Anesthesia secrets 4th ed

ANESTHESIA


ANESTHESIA
Fourth Edition
James Duke, MD, MBA

Associate Professor of Anesthesiology
University of Colorado Health Sciences Center
Aurora, Colorado
Associate Director, Department of Anesthesiology
Denver Health Medical Center
Denver, Colorado


1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
ANESTHESIA SECRETS

ISBN: 978-0-323-06524-5

Copyright © 2011, 2006, 2000 by Mosby, Inc., an affiliate of Elsevier Inc.
Copyright © 1996 by Hanley & Belfus
All rights reserved. No part of this publication may be reproduced or transmitted in any form or by
any means, electronic or mechanical, including photocopying, recording, or any information storage
and retrieval system, without permission in writing from the publisher. Permissions may be sought
directly from Elsevier’s Rights Department: phone: (þ1) 215 239 3804 (US) or (þ44) 1865 843830
(UK); fax: (þ44) 1865 853333; e-mail: You may also complete
your request on-line via the Elsevier website at />

NOTICE
Knowledge and best practice in this field are constantly changing. As new research and
experience broaden our knowledge, changes in practice, treatment, and drug therapy may
become necessary or appropriate. Readers are advised to check the most current information
provided (i) on procedures featured or (ii) by the manufacturer of each product to be
administered, to verify the recommended dose or formula, the method and duration of
administration, and contraindications. It is the responsibility of the practitioner, relying on his or
her own experience and knowledge of the patient, to make diagnoses, to determine dosages and
the best treatment for each individual patient, and to take all appropriate safety precautions. To
the fullest extent of the law, neither the Publisher nor the Editors assumes any liability for any
injury and/or damage to persons or property arising out of or related to any use of the material
contained in this book.
The Publisher

Library of Congress Cataloging-in-Publication Data
Anesthesia secrets / [edited by] James Duke. – 4th ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-0-323-06524-5
1. Anesthesiology–Examinations, questions, etc. I. Duke, James
[DNLM: 1. Anesthesia–Examination Questions. 2. Anesthesiology–methods–Examination
Questions. 3. Anesthetics–Examination Questions. WO 218.2 A578 2011]
RD82.3.D85 2011
617.9’6–dc22
2009040467
Acquisitions Editor: James Merritt
Developmental Editor: Barbara Cicalese
Publishing Services Manager: Hemamalini Rajendrababu
Project Manager: K Anand Kumar
Design Direction: Steve Stave

Printed in Canada
Last digit is the print number: 9

8 7 6 5

4 3 2

1


DEDICATION
Dedicated to Renee, my wife and constant companion, and to Desi, Audrey, Sailor, and Famous.

v


CONTRIBUTORS
Rita Agarwal, MD
Associate Professor of Anesthesiology, The Children’s Hospital, University of Colorado Health Sciences
Center; Pediatric Anesthesia Program Director, The Children’s Hospital, Aurora, Colorado

William A. Baker, MD
Associate Professor of Medicine, University of Colorado School of Medicine; Director, Coronary Care Unit
and Cardiology Clinic, Denver Health Medical Center, Denver, Colorado.

Jennifer F. Brunworth, MD
Pediatric Anesthesiology Fellow, University of Colorado Denver, Denver; Pediatric Anesthesiology Fellow,
The Children’s Hospital, Aurora, Colorado

Brenda A. Bucklin, MD
Professor of Anesthesiology, Department of Anesthesiology, University of Colorado Denver, Aurora
Colorado

Mark H. Chandler, MD
Assistant Professor of Anesthesiology, University of Colorado Health Sciences Center; Anesthesiologist,
Department of Anesthesiology, Denver Health Medical Center, Denver, Colorado

Christopher L. Ciarallo, MD
Assistant Professor of Anesthesiology, University of Colorado Denver, Denver; Anesthesiologist, Denver
Health Medical Center, Denver; Pediatric Anesthesiologist, The Children’s Hospital, Aurora, Colorado

Matthew D. Coleman, MD
Anesthesiology Critical Care Fellow, Department of Anesthesiology and Critical Care, Columbia University;
Anesthesiology Critical Care Fellow, Department of Anesthesiology and Critical Care, New YorkPresbyterian Hospital, New York

Heather Rachel Davids, MD
Pain Fellow, Interventional Pain Medicine, Department of Anesthesiology, University of Colorado, Aurora;
Colorado

James Duke, MD, MBA
Associate Professor of Anesthesiology, University of Colorado Health Sciences Center, Aurora, Colorado;
Associate Director, Department of Anesthesiology, Denver Health Medical Center, Denver, Colorado

Matthew J. Fiegel, MD
Assistant Professor, Department of Anesthesiology, University of Colorado Denver; Assistant Professor,
Department of Anesthesiology, University of Colorado Denver Hospital, Aurora, Colorado

Jacob Friedman, MD
Assistant Professor, Department of Anesthesiology, University of Colorado Denver Health Sciences

Center; Staff Anesthesiologist, Department of Anesthesiology, Denver Veteran’s Affairs Hospital, Denver,
Colorado

xiii


xiv CONTRIBUTORS
Robert H. Friesen, MD
Professor of Anesthesiology, University of Colorado Denver; Vice-Chair, Anesthesiology, The Children’s
Hospital, Aurora, Colorado

Andrea J. Fuller, MD
Assistant Professor of Anesthesiology, University of Colorado Health Sciences Center, Aurora, Colorado

James B. Haenel, RRT
Surgical Critical Care Specialist, Department of Surgery, Denver Health Medical Center, Denver, Colorado

Matthew Hall, MD
Anesthesiologist, University of Colorado Health Sciences Center, Aurora, Colorado

Joy L. Hawkins, MD
Professor of Anesthesiology and Associate Chair for Academic Affairs, University of Colorado
Denver School of Medicine; Director, Obstetric Anesthesia, University of Colorado Hospital, Aurora,
Colorado

Michelle Dianne Herren, MD
Pediatric Anesthesiologist, Department of Anesthesiology, University of Colorado Hospital;
Pediatric Anesthesiologist, Department of Anesthesiology, Denver Health Medical Center, Denver;
Pediatric Anesthesiologist, Department of Anesthesiology, The Children’s Hospital Denver, Aurora,
Colorado

