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ACE 11A
DISCUSSION FOR QUESTION 1
Somatosensory evoked potential (SSEP) latency is the time from initial stimulus of a peripheral nerve (tibial nerve) to the peak of the response (usually near the brainstem). An increase
in latency indicates slowed conduction of the SSEP response through the spinal cord. The differential diagnosis for an increase in latency includes the following:
Increasing inhaled anesthetic concentration

Changing from an intravenous anesthetic to an inhaled anesthetic
Hypothermia
Compression of the areas of the spinal cord that transmit the SSEP signal
Compromised blood supply in the areas of the spinal cord that transmit the SSEP signal
Excessive distraction of the spinal cord
It is important to recall that SSEPs propagate only through certain parts of the spinal cord; consequently, only certain parts of the spinal cord are tested. Compared to the lower
extremity, the upper extremity SSEP signal propagates through a different region of the spinal cord. Studies show that upper extremity (eg, the median or ulnar nerve) SSEP signals
propagate mainly through the dorsal column. In contrast, lower extremity (eg, the posterior tibial nerve) SSEP signals propagate mainly through the dorsal lateral funiculus, which
includes the spinocerebellar tract (Figure 1). The dorsal lateral funiculus is mainly supplied by the anterior spinal artery. Therefore, lower extremity SSEP signals will respond to
changes in anterior spinal cord blood supply. In contrast, upper extremity SSEP signals respond to changes in posterior spinal cord blood supply (ie, paired posterior spinal arteries).
An increase in SSEP latency alerts the surgeon and anesthesiologist that SSEP transmission through the spinal cord has been compromised.
Anterior spinal cord compression may not have any effect on SSEPs.
Changing to a total intravenous anesthetic would most likely decrease SSEP latency.
Discussion Media for Question 1
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Figure 1. Spinocerebellar tract. Image courtesy of Wikipedia users Polarlys and Mikael Häggström. http://commons.wikimedia.org/wiki/File:Spinal_cord_tracts_-_English.svg .
Accessed January 20, 2014. Used in accordance with the Creative Commons Attribution Share Alike 3.0 Unported license, available at http://creativecommons.org/licenses/by-
sa/3.0/deed.en .
References
1. Miller RD. Millerâ€™s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:1486-1488.
2. Sloan TB, Heyer EJ. Anesthesia for intraoperative neurophysiologic monitoring of the spinal cord. J Clin Neurophysiol. 2002;19(5):430-443.
3. Mendiratta A, Emerson RG. Neurophysiologic intraoperative monitoring of scoliosis surgery. J Clin Neurophysiol. 2009;26(2):62-69.
Taxonomy
I.C. BASIC: Organ-based Basic and Clinical Sciences, 1. Central and Peripheral Nervous Systems
II.A. ADVANCED: Basic Sciences, 1. Physics, Monitoring, and Anesthesia Delivery Devices
Cyclosporine is a calcineurin blocker, which causes the inhibition of synthesis of interleukin-2 (IL-2), a T-cell growth factor. This action provides a specific, noncytotoxic suppression of
T-cell activation.
Cyclosporine also appears to have a direct effect on the vascular system, resulting in derangements in several organ systems. Acute nephrotoxicity occurs in 25% to 38% of patients
receiving cyclosporine after transplantation; however, this effect is transient and reversible as long as the dosage is reduced or the drug is discontinued. Long-term treatment with
cyclosporine is associated with irreversible nephrotoxicity, which is reported to occur in 15% to 40% of patients.
Another consequence of cyclosporine administration is hypertension, which may be due to vasoconstriction in the kidney or to a direct effect on the systemic vasculature. Onset of
hypertension occurs within 2 weeks of cyclosporine administration. Treatment consists of sodium restriction or treatment with calcium channel blockers and diuretics. Cardiac toxicity is
not commonly associated with cyclosporine treatment. (Table 1)
Cyclosporine treatment is associated hyperglycemia, however the causality of this effect is confounded by the frequent coadministration of steroids. Toxicity or destruction of the
pancreas does not occur with cyclosporine administration.
Although cyclosporine has been reported to be associated with the development of bronchospasm, cough, and dyspnea, pulmonary sequelae occur less frequently than nephrotoxicity.

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Table 1. Pulmonary and cardiac complications associated with cyclosporine therapy.
References
1. Vincent JL, Abraham E, Moore FA, Kochanek P, Fink MP. Textbook of Critical Care. 6th ed. Philadelphia, PA: Elsevier Saunders; 2011:1310-1311.
2. Hammel L, Sebranek J, Hevesi Z. The anesthetic management of adult patients with organ transplants undergoing nontransplant surgery. In: McLoughlin TM, Johnson JO, Salinas
FV. Advances in Anesthesia.Vol 28. Philadelphia, PA: Elsevier Mosby; 2010:211-244.
3. Kahan B. Forty years of publication in Transplantation Proceedingsâ€”the second decade: the cyclosporine revolution. Transplant Proc. 2009;41(5):1423-1437.
Taxonomy
I.B. BASIC: Clinical Sciences: Anesthesia Procedures, Methods, and Techniques, 1. Evaluation of the Patient and Preoperative Preparation
Metabolism differs among the inhaled general anesthetic agents (Table 1).
Nitrous oxide has not demonstrated any degree of metabolism when administered.
Enflurane, desflurane, and isoflurane undergo metabolism to trifluoroacetylated (TFA) proteins via CYP2E1. TFA proteins are the antigens that stimulate formation of antibodies

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Enflurane, desflurane, and isoflurane undergo metabolism to trifluoroacetylated (TFA) proteins via CYP2E1. TFA proteins are the antigens that stimulate formation of antibodies
attributed with causing the immune response resulting in the hepatic necrosis initially reported with halothane (ie, “halothane hepatitis”). Modern halogenated volatile anesthetics
metabolized to TFA proteins are associated with hepatic necrosis, albeit at a much lower rate than that reported with halothane.
As would be expected since the metabolism of sevoflurane does not result in the creation of TFA proteins, there are no reports of immune-mediated hepatitis following the
administration of sevoflurane. (There are, however, case reports of hepatic necrosis following the administration of sevoflurane. An immune-mediated mechanism has not been
described in these cases.)
Sevoflurane biotransformation results from oxidative metabolism of a fluoromethoxy C–H bond. This biotransformation results in the formation of hexafluoroisopropanol and inorganic
fluoride (Figure 1).
Table 1. Metabolism of halogenated anesthetics to trifluoroacetylated proteins (TFA-proteins) and the incidence of immune-mediated hepatitis. Sevoflurane and methoxyflurane are not
metabolized to trifluoroacetylating species and do not cause immune hepatitis. © 2008. Modified by permission of Macmillan Publishers Ltd, from Kharasch ED. Adverse drug reactions
with halogenated anesthetics. Clin Pharmacol Ther. 2008;84(1):158-162.
Figure 1. In vivo metabolism of sevoflurane. © 2014 American Society of Anesthesiologists.
References
1. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:634-639.
2. Evers AS, Mace M, Kharasch ED. Anesthetic Pharmacology: Basic Principles and Clinical Practice. 2nd ed. New York, NY: Cambridge University Press; 2011:391-392.
3. Reichle FM, Conzen PF. Halogenated inhalational anaesthetics. Best Pract Res Clin Anaesthesiol. 2003;17(1):29-46.
4. Kharasch ED. Adverse drug reactions with halogenated anesthetics. Clin Pharmacol Ther. 2008;84(1):158-162.

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4. Kharasch ED. Adverse drug reactions with halogenated anesthetics. Clin Pharmacol Ther. 2008;84(1):158-162.
Taxonomy
I.D. BASIC: Special Problems or Issues in Anesthesiology, 2. Ethics, Practice Management, and Medicolegal Issues
The anesthesia machine receives high-pressure gas from the pipeline supply or from cylinders. The gas pressure is down-regulated and flows are controlled to supply gas to the low-
pressure circuit (Figure 1). There are 3 methods of checking the low-pressure circuit to detect leaks and oxygen flow problems:
The oxygen analyzer test

A circle system flow test
The low-pressure circuit leak test
Some anesthesia machines have a check valve between the oxygen flush valve and the flow meter/vaporizer assembly, while others (particularly older models) do not (Figure 2). If this
check valve is present, a commonly used test for the low-pressure circuit leak test (ie, the positive-pressure check) is not valid. Application of high pressure at the machine outlet or the
Y-piece closes the check valve and excludes the proximal portions of the low-pressure system. In those machines with a check valve, a negative-pressure leak test (using a suction
bulb) is required to ensure that there are no leaks in the vaporizers, the vaporizer mounts, or the flow tubes.
The negative-pressure leak test is accomplished by placing a suction bulb at the machine outlet (with all vaporizers closed and the gases off). When suction is applied (the bulb is
deflated fully), the bulb will not re-inflate for at least 10 seconds. During the low-pressure test, the check valve remains open and leaks proximal to the check valve would be detected
(Figure 2).
The oxygen analyzer is downstream from all other flow control devices and monitors the anesthesia circuit on a continuous basis throughout the case. The oxygen analyzer test is
performed by exposing the analyzer to room air (21% O2), and then re-exposing it to 100% O2 via the flush mechanism. Calibration of the oxygen analyzer does not depend on the
presence or absence of a check valve.
The circle system flow test (Table 1) evaluates leaks and the integrity of the unidirectional valves in the breathing system and does not depend on the presence or absence of a check
valve.
The pressure check in the piped gas supply is part of the high-pressure system and is independent of the presence of a check valve. This portion of the Anesthesia Apparatus
Checkout Recommendations includes both the oxygen cylinder supply and the central pipeline supply.
There are several short videos on the Web that illustrate the preoperative anesthesia machine safety check, including the low pressure leak test. An example (for the Dräger Aestiva
machine) may be viewed at http://www.youtube.com/watch?v=bs7N3BvFt40.

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Figure 1. Simplified gas supply through an anesthesia machine. Modified with permission, from American Society of Anesthesiologists. Check-out: A Guide for Preoperative Inspection
of an Anesthesia Machine. Park Ridge, IL: American Society of Anesthesiologists; 1987. © 2014 American Society of Anesthesiologists.

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Figure 2. Negative pressure leak test. Left: A negative pressure leak testing device is attached directly to the machine outlet. Squeezing the bulb creates a vacuum in the low-pressure
circuit and opens the check valve. Right: When a leak is present in the low-pressure circuit, room air is entrained through the leak and the suction bulb inflates. Used with permission,
from Andrews JJ. Understanding anesthesia machines. 1988 Review Course Lectures. Cleveland OH: International Anesthesia Research Society; 1988:78.
Table 1. Circle system flow test. Modified with permission, from US Food and Drug Administration. Anesthesia Apparatus Checkout Recommendations, 1993.
https://www.osha.gov/dts/osta/anestheticgases/#Appendix2. Accessed January 22, 2014.

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References
2. Dorsch JA, Dorsch SE. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2008:103-111.
3. Anesthesia Patient Safety Foundation Newsletter. Spring 2008;23(1). http://www.apsf.org/newsletters/html/2008/spring/05_new_guidelines.htm. Accessed January 13, 2014.
4. Arbous MS, Meursing AE, van Kleef JW, et al. Impact of anesthesia management characteristics on severe morbidity and mortality. Anesthesiology. 2005;102(2):257-268.
5. Occupational Safety and Health US Food and Drug Administration. Anesthesia Apparatus Checkout Recommendations, 1993.
http://www.osha.gov/dts/osta/anestheticgases/index.html#Appendix2. Accessed January 22, 2014.
6. Larson ER, Nuttall GA, Ogren BD, et al. A prospective study on anesthesia machine fault identification. Anesth Analg. 2007;104(1):154-156.
7. Weigel WA, Murray WB. Detecting unidirectional valve incompetence by the modified pressure decline method. Anesth Analg. 2005;100(6):1723-1727.
Taxonomy
I.B. BASIC: Clinical Sciences: Anesthesia Procedures, Methods, and Techniques, 7. Postoperative Period

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In 2005, the US Food and Drug Administration (FDA) revised the package insert for all COX-2 inhibitors and nonselective nonsteroidal antiinflammatory drugs (NSAIDs) to highlight the
potential for increased risk of cardiovascular events and the well-described, potentially life-threatening gastrointestinal bleeding associated with their use. Rofecoxib and valdecoxib
were voluntarily removed from the market at that time. Randomized clinical trial data and retrospective observational studies strongly suggested that rofecoxib in particular—and
especially at doses greater than 25 mg/day—was associated with a markedly increased risk of cardiovascular events compared to either placebo or celecoxib. In contrast, data on
celecoxib has been mixed, with some studies even indicating that it might have protective effects with regard to acute myocardial infarction (MI).
Naproxen, across studies, has shown a trend of being safer than diclofenac, ibuprofen, and celecoxib. Across the many studies of cardiovascular risk and overall mortality associated
with coxibs and NSAIDs, higher doses of each agent have been associated with marked increases in the relative risk of adverse outcomes. This highlights the need to use the lowest
dose possible. Furthermore, the cardiac risks associated with these agents are distributed disproportionately to patients at greater risk of cardiovascular events at baseline. For
example, in a study of 8,000 patients comparing rofecoxib and naproxen, only 4% of patients met FDA criteria for secondary prophylaxis of heart attack with aspirin (history of
myocardial infarction, angina, transient ischemic attack, cerebrovascular accident, coronary artery bypass, or angioplasty), but these patients experienced 38% of the MIs. Among the
other 96% of patients, the rate of MI did not significantly differ among patients given naproxen or rofecoxib compared to those receiving placebo.
References
1. Evers AS, Mace M, Kharasch ED. Anesthetic Pharmacology: Basic Principles and Clinical Practice. 2nd ed. New York, NY: Cambridge University Press; 2011:555-557.
2. Fishman SM, Ballantyne JC, Rathmell JP. Bonicaâ€™s Management of Pain. 4th ed. Baltimore, MD: Wolters Kluwer/Lippincott, Williams & Wilkins; 2010:1167.
3. Joshi GP, Gertler R, Fricker R. Cardiovascular thromboembolic adverse effects associated with cyclooxygenase-2 selective inhibitors and nonselective antiinflammatory drugs.
Anesth Analg. 2007;105(6):1793-1804.
4. Trelle S, Reichenbach S, Wandel S, et al. Cardiovascular safety of non-steroidal anti-inflammatory drugs: network meta-analysis. BMJ. 2011;342:c7086.
5. Bombardier C, Laine L, Reicin A, et al; VIGOR Study Group. Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. VIGOR
Study Group. N Engl J Med. 2000;343(21):1520-1528.
Taxonomy
II.D. ADVANCED: Clinical Subspecialties, 1. Painful Disease States
Acute intraoperative bronchospasm requires simultaneous treatment and evaluation of potential causes. Figure 1 illustrates treatment options for allergic and nonallergic
bronchospasm.
In a case of suspected asthma exacerbation, increasing depth of anesthesia, hand-ventilating with 100% oxygen, and administration of β2-agonists are the most important initial
therapeutic interventions.
Figure 2 illustrates the effect of volatile anesthetics on airway resistance.
In addition to the treatments described in Figure 1, consideration should be given to
administration of ketamine
use of volume-cycled ventilatory support with an increased expiratory time and an increase in the allowable peak pressure
ensuring the tracheal tube has not migrated distally to stimulate the carina
administration of epinephrine.
Long-term treatment of asthma proceeds in a stepwise fashion (Figure 3).
Therapeutic options are detailed in Table 1.
Agents that inhibit the leukotriene pathway, such as montelukast, are not used for the acute treatment of bronchospasm.

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Figure 1. Stepwise approach to treatment of perioperative bronchospasm according to the clinical scenario. Used with permission, from Dewachter P, Moulton-Faivre C, Emala CW,
Beloucif S. Case scenario: bronchospasm during anesthetic induction. Anesthesiology. 2011;114(5):1200-1210.

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Figure 2. Percent change in respiratory system resistance in patients after 5 and 10 minutes of maintenance anesthesia with either a continuous infusion of thiopental (0.25 mg • kg–1 •
min–1) in 50-50 nitrous and oxygen or a volatile anesthetic agent (1.1 minimum alveolar concentration [MAC] sevoflurane, halothane, or isoflurane or approximately 1 MAC desflurane).
Volatile anesthetics other than desflurane decrease respiratory system resistance. © 2014 American Society of Anesthesiologists.

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Figure 3. Stepped care approach to asthma treatment. This simplified stepped-care approach to asthma treatment is constructed around the central role of inhaled corticosteroids. For
each of the overlapping steps, the dose of the inhaled corticosteroid can be adjusted as needed to achieve the goal of well-controlled asthma while minimizing the long-term risks
associated with high doses. LABA denotes long-acting β-agonist, LTM leukotriene modifier, LTRA leukotriene-receptor antagonist, and SABA short-acting β-agonist. Used with
permission, from Fanta CH. Asthma. N Engl J Med. 2009;360(10):1002-1014. © 2014 Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.
Table 1. Therapeutic options in asthma. Used with permission of Oxford University Press, from Woods BD, Sladen RN. Perioperative considerations for the patient with asthma and
bronchospasm. Br J Anaesth. 2009;103(suppl 1):i57-i65. Adapted in part from Fanta CH. Asthma. N Engl J Med. 2009;360(10):1002-1014. ï¿½ 2009 Massachusetts Medical Society.
Reprinted with permission from the Massachusetts Medical Society.

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References
1. Miller RD. Millerâ€™s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:562.
2. Woods BD, Sladen RN. Perioperative considerations for the patient with asthma and bronchospasm. Br J Anaesth. 2009;103(suppl 1):i57-i65.
3. Fanta CH. Asthma. N Engl J Med. 2009;360(10):1002-1014.
4. Dewachter P, Moulton-Faivre C, Emala CW, Beloucif S. Case scenario: bronchospasm during anesthetic induction. Anesthesiology. 2011;114(5):1200-1210.
Taxonomy
II.C. ADVANCED: Organ-based Basic and Clinical Sciences, 2. Respiratory System
Successful resuscitation from cardiac arrest is built upon high-quality cardiopulmonary resuscitation and early defibrillation for pulseless ventricular tachycardia (VT) or ventricular
fibrillation (VF). A flow chart depicting adult advanced cardiovascular life support is available at the website for the American Heart Association (AHA) journals:
http://circ.ahajournals.org/content/122/18_suppl_3/S729/F1.expansion.html.
Upon recognition of the patient’s condition and activation of the emergency response system, early, high-quality external cardiac massage is now recommended. High-quality external
cardiac massage is characterized by effective, fast compressions (depressing the sternum > 5 cm, at a rate of 100 compressions/min) with minimal ventilation time or interruptions
between compressions.
Ventilation of the patient’s lungs—in particular, placement of an advanced airway device—should not delay or cause long interruptions in external cardiac massage.
The use of a precordial thump to convert an abnormal or absent cardiac rhythm to a normal sinus rhythm has been the stuff of television and movies. However, the AHA now considers
its use appropriate only in specific circumstances. A precordial thump may be considered in patients with witnessed, monitored, unstable VT (including pulseless VT) if a defibrillator is
not immediately available. It should not delay external cardiac massage. Additionally, in the given scenario, the cardiac arrest was unmonitored.
Attaching a monitor/defibrillator to the patient should be done as expeditiously as possible but should not delay the start of external cardiac massage.
References
2. Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care. Circulation. 2010;122(18 suppl 3):S729-S767.
Taxonomy
II.C. ADVANCED: Organ-based Basic and Clinical Sciences, 3. Cardiovascular System

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The effect of age on minimum alveolar concentration (MAC) is shown in Table 1. In the premature infant, MAC is lower than in the term neonate or the 3-month-old infant. MAC
decreases over the lifetime of the adult, at a rate of approximately 6% per decade over the age of 40.
Intravenous lidocaine decreases MAC by 10% to 28% depending upon the blood concentration achieved. As part of a balanced anesthetic, local anesthetics appear to decrease MAC
synergistically with inhaled anesthetics due to blockade of sodium channels.
Clonidine and dexmedetomidine have been shown to reduce MAC through their central α2 agonist action (Figure 1). In a study using dexmedetomidine in humans, a 17% reduction in
MAC was observed at the highest blood concentration used (0.6 ng/mL).
Although acute alcohol intoxication may result in a decrease in MAC, chronic alcohol intake (alcoholism) increases MAC, presumably through up-regulation of central nervous system
(CNS) responses due to chronically depressed CNS neurotransmitter levels.
Table 1. Effect of age on minimum alveolar concentration (MAC). Modified with permission of Oxford University Press, from Nickalls RW, Mapleson WW. Age-related iso-MAC charts for
isoflurane, sevoflurane and desflurane in man. Br J Anaesth. 2003;91(2):170-174.

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Figure 1. Changes in halothane MAC with time following intravenous clonidine, 5 µg/kg, in dogs. Control, time zero, represents pooled mean ± SEM, n = 30. Each remaining point is
shown as mean ± SEM, (n = 10). Used with permission, from Bloor BC, Flacke WE. Reduction in halothane anesthetic requirement by clonidine, an alpha-adrenergic agonist. Anesth
Analg. 1982;61(9):741-745.
References
2. Nickalls RW, Mapleson WW. Age-related iso-MAC charts for isoflurane, sevoflurane and desflurane in man. Br J Anaesth. 2003;91(2):170-174.
3. Himes RS Jr, DiFazio CA, Burney RG. Effects of lidocaine on the anesthetic requirements for nitrous oxide and halothane. Anesthesiology. 1977;47(5):437-440.
4. Bloor BC, Flacke WE. Reduction in halothane anesthetic requirement by clonidine, an alpha-adrenergic agonist. Anesth Analg. 1982;61(9):741-745.
5. Fragen RJ, Fitzgerald PC. Effect of dexmedetomidine on the minimum alveolar concentration (MAC) of sevoflurane in adults age 55 to 70 years. J Clin Anesth. 1999;11(6):466-
470.
Taxonomy
I.A. BASIC: Basic Sciences, 4. Pharmacology

II.A. ADVANCED: Basic Sciences, 2. Pharmacology

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Droperidol, a butyrophenone, was a commonly used antiemetic prior to the US Food and Drug Administration mandated “black box” warning label regarding prolongation of the QT
interval with a subsequent risk of torsade de pointes. The blockade of dopamine receptors achieved by droperidol may precipitate a worsening of Parkinson symptoms.
Ondansetron, a 5-HT3 antagonist, is a commonly used antiemetic in the perioperative period. Although it has been shown to be effective with few, if any, side effects in patients with
Parkinson disease, repeat dosing of ondansetron has not proven to be effective as a rescue antiemetic. Interestingly, ondansetron has been used as a treatment for psychosis that is
associated with chronic L-dopa therapy for Parkinson disease.
Diphenhydramine, an H1-blocker, is an antihistamine with weak anticholinergic properties. Its side effect profile includes the potential for drowsiness, so treatment may delay recovery.
Antihistamines are recognized as an appropriate medication in multimodal therapy for postoperative nausea and vomiting (Figure 1).
Prochlorperazine, a phenothiazine, may aggravate Parkinson disease symptoms through blockade of dopamine (D2) receptors. As an antiemetic, it blocks D2 receptors in the
chemoreceptor trigger zone.

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Figure 1. Neuronal pathways and factors associated to PONV. Used with permission, from Lages N, Fonseca C, Neves A, Landeiro N, Abelha FJ. Postoperative nausea and vomiting:
a review of the 'minor-major' problem [in Portuguese]. Rev Bras Anestesiol. 2005;55(5):575-585. Used in accordance with the Creative Commons Attribution-Noncommerical 3.0
Unported license available at http://creativecommons.org/licenses/by-nc/3.0/ .
References
2.
Gan TJ, Meyer TA, Apfel CC, et al; Society for Ambulatory Anesthesia. Society for Ambulatory Anesthesia Guidelines for the management of postoperative nausea and vomiting.
Anesth Analg. 2007;105(6):1615-1628.
3. Kovac Al, O'€™Connor TA, Pearman MH, et al. Efficacy of repeat intravenous dosing of ondansetron in controlling postoperative nausea and vomiting: a randomized, double-blind,
placebo-controlled multicenter trial. J Clin Anesth. 1999;11(6):453-459.
Taxonomy
II.C. ADVANCED: Organ-based Basic and Clinical Sciences, 1. Central and Peripheral Nervous Systems

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Succinylcholine can induce life-threatening hyperkalemia in many inherited muscular diseases. However, not all muscle diseases are susceptible to succinylcholine-induced life-
threatening hyperkalemia.
Myotonic dystrophy is an inherited muscular disorder characterized by distal limb and facial muscle weakness, periodic myotonia, frontal balding (in males), insulin resistance, and
cardiac conduction defects. There are 2 types of myotonic dystrophy, with myotonic dystrophy type 1 accounting for 98% of all cases. The defect has been localized to chromosome 19;
specifically, the dystrophia myotonica-protein kinase gene. The prevalence of myotonic dystrophy is 1 in 8,000. Succinylcholine administration to patients with myotonic dystrophy
causes sustained and diffuse muscle contraction lasting several minutes, making mask ventilation and opening the mouth for intubation very difficult. Administration of nondepolarizing
neuromuscular blockers does not relieve the muscle contractions. Succinylcholine does not induce life-threatening hyperkalemia in patients with myotonic dystrophy but is still
contraindicated because of the muscle contractions.
Familial periodic paralysis (PP) is divided into hyperkalemic and hypokalemic types. In the hyperkalemic type, sodium channel mutations, triggered by increased serum potassium,
cause attacks of flaccid paralysis. In the hypokalemic type, either abnormal calcium or sodium channels, triggered by low serum potassium levels, cause attacks of paralysis. Both PP
types are autosomal dominant. Exercise elevates serum potassium and triggers attacks in patients with hyperkalemic PP. Glucose-insulin infusions lower serum potassium and trigger
attacks of paralysis in patients with hypokalemic PP. Succinylcholine administration can cause prolonged muscle paralysis but does not trigger life-threatening hyperkalemia in these
patients.
Myotonia congenita is a congenital form of myotonic dystrophy that is caused by mutations in muscle chloride channels. The autosomal dominant form is also known as Thomsen
disease; the autosomal recessive form is also known as Becker myotonia. In both forms of myotonia congenita, intense myotonia is initiated by a forceful contraction, worsening with
repeated contractions, before gradually extinguishing with further contractions. Succinylcholine administration causes severe myotonia, similar to myotonic dystrophy patients, but not
life-threatening hyperkalemia.
Glycogen storage diseases (GSD) are divided into several types. In GSD type 1, the glucose-6-phosphate pathway is defective. Several different pathway defects are known. An
autosomal recessive defect, with a prevalence of 1 in 100,000, is found primarily in non-Ashkenazi Jews from North Africa. In GSD type 2, the enzyme, acid maltase, is defective. Acid
maltase catalyzes the breakdown of glycogen to glucose-6-phosphate. The infantile form of GSD type 2 is also known as Pompe disease. In all types of GSD, glycogen massively
accumulates in muscle tissue (including the heart), resulting in progressive myopathy. Succinylcholine administration should be avoided in these patients as life-threatening
hyperkalemia, rhabdomyolysis, and possibly malignant hyperthermia can result.
Although patients with end-stage renal disease may have elevated serum potassium, the increase in serum potassium that occurs following the administration of succinylcholine is not
of greater magnitude than that in patients without renal disease.
References
2. Longnecker DE, Brown DL, Newman MF, Zapol WM. Anesthesiology. 2nd ed. New York, NY: McGraw-Hill Medical; 2012:517.
3. Kishnani PS, Steiner RD, Bali D, et al. Pompe disease diagnosis and management guideline. Genet Med. 2006;8(5):267-288.
Taxonomy


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Epinephrine is commonly added to local anesthetic solutions to test for intravascular injection during the performance of regional anesthetic procedures. The test relies on recognition of
an increase in heart rate and blood pressure when epinephrine is introduced into the systemic circulation.
A variety of physiologic and pharmacologic states can alter the heart rate response. For example, the heart rate response is reduced, if not eliminated, in subjects who are acutely β-
blocked. Since α1-adrenergic effects are not affected, epinephrine-induced increases in systolic blood pressure will be unaffected and may be used as a marker of intravascular
injection. The effect of chronic β-blockade on epinephrine-related alterations in heart rate is unknown. The effect of epinephrine on heart rate when used as a marker for intravascular
injection is independent of the local anesthetic used.
The magnitude of the heart rate increase is also reduced as patients age, particularly after the age of 40. Some older patients may not demonstrate a heart rate increase in response to
15 µg of intravenous epinephrine. Blood pressure response is not significantly altered by age.
Furthermore, epinephrine-related heart rate and blood pressure responses are reduced when a patient undergoes general anesthesia.
Table 1 shows the hemodynamic responses to epinephrine test doses in different populations.
Table 1. Hemodynamic responses to epinephrine test doses in different populations based on 3 studies. Used with permission, from Mulroy MF, Bernards CM, McDonald SB, Salinas
FV. A Practical Approach to Regional Anesthesia. 4th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2009:Table 3.2.
References
1. Mulroy MF, Bernards CM, McDonald SB, Salinas FV. A Practical Approach to Regional Anesthesia. 4th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins;
2009:33.
2. Guinard JP, Mulroy MF, Carpenter RL, Knopes KD. Test doses: optimal epinephrine content with and without acute beta-adrenergic blockade. Anesthesiology. 1990;73(3):386-392.
Taxonomy

II.B. ADVANCED: Clinical Sciences (Procedures, Methods, Techniques), 1. Regional Anesthesia

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Sepsis, the systemic inflammatory response to an infectious process, is described in terms of increasing severity. Severe sepsis occurs when organ system dysfunction develops in a
patient with sepsis. Septic shock occurs when severe sepsis is accompanied by hypotension not responsive to fluid administration. Septic shock is caused by an overwhelming infection
that is usually due to a bacterial agent, though other agents (eg, viruses, fungi) can be involved. Septic shock is usually characterized by high cardiac output, low systemic vascular
resistance, intense and diffuse inflammatory response, and organ perfusion abnormalities. Altered mental status, oliguria, and lactic acidosis are common manifestations of septic
shock.
An international group of intensive care organizations is using the best available evidence to advocate for standardized treatment protocols for these critically ill patients. Two groups of
treatments and goals known as “bundles” have been proposed. The concept of bundles has been widely adopted, but it is difficult to determine which elements of a specific bundle are
the most important and it is certainly possible that some are superfluous. The reader is encouraged to review the references for more specific information and to recognize that
treatment of septic shock is an evolving area of medicine with recommendations changing as new scientific evidence emerges. A new, revised set of Surviving Sepsis Campaign
bundles was recently published (Table 1).
The authors of the Surviving Sepsis Campaign recommend AGAINST the administration of bicarbonate for purposes of improving hemodynamics or decreasing vasopressor
requirements in patients with hypoperfusion lactic acidemia with a pH equal to or greater than 7.15. There are no studies available that examine the effect of bicarbonate administration
upon patient outcome.
Initial resuscitation for sepsis-induced hypoperfusion includes volume expansion with crystalloid fluids. End points of adequate resuscitation include
CVP equal to or greater than 8 mm Hg

MAP 65 mm Hg or higher
Urine output 0.5 mL/kg/h or above
Mixed venous oxygen saturation 70% or higher.
Targeting these resuscitation milestones within the initial 6-hour window is known as early goal-directed therapy and has been shown to reduce mortality by 15%.
Measurement of serum lactate is an indicator of hypoperfusion, and reduction of serum lactate levels suggests achievement of adequate tissue perfusion.
Norepinephrine is recommended as a first-line drug for treatment of hypotension. Phenylephrine is not recommended except in instances where norepinephrine causes excessive
dysrhythmias.

