halothane.


    The central neurotoxicity of LA usually precedes CV effects as CNS toxic serum concentrations are approximately FOUR TIMES LOWER than those required for CV toxicity. Bupivicaine will produce CV toxicity at only TWO TIMES the concentrations required for CNS effects. When heavily premedicated with benzodiazepines, CNS effects may be masked or blunted to the point that toxicity first presents with CV effects.

    Low plasma concentrations of LA are likely to produce numbness of the tongue and circumoral tissues presumedly reflecting delivery of the drug to these highly vascular tissues. As plasma levels continue to increase, the LA will cross the BBB and produce a predictable pattern of CNS changes.

    SYMPTOMS begin with restlessness, vertigo, tinnitus and difficulty in focusing. Slurred speech and skeletal muscle twitching will follow. Skeletal muscle twitching is often first evident in the face and extremities and signals the imminence of tonic clonic seizures. Lidocaine and the other amides may cause drowsiness before the onset of seizures and symptoms may be limited to drowsiness alone.

    HYPERCARBIA may increase the CNS toxicity of LA by augmentation of CBF. It is important to remember that hypercarbia may also accentuate CV toxicity. HYPOKALEMIA (on the other hand) may greatly decrease the CNS toxicity of LA by hyperpolarizing the neurons.

    TREATMENT for neurotoxicity is by airway protection and oxygenation as well as immediate use of a benzodiazepine or barbiturate to terminate or prevent the progression to seizure. Appropriate DOSES include:

    thiopental 1-2 mg/kg
    midazolam 0.05-0.1 mg/kg
    propofol 0.5-1.5 mg/kg

    When CV changes are noted with LA injection, it may be recommended to provide low dose thiopental while closely monitoring CV status. The early use of SCH may allow for greater oxygenation and minimize acidosis that is secondary to motor seizures.

    DIRECT neurotoxic effects of LA are also of minor concern with placement of SAB or peripheral nerve blocks. See other information under SAB – COMPLICATIONS.

    LA: PKA

    The pKa is the DISSOCIATION CONSTANT which denotes the pH at which 50% of a moleculular mixture will be neutral and 50% will be in the charged or ionized form.

    The pKa of the LA is most closely related to the agents ONSET of ACTION but will also be related to the lipid solubility of the agent and hence loosely related to its potency. Decreasing the pKa of an agent will increase the uncharged lipid-soluble form. NOTE, however, that lidocaine is less potent than bupivicaine even though the pKa is lower.

    Agents with lower pKa values (such as lidocaine 7.9) act more quickly than agents with higher pKa values (bupicaine at 8.1). It is those agents with the lower pKa that exist at an optimal ratio of ionized to nonionized fraction at a physiologic pH. It is the more lipid-soluble uncharged free base form of the LA that diffuses through the cell membrane to take effect at the intracellular aspect of the sodium channels. Remember that bases ionize in acid so that the more basic molecules (such as bupivicaine) will be more ionized (and less penetrating) at a physiologic pH.

    procaine 8.9 slow 1
    chlorpro 8.7 fast 4
    tetracaine 8.5 slow 16
    lidocaine 7.9 fast 1
    etidocaine 7.7 slow 4
    prilocaine 7.9 slow 1
    mepivicaine 7.6 slow 1
    bupivicaine 8.1 slow 4
    ropivicaine 8.1 slow 4


    Most drugs used for anesthesia rapidly cross the placenta. Several factors influence placental transfer. Local anesthetics are weak bases with pKa values between 7.7-8.1. At this pH, drugs are present equally in ionized and un-ionized forms. It is the NON-IONIZED form that penetrates the placental tissue barrier.

    As fetuses are usually acidotic compared to the mother the local anesthetic that crosses over to the fetus as non-ionized form changes to ionized form and is then unable to cross back. This results in accumulation of local anesthetic in the fetus known as ION TRAPPING.

    Rate of transfer by FICK EQUATION

    Q/t = [K x A (Cm – Cf)] / D

    K drug specific diffusion constant
    A surface area
    Cm free drug in maternal blood
    Cf free drug in fetal blood
    D thickness of troph epithelium

    K is affected by molecular size, lipid solubility and degree of ionization.


    Tachyphylaxis to local anesthetic is a clinical phenomenon whereby repeated injection of the same dose leads to decreasing efficacy. It has been described with neuraxial and peripheral blocks.

    An interesting clinical feature is the relationship to dosing intervals. If intervals are SHORT enough, tachyphylaxis does not develop. Patients that develop pain between longer dosing intervals seem more likely to develop tachyphylaxis and there is speculation that a central spinal mechanism by spinal cord sensitization is responsible.

    Prolonged exposure of a nerve over time does not affect either the flux through sodium channels or propagation of the action potential over time. There are few pharmacokinetic or pharmacodynamic changes noted after repeated dosing of the local anesthetics.


    The toxicity of the local anesthetics involve direct effects on peripheral and central nervous structures as well as cardiovascular depressant effects.

    Determinants of toxicity include plasma concentrations, total concentration, free concentration (as determined by protein binding) and ionization (non-ionic form involved in CNS penetration but ionic forms are CNS toxic). Since these parameters are determined by lipid solubility, toxicity is directly related to LIPID SOLUBILITY.

    Systemic ABSORPTION will vary by site of injection. Absorption is highest following injection for intercostal blocks.

    caudal epidural
    lumbar epidural
    brachial plexus
    lumbar plexus

    Exogenous VASOCONSTRICTORS are known to be associated with decreased blood levels of local anesthetics, with peak levels occurring later and uptake being slower. With some agents in some locations, the vasoconstrictors are associated with a more prolonged duration of action. Epinephrine may also accentuate the quality of certain blocks as with isobaric bupivacaine spinal anesthesia. There are (nevertheless) adverse toxic effects associated with exogenously added vasoconstrictors in addition to those associated with the local anesthetics. These adverse effects are catecholamine-mediated adrenergic effects and include hypertension, tachycardia, cardiac arrhythmia, as well as ischemia of the cardiac system.

    The effects of local anesthetics on the central nervous system are associated with the agent used, injection site and uptake into CNS. The more lipid soluble the agent, the more rapid the onset and the more rapid the onset of toxic phenomena. The influence of specific agents on the manifestations of local anesthetic toxicity has to do with lipid solubility with the more lipid soluble agents having a more rapid onset of toxic phenomenon; the protein binding of the agents also determines the onset of CNS clinical phenomenon. The more protein bound the agent, the slower the time course to symptoms and the narrower the gap between the first symptoms of CNS toxicity and the signs of massive reaction to central nervous system local anesthetic exposure.

    Intra-arterial injection of even a tiny amount of local anesthetic into the carotid or vertebral artery is associated with a very rapid onset of massive central nervous system reaction.


    Labetalol or Normodyne (like carvedilol) is a commonly used PO and IV antihypertensive with beta-1 and 2 blocking as well as alpha-1 blocking capabilities. The presynaptic alpha-2 receptors are spared by labetalol such that released NE can continue to inhibit further release of the catecholamines by the negative feedback mechanism. The beta to alpha blocking ratio is 3:1 with the oral form and 7:1 with the IV form of the medication.

    PK Metabolism is by conjugation of glucoronic acid and the elimination half time is between 5-8 hours. The maximum effect of labetalol is present within 5-10 minutes of administration.

    DOSING by bolus is typically between 5-10 mg and up to 0.1-0.5 mg/kg. Doses up to 2 mg/kg are occasionally used but may be associated with undesirable decreases in BP. For HYPERTENSIVE EMERGENCY labetalol may be bolused at 20-80 mg and repeated as needed to a maximum of 300 mg or 2 mg/min IV infusion.


    The FIRST stage of labor is noted for visceral pain transmitted from uterine contractions and dilation of the cervix and is innervated by the spinal cord at levels T10 through L1. Somatic pain is characteristic of the SECOND stage of labor (vaginal and perineal pain) and is innervated through the pudendal nerves to sacral levels 2-4.

    Controversy remains as to whether or not epidural analgesia (by local anesthetic) can prolong the second stage of labor and lead to a higher cesarean section rate. It is most likely that the dilute concentrations typically used will not lead to higher cesarean rates.

    EPIDURAL Infusions typically used combine bupivicaine 0.04% with fentanyl 1.7 mcg/mL and 1:600K epinephrine. Patients are given 15 mL loading doses followed by 15 mL per hour (and possibly additional PCA doses of 5 mL every 30 minutes).

    CSE Sixty to 120 minutes of analgesia can be provided with spinal fentanyl 12.5-25 mcg or sufentanil 10 mcg. Duration can be extended with 2.5 mg of bupivicaine – recommended as 1 mL of 0.25% hyperbaric but isobaric is often utilized. Complications unique to the CSE are unusual but in one series the epidural catheter was thread to the SA space in 4 of 1650 placements.

    Although 2-chloroprocaine with bisulfite was avoided after CSE in the past, chlorprocaine with citrate preservative can now be safely used through the epidural catheter.


    albumin 3.6-5.0 g/dl
    alkaline phos 38-126 IU/L
    ACTH (fasting) < 60 pg/ml
    aldosterone 10-160 ng/L
    amylase 25-115 IU/L
    ALT or SGPT 7-53 IU/L
    AST or SGOT 11-47 IU/L
    ammonia 9-33 mgmol/L
    amitriptyline 150-250 mcg/L
    bleeding time 2.5-9.5 mins
    calcium total 8.6-10.3 mg/dl
    calcium ionized 4.5-5.1 mg/dL
    calcium ionized 1-1.3 mmol/L
    ceruloplasmin 24-46 mg/dl
    chloride 97-110 mmol/L
    cortisol (am) 6-30 mg/dl
    creatinine 0.5-1.7 mg/dl
    CK male 30-200 IU/L
    CK female 20-170 IU/L
    CK-MB less than 13 IU/L
    CK-MB fraction less than 5%
    digoxin 0.8-2.0 mcg/L
    ferritin male 20-323 ng/ml
    ferritin female 10-283 ng/ml
    fibrinogen 150-360 mg/dl
    haptoglobin 30-220 mg/dl
    iron (male) 45-160 mcg/dl
    iron (female) 30-160 mcg/dl
    iron-binding 220-420 mcg/dl
    transferrin sat 20-50%
    lactate 0.7-2.1 mmol/L
    LDH 100-250 IU/L
    lipase < 100 IU/dl
    magnesium 1.3-2.2 mEq/L
    osmolality 275-300 mOsm
    PTH 12-72 pg/ml
    phenobarbital 10-40 mg/L
    phenytoin 10-20 mg/L
    phosphate 2.5-4.5 mg/dl
    protein 6.5-8.5 g/dl
    PTT 21-32 secs
    PT 8.2-10.3 secs
    INR 0.9-1.13
    salicylate 20-290 mg/L
    thyroxine, total 4.5-12.0 mcg/dl
    thyroxine, free 0.7-1.8 ng/dl
    T uptake 30-46%
    triiodothyronine 45-132 ng/dl
    T4 index 1.5-4.5
    TSH 0.35-6 mcU/ml
    troponin < 0.6 ng/ml
    valproic acid 50-100 mg/L
    urea nitrogen 8-25 mg/dl
    uric acid 3-8 mg/dl

    CBC in light purple
    T&C in dark purple
    COAGS in light blue
    BMP in green top

    LAGASSE 2002

    Anesthesia Safety: Model or Myth? (Anesthesiology 2002 97:1609)


    Mean LAP exceeds mean CVP in normal patients although transient reversal may occur during the a wave of atrial contraction. The right sided a wave occurs prior to the left (80 msec or two squares versus 240 msec respectively). The v wave is generally more prominent on the left than the a wave. The a and c waves are less often distinct on the left.


    Numerous complications have been described. Most serious is acute hemorrhage from visceral damage. Adequate IV access is mandatory before adducting the arms.

    CO2 is used for insufflation because it is nonflammable, soluble and easily excreted by ventilation.

    Subcutaneous emphysema occurs in up to 2% of all cases and may contribute to an increased absorption. Hypercarbia can lead to acidosis, vasodilation and impaired contractility but the initial response is usually that of increased sympathetic tone.

    CO2 EMBOLUS (possibly by the portal system) may lead to a true pulmonary embolus and arrhythmias. Pulmonary embolus may be suggested by a sudden increase in the ETCO2, sudden hypoxemia, pulmonary HTN, pulmonary edema and CV collapse.

    Hemodynamic consequences of the PNEUMOPERITONEUM include an increase in afterload, increase in BP and decrease in cardiac index (by up to 30%) from a decrease in venous return. Vagal responses including asystole can occur if anesthesia is not deep enough. Maximum pressure should be below 12 mmHg.

    Other consequences of the pneumoperitoneum include atelectasis, decreased FRC, high PIP, decreased pulmonary compliance (by up to 40%) and an increased risk of GER. Tension PTX has been reported in those patients with a patent pleuroperitoneal canal.

    The TRENDELENBURG postion may increase venous return, CO and BP but it often will worsen the associated pulmonary complications. Endobronchial intubations are common after repositioning to the head down position.

    OTHER RISKS to pateints undergoing laparoscopic procedures include hypothermia and PONV.

    Nitrous oxide is usually not part of the anesthetic regimen for laparoscopic procedures but one large study (150 patients) revealed no differences in recovery periods, bowel dostension or PONV. There may be some theoretical risk of fire during electrocautery manuevers from the combination of nitrous oxide and methane (a natural gas).


    The law of LAPLACE describes the pressure relationships within the alveoli.

    T = (1/2)PR

    The pressure within a sphere is directly proportional to the tension of the wall and inversely proportional to the radius of the curvature. Surfactant which lines the alveoli decreases the surface tension as the radius becomes smaller. Without this stabilizing mechanism, the pressure would increase and the smaller alveoli would empty into the larger and alveolar stability would be LOST.