Daniel J. Janik, MD [Colonel (Retired), USAF, MC]
Associate Professor and Co-Director, Intraoperative Neuromonitoring, Department of Anesthesiology,
University of Colorado Denver School of Medicine; Attending Anesthesiologist, Department of
Anesthesiology, University of Colorado Hospital, Aurora, Colorado

Gillian E. Johnson, MBBChir, BSc
Anesthesiology Resident, University of Colorado Health Sciences Center, Aurora, Colorado

Jeffrey L. Johnson, MD
Assistant Professor of Surgery, University of Colorado Health Sciences Center, Aurora; Director, Surgical
Intensive Care, Denver Health Medical Center, Denver, Colorado

Alma N. Juels, MD
Assistant Professor of Anesthesiology, University of Colorado Denver, Aurora; Attending Physician,
Department of Anesthesiology, Denver Health Medical Center, Denver, Colorado

Lyle E. Kirson, DDS
Associate Professor of Anesthesiology, University of Colorado Health Sciences Center,
Aurora; Veterans Affairs Medical Center, Denver, Colorado

Renee Koltes-Edwards, MD
Clinical Instructor of Anesthesiology, University of North Dakota School of Medicine and Health Science;
Staff Anesthesiologist, Altru Health System, Grand Forks, North Dakota

Jason P. Krutsch, MD
Director, Interventional Pain Management, and Assistant Professor of Anesthesiology, University of
Colorado Health Sciences Center, Aurora, Colorado

Sunil Kumar, MD, FFARCS

Assistant Professor, Department of Anesthesiology, University of Colorado Health Sciences
Center, Aurora; Anesthesiologist, Department of Anesthesiology, Denver Health Medical Center, Denver,
Colorado


CONTRIBUTORS xv

Philip R. Levin, MD
Associate Clinical Professor, Department of Anesthesiology, David Geffen School of Medicine at UCLA,
Los Angeles; Medical Director of Perioperative services, Chief of Anesthesiology, Department of
Anesthesiology, Santa Monica/UCLA Medical Center and Orthopaedic Hospital, Santa Monica; Associate
Clinical Professor, Department of Anesthesiology, Ronald Reagan/UCLA Medical Center, Los Angeles,
California

Ana M. Lobo, MD, MPH
Assistant Professor of Anesthesiology, Obstetric Anesthesia, Yale University School of Medicine, Yale New
Haven Hospital, New Haven, Connecticut

Christopher M. Lowery, MD
Assistant Professor of Medicine, Department of Cardiology, University of Colorado Denver, Aurora;
Director of Cardiac Electrophysiology, Department of Cardiology, Denver Health Medical Center,
Denver; Staff Electrophysiologist, Department of Cardiology, University of Colorado Hospital, Aurora,
Colorado

Theresa C. Michel, MD
Senior Lecturer, Department of Anesthesiology, University of Colorado; Attending Anesthesiologist, Denver
Health and Hospital Authority, Denver, Colorado

Howard J. Miller, MD
Associate Professor of Anesthesiology, Denver Health Medical Center, Denver; Associate Professor of

Anesthesiology, University of Colorado Denver School of Medicine, Aurora, Colorado

Steven T. Morozowich, DO, FASE
Instructor of Anesthesiology, Mayo Clinic College of Medicine, Mayo Clinic Arizona, Phoenix; Staff
Anesthesiologist, Mercy Regional Medical Center, Durango, Colorado

Aaron Murray, MD
Anesthesiology Resident, University of Colorado Health Sciences Center, Aurora, Colorado

Sola Olamikan, MD
Pediatric Anesthesiology, University of Colorado, Denver; Anesthesiologist, The Children’s Hospital,
Aurora, Colorado

Luke Osborne, MD
Assistant Professor of Anesthesiology, University of Colorado Health Sciences Center, Aurora; Assistant
Professor of Anesthesiology, Veteran’s Affairs Medical Center, Denver, Colorado

Malcolm Packer, MD
Associate Professor of Anesthesiology, Department of Anesthesiology, University of Colorado Denver;
Attending Anesthesiologist, Department of Anesthesiology, Denver Health and Hospitals Authority,
Denver; Attending Anesthesiologist, Department of Anesthesiology, The Children’s Hospital,
Denver, Colorado

Gurdev S. Rai, MD
Assistant Professor of Anesthesiology, University of Colorado Denver; Anesthesiologist, Anesthesiology
Service, Eastern Colorado Health Care System, Veterans Affairs Medical Center, Denver, Colorado

Prairie Neeley Robinson, MD
Anesthesiology Resident, University of Colorado Health Sciences Center, Denver, Aurora, Colorado

Michael M. Sawyer, MD
Assistant Professor of Anesthesiology, Department of Anesthesiology, University of Colorado Denver
Health Hospital Association, Denver, Colorado


xvi CONTRIBUTORS
Tamas Seres, MD, PhD
Associate Professor of Anesthesiology, University of Colorado Denver, Aurora, Colorado

Marina Shindell, DO
Assistant Professor of Anesthesiology, University of Colorado, Aurora, Colorado

Robert H. Slover, MD
Associate Professor of Pediatrics, University of Colorado Denver, Aurora; Director of Pediatric Services,
The Barbara Davis Center for Childhood Diabetes, Aurora; Pediatric Endocrinologist, Department of
Endocrinology, The Children’s Hospital, Aurora, Colorado

Robin Slover, MD
Associate Professor of Anesthesiology, University of Colorado; Interim Director of Chronic Pain Service,
The Children’s Hospital; Chronic Pain Physician, Anschutz Outpatient Clinic, University of Colorado,
Aurora, Colorado

Mark D. Twite, MA, MB, BChir, FRCP
Director of Pediatric Cardiac Anesthesia, Department of Anesthesiology, The Children’s Hospital and
University of Colorado, Denver, Colorado

Ronald Valdivieso, MD
Assistant Professor of Anesthesiology, University of Colorado, Aurora; Assistant Professor of
Anesthesiology, Denver Health Medical Center, Denver, Colorado

Nathaen Weitzel, MD
Assistant Professor of Anesthesiology, University of Colorado Health Sciences Center; Faculty
Anesthesiologist, University of Colorado, Denver, Colorado