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Table 1. Surviving sepsis campaign bundles. Used with permission, from Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis Campaign Guidelines Committee including the
Pediatric Subgroup. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580-637.
References
1. Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Clinical Anesthesia. 6th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2009:1444-1472.
2. Society of Critical Care Medicine. Surviving Sepsis Campaign website. http://www.survivingsepsis.org/. Accessed January 13, 2014.
3. Marik PE. Surviving sepsis: going beyond the guidelines. Ann Intensive Care. 2011;1(1):17.
4. Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup. Surviving sepsis campaign: international guidelines
for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580-637.
5. Rivers E, Nguyen B, Havstad S; Early Goal-Directed Therapy Collaborative Group. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med.
2001;345(19):1368-1377.
Taxonomy
II.D. ADVANCED: Clinical Subspecialties, 12. Critical Care

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In 1952, at the height of the poliomyelitis epidemic, millions were affected globally and more than 57,000 new cases were reported in the United States alone. Approximately 25% to
50% of polio survivors have been diagnosed with postpolio syndrome, a constellation of signs and symptoms that can contribute to perioperative morbidity. The most frequent
symptoms are generalized fatigue, skeletal muscle weakness, cold intolerance, dysphagia, musculoskeletal pain, increased sensitivity to sedative agents, and respiratory difficulties,
including obstructive sleep apnea and frank respiratory failure. Symptoms typically manifest 15 to 40 years after the initial infection and are preceded by many years of stable
neurologic and muscular function.
The majority of patients with postpolio syndrome have a history of paralytic polio with residual motor neuron loss. However, patients who had an initial diagnosis of bulbar polio have
been shown to have recurrent weakness involving the pharynx and larynx, including vocal cord paralysis. The virus has also been shown to damage the reticular activation system in
the brain, and this may be the cause of increased sensitivity to anesthetic agents and opioids reported in postpolio syndrome patients.
Patients with postpolio syndrome may be at increased risk for perioperative complications. Increased sensitivity to nondepolarizing neuromuscular blocking agents and opioids in
combination with respiratory muscle weakness may increase the risk of postoperative respiratory failure. Dysphagia likely represents bulbar involvement and may increase the risk for
aspiration. Cold intolerance is common, and postoperative shivering can be exacerbated. Chronic pain syndromes are also common and often related to muscle weakness and
scoliosis.
Neither fever nor persistent vomiting are manifestations of postpolio syndrome.
References
1. Hines RL, Marschall KE. Stoeltingâ€™s Anesthesia and Co-Existing Disease. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:250.
2. Lambert DA, Giannouli E, Schmidt BJ. Postpolio syndrome and anesthesia. Anesthesiology. 2005;103(3)638-643.
Taxonomy
II.C. ADVANCED: Organ-based Basic and Clinical Sciences, 8. Neuromuscular Diseases and Disorders: Clinical Science
Superior hypogastric plexus blockade can alleviate pelvic pain associated with cancer (eg, cervical, bladder, rectal, prostate) or chronic nonmalignant conditions. Afferent fibers
innervating pelvic viscera travel with sympathetic nerves, trunks, ganglia, and rami back to the spinal cord.
The superior hypogastric plexus is located in the retroperitoneum bilaterally from the lower third of the L5 vertebral body to the upper third of the S1 vertebral body (Figure 1). The
plexus is bounded laterally by the iliac vessels. Innervation of the pelvic viscera continues from the superior hypogastric plexus through the hypogastric nerves to the inferior
hypogastric plexus. Typically, a local anesthetic block is performed first to confirm analgesia prior to a neurolytic block. The classic 2-needle technique for superior hypogastric plexus
blockade requires fluoroscopy and needle placement at the anterolateral aspect of the L5 to S1 intervertebral space (Figure 2). A superior hypogastric plexus block also can be
accomplished via a single needle technique (Figure 3). Superior hypogastric plexus neurolysis is capable of decreasing visceral pain and opioid consumption even in advanced stages
of cancer. However, neurolysis may not be as effective in the setting of significant retroperitoneal lymph node involvement.
A superior hypogastric plexus block is most likely to relieve this patient’s visceral pain and tenesmus from rectal cancer.
A celiac plexus block will relieve visceral pain secondary to cancer of the upper abdomen.
A lumbar sympathetic block will relieve pain due to conditions such as lower extremity complex regional pain syndrome and arterial insufficiency of the lower extremities.
Bilateral pudendal nerve blocks would result in analgesia of the skin of the penis, the perianal area, and the posterior surface of the scrotum.

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Figure 1. Superior hypogastric plexus. © 2014 The American Society of Anesthesiologists.

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Figure 2. Anteroposterior fluoroscopic view of final needle placement for superior hypogastric block. Used with permission, from Mauck WD, Rho RH. The role of neurolytic sympathetic
blocks in treating cancer pain. Techniques in Regional Anesthesia and Pain Management. 2010;14(1):31-39.

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Figure 3. Needle placement in superior hypogastric plexus block. Antero-posterior fluoroscopy view. Used with permission, from Bosscher H. Blockade of the superior hypogastric
plexus block for visceral pelvic pain. Pain Pract. 2001;1(2):162-170.
References
1. Benzon HT, Raja SN, Fishman SM, Liu S, Cohen SP. Essentials of Pain Medicine. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2011:528-529.
2. Fishman SM, Ballantyne JC, Rathmell JP. Bonicaâ€™s Management of Pain. 4th ed. Baltimore, MD: Wolters Kluwer/Lippincott, Williams & Wilkins; 2010:614-615.
3. Bosscher H. Blockade of the superior hypogastric plexus block for visceral pelvic pain. Pain Pract. 2001;1(2):162-170.
4. Peng PW, Tumber PS. Ultrasound-guided interventional procedures for patients with chronic pelvic painâ€”a description of techniques and review of literature. Pain Physician.
2008;11(2):215-224.
Taxonomy

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Most pulmonary function laboratories measure carbon monoxide diffusion capacity of the lung (DLCO) with the single-breath method. A patient takes a rapid, deep breath of 0.3%
carbon monoxide and 10% helium. The patient holds it for 10 s, then rapidly exhales the gas. The first 0.5 to 1 L of exhaled gas (dead space) is discarded and the next 1 L of gas
(alveolar gas) is sampled and analyzed. The average DLCO is 25 mL CO/min/mm Hg, but DLCO is also commonly reported as a percentage of predicted.
Any condition that impairs gas exchange across the alveolar membrane lowers the DLCO, including
chronic obstructive pulmonary disease

sarcoidosis
asbestosis
tuberculosis
heart failure
anemia.
Conditions that have been observed to increase DLCO include
exercise
asthma
polycythemia
left to right intracardiac shunting
pulmonary hemorrhage.
References
2. Enright PL. Diffusing capacity for carbon dioxide. UpToDate website. http://www.uptodate.com/contents/diffusing-capacity-for-carbon-monoxide. Updated July 10, 2013. Accessed
January 13, 2014.
Taxonomy
I.C. BASIC: Organ-based Basic and Clinical Sciences, 2. Respiratory System


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The increased metabolic demand during pregnancy due to the developing fetus increases maternal oxygen consumption by 30 to 40 mL/min. Compared to the nonpregnant state,
oxygen consumption increases by 40% by 8 to 11 weeks’ gestation and 60% immediately postpartum. The increased oxygen demand is associated with an increase in minute
ventilation due to the respiratory stimulation of progesterone and the leftward shift of the carbon dioxide response curve. This increase in minute ventilation is primarily due to an
increase in tidal volume, which increases by 40% from 500 mL to 700 mL. The respiratory rate remains more or less unchanged.
During pregnancy, functional residual capacity decreases by approximately 500 mL as a result of reductions in
residual volume (15% decrease due to cephalad shift of the diaphragm caused by the gravid uterus)
expiratory reserve volume (25% decrease).
Vital capacity is the summation of tidal volume, inspiratory reserve volume, and expiratory reserve volume. It is the maximum amount of air that could be exhaled after maximum
inhalation. There is no significant change in vital capacity during pregnancy.
The opposing effects of prostaglandin E (bronchodilation) and prostaglandin F2α (bronchoconstriction) keep the airway resistance unaltered during pregnancy. Consequently, there are
no significant changes in peak expiratory flow rate or forced expiratory volume in 1 second in pregnant patients.
References
1. Chestnut DH, Polley LS, Tsen LC, Wong CA. Chestnut’s Obstetric Anesthesia: Principles and Practice. 4th ed. Philadelphia, PA: Elsevier Mosby; 2009:19-21.
2. Carlin A, Alfirevic Z. Physiologic changes of pregnancy and monitoring. Best Pract Res Clin Obstet Gynaecol. 2008;22(5):801-823.
Taxonomy
II.D. ADVANCED: Clinical Subspecialties, 3. Obstetric Anesthesia

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Polyuria is usually deemed present when the volume of urine exceeds 50 mL • kg–1 • day–1 or 3,500 mL in a 70-kg patient. Several different pathological processes may contribute to
increased urine output in critical care; therefore, it is important to differentiate among these conditions. Diabetes insipidus (DI) presents with polyuria, polydipsia, hypovolemia, and
hypernatremia (serum sodium > 145 mmol/L). DI is characterized by impaired renal concentrating ability either due to decreased antidiuretic hormone (ADH) secretion (central) or to
decreased renal response to ADH. Central DI commonly manifests after head trauma, following neurosurgery, and with pituitary lesions (eg, craniopharyngioma, adenoma). Along with
hypernatremia, the serum osmolality in patients with DI is usually greater than 300 mOsm/kg and the urine osmolality is less than 300 mOsm/kg. The diagnosis of central DI is
confirmed with increased urine osmolality in response to exogenous ADH.
In patients with syndrome of inappropriate antidiuretic hormone secretion (SIADH), the serum sodium is less than 130 mmol/L, plasma osmolality is less than 270 mOsm/kg, and urine
is hypertonic relative to plasma. Urine output is usually low or normal in SIADH.
Cerebral salt wasting, also seen after head trauma and neurosurgery, is possibly due to hypersecretion of natriuretic peptides. It is accompanied by hyponatremia, with increased urine
output and increased urinary sodium.
Finally, diabetic ketoacidosis, an acute complication of diabetes, is associated with thirst, hyperglycemia, polyuria, normal or low serum sodium (125–135 mEq/L), and high serum
osmolality (300–320 mOsm/kg).
References
2. Fauci AS, Brauwald E, Kasper DL, et al. Harrison’s Principles of Internal Medicine. 17th ed. New York, NY: McGraw-Hill Medical; 2008:2218-2220.
3. Kliegman R, Behrman RE, Jenson HB, Stanton BF. Nelson Textbook of Pediatrics. 18th ed. Philadelphia, PA: Elsevier Saunders; 2007:2299-2303.
Taxonomy
I.C. BASIC: Organ-based Basic and Clinical Sciences, 5. Renal and Urinary Systems/ Electrolyte Balance
II.C. ADVANCED: Organ-based Basic and Clinical Sciences, 7. Endocrine and Metabolic Systems

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Forceps and vacuum extraction are the most commonly available modalities for operative vaginal deliveries. Depending on the position of the fetal skull in the birth canal, forceps
deliveries are classified as outlet (fetal skull at the pelvic floor), low (fetal skull at station < 2 cm), and midpelvic (station > 2 cm). Neonatal injuries, most commonly noted during
midforceps deliveries, include soft tissue trauma to the face, facial nerve injury, cephalohematoma, brachial plexus injury, intracranial hemorrhage, and retinal hemorrhage. Facial nerve
palsy due to forceps use is a relatively common complication. Most of the facial nerve palsies due to birth trauma are related to the use of forceps. Pressure is usually exerted by the
blades of the forceps onto the stylomastoid foramen or on the bone covering the nerve prior to its egress. In the majority of cases the paralysis resolves spontaneously within a few
weeks without any treatment. Decompression and surgical exploration are rarely necessary. Forceps delivery also increases the risk of brachial plexus injuries in the newborn,
especially among those who are born to diabetic mothers and weigh more than 4.5 kg.
Although the use of epidural analgesia for labor pain is not directly associated with increased neonatal injuries in forceps-assisted deliveries, several randomized clinical trials have
reported that effective epidural analgesia prolongs the second stage of labor and increases the risks of operative vaginal deliveries such as forceps and vacuum extraction. Maternal
epidural labor analgesia has not been demonstrated to have any impact on the risk of neonatal injuries with forceps deliveries.
References
2. Wen SW, Liu S, Kramer MS, et al. Comparison of maternal and infant outcomes between vacuum extraction and forceps deliveries. Am J Epidemiol. 2001;153(2):103-107.
Taxonomy
A patient who develops severe hypotension, tachycardia, and increased peak airway pressures is in a situation that requires prompt recognition and management; delaying intervention
for a stat chest radiograph is not warranted. Using only the limited clinical information presented in this scenario, strong consideration should be given to the possibility of a tension
pneumothorax.

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Patients receiving general anesthesia who develop a tension pneumothorax (Figure 1) will typically manifest many of the following signs:
Hypotension
Tachycardia
Decreased breath sounds on the side of the tension pneumothorax
Jugular venous distension (JVD)
Tracheal deviation to the side opposite (away from) the tension pneumothorax
Mediastinal shift to the side opposite (away from) the side of the tension pneumothorax
Increased peak airway pressures
It should be emphasized that not all patients will manifest all the signs listed. For example, hypovolemic patients may be more likely to develop hypotension but are less likely to
develop JVD.
Initial management of a tension pneumothorax includes
administering 100% oxygen

discontinuing nitrous oxide if it was being used
administering volume expanders and resuscitation medications as needed
notifying the surgeon
reducing or eliminating cardiac depressant agents, including inhaled anesthetic gases
performing needle decompression to the ipsilateral side of the tension pneumothorax.
Needle decompression is performed by placement of a large-bore needle (eg, a 14–16 G intravenous cannula) into the second intercostal space at the mid-clavicular line (Figure 2).
The needle is then advanced until air can be aspirated into a syringe; the needle is then removed and the cannula is left open to air. An immediate rush of air indicates the presence of
a tension pneumothorax. Chest tube placement would typically follow once the patient has been stabilized.
Withdrawing the tracheal tube would be appropriate management for a mainstem intubation. Although intubation of the right mainstem bronchus would result in increased peak airway
pressures and diminished breath sounds on the left, it is unlikely to cause severe hypotension and tachycardia.
The administration of albuterol would be appropriate management for a patient with bronchospasm. Although bronchospasm would cause increased peak airway pressure and could be
associated with tachycardia, it is unlikely to cause a unilateral decrease in breath sounds.

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Figure 1. Chest radiograph depicting a left tension pneumothorax, including tracheal deviation and mediastinal shift towards the patient's right side. Used with permission, from Dimov
V. Tension Pneumothorax. Clinical Cases and Images website. http://clinicalcases.org/2004/02/tension-pneumothorax.html. Published March 11, 2004. Updated November 1,
2009. Accessed November 7, 2013. Used in accordance with the Creative Commons Attribution Share Alike 2.5 Generic license, available
athttp://creativecommons.org/licenses/by-sa/2.5/deed.en. Image courtesy of Wikimedia. http://commons.wikimedia.org/wiki/File:Pneumothorax_CXR.jpg. Accessed January
20, 2014.
Figure 2. Needle decompression of tension pneumothorax. © 2014 American Society of Anesthesiologists.
References
1. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:1291.

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2. Giacomini M, Iapichino G, Armani S, Cozzolino M, Brancaccio D, Gallieni M. How to avoid and manage a pneumothorax. J Vasc Access. 2006;7(1):7-14.
Taxonomy
I.B. BASIC: Clinical Sciences: Anesthesia Procedures, Methods, and Techniques, 6. Complications (Etiology, Prevention, Treatment)
Heparin-induced thrombocytopenia (HIT) is caused by antibody-mediated platelet aggregation after exposure to heparin. Heparin is known to cause the expression of several different
glycoproteins on the platelet surface, including platelet factor 4 (PF4). It also causes release of PF4 from vascular endothelium. The heparin–PF4 complex forms the antigen
responsible for the immune response. Antibodies bind to this complex on the platelet surface and activate the platelet via the Fcy II receptor. Aggregation of activated platelets follows.
Severe and even fatal vascular thrombosis can occur. This is termed heparin-induced thrombocytopenia with thrombosis (HITT).
The classically described finding in HIT is a decrease in platelet count to less than 100,000/µL or to less than 50% of the baseline platelet count after exposure to heparin. Typically the
decrease in platelet count occurs several days after heparin exposure but can occur more rapidly in patients who have a history of prior heparin administration.
Thrombosis, most commonly venous, occurs in 75% of patients diagnosed with HIT. The most common presentation of HIT is pulmonary embolism. Arterial thrombosis, occurring
primarily at sites of endothelial damage or atherosclerotic plaque, occurs in approximately 20% of patients with HIT. Significant thrombosis can occur with platelet counts in excess of
100,000/µL and may even precede the development of thrombocytopenia. In the absence of a preexisting bleeding diathesis, spontaneous bleeding is rare in patients with HIT.

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References
1. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:1767-1775, 1902.
2. Lanzarotti S, Weigelt JA. Heparin-induced thrombocytopenia. Surg Clin North Am. 2012;92(6):1559-1572.
Taxonomy
I.C. BASIC: Organ-based Basic and Clinical Sciences, 6. Hematologic System

II.C. ADVANCED: Organ-based Basic and Clinical Sciences, 6. Hematologic System
Laryngotracheobronchitis (croup) is one of the most common infectious causes of acute airway obstruction in children aged 6 months to 6 years. Although croup occasionally causes
potentially life-threatening airway compromise necessitating tracheal intubation, one of the most important considerations in a child suspected of having croup is differentiation from
epiglottitis. Radiographic studies may be performed to assist in establishing the diagnosis. In croup, subglottic narrowing of the trachea produced by airway edema results in narrowing
of the air column of the trachea (steeple sign) on a radiograph of the neck (Figure 1).
The thumb (or thumbprint) sign (Figure 2) is seen on lateral neck radiographs in patients with epiglottitis. This contrasts with the normal sharp appearance of the epiglottis on lateral
neck radiographs (Figure 3).
The anteater nose sign is seen on radiographs of the foot/ankle in calcaneonavicular tarsal coalition (the abnormal fusion of 2 or more tarsal bones).
Hampton hump is a wedge-shaped area of pulmonary consolidation that is sometimes seen on chest radiographs in the presence of a pulmonary embolus. Hampton hump, which
represents an area of pulmonary infarction and atelectasis, is more specific (82%) than sensitive (22%).
In speaking about radiological signs, someone once said, “These are the things radiologists come up with when they sit in the dark too long.”

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Figure 1. In patients with croup, a radiograph of the neck usually demonstrates narrowing of the subglottic trachea with loss of the normally rounded subglottic area, the steeple sign.
Image by Frank Gaillard, MBBS, MMed, FRANZCR, courtesy of Wikipedia. Used in accordance with the Creative Commons Attribution Share Alike 3.0 Unported license, available at
http://creativecommons.org/licenses/by-sa/3.0/deed.en .

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Figure 2. Thumb sign. Used with permission, from Grover C. "Thumb sign" of epiglottitis. N Engl J Med. 2011;365(5):447. © 2011 Boston Massachusetts Medical Society. Reprinted
with permission from the Massachusetts Medical Society.

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Figure 3. Normal lateral neck radiograph demonstrating normal anatomy including the sharp appearance of the epiglottis. Used with permission, from Grover C. "Thumb sign" of
epiglottitis. N Engl J Med. 2011;365(5):447. © 2011 Boston Massachusetts Medical Society. Reprinted with permission from the Massachusetts Medical Society.
References
1. Coté CJ, Lerman J, Todres ID. A Practice of Anesthesia for Infants and Children. 4th ed. Philadelphia, PA: Elsevier Saunders; 2009:675-676.
2. Davis PJ, Cladis FP, Motoyama EK. Smith’s Anesthesia for Infants and Children. 8th ed. Philadelphia, PA: Elsevier Mosby; 2011:812.
3. Gregory GA. Pediatric Anesthesia. 4th ed. New York, NY: Churchill Livingstone; 2002:852-854.
4. Stankiewicz JA, Bowes AK. Croup and epiglottis: a radiologic study. Laryngoscope. 1985;95(10):1159-1160.
5. Rothrock SG, Pignatiello GA, Howard RM. Radiologic diagnosis of epiglottitis: objective criteria for all ages. Ann Emerg Med. 1990;19(9):978-982.
6. Diaz JH. Croup and epiglottitis in children: the anesthesiologist as diagnostician. Anesth Analg. 1985;64(6):621-633.
Taxonomy
II.D. ADVANCED: Clinical Subspecialties, 2. Pediatric Anesthesia

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Placement of a limb tourniquet during surgical procedures results in the development of ischemia to the extremity. Upon tourniquet release, acidotic metabolites are released into the
circulation. The release of the tourniquet can result in significant laboratory and physiologic changes. The degree of these changes is dependent on the amount of area exposed to the
tourniquet (eg, forearm vs entire lower extremity) and the duration of tourniquet inflation. However, many of these changes are mild, transient, and clinically insignificant, especially in
hemodynamically stable patients without comorbid medical disorders. Serum lactate would be likely to increase after release of the limb tourniquet, while central venous pressure,
arterial pH, systemic vascular resistance, and core body temperature would be expected to decrease (Table 1).
Table 1. Physiologic and laboratory changes after release of a limb tourniquet.
References
2. Tai TW, Lin CJ, Jou IM, Chang CW, Lai KA, Yang CY. Tourniquet use in total knee arthroplasty: a meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2011;19(7):1121-1130.
3. Townsend HS, Goodman SB, Schurman DJ, Hackel A, Brock-Utne JG. Tourniquet release: systemic and metabolic effects. Acta Anaesthesiol Scand. 1996;40(10):1234-1237.
Taxonomy
II.D. ADVANCED: Clinical Subspecialties, 8. Orthopedic Anesthesia; Tourniquet Management, Complications, Regional vs. General Anesthesia
Chronic obstructive pulmonary disease (COPD) is characterized by chronic cough, dyspnea, and sputum production with only partially reversible—and usually progressive—airflow
limitation. The National Heart, Lung, and Blood Institute estimates that 14 million Americans have been diagnosed with COPD; an equal number are thought to be afflicted but
undiagnosed.
Patients with COPD usually have features of both chronic bronchitis and emphysema. Chronic bronchitis is defined as excessive secretion of bronchial mucus manifesting as a daily
productive cough for 3 months or more in at least 2 consecutive years. Emphysema denotes abnormal permanent enlargement of air spaces distal to the terminal bronchiole, with
destruction of their walls and without obvious fibrosis.

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In the early stages of COPD, arterial blood gases may show an increased alveolar– arterial oxygen gradient but are usually otherwise normal. In advanced disease, hypoxemia
develops, especially when chronic bronchitis predominates. With increasing severity of COPD, when chronic respiratory failure develops, respiratory acidosis occurs, usually
compensated by metabolic alkalosis.
Two main patterns of disease have been identified in patients with advanced COPD: type A (“pink puffers”) and type B (“blue bloaters”) as shown in Table 1. Most patients have
pathologic evidence of both. Patients with type A disease are less likely to manifest carbon dioxide retention but will do so with advanced disease.
Consider the following arterial blood gases drawn in the preoperative clinic:
Patient
PaO2 PaCO2
pH HCO3-
(mm Hg) (mm Hg) (mEq/L)
A 85 29 7.40 19
B 64 60 7.35 31
C 100 28 7.52 24
D 100 40 7.40 24
The blood gases for patient A show a normal pH, a metabolic acidosis, and a respiratory alkalosis. They are not typical of a patient with COPD. The values for patient C show a primary
respiratory alkalosis with alkalemia. This situation is unlikely to be seen in a patient with COPD. The blood gases shown for patient D are normal. Only patient B has values congruent
with severe COPD.

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Table 1. Patterns of disease in advanced COPD. Used with permission, from Papadakis MA, McPhee SJ. Current Medical Diagnosis & Treatment 2013. New York, NY: McGraw-Hill;
2013:Table 9.7.
References
1. Chesnutt MS, Prendergast TJ, Tavan ET. Pulmonary disorders. In: Papadakis MA, McPhee SJ. Current Medical Diagnosis and Treatment 2013. New York, NY: McGraw-Hill; 2013.
2. Spieth PM, GÃ¼ldner A, de Abreu MG. Chronic obstructive pulmonary disease. Curr Opin Anaesthesiol. 2012;25(1):24-29.
Taxonomy

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Considerations for the anesthetic management of patients with chronic obstructive pulmonary disease (COPD) include the following:
Preoperative cardiopulmonary conditioning (“pulmonary rehabilitation”), which may decrease perioperative risk.
Smoking cessation, which may improve both short- and long-term outcomes.
Use of regional anesthesia techniques as a primary anesthetic to avoid the necessity for tracheal intubation.
Use of regional anesthesia as adjunctive therapy to provide optimal postoperative analgesia and potentially decrease postoperative pulmonary complications.
When tracheal intubation and mechanical ventilation are required, avoidance of pulmonary hyperventilation and intrinsic positive end-expiratory pressure is desirable. Pressure
and flow tracings should be monitored. Breath-by-breath increase in airway pressures and ventilator cycling at expiratory flow higher than zero suggest dynamic hyperinflation.
Efforts should be made to liberate the patient early from mechanical ventilation. Noninvasive ventilation (NIV) may be useful in this regard. NIV has been used to avoid tracheal
intubation during acute exacerbations of COPD and may be employed immediately after extubation in patients who might not meet criteria for extubation.
References
1. Chesnutt MS, Prendergast TJ, Tavan ET. Pulmonary disorders. In: Papadakis MA, McPhee SJ. Current Medical Diagnosis and Treatment 2013. New York, NY: McGraw-Hill; 2013.
2. Spieth PM, GÃ¼ldner A, de Abreu MG. Chronic obstructive pulmonary disease. Curr Opin Anaesthesiol. 2012;25(1):24-29.
Taxonomy
Anesthesiologists may be involved in the care of patients undergoing brain death testing in the intensive care unit or may care for brain dead organ donors undergoing organ
procurement for transplantation. It is vital from a medical, legal, ethical, and societal standpoint that brain death testing be performed properly. Neurologists or neurosurgeons usually
perform such testing, and such clinicians should be independent of any transplant teams that may procure organs.
Prior to brain death testing, conditions that may confound the results should be excluded. These conditions include
severe electrolyte, acid–base, or endocrine disturbances

hypothermia
hypotension
presence of drugs that may alter levels of consciousness
presence of neuromuscular blocking agents.
In addition to these stipulations, the cause of the coma should be known and should be deemed to be irreversible. Clinical criteria critical to the determination of brain death are listed in
Table 1. Steps in the physical examination to assess brain stem death are illustrated in Figure 1.
Decerebrate posturing is not seen in patients with brain death as it implies the presence of some brain stem function.
Although brain death cannot be assessed in the presence of neuromuscular blockade, assessment may proceed after 5 drug half-lives have passed and/or demonstration of recovery

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Although brain death cannot be assessed in the presence of neuromuscular blockade, assessment may proceed after 5 drug half-lives have passed and/or demonstration of recovery
of neuromuscular function.
If brain stem testing is impossible or inconclusive, a cerebral angiogram demonstrating no evidence of cerebral blood flow may be used as evidence of brain death.
Table 1. Clinical criteria for the determination of brain death. Used with permission, from Wijdicks EFM. The diagnosis of brain death. N Engl J Med. 2001;344(16):1215-1221. © 2001
Massachusetts Medical Society. Reprinted with permission from the Massachusetts Medical Society.