    SURFACTANT is produced by the type 2 alveolar epithelial cells and contains dipalmtoyl lecithin. It is a compostion which is 90% lipid and 10% protein.


    INCIDENCE Laryngospasm occurs in 8.7 of 1000 patients in the general population. It occurs twice as often (17.4 of 1000 patients) in patients less than 9 years of age and is three times as likely to occur in children less than three months of age. As many as 1 in 200 patients with laryngospasm may experience cardiac arrest.

    The PATHOPHYSIOLOGY involves apposition of structures at three levels including the (1) supraglottic folds, (2) false vocal cords and (3) true vocal cords. As translaryngeal pressure gradient increases during inspiration, soft tissues of the supraglottic region are drawn into the laryngeal inlet. The effect becomes progressively worse as the tissues continue to fold over the vocal cords with forceful inspiratory effort. Hypercarbia and hypoxia are known to eventually break laryngospasm.

    ETIOLOGY Laryngospasm occurs as a response to stimulation of visceral nerve endings in the pelvis, abdomen, thorax or larynx. Risk factors include

    extubation of the trachea
    NG tube or oral airway
    endoscopy or EGD
    upper respiratory infections
    light anesthesia

    MANAGEMENT Treatment depends on whether there is complete (absence of sound) or incomplete obstruction. Either type requires initial treatment with a patency preserving maneuver such as the survival position (a two-person technique) or modified jaw-thrust and chin-lift.

    For incomplete obstruction, gentle positive pressure with 100% oxygen is effectively delivered by fluttering the bag (in essence creating a manual high frequency ventilation). If the patient improves, one may eliminate the noxious stimulus (if any), increase or decrease the volatile anesthetic and resume anesthetic. If the patient fails to improve, one may quickly deepen anesthesia with an IV agent (such as thiopental or propofol) and further stabilize the airway. Further failure requires IV succinylcholine and atropine. Some centers advocate the use of IV lidocaine at 1 mg/kg as an alternative to SCh.

    Complete obstruction cannot be broken by simple PPV which may actually worsen the condition by forcing supraglottic tissues downward. It also may force air into the stomach further complicating ventilation. The treatment of complete obstruction is to lengthen the thyrohyoid muscle and unfold the supraglottic tissue. In the survival position one person holds the mask tightly and stretches the jaw (and larynx) while the other applies gentle PPV. If no air can be moved through the larynx, IV succinylcholine at 1.5 mg/kg (and atropine at 0.02 mg/kg for the pediatric patient) should be given. Rocuronium or mivacron (0.3 mg/kg) may be given IF an IV is available when succinylcholine is contraindicated. One report has revealed that mivacron has its initial effects at the cords within 40 seconds while succinylcholine relaxes the cords within 17 seconds. Without IV access, IM succinylcholine (4 mg/kg) is given.

    If laryngospasm is sustained in the face of severe hypoxia (especially with bradycardia), it may be necessary to intubate without relaxation. Direct application of lidocaine to the vocal cords may be helpful.

    If all above measures have failed, cricothyrotomy or emergency tracheostomy may be required.

    In the recovery room, 1 mL of 2.25% RACEMIC EPINEPHRINE (or 1 mL of 1:100 epinephrine) may be diluted in 3 mL NS and nebulized.




    Latex allergies are most often IgE-mediated reactions to latex (natural rubber) which may cause unexplained cardiovascular collapse during surgery and anesthesia. Patients at risk are those with frequent exposures including healthcare workers (7% incidence) and patients that require repeated bladder catheterization such as patients with myelomeningocele and spina bifida (40% incidence), spinal cord trauma, urogenital malformations and neurogenic bladder. Patients who have had surgery early in life are particularly at risk.

    Proteins in the rubber appear to be the source of the antigens, especially if there is contact with mucous membranes.

    HISTORY & DIAGNOSIS Careful history taking is paramount in those with co-existing atopy or multiple allergies. Cross-reactivity to latex occurs with avocado, apples, bananas, chestnuts, spinach and several other foods. Routine diagnostic testing for those at risk is not currently recommended but tests that exists include intradermal tests (most sensitive), skin prick and radioallergosorbent test (RAST) which is an in-vitro test for IgE antibodies (expensive with sensitivity of only 65-95%).

    MANAGEMENT It is advisable to schedule allergic patients as first cases of the day as latex is an aeroallergen and present in the OR for at least one hour after use of powdered latex gloves. Equipment to be used include glass syringes (unless latex-free plastic is available), latex-free drug vials, IV tubing without latex injection ports, neoprene reservoir bags, Webril as a barrier between rubber-containing items and the skin, non-latex gloves, and ambu or other resuscitation bags with silicone instead of latex valves. In addition, many surgical items contain latex and substitutes should be available.

    DIAGNOSIS of ANAPHYLAXIS Anaphylaxis has been reported despite prophylaxis with H1/H2 blockers (controversial benefit) and steroids in a purported latex-free environment. The anesthesiologist should always be prepared to treat. Onset is generally 20-60 minutes after exposure to the antigen and this often differentiates latex reactions from more common drug reactions. Anaphylaxis presents with the triad of hypotension (most common clinical sign), rash and bronchospasm. Serum mast cell TRYPTASE levels will be high and remain elevated for at least four hours after clinical events. Serial assessments of complement C3 and C4 will also increase over the initial four hours. These tests will identify anaphylaxis but not latex as the antigen.

    TREATMENT does not differ from treatment of severe allergic reaction by other antigens. Primary treatment involves maintaining the airway with 100% oxygen and discontinued use of all anesthetic agents. Intravascular volume should be restored with two to four liters of crystalloid and epinephrine (the cornerstone of successful treatment).

    A characteristic of anaphylaxis is the failure to respond to vasopressors other than EPINEPHRINE. Dosing should begin at 10 mcg (or 0.1 mcg/kg) and escalate rapidly to clinical response. Infusions at 5-10 mcg per minute can also be started. Cardiovascular collapse requires larger doses of 0.1 to 1 mg IV.

    If IV access is not available, epinephrine can be given subcutaneously at a dose of 3-5 mg or 50-100 mcg through the ETT.

    Note that starting with code doses of epinephrine may ironically cause life-threatening hypotension, myocardial ischemia and stroke.

    Secondary TREATMENT

    1) corticosteroids: 0.25-1 g hydrocortisone or 1-2 g methylprednisilone IV
    2) antihistamines: 0.5-1 mg per kg of diphenhydramine
    3) catecholamine infusions: epinephrine or norepinephrine at 4-8 mcg/minute
    4) aminophylline: 5-6 mg per kg over 20 minutes for persistent bronchospasm
    5) sodium bicarbonate: 0.5-1 mEq per kg for persistent hypotension with acidosis



    tricyclic antidepressants
    possibly nitrous oxide

    ranitidine and cimetidine


    CHIROCAINE contains a single enantiomer of bupivicaine described as the levo-enantiomer. The drug is most useful when large doses of LA are needed, hence it is more useful for peripheral nerve blocks and not epidural analgesia or anesthesia.

    The pKa for levobupivicaine (related to onset of action) is identical to that of bupivicaine (pKa 8.09). The potency of CHIROCAINE is equivalent to that of bupivicaine for epidural (surgical and postoperative) and peripheral nerve blocks (unlike ropivicaine).

    Levobupivicaine is thought to be less toxic than bupivicaine but this has yet to be clearly proven in humans. Studies in sheep have clearly demonstrated less cardiac and CNS toxicity thought it is slightly more toxic than ropivicaine on a milligram to milligram basis.

    The cost of levobupivicaine is roughly 60% more than the cost of bupivicaine. It is slightly less expensive than ropivicaine.


    LEVODOPA, the precursor to dopamine, is utilized for the treatment of Parkinson’s disease as DA itself does not readily cross the blood brain barrier. LD crosses the BBB and is converted to DA by the dopa decarboxylase enzyme to replenish the stores of DA in the basal ganglia. LD is usually administered with a peripheral decarboxylase inhibitor to maximize entrance of the precursor into the brain before it is converted and to minimize side effects (HTN and arrhythmias) that could occur with higher peripheral DA concentrations. The elimination half-time of LD is between 1-3 hours. An IV form of the drug is not available in the US. The benefit of LD typically diminishes over 2-5 years of therapy.

    Lidocaine is the most commonly used LA in the US. It is an amino amide with a pKa 7.7 and a commercial pH in the range of 5.6 when prepared without epinephrine. It has a rapid onset of action with intermediate duration.

    Its toxicity is intermediate with metabolism occurring in the liver. The alpha clearance half-life (redistribution) is thought to be 8-9 minutes and the ß half-life (elimination) is 45-60 minutes. Clinical TOXIC DOSE associated with lidocaine is thought to be in the 300 mg range (3 mg/kg) without epinephrine and in excess of 500 mg (7 mg/kg) when used with epinephrine. Toxicity may be observed with serum concentrations at 6-10 mcg/mL.

    Clinical uses include topical anesthesia when used in the 4% concentration liquid. It is also prepared as a gelatin or a viscous solution for mucous membrane use.

    It is used for IVRA at 0.5% concentration and is associated with a 45-60 minute duration of action.

    It is used in 5% concentration combined with glucose for SAB with 45-90 minutes duration depending on the age of the patient and the use of epinephrine in the solution. One recent study revealed an 22% incidence of transient neurologic symptoms following lidocaine SAB (versus no reports with mepivicaine).

    It is used for epidural anesthesia and analgesia in the 1-2% concentration and has a typical time to two segment regression of 45-60 minutes. Peripheral conduction block at all conduction sites is also performed with lidocaine with a duration of action typically between 1-3 hours but accentuated with the use of exogenously applied epinephrine.

    Controversy associated with lidocaine mainly relates to its use in obstetrics. In the late 1970s, Scanlon reported exaggerated effects of lidocaine on the fetus. His evaluation system was referred to as Early Neonatal Neurobehavioral Scoring and he found there to be depression using this scale of the newborn behavior when lidocaine was used epidurally for analgesia or cesarean-section. Subsequent work suggested the changes found in this system of scoring are very subtle, not clinically significant and, not reproducible from investigator to investigator. Subsequent studies have abolished lidocaine of morbidity associated with obstetric use. However, because of the low pKa of the agent and the propensity for ion trapping, lidocaine is not felt to be indicated in large doses for epidural anesthesia in mothers who have fetuses with any signs of fetal distress. This is because the fetal pH is already 0.1 of a pH unit lower than the mother in the normal state and any hypoxia or fetal stress may be associated with an even lower fetal pH and a higher propensity for ion trapping of lidocaine and hence higher toxicity of lidocaine in the newborn.


    Lidocaine is used principally for suppression of ventricular dysrhythmias and has minimal effects on supraventricular tachydysrhytmias. It is particularly effective at suppressing reentry dysrhythmias such as PVC and VT.

    MECHANISM Lidocaine delays the rate of spontaneous phase 4 depolarization by preventing or diminishing the gradual decrease in potassium ion permeability that normally occurs at this phase. Lidocaine decreases the automaticity of ectopic pacemakers and increases the threshold for VF. Lidocaine depresses cardiac contractility less than other drugs used to suppress ventricular dysrhythmias. Depressed contractility is marked in the presence of HYPERKALEMIA.

    Lidocaine has variable effects at the AV node sometimes slowing conduction but sometimes speeding conduction and causing CV collapse due to the increased rate. This outcome is particularly likely with rapid AFIB when wide complex Ashman beats (often seen with atrial fibrillation) are mistaken for ventricular premature beats.

    DOSING For adults with normal cardiac output, an initial dose at 2 mg per kg followed by an infusion at 1-4 mg per minute is usually sufficient. Decreased CO and hepatic flow (common with GA) may decrease requirements by 50%. Emergency administration of 4-5 mg per kg IM will produce therapeutic levels within 15 minutes.

    TOXIC levels may produce peripheral vasodilation and direct myocardial depression resulting in hypotension. Slowing of cardiac impulses may manifest as bradycardia, a prolonged PR and widened QRS on the EKG. Seizures progressing to CNS depression, apnea and cardiac arrest are possible at high serum levels.


    The light wand or TUBE-STAT device is useful for difficult intubations or in patients with suspected or proven cervical spine injuries.

    The ETT should be cut at 25 cm at a slight angle and the stylet should be inserted through the tube so that the light is just distal to the inflatable cuff. The apparatus should be bent at a point correlating with the patient’s mandibular-hyoid distance. The appropriate angle may range from 75 degrees (for a head in the neutral position) to 105 degrees (for the hyperextended neck).

    With extraneous lights out, the tongue should be lifted with the nondominant hand and the wand should be inserted to the point at which a bright midline glow is appreciated.

    The light wand may also be used for insertion of an ETT through a intubating LMA but would not be useful through the curve of a fast track LMA.


    A line isolation monitor (LIM) monitors the integrity of an isolated power system. Isolation transformers produce non-grounded power sources. All AC wiring and AC operated electrical devices have the potential for direct resisting capacitance or inductive leakage currents to occur via the casing of moat electrical devices, thus there are small leakage currents.

    The LIM, also known as the ground fault detector, indicates (in milliamperes not microamperes) the total leakage from the system. LIM readings of mA does not mean that current is actually flowing, but indicates how much current would flow in the event of a SECOND fault (usually caused by someone touching the non-earthed side of the circuit). Thus the alarm does not mean that there is a hazardous situation, however there is potential for it, should a second fault occur.

    The LIM reads zero amperes with no leakage current. If one side of the electrical current becomes relatively grounded, touching the current at the ungrounded side allows the current to make a complete path, thus causing an electric shock.

    MICROSHOCK involves current delivered directly to the heart. A current of 50 MICROAMPS can cause ventricular fibrillation (depending on current density). 10 MICROAMPS is considered to be the limit of safety and the potential for leak is routinely evaluated during formal equipment checks.