Joel E. Wilson, MD
Anesthesiology Resident, University of Colorado Health Sciences Center, Aurora, Colorado


PREFACE
In this fourth edition of Anesthesia Secrets, the goal continues to be concise presentation
of a wide range of topics important to anyone interested in anesthesiology. My goal has always been
to not merely offer a few words suitable for the sake of familiarity, but to provide suitable depth
to allow readers to integrate the concerns of this field into their wider knowledge of medicine
in general.
I am humbled by the reception Anesthesia Secrets has received since the first edition was
published in 1996. I take it as an affirmation that my contributors and I have a good idea of the
important concepts in the field, as much as they can be described in a text of this size. I thank my
contributors for this edition and all previous editions. Over the years my contributors have gone
on to successful careers across the country, yet their imprint remains throughout. Although they may
no longer be listed as authors, they nonetheless have my thanks.
And to you, the reader, thank you for making Anesthesia Secrets a part of your educational
program.
James Duke, MD, MBA

xvii


TOP 100 SECRETS
These secrets are 100 of the top board alerts. They summarize the concepts,
principles, and most salient details of anesthesiology.

1. Patients should take prescribed b-blockers on the day of surgery and continue them
perioperatively. Because the receptors are up-regulated, withdrawal may precipitate
hypertension, tachycardia, and myocardial ischemia. Clonidine should also be continued
perioperatively because of concerns for rebound hypertension.
2. Under most circumstances peri-induction hypotension responds best to administration of
intravenous fluids and the use of direct-acting sympathomimetics such as phenylephrine.
3. To determine the etiology of hypoxemia, calculate the A-a gradient to narrow the
differential diagnosis.
À
4. Calculating the anion gap (Naþ À [HCOÀ
3 þ Cl ]) in the presence of a metabolic acidosis
helps narrow the differential diagnosis.

5. Estimating volume status requires gathering as much clinical information as possible
because any single variable may mislead. Always look for supporting information.
6. Rapid correction of electrolyte disturbances may be as dangerous as the underlying
electrolyte disturbance.
7. When other causes have been ruled out, persistent and refractory hypotension in trauma
or other critically ill patients may be caused by hypocalcemia or hypomagnesemia.
8. There is no set hemoglobin/hematocrit level at which transfusion is required. The decision
should be individualized to the clinical situation, taking into consideration the patient’s
health status.
9. An outpatient with a bleeding diathesis can usually be identified through history (including
medications) and physical examination. Preoperative coagulation studies in asymptomatic
patients are of little value.
10. Thorough airway examination and identification of the patient with a potentially difficult
airway are of paramount importance. The “difficult-to-ventilate, difficult-to-intubate”
scenario must be avoided if possible. An organized approach, as reflected in the American
Society of Anesthesiologists’ Difficult Airway Algorithm, is necessary and facilitates highquality care for patients with airway management difficulties.

11. No single pulmonary function test result absolutely contraindicates surgery. Factors
such as physical examination, arterial blood gases, and coexisting medical problems also
must be considered in determining suitability for surgery.
12. Speed of onset of volatile anesthetics is increased by increasing the delivered
concentration of anesthetic, increasing the fresh gas flow, increasing alveolar ventilation,
and using nonlipid-soluble anesthetics.

1


2 TOP 100 SECRETS
13. Opioids depress the carbon dioxide–associated drive to breathe, resulting in
hypoventilation. Because of the active metabolites, patients with renal failure may
experience an exaggerated reaction to morphine.
14. Appropriate dosing of intravenous anesthetics requires considering intravascular volume
status, comorbidities, age, and medications.
15. Termination of effect of intravenous anesthetics is by redistribution, not biotransformation
and breakdown.
16. Although succinylcholine is the usual relaxant used for rapid sequence induction, agents
that chelate nondepolarizing relaxant molecule may alter this paradigm in the future.
17. Leave clinically weak patients intubated and support respirations until the patient can
demonstrate return of strength.
18. Lipid solubility, pKa, and protein binding of the local anesthetics determine their potency,
onset, and duration of action, respectively.
19. Local anesthetic-induced central nervous system toxicity manifests as excitation, followed
by seizures, and then loss of consciousness. Hypotension, conduction blockade, and
cardiac arrest are signs of local anesthetic cardiovascular toxicity.
20. There is sound scientific evidence that low-dose dopamine is ineffective for prevention and
treatment of acute renal injury and protection of the gut.
21. A preoperative visit by an informative and reassuring anesthesiologist provides useful

psychologic preparation and calms the patient’s fears and anxiety before administration of
anesthesia.
22. The risk of clinically significant aspiration pneumonitis in healthy patients having elective
surgery is very low. Routine use of pharmacologic agents to alter the volume or pH of
gastric contents is unnecessary.
23. The most important information obtained in a preanesthetic evaluation comes from a
thorough, accurate, and focused history and physical examination.
24. When compressed, some gases condense into a liquid (N2O and CO2) and some do not
(O2 and N2). These properties define the relationship between tank volume and pressure.
25. The semiclosed circuit using a circle system is the most commonly used anesthesia
circuit. Components include an inspiratory limb, expiratory limb, unidirectional valves, a
CO2 absorber, a gas reservoir bag, and a pop-off valve on the expiratory limb.
26. Every patient ventilated with an ascending bellows anesthesia ventilator receives
approximately 2.5 to 3 cm H2O of positive end-expiratory pressure (PEEP) because of the
weight of the bellows.
27. The output of traditional vaporizers depends on the proportion of fresh gas that bypasses
the vaporizing chamber compared with the proportion that passes through the vaporizing
chamber.
28. A conscientious approach to positioning is required to facilitate the surgical procedure,
prevent physiologic embarrassment, and prevent neuropathy and injury to other aspects of
the patient’s anatomy.


TOP 100 SECRETS 3
29. The first step in the care of the hypoxic patient fighting the ventilator is to ventilate the
patient manually with 100% oxygen.
30. Risk factors for auto-PEEP include high minute ventilation, small endotracheal tube,
chronic obstructive pulmonary disease, and asthma.
31. When determining whether an abnormal electrocardiogram (ECG) signal may be an artifact,
look to see if the native rhythm is superimposed on (marching through) the abnormal tracing.