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Massachusetts Medical Society. Reprinted with permission from the Massachusetts Medical Society.
Figure 1. The steps in a clinical examination to assess brain stem death. In step 1, the physician determines that there is no motor response and the eyes do not open when a painful
stimulus is applied to the supraorbital nerve or nail bed. In step 2, a clinical assessment of brain-stem reflexes is undertaken. The tested cranial nerves are indicated by Roman
numerals; the solid arrows represent afferent limbs, and the broken arrows efferent limbs. Depicted are the absence of grimacing or eye opening with deep pressure on both condyles
at the level of the temporomandibular joint (afferent nerve V and efferent nerve VII), the absent corneal reflex elicited by touching the edge of the cornea (V and VII), the absent light
reflex (II and III), the absent oculovestibular response toward the side of the cold stimulus provided by ice water (pen marks at the level of the pupils can be used as reference) (VIII and
III and VI), and the absent cough reflex elicited through the introduction of a suction catheter deep in the trachea (IX and X). In step 3, the apnea test is performed; the disconnection of
the ventilator and the use of apneic diffusion oxygenation require precautionary measures. The core temperature should be 36.5°C or higher, the systolic blood pressure should be 90
mm Hg or higher, and the fluid balance should be positive for 6 hours. After preoxygenation (the fraction of inspired oxygen should be 1.0 for 10 minutes), the ventilation rate should be
decreased. The ventilator should be disconnected if the partial pressure of arterial oxygen reaches 200 mm Hg or higher and if the partial pressure of arterial carbon dioxide reaches 40
mm Hg or higher. The oxygen catheter should be at the carina (delivering oxygen at a rate of 6 L/min). The physician should observe the chest and the abdominal wall for respiration for
8 to 10 minutes and should monitor the patient for changes in vital functions. If there is a Paco2 of 60 mm Hg or higher or an increase of more than 20 mm Hg from the normal baseline
value, apnea is confirmed. ABP denotes arterial blood pressure, HR heart rate, RESP respirations, and Spo2 oxygen saturation measured by pulse oximetry. By permission of Mayo
Foundation for Medical Education and Research. All rights reserved. Wijdicks EFM. Brain Death. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.
References
2. Wijdicks EF. The diagnosis of brain death. N Engl J Med. 2001;344(16):1215-1221.

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Taxonomy
II.E. ADVANCED: Special Problems or Issues in Anesthesiology, 2. Organ Donors: Pathophysiology and Clinical Management
Carbon monoxide (CO) is produced when potent inhaled anesthetics react with certain carbon dioxide (CO2) absorbents under certain conditions. Specifically, CO is produced when
potent inhaled anesthetics are exposed to desiccated and alkaline CO2 absorbents (Figure 1).
Figure 2 shows CO concentration versus time when approximately one-half minimum alveolar concentration (MAC) of potent inhaled agent is passed over desiccated soda lime CO2
absorbent. Fifteen L/min oxygen was flowed through soda lime absorbent until desiccated. Under these conditions, desflurane 3.0%/desiccated soda lime produced the maximum
amount of CO, peaking at 14,000 ppm after about 15 minutes. Enflurane, followed by isoflurane, produced the next highest CO amounts. A 1-hour exposure to 1,500 ppm CO is
considered dangerous to life.
Desiccated CO2 absorbents containing alkali (eg, barium, potassium, or sodium hydroxide) produce the largest amounts of CO. Desiccated CO2 absorbents that do not contain any
alkali do not produce appreciable amounts of CO. Figure 3 shows the CO production versus time for desflurane 3.0% when passed through 3 different CO2 absorbents. Absorbents that
are devoid of alkali produce low or no CO.
Temperature is not a good indicator of CO production; in the desiccated soda lime experiments, temperatures increased on average from 24°C to 32.9°C. Despite being a low CO
producer (Figure 4) for the sevoflurane/desiccated soda lime interaction, temperature increased from 26°C to 67.7°C.

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Figure 1. Proposed mechanism of carbon monoxide formation from difluoromethyl–ethyl ether anesthetics. Shown is the backbone structure for isoflurane (X = CI) and desflurane (X =
F). Also shown is a putative mechanism for the concomitant formation of trifluoromethane. Water in line 3 may also react as OH –. Used with permission, from Baxter PJ, Garton K,
Kharasch ED. Mechanistic aspects of carbon monoxide formation from volatile anesthetics. Anesthesiology. 1998;89(4):929-941.

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Figure 2. Carbon monoxide production of desflurane, enflurane and isoflurane in desiccated soda lime. Carbon monoxide was measured in parts per million (ppm). Used with
permission of BioMed Central, from Keijzer C, Perez RS, De Lange JJ. Carbon monoxide production from five volatile anesthetics in dry sodalime in a patient model: halothane and
sevoflurane do produce carbon monoxide; temperature is a poor predictor of carbon monoxide production. BMC Anesthesiol. 2005;5(1):6.

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Figure 3. Carbon monoxide concentrations in parts per million (ppm) from 3.0 vol% desflurane in, respectively, completely dry Medisorb, Spherasorb, and Loflosorb. Because of the
distinctly lower or absent CO concentrations for Superia, Amsorb, and lithium hydroxide, these measurements are not depicted. Medisorb contains potassium hydroxide (KOH);
Spherasorb contains both KOH and sodium hydroxide (NaOH); Loflosorb contains neither KOH nor NaOH. Used with permission, from Keijzer C, Perez RS, de Lange JJ. Carbon
monoxide production from desflurane and six types of carbon dioxide absorbents in a patient model. Acta Anaesthesiol Scand. 2005;49(6):815-818.
Figure 4. Carbon monoxide production of halothane and sevoflurane in desiccated soda lime. Carbon monoxide was measured in parts per million (ppm). Used with permission of
BioMed Central, from Keijzer C, Perez RS, De Lange JJ. Carbon monoxide production from five volatile anesthetics in dry sodalime in a patient model: halothane and sevoflurane do
produce carbon monoxide; temperature is a poor predictor of carbon monoxide production. BMC Anesthesiol. 2005;5(1):6.

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References
2. Keijzer C, Perez RS, De Lange JJ. Carbon monoxide production from five volatile anesthetics in dry sodalime in a patient model: halothane and sevoflurane do produce carbon
monoxide; temperature is a poor predictor of carbon monoxide production. BMC Anesthesiol. 2005;5(1):6.
3. Keijzer C, Perez RS, de Lange JJ. Carbon monoxide production from desflurane and six types of carbon dioxide absorbents in a patient model. Acta Anaesthesiol Scand.
2005;49(6):815-818.
Taxonomy
I.A. BASIC: Basic Sciences, 2. Physics, Monitoring, and Anesthesia Delivery Devices
Parathyroidectomy is usually performed to remove a single, overactive parathyroid adenoma. This procedure can be performed under general anesthesia or with local anesthesia. After
parathyroid resection, some surgeons measure a rapid intraoperative parathyroid hormone (PTH) level to document a reduction in serum concentration. Propofol has been shown in
vitro to interfere with serum PTH measurement. Therefore, some surgeons may request that propofol not be administered for at least 15 minutes prior to blood draw. However, recent
studies show that propofol does not interfere with PTH measurement.
Complications of parathyroidectomy include hematoma, hypoparathyroidism, and unilateral recurrent laryngeal nerve palsy characterized by hoarseness. Bilateral recurrent laryngeal
nerve palsy is extremely rare in this procedure and is characterized by severe airway obstruction (due to vocal cord paralysis in the closed position) requiring intubation.
In the postoperative period, serum calcium levels will gradually decrease over approximately 24 hours, with the nadir of serum calcium occurring 3 to 10 days after resection. Patients
with serious bone demineralization will develop significant hypocalcemia as bone rapidly remineralizes (hungry bone syndrome). Because of the potential for rapid changes in calcium,
phosphate, and magnesium levels, these patients should have serum calcium levels monitored postoperatively.
References
1. Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC, Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2013:1334.
2. Carty SE. Prevention and management of complications in parathyroid surgery. Otolaryngol Clin North Am. 2004;37(4):897-907.
3. Fewins J, Simpson CB, Miller FR. Complications of thyroid and parathyroid surgery. Otolaryngol Clin North Am. 2003;36(1):189-206.
4. Kivela JE, Sprung J, Richards ML, et al. Effects of propofol on intraoperative parathyroid hormone monitoring in patients with primary hyperparathyroidism undergoing
parathyroidectomy: a randomized control trial. Can J Anaesth. 2011;58(6):525-531.
Taxonomy
I.C. BASIC: Organ-based Basic and Clinical Sciences, 7. Endocrine and Metabolic Systems

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The potency of local anesthetic agents is directly proportional to their central nervous system (CNS) and cardiovascular toxicity.
Initial CNS manifestations of local anesthetic toxicity include dizziness or lightheadedness. Patients may also complain of tinnitus or problems focusing their vision; drowsiness may
also occur. Physical manifestations of CNS toxicity include increased motor activity described as shivering, tremors, or twitching. Eventually generalized tonic–clonic convulsions occur.
If local anesthetic concentrations in the brain are sufficiently high, CNS depression including hypoventilation or apnea may occur. Acidosis, whether respiratory or metabolic, decreases
protein binding of local anesthetics, thus increasing the amount of the drug available for diffusion into the brain and increasing the risk of local anesthetic–induced CNS toxicity.
Hypercapnia is particularly detrimental because it results in increased delivery of local anesthetic to the brain via increased cerebral blood flow as well as decreasing intracellular pH,
which produces a greater percentage of ionized drug that cannot diffuse across the cellular membrane (ion trapping).
All local anesthetics produce a dose-dependent blockade of sodium channels, causing blockade of the cardiac conduction system and severe myocardial depression. Overall, the more
potent local anesthetics (eg, bupivacaine, levobupivacaine, ropivacaine) create dysrhythmias at lower concentrations than less potent local anesthetics such as lidocaine and
mepivacaine. However, bupivacaine has a much stronger binding affinity for resting and inactivated sodium channels in the cardiac myocyte than less potent local anesthetics. Similarly,
bupivacaine dissociates from sodium channels during cardiac diastole at a much slower rate than less potent local anesthetics. Bupivacaine’s dissociation rate from sodium channels
does not allow recovery and predisposes to cumulative conduction blockade.
Although vasoconstriction may be present at low concentrations of local anesthetics, vasodilation will be the predominant vascular response in circumstances of local anesthetic
toxicity.
The ratio of the dosage that induces cardiovascular collapse to the dosage that will produce seizures is lower for bupivacaine than other local anesthetics.
Prevention of local anesthetic systemic toxicity is paramount. Consideration should be given to using the lowest-effective dose of local anesthetic, incremental injection of local
anesthetic, aspiration of needles or catheters prior to injection, and use of an intravascular marker (epinephrine or fentanyl). Administration of a benzodiazepine prior to administration
of a local anesthetic is likely to decrease the possibility of a local anesthetic–induced seizure.
The American Society of Regional Anesthesia and Pain Medicine has developed a practice advisory on the treatment of local anesthetic systemic toxicity. As part of the approach, lipid
emulsion (20%) therapy is recommended in the management of local anesthetic toxicity involving cardiac dysrhythmias. It is hypothesized that lipid emulsion binds the highly lipid-
soluble local anesthetics (eg, bupivacaine) resulting in lower drug levels in the cardiac tissue. Lipid emulsion should be administered by bolus followed by a continuous infusion.
Propofol is not an appropriate substitute for lipid emulsion therapy to treat local anesthetic systemic toxicity. It has a low lipid concentration (10%), requires larger volumes for use as a
lipid therapy, and causes direct cardiac depression.
References
1. Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC, Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2013:572-575.
2. Neal JM, Bernards CM, Butterworth JF, et al. ASRA practice advisory on local anesthetic systemic toxicity. Reg Anesth Pain Med. 2010; 35(2):152-161.
3. Neal JM, Mulroy MF, Weinberg GL; American Society of Regional Anesthesia and Pain Medicine. American Society of Regional Anesthesia and Pain Medicine checklist for
managing local anesthetic systemic toxicity: 2012 version. Reg Anesth Pain Med. 2012;37(1):16-18.
Taxonomy
It is possible to perform an isolated cephalic stellate ganglion block that produces sympathetic blockade of upper cervical segments resulting in a Horner syndrome (ie, ptosis, miosis,
anhidrosis, enophthalmos), ipsilateral nasal stuffiness (Guttmann sign), and facial warmth. However, the presence of these signs does not assure successful sympathetic blockade of
the upper extremity. Increase in ipsilateral upper extremity skin temperature is the most commonly used clinical sign of sympathetic blockade of the upper limb.
The first and second (and sometimes third) intercostal nerves may provide an alternate pathway for postganglionic nerves to pass from the upper thoracic ganglia to the brachial plexus
through interconnected postganglionic fibers from their gray rami. These anomalous pathways are referred to as Kuntz nerves and may explain inadequate relief of sympathetically
maintained pain despite successful stellate ganglion block.
References
1. Benzon HT, Raja SN, Fishman SM, Liu S, Cohen SP. Essentials of Pain Medicine. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2011:621, 626-627.
2. Fishman SM, Ballantyne JC, Rathmell JP. Bonica’s Management of Pain. 4th ed. Baltimore, MD: Wolters Kluwer/Lippincott Williams & Wilkins; 2010:1932-1933.
Taxonomy
II.B. ADVANCED: Clinical Sciences (Procedures, Methods, Techniques), 1. Regional Anesthesia

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Buprenorphine is a µ-receptor partial agonist and a κ-receptor antagonist. Given its high affinity for the µ receptor and low intrinsic activity, buprenorphine can induce withdrawal in
opioid-dependent patients by displacing opioids from the receptor. Buprenorphine has a slow onset of action, a peak effect as late as 3 hours after administration, and a prolonged
duration of action (due to high affinity and slow dissociation from the receptor). The half-life of sublingual buprenorphine is 24 to 60 hours. In addition, metabolism through the CYP 3A4
system creates various metabolites, including active norbuprenorphine. Full opioid agonists are much less effective in the presence of buprenorphine use since few receptors are
available for binding. Typically, patients on buprenorphine maintenance require much higher doses of opioid agonists to achieve adequate analgesia in the setting of acute pain.
Buprenorphine is administered sublingually once daily to thrice weekly. Both buprenorphine and a buprenorphine/naloxone combination (Suboxone) are approved by the US Food and
Drug Administration (FDA) for patients with opioid dependence. Naloxone has minimal bioavailability via the sublingual route and no effect. However, if the combination medication is
dissolved and injected intravenously, the naloxone will result in withdrawal given its high affinity for the µ receptor. The American Society of Addiction Medicine recommends the
buprenorphine/naloxone combination to treat all patients with opioid addiction with the exception of pregnant patients. Both methadone and buprenorphine are Category C drugs
(insufficient evidence to establish safety) for parturients. Since methadone is the “gold standard” for management of opioid addiction during pregnancy, buprenorphine should be a
reasonable alternative. Combination therapy (combined buprenorphine/naloxone) has not been evaluated in this patient population, however.
Expected side effects of buprenorphine include sedation, constipation, headache, nausea, vomiting, and dizziness. There is a much lower risk for respiratory depression with
buprenorphine compared to full µ-receptor agonists. Buprenorphine can cause depression of minute ventilation, leveling out to 50% of baseline at higher doses without the production
of apnea.
Administration of buprenorphine to patients who are physically dependent on opioids and not in moderate opioid withdrawal would likely precipitate opioid withdrawal, including
symptoms such as nausea, vomiting, diaphoresis, yawning, fatigue, aches and pain, diarrhea, mydriasis, and piloerection. Buprenorphine would displace the full µ agonist from the
opioid receptors to cause opioid withdrawal. Sedation and respiratory depression are symptoms of opioid overdose.
References
2. Fishman SM, Ballantyne JC, Rathmell JP. Bonicaâ€™s Management of Pain. 4th ed. Baltimore, MD: Wolters Kluwer/Lippincott Williams & Wilkins; 2010:1661.
3. Ducharme S, Fraser R, Gill K. Update on the clinical use of buprenorphine: in opioid-related disorders. Can Fam Physician. 2012;58(1):37-41.
4. Kraus ML, Alford DP, Kotz MM, et al; American Society of Addiction Medicine. Statement of the American Society of Addiction Medicine Consensus Panel on the use of
buprenorphine in office-based treatment of opioid addiction. J Addict Med. 2011;5(4):254-263.
Taxonomy

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Typical tumescent local anesthetic solutions are a mixture of lidocaine, epinephrine, sodium bicarbonate, and normal saline. Lidocaine concentrations are typically 0.1%, 0.075%, or
0.05%. Epinephrine ranges from 0.5 to 1.5 mg/L, and the total dose should not exceed 50 µg/kg. Sodium bicarbonate is typically added at a concentration of 10 mEq/L. Normal saline is
used to create the dilute lidocaine concentrations.
Cytochrome P450 3A4 and P450 1A2 metabolize lidocaine. Reduced activity of the enzymes may result in increased serum lidocaine levels; greater activity of the enzymes may result
in more rapid elimination of lidocaine and therefore lower blood levels.
Because elevated blood levels of lidocaine may occur in patients taking drugs that inhibit the 3A4 or 1A2 isoenzymes of the cytochrome P450 system, the maximum dose of lidocaine
for tumescent liposuction should be decreased in patients taking these drugs. Table 1 lists some foods and drugs that inhibit or induce the cytochrome P450 system.
A comprehensive resource for cytochrome–drug interactions can be found at http://bioinformatics.charite.de/supercyp.
Table 1. Select foods and drugs that inhibit or induce the cytochrome P450 system.
References
2. Svedman KJ, Coldiron B, Coleman WP III, et al. ASDS guidelines of care for tumescent liposuction. Dermatol Surg. 2006;32(5):709-716.
3. Venkataram J. Tumescent liposuction: a review. J Cutan Aesthet Surg. 2008;1(2):49-57.
4. Habbema L. Efficacy of tumescent local anesthesia with variable lidocaine concentration in 3430 consecutive cases of liposuction. J Am Acad Dermatol. 2010;62(6):988-994.
5. Preissner S, Kroll K, Dunkel M, et al. SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids
Res. 2010;38(database issue):D237-D243.

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Res. 2010;38(database issue):D237-D243.
6. Larson AM. Drugs and the liver: Metabolism and mechanisms of injury. UpToDate website. http://www.uptodate.com/contents/drugs-and-the-liver-metabolism-and-
mechanisms-of-injury. Updated October 15, 2012. Accessed January 14, 2014.
Taxonomy
II.D. ADVANCED: Clinical Subspecialties, 5. Anesthesia for Plastic Surgery, Liposuction
Postdural puncture headache (PDPH) is a frequent complication of accidental dural puncture during epidural catheter placement. Younger women (20–30 years old) are at higher risk
than patients older than 60 years. Patients with morbid obesity are at lesser risk than patients with lower body mass index. Relatively less leakage of cerebrospinal fluid after dural
puncture in morbidly obese patients due to their increased abdominal pressure has been proposed to be a protective factor. Patients who have a previous history of PDPH or a previous
history of chronic headache are at higher risk for developing PDPH; this relationship indicates the possibility of some predisposing factors for development of headache in these
patients.
Both saline and air are used for loss-of-resistance technique during epidural placement. The use of saline for location of epidural space has not been found to be a risk factor for
development of PDPH following inadvertent dural puncture. However, some controversy exists regarding a higher risk of PDPH when air, instead of saline, is used for loss of resistance
technique.
References
2. Bezov D, Lipton RB, and Ashina S. Post-dural puncture headache: part I diagnosis, epidemiology, etiology and pathophysiology. Headache. 2010;50(7):1144-1152.

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Superior vena cava syndrome (SVCS) is caused by a compromised venous return from the superior vena cava (SVC) to the right atrium. SVCS is most often secondary to
malignancies, such as bronchial carcinomas and lymphoma. Diminished venous return from the SVC can result in increased intracranial pressure, venous engorgement in the face, and
dyspnea. Edema of the face, neck, and laryngeal structures may result in a difficult laryngoscopy examination or mask ventilation. Similarly, the potential for tracheal compression
warrants the use of an armored tracheal tube, as standard tubes can be compressed.
Anesthetic management includes placement of lower extremity intravenous (IV) access. Upper extremity IV access should be avoided in patients with superior vena cava syndrome due
to impaired blood flow from the upper body. Maintenance of preload is important to attenuate venous collapse, thus diuretics are not recommended in patients with SVCS. Similarly,
maintaining spontaneous ventilation is recommended, as positive pressure ventilation can further compromise venous return. A reverse Trendelenburg or semi-Fowler position (Figure
1) is recommended to facilitate venous return from the upper body and prevent increases in intracranial pressure. Placement of the patient in the Trendelenburg position increases
upper body and cerebral venous engorgement and should therefore be avoided.
Figure 1. Reverse Trendelenburg or semi-Fowler position. Used with permission, from Allport-Settle MJ; US Army. Nursing Fundamentals II, Subcourse MD0906. Edition 100. Willow
Spring, NC: PharmaLogika; 2011:Figure 1-3.
References
1. Hines RL, Marschall KE. Stoeltingâ€™s Anesthesia and Co-Existing Disease. 5th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2008:183, 506.
2. Chaudhary K, Gupta A, Wadhawan S, Jain D, Bhadoria P. Anesthetic management of superior vena cava syndrome due to anterior mediastinal mass. J Anaesthesiol Clin
Pharmacol. 2012;28(2):242-246.
Taxonomy

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Parkinson disease affects 3% of patients over 65 years of age. Treatment revolves around increasing dopamine levels in the central nervous system while attempting to avoid adverse
dopaminergic effects in peripheral systems. Levodopa is a mainstay of therapy. Side effects of levodopa include nausea, vomiting, hypotension, and dyskinesia (ie, dystonic and
myoclonic involuntary muscle movement). Carbidopa is often given in conjunction with levodopa as it does not cross the blood-brain barrier and can attenuate some of the
dopaminergic symptoms caused by levodopa.
Acute discontinuation of levodopa, as can occur in the perioperative period, places the patient with Parkinson disease at risk for exacerbation of symptoms, especially dysphagia and
chest wall rigidity, and has been reported to precipitate a constellation of symptoms similar to neuroleptic malignant syndrome (ie, autonomic instability, altered mental status, muscle
rigidity, and fever). Some authors have termed this constellation of signs and symptoms parkinsonism–hyperpyrexia syndrome or neuroleptic malignant-like syndrome because of the
association with Parkinson disease rather than neuroleptic medications.
Acute exacerbation of symptoms in these patients, who are usually elderly, increases the risk of aspiration, respiratory compromise, and the sequelae of immobility.
Nausea is a side effect of levodopa therapy and is not necessarily a symptom of levodopa withdrawal.
References

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1. Miller RD. Millerâ€™s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:1032, 1113, 2265.
2. Nicholson G, Pereira AC, Hall GM. Parkinsonâ€™s disease and anaesthesia. Br J Anaesth. 2002;89(6):904-916.
Taxonomy
Hypotensive epidural anesthesia is an effective method to reduce perioperative blood loss. This method is achieved by providing an epidural dermatome block at least as high as the
T2 level, blocking the cardioaccelerator fibers of the thoracic sympathetic chain. Any resulting bradycardia can be prevented by using anticholinergics or a continuous intravenous
infusion of a direct β1 agonist (eg, low-dose epinephrine). Reducing arterial pressure while maintaining other cardiovascular parameters within the normal range can decrease
intraoperative blood loss by up to 40%.
Hypothermia has been shown to negatively affect both platelet aggregation and bleeding time. Even a slight decrease in core body temperature of 1.5°C has been associated with
increased blood loss of about 50% during total hip replacement. The mechanism appears to be primarily the effect of hypothermia on platelet aggregation.
Erythropoietin is mainly formed in the human kidney by changes in tissue oxygenation. When injected subcutaneously weekly for 3 weeks before surgery, a mean increase in
preoperative hemoglobin of approximately 1.9 g/dL can be expected. The maximum action of erythropoietin injections is achieved only when patients’ iron stores are adequate;
therefore, patients should also receive supplemental iron orally. The use of preoperative erythropoietin has been demonstrated in many studies to reduce allogenic blood transfusions in
hip replacement surgery.
One method to achieve acute normovolemic hemodilution is to
collect 2 to 3 units of whole blood preoperatively (with crystalloid replacement)

lose diluted blood intraoperatively
re-infuse the preoperatively donated blood postoperatively.
Besides saving red blood cells, acute normovolemic hemodilution returns the patient’s own clotting factors and contributes to hemostasis, which decreases postoperative blood loss.
References
1. Miller RD. Millerâ€™s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010: 2248.
2. Kleinert K, Theusinger OM, Nuernberg J, Werner CM. Alternative procedures for reducing allogeneic blood transfusion in elective orthopedic surgery. HSS J. 2010;6(2):190-198.
3. Moonen AF, Neal TD, Pilot P. Peri-operative blood management in elective orthopaedic surgery. A critical review of the literature. Injury. 2006;37(suppl 5):S11-S16.
Taxonomy

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The most common causes of mortality associated with blood transfusion are noninfectious, many of which are immune-mediated. The term noninfectious serious hazards of transfusion
(NISHOT) is often used to encompass all noninfectious complications of transfusion. A list of both immune- and nonimmune-mediated NISHOTs can be found in Table 1.
Transfusion-associated graft versus host disease (TA-GVHD) is rare but often fatal (>90% mortality). It is caused by engraftment and proliferation of donor T-lymphocytes typically in an
immunocompromised recipient. Patients who have a history of a bone marrow transplant, a stem cell transplant, Hodgkin lymphoma, intensive chemotherapy, or other
immunodeficiency are considered to be at increased risk. Immunocompetent recipients can suffer from TA-GVHD as well if their human leukocyte antigen (HLA) type closely matches
that of the donor; for example, when donor cells are homozygous for an HLA type and the recipient is heterozygous for the same HLA type. Risk factors among immunocompetent
recipients are considered to be receipt of donor-directed blood or HLA-matched blood products, intrauterine transfusion, and erythroblastosis fetalis. Symptoms include fever, rash, liver
dysfunction, diarrhea, and pancytopenia that develops 1 to 6 weeks after transfusion.
TA-GVHD occurs most commonly in patients over age 60 years.