    MACROSHOCK involves current delivered through the skin or tissue remote from the heart. Macroshock of 100 MILLIAMPS is required to cause heart fibrillation.

    6.0 Amps causes sustained myocardial contraction followed by normal rhythm. This current is usually associated with temporary respiratory paralysis if J >100 mA/cm.

    8-20 milliamps causes muscle contraction and 20 mA is considered to be the “let go” current level.

    1-2 milliamps causes pain and is considered to be the threshold for perception.

    The LIM is set to trigger an alarm at 2 or 5 milliamps, depending on the age and type of system. 5 mAmps is current standard. The LIM will not warn of microshock range leakage current, so equipment coming in direct contact with the heart (including the ECG monitor when placing a central venous catheter) should be pre-checked for leakage current during routine maintenance.

    10 microamps microshock safety
    50 microamps microshock VF
    1-2 milliamps pain sensation
    5 milliamps LIM alarm
    20 milliamps let-go current
    100 milliamps macroshock VF
    6 amperes sustains contraction


    In the event of LA-induced cardiac arrest that is unresponsive to standard therapy, in addition to standard CPR, INTRALIPID 20% should be given IV in the following dose regime: 1.5 mL/kg over 1 minute followed immediately with an infusion at a rate of 0.25 mL/kg/min. Continue chest compressions (lipid must circulate)
    and repeat bolus every 3-5 minutes up to 3 mL/kg total dose until circulation is restored. Continue infusion until HD stability is restored. Increase the rate to 0.5 mL/kg/min if BP declines. A maximum total dose of 8 mL/kg is recommended.

    In practice, in resuscitating an adult weighing 70kg: take a 500 mL bag of Intralipid 20% and a 50 mL syringe. Draw up 50 mL and give stat IV times 2 (100 mL). Then attach the Intralipid bag to an administration set and run it over the next 15 minutes. Repeat the initial bolus up to twice more – if spontaneous circulation has not returned.


    Liposuction is generally categorized as dry (without tumescent injection), wet (less than 1 mL of injectate per 1 mL of expected aspirate) or superwet (more than 1 mL of injectate per expected aspirate).

    A search of the literature shows multiple reports of complications ranging from LA toxicity, fluid overload and pulmonary edema, labile BP, tachyarrhythmias and death. At first glance, it may be easy to place to cause of complications on the content and volume of the tumescent fluid. This fluid is usually made up of LR, lidocaine at 500-1000 mg per liter and epinephrine but variations occur widely to included the use of bupivacaine, bicarbonate, Wydase, norepinephrine, verapamil, potassium chloride and other substances.

    Most if not all of the deaths have occurred with the concurrent use of systemic anesthesia. One of the pioneer surgeons in this field insists that GA is unnecessary and could even lead to excessive surgical trauma. Many have recommended the elimination of lidocaine or other LA all together if the patient is to have a GA. It is thought that the use of up to 35-55 mg/kg of LIDOCAINE is safe and that peak absorption of the tumescent fluid is over 8-12 hours following injection. One to 15 liters of tumescent infusion may be utilized and studies have shown that this fluid is absorbed over a 48 hour postoperative period.

    Contraindications to large volume liposuction may include repiratory insufficiency, pulmonary HTN, history of CHF or MVP.


    Lithium has many bilogical effects useful for the treatment of bipolar disorders and depression. Lithium attenuates the supersensitivity of the DA receptor, increases activity of the inhibitory neurotransmitter GABA and enhances responsiveness to acetylcholine. Serotinin activity is enhanced and there is decreased beta-adrenergic receptor stimulation of adenylate cyclase. At high concentrations, this inhibition of adenylate cyclase may explain its thyrotoxic properties and its antagonism of ADH on the renal tubules.

    SIDE EFFECTS most commonly include renal effects leading to polydipsia and polyuria. Changes in the EKG include reversible T wave flattening or inversion without clinical consequences. Conduction disturbances are rare but SA node dysfunction and block have been described.

    HYPOTHYROIDISM develops in 5% of the patients treated with lithium and TSH levels should be checked every six months in those on chronic therapy.

    Lithium may PROLONG the effects of the depolarizing AND nondepolarizing neuromuscular blockers. Lithium is known to DECREASE the MAC of the volatile agents.

    Patients are often prescribed ß blockers which decrease the common tremorogenic effects of lithium. Pseudotumor cerebri and seizures are rare side effects of lithium.

    TOXICITY is common because of the narrow therapeutic index. Mld toxicity is reflected by sedation, nausea, weakness and EKG changes including widened QRS complexes. AV block, hypotension, cardiac dysrhythmias and seizures may occur at higher serum levels (over 2 mEq/L).

    Significant toxicity is a medical emergency requiring hemodialysis. If renal function is good, excretion may be accelerated by osmotic diuresis and sodium bicarbonate.


    SIDE EFFECTS of the immersion lithotripsy procedure include peripheral venous compression resulting in an increase in central blood volume and CVP (about 8-11 mmHg). Some patients experience hypotension owing to vasodilation from the warm water.

    In patients with cardiac disease, immersion should be achieved slowly. During immersion or emersion, cardiac dysrhythmias may occur reflecting changes in right atrial pressure. Shock waves are triggered from the EKG to occur 20 msec after the R wave to minimize the risk of dysrhythmias.

    Immersion lithotripsy increases the work of breathing.

    ANESTHESIA Regional anesthesia has the advantage of maintaining an awake and cooperative patient. Regional anesthetic requires a T6 sensory level. Monitors, epidural catheter insertion site, vascular access sites should be protected with water impermeable dressings. Maintenance of adequate urine output with IV fluids to help facilitate passage of disintegrated stones. Monitoring of body temperate is useful to detect changes secondary to water immersion.


    TYPICAL OR SETUP for well-functioning ESLD patients.

    DRUGS Infusions (ready before starting case) should include infusion pumps with NTG, phenylephrine, DA and carrier. Medfusion pumps are set up for calcium and possibly fentanyl.

    Syringes with standard drugs (STP, succinylcholine, d-tubocurarine) and epinephrine (10 and 100 mcg/mL), calcium chloride and pancuronium (frequently used unless extubation is possible).

    Also have sodium bicarbonate, Amicar (at least 2 vials), mannitol 0.25-0.5 gm/kg, albumin 5% (1 box of 6 bottles), insulin, KCl in 20 mEq bags, cisatracurium (infused at 1-3 mcg/kg/min if planning to extubate), Lasix and SoluMedrol.

    LINES include arterial catheter, introducer with PA catheter in most patients for fluid management, three additional large bore IVs (14-16 gauge PIV, 7 French RIS catheter or additional 8.5 French introducer). More access is necessary if significantly higher blood loss is expected. Patients generally have easy IV access. If not plan to double cannulate one or both internal or external jugulars.

    EQUIPMENT to have available include rapid infuser (rarely needed – know where it is), three standard sized pressure bags and blood filters.

    ANESTHETIC PLAN All large bore IVs should run through fluid warmers. The GANG OF 5-10 should be hooked up to sideport of the cordis that has the PAC through it. Once the case is started, this can simply hang off the side – all infusions should be hooked up at beginning of case. Transducers should be on free standing pole, not attached to the bed (to avoid artifacts from constantly tilting bed one way or another).

    Program weight and HEIGHT (to calculate CI, SVRI). UE and LE warming blankets are useful. Place the machines at foot of bed and on RIGHT side of patient, under armboard (and out of the way). All electrical cords should be on the RIGHT, so that wheeled items can easily roll in and out of the anesthesia area.

    INDUCTION is usually by RSI. Place all lines (but one) after induction.

    MAINTENANCE includes fentanyl and dopamine (renal dose) infusions usually throughout the case – cisatracurium if planning to extubate. Isoflurane and pancuronium are commonly used. Calcium infusions are useful when starting to give blood products. Lasix boluses or infusions can be used if urine output is low. AMICAR is dosed at 0.25 mg/kg over first hour followed by a 1 mg/hour infusion if primary fibrinolysis is suspected.

    LABS An ABG is obtained every 30 minutes. CBC, PT/PTT/fibrinogen are obtained every hour. Labs made be drawn less often if the patient is stable.

    FLUID MANAGEMENT Limit crystalloid (NS) use. FFP, RBC and platelets are given based on lab results. Target Hgb 9-10, INR 1.5, platelet count at 70-100K. FFP is usually the primary fluid given – the rate depends on coagulation (2-6 units/hr). Albumin 5% can be given if the patient needs volume and labs are within target ranges.

    PREANHEPATIC PHASE Keep up with blood loss. Be aware that you will have problems when the IVC is CLAMPED if you limit fluids too much and are unable to catch up. Patient may be volume loaded 10-15 minutes prior to IVC clamp. Phenylephrine may also be useful. Mannitol and Solumedrol 250 mg are often required.

    ANHEPATIC PHASE Maintain ABP and minimize fluids in anticipation of an increase in venous return with reperfusion. Expect oliguria. Solumedrol 250 mg.

    At REPERFUSION, give fluids to increase preload in advance, in anticipation of possible CV collapse.
    Beware of possible dysrhythmias, acidosis/hyperkalemia – remember calcium, HCO3, hyperventilation, maybe glucose and insulin.

    NEOHEPATIC PHASE Surgeons prefer low CVP. NTG as necessary to lower CVP while maintaining ABP. UOP should increase.

    Plan for transport to ICU when closure starts, heplock all IVs except one (central), hang all fluids and IMED pump off one pole. Maintain FFP at previous rates – PT and PTT will often remain high as liver starts to work.


    EVALUATION Preoperative evaluations should be placed in patient chart and the yellow copy in the Liver Preop Notebook in the monitoring room between OR 5 & 6.

    1) CVP infusion line required is the double lumen 5F Cook catheter kit
    (5 cm for infants and toddlers, 8 cm for the small child and 12 cm for larger children). A 15-30 cm line can be used for femoral access.
    2) large bore access requires at least one 5F (Cordis) or 6F (Arrow pediatric introducer or Arrow emergency infusion device)
    3) other peripheral access should include at least one, but preferably two 22-gauge or larger IVs
    4) arterial access is by radial or axillary line on either side – occasionally two arterial lines may be required
    5) triple transducer should be set up with T-connectors on each of the three lines

    1) for the child less than 1 year or 10 kg, set up NS through a dial-a-flow (or Medfusion pump) and a gang of four to a T-connector
    2) NS through a buretrol and a dial-a-flow to double stopcock to short (non high-pressure) extension tubing (to one of two large bore central or peripheral lines)
    3) NS through a buretrol and a dial-a-flow to double stopcock to long extension tubing (to one of two large bore central or peripheral lines)
    4) D5 1/4 NS through a buretrol and a dial-a-flow to an extension set to T-connector (to a peripheral IV)
    5) standard blood administration set up (blood administration with hot line to extension set) – do not hang any fluids with this blood line
    6) level one warmer in the room or readily available

    For the child weighing from 11-20 kg the dial-a-flows can be omitted. For the child weighing from 21-40 kg, omit the dial-a-flows and the buretrols but use minidrips instead. For the child over 40 kg, use the standard adult setup (no minidrips except for carrier and include a PA catheter setup)

    INFUSIONS (50 milliliter syringes)
    1) calcium chloride – dilute 10 mL of 10% CaCI in 40cc NS for a 20mg per mL solution equating to 0.5 cc/kg/hr providing 10 mg CaCl/kg/hr
    2) dopamine – 6 x wt(kg) = mg of drug in total of 50 mL NS so that 1 cc/hr = 1 mcg/kg/min
    3) lasix – 12 x wt(kg) = mg of drug in total of 50 mL NS so that 1 cc/hr = 4 mcg/kg/min or 0.24 mg/kg/hr
    4) KCl – use the standard 2 meq per mL concentration so that 0.5 mEq/kg/hr = 0.25 cc/kg/hr (NOTE that this can only be given centrally and must be through a port proximal to the patient and with a continuous carrier)

    1) 100-250 mL of 5% albumin
    2) epinephrine 10 mcg per mL
    3) 10% CaCI undiluted
    4) sodium bicarbonate
    5) Amicar
    6) phenylephrine 40 mcg per mL
    7) mannitol – plan to give 0.5-1 gm per kg just prior to anhepatic phase
    8) insulin
    9) D50

    EQUIPMENT warming blanket, warm the room, plastic wrap, pediatric ABG syringes, CBC and coagulation tubes.

    BLOOD PRODUCTS in the room
    1) have more than the patient’s total blood volume in the room (estimate 250 mL per unit of blood)
    2) have more than the patient’s total blood volume of FFP in the room
    3) the blood bank should have at least an equivalent (to what is in the room) in PRBC and FFP
    4) platelets and cryoprecipitate should also be available in the blood bank – have 2 units per 5 kg of platelets available (single pheresis unit equals six random donor units) – 20 mL per kg pf cryoprecipitate should also be available

    For INDUCTION, if IV access is in place, then standard rapid sequence induction. If no IV is available, induction will vary depending on the patient and anesthesia team.
    MAINTENANCE is by volatile agent and narcotic technique – muscle relaxant of choice (renal route of excretion may be preferable).


    Complications of using the LMA generally are few and minor. Using the LMA does not guarantee a patent airway. Hypoxemia and hypoventilation as a result of nonpatency (0.4%-6%) can result from occlusion of the glottis by the distal tip of the cuff, backfolding of the epiglottis, rotation of the LMA along the long axis due to misplacement or displacement or as a result of kinking of the tube on insertion.

    The smaller LMAs used in the pediatric population are more prone to kinking and the smallest LMAs (sizes less than 2) are subsequently not available in flexible models.