32. A patient with new ST-segment depression or T-wave inversion may have suffered a non–
ST-elevation myocardial infarction.
33. Pulse oximetry measures arterial oxygenation using different wavelengths of light shone
through a pulsatile vascular bed. Pulse oximetry can detect hypoxemia earlier, providing
an early warning sign of potential organ damage.
34. Below a hemoglobin saturation of 90%, a small decrease in saturation corresponds to a
large drop in PaO2.
35. Except for visualization with bronchoscopy, CO2 detection is the best method of verifying
endotracheal tube location.
36. Analysis of the capnographic waveform provides supportive evidence for numerous
clinical conditions, including decreasing cardiac output; altered metabolic activity; acute
and chronic pulmonary disease; and ventilator, circuit, and endotracheal tube malfunction.
37. Trends in central venous pressures are more valuable than isolated values and should
always be evaluated in the context of the patient’s scenario.
38. Pulmonary catheterization has not been shown to improve outcome in all patient subsets.
39. The risks of central venous catheterization and pulmonary artery (PA) insertion are many
and serious, and the benefits should be identified before initiation of these procedures to
justify their use.
40. To improve accuracy in interpretation of PA catheter data, always consider the timing of
the waveforms with the ECG cycle.
41. Ipsilateral ulnar arterial catheterization should not be attempted after multiple failed
attempts at radial artery catheterization.
42. With the exception of antagonists of the renin-angiotensin system and possibly diuretics,
antihypertensive therapy should be given up to and including the day of surgery.
43. Symptoms of awareness may be very nonspecific, especially when muscle relaxants are used.
44. When a patient with structural heart disease develops a wide-complex tachycardia,
assume that the rhythm is ventricular tachycardia until proven otherwise. When a patient
develops tachycardia and becomes hemodynamically unstable, prepare for cardioversion
(unless the rhythm is clearly sinus!).
45. When a patient develops transient slowing of the sinoatrial node along with transient

atrioventricular block, consider increased vagal tone, a medication effect, or both.


4 TOP 100 SECRETS
46. Even mild hypothermia has a negative influence on patient outcome, increasing rates of
wound infection, delaying healing, increasing blood loss, and increasing cardiac morbidity
threefold.
47. If a patient’s exercise capacity is excellent, even in the presence of ischemic heart disease,
the chances are good that the patient will be able to tolerate the stresses of surgery. The
ability to climb two or three flights of stairs without significant symptoms (e.g., angina,
dyspnea, syncope) is usually an indication of adequate cardiac reserve.
48. Patients with decreased myocardial reserve are more sensitive to the cardiovascular
depressant effects caused by anesthetic agents, but careful administration with close
monitoring of hemodynamic responses can be accomplished with most agents.
49. For elective procedures, the most current fasting guidelines are as follows:
Clear liquids (water, clear juices)
2 hours
4 hours
Nonclear liquids (Jello, breast milk)
Light meal or snack (crackers, toast, liquid) 6 hours
Full meal (fat containing, meat)
8 hours
50. “All that wheezes is not asthma.” Also consider mechanical airway obstruction, congestive
failure, allergic reaction, pulmonary embolus, pneumothorax, aspiration, and
endobronchial intubation.
51. Patients with significant reactive airway disease require thorough preoperative preparation,
including inhaled b-agonist therapy and possibly steroids, methylxanthines, or other
agents.
52. The necessary criteria for acute lung injury/acute respiratory distress syndrome (ALI/
ARDS) include:

(1) Acute onset
(2) PaO2/FiO2 ratio of 300 for ALI
(3) PaO2/FiO2 ratio of 200 for ARDS
(4) Chest radiograph with diffuse infiltrates
(5) Pulmonary capillary wedge pressure of 18 mm Hg
53. Mechanical ventilation settings for patients with ARDS or ALI include tidal volume of at
6 to 8 ml/kg of ideal body weight while limiting plateau pressures to <30 cm H2O. PEEP
should be adjusted to prevent end-expiratory collapse. FiO2 should be adjusted to maintain
oxygen saturations between 88% and 92%.
54. Acute intraoperative increases in PA pressure may respond to optimizing oxygenation and
ventilation, correcting acid-base status, establishing normothermia, decreasing the
autonomic stress response by deepening the anesthetic, and administering vasodilator
therapy.
55. The best way to maintain renal function during surgery is to ensure an adequate
intravascular volume, maintain cardiac output, and avoid drugs known to decrease renal
perfusion.
56. Measures to acutely decrease intracranial pressure (ICP) include elevation of the head
of the bed; hyperventilation (PaCO2 25 to 30 mm Hg); diuresis (mannitol and/or
furosemide); and minimized intravenous fluid. In the setting of elevated ICP, avoid
ketamine and nitrous oxide.


TOP 100 SECRETS 5
57. Airway comes first in every algorithm; thus succinylcholine is the agent of choice for a
rapid-sequence induction for the full-stomach, head-injured patient, despite the
transient rise in ICP seen with succinylcholine. Succinylcholine must be avoided in
children with muscular dystrophy and should be avoided except in airway emergencies
in young males.
58. Malignant hyperthermia (MH) is an inherited disorder that presents in the perioperative
period after exposure to inhalational agents and/or succinylcholine. The disease may be

fatal if the diagnosis is delayed and dantrolene is not administered. The sine qua non of
MH is an unexplained rise in end-tidal carbon dioxide with a simultaneous increase in
minute ventilation in the setting of an unexplained tachycardia.
59. Patients with Alzheimer’s disease may become more confused and disoriented with
preoperative sedation.
60. In patients with multiple sclerosis spinal anesthesia should be used with caution and only
in situations in which the benefits of spinal anesthesia over general anesthesia are clear.
61. Patients with diabetes have a high incidence of coronary artery disease with an atypical or
silent presentation. Maintaining perfusion pressure, controlling heart rate, continuous ECG
observation, and a high index of suspicion during periods of refractory hypotension are
key considerations.
62. The inability to touch the palmar aspects of the index fingers when palms touch (the
prayer sign) can indicate a difficult oral intubation in patients with diabetes.
63. Thyroid storm may mimic MH. It is confirmed by an increased serum tetraiodothyronine
(T4) level and is treated initially with b-blockade followed by antithyroid therapy.
64. Perioperative glucocorticoid supplementation should be considered for patients receiving
exogenous steroids.
65. Obese patients may be difficult to ventilate and difficult to intubate. Backup strategies
should always be considered and readily available before airway management begins.
66. A patient with a Glasgow Coma Scale of 8 is sufficiently depressed that endotracheal
intubation is indicated.
67. The initial goal of burn resuscitation is to correct hypovolemia. Burns cause a generalized
increase in capillary permeability with loss of significant fluid and protein into interstitial tissue.
68. From about 24 hours after injury until the burn has healed, succinylcholine may cause
hyperkalemia because of proliferation of extrajunctional neuromuscular receptors. Burned
patients tend to be resistant to the effects of nondepolarizing muscle relaxants and may
need two to five times the normal dose.
69. Abrupt oxygen desaturation while transporting an intubated pediatric patient is probably
the result of main stem intubation.
70. Because children have stiff ventricles and rely on heart rate for cardiac output, maintain