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Table 1. Noninfectious serious hazards of transfusion. Modified from Hendrickson JE, Hillyer CD. Noninfectious serious hazards of transfusion. Anesth Analg. 2009;108(3):759-769.
References
2. Hendrickson JE, Hillyer CD. Noninfectious serious hazards of transfusion. Anesth Analg. 2009;108(3):759-769.
Taxonomy


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The lithotomy position is commonly used for gynecological, urological, and lower abdominal procedures. Typically, the hips are flexed 80 to 100 degrees and the legs are abducted 30
to 45 degrees from the midline. The knees are flexed, positioning the lower legs approximately parallel to the body, and the legs are held in place by some type of mechanical support
(Figure 1). The common peroneal nerve can be compressed by the supporting structure, most frequently at the level of the head of the fibula, resulting in a neuropathy.
In a large retrospective review of patients who underwent surgery in the lithotomy position, the most common nerve injury was to the common peroneal. Patients with common peroneal
nerve injury were also more likely to be smokers, have a lower body mass index, and have undergone longer procedures.
The common peroneal nerve contains nerve fibers originating at L4 to S2, and a motor neuropathy of this nerve can result in an inability to dorsiflex the foot (foot drop).
Figure 1. Lithotomy position. Image by Saltanat Ebli, courtesy of Wikipedia. http://en.wikipedia.org/wiki/File:Lithotomy_position.jpg . Accessed January 20, 2014. Used in
accordance with the Creative Commons Attribution Share Alike 3.0 Unported license, available at http://creativecommons.org/licenses/by-sa/3.0/deed.en .
References
2. Warner MA, Martin JT, Schroeder DR, Offord KP, Chute CG. Lower-extremity motor neuropathy associated with surgery performed on patients in a lithotomy position.
Anesthesiology. 1994;81(1):6-12.

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Taxonomy
Multiple sclerosis (MS) is an autoimmune disorder that affects the central nervous system (CNS). While the exact cause is unknown, there is speculation that some combination of
environmental factors and genetic predisposition may play a role in the etiology of this disease.
Typically, the symptoms of MS are related to the presence and degree of demyelination within the CNS. Symptoms can be exacerbated by emotional and physiological stress, which is
certainly an issue in the perioperative period.
Autonomic dysfunction as well as motor weakness can occur. Symptoms can be chronic and slowly progressive or acute and intermittent with periods of apparent recovery or
remission. The extreme unpredictability and variability of signs and symptoms can make diagnosis and treatment difficult.
Patients with MS are sensitive to increases in body temperature, and even modest elevations in temperature (1°C) have been associated with exacerbations of symptoms. Acute
exacerbations of MS symptoms are treated with immunosuppressant medications, including corticosteroids. All immunosuppressants should be continued throughout the perioperative
period.
The use of nondepolarizing neuromuscular blockers in patients with MS is considered safe. However, as with some other neuromuscular disorders, response to nondepolarizing
neuromuscular blockade can be variable, and both significant increased sensitivity and apparent resistance to these drugs have been reported. Exaggerated release of potassium from
demyelinated muscle in response to administration of succinylcholine has been reported in patients with MS, and some sources recommend that its use be avoided if possible.
Spinal anesthesia has been associated with exacerbation of symptoms in some patients with MS. The precise mechanism of this phenomenon is unknown; however, it has been
suggested that demyelination within the CNS may predispose the spinal cord to the neurotoxic effects of local anesthetics. Epidural anesthesia may be associated with less risk. Some
authors recommend using lower concentrations of bupivacaine for labor epidurals in patients with MS. It is important to note that both spinal and epidural anesthesia have been used
successfully and without adverse sequelae in patients with MS.
References
1. Hines RL, Marschall KE. Stoelting’s Anesthesia and Co-Existing Disease. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:248-250.
2. Hebl JR, Horlocker TT, Schroeder DR. Neuraxial anesthesia and analgesia in patients with preexisting central nervous system disorders. Anesth Analg. 2006;103(1):223-228.

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Taxonomy
I.B. BASIC: Clinical Sciences: Anesthesia Procedures, Methods, and Techniques, 2. Regional Anesthesia
Electroconvulsive therapy (ECT) is an important modality in the treatment of medication-resistant, severe depression. The efficacy of ECT in treating patients with severe depression is
related to the duration of seizure activity, with the best therapeutic response reportedly associated with a seizure lasting 25 to 50 seconds. The choice of induction agent can affect both
the quality and duration of the therapeutic seizure and so may affect the efficacy of treatment. The “gold standard” for induction agents is methohexital. It has a short duration of action
and has little to no effect on seizure duration. The effects of other induction agents are often discussed in comparison with methohexital.
Propofol has been shown to shorten seizure duration significantly, unless given in subhypnotic doses.
Etomidate is associated with longer seizure duration compared to methohexital and is often chosen as the induction agent for patients with a history of suboptimal seizure duration.
Etomidate also has been associated with post-ECT confusion and an increased risk for nausea and vomiting compared with methohexital.
Compared with other induction agents, the sympathetic response to ECT is exaggerated when ketamine is used for induction. Ketamine is also associated with a significantly shortened
seizure duration compared with methohexital.
References
2. Ding Z, White PF. Anesthesia for electroconvulsive therapy. Anesth Analg. 2002;94(5):1351-1364.
3. Forman SA. Clinical and molecular pharmacology of etomidate. Anesthesiology. 2011;114(3):695-707.
Taxonomy
II.E. ADVANCED: Special Problems or Issues in Anesthesiology, 1. Electroconvulsive Therapy

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A pulmonary embolus mechanically obstructs blood flow to part of the lung. The resulting absence of perfusion to a ventilated area of the lung constitutes increased dead space. An
increase in alveolar dead space results in an increased difference between the PaCO2 and end-tidal gas.
In addition to the mechanical obstruction of blood flow, pulmonary thromboembolism commonly results in platelet activation with a consequent release of serotonin and thromboxane
A2, resulting in bronchospasm. Accordingly, pulmonary embolism is commonly associated with an increase in peak inspiratory pressure.
Tachycardia is reported to occur in 71% of patients with pulmonary embolism.
The effect of a pulmonary embolism on PaCO2 depends on the ventilatory status of the patient. Patients who are unable to increase minute ventilation sufficiently to compensate for the
increase in dead space will manifest an increase in PaCO2. Because end-tidal gas results from a mixture of gas from normal alveoli as well as from alveoli lacking perfusion as a result
of the embolus, end-tidal carbon dioxide concentrations decrease with pulmonary embolism. Accordingly, the difference between PaCO2 and end-tidal gas will be increased.
References
1. Lumb AB. Nunnâ€™s Applied Respiratory Physiology. 7th ed. Edinburgh, Scotland: Elsevier Churchill Livingstone; 2010:425-426.
2. Vidal Melo MF, Harris RS, Layfield D, Musch G, Venegas JG. Changes in regional ventilation after autologous blood clot pulmonary embolism. Anesthesiology. 2002;97(3):671-
681.
3. Schmitt HJ, Beckmann T, Lang W. Small change in capnography led to the detection of an intravascular thrombus. J Clin Anesth. 2004;16(4):286-288.
4. Desciak MC, Martin DE. Perioperative pulmonary embolism: diagnosis and anesthetic management. J Clin Anesth. 2011;23(2):153-165.
Taxonomy

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Stent thrombosis is a devastating complication of drug-eluting stents (DES) placed in patients with coronary artery disease. The risk of stent thrombosis is increased in the perioperative
setting due to the inflammatory response and platelet activation associated with surgery. The risk of perioperative stent thrombosis decreases when surgical procedures are performed
12 months or more after DES placement. Therefore, it is recommended that elective procedures be postponed for at least 12 months following DES placement (Figure 1). If surgery
must commence during this time period, continuation of dual antiplatelet therapy with aspirin and a thienopyridine (eg, clopidogrel) is recommended throughout the entire perioperative
period to reduce the risk of late stent thrombosis. For surgical procedures associated with a high risk of bleeding, clopidogrel may be discontinued for 5 days preoperatively and
reloaded postoperatively once the bleeding risk has diminished. Aspirin, however, should be continued.
The evidence to support the recommendation for “bridging therapy” is tenuous.
Figure 1. Algorithm of perioperative management of patients with drug-eluting stents. COX = cyclooxygenase; DES = drug-eluting stent(s); LMWH = low molecular weight heparin;
NSAID = nonsteroidal antiinflammatory drug; PCI = percutaneous coronary intervention; ST = stent thrombosis; UFH = unfractionated heparin. Used with permission, from King SB III,
Smith SC Jr, Hirshfeld JW Jr, et al. 2007 focused update of the ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2008;51(2):172-209. © Elsevier Inc. All rights reserved.
References
2. Abualsaud AO, Eisenberg MJ. Perioperative management of patients with drug-eluting stents. JACC Cardiovasc Interv. 2010;3(22):131-142.
3. King SB III, Smith SC Jr, Hirshfeld JW Jr, et al. 2007 focused update of the ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention: a report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2008;51(2):172-209.
Taxonomy

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Cor pulmonale is defined as right ventricular dysfunction secondary to pulmonary hypertension. The pathophysiology of pulmonary hypertension specific to patients with respiratory
disorders includes hypoxic pulmonary vasoconstriction, remodeling and decreased cross-sectional area of small pulmonary arteries, and endothelial dysfunction. These changes result
in increased right ventricular afterload, right ventricular hypertrophy, and, ultimately, right ventricular failure. Signs of respiratory-induced pulmonary hypertension and cor pulmonale
include lower extremity edema and jugular venous distension. Respiratory disease results in precapillary pulmonary hypertension with a normal pulmonary artery occlusion pressure
(PAOP).
An elevated PAOP represents pulmonary venous hypertension, most often from left ventricular failure.
References
1. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:941, 942, 1825.
2. Weitzenblum E. Chronic cor pulmonale. Heart. 2003;89(2):225-230.
3. Shujaat A, Minkin R, Eden E. Pulmonary hypertension and chronic cor pulmonale in COPD. Int J Chron Obstruct Pulmon Dis. 2007;2(3):273-282.
Taxonomy


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Cortisol levels are usually obtained in the morning to account for normal circadian variation (Table 1). The patient without a history of exogenous glucocorticoid intake with a normal
plasma cortisol level is not at increased risk for adrenal insufficiency. Stress (which may occur due to preoperative anxiety) may increase the plasma cortisol level.
The risk of adrenal suppression secondary to exogenous steroid administration is dependent on several factors in addition to the dose and the duration of steroid administration,
including age of the patient (elderly patients are more likely to experience adrenal suppression from a given dose) and dosing regimen (alternate-day dosing is less likely to result in
adrenal suppression than daily dosing). Adults taking 5 mg every other day of a morning dose of prednisone for 3 doses are not likely to have suppression of the hypothalamic pituitary
axis and do not require additional supplementation of their usual daily dose. These patients are not at increased risk for adrenal insufficiency.
Inadequate steroid replacement in a patient with adrenal insufficiency or adrenal suppression may lead to an Addisonian crisis or even death. In the patient taking steroids, a
medication history of chronic glucocorticoid intake may be inaccurate. Thus, in a patient where there is an elevated suspicion for adrenal suppression, a preoperative
adrenocorticotropic hormone (ACTH) stimulation test has been advocated (Figure 1).
More often in the preoperative period it is disadvantageous to obtain an ACTH stimulation test. Prophylactic treatment with perioperative steroids is not associated with significant
adverse effects. In particular, wound healing after supraphysiologic doses of hydrocortisone has been investigated in a primate model and found not to be affected by short-term dosing.
After prolonged use of glucocorticoids, it may take 6 to 12 months for adrenal glands to recover fully. Most recommendations include perioperative steroid coverage for patients taking
suppressive doses of steroids in the previous year.
Patients requiring perioperative steroids should receive their baseline steroid dose and supplementation with a glucocorticoid such as hydrocortisone. Recommendations for dosing,
which have not substantively changed in almost 40 years, are presented in Table 2.
Testosterone therapy for androgen deficiency does not increase the risk of adrenal insufficiency.
Etomidate induction during intubation of the trachea may result in acute suppression of the adrenal response to stress. In the septic patient, etomidate induction may lead to increased
mortality. The multicenter Corticosteroid Therapy of Septic Shock trial found that 61% of patients receiving etomidate developed adrenal insufficiency, while 45% of patients not
receiving etomidate developed adrenal insufficiency. Thus, while adrenal insufficiency is common in severely septic patients, etomidate administration leads to a significantly increased
risk. This is borne out by the fact that etomidate use predicted death in both univariable (odds ratio 1.7) and multivariable (odds ratio 1.75) analyses.
Table 1. Normal diurnal cortisol range. Data from Dmitrieva NO, Almeida DM, Dmitrieva J, Loken E, Pieper CF. A day-centered approach to modeling cortisol: diurnal cortisol profiles
and their associations among U.S. adults. Psychoneuroendocrinology. 2013;38(10):2354-2365.

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Figure 1. Ruling out adrenal insufficiency (AI). Reproduced with permission of the Cleveland Clinic Center for Continuing Education. Ioachimescu AG, Hamrahian AH. Diseases of the
adrenal gland. Disease management project. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/diseases-of-the-adrenal-gland/ . © 2010
The Cleveland Clinic Foundation. All rights reserved.
Table 2. Stress and glucocorticoid supplementation. Data from Salem M, Tainsh RE Jr, Bromberg J, Loriaux DL, Chernow B. Perioperative glucocorticoid coverage. A reassessment 42
years after emergence of a problem. Ann Surg. 1994;219(4):416-425.
References
1. Hines RL, Marschall KE. Stoeltingâ€™s Anesthesia and Co-Existing Disease. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:398-400.
3. de la Grandville B, Arroyo D, Walder B. Etomidate for critically ill patients. Con: do you really want to weaken the frail? Eur J Anaesthesiol. 2012;29(11):511-514.
4. Salem M, Tainsh RE Jr, Bromberg J, Loriaux DL, Chernow B. Perioperative glucocorticoid coverage. A reassessment 42 years after emergence of a problem. Ann Surg.
1994;219(4):416-425.

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1994;219(4):416-425.
Taxonomy
In any upright position, including the sitting position, the blood pressure (BP) measured in the arm will be higher than the BP in the brain. The difference between these two is the
hydrostatic pressure gradient between the brain and the location in which the BP is being measured. There is approximately a 0.77 mm Hg decrease in BP for each cm difference in
height. In the sitting position, the circle of Willis is located 10 to 12 cm above the base of the brain, resulting in a BP that is about 9 mm Hg lower at the circle of Willis than at the
external auditory meatus and up to 33 mm Hg lower than that measured in the arm. Because the vertical distance between a BP cuff placed on the lower extremity and any cerebral
structure is even greater, the magnitude of this difference becomes even more critical. For example, if a BP cuff on the leg is 36 cm below the external auditory meatus, the cuff will
record a pressure 28 mm Hg higher than will be present at the base of the brain and 37 mm Hg lower than at the circle of Willis. Failure to recognize this difference in BP, especially in
patients with cerebrovascular disease or those in whom controlled hypotension is requested by the surgeon, may easily result in cerebral perfusion pressures below the lower limit of
autoregulation.
Autopsy studies show that more than 45% of the adult population has an incomplete circle of Willis.
Although the height difference between the brain and the location in which the blood pressure is being measured is not as great with the patient in the “beach chair” position as in the
full sitting position, the same considerations apply.
References
2. Lobato EB, Gravenstein N, Kirby RR. Complications in Anesthesiology. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2008:850-852.
3. Martin JT, Warner MA. Positioning in Anesthesia and Surgery. 3rd ed. Philadelphia, PA: WB Saunders; 1997:71-88.
4. Cullen DJ, Kirby RR. Beach chair position may decrease cerebral perfusion. Anesthesia Patient Safety Foundation Newsletter. Summer 2007;22(2).
http://www.apsf.org/newsletters/html/2007/summer/01_beach_chair.htm. Accessed January 14, 2014.
5. Pohl A, Cullen DJ. Cerebral ischemia during shoulder surgery in the upright position: a case series. J Clin Anesth. 2005;17(6):463-469.
6. Papadonikolakis A, Wiesler ER, Olympio MA, Poehling GG. Avoiding catastrophic complications of stroke and death related to shoulder surgery in the sitting position. Arthroscopy.
2008;24(4):481-482.
7. Drummond JC, Lee RR, Howell JP Jr. Focal cerebral ischemia after surgery in the '€œbeach chair' position: the role of a congenital variation of circle of Willis anatomy. Anesth
Analg. 2012;114(6):1301-1303.
8. Murphy GS, Szokol JW Marymont JH, et al. Cerebral oxygen desaturation events assessed by near-infrared spectroscopy during shoulder arthroscopy in the beach chair and
lateral decubitus positions.Anesth Analg. 2010;111(2):496-505.
9. Lam AM, Baldwin G. Blood pressure and adverse perioperative neurologic outcomes: an uncomfortable position. Anesth Analg. 2012;114(6):1156-1159.
10. Lee L, Caplan R. APSF workshop: cerebral perfusion experts share views on management of head-up cases. Anesthesia Patient Safety Foundation Newsletter. 2010; Winter
2009â€“2010. http://www.apsf.org/newsletters/html/2010/winter/01_workshop.htm. Accessed January 14, 2014.
Taxonomy

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Malignant hyperthermia (MH) is a disorder of muscle hypermetabolism occurring upon exposure to certain drugs used during anesthesia (eg, volatile anesthetic agents and
succinylcholine). In the pediatric population, the rate of MH is has been reported to be as high as 1 in 3,000 to 1 in 15,000 anesthetics. The reported rate in adults is 1 in 50,000
anesthetics. This range may be due to the multiple inheritance patterns that have been reported as well as variable penetrance and expression. Some of the variability is due to the
multiple loci of the gene for ryanodine receptor on chromosome 19.
Central core disease, King-Denborough syndrome, and Evans myopathy are clearly linked to MH.
Often, the first signs of MH in the anesthetized patient are tachycardia and/or tachypnea (if the patient is breathing spontaneously). The tachypnea is driven by hypercapnia secondary
to hypermetabolism. Increases in core temperature may be seen within 15 minutes, but hyperthermia is considered an intermediate sign. Late signs include generalized skeletal muscle
rigidity and dark-colored urine (myoglobinuria).
Medical treatment for MH consists of an initial dose of dantrolene 2.5 mg/kg. The anesthetic trigger should be removed, the patient hyperventilated with 100% oxygen at high flow rates,
and active cooling should be initiated. Hydration and diuresis to treat myoglobinuria should be initiated. An arterial catheter may be placed to regularly sample blood, and metabolic
abnormalities should be addressed. Additional information on emergency therapy for MH is available on the website of the Malignant Hyperthermia Association of the United States
(MHAUS) at http://www.mhaus.org/.
In the event of an MH crisis, the MH 24-hour hotline (800-644-9737) may be accessed.
References
2. Lerman J. Perioperative management of the paediatric patient with coexisting neuromuscular disease. Br J Anaesth. 2011;107(suppl 1):i79-i89.
Taxonomy

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Abnormal movements, including generalized tonic–clonic seizure activity, focal motor seizures, myoclonus, opisthotonus, and choreoathetoid movements, have been reported to occur
upon induction and emergence after administration of propofol. Of these, myoclonus is reported most frequently, occurring in 15% to 85% of pediatric patients.
Seizure-like movements after administration of etomidate, including tonic–clonic and focal motor (dystonic) activity, have been associated with electroencephalographic (EEG)
abnormalities (Table 1).
The absence of abnormal cortical activity in the majority of patients has led to several theories regarding the origin of these seizure-like movements. The predominant thought is that
propofol potentiates γ-aminobutyric acid (GABA)-mediated pre- and postsynaptic inhibition, thereby impeding inhibitory circuitry. This leads to subcortical or brainstem excitation. In
addition, propofol acts as a glycine antagonist at low doses and a glycine agonist at high doses. Since glycine is the major inhibitory neurotransmitter in the central nervous system,
varying concentrations of propofol (as seen during induction and emergence) may lead to an imbalance in inhibitory versus excitatory effects. Finally, it has been postulated that
propofol stimulates subcortical dopaminergic sites.
Opisthotonus is caused by a severe spasm of back and neck muscles (Figure 1). Experimentally it may be produced in animals by transection at the level of the midbrain, leading to a
decerebrate state. There are a few case reports describing this striking side effect after induction with propofol, during emergence, and in the postoperative care unit.
Case reports of choreoathetoid movements after propofol administration are rare.
Myoclonic movements in the pediatric population have been reported to range from 15% to 85% upon induction using propofol. The reported rate of myoclonic activity in adult patients
induced with etomidate (20%–70%) greatly exceeds that reported for propofol (1.8%).
Pretreatment to prevent abnormal movements after propofol administration has been studied. Dopaminergic medications such as metoclopramide and droperidol have not been shown
to be effective; midazolam also has not been shown effective. There is some evidence that fentanyl decreases the frequency of abnormal movements.

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Table 1. Relationship of abnormal electroencephalographic (EEG) activity to seizure-like movements using various induction agents. Data from Reddy RV, Moorthy SS, Dierdorf SF,
Deitch RD Jr, Link L. Excitatory effects and electroencephalographic correlation of etomidate, thiopental, methohexital, and propofol. Anesth Analg. 1993;77(5):1008-1011.
Figure 1. Opisthotonus. Image courtesy of Wikipedia.
References
2. Voss LJ, Sleigh JW, Barnard JP, Kirsch HE. The howling cortex: seizures and general anesthetic drugs. Anesth Analg. 2008;107(5):1689-1703.
3. Walder B, Tramèr MR, Seeck M. Seizure-like phenomena and propofol: a systematic review. Neurology. 2002;58(9):1327-1332.
4. Ries CR, Scoates PJ, Puil E. Opisthotonos following propofol: a nonepileptic perspective and treatment strategy. Can J Anaesth. 1994;41(5 Pt 1):414-419.
5. Reddy RV, Moorthy SS, Dierdorf SF, Deitch RD Jr, Link L. Excitatory effects and electroencephalographic correlation of etomidate, thiopental, methohexital, and propofol. Anesth
Analg. 1993;77(5):1008-1011.
Taxonomy


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Identifying patients who are at risk for acute cognitive changes (eg, delirium), late-onset cognitive changes such as postoperative cognitive dysfunction (POCD), or progression of
preexisting cognitive dysfunction (eg, dementia) leads to better outcomes for the patient and the facility. Delirium is a serious postoperative complication in 5% to 15% of elderly patients
after general anesthesia and up to 64% of these patients after total joint replacement. It is estimated that at least 20% or 12.5 million individuals aged 65 years or older will experience
delirium at an annual cost to the health care system of about $152 billion. Anesthetic management that alters these statistics would make a substantial contribution to controlling health
care costs.
Current data strongly suggest that preoperatively identifying patients with cognitive impairment and preemptively managing it in patients scheduled for inpatient procedures will
decrease
the duration of stay

the risk of intensive care unit admission
complications
the need for long-term institutional care
one-year postprocedure mortality.
The initial step in assessing risk is establishing the preoperative presence and severity of the cognitive changes. Dementia is a disturbance of higher cortical function, memory, thinking,
learning capacity, and judgment. When a clinician is suspicious of significant undiagnosed dementia, the inclusion of elements of a Mini-Mental Status Exam (MMSE) in the interview
can be useful in discussing expectations with family and adjusting anesthetic management.
The National Center for Emergency Medicine Informatics provides a simplified MMSE form that can be used to guide the physician interview or be administered by a nurse. Table 1
shows some sample questions. The maximum MMSE score is 30; any patient who scores below 23 has mild dementia, a situation that is often hard to detect without formal evaluation.
Patients with preexisting cognitive disorders have a higher risk for postoperative cognitive complications than other patients. The most common complication is delirium, which occurs in
about 40% of elderly surgical patients with preexisting cognitive impairment. Delirium is characterized by fluctuating changes in attention, thinking, and levels of consciousness. Risk
factors for delirium include

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use of central nervous system (CNS) depressant drugs (eg, benzodiazepines)

inadequate hydration (eg, inadequate oral intake)
unfamiliar environment and caregivers
sleep deprivation
anxiety.
Patients generally recover from the acute cognitive changes, although in extreme instances only a return to familiar surroundings restores mental functioning to baseline. Discussion
has occurred in the anesthesiology literature and the lay press about residual cognitive dysfunction as a complication of surgery. Unfortunately, cognitive changes, especially long-term
changes such as POCD, are often assumed to be caused by anesthetic management, which makes patients and families anxious and, at times, hostile about receiving anesthesia
care.
POCD is a more subtle intellectual dysfunction than delirium or exacerbation of preexisting cognitive disease. Characterized by a lingering decline in memory, concentration, and
information processing, POCD is often not identified at the time of hospital discharge but months later. It is initially attributed by the family, the patient, and the primary care physician to
medications and stress. The frequency of POCD is associated with severity of surgery and the number of perioperative complications that occur. Table 2 describes the primary
differences between delirium and POCD.
No causal relationship between specific anesthetic management or drug toxicity and POCD has been identified despite efforts to develop an animal model in both elderly and neonatal
rodents. There remains only an association with low processed electroencephalographic scores and POCD. There is an association with POCD and postoperative mortality at 1 year.
This may reflect an underlying CNS disease, including depression, or the severity of comorbid conditions. Addressing the issue with patients and their families will be necessary.
The only consistent method to prevent either dementia or POCD is through identifying patients at risk and initiating preemptive treatment. The only established prevention strategy for
perioperative cognitive changes is a preemptive geriatric consultation. Treatment of preexisting mental health issues, particularly depression and early dementia, allows early
appropriate intervention by primary care or other health care providers.
Table 2. Key differences between delirium and POCD. Used with permission, from Funder KS, Steinmetz J, Rasmussen LS. Anaesthesia for the patient with dementia undergoing
outpatient surgery. Curr Opin Anaesthesiol. 2009;22(6):712-717.
References
2. Funder KS, Steinmetz J, Rasmussen LS. Anaesthesia for the patient with dementia undergoing outpatient surgery. Curr Opin Anaesthesiol. 2009;22(6):712-717.
3. Schultz-Larsen K, Lomholt RK, Kreiner S. Mini-Mental Status Examination: a short form of MMSE was as accurate as the original MMSE in predicting dementia. J Clin Epidemiol.
2007;60(3):260-267.
4. Dasgupta M, Dumbrell AC. Preoperative risk assessment for delirium after noncardiac surgery: a systematic review. J Am Geriatr Soc. 2006;54(10):1578-1589.
5. Greene NH, Attix DK, Weldon BC, Smith PJ, McDonagh DL, Monk TG. Measures of executive function and depression identify patients at risk for postoperative delirium.
Anesthesiology. 2009;110(4):788-795.
6. Monk TG, Weldon BC, Garvan CW, et al. Gravenstein JS. Predictors of cognitive dysfunction after major noncardiac surgery. Anesthesiology. 2008;108(1):18-30.
Taxonomy
II.D. ADVANCED: Clinical Subspecialties, 11. Geriatric Anesthesia/Aging

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Metoclopramide, a medication commonly used to treat nausea, vomiting, and gastroparesis, is a dopamine antagonist.
A well-known side effect from the administration of metoclopramide is the development of extrapyramidal symptoms (EPS). Large doses of metoclopramide have been reported to
cause EPS in more than 10% of patients. Examples of EPS include restlessness, involuntary movements, uncontrollable speech, akinesia (inability to initiate movement), and akathisia
(inability to remain motionless). EPS can be effectively managed by the administration of medications with anticholinergic effects (such as benztropine or diphenhydramine) as well as
benzodiazepines.
Flumazenil, neostigmine, and physostigmine are not appropriate medications for management of a patient with EPS. Flumazenil is a benzodiazepine antagonist and would not be
expected to be effective in the management of extrapyramidal symptoms. Neostigmine and physostigmine are acetylcholinesterase inhibitors; administration of either of these drugs
results in an increase in acetylcholine and would not be expected to be effective in the management of extrapyramidal symptoms.
References
2. Jo YY, Kim YB, Yang MR, Chang YJ. Extrapyramidal side effects after metoclopramide administration in a post-anesthesia care unit—a case report. Korean J Anesthesiol.
2012;63(3):274-276.
Taxonomy

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In late 2010, the American Heart Association (AHA) released updates to the pediatric basic life support (BLS) algorithm
(http://circ.ahajournals.org/content/122/18_suppl_3/S862/F3.expansion.html). A major change in the 2010 Pediatric BLS guidelines is regarding the order of cardiopulmonary
resuscitation. The previous “ABC” order of airway, breathing, and then circulation has been replaced with “CAB”; this sequence requires chest compressions to be started before
providing airway management.
The change from “ABC” to “CAB” was made by the AHA for the following reasons:
Better outcome in adults if compressions are started early

Less delay in ability to start compressions due to
head positioning/opening airway
unwillingness to provide rescue breaths
Although the new pediatric BLS guidelines provide consistency with adult guidelines, the delay in initiating ventilation may be more problematic in children. The consensus was that the
consequences of the minimal delay would be offset by the advantage of consistency.
When in the situation of having a child who is unresponsive and apneic, if more than one rescuer is present, one should be sent to activate the emergency response system and obtain
an automatic external defibrillator (AED). The primary health care provider should check for a pulse; this should take less than 10 seconds. If no pulse is present or if the provider is
unsure, chest compressions should be initiated. For a single rescuer, opening the airway and rescue breathing should occur after 30 chest compressions have been delivered. If 2
rescuers are present, opening the airway and rescue breathing should occur after 15 chest compressions. Five cycles of chest compressions and rescue breaths should be delivered in
the ratio of 30:2 by a single rescuer or 15:2 for a 2-person team. After 5 cycles have occurred (about 2 min), the patient’s rhythm should be evaluated by an AED, if available, to
determine if a shock is indicated. If an AED is not available or the AED does not indicate the patient should be defibrillated, 5 cycles of chest compressions and rescue breaths should
be repeated. This 2-minute cycle should be repeated until the patient starts to move or advanced life support personnel and equipment are present.
References
1. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010: 691-698.
2. Berg MD, Schexnayder SM, Chameides L, et al. Part 13: pediatric basic life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care. Circulation. 2010;122(18)(suppl 3):S862-S875.
Taxonomy

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Mediastinoscopy and mediastinotomy are frequently performed to diagnose as well as stage lung cancers. However, lymphadenopathy from other causes such as lymphoma and
sarcoidosis are also possibilities. The most common diagnosis associated with these procedures is bronchogenic carcinoma. Frequently these carcinomas will spread via the
lymphatics of the lung to the paratracheal, subaortic, and bronchial lymph nodes. These procedures allow the surgeon to gain access to these nodes and take biopsies. The most likely
path of spread for metastatic disease determines the surgical approach taken. For lesions affecting the right upper and middle lobes (and to some extent left lower lobes), a cervical
mediastinal exploration (mediastinoscopy) is the preferred approach. In the case of left upper lobe lesions, an anterior mediastinotomy is recommended.
Mediastinoscopy is performed with the patient in the supine position and neck extended. A small incision is made in the suprasternal notch and a tunnel is created by blunt dissection
just anterior and slightly lateral to the trachea. The rigid mediastinoscope is inserted into the mediastinum along a plane running anterior to the trachea. It passes posterior to the
innominate artery and thoracic aorta. Several anatomic structures can be inadvertently compressed or damaged by the mediastinoscope during the procedure (Figure 1). These
structures (and damage) include the following:
Thoracic aorta (reflex bradycardia or rupture/hemorrhage)

Innominate artery (decreased carotid blood flow and decreased cerebral flow)
Trachea (an inability to ventilate)
Vena cava (hemorrhage)
Lung (tension pneumothorax)
As part of the anesthetic management during mediastinoscopy, the anesthesiologist focuses on early detection of these potential complications. The most commonly compressed
vessel is the innominate artery with blood flow decreasing to the right subclavian and right carotid arteries. This can lead to significant reductions in cerebral blood flow. In order to
detect compression of this vessel early, it is recommended that the pulse oximeter or arterial line be placed on the right upper extremity. The pulse is monitored, and compression can
be immediately detected by a decrease in the pressure waveform. The anesthesiologist can then inform the surgeon that flow appears compromised, and the scope position can be
corrected. A noninvasive blood pressure monitor would be best utilized on the left upper extremity rather than on the right to avoid overtreating low blood pressure readings. Placement
of lower extremity intravenous access has been suggested by some, especially in the case of superior vena cava syndrome or a mediastinal mass where damage to the superior vena
cava or compression of upper extremity vessels might impede a resuscitation. However, the placement of an arterial line in a lower extremity for this case is not indicated, nor is a lower

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cava or compression of upper extremity vessels might impede a resuscitation. However, the placement of an arterial line in a lower extremity for this case is not indicated, nor is a lower
extremity the most appropriate site.
Figure 1. Mediastinoscopy and surrounding structures. Used with permission, from Longnecker DE, Brown DL, Newman MF, Zapol WM. Anesthesiology. New York, NY: McGraw-Hill
Medical; 2008:Figure 53-30. © 2008 The McGraw-Hill Companies, Inc. All rights reserved.

