AMERICAN SOCIETY OF ANESTHESIOLOGISTS
Anesthesiology Continuing Education Program
Answer Key
Issue 3B
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B
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B
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B
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B
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A
ITEM 1
Over 400 million people worldwide are actively infected with the hepatitis B virus. In areas where
hepatitis B is hyperendemic (China, southeast Asia, sub-Saharan Africa), over 8% of adults are carriers
and transmission from mother to child is common during parturition. In the US hepatitis B is the sixth
leading indication for liver transplantation. The double-stranded DNA virus can remain viable outside the
body for seven days.
Hepatitis B is transmitted by exposure to blood or other bodily fluids via contaminated needles (including
tattooing or body-piercing implements), sexual contact, or even toothbrushes. In the United States, the
most frequent modes of transmission are sexual contact (50%) and intravenous drug use (15%); in
approximately 30% of cases no risk factor can be identified. Prior to the development of an effective
vaccine, the risk of transmission of hepatitis B via an occupational needlestick was estimated to be as high
as 30%. In the 1980s and 1990s studies demonstrated the presence of serologic markers for hepatitis B in
as many of 49% of anesthesia personnel in the United States and other countries.
The risk of transmission via transfusion has been almost eliminated with donor screening and testing of
blood. Accordingly, exposure to the blood of an infected patient is currently a greater risk factor for an
anesthesia provider than exposure to a unit of blood.
Hepatitis B vaccine, administered in a series of three doses over a four-month period, provides lifelong
immunity for the majority of those vaccinated. Monitoring of surface antibodies will detect the small
percentage of people who do not respond to vaccination. The vaccination series may be repeated once on
these patients, but failure to develop adequate titers in response to a second round of immunizations
should result in testing for the presence of hepatitis B surface antigen in the blood to determine if they
have chronic hepatitis B infection or are simply nonresponders.
The incubation period for hepatitis B is as long as six months; almost one third of individuals who
become infected with hepatitis B fail to develop the classic symptoms of rash, joint pain, anorexia,
nausea, vomiting, weight loss, jaundice, light colored stools, or fatigue and flu-like symptoms. Most
adults who become acutely infected will recover completely. Antiviral therapy is not indicated for the
majority of patients with hepatitis B. Indications for antiviral therapy include active hepatic inflammation,
a high replicative phase of hepatitis B infection, and an increased serum alanine-lysine transferase (ALT)
concentration. Patients who are positive for the hepatitis B surface antigen should be monitored for the
development of cirrhosis or hepatocellular carcinoma, which develop in approximately 30% of patients
with chronic infection.
REFERENCES
1.
Jackson SH, Cheung EC. Hepatitis B and hepatitis C: Occupational considerations for the
anesthesiologist. Anesthesiol Clin North America. 2004; 22:357-377.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:31573158.
1
ITEM 2
Clinical scenario: The husband of a patient with confirmed diagnosis of botulism contracted through
ingestion of contaminated food presents with a history of having consumed the same foods. The husband
is currently asymptomatic.
Suspected cases of botulism must be reported to local and state health department as well as the hospital
infection control officer/epidemiologist.
Since botulism is due to the toxin rather than the organism, neither antibiotics nor antiviral agents are
effective in treating a victim of biologic intoxication. Antibiotics are indicated for patients with botulism
associated with wound contamination. Similarly, gastrointestinal decontamination may be indicated for
patients with food-borne disease, but in this situation antibiotic administration would be enteral rather
than intravenous. Charcoal administration, cathartics, and enemas have also been advocated in an attempt
to minimize exposure in cases of food-borne disease.
Botulinum antitoxin is the gold standard for patients who become symptomatic. Although a heptavalent
antitoxin is under investigation by the US military, currently the trivalent antitoxin, effective against
neurotoxin types A, B, and E, is stockpiled in six cities in the United States. Release of the antitoxin
requires authorization by officials from the Centers for Disease Control and Prevention (CDC).
Administration of antitoxin should occur early in the disease; it is targeted against circulating toxin and is
ineffective after the toxin enters the nerve. Because antitoxin is derived from hyperimmunized horses,
there is a fairly high incidence of allergic reactions—a 2% incidence of anaphylaxis and a 9% incidence
of serum sickness or other hypersensitivity reactions. Accordingly, antitoxin is generally not
recommended for asymptomatic patients. Dosing of antitoxin is undergoing re-evaluation; CDC
recommendations should be reviewed prior to administration.
Current CDC recommendations include close monitoring of respiratory function—generally described as
negative inspiratory force, peak expiratory flow rate, or vital capacity—in asymptomatic individuals with
a credible history of exposure. Antitoxin is initiated at the earliest evidence of decreased respiratory
muscle strength. There have been reports of abrupt respiratory arrest occurring within the first two days
following exposure. Once mechanical ventilation is necessary, ventilatory support is routinely needed for
up to eight weeks but has been required for as long as seven months.