heart rate at all costs by avoiding hypoxemia and administering anticholinergic agents
when appropriate.


6 TOP 100 SECRETS
71. Infants may be difficult to intubate because they have a more anterior larynx, relatively
large tongues, and a floppy epiglottis. The narrowest part of the larynx is below the vocal
cords at the cricoid cartilage.
72. Hyperventilation with 100% oxygen is the best first step in treating a pulmonary
hypertensive event.
73. If a child with tetralogy of Fallot has a hypercyanotic spell during induction of anesthesia,
gentle external compression of the abdominal aorta can reverse the right-to-left shunt
while pharmacologic treatments are being prepared.
74. The patient with a ventricular obstructive cardiac lesion is at high risk for perioperative
cardiac failure or arrest because of ventricular hypertrophy, ischemia, and loss of
contractile tissue.
75. Pregnant patients can pose airway management problems because of airway edema, large
breasts that make laryngoscopy difficult, full stomachs rendering them prone to aspiration,
and rapid oxygen desaturation caused by decreased functional residual capacity.
76. In preeclampsia hypertension should be treated, but blood pressure should not be
normalized. Spinal anesthesia may be preferable to general anesthesia when the
preeclamptic patient does not have an existing epidural catheter or there is insufficient
time because of nonreassuring fetal heart rate tracing.
77. Intrauterine fetal resuscitation and maternal airway management are of overriding
importance in patients with eclamptic seizures.
78. Basal function of most organ systems is relatively unchanged by the aging process per se,
but the functional reserve and ability to compensate for physiologic stress are reduced.
79. In general, anesthetic requirements are decreased in geriatric patients. There is an
increased potential for a wide variety of postoperative complications in the elderly, and
postoperative cognitive dysfunction is arguably the most common.

80. Anesthesiologists increasingly are asked to administer anesthesia in nontraditional
settings. Regardless of where an anesthetic is administered, the same standards apply for
safety, monitors, equipment, and personnel.
81. O-negative blood is the universal donor for packed red blood cells; for plasma it is AB positive.
82. If a patient is pacemaker dependent, the interference by electrocautery may be interpreted
by the device as intrinsic cardiac activity, leading to profound inhibition of pacing and
possible asystole. Devices should be programmed to the asynchronous mode before
surgery.
83. Pacemaker-mediated tachycardia is an endless-loop tachycardia caused by retrograde
atrial activation up the conduction system, with subsequent tracking of this atrial signal
and then pacing in the ventricle. It can be terminated by application of a magnet that
prevents tracking.
84. Loss of afferent sensory and motor stimulation renders a patient sensitive to sedative
medications secondary to deafferentiation. For the same reason neuraxial anesthesia
decreases the minimum alveolar concentration of volatile anesthetics.


TOP 100 SECRETS 7
85. Patients with sympathectomies from regional anesthesia require aggressive resuscitation,
perhaps with unusually large doses of pressors, to reestablish myocardial perfusion after
cardiac arrest.
86. Although patients with end-stage liver disease have a hyperdynamic circulation characterized
by increased cardiac index and decreased systemic vascular resistance, impaired myocardial
function, coronary artery disease, and pulmonary hypertension are common.
87. Patients with liver disease commonly have an increased volume of distribution,
necessitating an increase in initial dose requirements. However, because the drug
metabolism may be reduced, smaller doses are subsequently administered at longer
intervals.
88. There is no best anesthetic technique during cardiopulmonary bypass. Patients with
decreased ejection fraction will not tolerate propofol infusions or volatile anesthesia as

well as patients with preserved stroke volume and will probably require an opioid-based
technique.
89. Always reassess optimal positioning of any lung-isolation device after repositioning the
patient. A malpositioned tube is suggested by acute increases in ventilatory pressures and
decreases in oxygen saturation.
90. Methods to improve oxygenation during one-lung ventilation include increasing FiO2,
adding PEEP to the dependent lung, adding continuous positive airway pressure to the
nondependent lung, adjusting tidal volumes, and clamping the blood supply to the
nonventilated lung.
91. To decrease airway pressures, always use the largest double-lumen endotracheal tube
available.
92. If ICP is high, as evidenced by profound changes in mental status or radiologic evidence of
cerebral swelling, avoid volatile anesthetics and opt instead for a total intravenous
anesthetic technique.
93. If PaCO2 significantly increases after 30 minutes of pneumoperitoneum, search for another
cause of hypercapnia such as capnothorax, subcutaneous PaCO2, CO2 embolism, or
endobronchial intubation.
94. Pulmonary arterial occlusion pressure is an unreliable indicator of cardiac filling pressures
during pneumoperitoneum.
95. Postoperative nausea and vomiting are common after laparoscopic surgery; they should
be anticipated and treated prophylactically.
96. Methohexital should be considered the drug of choice for the induction of anesthesia for
electroconvulsive therapy (ECT). ECT causes pronounced sympathetic activity, which may
result in myocardial ischemia or even infarction in patients with coronary artery disease.
97. To perform ECT safely it is necessary to complete a preoperative history and physical
examination, use standard monitors, have readily available equipment and medications
appropriate for full cardiopulmonary resuscitation, use an induction agent (e.g.,
methohexital) and muscle relaxant (e.g., succinylcholine), and have a b-blocker readily
available (e.g., esmolol).