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References
1. Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC, Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2013:1060-
1061.
2. Longnecker DE, Brown DL, Newman MF, Zapol WM. Anesthesiology. New York, NY: McGraw-Hill Medical; 2008:1252-1259.
3. ErdÃ¶s G, Tzanova I. Perioperative anaesthetic management of mediastinal mass in adults. Eur J Anaesthesiol. 2009;26(8):627-632.
4. BÃ©chard P, LÃ©tourneau L, Lacasse Y, CÃ´tÃ© D, BussiÃ¨res JS. Perioperative cardiorespiratory complications in adults with mediastinal mass: incidence and risk factors.
Anesthesiology. 2004;100(4):826-834.
Taxonomy
Preoperative assessment of the patient scheduled for thoracotomy and lung resection surgery provides important information for postoperative and long-term morbidity and mortality.
Specifically, pulmonary function studies are routinely used to determine feasibility of surgery. The combination of tests performed focuses on respiratory mechanics, cardiopulmonary
reserve, and lung parenchymal function (Table 1).
Of all the preoperative tests, maximal oxygen consumption (V̇ O2max), obtained in the exercise laboratory, is the best predictor of post-thoracotomy morbidity and mortality. While few
patients with V̇ O2max greater than 20 mL • kg–1 • min–1 have respiratory complications, those with a V̇ O2max less than 12 mL • kg–1 • min–1 are at severalfold increased risk for
perioperative cardiopulmonary complications and mortality. Interestingly, stair climbing correlates with V̇ O2max:
5 flights equates to greater than 20 mL • kg–1 • min–1

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5 flights equates to greater than 20 mL • kg–1 • min–1

less than 1 flight equates to less than 10 mL • kg–1 • min–1.
A preoperative Paco2 level greater than 60 mm Hg has been a traditional cutoff for pulmonary resection. However, alone, it is not a sensitive predictor of postoperative complications.
Lung diffusion capacity for carbon monoxide (DLCO) measures the gas exchange or functional surface area of the lung. Predicted postoperative DLCO less than 40% of normal is
predictive of perioperative, but not long-term, mortality. Resection of only the right upper lobe should not decrease DLCO to less than 40% of predicted from a preoperative value of 80%
of predicted.
Of the respiratory mechanics tests, a forced expiratory volume in 1 second less than 40% is predictive of postoperative respiratory complications.
Table 1. The "three-legged" stool of prethoracotomy respiratory assessment. * = Most valid test; DLCO = diffusing capacity of the lung for carbon monoxide; V̇ o2max = maximum
oxygen consumption; FVC = forced vital capacity; MVV = maximum ventilatory volume; ppo = predicted postoperative; RV/TLC = residual volume/total lung capacity. Used with
permission, from slinger PD, Johnston MR. Preoperative assessment for pulmonary resection. Anesthesiol Clin North America. 2001;19(3):411-433. © Elsevier Inc. All rights reserved.
References
1. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:1820-1822
2. Brunelli A, Belardinelli R, Refai M, et al. Peak oxygen consumption during cardiopulmonary exercise test improves risk stratification in candidates to major lung resection. Chest.
2009;135(5):1260-1267.
3. Beckles MA, Spiro SG, Colice GL, et al. The physiologic evaluation of patients with lung cancer being considered for resectional surgery. Chest. 2003;123(1 suppl):105S-114S.
Taxonomy

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The porphyrias are a group of inherited disorders that result from deficiencies in enzymes in the heme synthetic pathway. There are multiple different porphyrias, but the most common
is acute intermittent porphyria (AIP), which has a prevalence of about 1:15,000.
Patients with AIP have a deficiency of porphobilinogen deaminase, which leads to increased levels of cellular 5-aminolevulinic acid (ALA). Most patients will be asymptomatic until an
event that stimulates the production of ALA, producing a porphyric crisis.
Factors that can stimulate a porphyric crisis include
induction of ALA synthetase production in the liver

endocrine factors (eg, menstrual cycle)
fasting and dehydration
emotional stress (eg, undergoing surgery).
An acute attack is usually manifested by the onset of colicky abdominal pain, nausea, and vomiting, followed by darkening of the urine. If left untreated, neurologic symptoms, including
neuropathy and seizures, may develop.
Treatment begins with eliminating any precipitating factors, then administering glucose and/or heme arginate, both of which act to reduce ALA synthetase activity.
Careful planning is needed when scheduling a patient with a history of AIP for surgery. It is recommended that the patient be admitted the night before surgery to ensure proper
hydration with a glucose-containing solution.
There is no single anesthetic technique that has been proven to be safer for these patients; both general and regional anesthesia have been used successfully. Determination of which
drugs are safe or not safe in patients with AIP is largely based on case reports. Determining the safety of anesthetic drugs is particularly challenging since other factors (eg,
dehydration, stress) are likely to be present in patients undergoing anesthesia. Although mechanisms exist for testing drugs in both cell cultures and animal models, both of these
techniques tend to overestimate the likelihood of a drug to precipitate an attack in a human. A database for drugs in patients with porphyria is maintained at
http://www.porphyriafoundation.com/. Table 1 classifies drugs commonly administered in the perioperative period.
Barbiturates used for induction of anesthesia (eg, methohexital, thiopental) are clearly labeled as being unsafe in patients with AIP. Although propofol is considered safe in these
patients, etomidate is not. Succinylcholine is also classified as being safe in these patients, but ketorolac is considered to be possibly porphyrogenic.

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Table 1. Perioperative drug recommendations for patients with acute porphyria. Data from James MFM, Hift RJ. Porphyrias. Br J Anaesth. 2000;85(1):143-153.
References
1. Fleisher LA. Anesthesia and Uncommon Diseases. 5th ed. Philadelphia, PA: Elsevier Saunders; 2006:171-172.
3. Jensen NF; Fiddler DS, Striepe V. Anesthetic considerations in porphyrias. Anesth Analg. 1995;80(3):591-599.
4. James MF, Hift RJ. Porphyrias. Br J Anaesth. 2000;85(1):143-153.
Taxonomy

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Magnetic resonance imaging (MRI) presents unique challenges for the anesthesiologist and hazards for the patient. Since the MRI magnet is always “on,” any ferromagnetic object
brought into the MRI environment can become a missile, injuring or killing the patient or staff. Therefore, all objects brought into the MRI environment must be MRI-compatible.
MRI-compatible anesthesia equipment exists, including oxygen cylinders, anesthesia machines, monitoring equipment, supraglottic airways (including standard laryngeal mask
airways), and laryngoscopes. However, most, if not all, video-assisted airway devices are not MRI-compatible and if brought into the MRI environment could become mobile or
unusable when exposed to the strong magnetic fields. In addition, most code carts and all defibrillators lack MRI compatibility. Therefore, should the need arise to use a defibrillator,
code cart, or video laryngoscope, it is paramount to remove the patient from the MRI room prior to the use of any equipment that is not MRI-compatible.
References
2. Schmitz B, Nimsky C, Wendel G, et al. Anesthesia during high-field intraoperative magnetic resonance imaging experience with 80 consecutive cases. J Neurosurg Anesthesiol.
2003;15(3):255-262.
3. Gooden CK, Dilos B. Anesthesia for magnetic resonance imaging. Int Anesthesiol Clin. 2003; 41(2):29-37.
Taxonomy
II.E. ADVANCED: Special Problems or Issues in Anesthesiology, 3. Radiologic Procedures; CT Scan; MRI-Anesthetic Implications/Management, Anesthesia in Locations Outside the
Operating Rooms

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For many years, thoracic epidural analgesia (TEA) has been considered to be the gold standard for post-thoracotomy pain relief. Though introduced in the early 1900s and reintroduced
in the late 1970s, paravertebral blocks (PVB) for thoracotomy (Figure 1 and Figure 2) have become more popular as ultrasound guidance, catheters, and placement equipment have
been refined. PVB is shown to be equivalent to or better than TEA in providing postoperative pain relief in both single shot and continuous infusions. Advantages of placing PVB
compared to TEA include less restrictive anticoagulation guidelines and the ability to place the catheter intraoperatively or postoperatively. PVB has a similar pulmonary function profile
as TEA for the same procedure, except most studies demonstrate a better forced expiratory volume in 1 second with PVB. Pulse oximetry recordings were marginally (but statistically)
better in patients with PVB compared to TEA. However, the occurrence of atelectasis and pneumonia has been reported to be much higher in TEA patients by severalfold. Likewise, the
occurrence of hypotension has been shown to be up to 10 times higher in TEA patients compared with PVB patients (Table 1).
The occurrence of nausea and vomiting is reported in 7% to 17% of patients receiving a thoracic PVB. The volume of local anesthetic has not been reported to influence the occurrence
of nausea and vomiting in these patients.
Neuraxial spread of local anesthetic is related to the volume of local anesthetic injected. In volumes of 15 mL or higher in a single injection, the risk is reported to be as high as 70%.
Multiple injections of less than 5 mL each dramatically reduce the occurrence of neuraxial spread in the thoracic areas.
Hypotension is present in approximately 4% of patients receiving a PVB without neuraxial spread. In patients who experience a neuraxial spread of the local anesthetic from a thoracic
PVB, some may experience transient hypotension, but the overall risk of hypotension is less than the risk of neuraxial spread. The volume of injected solution has not been shown to be
a contributing factor for the development of hypotension in thoracic PVB.
Even though pleural punctures occur in approximately 1% of thoracic PVBs placed between T1 and T8, an actual pneumothorax only occurs in approximately half of these patients. A
pneumothorax from a PVB placed between T10 and L3 is a very rare occurrence. The volume of local anesthetic has nothing to do with the development of a pneumothorax. In centers
that place a large number of thoracic PVBs, the rate of pneumothorax has been reported to be as low as 0.1%. Placement of bilateral PVB increases the risk of a pneumothorax.

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Figure 1. Anatomy of paravertebral space. Used with permission, from Karmakar MK. Thoracic paravertebral block. Anesthesiology. 2001;95(3):771-780.

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Figure 2. Needle placement for paravertebral block. Used with permission, from Karmakar MK. Thoracic paravertebral block. Anesthesiology. 2001;95(3):771-780.
Table 1. Complications associated with thoracic epidural analgesia and paravertebral block.
References
2. Groeben H. Epidural anesthesia and pulmonary function. J Anesth. 2006;20(4):290-299.
3. PÃ¶pping DM, Elia N, Marret E, Remy C, TramÃ¨r MR. Protective effects of epidural analgesia on pulmonary complications after abdominal and thoracic surgery: a meta-analysis.
Arch Surg. 2008;143(10):990-999.
4. Edrich T, Sadovnikoff N. Anesthesia for patients with severe chronic obstructive pulmonary disease. Curr Opin Anaesthesiol. 2010;23(1):18-24.
5. Daly DJ, Myles PS. Update on the role of paravertebral blocks for thoracic surgery: are they worth it? Curr Opin Anaesthesiol. 2009;22(1):38-43.
6. Scarci M, Joshi A, Attia R. In patients undergoing thoracic surgery is paravertebral block as effective as epidural analgesia for pain management? Interact Cardiovasc Thorac
Surg. 2010;10(1):92-96.
7. Chelly JE. Paravertebral blocks. Anesthesiol Clin. 2012;30(1):75-90.
8. Thavaneswaran P, Rudkin GE, Cooter RD, et al. Brief reports: paravertebral block for anesthesia: a systematic review. Anesth Analg. 2010;110(6):1740-1744.
9. Karmakar MK. Thoracic paravertebral block. Anesthesiology. 2001;95(3):771-780.

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10. Vila H Jr, Liu J, Kavasmaneck D. Paravertebral block: new benefits from an old procedure. Curr Opin Anaesthesiol. 2007;20(4):316-318.
Taxonomy
A patient who is dependent on opioids will begin to exhibit the signs of withdrawal anywhere from 12 hours after taking heroin or 30 hours after methadone. The initial symptoms mimic
flu symptoms and include agitation, anxiety, muscle aches, increased tearing, insomnia, runny nose, sweating, and yawning. Late symptoms and complications of withdrawal include
cramping, nausea, vomiting (with the potential for aspiration), and diarrhea, which can cause dehydration and electrolyte disturbances. Patients who have been taking the equivalent of
30 mg of morphine daily for more than 4 weeks should be considered at risk for opioid withdrawal.
Though opioid withdrawal is not life-threatening (unlike alcohol and benzodiazepine withdrawal) treatment should be given in order to avoid the complications. In the acute setting, mu
receptor agonist/antagonists (eg, buprenorphine) have been used successfully to treat withdrawal. Giving buprenorphine to patients too early after their last intake of opioids or to
patients chronically consuming high doses of opioids can precipitate or exacerbate opioid withdrawal symptoms.
Administration of α-antagonists is not indicated in the treatment of opioid withdrawal. Beta-antagonists can be used to treat any tachycardia or hypertension associated with opioid
withdrawal. Alpha2-agonists (eg, clonidine) are also useful in the treatment of opioid withdrawal symptoms by reducing anxiety, agitation, muscle aches, sweating, runny nose, and
cramping. Other drugs are necessary for treating vomiting and diarrhea.
Mu receptor agonists should be considered for treatment of withdrawal and for perioperative pain control. The longer the time since onset of symptoms, the lower the dose of opioids
required to abate the symptoms of withdrawal.
Regional anesthesia and N-methyl-D-aspartate (NMDA) receptor antagonists (eg, ketamine) are good anesthesia management options for perioperative anesthesia and pain
management but do not treat opioid withdrawal symptoms.
References
2. Doyon S. Opioids. In: Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York, NY: McGraw-Hill; 2004.
3. Gordon D, Inturrisi CE, Greensmith JE, Brennan TJ, Goble L, Kerns RD. Perioperative pain management in the opioid-tolerant individual. J Pain. 2008;9(5):383-387.
4. Kopf A, Banzhaf A, Stein C. Perioperative management of the chronic pain patient. Best Pract Res Clin Anaesthesiol. 2005;19(1):59-76.
Taxonomy

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Carcinoid tumors, which occur at the rate of approximately 10 cases per million people annually, generally originate from the bronchus, the small bowel, or the colon. Carcinoid tumors,
which are capable of secreting a wide variety of amines and polypeptides, have been classified based on their site of origin as foregut (originating in bronchus or stomach), midgut
(originating in the small bowel, appendix, or ascending colon), or hindgut (originating in distal colon or rectum). The location of the tumor is important in determining not only
presentation but also the types of substances produced by the tumor.
A partial list of substances reported to be released by carcinoid tumors includes the following:
Gastrin
Gastrin-releasing peptide
Ghrelin
Calcitonin
Pancreatic polypeptide
Adrenocorticotropic hormone (ACTH)
Corticotropin-releasing hormone (CRH)
Growth hormone-releasing hormone (GHRH)
Somatostatin
Glucagon
Calcitonin gene-related peptide
Chromogranin A
5-Hydroxytrytophan
Kallikrein
Prostaglandins E1, E2, F1, F2
Histamine
Dopamine
Norepinephrine
Substance P
Neurokinin A
Neuropeptide K
Eledoisin
Insulin
Polypeptide YY
Human chorionic gonadotropin alpha-subunit
Motilin
Vasoactive intestinal peptide
Endorphins
The clinical presentation of a patient with a carcinoid tumor is largely determined by the location of the tumor (Table 1)
Carcinoid syndrome, which consists primarily of episodic flushing, diarrhea, and right-sided heart disease, occurs in only about 20% of patients with carcinoid tumors. Other
manifestations may include wheezing, retroperitoneal fibrosis (which may lead to ureteral obstruction), weight loss, sweating, and arthropathy. The location of the tumor is a major
determinant of the likelihood of developing carcinoid syndrome; rectal tumors, for example, less commonly secrete mediators that can produce the carcinoid syndrome. The presence of
metastases is another important determinant of the likelihood of developing carcinoid syndrome. The liver is very effective at inactivating most of the substances released by carcinoid
tumors. Since the venous drainage of the bowel enters the portal circulation, the presence of carcinoid syndrome in a patient with a carcinoid tumor of the small bowel suggests the
presence of hepatic metastases. Because ovarian and intrathoracic tumors release mediators directly into the systemic circulation (as opposed to into the portal circulation), carcinoid
syndrome is more common in patients with these types of tumors.
Secretion of GHRH, which occurs primarily in intrathoracic carcinoid tumors and those originating in the stomach or duodenum, may result in acromegaly. Intrathoracic carcinoid
tumors, which can release ACTH or CRH, have been associated with the development of Cushing syndrome. In fact, approximately 1% of all cases of Cushing syndrome are
associated with an intrathoracic carcinoid tumor.
Carcinoid tumors derive from enterochromaffin cells and frequently secrete large quantities of serotonin. Carcinoid tumors can be diagnosed by the presence of excessive amounts of
the serotonin metabolite 5-hydroxyindoleacetic acid in urine. Carcinoid tumors may also secrete multiple types of vasoactive substances, including histamine, bradykinin, tachykinin,
substance P, prostaglandins, and catecholamines. Nonmetastatic carcinoid tumors of the bowel release their substances into the portal system where they are inactivated by the liver.
When it metastasizes outside the portal system, carcinoid tumor will release vasoactive substances directly into the systemic circulation, causing marked symptoms of cutaneous
flushing, bronchospasm, hypotension, and diarrhea. Hypertension may also result because serotonin has inotropic and chronotropic activity. The classic carcinoid triad is described by
flushing, diarrhea, and cardiac involvement. Of those patients who develop carcinoid syndrome, approximately 60% develop carcinoid heart, characterized by plaque deposition in the
right ventricular endocardium and the tricuspid and pulmonic valves, typically resulting in regurgitant valvular lesions, but stenotic valvular lesions also occur. This represents only about
12% of patients with carcinoid tumors.
The cell surface of carcinoid tumor has high densities of somatostatin receptors. Activation of somatostatin receptors results in the reduced production of vasoactive substances.
Octreotide is a somatostatin analog with a long half-life. Administered preoperatively, octreotide helps control the symptoms caused by release of vasoactive substances from carcinoid
tumor during surgical manipulation.

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Table 1. Presentation based on location of tumor.
References
1. Kronenberg HM, Melmed S, Polonsky KS, Larsen PR, Kronenberg HM. Williams Textbook of Endocrinology. 12th ed. Philadelphia, PA: Elsevier Saunders; 2011:1809-1828.
2. Pasieka JL. Carcinoid tumors. Surg Clin North Am. 2009; 89(5):1123-1137.
3. Mancuso K, Kaye AD, Boudreaux JP, et al. Carcinoid syndrome and perioperative anesthetic considerations. J Clin Anesth. 2011;23(4):329-341.
Taxonomy
Systemic lupus erythematosus (SLE) is primarily a disease of autoimmunity against multiple cellular components. Even though there is a large genetic predisposition for developing
SLE, the variable expression of the genomics does not allow SLE to be classified as a genetically inherited disease as yet.

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Because of the multiple ways in which SLE can present, the American College of Rheumatology provided an updated consensus set of guidelines for an accurate and standardized
diagnosis for SLE (Table 1). The presence of any 4 of the 11 criteria either consecutively or concurrently confirms the diagnosis.
Atlantoaxial subluxation is present in 8.5% of patients with SLE at autopsy. Even though the cervical vertebrae are usually spared in SLE, the atlantoaxial joint is not, and patients who
present with severe forms of the disease should be evaluated for neurologic changes, as should any patient with SLE and a complaint of neck pain.
Patients with SLE have a restrictive pulmonary disease due to the chronic fibrosis resulting from the repeated inflammatory and immune-related insults to interstitial and pleural tissues.
Pneumonitis and pleural effusions are common, and chest radiographs are recommended for preoperative evaluation. SLE patients with a history of recent increase in dyspnea, new
ground glass opacities on radiographs, or decreases in blood hemoglobin/hematocrits should be evaluated for diffuse alveolar hemorrhage as this condition carries a 50% mortality. A
decrease in hemoglobin/hematocrit may be the result of an autoimmune attack and not diffuse alveolar hemorrhage.
Tracheal stenosis, not tracheomalacia, is present in up to 30% patients with SLE. Vocal cord paralysis and laryngeal edema also may complicate the presentation and management of
these patients.
Pituitary hyperactivity is not associated with SLE.
Table 1. Reported prevalence of criteria used for diagnosis of systemic lupus erythematosus.
References
2. Hines RL, Marschall KE. Stoelting’s Anesthesia and Co-Existing Disease. 5th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2008:445-446.
3. Ben-Menachem E. Review article: systemic lupus erythematosus: a review for anesthesiologists. Anesth Analg. 2010;111:665-676.
4. Wetzl RG. Anaesthesiological aspects of pregnancy in patients with rheumatic diseases. Lupus. 2004;13:699-702.
Taxonomy

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Lambert–Eaton myasthenic syndrome (LEMS) is an autoimmune disorder with antibodies against voltage-gated calcium channels in presynaptic nerve terminals (Figure 1, step 1).
LEMS is often associated with underlying malignancies (especially small cell carcinoma of the lung), thyroiditis, collagen-vascular disorders, and sarcoidosis.
Autoimmune antibodies inhibit the release of acetylcholine into the neuromuscular junction causing proximal skeletal muscle weakness, particularly in the lower extremities. Autonomic
dysfunction, including orthostatic hypotension and gastroparesis, is present in some patients. Similarly, repetitive activity causes an accumulation of acetylcholine, resulting in increased
muscle strength (Figure 2). Tumor resection or tumor response to chemotherapy may result in improved strength.
Patients with LEMS manifest increased sensitivity to both depolarizing and nondepolarizing neuromuscular blocking agents. As patients with LEMS also respond poorly to
acetylcholinesterase inhibitors, prolonged neuromuscular blockade has been reported in this population.

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Figure 1. Diagrammatic representation of neuromuscular transmission. (1) Action potential arriving at nerve terminal triggers opening of voltage-gated calcium channels (VGCCs) and
entry of calcium. (2) Rise in intracellular calcium triggers release of packets of acetylcholine (ACh). (3) Interaction of ACh with ACh receptors (AChR) depolarizes postsynaptic
membrane. (4) Voltage-gated sodium channels (VGSCs) open, triggering muscle action potential. (5) ACh esterase (AChE) breaks ACh into acetyl and choline, which are taken up by
the nerve terminal to be reformed into ACh. (6) Opening of voltage-gated potassium channels (VGKCs) repolarizes nerve terminal. Reproduced from Hill M. The neuromuscular junction
disorders. J Neurol Neurosurg Psychiatry. 2003;74(suppl 2):ii32-ii37 with permission of BMJ Publishing Group Ltd.

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Figure 2. Electromyography shows incremental response (>200%) at 30 Hz of stimulation in the abductor hallucis muscle. Used with permission, from Morimoto M, Osaki T, Nagara Y,
Kodate M, Motomura M, Murai H. Thymoma with Lambert-Eaton myasthenic syndrome. Ann Thorac Surg. 2010;89(6):2001-2003. © Elsevier Inc. All rights reserved.
References
1. Miller RD. Millerâ€™s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:1033, 1116, 1828.
2. Dalmau J, Rosenfeld MR. Paraneoplastic syndromes and the CNS. Lancet Neurol. 2008;7(4):327-340.
3. Morimoto M, Osaki T, Nagara Y, Kodate M, Motomura M, Murai H. Thymoma with Lambert-Eaton myasthenic syndrome. Ann Thorac Surg. 2010;89(6):2001-2003.
4. Hill M. The neuromuscular junction disorders. J Neurol Neurosurg Psychiatry. 2003;74(suppl 2):ii32-ii37.
5. Briggs ED, Kirsch JR. Anesthetic implications of neuromuscular disease. J Anesth. 2003;17(3):177-185.
Taxonomy
Local anesthetics are made from a lipid-soluble benzene ring connected to a water-soluble amide group (Figure 1). Local anesthetics are grouped based on the type of linkage that
exists between these 2 physiologically active parts. Some of the physicochemical properties of the local anesthetics, such as elimination, are determined by the type of this linkage.
Amino esters (often referred to simply as “esters”) are connected by an ester linkage. These local anesthetics are primarily hydrolyzed by plasma cholinesterase within the blood.
Common examples include

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chloroprocaine
procaine
tetracaine.
Amino amides (often referred to simply as “amides”) are connected by an amide linkage. These local anesthetics are primarily eliminated through hepatic biotransformation and include
bupivacaine
etidocaine
lidocaine
mepivacaine
prilocaine
ropivacaine.
A number of additional local anesthetic physicochemical properties are also clinically important. Knowing these properties and their clinical effect should allow clinicians to tailor the
choice of local anesthetic to the desired effect. These properties include
lipid solubility, which is directly related to local anesthetic potency (high solubility = high potency)
pKa, which is directly related to local anesthetic time to onset (low pKa = fast onset)
protein binding, which is directly related to local anesthetic duration (high protein binding = long duration).
When applied to a peripheral nerve, the addition of epinephrine is not associated with a shortened time to onset of block but is associated with increased block intensity, prolonged
duration of block, and decreased systemic absorption of local anesthetic.