    Inadequate levels of anesthesia may contribute to difficulty in inserting the device, resulting in repeated attempts, airway trauma, cough, vomiting and laryngospasm. Repeated anesthetics using an LMA may result in cumulative tissue trauma as well.

    Gastric distention and regurgitation of stomach contents as a result of airway pressures exceeding the sealing pressure of the LMA may result in aspiration even if the LMA is properly seated. Aspiration of oral secretions and blood may also occur. Although aspiration of gastric contents in elective procedures has been reported, the overall incidence appears to be low and comparable to the risk of aspiration in outpatient procedures without LMA use (recall that aspiration is possible even with conventional ETT).

    Despite a routine single-attempt placement, using the LMA can potentially result in trauma to the structures of the oral cavity and larynx, including abrasion of mucosa, avulsion of the uvula or compression causing ischemia to soft tissues and nerves.

    Dislodgement and misplacement of loose deciduous teeth should be of concern in any manipulation of the pediatric airway.

    Once in place, the LMA can be displaced more readily in pediatric patients than in adults and therefore must be secured properly. Using the size 1 LMA in 50 infants, Mizushima found that in 12 of these patients complete or partial obstruction developed after an initial patent placement. The investigators concluded that the size 1 LMA is prone to dislodgement and loss of satisfactory air exchange.

    For laser facial surgery, while the LMA is less flammable than the standard mask, the area between the oropharynx and the tube should be packed with wet gauze to prevent airway fire, as oxygen may leak around the LMA cuff.


    1 3.5 2.7
    2 4.5 3.5
    2.5 5.0 4.0
    3 6.0 5.0
    4 6.0 5.0
    5 7.0 5.0
    6 7.0 5.0

    See related information under [LMA – FASTRACH]


    The LMA-FASTRACH introduced in 1997 is a silicone LMA designed to accomadate the insertion of a specialized silicone ETT (up to size 9.0) either blindly or with the aid of a FOB. The cuff of the ETT is a low volume cuff that does not entail risk of mucosal injury secondary to the nature of the silicone.


    1) previous difficult intubation by conventional laryngoscopy
    2) immobilized cervical spines either by surgical fixation or Philadelphia collars that may be left in place
    3) distorted airway secondary to tumor, surgery or radiation therapy
    4) presence of a stereotactic head frame that limits access to airway

    Anesthesia for placement of the LMA has been described successfully with standard IV induction agents, inhalation inductions to maintain spontaneous respirations and topical anesthesia with 4% lidocaine spray to the oropharynx and 4% lidocaine through the transtracheal approach.

    In one series of 250 utilizations of the LMA-Fastrach (Anes 2001), the LMA was placed in all cases with three or fewer attempts. The ETT was then inserted blindly with a success rate of 95% and with FOB assistance at a success rate of 100%.

    Two maneuvers known as the CHANDY maneuvers often ease placement of the ETT. The first movement involves subtle rotation of the LMA in the sagittal plane until the least resistance is felt with BMV. The second maneuver performed in conjunction with ETT placement involves using the metal handle on the Fastrach to slightly lift but not tilt the LMA away from the posterior pharyngeal wall during insertion.

    The COVENTIONAL LMA may be used when the Fastrach is not available. A 6.0 ETT may be passed over a FOB and through the shaft of the size 3-4 LMA and a 7.0 ETT may be passed over the FOB and through the shaft of the size 5 LMA. If a 4.0 OD or smaller fiberscope is used with the 6.0-7.0 ETT, the lungs can be continuously ventilated around the fiberscope but within the ETT by passing the fiberscope through the self-sealing diaphragm of a bronchoscopy elbow adapter. Sizes for ETT (ID) and FOB (mm) are as follows:

    1 3.5 2.7
    2 4.5 3.5
    2.5 5.0 4.0
    3 6.0 5.0
    4 6.0 5.0
    5 7.0 5.0
    6 7.0 5.0


    1 <5 kg 4
    1.5 5-10 kg 7
    2 10-20 kg 10
    2.5 20-30 kg 14
    3 >30 kg 20
    4 adults 30
    5 ADULTS 40

    When in proper position, the body of the mask of the LMA is designed to lie in the hypopharynx, with the distal tip of the mask just above the upper esophageal sphincter, the proximal aspect of the mask juxtaposed with the base of the tongue and the sides of the mask facing the pyriform fossae. As the cuff is inflated, a low-pressure seal is created around the periphery of the laryngeal inlet.

    Propofol is typically chosen for elective LMA placement because of the superior ability in blocking the airway reflexes (laryngospasm and bronchospasm). While LMA placement is far less stimulating than laryngoscopy, the occurrence of bronchospasm or laryngospasm is more detrimental..

    ADVANTAGES One of the major advantages of the LMA is that it allows rapid establishment of an airway in the patient without the necessity for muscle relaxation. The LMA can provide rescue ventilation in 94% of unanticipated CVCI patients (incidence 1:5000 anesthetics). It provides a more suitable and trouble-free airway than the face mask for brief GA.

    The LMA is easier to insert than the ETT, will not injure the trachea or vocal cords, does not cause the same hemodynamic response associated with intubation, does not affect intraocular pressure and is less likely to stimulate bronchospasm in susceptible patients.

    The spontaneously breathing patient may continue to preserve hemodynamic stability better than the mechanically ventilated patient. The larger lumen of the LMA also provides less airway resistance during spontaneous respiration.

    DISADVANTAGES Air leak around the LMA must be limited to avoid insufflation of the stomach. This restricts the amount of positive pressure that can be applied to the lungs to 20-25 mmHg.

    Leak fraction around the LMA increases with increasing peak airway pressures (at 15 to 30 cm H2O) from 13 to 27% of the delivered volume. Even with minimal PPV, a small percentage of insertions will result in the esophagus being within the lumen of the mask – more readily resulting in gastric distention.

    While using an LMA, it may be more difficult to differentiate laryngospasm or bronchospasm from incorrect placement and more difficult to apply positive pressure to break laryngospasm, although the LMA can be useful as a spacer to deliver inhaled bronchodilator.

    Although the larger size of the airway tube reduces airway resistance in the LMA compared with an endotracheal tube, it may increase dead space and the amount of rebreathing.

    Although conventionally not used in the obese patient, one recent study of 300 patients in Britain demonstrated relatively safe use of the LMA in patients with BMI less than 40.

    LMA REMOVAL during deep anesthesia is routinely performed by many clinicians. Most patients with elective LMA placements will have no contraindications to deep removal. The one exception may be the patient that is difficult to mask ventilate.


    Studies in healthy volunteers show that in single high doses lorazepam has a tranquilizing action on the CNS with no appreciable effect on the respiratory or cardiovascular systems.

    IV or IM administration of the recommended dose of 2-4 mg of lorazepam injection to adult patients is followed by dose-related effects of sedation, relief of preoperative anxiety and lack of recall of events related to the day of surgery in the majority of patients. The clinical sedation thus noted is such that the majority of patients are able to respond to simple instructions whether they are give the appearance of being awake or asleep. The lack of recall is relative rather than absolute, as determined under conditions of careful patient questioning and testing, using props designed to enhance recall. The majority of events or recognizing props from before surgery. The lack of recall and recognition was optimum within 2 hours following IM administration and 15-20 minutes after IV injection.

    DOSING For the primary purpose of sedation and relief of anxiety, the usual recommended initial dose of lorazepam for intravenous injection is 2 mg total or 0.04 mg per kg, whichever is smaller. This dose will suffice for sedating most adult patients and should not ordinarily be exceeded in patients over 50 years of age. In those patients in whom a greater likelihood of lack of recall for perioperative events would be beneficial, larger doses as high as 0.05 mg/kg up to a total of 4 mg may be administered.

    For STATUS EPILEPTICUS in children, give 0.05 to 0.1 mg/kg IV or IM and repeat doses every 10-15 minutes for clinical effect.


    LFA is a technique that minimizes the fresh gas flow needed to maintain the desired alveolar concentration of anesthetic vapor. For most adults, a total fresh gas flow of 500-600 mL per minute including 400 mL of oxygen should replace the oxygen consumed and other gases removed while avoiding hypoxemia. Use of these extremely low flows can technically be considered MINIMAL flow anesthesia while LFA generally refers to flows below 1500 mL per minute. LFA can be safely used in the spontaneously breathing patient and the pediatric population.

    Normal oxygen consumption is roughly 3-5 mL/kg/minute in adults and gas analyzers typically require 150-250 mLs per minute.

    TECHNIQUES for administration of LFA mandate an initial period of higher gas flows to prime the circuit and patient with anesthetic agent. When nitrous oxide is utilized, a longer period of priming is neccessary for purging the system of nitrogen. Purging can be individualized until inspired and expired concentrations of nitrous oxide are within 3-4%.

    The FRC contains about 1600 mL of nitrogen and there is an additional 2000 mL dissolved in the tissues.

    When analyzed gas is returned to the circuit, it is actually possible to turn off the vaporizers and nitrous oxide after the first hour of anesthesia.

    ADVANTAGES of LFA include cost reduction, temperature preservation and decreases in environmental pollution. The provided humidity in the circuit should attenuate the production of carbon monoxide from the reactions between desflurane and soda lime.

    DISADVANTAGES include the possiblity of delivering less than the required oxygen consumption (especially when nitrous oxide is used), discrepancy between the inspired vapor concentrations and the dial settings (dial readings are significantly higher than inspired concentrations) and an increased tendency for moisture accumulation in anesthesia circuit that can interfere with gas sampling, flow and volume sensors and the function of the valves.


    There are two major plexuses of the lower extremity. The LUMBAR PLEXUS is formed from the anterior rami of the L1-4 spinal nerves (often with a contribution of T12) and the SACRAL PLEXUS is formed from the anterior rami of the L4-5 and the S1-3 sacral nerves.

    LUMBAR PLEXUS divides into SIX primary branches. The most cephalad three pierce the abdominal musculature anteriorly to supply the skin of the hip and groin. (1) ILIOHYPOGASTRIC, (2) ILIOINGUINAL & (3) GENITOFEMORAL. The (4) LATERAL FEMORAL CUTANEOUS passes under the inguinal ligament to supply sensation to the lateral thigh and buttock & the (5) FEMORAL nerve passes under the ligament lateral to the artery to supply the muscles and skin of the anterior thigh as well as the hip and knee joints. The SAPHENOUS nerve is the cutaneous termination of the femoral supplying the skin of the medial leg and part of the foot. The (6) OBTURATOR nerve exits the pelvis through the obturator canal to innervate the adductors, the hip and knee joints and a portion of the skin of the medial thigh.

    SACRAL PLEXUS divides into TWO major nerves: the (1) POSTERIOR CUTANEOUS nerve of the thigh supplies the skin of the posterior thigh, and the (2) SCIATIC nerve which becomes superficial at the posterior aspect of the gluteus maximus, travels along the femur to supply the hamstrings and then becomes superficial a second time at the popliteal fossa.

    The SCIATIC then branches onto two secondary nerves: (1) the TIBIAL nerve travels down the posterior calf under the medial malleolus to supply the skin of the medial and plantar foot and the muscles of plantar flexion, and the (2) COMMON PERONEAL nerve winds laterally around the head of the fibula before dividing into the superficial and deep peroneal nerves (which is responsible for dorsiflexion).

    The SURAL nerve is a sensory nerve that is formed from branches of the common peroneal and tibial nerves. It passes under the lateral malleolus to supply the lateral area of the foot.

    INDICATIONS LE blocks prove most useful as combined techniques and for postoperative analgesia using lower concentrations of LA.

    1) HIP operations require anesthesia of the entire lumbar plexus with the exception of the ilioinguinal and iliohypogastric nerves. This is may be accomplished with a lumbar plexus block but more consistently with neuraxial anesthesia.
    2) ANTERIOR THIGH procedures may be performed with a combined LFC and femoral block or together with a three-in-one block. An isolated femoral block is useful for postoperative analgesia for a femoral shaft fracture.
    3) thigh TOURNIQUET pain may be controlled with a femoral nerve block combined with a sciatic block. The contribution of the obturator nerve is rather small but should be covered with 75% of the femoral nerve blocks.
    4) KNEE operations that are open procedures require anesthesia of the LFC, femoral and obturator (often by lumbar plexus block) as well as the sciatic nerves. Arthroscopy alone can often be performed with local infiltration and IV sedation (propofol or remifentanil).


    LGL syndrome is considered in a class of preexcitation syndromes that includes the WPW, LGL, and Mahaim-type preexcitation. Little is known regarding the structural anomalies underlying LGL. Theories proposed to explain LGL have centered around the possible existence of intranodal or paranodal fibers that bypass all or part of the AV node.

    CRITERIA for LGL include PR interval less than or equal to 120 msec (normal being 120-200 msec or 3-5 small blocks), a normal QRS complex duration and occurrence of supraventricular tachycardia but not atrial fibrillation or atrial flutter. Patients with an isolated finding of short PR interval may be characterized as having accelerated atrioventricular nodal conduction.

    In the outpatient setting, empiric therapies for recurrent PSVT may be instituted. These therapies may include beta-blockers, calcium channel blockers and digoxin.

    ANESTHESIA Atrial fibrillation and flutter are the dysrhythmias most often associated with LGL though many patients are aymptomatic. Management is identical to that of the patient with WPW.

    Lown described tachyarrhythmias in 17% of patients with a short PR interval. Some 2-4% of the adult population has a PR interval less than or equal to 120 msec. These data provide an estimate of the frequency of LGL as 0.5% of the adult population.

    The modern view of LGL is that no convincing evidence suggests that this is a syndrome separate from other known phenomena. LGL was identified as a syndrome prior to the advent of catheter-based electrophysiologic (EP) studies. EP studies have led to several realizations. The short PR interval of LGL likely represents one end of the spectrum of normal PR intervals. Most patients with putative LGL are found at EP study to have another basis for paroxysmal tachycardia. Most have AV nodal reentrant tachycardia. Others have concealed accessory pathways, usually near the septum.