8 TOP 100 SECRETS
98. Doses of morphine differ by a factor of 10 between intravenous, epidural, and intrathecal
routes.
99. Chronic pain is best treated by using multiple therapeutic modalities, including physical
therapy, psychologic support, pharmacologic management, and rational use of more
invasive procedures such as nerve blocks and implantable technologies.
100. Neuropathic pain is usually less responsive to opioids than pain originating from
nociceptors.


AUTONOMIC NERVOUS SYSTEM
James Duke, MD, MBA

CHAPTER 1

I. BASICS OF PATIENT MANAGEMENT

1. Describe the autonomic nervous system.
The autonomic nervous system (ANS) is a network of nerves and ganglia that controls involuntary
physiologic actions and maintains internal homeostasis and stress responses. The ANS
innervates structures within the cardiovascular, pulmonary, endocrine, exocrine, gastrointestinal,
genitourinary, and central nervous systems (CNS) and influences metabolism and thermal
regulation. The ANS is divided into two parts: the sympathetic (SNS) and parasympathetic (PNS)
nervous system. When stimulated, the effects of the SNS are widespread across the body. In
contrast, PNS stimulation tends to produce localized, discrete effects. The SNS and PNS generally
have opposing effects on end-organs, with either the SNS or the PNS exhibiting a dominant
tone at rest and without exogenous stimulating events (Table 1-1). In general the function of the
PNS is homeostatic, whereas stimulation of the SNS prepares the organism for some stressful
event (this is often called the fight-or-flight response).

TABLE 1-1. A U T O N O M I C D O M I N A N C E P A T T E R N S A T E F F E C T O R S I T E S
Sympathetic Nervous System

Parasympathetic Nervous System

Arterioles

Sinoatrial node

Veins

Gastrointestinal tract

Sweat glands

Uterus
Urinary bladder
Salivary glands
Iris
Ciliary muscle

KEY POINTS: AUTONOMIC NERVOUS SYSTEM
1. Patients should take b-blockers on the day of surgery and continue them perioperatively.
Because the receptors are up-regulated, withdrawal may precipitate hypertension,
tachycardia, and myocardial ischemia.
2. Clonidine should also be continued perioperatively because of concerns for rebound
hypertension.
3. Indirect-acting sympthomimetics (e.g., ephedrine) depend on norepinephrine release to be
effective. Norepinephrine-depleted states will not respond to ephedrine administration.

9


10 CHAPTER 1 AUTONOMIC NERVOUS SYSTEM

4. Under most circumstances peri-induction hypotension responds best to intravenous fluid
administration and the use of direct-acting sympathomimetics such as phenylephrine.
5. Orthostatic hypotension is common after surgery and may be caused by the use of any or all
anesthetic agents and lying supine for extended periods. It is necessary to be cognizant of this
potential problem when elevating a patient’s head after surgery or even when moving the patient
from the operating room table to a chair (e.g., procedures requiring only sedation and monitoring).

2. Review the anatomy of the sympathetic nervous system.
Preganglionic sympathetic neurons originate from the intermediolateral columns of the
thoracolumbar spinal cord. These myelinated fibers exit via the ventral root of the spinal nerve
and synapse with postganglionic fibers in paravertebral sympathetic ganglia, unpaired
prevertebral ganglia, or a terminal ganglion. Preganglionic neurons may ascend or descend the
sympathetic chain before synapsing. Preganglionic neurons stimulate nicotinic cholinergic
postganglionic neurons by releasing acetylcholine. Postganglionic adrenergic neurons synapse
at targeted end-organs and release norepinephrine (Figure 1-1).

Ganglion
Preganglionic

Postganglionic
ACh

SYMPATHETIC

Heart
N.E. Smooth muscle
Glands

Ganglion
Preganglionic
SYMPATHETIC

Postganglionic

ACh Sweat glands

ACh
Ganglion

Preganglionic
SYMPATHETIC

Adrenal medulla
N.E.
Epi.

ACh
Ganglion

Preganglionic
PARASYMPATHETIC

Postganglionic

Heart
ACh Smooth muscle
Glands

Figure 1-1. Neuronal anatomy of the autonomic nervous system with respective neurotransmitters.
Ach, Acetylcholine; NE, norepinephrine. (Moss J, Glick D: The autonomic nervous system. In Miller RD,
editor: Miller’s Anesthesia, ed 6, Philadelphia, 2005, Churchill Livingstone, p 618.)

3. Elaborate on the location and names of the sympathetic ganglia. Practically
speaking, what is the importance of knowing the name and location of these
ganglia?
Easily identifiable paravertebral ganglia are found in the cervical region (including the stellate
ganglion) and along thoracic, lumbar, and pelvic sympathetic trunks. Prevertebral ganglia
are named in relation to major branches of the aorta and include the celiac, superior and inferior
mesenteric, and renal ganglia. Terminal ganglia are located close to the organs that they serve. The
practical significance of knowing the location of some of these ganglia is that local anesthetics can
be injected in the region of these structures to ameliorate sympathetically mediated pain.


CHAPTER 1 AUTONOMIC NERVOUS SYSTEM 11
4. Describe the postganglionic adrenergic receptors of the sympathetic nervous
system and the effects of stimulating these receptors.
There are a1, a2, b1, and b2 adrenergic receptors. The A1, A2, and B2 receptors are
postsynaptic and are stimulated by the neurotransmitter norepinephrine. The A2 receptors are
presynaptic, and stimulation inhibits release of norepinephrine, reducing overall the autonomic
response. Molecular pharmacologists have further subdivided these receptors, but this is
beyond the scope of this discussion. Dopamine stimulates postganglionic dopaminergic
receptors, classified as DA1 and DA2. The response to receptor activation in different sites is
described in Table 1-2.