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Figure 1. Local anesthetic structures. Image courtesy of Wikipedia. http://commons.wikimedia.org/wiki/File:Struktur-LokalanÃ¤sthetika.png . Accessed January 20, 2014. Used in
accordance with the Creative Commons Attribution Share Alike 3.0 Unported license, available at http://creativecommons.org/licenses/by-sa/3.0/deed.en.
References
2. Mercado P, Weinberg GL. Local anesthetic systemic toxicity: prevention and treatment. Anesthesiol Clin. 2011;29(2):233-242.
3. Yanagidate F, Strichartz GR. Local anesthetics. Handb Exp Pharmacol. 2007;(177):95-127.
Taxonomy

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Implantable cardioverter defibrillators (ICDs) are placed for prevention of sudden death in patients with moderate to severe heart failure. Biventricular ICD leads are most commonly
placed percutaneously into the subclavian vein and directed to the right atrium, right ventricle, and coronary sinus (Figure 1).
Placement of biventricular ICD devices is associated with a 4.1% adverse event rate; the most serious events are related to vascular and thoracic complications (Table 1). Cardiac
tamponade is one of the most life-threatening complications and should be suspected in patients with hypotension and tachycardia following the procedure. Tamponade occurs in the
event of inadvertent puncture of great vessels or the atrium by a lead, resulting in accumulation of blood in the pericardium. Diagnosis of cardiac tamponade can be rapidly achieved
with a bedside transthoracic echocardiogram. Emergency decompression is warranted following the diagnosis of cardiac tamponade.
Pneumothorax or hemopneumothorax should also be suspected in this scenario. Physical examination and, if needed, an emergency bedside chest radiograph should be performed. In
the event of a pneumothorax or hemothorax, chest tube insertion and/or surgical exploration should commence immediately.
Computed tomography scan of the chest is sensitive for pneumothorax, hemopneumothorax, and pericardial effusion. However, in this patient with hemodynamic instability, rapid
bedside diagnosis and return to the operating room is the appropriate course of action.
Left-sided heart catheterization for detecting coronary obstruction would be a lower priority in this patient. This should be performed only after ruling out the other causes mentioned.
Placing a magnet on modern ICDs will disable the tachycardia therapies and is not warranted at this time.

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Figure 1. Lead placement for a biventricular pacing system. © 2013 Boston Scientific Corporation or its affiliates. All rights reserved. Used with permission of Boston Scientific
Corporation.
Table 1. Complications following placement of an implantable cardioverter defibrillator or pacemaker. Modified from table in Pavia S, Wilkoff B. The management of surgical
complications of pacemaker and implantable cardioverter-defibrillators. Curr Opin Cardiol. 2001;16(1):66-71.
References
2. Hall MC, Todd DM. Modern management of arrhythmias. Postgrad Med J. 2006;82(964):117-125.
3. Pavia S, Wilkoff B. The management of surgical complications of pacemaker and implantable cardioverter-defibrillators. Curr Opin Cardiol. 2001;16(1):66-71.
Taxonomy

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Nonsteroidal antiinflammatory drugs (NSAIDs) possess analgesic properties that make them particularly useful in the postsurgical period. Their primary analgesic effect results from an
ability to inhibit prostaglandin synthesis in peripheral tissues, nerves, and the central nervous system. NSAIDs are useful adjuncts in multimodal analgesia, and a Cochrane review
demonstrated efficacy among NSAIDs when given as a single-dose for reducing acute postsurgical pain. Moreover, a meta-analysis demonstrated that NSAIDs not only reduce
postoperative pain scores but also reduce opioid consumption and, when given in conjunction with opioids, significantly reduced postoperative pain, nausea, vomiting, and sedation.
Preventative effects of NSAIDS on the progression of acute to chronic pain have not been well studied, as few studies report long-term follow-up. Some long-term data that appeared
promising have since been retracted from the literature. One well-done, highly powered study randomized 902 patients who had undergone hip replacement to receive placebo or 400
mg of ibuprofen 3 times a day starting within 24 hours of completing surgery and continuing for 14 days. No significant differences in chronic pain were observed 6 and 12 months after
surgery. This study reported 90% power to detect a difference of greater than 10% in the amount of pain that patients experienced 6 to 12 months after surgery. Perioperative NSAID
administration has also failed to demonstrate a reduction in the incidence of postmastectomy pain syndrome in 1 small trial of 30 patients at 12 months.
In summary, there are good data that use of nonselective NSAIDs or COX-2 inhibitors reduces pain, opioid use, and opioid-related side effects in the immediate postoperative period.
However, the available data, including at least 1 large, well-powered, randomized clinical trial, indicate with 90% confidence that any protective effect of postoperative ibuprofen for
preventing chronic pain is of a magnitude that is clinically insignificant if it exists at all.
Perioperative administration of NSAIDs is not associated with either hepatic dysfunction or an increased rate of postoperative hallucinations.
References
1. Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC, Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2013:1556,
1558-1560.
2. Fransen M, Anderson C, Douglas J, et al; HIPAID Collaborative Group. Safety and efficacy of routine postoperative ibuprofen for pain and disability related to ectopic bone
formation after hip replacement surgery (HIPAID): randomised controlled trial. BMJ. 2006;333(7567):519.
3. 3. Derry C, Derry S, Moore RA, McQuay HJ. Single dose oral ibuprofen for acute postoperative pain in adults. Cochrane Database Syst Rev. 2009;(3):CD001548.
4. Derry C, Derry S, Moore RA, McQuay HJl. Single dose oral naproxen and naproxen sodium for acute postoperative pain in adults. Cochrane Database Syst Rev. 2009;
(1):CD004234.
5. 5. Lakdja F, Dixmérias F, Bussières E, Fonrouge JM, Lobéra A. Preventive analgesic effect of intraoperative administration of ibuprofen-arginine on postmastectomy pain
syndrome [in French]. Bull Cancer. 1997;84(3):259-263.
Taxonomy

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During surgical procedures where there is an increased risk of brain ischemia, such as open-heart surgery and carotid endarterectomy, there has been great interest in determining if
electroencephalographic (EEG) monitoring can reduce neurologic complications.
When cerebral blood flow (CBF) is decreased below a critical threshold (usually 20 mL • 100 g–1 • min–1), there is an immediate decrease in neuronal activity, which can be detected
within seconds on an EEG. The characteristic EEG findings representing cerebral ischemia include slowing of the EEG, with initial preservation of amplitude (in mild to moderate
ischemia), progressing to loss of amplitude (in severe ischemia) (Figure 1).
EEG monitoring is not without limitations. EEG monitoring generally requires placement of 16 or more electrodes on the patient’s head, in addition to requiring personnel trained in
monitoring to the EEG.
Several studies have been done to try and prove that routine EEG monitoring reduces the occurrence of stroke in patients undergoing carotid endarterectomy. However, none of these
studies definitively showed that routine use of EEG monitoring reduces the risk of ischemic stroke.

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Figure 1. Characteristic electroencephalogram (EEG) findings representing cerebral ischemia during decreases in cerebral blood flow or hypoxia. Used with permission, from Marsh
ML, Marshall LF, Shapiro HM. Anesthesiology. 1977;47(2):149-163.
References
2. Florence G, Guerit JM, Gueguen B. Electroencephalographic (EEG) and somatosensory evoked potentials (SEP) to prevent cerebral ischaemia in the operating room.
Neurophysiol Clin. 2004;34(1):17-32.
3. Friedman D, Claassen J. Quantitative EEG and cerebral ischemia. Clin Neurophysiol. 2010;121(10):1707-1708.
Taxonomy

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Transesophageal echocardiography (TEE) is a sensitive tool for detecting myocardial ischemia. While there are 4 standard views for monitoring left ventricular function, only the
transgastric mid short-axis view of the left ventricle provides information on areas of the myocardium perfused by all 3 major coronary arteries: left anterior descending, left circumflex,
and right.
The arrow shown in the TEE is pointing to the septal wall of the left ventricle. The majority of the septal wall is supplied by the left anterior descending coronary artery after it divides
from the left main coronary artery.
The right coronary artery supplies the right ventricle and inferior wall of the left ventricle (Figure 1). The circumflex artery supplies the lateral and inferolateral or posterior walls. The
obtuse marginal artery, a branch of the circumflex artery, also supplies the lateral and inferolateral walls of the left ventricle.

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Figure 1. Four standard views of the left ventricle demonstrating the areas of myocardium supplied by each of the coronary arteries. LAD, left anterior descending; LCx, left circumflex;
RCA, right coronary artery. Used with permission of Oxford University Press, from Kneeshaw JD. Transoesophageal echocardiography (TOE) in the operating room. Br J Anaesth.
2006;97(1):77-84.
References
1. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:1339-1342
2. Kneeshaw JD. Transoesophageal echocardiography (TOE) in the operating room. Br J Anaesth. 2006;97(1):77-84.
Taxonomy

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The American Society of Anesthesiologists (ASA) has defined both general anesthesia and levels of sedation in order to provide a consistent working vocabulary (Table 1).
One of the key concepts is that providers who administer sedation need to be trained to rescue patients whose level of sedation becomes deeper than intended (ie, those administering
moderate sedation need to be trained to rescue patients from deep sedation).
Table 1. Definitions of levels of sedation and general anesthesia. Used with permission, from American Society of Anesthesiologists. Continuum of depth of sedation: definition of
general anesthesia and levels of sedation/analgesia. http://www.asahq.org/For-
Members/~/media/For%20Members/Standards%20and%20Guidelines/2012/CONTINUUM%20OF%20DEPTH%20OF%20SEDATION%20442012.ashx . Committee of Origin:
Quality Management and Departmental Administration. Approved by the ASA House of Delegates on October 27, 2004, and amended on October 21, 2009. Accessed January 14,
2014.
References
2. American Society of Anesthesiologists? Continuum of depth of sedation: definition of general anesthesia and levels of sedation/analgesia. http://www.asahq.org/For-
Members/~/media/For Members/Standards and Guidelines/2012/CONTINUUM OF DEPTH OF SEDATION 442012.ashx. Updated October 21, 2009. Accessed January 14, 2014.
Taxonomy
I.B. BASIC: Clinical Sciences: Anesthesia Procedures, Methods, and Techniques, 4. Monitored Anesthesia Care and Sedation: ASA Guidelines for Sedation, Sedation Guidelines for
Non-Anesthesiologists

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The epidemic of obesity is a well-publicized phenomenon in the US population.
One of the potential consequences of morbid obesity is obesity hypoventilation syndrome (OHS). The exact prevalence of OHS in the morbidly obese population is unknown, in part
because it is often assumed that obstructive sleep apnea (OSA) and OHS are the same disease. OHS is associated with a much higher perioperative and general medical morbidity
and mortality than OSA. The diagnostic criteria for OHS are
body mass index (BMI) more than 30 kg/m2

awake arterial hypercapnia (Paco2 > 45 mm Hg)
no other cause for chronic hypoventilation
abnormal polysomnography findings that include hypoventilation with nocturnal hypercapnia with or without obstructive apnea or hypopnea events.
Other associated characteristics of this patient population include the presence of central obesity (waist greater than thighs or “apple” fat distribution). Patients with central obesity are
assessed by establishing a waist-to-hip ratio, which will be greater than for patients with a similar BMI but a weight distribution in the lower body (hips, thighs, or “pear-like” fat
distribution) or weight evenly distributed in extremities and abdomen.
Distribution of body fat does not affect the increased oxygen consumption and carbon dioxide production seen with all comparably obese patients due to the increased work of
breathing and the additional metabolic effort required for general living even at rest. Individuals with central obesity are more likely to have closure of the dependent airways (dependent
atelectasis) in the range of tidal volume, causing significant pulmonary ventilation/perfusion defects, hypoxemia, and hypercapnia. In these patients, central ventilatory response to
hypercapnia and hypoxemia is markedly reduced compared to that of normal eucapnic obese or normal-weight individuals.

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Other characteristics that are associated with OHS are
male sex
age between 50 and 70 years
history of chronic fatigue
mood disorders
morning and nocturnal headaches
dyspnea with minimal exertion
hypersomnolence.
Patients in the OHS population are often not diagnosed until an acute medical event. Furthermore, OHS may deteriorate to respiratory failure when an acute illness or other medical
stress occurs.
References
2. BaHammam A. Acute ventilatory failure complicating obesity hypoventilation: update on a ‘critical care syndrome’. Curr Opin Pulm Med. 2010;16(6):543-551.
3. Berger KI, Goldring RM, Rapoport DM. Obesity hypoventilation syndrome. Semin Respir Crit Care Med. 2009;30(3):253-261.
Taxonomy
II.C. ADVANCED: Organ-based Basic and Clinical Sciences, 4. Gastrointestinal / Hepatic Systems
Carbon monoxide (CO) is an odorless, colorless, and nonirritating toxic gas that has a 200 times greater affinity for hemoglobin than does oxygen. It is produced whenever incomplete
combustion of carbon compounds occurs and is responsible for thousands of deaths each year in the United States.
Carbon monoxide has 3 primary modes of toxicity:
Due to the high affinity of hemoglobin for CO, all the hemoglobin binding sites occupied by CO are unavailable for oxygen transport, thus producing a functional anemia.
Hemoglobin has 4 oxygen binding sites. When one of these sites is occupied by carbon monoxide, the remaining sites have an increased affinity for oxygen, therefore a shift of
the oxyhemoglobin disassociation curve to the left occurs (Figure 1). The increased affinity of carboxyhemoglobin (COHB) for oxygen results in less oxygen delivery at the
tissues and is reflected by a lower partial pressure of oxygen needed to saturate 50% of the hemoglobin binding sites (decreased P50).
CO binds directly to intracellular pigments and can uncouple oxidative phosphorylation thus causing direct mitochondrial toxicity. This direct cellular toxicity may explain some of
the long-term neurologic complications that can occur despite prompt treatment in patients with severe CO poisoning.
Table 1 presents signs and symptoms of CO toxicity.
Cherry-red colored blood is usually absent in patients with CO poisoning because it usually only occurs at COHB levels greater than 40%. The majority of patients with CO poisoning
who survive and present for treatment have COHB levels less than 40%.

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Figure 1. Oxygen–Hemoglobin dissociation curve. The presence of carboxyhemoglobin shifts the curve to the left and changes it to a more hyperbolic shape. This results in a decrease
in oxygen-carrying capacity and impaired release of oxygen at the tissue level. Used with permission, from Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med.
1998;339(22):1603-1608. © 2014 Massachusetts Medical Society. Reprinted with permission from the Massachusetts Medical Society.

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Table 1. Signs and symptoms of CO toxicity.
References
2. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med. 1998;339(22):1603-1608.
3. Harvey WR, Hutton P. Carbon monoxide: chemistry, role, toxicity and treatment. Curr Anaesth Crit Care. 1999;10(3):158-163.
4. Clinical guidance for carbon monoxide (CO) poisoning after a disaster. Centers for Disease Control and Prevention website. http://emergency.cdc.gov/disasters/co_guidance.asp.
Updated September 19, 2008. Accessed January 22, 2014.
Taxonomy
While no longer required by code, many operating rooms still have isolated electrical power supplies. An isolated electrical power supply provides alternating current with no direct
connection to ground. This is accomplished by the use of an induction transformer (Figure 1).
Since the isolated power does not have a potential relative to ground, contacting an electrically hot line will not result in a shock. The type of shock that an isolated power supply helps
to protect against is known as macroshock. Macroshock is electrocution where electricity enters through the skin and flows through a large portion of the body. The lowest lethal
macroshock currents (ie, those that produce ventricular fibrillation) are on the order of 100 to 300 mA. In contrast, microshock occurs when a shock is delivered via an indwelling line
(eg, pulmonary artery catheter or pacemaker leads). The current needed to produce ventricular fibrillation in this setting is on the order of 100 µA, that is 3 orders of magnitude less
than the than the macroshock current. An isolated operating room (OR) power supply will not reduce the risk of microshock. Advances in equipment that help isolate the patient from
stray currents (eg, patient isolated electrocardiography leads) are the best protection available against microshock.
The use of an isolated power supply does not preclude metal chassis grounding that is provided by a 3-prong grounded plug. This third wire, which is required on all OR equipment,
provides a low resistance pathway for electricity to flow should there be a fault. An isolated power supply does not provide uninterruptible power; rather it provides a source of power
that has no potential relative to ground, thus reducing the risk of macroshock.

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Figure 1. Isolated electrical power supply. © 2014 American Society of Anesthesiologists.
References
1. Lobato EB, Gravenstein N, Kirby RR. Complications in Anesthesiology. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2008:780-789.
3. Morell RC, Eichhorn JH. Patient Safety in Anesthetic Practice. New York, NY: Elsevier Churchill Livingstone; 1997:56-68.

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Taxonomy
I.A. BASIC: Basic Sciences, 2. Physics, Monitoring, and Anesthesia Delivery Devices
Risk factors for corneal abrasion include
general anesthesia
case duration more than 90 minutes
head and neck procedures
prone or lateral patient positioning (the rate is higher in the more dependent eye)
lagophthalmos (incomplete lid closure), which occurs in about 5% of the normal population and in about 60% of patients undergoing general anesthesia
preexisting proptosis.
The anesthesiologist must be careful to tape the eyelids shut during general anesthesia. This is satisfactory for many cases. The predisposing factors listed increase the likelihood that
applied tape will be dislodged, potentially leading to corneal injury. If risk factors are present, consideration should be given to placing ointment into the eyes and then taping the lids
shut. A methylcellulose-based lubricant (eg, Celluvisc) is suitable for use in short cases, but a petroleum-based lubricant (eg, Lacri-Lube) lasts longer and is more suitable for cases of
longer duration.

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References
2. Roth S, Thisted RA, Erickson JP, Black S, Schreider BD. Eye injuries after nonocular surgery. A study of 60,965 anesthetics from 1988 to 1992. Anesthesiology. 1996;85(5):1020-
1027.
3. Gild WM, Posner KL, Caplan RA, Cheney FW. Eye injuries associated with anesthesia. A closed claims analysis. Anesthesiology. 1992;76(2):204-208.
Taxonomy
Delayed cerebral ischemia (DCI) is the single most important cause of morbidity and mortality in patients with subarachnoid hemorrhage (SAH) who survive the initial bleed. If it occurs,
DCI presents 3 to 14 days after the initial hemorrhage. Although the exact cause of DCI is not fully understood, it is thought that breakdown products from released blood in the brain
parenchyma and cerebrospinal fluid cause vasoconstriction.
The mainstay treatment for cerebral vasospasm after SAH is triple-H therapy, which consists of promoting hypertension, hypervolemia, and hemodilution. The rationale for triple-H
therapy is improvement in cerebral blood flow. Extravascular blood causes cerebral arterial vasospasm, which shifts cerebral vascular resistance towards more proximal arteries. This
shift may result in decreased perfusion in the more distal arterial segments, resulting in further cerebral ischemia or stroke. With loss of cerebral autoregulation, brain perfusion in the
area beyond the site of SAH becomes completely dependent upon the Hagen–Poiseuille law. Hemodilution lowers viscosity and flow resistance. Hypertension and hypervolemia have
been thought to contribute to more favorable hemodynamics, leading to improved brain perfusion beyond the SAH site.
Recently, the efficacy of hypervolemia has been questioned. A Cochrane review of hypervolemia therapy in SAH failed to identify benefit and instead found that hypervolemia may lead
to more complications and a worsened outcome. Furthermore, a meta-analysis failed to identify benefit from any of the components of triple-H therapy. A 2011 consensus guideline by
the Neurocritical Care Society states that stabilizing or increasing systemic arterial pressure and avoiding hypervolemia is likely to benefit SAH patients.
While hypothermia has not been shown to improve patient outcome in SAH patients, the calcium channel blocker nimodipine (not diltiazem) remains the only drug demonstrating SAH
patient benefit.
Barbiturate coma may be indicated for the treatment of refractory status epilepticus but is not routinely indicated for treatment of SAH.
References
2. Mocco J, Zacharia BE, Komotar RJ, Connolly ES Jr. A review of current and future medical therapies for cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
Neurosurg Focus. 2006;21(3):E9.
3. Rowland MJ, Hadjipavlou G, Kelly M, Westbrook J, Pattinson KT. Delayed cerebral ischaemia after subarachnoid haemorrhage: looking beyond vasospasm. Br J Anaesth.
2012;109(3):315-329.
4. Weyer GW, Nolan CP, Macdonald RL. Evidence-based cerebral vasospasm management. Neurosurg Focus. 2006;21(3):E8.
5. Todd MM, Hindman BJ, Clarke WR, Torner JC. Mild intraoperative hypothermia during surgery for intracranial aneurysm. N Engl J Med. 2005;352(2):135-145.
6. Dankbaar JW, Slooter AJ, Rinkel GJ, Schaaf IC. Effect of different components of triple-H therapy on cerebral perfusion in patients with aneurysmal subarachnoid haemorrhage: a

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6. Dankbaar JW, Slooter AJ, Rinkel GJ, Schaaf IC. Effect of different components of triple-H therapy on cerebral perfusion in patients with aneurysmal subarachnoid haemorrhage: a
systematic review. Crit Care. 2010;14(1):R23.
7. Diringer MN, Bleck TP, Claude Hemphill J III, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical
Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care. 2011;15(2):211-240.
8. Rinkel GJ, Feigin VL, Algra A, van Gijn J. Circulatory volume expansion therapy for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev. 2004;(4):CD000483.
Taxonomy
All inhaled anesthetic agents produce dose-dependent respiratory depression. It is believed that pulmonary stretch receptors are activated by inhaled agents, leading to decreased tidal
volume and increased respiratory rate. The increased respiratory rate is not enough to offset the decreased tidal volume, and this leads to a rise in PaCO2. Desflurane, at concentrations
at or above 1.5 minimum alveolar concentration produces the highest arterial PaCO2 (Figure 1).
Similar to their action upon pulmonary stretch receptors, inhaled anesthetic agents increase laryngeal irritant receptor activity, which can lead to laryngospasm during inhalation
anesthesia.
Figure 1. Comparison of mean changes in resting Paco2, tidal volume, respiratory rate, and minute ventilation in patients anesthetized with either halothane, isoflurane, enflurane,
sevoflurane, desflurane, nitrous oxide, or xenon. Anesthetic-induced tachypnea compensates in part for the ventilatory depression caused by all volatile anesthetics (decrease in minute
ventilation and tidal volume and concomitant increase in Paco2). Desflurane results in the greatest increase in Paco2with corresponding reductions in tidal volume and minute
ventilation. Isoflurane, like all other inhaled agents, increases the respiratory rate; however, isoflurane does not result in dose-dependent tachypnea. MAC, minimum alveolar
concentration. Used with permission, from Miller RD. Miller's Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:Figure 22-15. © Elsevier Inc. All rights reserved.

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concentration. Used with permission, from Miller RD. Miller's Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:Figure 22-15. © Elsevier Inc. All rights reserved.
Reference
Taxonomy

Although the lung is commonly considered essentially only as an organ of gas exchange, it also functions as a filter to minimize the probability of arterial embolization by eliminating
particulate matter from systemic venous blood and as an organ of defense to minimize entry of noxious substances into the circulation. The lung also provides a metabolic function by
activating some compounds and inactivating others.
The endothelial cells in the lung contain substantial quantities of the enzymes (ie, monoamine oxidase and catechol-O-methyl transferase) that metabolize amines. Because the
pulmonary endothelial membrane selectively takes up norepinephrine and serotonin, those compounds are metabolized to a much greater degree than the other amines. Epinephrine,
dopamine, and isoproterenol are unaltered by the lung, but approximately 30% of norepinephrine is removed in a single pass through the lung.
References
1. Lumb AB. Nunn’s Applied Respiratory Physiology. 7th ed. Edinburgh, Scotland: Elsevier Churchill Livingstone; 2010:225-226.
2. Wojciak-Stothard B, Haworth SG. Perinatal changes in pulmonary vascular endothelial function. Pharmacol Ther. 2006;109(1-2):78-91.
Taxonomy

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Laryngeal closure, swallowing, coughing, and apnea are reflexes that protect the airway. Under normal circumstances, the laryngeal closure and swallowing reflexes are coordinated.
The laryngeal closure reflex is responsible for the development of laryngospasm.
Stimulation of the oropharynx and hypopharynx trigger the swallowing reflex; the afferent limb of the swallowing reflex primarily involves the glossopharyngeal nerve. Direct stimulation
of the larynx triggers the laryngeal closure reflex; the superior laryngeal nerve is the primary afferent nerve involved in this reflex.
The lateral cricoarytenoid, cricothyroid, and thyroarytenoid muscles produce adduction of the vocal folds (ie, laryngospasm). The recurrent laryngeal nerve is the primary efferent nerve
for these muscles.
The trigeminal nerve, the primary afferent nerve for stimuli in the nasopharynx, may contribute to laryngospasm.
References
1. Hagberg CA. Benumof and Hagberg’s Airway Management. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2013:14.
2. Orliaguet GA, Gall O, Savoldelli GL, Couloigner V. Case scenario: perianesthetic management of laryngospasm in children. Anesthesiology. 2012;116(2):458-468.
Taxonomy

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Clinical manifestations of hypophosphatemia are uncommon unless the serum phosphate concentration is less than 1.0 mg/dL (Table 1), but severe hypophosphatemia in intensive
care unit patients may cause muscle weakness to the point of respiratory failure.
Hypophosphatemia may occur as a result of a shift of phosphate into the cells (due to insulin administration or respiratory alkalosis), increased renal losses (eg, diuretic therapy,
hyperparathyroidism), or inadequate absorption (eg, malnutrition, nasogastric suctioning, malabsorption syndromes).
One cause of hypophosphatemia merits particular consideration. Initiation of nutritional support may result in hypophosphatemia in patients with chronic malnutrition (eg, patients with
alcohol abuse). Provision of significant amounts of carbohydrates can result in increased release of insulin with the change from catabolism to anabolism. The increased levels of
insulin result in a shift of phosphate into the cells, potentially producing a rapid, dramatic decrease in serum phosphate concentration. This potentially fatal phenomenon, termed
refeeding syndrome, is commonly accompanied by hypokalemia and hypomagnesemia.
In addition to ventilatory failure (which may present as difficulty in weaning from the ventilator), severe hypophosphatemia may cause decreased myocardial contractility,
cardiomyopathy, generalized muscle weakness, rhabdomyolysis, hemolysis, or altered mental status.
Severe hypophosphatemia will result in decreased levels of 2,3-diphosphoglycerate (2,3-DPG); decreased levels of 2,3-DPG result in a leftward shift of the oxyhemoglobin dissociation
curve with impaired oxygen delivery.
Hyperphosphatemia (serum phosphate level > 4.5 mg/dL) occurs most frequently as a result of renal failure. The manifestations of hyperphosphatemia can generally be related to the
concurrent hypocalcemia. Hypocalcemia produces a prolonged QT interval, hyperreflexia/tetany, and bronchospasm.
Table 1. Classification of hypophosphatemia.
References
2. Kilic O, Demirkol D, Ucsel R, Citak A, Karabocuoglu M. Hypophosphatemia and its clinical implications in critically ill children: a retrospective study. J Crit Care. 2012;27(5):474-
479.
Taxonomy
II.C. ADVANCED: Organ-based Basic and Clinical Sciences, 5. Renal and Urinary Systems/ Electrolyte Balance

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While the pathophysiological mechanisms of acquired von Willebrand syndrome (aVWS) are different from those of hereditary von Willebrand disease (vWD), the clinical signs are
similar. Typically, aVWS occurs in patients with some other underlying disease process who have no family history of bleeding diathesis and are without any prior history of unexpected
or pathological bleeding after invasive procedures.
von Willebrand factor (vWF) is synthesized and stored in vascular endothelial cells and megakaryocytes. It functions as the carrier for factor VIII in the plasma, inhibiting degradation by
plasma enzymatic processes and thus prolonging the half-life of factor VIII in the circulation. vWF also promotes platelet adhesion to exposed subendothelial tissue in injured blood
vessels and causes platelet aggregation in response to high shear stress. aVWS is thought to occur secondary to decreased production and release of vWF or increased clearance of
vWF or its active subunits from the circulation.
The presence of autoantibodies to different subunits of vWF, uptake of vWF by tumor cells, and increased degradation or loss of the more hemostatically active subunits under
conditions of high shear stress (eg, in patients with severe aortic stenosis) have all been implicated in the etiology of aVWS (Figure 1).
Some of the underlying disorders associated with aVWS are
lymphoproliferative disorders
myeloproliferative disorders such as multiple myeloma
monoclonal gammopathies
malignancy
systemic lupus erythematosus
severe aortic stenosis
mitral valve prolapse
presence of an axial-flow (nonpulsatile) left ventricular assist device (eg, HeartMate II)
congenital heart disease (atrial septic defect or ventricular septal defect)
hypothyroidism (decreased production and storage of vWF).
Drugs associated with the development of aVWS include
valproic acid
ciprofloxacin
tetracycline
griseofulvin.
The first step in treatment of aVWS is to address the underlying cause. Pharmacologically, the treatment is essentially the same as that for the hereditary form. Both desmopressin
(DDAVP) and factor VIII/vWF concentrates have been used successfully to treat acquired vWD and as prophylaxis prior to surgical procedures.