    Possible complications from the lumbar drain include retained catheter, meningitis, abduscens nerve palsy and PDPHA. One study of drains used during TAAA repair reported a complication rate of 3.5%.


    Otherwise known as the PSOAS COMPARTMENT block, this form of anesthesia is often used in conjunction with a sciatic nerve block for ACL repairs. The lumbar plexus block produces a block of all lumbar and some sacral components, thus providing anesthesia to the entire anterior thigh with extension to the medial malleolus.

    The lumbar plexus block is LESS successful in blocking the OBTURATOR nerve than the three-in-one anterior technique because the obturator nerve will often occupy a separate fascial sheath from the femoral and LFC. The femoral block is also preferred to preserve hip flexion when postoperative ambulation on crutches is desirable.

    ANATOMY The lumbar plexus is made up of the ventral roots of the first four lumbar nerves. The plexus is deep within the psoas muscle and anterior to the transverse process of each of these lumbar vertebrae.

    The various branches of the plexus include the iliohypogastric, ilioinguinal, genitofemoral, lateral femoral cutaneous, obturator, accesory obturator (50% incidence) and FEMORAL nerves. It is the femoral nerve that innervates the anterior thigh and the medial aspect of the lower leg.

    TECHNIQUE A line is drawn across the posterior iliac crests (TUFFIER’S LINE) and the stimulator needle is placed 5 cm lateral to the midline. Alternatively, the needle may be introduced 3 cm caudal to Tuffier’s line at the level of the L5 transverse process – the needle can then be slid just cephalad to the transverse process.

    The psoas compartment is generally encountered at about 8-12 cm in depth. With a STIMULATOR, the needle placement can be confirmed by contraction of the quadricep muscles (femoral), hip flexion (L1-4) or possibly hip adduction (obturator). Hamstring stimulation indocates placement too medial.

    Commonly used agents include 35 mL of 0.5% levobupivicaine often with epinephrine as a marker and attenuation of systemic absorption peaks. Lower concentrations are appropriate for postoperative analgesia. Longer needles (6-8 inch) are required and the original description made use of a 20 gauge 15 cm peripheral block needle.



    MOTOR examination may provide information about specific nerve root compromise.

    L1-2 hip flexion
    L3 knee flexion
    L4 ankle dorsiflexion
    L5 toe extension
    S1 plantar flexion, hip extension, knee flexion
    S2 knee flexion

    SENSORY dermatomes are complex to examine without visual guides. The anterior thigh progresses from L1 through L3 at the knee. The medial calf is innervated by L4 and the lateral is L5. The sacral dermatomes begin with S1 and the lateral foot and posterior calf. S2 innervates the popliteal region. S3 through S5 innervate circular dermatomes in toward the anus.

    DTR or more properly muscle stretch reflexes since the reflex occurs after a muscle stretch is obtained (most commonly by tapping the distal tendon of a muscle), are helpful in the evaluation of patients presenting with limb symptoms suggestive of a radiculopathy. There are no specific reflexes for L1 through L3.

    L4 quadricep reflex
    L5 medial hamstring jerk
    S1 ankle jerk

    Patients with MYELOPATHY may demonstrate

    LE hypertonia
    LE hyperreflexia
    toe up Babinski reflexes
    Hoffman reflexes
    difficult tandem walking

    PROVACATIVE TESTS include the STRAIGHT LEG RAISE test that is sensitive to herniation at the L4-5 or L5-S1 disk which can cause pressure on the L5 or S1 nerve roots. Pain should be differentiated from normal hamstring stretch pain that can be caused by flexing the hip beyond 70 degrees.


    LUMBOSACRAL STRAIN implies muscular or ligamentous injury similar to ankle sprain.

    DISK HERNIATION is diagnosed when the nucleus pulposus has been displaced from the intervetebral space and lies outside the foramen.

    DISCOGENIC SYNDROME suggests that the pain originates from the lumbar disk itself secondary to tears in the annulus and release of chemical mediators.

    SPONDYLOSIS is a general term describing all the changes associated with degenerative disk disease including dessication of the disk, allowing narrowing of the interspace, inflammatory and degenerative changes of the bone, ligament hypertrophy and bone spurring. In persons with spondylolysis, 30-50% are believed to progress to spondylolisthesis.

    SPONDYLOLISTHESIS describes the forward slippage of one vertebral body with respect to the one beneath it. This most commonly occurs at the lumbosacral junction with L5 slipping over S1, but it can occur at higher levels as well. It is classified based on etiology into 5 types: congenital or dysplastic, isthmic, degenerative, traumatic and pathologic.

    SPONDYLOLYSIS indicates a structural defect in the pars interarticularis.

    FACET SYNDROME pain is located only in the back and is aggravated by movement and particularly rotational movement. Percutaneous denervation has been advocated for this syndrome.

    SPINAL STENOSIS describes the condition of spinal canal narrowing secondary to congenital disorders or from spondylosis. The narrowing may apply to the whole canal or to the lateral recess or be isolated to the neural foramina. Stenosis of the central cervical and thoracic spine may result in myelopathy from cord compression. Canal stenosis in the lumbosacral region often results in pain, neurogenic claudication, or both.

    SPINAL INSTABILITY refers to instability and movement of the bony elements on flexion extension or motion films.

    FAILED BACK SYNDROME is a term given to patients who have undergone more than one spinal surgery and still have incapacitating complaints.


    The MICRODISCECTOMY procedure generally takes less than one hour and does not mandate the use of invasive monitors.

    The ALIF or anterior lumbar interbody fusion is generally performed through a small anterior incison and is associated with minimal blood loss and hemodynamic disturbance.

    The PLIF or posterior lumbar interbody fusion may be performed with bone grafts or instrumentation and is often performed in conjunction with discectomy. Arterial lines and CVC are used though CXR is not mandatory as it is with sitting craniotomy or cervical spine procedures.

    The IDET or intradiscal electrothermal therapy involves inserting a small catheter into the damaged vertebral disc and heating to a temperature of 90 degrees Celsius.

    KYPHOPLASTY requires no invasive lines though arterial lines may be helpful for those with cardiopulmonary disease.



    The rate of Pancoast tumors varied from 1-3% of all lung cancers.

    Lyme disease is caused by the spirochete Borrelia burgdorferi, which is transmitted to humans by tick bites. Like other spirochetal infections, Lyme disease is characterized by multisystem involvement and occurrence in clinically distinct stages with manifestations that undergo remissions and exacerbations.

    Erythema chronicum migrans is the initial unique clinical marker for Lyme disease. This classic cutaneous manifestation begins as an area of redness, which expands to a diameter ranging from 3-6 cm. Malaise and fatigue, HA, fever and chills often accompany skin involvement. Some patients have evidence of meningeal irritation, encephalopathy, lymphadenopathy and hepatitis. Cranial neuritis, including bilateral FACIAL PALSY, may occur. Neurologic abnormalities typically last for months but usually resolve completely. Within several weeks after the onset of illness 8% of patients develop cardiac involvement, most often manifested as fluctuating degrees of atrioventricular HEART BLOCK lasting 7-10 days. Rarely, mild LV dysfunction occurs. Duration of cardiac involvement is usually brief (3 days to 6 weeks) but it may recur. From a few weeks to as long as 2 years after the onset of illness, about 60% of patients develop ARTHRITIS. Typically, this arthritis consists of migratory musculoskeletal pain, which may recur for years. In about 10% of patients with arthritis, involvement of the large joints becomes chronic, with erosion of cartilage and bone.

    Laboratory abnormalities early during the course of Lyme disease include a high sedimentation rate, elevated plasma concentration of transaminase enzymes and immunoglobulin M proteins. These levels generally return to normal within several weeks. Mild anemia may be present. Renal function tests are not altered. Treatment is initially with tetracyclines, followed by penicillin and erythromycin. Despite antibiotic therapy, nearly one-half of patients continue to experience minor complications such as HA, fatigue or musculoskeletal pain.


    MAC awake is the anesthetic concentration that prevents responsiveness to commands in 50% of patients. MAC awake may be slightly higher than MAC aware or recall. For such desirable outcomes, the ED95 would be more useful.

    To prevent recall, one should probably maintain 0.6-0.8 MAC of any of the modern volatile agents.

    As percentage of surgical MAC:

    propofol 18%
    isoflurane 38%
    sevoflurane 33%
    desflurane 36%
    N2O 64%
    halothane 52%
    methoxyflurane 52%
    ether 60%


    INCREASED MAC with hyperthermia, hypernatremia, increased catecholamines (MAOI, TCA, ephedrine, acute cocaine or amphetamine) and CHRONIC ethanol abuse.

    DECREASED MAC with hypothermia, hyponatremia, hypoosmalility, metabolic acidosis, anemia with Hgb below 4.3, pregnancy, lithium, lidocaine, alpha-2 agonist, hypoxemia with PaO2 < 38, hypotension with MAP < 40, elderly, decreased catecholamines (clonidine, chronic amphetamines and alpha-methyl dopa), acute ethanol, ketamine, pancuronium (possibly other neuromuscular blockers), barbiturates, chlorpromazine, diazepam, THC, verapamil and opioids.

    Thyoid disese does NOT inflence MAC. Hypothyroidism causes a decrease in MAC only if concomitant with hypothermia.

    The OIL:GAS partition coefficients parallel anesthetic requirements of the various volatile agents. An estimated MAC can be calculated as 150 divided by the oil:gas partition coefficient.


    There are FOURTEEN routine steps to performing a thorough machine check. Some variation between machines might alter the steps in various ways.


    1) verify backup ventilation equipment is available


    2) check oxygen cylinder supply by opening oxygen cylinder and verifying that it is at least half full (1000 psi) and then closing
    3) check central pipeline supplies by verifying that hoses are connected and pipeline gauges read about 50 psi


    4) check initial status of low pressure system by closing flow control valves and turning vaporizers off – also check the fill level and tighten vaporizer fill caps
    5) perform leak check of machine by verify that the machine master switch and flow control valves are OFF before attaching suction bulb to the common fresh gas outlet and squeezing the bulb repeatedly until fully collapsed for at least 10 seconds
    6) open one vaporizer at a time and repeat the bulb suctioning technique
    7) turn on machine master switch and all other electrical equipment
    8) test flowmeters by adjusting flow of all gases through their full range, checking for smooth operation of floats and undamaged flowtubes – attempt to create a hypoxic mixture to verify changes in flow or alarm


    9) adjust and check scavenging system by ensuring proper connections between the scavenging system and both APL (pop-off) valve and ventilator relief valve – adjust waste gas vacuum (if possible) – fully open APL valve and occlude Y-piece – with minimum oxygen flow, allow scavenger reservoir bag to collapse completely and verify that absorber pressure gauge reads about zero – with the oxygen flush activated allow the scavenger reservoir bag to distend fully and then verify that absorber pressure gauge reads less than 10 cm H20



    9) calibrate oxygen monitor – verify that low oxygen alarm is enabled and functioning – reinstall sensor into circuit and flush breathing system with oxygen – verify that monitor now reads greater than 90%
    10) check initial status of breathing system by setting selector switch to bag mode – check that breathing circuit is complete, undamaged and unobstructed – verify that C02 absorbent is adequate
    11) perform leak check of the breathing system – set all gas flows to zero – close APL valve and occlude Y piece – pressurize breathing system to about 30 cm H20 with oxygen flush – ensure that pressure remains fixed for at least 10 seconds then open APL valve and ensure that pressure decreases


    12) test ventilation systems and unidirectional valves – place a second breathing bag on Y piece – set appropriate ventilator parameters for next patient – switch to automatic ventilation mode – fill bellows and breathing bag with oxygen flush and then turn ventilator ON – set oxygen flow to minimum and other gas flows to zero – verify that during inspiration bellows delivers appropriate tidal volume and that during expiration bellows fill completely – set FGF to about 5 LPM – verify that the ventilator bellows and simulated lungs fill and empty appropriately without sustained pressure at end expiration – check for proper action of unidirectional valves – turn ventilator OFF and switch to manual ventilation mode – ventilate manually and assure inflation and deflation of artificial lungs and appropriate feel of system resistance and compliance


    13) check, calibrate and set alarm limits of all monitors – capnometer, pulse oximeter, oxygen analyzer, respiratory volume monitor, pressure monitor with high and low airway alarms


    14) check final status of machine by turning vaporizers off, leaving APL valve open – selector switch to bag and all flowmeters to zero – patient suction level adequate

    Serum magnesium has a normal range of 1.6-2.2 mg/dL (0.8-1.2 mMol/L). Magnesium strongly influences cardiac cell membrane ion transport function and is essential for activating approximately 300 enzyme systems including most of the enzymes involved in energy metabolism.

    Various effects include decreasing calcium activity intracellularly, decreased ACh release at the NMJ and decreased sensitivity of the motor end plate. Recent evidence also has revealed an ability to antagonize the NMDA receptor like ketamine.

    DOSING for severe depletion and polymorphic tachycardia consists of 2-4 gm IV over 5-10 minutes followed by 8-12 gm infused over 24 hours. Pediatric patients may receive 25-30 mg/kg. See HYPOMAGNESEMIA for other dosing regimens.

    ANALGESIA dosing is generally by 5 mg/kg loaded and followed by 500 mg per hour for 24 hours following surgery.

    SIDE EFFECTS include chest pain (epecially when given with beta agonists), palpitations, nausea, transient hypotension, sedation and pulmonary edema.

    Serum LEVELS correlate with certain physical findings.