TABLE 1-2. E N D - O R G A N E F F E C T S O F A D R E N E R G I C R E C E P T O R S T I M U L A T I O N
Receptor

Organ

Response

b1

Heart

Increases heart rate, contractility, and

Fat cells

Lipolysis

Blood vessels

Dilation

Bronchioles

Dilation

Uterus
Kidneys

Relaxation
Renin secretion

Liver

Gluconeogenesis, glycogenolysis

Pancreas

Insulin secretion

Blood vessels

Constriction

conduction velocity
b2

a1

Pancreas

Inhibits insulin release

Intestine, bladder

Relaxation but constriction of sphincters

a2

Presynaptic nerve endings

Inhibits norepinephrine release

Dopamine-1
Dopamine-2

Blood vessels
Presynaptic endings

Dilates renal, coronary, and splanchnic vessels
Inhibits norepinephrine release

Central nervous system

Psychic disturbances

5. Review the anatomy and function of the parasympathetic nervous system.
Preganglionic parasympathetic neurons originate from cranial nerves III, VII, IX, and X and
sacral segments 2-4. Preganglionic parasympathetic neurons synapse with postganglionic
neurons close to the targeted end-organ, creating a more discrete physiologic effect. Both
preganglionic and postganglionic parasympathetic neurons release acetylcholine; these
cholinergic receptors are subclassified as either nicotinic or muscarinic. The response to
cholinergic stimulation is summarized in Table 1-3.
6. What are catecholamines? Which catecholamines occur naturally? Which are
synthetic?
Catecholamines are hydroxy-substituted phenylethylamines and stimulate adrenergic nerve
endings. Norepinephrine, epinephrine, and dopamine are naturally occurring catecholamines,
whereas dobutamine and isoproterenol are synthetic catecholamines.
7. Review the synthesis of dopamine, norepinephrine, and epinephrine.
The amino acid tyrosine is actively transported into the adrenergic presynaptic nerve terminal
cytoplasm, where it is converted to dopamine by two enzymatic reactions: hydroxylation of

tyrosine by tyrosine hydroxylase to dopamine and decarboxylation of dopamine by aromatic


12 CHAPTER 1 AUTONOMIC NERVOUS SYSTEM
TABLE 1-3. E N D - O R G A N E F F E C T S O F C H O L I N E R G I C R E C E P T O R S T I M U L A T I O N
Receptor

Organ

Response

Muscarinic

Heart

Decreased heart rate,

Bronchioles

contractility, conduction velocity
Constriction

Salivary glands

Stimulates secretion

Intestine

Contraction and relaxation of

Bladder

Contraction and relaxation of sphincters

Neuromuscular junction

Skeletal muscle contraction

Autonomic ganglia

SNS stimulation

sphincters, stimulates secretions
Nicotinic

SNS, Sympathetic nervous system.

L-amino acid decarboxylase. Dopamine is transported into storage vesicles, where it is
hydroxylated by dopamine b-hydroxylase to norepinephrine. Epinephrine is synthesized in
the adrenal medulla from norepinephrine through methylation by phenylethanolamine
N-methyltransferase (Figure 1-2).

8. How is norepinephrine metabolized?
Norepinephrine is removed from the synaptic junction by reuptake into the presynaptic nerve
terminal and metabolic breakdown. Reuptake is the most important mechanism and allows reuse
of the neurotransmitter. The enzyme monoamine oxidase (MAO) metabolizes norepinephrine
within the neuronal cytoplasm; both MAO and catecholamine O–methyltransferase (COMT)
metabolize the neurotransmitter at extraneuronal sites. The important metabolites are
3-methoxy-4-hydroxymandelic acid, metanephrine, and normetanephrine.
9. Describe the synthesis and degradation of acetylcholine.

The cholinergic neurotransmitter acetylcholine (ACh) is synthesized within presynaptic neuronal
mitochondria by esterification of acetyl coenzyme A and choline by the enzyme choline
acetyltransferase; it is stored in synaptic vesicles until release. After release, ACh is principally
metabolized by acetylcholinesterase, a membrane-bound enzyme located in the synaptic
junction. Acetylcholinesterase is also located in other nonneuronal tissues such as erythrocytes.
10. What are sympathomimetics?
Sympathomimetics are synthetic drugs with vasopressor and chronotropic effects similar to
those of catecholamines. They are commonly used in the operating room to reverse the
circulatory depressant effects of anesthetic agents by increasing blood pressure and heart rate;
they also temporize the effects of hypovolemia while fluids are administered. They are effective
during both general and regional anesthesia.
11. Review the sympathomimetics commonly used in the perioperative
environment.
Direct-acting sympathomimetics are agonists at the targeted receptor, whereas indirect-acting
sympathomimetics stimulate release of norepinephrine. Sympathomimetics may be mixed in
their actions, having both direct and indirect effects. Practically speaking, phenylephrine (direct
acting) and ephedrine (mostly indirect acting) are the sympathomimetics commonly used


O
OH

L-Tyrosine

NH2

HO
O2, Tetrahydrobiopterin

Tyrosine hydroxylase

H2O, Dihydrobiopterin

O
HO

OH
NH2

HO

L-Dihydroxyphenylalanine

(L-DOPA)

DOPA decarboxylase
Aromatic L-amino acid decarboxylase
CO2

HO

Dopamine
NH2

HO
O2, Ascorbic
acid

Dopamine ␤-hydroxylase
H2O, Dehydroascorbic acid

OH
HO

HO
S-adenosylmethionine

Norepinephrine
NH2

Phenylethanolamine
N-methyltransferase

Homocysteine

OH
HO

HO

Epinephrine
HN

CH3

Figure 1-2. The catecholamine synthetic pathway. (From wers
.com/topic/epinephrine.)


14 CHAPTER 1 AUTONOMIC NERVOUS SYSTEM
perioperatively. Also, epinephrine, dopamine, and norepinephrine may be used perioperatively