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(DDAVP) and factor VIII/vWF concentrates have been used successfully to treat acquired vWD and as prophylaxis prior to surgical procedures.
Plasmapheresis is one of the recommended forms of therapy for aVWS.
Figure 1. A, Normal synthesis of von Willebrand factor (vWF) by endothelial cells and storage in Weibel-Palade bodies. The highly adhesive ultra-large vWF multimers are cleaved into
smaller forms as they are secreted from their storage pools. The size of circulating vWF multimers is controlled by limited proteolytic cleavage by a specific plasma protease, ADAMTS-
13. In the plasma, vWF circulates as smaller, less-adhesive multimers of different sizes; thereby, high-molecular-weight (HMW) vWF multimers present the hemostatically most relevant

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form. B, Several pathophysiological mechanisms have been described as responsible for acquired vWD including accelerated removal of the protein through autoantibodies to vWF,
adsorption of vWF onto tumor cells, and increased proteolytic degradation of vWF and/or loss of HMW vWF multimers under conditions of high shear stress (eg, aortic stenosis). Used
with permission, from Lison S, Dietrich W, Spannagl M. Unexpected bleeding in the operating room: the role of acquired von Willebrand disease. Anesth Analg. 2012;114(1):73-81.
References
1. Hines RL, Marschall KE. Stoelting’s Anesthesia and Co-Existing Disease. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:429.
2. Lison S, Dietrich W, Spannagl M. Unexpected bleeding in the operating room: the role of acquired von Willebrand disease. Anesth Analg. 2012;114(1):73-81.
Taxonomy
The respiratory response to altitude is characterized as having 2 components—acclimatization and adaptation. Acclimatization describes the acute responses of an individual
accustomed to living at normal altitude who ascends to a markedly higher altitude; these changes occur over a period of hours to weeks. A person living at a high altitude for a
prolonged period develops physiologic changes that are termed adaptation.
The primary respiratory consequence of high altitude is the decrease in the partial pressure of inspired oxygen (PIo2) which occurs as barometric pressure decreases at increasing
heights (Table 1). The decrease in PIo2 produces a decrease in the alveolar partial pressure of oxygen (Pao2) that results in a decrease in the partial pressure of oxygen in arterial
blood (Pao2) (Table 1).
Acclimatization may be viewed as occurring in 2 parts (Figure 1). Abrupt ascent to a higher altitude causes an increased hypoxic drive with an initial phase of hyperventilation resulting
in a decrease in the partial pressure of carbon dioxide in the alveolus (Paco2) with a reciprocal increase in Pao2 and, in most circumstances, an increase in Pao2 toward normal values.
The majority of this effect lasts only about 30 minutes, at the end of which time ventilation is only minimally greater than prior to exposure to altitude. Depending on the altitude (and the
associated barometric pressure), in the absence of supplemental oxygen this failure to sustain increased ventilation may result in a significant decrease in Pao2. Remaining at high
altitude for several days results in the second phase of acclimatization—a gradual increase in ventilation. The rate at which the second phase of hyperventilation occurs is influenced by
the altitude achieved and the amount to time over which this change occurs, but in most subjects the second phase of acclimatization is complete at 1 week.
The acute respiratory alkalosis occurring as a result of ascent to a higher altitude results in a leftward shift of the oxyhemoglobin dissociation curve, which is reflected in a decreased
Po2 at which hemoglobin is 50% saturated.

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Table 1. Effect of increasing altitude on barometric pressure and the partial pressure of oxygen in the inspired gas mixture.

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Figure 1. Effects of prolonged hypoxia. A. Acute hypoxemia produces an initial increase in minute ventilation that lasts for about 30 minutes. After the acute response, ventilation
decreases towards normal. B. The acute decrease in Paco2 occurs with the initiation of hypoxemia-induced increased ventilation. As ventilation is decreased, Paco2 returns toward
more normal values. C. The value of Pao2 is a mirror-image of the value of Paco2. Increased minute ventilation produces a decrease in Paco2 with a reciprocal increase in Pao2,
resulting in an increase in Pao2. The subsequent reduction in ventilation produces an increase in Paco2 with a decrease in Pao2. As acclimatization occurs, minute ventilation increases
with the predictable changes in Paco2 and Pao2. © 2014 American Society of Anesthesiologists.
References
1. Mason RJ, Broaddus VC, Martin TR, et al. Murray and Nadel’s Textbook of Respiratory Medicine. 5th ed. Philadelphia, PA: Elsevier Saunders; 2010:1651-1653.
2. Lumb AB. Nunn’s Applied Respiratory Physiology. 7th ed. Edinburgh, Scotland: Elsevier Churchill Livingstone; 2010:279-283.
3. Burtscher M. Arterial oxygen saturation during ascending to altitude under various conditions: lessons from the field. J Sci Med Sport. 2008;11(6):535-537.
Taxonomy

II.B. ADVANCED: Clinical Sciences (Procedures, Methods, Techniques), 2. Special Techniques
Clinical situations that prolong labor or overly distend the uterus (eg, multiple gestations, large for gestational age fetus, polyhydramnios) can increase the risk for postpartum
hemorrhage due to uterine atony. Pharmacologic agents that increase uterine smooth muscle contractions and tone are used to palliate or prevent this (Table 1).
Carboprost tromethamine (Hemabate) is an analog of prostaglandin F2α; it can be administered intramuscularly (IM) or injected directly into the uterus. The side effects include
increased temperature, shivering, diarrhea, severe nausea and vomiting, bronchoconstriction, and increased intrapulmonary shunt fraction resulting in hypoxemia.

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increased temperature, shivering, diarrhea, severe nausea and vomiting, bronchoconstriction, and increased intrapulmonary shunt fraction resulting in hypoxemia.
Methylergonovine (Methergine) and ergonovine (Ergotrate) are ergot derivatives that are administered IM. They can precipitate significant hypertension, increased pulmonary artery
pressure, and coronary artery vasoconstriction. Their use is typically avoided in patients with severe pregnancy-induced hypertension or preexisting hypertensive disease.
Oxytocin (Pitocin) is administered by intravenous (IV) infusion to increase uterine contractions to induce labor and to decrease uterine bleeding postpartum/postcesarean delivery. Side
effects include hypotension, especially if administered in bolus doses, and decreased systemic vascular resistance.
Terbutaline, along with magnesium sulfate, nitroglycerine, and inhaled inhalation anesthetics, relaxes uterine smooth muscle. Clinical situations in which uterine smooth muscle
relaxation is desired include inhibition of uterine contractions in preterm labor, persistent uterine hypertonus, or to provide uterine relaxation for removal of retained placenta.
Table 1. Drugs commonly used to increase uterine tone. N/V = nausea/vomiting.
References
2. Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Clinical Anesthesia. 6th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2009:1153-1158.
3. Chestnut DH, Polley LS, Tsen LC, Wong CA. Chestnut’s Obstetric Anesthesia: Principles and Practice. 4th ed. Philadelphia, PA: Elsevier Mosby; 2009:271, 757, 819-820.
4. Oyelese Y, Scorza WE, Mastrolia R, Smulian JC. Postpartum hemorrhage. Obstet Gynecol Clin North Am. 2007;34(3):421-441.
Taxonomy

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Side effects associated with chronic lithium therapy include:
General: weight gain, leukocytosis, systemic lupus erythematosus (rare)

Central nervous system: altered cognition, impaired coordination, encephalopathy, delirium, movement disorders
Cardiovascular: atrioventricular block, flattened T waves
Renal: decreased renal concentrating ability (diabetes insipidus), renal tubular damage, acute renal failure, glomerulosclerosis, nephrotic syndrome
Endocrine: hypothyroidism, hyperthyroidism (rare)
Lithium can inhibit the release of thyroid hormones. Up to 5% of patients have clinical manifestations of hypothyroidism, but approximately 35% of patients receiving chronic lithium
therapy develop laboratory evidence of hypothyroidism. Rarely, patients receiving lithium have been reported to develop hyperthyroidism.
Nephrotoxicity associated with lithium may occur after either short-term or long-term therapy. Although up to 20% of patients receiving chronic lithium therapy experience a decrease in
glomerular filtration rate, development of end-stage renal disease is uncommon. Up to 20% of patients receiving lithium therapy develop nephrogenic diabetes insipidus; they are not at
risk for developing syndrome of inappropriate antidiuretic hormone secretion.
Patients receiving chronic lithium therapy have been reported to develop a leukocytosis with white blood cell counts as high as 14,000/mm3 attributed solely to lithium.
References
1. Fleisher LA. Anesthesia and Uncommon Diseases. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:453.
2. Hemmings HC Jr, Egan TD. Pharmacology and Physiology for Anesthesia: Foundations and Clinical Applications. Philadelphia, PA: Elsevier Saunders; 2013:194-195.
3. Smith FA, Wittmann CW, Stern TA. Medical complications of psychiatric treatment. Crit Care Clin. 2008;24(4):635-656.
Taxonomy

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Long-term alcohol abuse can lead to chronic liver disease, cirrhosis, and portal hypertension. Hypoxemia in patients with portal hypertension is a well-described phenomenon, and
approximately 50% to 70% of patients with chronic liver disease complain of dyspnea. The differential diagnosis includes a wide range of pathologic processes, including intrinsic
underlying lung disease with an increase in the intrapulmonary shunt fraction, pleural effusion, loss of lung volume secondary to large amounts of ascites, fluid retention, and
metabolic/hereditary disorders such as cystic fibrosis and alpha-1 antitrypsin deficiency that affect both the liver and the lung.
There are also 2 pulmonary conditions that are unique to patients with portal hypertension:
Hepatopulmonary syndrome (HPS) is defined by the presence of liver dysfunction, unexplained hypoxemia, and abnormal vasodilation of intrapulmonary vessels. The
pulmonary vascular abnormalities range from precapillary dilations at the alveolar level to larger pulmonary vascular dilations, which are centrally located within the lung and act
as true arteriovenous shunts (Table 1). The positional hypoxemia that is associated with HPS is called orthodeoxia. Because the vascular abnormalities associated with HPS
occur more frequently at the base of the lungs, the hypoxia improves when the patient is supine and blood flow to the lungs is redistributed away from the bases. Among
candidates for liver transplantation, those with HPS have a higher mortality rate than those who do not. The hypoxemia resolves in approximately 85% of patients after liver
transplant, but the process may take up to 12 months. Without liver transplant, the 5-year survival for patients with HPS is only 23%.
Portopulmonary hypertension (PPHTN) is defined as the presence of otherwise idiopathic pulmonary hypertension in a patient with portal hypertension. The prevalence among
liver transplant candidates is approximately 4% to 6%. The presence of PPHTN does not appear to correlate with the severity of liver disease or portal hypertension. There may
be an immune or hormonal contribution to the etiology of PPHTN as it is more prevalent in female patients and in patients with autoimmune hepatitis. The presence of severe
PPHTN is a contraindication to liver transplantation.
While chronic pulmonary emboli can lead to both chronic hypoxemia and pulmonary hypertension, they are not the most likely cause of positional hypoxemia in this patient. Creation of
a splenorenal shunt is employed to relieve portal hypertension. None of these explain the presence of orthodeoxia in this patient.

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Table 1. Diagnostic criteria for the hepatopulmonary syndrome. Used with permission, from Rodríguez-Roisin R, Krowka MJ. Hepatopulmonary syndrome—a liver-induced lung
vascular disorder. N Eng J Med. 2008;358(22):2378-2387. © 2008 Boston Massachusetts Medical Society. Reprinted with permission from the Massachusetts Medical Society.
References
1. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010: 2148.
3. Muilenburg DJ, Singh A, Torzilli G, Khatri VP. Surgery in the patient with liver disease. Anesthesiol Clin. 2009;27(4):721-737.
Taxonomy
Fenoldopam is a selective dopamine type 1 receptor agonist. It lacks effect at alpha, beta, and dopamine type 2 receptors. Initially approved for treatment of hypertension, fenoldopam
has shown promise for nephroprotection in high-risk settings. The effects of fenoldopam are dose-dependent; most experts recommend starting at a dose of 0.05 µg • kg–1 • min–1 and
increasing to a maximum dose of 0.3 µg • kg–1 • min–1.
Most studies are conducted at a dose of 0.1 µg • kg–1 • min–1. At this dose, fenoldopam has been demonstrated to decrease renal vascular resistance and increase renal blood flow,
glomerular filtration rate, creatinine clearance, urine output, and excretion of sodium, potassium, and calcium.

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glomerular filtration rate, creatinine clearance, urine output, and excretion of sodium, potassium, and calcium.
References
1. Longnecker DE, Brown DL, Newman MF, Zapol WM. Anesthesiology. 2nd ed. New York, NY: McGraw-Hill Medical; 2012:747.
2. Meco M, Cirri S. The effect of various fenoldopam doses on renal perfusion in patients undergoing cardiac surgery. Ann Thorac Surg. 2010;89(2):497-503.
3. Nigwekar SU, Waikar SS. Diuretics in acute kidney injury. Semin Nephrol. 2011;31(6):523-534.
4. Jones DR, Lee HT. Perioperative renal protection. Best Pract Res Clin Anaesthesiol. 2008;22(1):193-208.
Taxonomy

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Physiologic anemia of infancy is a common and normal finding in full-term infants. Initial hemoglobin (Hb) values in the newborn are approximately 18 to 19 g/dL. In full-term infants, Hb
typically decreases during the first 2 to 3 months of life to reach a nadir as low as 8 g/dL.
Several factors are responsible for the physiologic anemia of infancy. The severe hypoxemia in utero provides a potent stimulus for erythropoietin production resulting in the high
hemoglobin concentration at birth. This stimulus is removed with the dramatic increase in oxygen content at birth. In addition to the decreased erythropoiesis, the shortened red cell
survival (80–100 days vs 120 days for an adult) results in the decrease in hemoglobin concentration. The rapid growth of the infant and blood volume results in hemodilution and the
development of physiologic anemia.
Treatment of physiologic anemia of infancy is usually not required. It is reasonable to proceed with surgery with a reduced Hb level for a surgical procedure with minimal expected blood
loss as long as the patient is asymptomatic.
Administration of supplemental iron is not indicated, but if initiated it would take at least 2 weeks for the therapy to produce a significant increase in hemoglobin concentration.
A hemoglobin electrophoresis would not be expected to give additional information for the preoperative evaluation of this patient; however, it could be useful if a hemoglobinopathy was
strongly suspected.
The transfusion of packed red blood cells is not indicated for this minor surgical procedure.
References
1. Coté CJ, Lerman J, Anderson B. A Practice of Anesthesia for Infants and Children. 5th ed. Philadelphia, PA: Elsevier Saunders; 2013:18.
2. Olson RP, Stone A, Lubarsky D. The prevalence and significance of low preoperative hemoglobin in ASA 1 or 2 outpatient surgery candidates. Anesth Analg. 2005;101(5):1337-
1340.
Taxonomy
Opioid-induced “rigidity” severe enough to cause inability to ventilate has been reported with all opioids. Factors associated with an increased risk of opioid-induced rigidity include
increased dose
increased rate of administration
absence of other anesthetic agents
The mechanism for opioid-induced rigidity is not clear. The fact that rigidity can be prevented or treated by neuromuscular blocking drugs provides evidence that the rigidity is not due to
a direct effect on muscle cells themselves. A central mechanism of action was convincingly demonstrated by a study in which a tourniquet was inflated on an upper extremity prior to
administration of alfentanil that produced generalized rigidity, including that of the isolated extremity. The specific site of the central effect is debated; hypotheses include central mu
receptor activation and involvement of basal ganglia.
Vocal cord closure is hypothesized to be the primary factor in situations where opioid-induced rigidity compromises positive pressure ventilation (Figure 1). Administration of
neuromuscular blocking drugs is the only intervention with documented efficacy in resolving the inability to ventilate.
Neither placement of a supraglottic airway device or a nasal airway nor administration of albuterol would be expected to improve ventilation in this circumstance.

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Figure 1. Changes in laryngeal conformation associated with opioid administration. A. Prior to opioid administration. B. Following opioid administration, demonstrating glottic closure. C.
Following administration of neuromuscular blocking drugs, demonstrating relief of glottic closure. Used with permission, from Bennett JA, Abrams JT, Van Riper DF, Horrow JC. Difficult
or impossible ventilation after sufentanil-induced anesthesia is caused primarily by vocal cord closure. Anesthesiology. 1997;87(5):1070-1074.
References
1. Coté CJ, Lerman J, Anderson BJ. A Practice of Anesthesia for Infants and Children. 5th ed. Philadelphia, PA: Elsevier Saunders; 2013:133.
2. Fahnenstich H, Steffan J, Kau N, Bartmann P. Fentanyl-induced chest wall rigidity and laryngospasm in preterm and term infants. Crit Care Med. 2000;28(3):836-839.
3. Dewhirst E, Naguib A, Tobias JD. Chest wall rigidity in two infants after low-dose fentanyl administration. Pediatr Emerg Care. 2012;28(5):465-468.
4. Bennett JA, Abrams JT, Van Riper DF, Horrow JC. Difficult or impossible ventilation after sufentanil-induced anesthesia is caused primarily by vocal cord closure. Anesthesiology.
1997;87(5):1070-1074.
Taxonomy


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The plasma concentration of local anesthetics is dependent on the total dose administered, pharmacologic profile, and systemic absorption. The site of injection can produce varying
local anesthetic plasma concentrations for the same total dose administered.
Absorption of local anesthetics depends on the vascularity of the injection site. An injection site with high vascularity such as the intercostal region results in the highest plasma
concentrations for local anesthetics. Maximum serum local anesthetic concentrations based on injection site (listed from greatest serum concentration to least serum concentration) are
intercostal
caudal epidural
lumbar epidural
peripheral nerve blocks (eg, brachial plexus, femoral/sciatic).
References
1. Coté CJ, Lerman J, Anderson BJ. A Practice of Anesthesia for Infants and Children. 5th ed. Philadelphia, PA: Elsevier Saunders; 2013:839.
2. Dillane D, Finucane BT. Local anesthetic systemic toxicity. Can J Anaesth. 2010;57(4):368-380.
Taxonomy
I.B. BASIC: Clinical Sciences: Anesthesia Procedures, Methods, and Techniques, 2. Regional Anesthesia

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Several characteristics are present in patients previously receiving cardiac transplantation:
Lack of cardiac innervation

Increased risk for allograft rejection
Accelerated coronary artery disease (CAD)
Increased risk for malignancy
Chronic administration of corticosteroids
Chronic administration of immunosuppressive agents
After cardiac transplantation, the donor heart is denervated. The lack of innervation restricts the ability of the new donor heart to increase heart rate in response to conditions such as
hypotension or hypovolemia. Due to this lack of innervation, patients with a transplanted heart are considered to be preload dependent. An intraoperative goal would be to maintain
normovolemia and not restrict intravenous fluids. Patients may regenerate cardiac innervation after approximately 1 year.
Premedication with atropine is not routinely required for patients after cardiac transplantation. If a medication is required for increasing heart rate, it is recommended to administer a
direct-acting agent (eg, epinephrine).
Corticosteroids are commonly administered chronically to patients after cardiac transplantation. Many patients will have the associated side effects from long-term administration,
including hypertension and diabetes mellitus. Strong consideration should be given to providing a stress dose of corticosteroids in the preoperative period or soon after induction of
anesthesia to reduce the risk of acute adrenal insufficiency.
Patients with a transplanted heart are at increased risk for accelerated CAD. The detection of myocardial ischemia can be challenging if the patient is unable to perceive ischemia-
related chest pain because of denervation. The detection of CAD in patients after cardiac transplantation is typically determined by cardiac angiography. The presence of CAD in a
patient with a transplanted heart generally increases proportionally from the time of cardiac transplantation. Due to an increased risk for CAD, monitoring the ST segments closely in the
perioperative period is strongly suggested.
References
1. Coté CJ, Lerman J, Anderson BJ. A Practice of Anesthesia for Infants and Children. 5th ed. Philadelphia, PA: Elsevier Saunders; 2013:617-618.
2. Schure AY, Kussman BD. Pediatric heart transplantation: demographics, outcomes, and anesthetic implications. Paediatr Anaesth. 2011;21(5):594-603.
Taxonomy

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Pyloric stenosis (PS) is among the most common gastrointestinal conditions that require surgical intervention in infants. PS occurs due to the development of hypertrophic muscle at the
pyloric region of the stomach, resulting in gastric outlet obstruction. The prevalence of PS is estimated to be 1 in 500 to 1 in 2,000 live births. PS is more common in males and typically
presents at an age of 3 to 6 weeks.
An important component of the anesthetic management centers on the concept that PS is not a surgical emergency. Appropriate volume resuscitation, including correction of electrolyte
disorders, should occur prior to surgical intervention. Anesthetic implications for the patient undergoing a pyloromyotomy should focus on management strategies for the neonate in
addition to the increased risk for pulmonary aspiration of gastric contents.
Anesthetic management for pyloromyotomy commonly includes
anticholinergic administration (eg, atropine) to reduce the risk of bradycardia

gastric decompression using an orogastric tube that is repeated several times after anticholinergic administration but prior to induction of anesthesia
rapid-sequence induction and tracheal intubation
infiltration of the incision site with local anesthetic agent
minimal or no use of opioids
awake extubation.
Gastric decompression prior to induction is beneficial in reducing the contents from the stomach but does not reliably assure it to be completely empty. Most experts recommend that a
large-bore orogastric tube be inserted for suctioning the stomach in right and left lateral positions as well as in the supine position. Because residual gastric contents often remain even
after this technique, the child should still be considered at risk for regurgitation and aspiration of gastric contents. Accordingly, tracheal intubation is indicated. Although most experts
recommend rapid-sequence induction, awake intubation is considered acceptable. An inhalation induction would not be the most acceptable approach for an otherwise healthy 5-week-
old boy scheduled for a pyloromyotomy who has fasted for 8 hours.
Although the use of succinylcholine is controversial in pediatric patients, most experts recognize it is an acceptable agent for infants undergoing pyloromyotomy.
Opioids are generally avoided due to the increased risk of respiratory depression in infants with metabolic alkalosis. It is proposed that the increased risk of respiratory depression is
due to the compensatory hypoventilation stemming from the preexisting metabolic alkalosis. Furthermore, adequate postoperative analgesia is usually obtained with local infiltration of a
long-acting anesthetic into incision sites along with the administration of acetaminophen.
References
1. Coté CJ, Lerman J, Anderson BJ. A Practice of Anesthesia for Infants and Children. 5th ed. Philadelphia, PA: Elsevier Saunders; 2013:760-761.
2. Bissonnette B, Sullivan PJ. Pyloric stenosis. Can J Anaesth. 1991;38(5):668-676.
Taxonomy

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Hepatic metabolism of meperidine results in several metabolites, including normeperidine. The half-life of normeperidine is up to 30 hours. Normeperidine, which is eliminated by both
the liver and kidneys, may accumulate to toxic levels in patients with renal failure or hepatic insufficiency. In addition to respiratory depression, normeperidine produces central nervous
system (CNS) excitation manifested as myoclonic jerking or seizures. While naloxone will reverse the respiratory depression, it has been reported that administration of naloxone to
patients with normeperidine toxicity can result in worsening CNS excitation, including precipitation of seizures.
Metabolism of morphine results in morphine-3-glucuronide and morphine-6-glucuronide. Morphine-6-glucuronide, an active metabolite that causes respiratory depression, undergoes
renal excretion. Patients with renal failure may develop life-threatening respiratory depression from high levels of morphine-6-glucuronide. Neither morphine nor its metabolites cause
CNS excitation.
Propofol is metabolized to inactive metabolites; neither hepatic nor renal disease substantially alters the pharmacokinetics of propofol. Propofol is a potent anticonvulsant; however,
sedative doses have been reported to cause myoclonus.
The pharmacokinetics of dexmedetomidine, which undergoes hepatic metabolism, are only minimally altered by renal failure. Administration of dexmedetomidine results in an
electroencephalogram (EEG) that resembles normal sleep. Although dexmedetomidine has been shown to lower the seizure threshold in animal models, it has proven to have minimal
effects on the EEGs of children sedated for EEG or on patients undergoing either electroconvulsive therapy or craniotomy for seizure focus resection.
References
3. Geller RJ. Meperidine in patient-controlled analgesia: a near-fatal mishap. Anesth Analg. 1993;76(3):655-657.
Taxonomy
The refeeding syndrome is a constellation of signs and symptoms that occurs after the abrupt provision of nutrition to patients who have been in a state of starvation. It was initially
noted during World War II when administration of a normal diet to emaciated former prisoners-of-war led to sudden deaths. Refeeding syndrome may be observed in a variety of patient
populations including those with eating disorders such as anorexia nervosa and in malnourished critically ill patients to whom nutritional supplementation is administered (Table 1).
The pathophysiology of refeeding syndrome is related to a change in the hormonal milieu during the transition from the starving to the fed state. As nutrition is introduced, insulin
secretion is increased, glucagon release is inhibited, previously slowed anabolic pathways are activated, and there is a shift from lipolysis to lipogenesis. Such hormonal changes can
lead to profound hypophosphatemia with concomitant hypokalemia and hypomagnesemia. Hyperglycemia and hypervolemia may also occur. Heart failure may occur as a result of the
combination of hypophosphatemia and sodium retention. Cardiac dysrhythmias, muscle weakness, and dysfunction of other organs may also occur (Figure 1).
The clinical presentation described is not consistent with hypoparathyroidism, which does not occur acutely unless the parathyroids are removed during a surgical procedure.
Kwashiorkor is characterized by marked muscle atrophy with normal or increased body fat and is typically seen in malnourished individuals in developing countries. Patients usually
have anasarca, dry and atrophic skin, hepatomegaly, and a distended abdomen with dilated intestinal loops.
Hypervitaminosis D typically occurs after long-term administration of vitamin D rather than in the clinical situation described.

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Table 1. Conditions and symptoms associated with the risk of the refeeding syndrome.
Modified from Byrnes MC, Stangenes J. Refeeding in the ICU: an adult and pediatric problem. Curr Opin Clin Nutr Metab Care. 2011;14(2):186-192.
Figure 1. Steps in the refeeding syndrome. Modified with permission, from Byrnes MC, Stangenes J. Refeeding in the ICU: an adult and pediatric problem. Curr Opin Clin Nutr Metab
Care. 2011;14(2):186-192.

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References
3. Byrnes MC, Stangenes J. Refeeding in the ICU: an adult and pediatric problem. Curr Opin Clin Nutr Metab Care. 2011;14(2):186-192.
4. Ormerod C, Farrer K, Harper L, Lal S. Refeeding syndrome: a clinical review. Br J Hosp Med (Lond). 2010;71(12):686-690.
Taxonomy

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Thrombotic thrombocytopenic purpura (TTP) is an acute multisystem disease, the manifestations of which include hemolytic anemia and thrombocytopenia. The disorder overlaps with
hemolytic uremic syndrome.
TTP should be suspected when a patient presents with a pentad of laboratory and clinical findings, including
microangiopathic hemolytic anemia (a nonimmune hemolysis in which the direct antiglobulin test is negative and schistocytes are observed on the peripheral blood smear)
renal dysfunction
mental status changes
thrombocytopenia (which is often accompanied by purpura)
fever.
The presence of both microangiopathic hemolytic anemia and thrombocytopenia is required to make the diagnosis. Therapeutic interventions mean that the development of the
characteristic pentad is now unusual. A deficiency of ADAMTS13, a protease that cleaves von Willebrand factor, or the presence of an inhibitor of ADAMTS13 is common in patients
with TTP.
The mainstay of treatment of TTP is plasma exchange, which should be initiated even if there is some uncertainty about the diagnosis of TTP. Plasma exchange reverses the
microvascular thrombus formation (and the resulting signs and symptoms) by depleting circulating autoantibody to ADAMTS13 (when present) and the circulating very high molecular
weight multimers. The missing ADAMST13 protease is replenished by the administration of donor plasma.
In addition to plasma exchange, steroids and/or other immunosuppressant agents may be indicated. Figure 1 shows a schema for treatment.
Anticoagulants, including heparin, are not used to treat the microvascular thrombi of TTP, which are mostly composed of platelets rather than fibrin. If heparin is indicated for an acute
thrombotic event, the presence of TTP is not an absolute contraindication.
Ciprofloxacin has no role in the treatment of TTP.
Platelet transfusion has been associated anecdotally with worsening of TTP symptoms, although more recent investigations have cast doubt on this impression. Nonetheless, platelet
transfusion should not be administered to patients with TTP unless significant bleeding occurs.