    8-10 mg/dL decreased DTR
    10-15 mg/dL resp depression
    >15 mg/dL wide QRS, increase PR

    ANESTHETIC CONCERNS include the possibilty of potentiated neuromuscular block. Standard doses of SCh should still be used but reduced doses of nondepolarizing agents may be utilized. MAC is somewhat decreased (by about 20% with levels between 7-11 mg/dL) but this is not consistently reported.

    MANGANO ET AL 1990

    Association of perioperative myocardial ischemia with cardiac morbidity and mortality in men undergoing noncardiac surgery (NEJM 1990).

    Adverse cardiac events are a major cause of morbidity and mortality after noncardiac surgery. It is necessary to determine the predictors of these outcomes in order to focus efforts on prevention and treatment. Patients undergoing noncardiac surgery sometimes have postoperative cardiac events and it would be helpful to know which patients are at highest risk.

    Mangano prospectively studied 474 men with coronary artery disease (243) or at high risk for it (231) who were undergoing elective noncardiac surgery. Historical, clinical, laboratory and physiologic data were gathered during hospitalization and for 6-24 months after surgery. Myocardial ischemia was assessed by continuous electrocardiographic monitoring, beginning two days before surgery and continuing for two days after.

    Eighty-three patients (18%) had postoperative cardiac events in the hospital that were classified as ischemic events (15 patients with cardiac death, myocardial infarction or unstable angina), congestive heart failure (30 patients) or ventricular tachycardia (38 patients). Postoperative myocardial ischemia occurred in 41 percent of the monitored patients and was associated with a 2.8-fold increase in the odds of all adverse cardiac outcomes (95% CI of 1.6-4.1 and p less than 0.0002) and a 9.2-fold increase in the odds of an ischemic event (95% CI between 2.0-42.0 and p less than 0.004). Multivariate analysis showed no other clinical, historical or perioperative variable to be independently associated with ischemic events, including cardiac-risk index, a history of previous myocardial infarction or congestive heart failure or the occurrence of ischemia before or during surgery.

    In high-risk patients undergoing noncardiac surgery, early postoperative myocardial ischemia is the most important correlate of adverse cardiac outcomes.

    MANGANO ET AL 1996

    Effect of ATENOLOL on mortality and cardiovascular morbidity after noncardiac surgery (NEJM 1996 335:1713)

    Perioperative myocardial ischemia is the single most important potentially reversible risk factor for mortality and cardiovascular complications after noncardiac surgery. Although more than 1 million patients (of 27 million total anesthetics provided) have such complications annually, there is no effective preventive therapy.

    Mangano performed a randomized, double-blind, placebo-controlled trial to compare the effect of atenolol with that of a placebo on overall survival and cardiovascular morbidity in patients with or at risk for coronary artery disease who were undergoing noncardiac surgery. ATENOLOL (5-10 mg) was given intravenously IMMEDIATELY BEFORE and for seven days after surgery. Patients were followed over the subsequent two years.

    A total of 200 patients were enrolled with ninety-nine were assigned to the atenolol group and 101 to the placebo group. One hundred ninety-four patients survived to be discharged from the hospital and 192 of these were followed for two years. Overall MORTALITY after discharge from the hospital was significantly lower among the atenolol-treated patients than among those who were given placebo over the six months following hospital discharge (0 versus 8% with p less than 0.001), over the first year (3% versus 14% with p at 0.005) and over two years (10% versus 21% with p at 0.019). The principal effect was a reduction in deaths from cardiac causes during the first six to eight months. Combined cardiovascular outcomes were similarly reduced among the atenolol-treated patients and event-free survival throughout the two-year study period was 68 percent in the placebo group and 83 percent in the atenolol group (p at 0.008).

    In patients who have or are at risk for coronary artery disease who must undergo noncardiac surgery, treatment with atenolol during hospitalization can reduce mortality by FIFTY PERCENT and the incidence of cardiovascular complications for as long as TWO YEARS after surgery.


    Mannitol is usually dosed at 0.5-1.0 grams per kg for control of intracranial HTN. Effects begin within 10-15 minutes and persist for about 2 HOURS.

    The drug may be detrimental to ICP if it is given too rapidly or the BBB is disrupted. It may also lead to CHF and irreversible cardiac arrest.

    Mannitol may cause vasodilation of vascular smooth muscle. This effect is dependent on rate of infusion. It is possible to actually increase ICP while lowering SBP thus greatly reducing CPP. It is advisable to give mannitol slowly while using other maneuvers to lower intracranial volume.

    Mannitol is preferable to urea because of its longer duration of action, higher molecular weight and lesser propensity for rebound effects.

    Plasma osmolarity should be kept below 320 mOsmol/L to avoid renal injury. Sodium should not exceed 150. Furosemide may be beneficial to avoid rebound brain swelling. Furosemide inihibits chloride channels in brain cells to prevent accumulation of idiogenic osmoles.

    Administration is recommended through…

    MAOIs are drugs that prevent the oxidative deamination of naturally occurring monoamines in the central and peripheral autonomic nervous systems. They are classified as hydrazine or non-hydrazine compounds.

    CLINICAL USE The use of MAOI are limited due to serious drug interactions and hepatotoxicity. They are used for the treatment of depression, obsessive-compulsive disorder, eating disorders, essential hypertension (pargyline), chronic pain syndromes and migraine headaches. Tranylcypromine and phenelzine account for over 90% of all MAOI currently prescribed.

    MECHANISM MAOI form a stable and irreversible complex with the MAO enzyme. Synthesis of new monoamine oxidase is a slow process, accounting for the prolonged affect of MAOI following their discontinuation.

    Inhibition of monamine oxidase by MAOI results in accumulation of amine neurotransmitters in the brain within a few hours. This activates a feedback loop that leads to decreased synthesis of these amines and delayed antidepressant effects. With chronic MAOI therapy, there is a reduction in the responsiveness of alpha, beta and serotonergic receptors manifesting as a general reduction in sympathetic nervous system activity.

    Hypotensive effects of MAOI are attributed to accumulation of a false neurotransmitter OCTOPAMINE, in postganglionic sympathetic nerve endings. This causes less vasoconstriction than norepinephrine and blood pressure declines due to decreased SVR (this is the presumed mechanism of action of pargyline in the treatment of hypertension).

    Two FORMS of monoamine oxidase (MAO-A and MAO-B) have been defined on the basis of differences in substrate preferences. Type A enzyme preferentially deaminates serotonin, dopamine and norepinephrine. Type B preferentially deaminates phenethylamine and tyramine. Human brain contains approximately 60% MAO-A. Substrate specificity is concentration dependent and both subtypes are capable of metabolizing all substrates if presented in appropriate concentrations.

    SIDE EFFECTS The most common side effects are sedation, blurred vision, dryness of the mouth and orthostatic hypotension. A common recommendation is the discontinuation of MAOI 14-21 days prior to elective surgery but this is based upon anecdotal reports rather than studies. This practice can increases the risk of suicide significantly. There is now growing evidence that anesthesia may be safely administered in the presence of chronic MAOI use.

    OVERDOSE is reflected in signs of excessive sympathetic nervous system activity (tachycardia, hyperthermia, mydriasis), seizures and coma. MAOI delay gastric emptying. Dantrolene has been used to treat OD.


    SYMPATHOMIMETICS Action of indirect-acting and, to a lesser extent, direct-acting sympathomimetics, including those in cold or asthma remedies, may be exaggerated by MAOI. Many of the synthetic catecholamines (isoproterenol, dobutamine) and non-catecholamines (ephedrine, phenylephrine, amphetamine) are dependent on MAO for their metabolism.

    If HYPOTENSION occurs in those taking MAOIs, the direct-acting sympathomimetics, such as phenylephrine, at carefully titrated doses, are recommended.

    TYRAMINE in FOOD Ingestion of tyramine containing foods (cheese, chicken liver, chocolate, beer, wine) by patients taking MAOI may evoke hyperthermia and a hypertensive crisis since tyramine is not inactivated in the GI tract or liver. Tyramine will evoke the release of endogenous catecholamines that are present in excess amounts.

    HYPERTHEMIA and fatal excitatory reactions may accompany the administration of MEPERIDINE to patients receiving an MAOI. This is most likely due to the ability of meperidine to impair neuronal uptake of serotonin. In addition, there may be hypertension, hypotension, depression of ventilation, muscle rigidity, seizures and coma. Morphine and fentanyl are safe, however ventilatory depression with morphine may be exaggerated.

    OPIOIDS and BARBITURATES Inhibition of hepatic enzymes has been a proposed explanation of the prolonged depressant effects of opioids and barbiturates. The dose of opioids should be decreased to one fourth of the usual amount.

    Exaggerated effects of antihistamines, anticholinergics and tricyclic antidepressants may also be seen. There is one case report of prolonged apnea following succinylcholine and plasma cholinesterases levels were subsequently found to be decreased in 40% of patients treated with phenelzine but in no patients receiving other MAOI.

    MAC Anesthetic requirements are generally increased, reflecting accumulation of NE in the CNS.


    The Mapleson A circuit (MAGILL circuit) consists of a corrugated tube, a reservoir bag, a fresh gas inflow near the reservoir bag and a spring loaded expiratory valve near the patient.

    Rebreathing during SPONTANEOUS ventilation in this circuit can be prevented with relatively low gas flows. Upon exhalation, the patient end of the tubing is filled with dead space gas followed by the alveolar gas. This stream travels up the tubing and meets the fresh gas flowing into the circuit. The pressure in the circuit increases and forces the expiratory valve to open, allowing alveolar gas to escape. Most of the dead space gas is washed out if the fresh gas flow is adequate. During the inspiratory phase, the fresh gas flushes the dead space gas through the tubing toward the patient. Rebreathing of dead space gas poses no problem because the gas does not contain any carbon dioxide.

    Several studies have confirmed Mapleson’s original finding that rebreathing of alveolar gas can be prevented if the fresh gas flow equals or exceeds the patients minute ventilation. Rebreathing does not occur with spontaneous ventilation until the fresh gas flow is BELOW 70% of the minute ventilation.

    The Mapleson A circuit is innefficient during CONTROLLED ventilation. Expiratory valve resistance must be increased to ventilate the patient. Venting the gas in the circuit occurs during the inspiratory phase and the alveolar gases are retained in the tubing during the expiratory phase. Thus, alveolar gas is rebreathed with the ensuing breath before the pressure in the system increases enough to force the expiratory valve open, which causes an increase in arterial carbon dioxide tension. Adequate carbon dioxide elimination by using controlled ventilation with a Mapleson A system requires a fresh gas flow greater than three times the minute ventilation in children or over 20 L/minute in adults. In practice, controlled ventilation should be avoided with this system.


    The Mapleson D system is configured with the fresh gas flow at the airway and the popoff at the bag (precisely the reverse configuration of the Mapleson A). It is essentially a modification of the T-piece in which a breathing bag and an overflow valve (or a slit cut into the bag) have been added to the distal expiratory limb.

    This system has become the most widely used of the Mapleson circuits for pediatric anesthesia and may be most useful for transports in which spontaneously respirations have resumed.

    In contrast to the Mapleson A system, ALVEOLAR gas is the LAST gas to be expelled from the circuit in Mapleson D and E systems so it is more important to prevent rebreathing with adequate flows. With the Mapleson A, if any gas is rebreathed, it is more likely to be the anatomical deadspace gas which is most often fairly acceptable.

    This system is IDEAL during CONTROLLED VENTILATION since the possibility of rebreathing is minimized with fresh gas at only 70 mL/kg per minute provided that minute ventilation is adequate and over 120 mL/kg/minute. Flow must nevertheless be increased as respiratory rate increases as higher rates paradoxically increase the amount of rebreathing (reduce wash out) and will increase the PaCO2.

    Higher flow is needed in the SPONTANEOUSLY breathing patient at 200-300 mL/kg per minute to minimize rebreathing. These high flows correlate with the mean inspiratory flow rate which is about THREE times the minute ventilation with an I:E ratio of 1:2 to 1:3. The MINIMUM flow at 100 mL/kg/min will enable the pediatric patient to remain normocarbic at the expense of an increased minute ventilation. Remember VE as 180 mL per kg in the neonate, 120 for pediatrics and 80 for the adult.

    The BAIN modification is essentially a coaxial version of the Mapleson D with a fresh gas supply enclosed within the expiratory limb.

    A unique hazard of the use of the Bain circuit is occult disconnection or kinking of the inner, fresh gas delivery hose. To perform the PETHICK test, use the following steps.

    1) occlude the circuit at the elbow
    2) close the APL valve
    3) fill circuit using oxygen flush
    4) release the occlusion at elbow

    A Venturi effect will flatten the reservoir bag if the inner tube is patent.


    The MAPLESON E and F are valveless T piece arrangements. The E system is modified from AYRE’S original T piece by the addition of corrugated tubing to the expiratory limb which therby becomes a resevoir of fresh gas during inspiration. During inspiration, the patient breathes FGF from the machine and expiratory limb which must have a
    capacity greater than expected tidal volume (6 mL/kg in neonates and adults). During exhalation, exhaled gas enters the expiratory limb and is flushed out during the expiratory pause. The E system may be used for spontaneous or controlled ventilation (with what is known as a mechanical thumb) with FGF at three times the minite ventilation to prevent rebreathing.

    The MAPLESON F is known as the JACKSON REES modification of the Mapleson E system. In this system a two tailed resevoir bag and a means for venting gases are added to the end of the expiratory limb. The venting piece is usually an adjustable valve that is connected to a scavenging system. The Mapleson F functions similarly to the E except that during exhalation a mixture of exhaled and FGF collects in the bag. On the next inspiration the patient inhales FGF from the machine and that stored in the expiratory limb. The addition of the resevoir bag provides a means to qualitatively MONITOR VENTILATION during spontaneous breathing as well as a means to control ventilation by manually squeezing the resevoir bag. Rebreathing is prevented by using FGF at two to three times the minute ventilation. The Mapleson E and F and popular for pediatrics because they are simple and valveless which provides for low resistance.