and most often by infusion since their effects on blood pressure, heart rate, and myocardial
oxygen consumption can be profound. Dopamine is discussed in Chapter 15.
12. Discuss the effects of phenylephrine and review common doses of this
medication.
Phenylephrine stimulates primarily A1 receptors, resulting in increased systemic vascular
resistance and blood pressure. Larger doses stimulate A2 receptors. Reflex bradycardia may
be a response to increasing systemic vascular resistance. Usual intravenous doses of
phenylephrine range between 50 and 200 mcg. Phenylephrine may also be administered by
infusion at 10 to 20 mcg/min.
13. Discuss the effects of ephedrine and review common doses of this medication.
Give some examples of medications that contraindicate the use of ephedrine
and why.
Ephedrine produces norepinephrine release, stimulating mostly A1 and B1 receptors; the effects
resemble those of epinephrine although they are less intense. Increases in systolic blood
pressure, diastolic blood pressure, heart rate, and cardiac output are noted. Usual intravenous
doses of ephedrine are between 5 and 25 mg. Repeated doses demonstrate diminishing
response known as tachyphylaxis, possibly because of exhaustion of norepinephrine supplies or
receptor blockade. Similarly, an inadequate response to ephedrine may be the result of already
depleted norepinephrine stores. Ephedrine should not be used when the patient is taking drugs
that prevent reuptake of norepinephrine because of the risk of severe hypertension. Examples
include tricyclic antidepressants, monoamine oxidase inhibitors, and acute cocaine intoxication.
Chronic cocaine users may be catecholamine depleted and may not respond to ephedrine.
14. What are the indications for using b-adrenergic antagonists?
b-Adrenergic antagonists, commonly called b-blockers, are antagonists at b1- and
b2- receptors. b-blockers are mainstays in antihypertensive, antianginal, and antiarrhythmic
therapy. Perioperative b-blockade is essential in patients with coronary artery disease,
and atenolol has been shown to reduce death after myocardial infarction.
15. Review the mechanism of action for b1-antagonists and side effects.
b1-Blockade produces negative inotropic and chronotropic effects, decreasing cardiac
output and myocardial oxygen requirements. b1-Blockers also inhibit renin secretion and

lipolysis. Since volatile anesthetics also depress contractility, intraoperative hypotension is a risk.
b-Blockers can produce atrioventricular block. Abrupt withdrawal of these medications is not
recommended because of up-regulation of the receptors; myocardial ischemia and hypertension
may occur. b-Blockade decreases the signs of hypoglycemia; thus it must be used with caution
in insulin-dependent patients with diabetes. b-Blockers may be cardioselective, with relatively
selective B1 antagonist properties, or noncardioselective. Some b-Blockers have membranestabilizing (antiarrhythmic effects); some have sympathomimetic effects and are the drugs of
choice in patients with left ventricular failure or bradycardia. b-Blockers interfere with the
transmembrane movement of potassium; thus potassium should be infused with caution.
Because of their benefits in ischemic heart disease and the risk of rebound, b-blockers should be
taken on the day of surgery.
16. Review the effects of b2-antagonism.
b2-Blockade produces bronchoconstriction and peripheral vasoconstriction and inhibits insulin
release and glycogenolysis. Selective b1-blockers should be used in patients with chronic
or reactive airway disease and peripheral vascular disease because of respective concerns for
bronchial or vascular constriction.


CHAPTER 1 AUTONOMIC NERVOUS SYSTEM 15
17. How might complications of b-blockade be treated intraoperatively?
Bradycardia and heart block may respond to atropine; refractory cases may require the
b2-agonism of dobutamine or isoproterenol. Interestingly, calcium chloride may also be
effective, although the mechanism is not understood. In all cases expect to use larger than
normal doses.
18. Describe the pharmacology of a-adrenergic antagonists.
a1-Blockade results in vasodilation; therefore a-blockers are used in the treatment of
hypertension. However, nonselective a-blockers may be associated with reflex tachycardia.
Thus, selective a1-blockers are primarily used as antihypertensives. Prazosin is the
prototypical selective a1-blocker, whereas phentolamine and phenoxybenzamine are examples
of nonselective a-blockers. Interestingly, labetalol, a nonselective b-blocker, also has selective
a1-blocking properties and is a potent antihypertensive.

19. Review a2-agonists and their role in anesthesia.
When stimulated, a2-receptors within the CNS decrease sympathetic output.
Subsequently, cardiac output, systemic vascular resistance, and blood pressure decrease.
Clonidine is an a2-agonist used in the management of hypertension. It also has significant
sedative qualities. It decreases the anesthetic requirements of inhaled and intravenous
anesthetics. It has also been used intrathecally in the hopes of decreasing postprocedural pain,
but unacceptable hypotension is common after intrathecal administration, limiting its usefulness.
Clonidine should be continued perioperatively because of concerns for rebound hypertension.
20. Discuss muscarinic antagonists and their properties.
Muscarinic antagonists, also known as anticholinergics, block muscarinic cholinergic
receptors, producing mydriasis and bronchodilation, increasing heart rate, and inhibiting
secretions. Centrally acting muscarinic antagonists (all nonionized, tertiary amines with the ability
to cross the blood-brain barrier) may produce delirium. Commonly used muscarinic antagonists
include atropine, scopolamine, glycopyrrolate, and ipratropium bromide. Administering
muscarinic antagonists is a must when the effect of muscle relaxants is antagonized by
acetylcholinesterase inhibitors, lest profound bradycardia, heart block, and asystole ensue.
Glycopyrrolate is a quaternary ammonium compound, cannot cross the blood-brain barrier, and
therefore lacks CNS activity. When inhaled, ipratropium bromide produces bronchodilation.
21. What is the significance of autonomic dysfunction? How might you tell if a
patient has autonomic dysfunction?
Patients with autonomic dysfunction tend to have severe hypotension intraoperatively.
Evaluation of changes in orthostatic blood pressure and heart rate is a quick and effective way
of assessing autonomic dysfunction. If the autonomic nervous system is intact, an increase in
heart rate of 15 beats/min and an increase of 10 mm Hg in diastolic blood pressure are
expected when changing position from supine to sitting. Autonomic dysfunction is suggested
whenever there is a loss of heart rate variability, whatever the circumstances. Autonomic
dysfunction includes vasomotor, bladder, bowel, and sexual dysfunction. Other signs include
blurred vision, reduced or excessive sweating, dry or excessively moist eyes and mouth, cold
or discolored extremities, incontinence or incomplete voiding, diarrhea or constipation, and
impotence. Although there are many causes, it should be noted that people with diabetes and

chronic alcoholics are patient groups well known to demonstrate autonomic dysfunction.
22. What is a pheochromocytoma, and what are its associated symptoms? How is
pheochromocytoma diagnosed?
Pheochromocytoma is a catecholamine-secreting tumor of chromaffin tissue, producing
either norepinephrine or epinephrine. Most are intra-adrenal, but some are extra-adrenal (within the
bladder wall is common), and about 10% are malignant. Signs and symptoms include paroxysms of