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Figure 1. The clinical course of patients with TTP may be complex and cannot be easily represented by a single diagram. Continued search for alternative etiologies for the patient's
clinical features is critical, even after beginning plasma exchange. Exacerbations of TTP, either while continuing daily plasma exchange or after plasma exchange is stopped, and
relapses rarely occur in patients without ADAMTS13 deficiency. Broken lines represent complications that occur in a minority of patients. PEX indicates plasma exchange. CVC
indicates central venous catheter. Used with permission, from George JN. How I treat patients with thrombotic thrombocytopenic purpura: 2010. Blood. 2010;116(20):4060-4069.
References
2. George JN. How I treat patients with thrombotic thrombocytopenic purpura: 2010. Blood. 2010;116(20):4060-4069.
3. Scully M, Hunt BJ, Benjamin S, et al. Guidelines on the diagnosis and management of thrombotic thrombocytopenic purpura and other thrombotic microangiopathies. Br J
Haematol. 2012;158(3):323-325.
4. Youngblood SC, Deng Y, Chen A, Collard CD. Perioperative therapeutic plasmapheresis. Anesthesiology. 2013;118(3):722-728.
Taxonomy

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During plasmapheresis, plasma is separated from cellular blood components and discarded. In plasma exchange, along with return of erythrocytes, leucocytes, and platelets,
replacement fluid is administered to the patient in a volume equal to the volume of plasma removed.
The use of perioperative plasmapheresis may alter intravascular volume, coagulation, serum electrolyte concentration, and drug pharmacokinetics. A volume equal to 120% of the
patient’s calculated plasma volume is typically removed at each procedure. Multiple procedures are usually required because immunoglobulin G and other small proteins are distributed
throughout interstitial fluid and re-equilibrate with the intravascular space after the procedure.
Centrifugal plasmapheresis separates blood components based on variations in specific gravity (Figure 1). It is an efficient process that may be performed at low rates of blood flow into
the device, making it possible to perform using peripheral veins. Approximately 1.5 blood volumes must be processed to remove 120% of predicted plasma volume. Citrate is used as
an anticoagulant, rarely leading to citrate toxicity. Membrane filtration plasmapheresis requires higher flow rates and 3 to 4 blood volumes are needed to eliminate 120% of the
predicted plasma volume. It often requires central venous access. Heparin anticoagulation is used. Immunoadsorption techniques can be added to specifically remove pathologic
proteins.
Albumin is commonly used as a replacement fluid, either alone or in combination with crystalloid. If the replacement fluid is devoid of coagulation factors, a coagulopathy may develop.
Use of fresh frozen plasma as a replacement fluid avoids this problem and is most often used perioperatively. Fresh frozen plasma is associated with allergic and infectious risks.
Although plasmapheresis is a relatively safe procedure (overall complication rate <5%), it does have associated complications, including
hypervolemia
hypovolemia
hypotension
rigors
chills
paresthesias
muscle cramps
coagulopathy
citrate intoxication
hypocalcemia
thrombocytopenia
hypogammaglobulinemia
transfusion-associated acute lung injury (especially with fresh frozen plasma use).
Red blood cell administration is not routinely required in patients undergoing plasmapheresis.
Heparin is a highly charged molecule and is readily removed by plasmapheresis. Furthermore, plasmapheresis-mediated reduction in antithrombin may cause heparin resistance. If a
patient is receiving therapeutic anticoagulation with heparin (eg, for a pulmonary embolism), redosing or alteration of infusion rate may be required after plasmapheresis.
Most antibiotics are cleared, at least partially, by plasmapheresis. Although cefepime does not appear to be cleared, ceftriaxone, ampicillin, gentamicin, tobramycin, and vancomycin
are removed. Consideration should be given to redosing antibiotics after the procedure.

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Figure 1. Photograph of centrifugal plasmapheresis procedure and schematic of blood component separation. Used with permission, from Youngblood SC, Deng Y, Chen A, Collard
CD. Perioperative therapeutic plasmapheresis. Anesthesiology. 2013;118(3):722-728.
References
2. Youngblood SC, Deng Y, Chen A, Collard CD. Perioperative therapeutic plasmapheresis. Anesthesiology. 2013;118(3):722-728.
3. Szczepiorkowski ZM, Winters JL, Bandarenko N, et al. Guidelines on the use of therapeutic apheresis in clinical practice—evidence-based approach from the Apheresis
Applications Committee of the American Society for Apheresis. J Clin Apher. 2010;25(3):83-177.
Taxonomy

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Hypoxic pulmonary vasoconstriction (HPV) is an important element of ventilation/perfusion matching. HPV causes diversion of blood flow away from areas of the lung with a low partial
pressure of oxygen (PO2) in the alveolus (PAO2). As might be predicted, the single most important stimulus for HPV is the PAO2.
The PO2 of pulmonary artery blood (mixed venous blood, Pv̅ o2) contributes a relatively small portion of the stimulus for HPV. The relationship between the effect of PAO2 and the effect
of Pv̅ o2 is described in equation 1.
Equation 1. Formula describing the relationship between PAO2 and Pv̅ o2 on HPV.
The PO2 in the bronchial arteries is a stimulus for vasoconstriction in the larger pulmonary arteries but is not a major contributor to hypoxic pulmonary vasoconstriction. The PO2 in the
aortic sinus has an impact on hypoxic pulmonary vasoconstriction only to the degree that it reflects the PO2 in the bronchial artery.
References
1. Lumb AB. Nunn’s Applied Respiratory Physiology. 7th ed. Edinburgh, Scotland: Elsevier Churchill Livingstone; 2010:108.
2. Vidal Melo MF, Musch G, Kaczka DW. Pulmonary pathophysiology and lung mechanics in anesthesiology: a case-based overview. Anesthesiol Clin. 2012;30(4):759-784.
Taxonomy


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A patient with an acute cervical spine injury may present with myriad physiologic abnormalities, particularly related to the cardiovascular system. Left ventricular (LV) dysfunction may
be due to direct cardiac myocyte injury or Takotsubo cardiomyopathy, a transient yet profound decrease in LV systolic function. Further, decreased sympathetic stimulation often results
in profound bradycardia.
Pulmonary edema following cervical spine injury may be due to LV dysfunction or a noncardiogenic variety called neurogenic pulmonary edema (NPE). NPE is thought to be due to
increased pulmonary hydrostatic pressure in combination with pulmonary endothelial damage.
Loss of sympathetic stimulation below the spinal cord lesion results in decreased peripheral vascular resistance and hypotension (sometimes referred to as spinal shock).
References
2. Davison DL, Terek M, Chawla L. Neurogenic pulmonary edema: review. Crit Care. 2012,16(2):212.
Taxonomy
I.C. BASIC: Organ-based Basic and Clinical Sciences, 1. Central and Peripheral Nervous Systems
Patients with mitral valve prolapse and significant mitral regurgitation have an increased risk of atrial and ventricular dysrhythmias. Atrial dysrhythmias, such as atrial fibrillation and
paroxysmal supraventricular tachycardia, are more common than ventricular dysrhythmias, presumably due to left atrial dilation from chronic mitral regurgitation. Ventricular premature
beats and ventricular ectopy have been associated with mitral valve prolapse. In some studies of patients with more malignant dysrhythmias, such as ventricular tachycardia and
ventricular fibrillation, mitral valve prolapse was the only cardiac abnormality found, even on autopsy. Complete heart block is not typically associated with mitral valve prolapse.
References
2. St John Sutton M, Weyman AE. Mitral valve prolapse prevalence and complications: an ongoing dialogue. Circulation. 2002;106(111):1305-1307.
3. Anders S, Said S, Schulz F, Püschel K. Mitral valve prolapse syndrome as cause of sudden death in young adults. Forensic Sci Int. 2007;171(2-3):127-130.
4. Vohra J, Sathe S, Warren R, Tatoulis J, Hunt D. Malignant ventricular arrhythmias in patients with mitral valve prolapse and mild mitral regurgitation. Pacing Clin Electrophysiol.
1993;16(3 Pt 1):387-393.
Taxonomy

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Mannitol is generally given as a 20% solution with an osmolality of 1098 mOsm at doses up to 1 g/kg. It reduces brain swelling and decreases brain volume, enabling the neurosurgeon
to obtain better exposure without excessive retractor pressure. Administration should take place 30 minutes prior to dural opening, and a brisk response in urine output should be noted.
The large osmotic load from a standard dose of mannitol results in
no change or a mild increase in serum osmolality

a transient increase in central venous pressure (CVP) (Figure 1)
a transient increase in intracranial pressure (ICP), possibly due to vasodilation of cerebral vessels in response to the increased osmolality (Figure 2)
no change or a mild decrease in serum sodium and bicarbonate due to osmotic expansion of the extracellular volume.
Mannitol’s osmotic diuresis begins within 4 to 5 minutes and peaks at 30 to 45 minutes. The transient increase in ICP occurs soon after the onset of the infusion, possibly due to
vasodilation of the cerebral vessels in response to the increased osmolality. The response of the CVP to mannitol is biphasic; there is an initial increase with a subsequent decrease as
the diuretic action commences.
The effect of mannitol on serum potassium has been studied by a number of investigators with conflicting results. At doses around 1 g/kg, serum potassium may change from –0.5 to
0.5 mEq/L. There is a significant increase in serum potassium with an infusion of 2 g/kg, possibly due to osmotic disruption of red blood cells during the infusion.

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Figure 1. Effect of mannitol on central venous pressure (CVP), including patients with a high cerebral spinal fluid pressure (CSFP) and those with a normal CSFP. Used with
permission, from Ravussin P, Abou-Madi M, Archer D, et al. Changes in CSF pressure after mannitol in patients with and without elevated CSF pressure. J Neurosurg. 1988;69(6):869-
876.

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Figure 2. Effect of mannitol on intracranial pressure (ICP), including patients with a high cerebral spinal fluid pressure (CSFP) and those with a normal CSFP. Modified with permission,
from Ravussin P, Abou-Madi M, Archer D, et al. Changes in CSF pressure after mannitol in patients with and without elevated CSF pressure. J Neurosurg. 1988;69(6):869-876.
References
1. Cottrell JE, Young WL. Cottrell and Young’s Neuroanesthesia. 5th ed. Philadelphia, PA: Elsevier Mosby; 2010:155.
2. Manninen PH, Lam AM, Gelb AW, Brown SC. The effect of high-dose mannitol on serum and urine electrolytes and osmolality in neurosurgical patients. Can J Anaesth.
1987;34(5):442-446.
3. Ravussin P, Abou-Madi M, Archer D, et al. Changes in CSF pressure after mannitol in patients with and without elevated CSF pressure. J Neurosurg. 1988;69(6):869-876.
Taxonomy

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Wolff-Parkinson-White syndrome (WPW) is due to rapidly firing accessory electrical pathways located between the atria and ventricles. Antegrade and retrograde conduction through
the accessory pathway, atrioventricular node, and Purkinje fibers occurs in a circular or reentrant manner (Figure 1). Conduction through the accessory pathway results in the
characteristic electrocardiogram (ECG) findings in patients with WPW, including a short PR interval and a delta wave or slow upstroke of the QRS complex, consistent with pre-
excitation (Figure 2). Aberrant conduction may also result in negative or isoelectric p waves.
ECG findings of atrial flutter include multiple p waves between each QRS complex.
ECG findings that would indicate a second-degree heart block include a “dropped” or missing QRS following a p wave.
ECG findings of a right bundle branch block include an rSR’ pattern in V1 and a slurred S wave in V6.

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Figure 1. Normal and accessory conduction pathways. Image by Tom Lück, courtesy of Wikipedia. http://en.wikipedia.org/wiki/File:WPW.jpeg . Accessed January 20, 2014. Used in
accordance with the Creative Commons Attribution 3.0 Unported license, available at http://creativecommons.org/licenses/by/3.0/deed.en .
Figure 2. Characteristic electrocardiographic finding in WPW syndrome. The red bar represents the PR interval of 0.1 seconds (100 ms). The blue bar represents the slurred upstroke
in the QRS complex that is found in WPW syndrome, known as the delta wave. The combination of the blue bar and the green bar make up the QRS complex, which is prolonged (160
ms). Image courtesy of Wikipedia user Ksheka. Available at http://en.wikipedia.org/wiki/File:WPW_EKG_leadV2.png . Used in accordance with the Creative Commons Attribution
Share Alike 2.0 Generic license, available at http://creativecommons.org/licenses/by-sa/2.0/deed.en .

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References
1. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:1018, 1368.
2. Fengler BT, Brady WJ, Plautz CU. Atrial fibrillation in the Wolff-Parkinson-White syndrome: ECG recognition and treatment in the ED. Am J Emerg Med. 2007;25(5):576-583.
Taxonomy
Normal atrioventricular (AV) node conduction limits the number of electrical impulses that reach the ventricle. However, rapid, reentrant conduction through accessory pathways in

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Normal atrioventricular (AV) node conduction limits the number of electrical impulses that reach the ventricle. However, rapid, reentrant conduction through accessory pathways in
patients with Wolff-Parkinson-White syndrome (WPW) can manifest as a wide-complex tachycardia (Figure 1). While the rhythm resembles ventricular tachycardia, this is typically a
supraventricular tachycardia such as atrial fibrillation or atrial flutter. Agents that inhibit AV nodal conduction will promote conduction through the accessory pathway. Administration of
beta-blockers, calcium channel blockers, and digoxin can lead to ventricular fibrillation in patients with WPW and should be avoided.
Pharmacologic treatment for wide-complex supraventricular tachycardia associated with WPW includes lidocaine, amiodarone, or procainamide.
Figure 1. Twelve-lead surface ECG (25 mm/s) of an irregular wide QRS-complex tachycardia during atrial fibrillation in the presence of a rapidly conducting accessory pathway. ECG,
electrocardiogram. Used with permission, from Blank R, Dieterle T, Osswald S, Sticherling C. Images in cardiovascular medicine. Wolff-Parkinson-White syndrome and atrial fibrillation
in a patient with a coronary sinus diverticulum. Circulation. 2007;115(20):e469-e471.

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References
1. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:1018, 1368.
2. Fengler BT, Brady WJ, Plautz CU. Atrial fibrillation in the Wolff-Parkinson-White syndrome: ECG recognition and treatment in the ED. Am J Emerg Med. 2007;25(5):576-583.
3. Blank R, Dieterle T, Osswald S, Sticherling C. Images in cardiovascular medicine. Wolff-Parkinson-White syndrome and atrial fibrillation in a patient with a coronary sinus
diverticulum. Circulation. 2007;115(20):e469-e471.
Taxonomy
Guillain-Barré syndrome is an acute neurologic disorder that is characterized by skeletal muscle weakness and paralysis. The pathophysiology is believed to be a cell-mediated
immunologic reaction against peripheral nerves that results in demyelination. Muscle weakness typically begins bilaterally in the lower extremities and may be preceded by
paresthesias. The disease can then progress to involve the upper extremities, trunk, neck, and facial muscles. When pharyngeal muscles are involved, difficulty swallowing and risk of
aspiration are serious concerns. Likewise, involvement of the muscles of respiration can lead to ventilatory insufficiency. Disease progression usually occurs over 2 to 4 weeks. Other
diagnostic features include areflexia and flaccid paralysis. Cranial nerve involvement and autonomic nervous system dysfunction are present in some patients with Guillain-Barré
syndrome. Hypotension or hypertension, diaphoresis, tachycardia, and cardiac conduction abnormalities may all be problems encountered in patients with associated autonomic
dysfunction. The risk of thromboembolism is also increased with this disease.
A mortality rate of 3% to 8% has been reported for Guillain-Barré syndrome, primarily due to complications, such as pulmonary embolism or respiratory failure. Complete recovery,
however, occurs over several weeks in the vast majority of patients. A minority of patients may have some residual weakness. Treatment during the acute illness is primarily focused on
supportive therapy and prevention of disease progression. The patient’s ventilatory status, including measurement of vital capacity, must be closely monitored. If vital capacity is less
than 15 mL/kg, mechanical support of ventilation is often required. When pharyngeal muscle weakness places the patient at risk for aspiration, tracheal intubation may be necessary for
airway protection.
Plasmapheresis can shorten the duration of Guillain-Barré syndrome and reduce the progression of symptoms if it is initiated within a week of the onset of symptoms. Serious
complications can occur with this therapy, including hypotension and pulmonary edema. Therefore, it is usually reserved for patients with ventilatory compromise. It has been used
safely in parturients and is not contraindicated in pregnancy. Intravenous immunoglobulin is also effective at preventing disease progression, has been used in pregnancy, and is not
contraindicated. The risk of complications is lower and the ease of administration is greater compared to plasmapheresis. Therefore, it is generally considered the preferred initial
treatment for Guillain-Barré syndrome. Corticosteroid therapy has not been an effective treatment for Guillain-Barré syndrome.
References
2. Kocabas S, Karaman S, Firat V, Bademkiran F. Anesthetic management of Guillain-Barré syndrome in pregnancy. J Clin Anesth. 2007;19(4):299-302.

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3. Brooks H, Christian AS, May AE. Pregnancy, anaesthesia and Guillain Barré syndrome. Anaesthesia. 2000;55(9):894-898.
Taxonomy
Peripartum management of the woman with Guillain-Barré syndrome will be determined by her condition at the time of delivery. Presence of the disease is not an absolute indication for
cesarean delivery. Uterine contractions remain normal, and labor and vaginal delivery may be attempted. If the patient still has muscle weakness during the peripartum period, an
instrument-assisted vaginal delivery may be necessary.
There has been some controversy regarding the use of neuraxial anesthesia in patients with Guillain-Barré syndrome. One case report suggested that a postpartum exacerbation of the
disorder may have been precipitated by epidural labor analgesia. However, there was no evidence of a cause-and-effect relationship. There have been several reports of successful
epidural and combined spinal-epidural anesthesia use in parturients with Guillain-Barré syndrome without worsening of symptoms. Therefore, neuraxial anesthesia is not
contraindicated in these women. If the patient is demonstrating signs of autonomic dysfunction due to Guillain-Barré syndrome, the anesthesiologist should be aware that serious
hypotension could develop with the administration of epidural or spinal anesthesia. If treatment of neuraxial anesthesia–induced hypotension is required, the use of a direct-acting
adrenergic drug is generally recommended. Patient response to an indirect-acting sympathomimetic drug may be exaggerated due to up-regulation of the postsynaptic receptors.
Autonomic dysfunction can also complicate the administration of general anesthesia in parturients with Guillain-Barré syndrome. Significant hypertension may develop during
laryngoscopy or surgical stimulation. Likewise, severe hypotension could be associated with blood loss or positive pressure ventilation. Therefore, preoperative placement of an
intraarterial catheter to allow close hemodynamic monitoring should be considered. Succinylcholine should not be administered to patients with Guillain-Barré syndrome. They are at
risk for a hyperkalemic response to the drug due to the proliferation of postsynaptic receptors that occurs with the disease. Hyperkalemia also has been reported in a patient who
received succinylcholine a few weeks after recovery from the syndrome. Patients with Guillain-Barré syndrome may have an increased sensitivity to nondepolarizing neuromuscular
blocking drugs. If these drugs are used during general anesthesia, the dose should be decreased. Careful monitoring with a peripheral nerve stimulator is indicated. If there are any
signs of residual neuromuscular blockade at completion of surgery, postoperative mechanical ventilation may be required.
References
3. Brooks H, Christian AS, May AE. Pregnancy, anaesthesia and Guillain Barré syndrome. Anaesthesia. 2000;55(9):894-898.
Taxonomy

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Organophosphates function by inhibiting acetylcholinesterase and plasma cholinesterase (Figure 1). The inhibition of acetylcholinesterase causes an accumulation of acetylcholine at
muscarinic and nicotinic receptors that is responsible for the signs and symptoms of organophosphate poisoning (Table 1).
Treatment of organophosphate poisoning has 2 primary aims:
Control the muscarinic effects. This is accomplished by the administration of atropine, which is notable for its long half-life and ability to cross the blood-brain barrier.
Attempt to reactivate the enzymes. Oximes, such as 2-praladoxime, are agents that can bind to the cholinesterase enzyme and potentially cause the nerve agent to unbind from
the enzyme.
It is recommended that both classes of drugs be administered simultaneously.
Cyanide, which inhibits oxidative metabolism, is a cellular toxin. Exposure primarily causes manifestations of hypoxia in the central nervous system (ie, confusion and disorientation
progressing to seizures or coma) and cardiovascular system (ie, hypertension and tachycardia progressing to hypotension and bradycardia ultimately leading to cardiovascular
collapse). Increased minute ventilation (tachypnea and hyperpnea) may ultimately progress to apnea.
Phosgene, which has many manufacturing uses, is known as a lung-damaging agent. Exposure initially produces coughing, choking, chest tightness, and eye irritation. Approximately 2
to 24 hours after initial exposure there is a secondary phase marked by pulmonary edema and severe cellular lung damage.
Chlorine is also classified as a lung-damaging agent. Exposure usually results in coughing, nausea, pulmonary edema, and burning in the nose, throat, and mouth.
Sarin, the agent used in the 1995 Tokyo subway terrorist attack, is an organophosphate.
Figure 1. Mechanism of action of organophosphates. © 2014 The American Society of Anesthesiologists.

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Table 1. Manifestations of organophosphate poisoning. Used with permission, from US Army Training (and Education) Network website.
https://rdl.train.army.mil/catalog/view/100.ATSC/F6FE4C1D-AD48-4A96-AD22-F9FD82298F2A-1274564646370/4-02.285/image006.gif . Accessed January 22, 2014.
References
2. Nerve agent and organophosphate pesticide poisoning. Centers for Disease Control and Prevention website. http://www.bt.cdc.gov/agent/nerve/tsd.asp. Updated February 14,
2013. Accessed January 20, 2014.
3. Facts about chlorine. Centers for Disease Control and Prevention website. http://www.bt.cdc.gov/agent/chlorine/basics/facts.asp. Updated April 10, 2013. Accessed January 20,
2014.
4. Facts about phosgene. Centers for Disease Control and Prevention website. http://www.bt.cdc.gov/agent/phosgene/basics/facts.asp. Updated April 12, 2013. Accessed January
20, 2014.
5. Facts about cyanide. Centers for Disease Control and Prevention website. http://www.bt.cdc.gov/agent/cyanide/basics/facts.asp. Updated June 27, 2013. Accessed January 20,
2014.
Taxonomy

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Organophosphates are a class of compounds that bind to and inhibit acetylcholinesterase and plasma cholinesterase. Administration of succinylcholine, which is predominately broken
down by plasma cholinesterase, to a patient with organophosphate poisoning would be expected to result in a significant increase in the duration of action. While the exact increase in
duration of block may vary, some insight can be gained from considering the effect of succinylcholine administration after neostigmine has been given, where the duration of block can
be as long as 60 minutes.
Neither ventricular tachycardia nor hyperkalemic arrest is a known effect after administering succinylcholine to a patient with organophosphate poisoning. Increased resistance to the
effect of succinylcholine is seen with myasthenia gravis.
References
2. Sener EB, Ustun E, Kocamanoglu S, Tur A. Prolonged apnea following succinylcholine administration in undiagnosed acute organophosphate poisoning. Acta Anaesthesiol
Scand. 2002;46(8):1046-1048.
Taxonomy


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Although thyroid storm following elective thyroid surgery has become uncommon due to preoperative preparation of the patient, non–thyroid surgery is still a recognized trigger for
thyroid storm in a patient with undiagnosed or inadequately treated hyperthyroidism. Infections, pregnancy, burns, aspirin overdose, and ketoacidosis are also conditions known to be
associated with thyroid storm.
Presenting manifestations of thyroid storm are listed in Table 1.
Hypercalcemia occurs as a result of hemoconcentration and because thyroid hormone stimulates bone resorption.
Hypovolemia occurs as a result of fever and diaphoresis as well as nausea/vomiting and diarrhea.
Myxedema coma is associated with hyponatremia and a decreased ventilatory response to both hypoxemia and hypercapnia. Cardiac tamponade due to accumulation of
mucopolysaccharide-containing fluid in the pericardium occurs with myxedema coma. There are no associations between hyperthyroidism or thyroid storm and cardiac tamponade or
altered ventilatory responses.

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Table 1. Manifestations of thyroid storm.
References
1. Hemmings HC Jr, Egan TD. Pharmacology and Physiology for Anesthesia: Foundations and Clinical Application. Philadelphia, PA: Elsevier Saunders; 2013:543-544.
2. Klubo-Gwiezdzinska J, Wartofsky L. Thyroid emergencies. Med Clin North Am. 2012;96(2):385-403.
Taxonomy

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Treatment of thyroid storm has been categorized as having 4 separate elements:
Reduction of thyroid hormone production and release by antithyroid drugs

Blocking effects of existing thyroid hormones in the blood
Treatment of systemic decompensation
Treatment of precipitating condition
Thionamide antithyroid drugs are the first step in decreasing thyroid hormone production and release. Thionamides block synthesis of new thyroid hormones but do not block release of
hormone already present in the thyroid gland. Propylthiouracil (PTU) is preferred over methimazole or carbimazole because in this class of drugs only PTU inhibits conversion of T4 to
T3. Inorganic iodine blocks the continuing release of thyroid hormones from the gland. When administered after antithyroid drugs such as thionamides (eg, propylthiouracil), it produces
rapid decreases in serum levels of T4. If administered prior to antithyroid therapy, iodine will enhance the synthesis of thyroid hormones, leading to increased stores in the gland.
Beta-blockers decrease most manifestations of excess thyroid hormones; administration of beta-blockers has been reported to result not only in a decrease in heart rate (and the
associated myocardial oxygen demand) but also in some improvement in central nervous system manifestations (including agitation, tremor, psychotic behavior, and seizures) as well
as decreasing temperature, diarrhea, and diaphoresis. Propranolol has a theoretical benefit compared with other beta-blockers because it is more effective in inhibiting conversion of T4
to T3.
Plasmapheresis can acutely reduce levels of T4 and T3; the plasma or albumin administered during plasmapheresis provides additional binding sites, thereby decreasing circulating
levels of free thyroid hormones. Peritoneal dialysis and oral cholestyramine have also been used to decrease circulating levels of thyroid hormone.
Corticosteroids are indicated because of the potential for adrenal insufficiency to occur in conjunction with the increased metabolic demands and rapid turnover of cortisol due to thyroid
storm. Steroids may also be indicated if there is an autoimmune element to the disease.
Salicylates, including aspirin, are considered contraindicated in patients with hyperthyroidism because they inhibit binding of thyroid hormone and can increase levels of free T4 and T3.
Acetaminophen is preferred as an antipyretic.
References
1. Hemmings HC, Egan TD. Pharmacology and Physiology for Anesthesia: Foundation and Clinical Application. Philadelphia, PA: Elsevier Saunders; 2013:543-544.
2. Klubo-Gwiezdzinska J, Wartofsky L. Thyroid emergencies. Med Clin North Am. 2012;96(2):385-403.
Taxonomy

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DISCUSSION FOR QUESTION 1

Increasing inhaled anesthetic concentration

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DISCUSSION FOR QUESTION 2

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Table 1. Pulmonary and cardiac complications associated with cyclosporine therapy.

DISCUSSION FOR QUESTION 3

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Figure 1. In vivo metabolism of sevoflurane. © 2014 American Society of Anesthesiologists.

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DISCUSSION FOR QUESTION 4

The oxygen analyzer test

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DISCUSSION FOR QUESTION 5

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II.D. ADVANCED: Clinical Subspecialties, 1. Painful Disease States

DISCUSSION FOR QUESTION 6

Figure 2 illustrates the effect of volatile anesthetics on airway resistance.

In addition to the treatments described in Figure 1, consideration should be given to

Long-term treatment of asthma proceeds in a stepwise fashion (Figure 3).

Therapeutic options are detailed in Table 1.

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3. Fanta CH. Asthma. N Engl J Med. 2009;360(10):1002-1014.

II.C. ADVANCED: Organ-based Basic and Clinical Sciences, 2. Respiratory System

DISCUSSION FOR QUESTION 7

II.C. ADVANCED: Organ-based Basic and Clinical Sciences, 3. Cardiovascular System

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DISCUSSION FOR QUESTION 8

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I.A. BASIC: Basic Sciences, 4. Pharmacology

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DISCUSSION FOR QUESTION 9

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DISCUSSION FOR QUESTION 10

I.A. BASIC: Basic Sciences, 4. Pharmacology

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DISCUSSION FOR QUESTION 11

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DISCUSSION FOR QUESTION 12

CVP equal to or greater than 8 mm Hg

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II.D. ADVANCED: Clinical Subspecialties, 12. Critical Care

DISCUSSION FOR QUESTION 13

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Neither fever nor persistent vomiting are manifestations of postpolio syndrome.

DISCUSSION FOR QUESTION 14

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