    It is the MAPLESON F or simply the T-PIECE that is most commonly used for TRANSPORTING the pediatric patient when it is assumed that spontaneous ventilation will resume. This is useful for physiologic conditions that may benefit from early extubation and the benefit of negative intrathoracic pressures during inspiration. A small slit is cut into the end of the anesthesia bag and a blue clip may be applied or partially applied to allow for bagy inflation and to visualize spontaneous ventilation.


    A (MAGILL) has the fresh gas flow at the bag and popoff at the airway. The resevoir tube must be larger than the patient’s tidal volume or expired gas will enter the bag and contaminate the inspired gas. There is virtually no rebreathing during spontaneous ventilation if the fresh gas flow is 75% of the minute ventilation as the FGF will force expired gases through the popoff (remember VE as 180 mL per kg in the neonate, 120 for pediatrics and 80 for the adult – alveolar ventilation VA is approximately 70% of minute ventilation). The Mapleson A requires extremely high gas flows (three times VE) for controlled ventilation. The design is impractical during anesthesia because of the proximal location of the overflow valve and the need for scavenging wasted gas.

    B (bigger than C) is characterized by having the fresh gas and the popoff at the airway. In Mapleson B and C systems, the site of FGF and the pop off valve are near the patient whereas the circuit tubing and resevoir bag form a cul-de-sac in which a mixture of dead space, alveolar and FGF may collect. Both the B and C systems function similarly with spontaneous and controlled ventilation (the profile pictures are similar) and rebreathing is prevented with flow rates at least twice the minute ventilation.

    C (cute and smaller than B) also has the fresh gas and popoff at the airway. This circuit is useful only for transport in lieu of an ambulatory bag or Laerdahl system but neither the Mapleson B or C are commonly used by anesthesia.

    D (BAIN) has the fresh gas at the airway and the popoff at the bag (opposite of the A). The corrugated hose runs distally from the patient to a resevoir breathing bag. This system is IDEAL during controlled ventilation since the possibility of rebreathing is minimized (requires fresh gas at 70 mL/kg). Higher flow is needed in the spontaneously breathing patient at 200-300 mL/kg (reverse of the Mapleson A system requirements).

    E is also known as the Ayre’s T-piece (behaves like a Mapleson D) which has the fresh gas at the airway and an expiratory limb without a popoff valve. As with the Mapleson A, the volume of the resevoir tube must be greater than the patient’s tidal volume, otherwise the inspired gas will be contaminated by the surrounding air. Note that intermittent PPV can be accomplished by occluding the end of the resevoir tube or by a mechanical thumb type ventilator.

    F circuits are the Jackson-Rees modification of an Ayre’s T-piece and were not originally described by Mapleson. A bag with a small slit that is used as a pop-off is connected to the expiratory limb of the circuit which allows visualization of the respiratory movements. This is the system that is commonly used to transport patients when spontaneous ventilation is likely to resume.

    EFFICIENCY of the Mapleson systems is as follows.

    CONTROLLED D > B > C > A

    Remember the two mnemonics “all dogs can bark” and “do bag cautiously always.”

    Proponents advocate the use of the Mapleson and Bain circuits for the reduction of RESISTANCE to breathing that they provide. The primary sources of resistance in our circle systems are within the ETT, through the valves and the CO2 absorber. With modern equipment, the ETT actually represents a tenfold greater resistance to the neonate compared to the adult. The commonly used circle system has a total resistance of about 3 cm H2O (much less than the ETT itself).


    Marfan syndrome is a disorder of connective tissue inherited as an autosomal dominant trait. The incidence is 4-6 per 100,000 births and the mean age of survival is 32 years. Patients have long tubular bones, high arched palates, pectus excavatum, hyphoscoliosis and hyperextensibility of the joints. Early development of pulmonary emphysema is characteristic and may further accentuate the impact of restrictive lung disease that is secondary to the kyphoscoliosis. There is a high incidence of spontaneous pneumothorax. Cardiac manifestations include aortic root dilation and AI & aortic aneurysms. Ocular changes include lens dislocation, myopia and detachment of the retina.

    Pregnant Marfan patients are monitored for root dilation over 4 cm, may be started on beta blockade and usually should be scheduled for early cearean to lessen risk of dissection. Ephedrine should be avoided.


    Mark/Space Notebook is the perfect application to keep notes, lists, etc.

    Key Features:

    • New note from clipboard
    Click the Clipboard icon in the toolbar to create a new note using the text from your Clipboard.

    • Categories
    Create categories to help organize your notes.

    • Web Links
    Add a hypertext link to a note by entering the URL starting with www or http. For example, http://www.markspace.com

    • Search & Spotlight Support
    Enter text in the Toolbar search field or use Apple’s Spotlight.

    • Drag-n-Drop Import/Export
    Drag text files into Notebook to create notes, or drag a note out to the desktop to export a note.

    • Sync Notes
    Use your .Mac account to sync notes to another Mac with Mark/Space Notebook or sync notes to other Missing Sync products that include Mark/Space Notebook, like The Missing Sync for Sony PSP.


    MMR is a sustained contracture of the jaw muscles following the use of SUCCINYLCHOLINE that may be a forewarning of MH. A mild increase in masseter muscle tone following SCh with limb flaccidity may be a normal response to SCh (4.4% incidence in the pediatric population) and is more common after mask induction with the volatile agents particularly halothane. Those with isolated MMR are generally at little risk for MH and those with total body rigidity may or may not be at risk. In general, patients with MMR have a 20-50% risk of being MH susceptible as determined by positive muscle biopsy.

    When accompanied by total body rigidity, MH is likely enough that the anesthesiologist must immediately check serum potassium by ABG and place Foley for urinalysis and hydration. CVC and arterial catheters should also be considered. Signs of general hypermetabolism suggesting MH may follow immediately or be delayed for several HOURS. The diagnosis of MH is most clearly made when arterial CO2 is greater than 50 mmHg, pH is less than 7.25 and the base deficit is more negative than 8 mEq per liter.

    MYOGLOBINURIA is likely with MMR (without fulminant MH) and should be treated with fluids to maintain urine output greater than 3 mL/kg/hour, mannitol and possibly with alkalinization and furosemide to prevent ATN. Rapidly developing rhabdomyolysis will cause hyperkalemia while slowly developing rhabdomyolysis is safer as potassium is gradually redistributed.

    DANTROLENE is NOT recommended following the occurrence of MMR alone and is reserved for those cases in which MH is considered more likely.

    Patients experiencing MMR with or without clinical signs of MH should be observed closely for at least 24 hours whether or not surgery continues as planned. Myalgia and occasional muscle weakness may be present for 36 hours following the anesthetic. CK and urine color should be checked every six hours until returning to normal. CK may be elevated as high as 40 times the normal value even in patients that are subsequently found not to be susceptible to MH.

    Experts are divided as to how to proceed after isolated MMR is observed. In urgent cases and some elective cases, surgery may procede with anesthetic agents that will not trigger MH. Patients may require reawakening followed by nasal fiberoptic intubations. Many elective cases can be postponed for 24 hours and followed by non-triggering anesthetics or muscle biopsy though postponement is not mandated unless signs of hypermetabolism occur.

    The need for BIOPSY should be discussed with an MH expert. The halothane caffiene contracture test is abnormal in 20-50% of these patients and the advantage of testing primarily involves the elucidation of possible risks to family members and offsping of the patient.

    The DIFFERENTIAL DIAGNOSIS for MMR includes myotonic syndrome, TMJ dysfunction or simply not using enough succinylcholine.


    Methlyenedioxymethamphetamine or ECSTASY is a stimulant and hallucinogenic drug. Idiosyncratic reactions to ingestion include hyperthermia, rhabdomylysis, renal failure, CV collapse and DIC. TOXICITY presents as hyperthermia, rigidity and a rise in serum CK. Active cooling and DANTROLENE are used for therapy.

    It has been suggested that serum MDMA concentrations should be measured in patients who develop hyperthermia during GA. It is also possible that patients who have become hyperthermic with ecstasy could be at greater risk for MH.


    Adults presenting with mediastinal masses often have thymomas (risk for myasthenia gravis), bronchial carcinoma, thyroid and parathyroid tumors and lymphomas. Pediatric patients present with benign bronchial cysts, esophageal duplications or teratomas.

    While obstruction of the SVC may produce obvious symptoms, compression of the major airways or heart itself may not be apparent until after induction.

    TRACHEOBRONCHIAL COMPRESSION has been reported during induction, intubation, positioning, maintenance and recovery. Only 25% of these patients have signs or symptoms preoperatively. If the patient scheduled for biopsy presents with dyspnea or positional dyspnea, the procedure should be done under local anesthesia. Compression of 35% produces severe symptoms in 50% of all patients. Compression of 50% in children will guarantee complete obstruction during induction.

    If the tumor is felt to be chemosensitive or radiosensitive, these therapies should be undertaken before any surgical procedure is undertaken. Therapy will nevertheless make tissue diagnoses more difficult.

    If ASYMPTOMATIC, pulmonary function tests with flow volume loops should be performed in a sitting and supine position to evaluate for potentially obstructing lesions and differentiation of intra and extrathoracic obstructions. Other studies include CT scans, EKG (upright and supine) and echocardiography to evaluate the effect the tumor may have on the heart. If all studies are negative, the patient may proceed to GA but local anesthesia should still be considered given the possibility of FN tests. Some debate the use of these preoperative tests in the patient without symptoms, but many complications have been reported in the healthy appearing patient.

    When possible, FIBEROPTIC intubation with spontaneous ventilation in the semi-FOWLER position is desirable. Some advocate intubation in the LATERAL decubitus position so that the mass may fall away from the airway but a potential need for changing the position should be thought out before induction. INHALATION inductions are inadvisable because of the additional risk of laryngospasm and the inability to examine the airway as possible with FOB. With spontaneous inspiration, the transpulmonary pressures may distend the airway and maintain its patency. Neuromuscular blockers should be avoided throughout the case.

    Personnel and equipment should be available for intubation distal to an obstruction, independent cannulation in each mainstem bronchus, rigid ventilating bronchoscopy and femorofemoral CPB.

    CARDIAC INVOLVEMENT Compression of the SVC is most often a result of malignancy or thrombosis secondary to PA catheter. SVC syndrome consists of dilated venous systems, possible dyspnea, cough, orthopnea and difficult intubation secondary to edema. Mental status changes may also occur secondary to increase in CVP. Vasodilation with anesthesia coupled with decreased venous return may result in profound hypotension. Large mediastinal lymphomas have been associated with dysrhythmias and possible tamponade.

    When severe and potentially untreatable cardiac compression is likely, femorofemoral CPB should be available. Patients with SVC obstruction should be brought to the OR in the upright position to reduce airway edema. Arterial access and femoral CVC are usually helpful. Large bore access in the LOWER extremeties is generally advisable. Awake fiberoptic intubations in the upright position are often performed taking great care to avoid airway trauma. Nebulized lidocaine may avoid the coughing associated with transtracheal injection. Diuretics and steroids may be beneficial for an exacerbation of SVC symptoms during GA.

    Respiratory obstruction should also be anticipated with EMERGENCE especially following diagnostic only procedures. Airway edema may be worsened with manipulation and fluids.


    DOSING Adults may be given 50-75 mg IM. IV dosing for adults is typically in alliquots of 25 mg maximum with continued dosing at up to 100 mg (0.75 mg/kg) every three hours. The 24 hour limit is at 600 mg and the drug should not be used for longer than 48 hours. PEDIATRIC patients may receive 1-2 mg/kg IM or 0.5 mg/kg IV generally every 3-4 hours.

    There is some evidence which suggests that meperidine may produce less smooth muscle spasm, constipation and depression of the cough reflex than equianalgesic doses of morphine. Meperidine 60-100 mg IV is equinalgesic to 10 mg of morphine. The onset of action is lightly more rapid and the duration of action is slightly shorter. Meperidine is less effective by the ORAL route and exact PO:IV ratio of effectiveness is unknown. It is generally observed that oral doses should be four times those given IV.

    Meperidine has a low therapeutic index (LD50:ED50) at 5-7. Other narcotics have indices ranging from 70-90 for morphine, 400 for fentanyl and 33,000 for remifentanil.

    PK The duration of action is approximately 2-4 hours (similar to hydrocodone and less than morphine) though the serum half-life ranges between 15-20 hours. Approximately 90% of the drug is demethylated to normeperidine which has a half-life of 15 hours (up to 35 hours in those with renal failure). NORMEPERIDINE may cause irritability, agitation, tremors, lower seizure thresholds and lead to delirium. The seizures are not reversible with naloxone. Normeperidine is eliminated by the kidneys and should be avoided in those with renal disease, sickle cell disease and elderly.

    PHARMACODYNAMICS Meperidine is structurally similar to atropine and it does possess a mild ATROPINE like antispasmodic effect. Other effects related to this structure include tachycardia, mydriasis and dry mouth. Meperidine is more likely to cause orthostatic hypotension and respiratory depression than morphine. Meperidine is not used in high doses because of significant negative inotropic effects plus histamine release in a substantial number of patients.

    The antishivering effects of the drug are likely due to stimulation of the KAPPA receptors which represents 10% of the activity. This mechanism is supported by the fact that naloxone (a pure antagonist at the mu receptor) will not completely inhibit this beneficial effect.

    Meperidine is contraindicated in patients who are receiving MAO inhibitors and may be avoided in patients on SSRI. Therapeutic doses of meperidine have occasionally precipitated severe and occasionally fatal reactions with a diversity of manifestations in patients who have received such agents within 14 days. The mechanism of these reactions is unclear but may be related to a preexisting hyperphenylalaninemia. Some reactions have been characterized by coma, respiratory depression, cyanosis and hypotension resembling the syndrome of acute narcotic overdose. Other reactions are characterized by hyperexcitability, convulsions, tachycardia, hyperpyrexia and HTN. SEROTONIN SYNDROME is associated with combinations of meperidine, tramadol, dextromethorphan, SSRI, & SNRI (serotonin and NE reuptake inhibitors such as Effexor).

    Also known as pethidine in the UK.


    Mephenteramine is a synthetic noncatecholamine sympathomimetic that stimulates alpha and beta receptors. It acts by directly and indirectly releasing norepinephrine from neuronal storage sites. The medication increases blood pressure, HR and contractility primarily by an increase in myocardial contractility and to a lesser degree by an increase in vascular tone. It increase cerebral blood flow and produces CNS stimulation.

    DOSING is at 15-45 mg (0.4 mg/kg) IV or IM. Infusions are administered at 0.2-5 mg per minute (4-100 mcg/kg/minute).


    MEPIVICAINE or CARBOCAINE is an amino amide with a pKa of 7.6 and a pH of 5.5 in commercial preparations. It is a rapid onset, intermediate duration, intermediate toxicity LA. The potency of mepivicaine is 1.3 times that of of lidocaine (Anes 2001 94:888).

    Textbooks often suggest that the TOXICITY of mepivicaine is higher than that of lidocaine, but the clinical experience suggests the opposite. The toxic dose is 400 mg without epinephrine and 500-600 mg with the use of epinephrine, but the basis for this is anecdotal and many of the clinical studies report the safe use of considerably larger doses of mepivicaine without signs of toxicity when used with epinephrine.

    FETAL metabolism of mepivacaine (unlike that of lidocaine) is specifically limited and mepivacaine is contraindicated for use in obstetrics.

    Clinical uses include INFILTRATION of the skin at the 1% concentration which is associated with 1.5-3 hour duration. EPIDURAL anesthesia with a 2% concentration with a 70-90 minute duration to two segment regression (slightly longer lasting than lidocaine). SPINAL anesthesia at the 4% concentration was used historically with a duration of 60-90 minutes but spinal mepivicaine is not currently used in the US. The risk of TNS with SA mepivicaine is thought to be similar to that of lidocaine.

    PERIPHERAL conduction blocks may be performed at the 1-1.5% concentration and are associated with an approximate 3 hour duration of anesthetic blockade. MEPIVICAINE is probably the agent of choice for peripheral blocks in the patient with coronary disease.


    Also known as lateral femoral cutaneous neuralgia, this syndrome is characterized by a constant burning and tingling sensation associated with variable degrees of numbness over the anterolateral aspect of the thigh. Entrapment occurs near the anterior superior iliac spine where the nerve passes through the ilioinguinal ligament.

    The cause is mostly mechanical and is related to weight gain or tight clothes, but nerve irritation at its spinal origin or during its course through the pelvis must be ruled out. Diabetes and prolonged positioning in lithotomy position during labor may predispose patients to developing symptoms.

    Neural blockade (lateral femoral cutaneous nerve block) may be helpful in the diagnosis and therapy of nerve entrapment syndromes such as this one. Toradol and LIDODERM 5% patch in place for only 12 hours each day may also be beneficial.


    0.7 mmHg equals 1 cmH2O
    1 mmHg equals 1.4 cmH2O

    The density of mecury is 13 times the density of water. Density is the ratio of mass to volume.


    INCREASED ANION GAP The DX of metabolic acidosis can be reliably made whenever the anion gap (Na – Cl – HCO3) is over 20. Normal AG is less than 8 or 12 if K is included in the formula.

    uremia (usually with ESRD)
    DKA or alcoholic ketoacidosis
    starvation ketoacidosis
    paraldehyde or metformin
    iron or isoniazid
    lactic acidosis (cyanide, CO, metHb)
    ethylene glycol

    LACTIC ACIDOSIS will lead to an anion gap acidosis and may be secondary to shock (cardiogenic, hypovolemia, sepsis), regional ischemia, severe hypoxemia, severe anemia, toxins (CO, methanol, salicylates, ethylene glycol, paraldehyde) and
    hypermetabolism (seizures, shivering and MH).

    Other ANION GAP acidoses include ketoacidosis (diabetic, alcoholic, starvation) and chronic renal failure.

    NORMAL ANION GAP acidosis is caused by bicarbonate loss whether by chronic diarrhea, biliary loss, ARF, chloride administration or renal tubular acidosis.

    The TOTAL CO2 on the electrolyte panel is equal to the bicarbonate plus dissolved CO2 (which adds about 2). A low number correlates with chronic metabolic acidosis while a high number may indicate metabolic compensation for chronic hypercarbia.


    MA is the most common acid-base disorder in the hospitalized patient. Most frustrating is the SELF-SUSTAINING potential of alkalosis after CHLORIDE IS DEPLETED.


    1) gastric acid secretion is usually counterbalanced by the bicarbonate produced by the pancreas and this balance is shifted when the acid is lost by NG SUCTION
    2) DIURETICS promote alkalosis by chloride excretion (as chloride follows the sodium that is lost in the urine) – the chloride loss is balanced by HCO3 absorption across the renal tubules. As a rule of thumb, the serum bicarbonate plus 15 equals the last two digits of the serum pH. Potassium is lost because of the increased sodium delivered to the distal tubules. Magnesium is lost in the urine which promotes further potassium depletion by unclear mechanisms.
    3) VOLUME DEPLETION promotes alkalosis in two ways. Bicarbonate is increased in extracellular fluid by concentrating effects. A small circulating blood volume also stimulates the renin-angiotensin-aldosterone axis and aldosterone promotes release of potassium and hydrogen ions by the distal tubule. The other side of this argument is that a decreased GFR (as occurs with renal failure) should produce a metabolic acidosis.
    4) ORGANIC IONS such as lactate in Ringer’s solution or citrate in stored blood can produce a metabolic alkalosis though at least 8 UNITS of blood is required before bicarbonate begins to rise.
    5) the compensation for HYPERCAPNIA is a decrease in renal bicarbonate excretion. If respiratory acidosis is corrected acutely, the compensatory disorder can become a primary acid-base disorder.

    SYMPTOMS of metabolic alkolosis include hypokalemia, hypocalcemia, dysrhythmias, bronchoconstriction and hypotension. Metabolic alkalosis may increase cerebral blood flow unlike the effects of a respiratory alkalosis.

    EVALUATION is made by measuring the urine chloride concentration. Chloride-responsive alkalosis (most common) is characterized by low urinary chloride (less than 15 mEq/L). Chloride-resistant alkalosis (caused by mineralocorticoid excess and potassium depletion) is characterized by high urinary chloride (greater than 25 mEq/L).

    The only exception to these rules occurs in the early stages of diuretic therapy, when urinary chloride concentration is elevated but the metabolic alkalosis may be chloride sensitive.

    CHLORIDE DEFICIT can be estimated by the following.

    mEq = 0.3 x kg x (100 – Cl)

    As an illustration, an 80 kg man with a chloride of 80 would have a deficit of 480 mEq of chloride requiring 3.1 liters of normal saline (which contains 154 mEq of both sodium and chloride per liter).

    URINE ALKALINIZATION may be induced with acetazolamide (Diamox) as an alternative therapy.


    An overview of MET is probably the single best indicator for risks of perioperative cardiac morbidity.

    POOR prognosis
    1 watches TV at basal oxygen
    2 dresses, walking 2 mph
    3 level ground walking

    MODERATE prognosis
    4 cart golfing or bowling
    5 eight stairs, walking 4 mph
    6 stairs with groceries

    GOOD prognosis
    7 running or bag golfing
    8 jogging 8 mph
    12 vigorous stationary biking
    16 scuba diving



    One study in Anesthesiology 2001 revealed better blood pressure control and less neonatal acidosis when metaraminol (0.25 mg per minute) was compared to ephedrine (5 mg per minute) for SAB cesarean sections.


    GLUCOPHAGE (metformin) is a

    Various recommendations for the discontinuation of metformin prior to GA or procedures requiring the use of IV dye have been made since the medications introduction and the initial observations.

    IV METHADONE is equianalgesic to IV morphine but PO METHADONE is 2-3 times more potent than PO morphine. The IV:PO ratio is 1:2.

    The half-life of methadone is unusually long & highly variable. The range of half-lives reported is between 12 hours to FIVE DAYS. Many days or even weeks can be required before a steady state condition is reached.

    The use of methadone for chronic pain states requires multiple daily doses. It appears that cancer pain patients require 3-4 doses of methadone daily to maintain adequate freedom from pain. For this reasons, methadone is considered a second-line drug for cancer pain.

    DOSING Typical PO dosing begins at 5 mg (0.2 mg/kg) every 6-8 hours. Typical IV dosing begins at 2.5 mg (0.1 mg/kg) every 6-8 hours. Methadone may also be provided by PCA.

    When IV methadone is not available during the perioperative period, patients may be adequately treated with equivalent opioids, ketamine and magnesium infusions.

    At diurnal doses over 60 mg per day, methadone may be associated with prolonged QT and TDP.

    INCREASED serum levels may be secondary to ciprofloxacin, INH, amiodarone, fluoxetine, propafenone, cimetidine, erythromycin, diazepam, diltiazem, grapefruit juice, ketoconazole and verapamil.

    DECREASED serum levels may be secondary to barbiturates, carbamazepine, phenytoin, rifampin, spirinolactone and protease inhibitors.


    Methemoglobin is an oxidized adult hemoglobin molecule (with iron oxidized from the ferrous to FERRIC form). Because methemoglobin is UNABLE TO BIND oxygen and has an impaired ability to bind CO2, it causes cyanosis and hypoxemia despite a normal PO2. Pulse oximetry is read at 85% despite the actual concentration of oxyhemoglobin.

    SYMPTOMS Patients may become cyanotic with methemoglobin levels as low as 2.5% but usually greater than 10% concentrations are required. Concentrations higher than 35% will lead to lethargy and dyspnea and 70% may be fatal.

    DIAGNOSIS is made by the four wavelengths of COOXIMETRY and should be considered in any patient with unexplained cyanosis. The typical patient will be cyanotic while routine blood gas analysis will indicate normal oxygen tension and saturation. Cooximetry will give more accurate diagnosis read as oxygenated hemoglobin and methemoglobin concentrations comprising 100%. Blood will appear chocolate brown and will not change to red when exposed to air.

    ETILOGIES of metHgb include congenital absence of metHgb reductase, NITRATE containing compounds and O-TOLUDINE (a product of prilocaine metabolism). Other medications responsible for methemoglobin formation include chlorates, nitrobenzenes, antimalarial drugs, amyl nitrate, silver nitrate and benzocaine -reported with as little as 2-3 sprays of Hurricaine topical. Lidocaine and procaine also produce variable degrees of metHgb.

    SNP and NTG are metabolized within the RBC by a nonenzymatic reaction which REQUIRES oxidation of oxyhemoglobin to methemoglobin. Extremely high doses of these drugs are required to produce problems.

    Patients become symptomatic when the fomation of methemoglobin outpaces the RBC capacity to reduce the molecule. Normal red cells contain less than 1-1.5% methemoglobin.

    TREATMENT for methemoglobinemia is by METHYLENE BLUE most often in doses of 1-2 mg per kg. Methylene blue accelerates the action of NADPH methemoglobin reductase which is an alternative pathway for methemoglobin reduction. The methemoglobin level is usually reduced by at least 50% within one hours. Supplemental oxygen should be administered and bronchodilators may be of value.

    Alternative therapies include hyperbaric oxygen therapy and exchange transfusion.


    Methohexital is a barbiturate that is 2.7 times more potent than STP. It is most commonly used for the brief anesthetics required for electroconvulsive therapy. Methohexital is less likely than thiopental to cause allergic reactions and may be the prefered induction agent for the patient with multiple allergies.

    DOSING Given for induction at 1.5 mg/kg (which is equivalent to 4 mg/kg of thiopental). The onset of action is less than 30 seconds and duration of action is between 5-10 minutes.

    PHARMACOKINETICS The clearance of methohexital is approximately 11 mL/kg/min. The beta half-life is 3-6 hours and the volume of distribution is calculated at 2.5 L/kg. The hepatic extraction ratio is 0.5.

    PHARMACODYNAMICS Methohexital has epileptogenic effects but less than occurs in normal sleep for epileptic patients. It is stated by others that methohexital (like propofol) may lower the seizure threshold in patients with seizure disorders but will raise seizure thresholds in most normal patients. The medication may decrease CO, BP and SVR primarily by venous pooling. The drug causes less hypotension than STP because of greater reflexive tachycardia that accompanies its use.

    Methohexital is metabolized in liver to inactive hydroxyderivatives.


    Methoxyflurane (a methyl ethyl ether) was introduced for clinical use in 1960 because of the dysrhythmogenic effects related to the older alkane derivatives such as halothane. Characteristics are as follows.

    VP 22.5
    MAC 0.16
    B:G 12

    Methoxyflurane (no longer used clinically for several reasons) is best known for its potential to cause renal toxicity. The toxic effects were characterized by high-output renal failure, dilute polyuria, inability to concentrate the urine despite ADH administration and elevated BUN to creatinine ratio essentially producing a clinical picture similar to nephrogenic diabetes insipidus. Patients lost free water and were prone to the development of hypernatremia, hyperosmolarity and dehydration. While reversible in many cases, permanent renal impairment was widely reported as well. In experimental methoxyflurane toxicity, no histological renal pathology is evident.

    The mechanism of methoxyflurane renal toxicity is not completely clear. The degree of toxicity is related to the degree of hepatic metabolism of methoxyflurane and the level of serum fluoride ions that are produced. Fluoride itself is known to be toxic to the kidney and can cause high-output renal failure, s