Electromyography may provide useful information in establishing the diagnosis but is not sufficiently
reliable to direct therapy.
REFERENCES
1.
Marks JD. Medical aspects of biologic toxins. Anesthesiol Clin North America. 2004; 22:509532.
2.
Ford MD, Delaney KA, Ling LJ, et al. Clinical Toxicology. Philadelphia: WB Saunders;
2001:934-939.
2
ITEM 3
A 3-year-old boy is scheduled for an elective outpatient right inguinal hernia repair. The patient is very
anxious but has no other medical history and has never received general anesthesia. Family history is
positive for malignant hyperthermia (MH) in his father.
The understanding of the genetics of malignant hyperthermia (MH) is constantly evolving. In over 50% of
MH-susceptible patients, a mutation of the RYR1 receptor on skeletal muscle can be identified; over 30
different mutations have been identified to date. Prior to the use of dantrolene, mortality from MH
approached 80%; mortality from MH is currently estimated at less than 10%.
Patients with a history of MH, a family history of MH, muscular dystrophy, or central core disease are at
increased risk for developing manifestations of MH. Immediate family members of patients with a
previous MH episode should receive a nontriggering anesthetic or obtain a muscle biopsy to exclude MH
susceptibility. The only known pharmacological triggers of MH are succinylcholine and all volatile
anesthetic agents. Placement of intravenous access can be achieved using sedation with oral midazolam
and nitrous oxide/oxygen administered by mask. Nitrous oxide is not a pharmacological trigger for MH.
General anesthesia with propofol and nitrous oxide is an appropriate choice for this patient.
Preoperative dantrolene administration is not recommended for the prevention of MH. Safely performing
a spinal anesthetic on an unsedated 3 year old would be very challenging.
Molecular genetic testing for malignant hyperthermia using a routine blood sample has recently become
available. This genetic test identifies ryanodine receptor mutations that are estimated to be present in 25%
of MH-susceptible patients. The Malignant Hyperthermia Association of the United States (MHAUS)
recommends that only certain individuals should be considered for genetic testing at this time:





patients with a positive in vitro contracture test (IVCT)
relatives of patient with a positive IVCT
patients with a mutation causative for MH currently being investigated by a research protocol
relatives of patients with a known mutation for MH
patients who have experienced an episode believed to have been MH
The genetic test for MH is indicated for susceptible patients or patients with questionable susceptibility
status to identify if they indeed have the ryanodine receptor mutation. If so, other family members could
avoid muscle biopsy testing to evaluate MH susceptibility due to these specific ryanodine receptor
mutations. The genetic test for MH should not replace the traditional muscle biopsy or the use of
nontriggering anesthetic agents in ambiguous or uncertain clinical situations.
REFERENCES
1.
Litman RS, Rosenberg H. Malignant hyperthermia: Update on susceptibility testing. JAMA. 2005;
293-2918-2924.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:11841185.
3
ITEM 4
Clinical scenario: An 8-year-old boy with no other medical history is scheduled for an elective revision of
cleft palate repair. The patient is receiving sevoflurane via inhalational induction for intravenous catheter
placement. Intraoperative laryngospasm is noted and treated with intravenous succinylcholine (2mg/kg).
Masseter muscle rigidity occurs.
Masseter muscle rigidity is defined as inability to open the mouth after administration of succinylcholine.
Prolonged rigidity of the masseter muscles may represent an early manifestation of MH. The risk of MH
may be related to the presence of rigidity of other muscles; the risk of development of MH manifestations
is high if masseter muscle rigidity is accompanied by generalized rigidity.
To consider that an episode constitutes masseter muscle rigidity, an appropriate dose of succinylcholine
must have been administered and an appropriate amount of time must have passed before direct
laryngoscopy is attempted. Absence of response to peripheral nerve stimulator would also be supportive
of the diagnosis of masseter muscle rigidity. During an episode of masseter muscle rigidity, failure to
open the mouth prevents oral intubation. However, most of these patients can be ventilated adequately by
mask until the rigidity resolves.
Masseter muscle rigidity, which is difficult to define since the diagnosis is made on a clinical basis, has
been estimated to occur in approximately 1% of patients after receiving halothane and succinylcholine. It
is unclear if masseter muscle rigidity is just a variant in the spectrum of responses to succinylcholine or is
truly a pathologic condition. Masseter muscle rigidity has been associated with an increased incidence of
malignant hyperthermia, with up to 50% of patients with masseter muscle rigidity having muscle biopsies
positive for malignant hyperthermia susceptibility.
Controversy surrounds the management of masseter muscle rigidity. The two most conservative options
are to either abort the surgical procedure or continue using only nontriggering anesthetic agents (ie,
avoiding volatile anesthetic agents and succinylcholine). Regardless of the option selected, patients who
have experienced masseter muscle rigidity must be closely monitored for the development of malignant
hyperthermia. Dantrolene is not indicated in the initial treatment of masseter muscle rigidity unless signs
of malignant hyperthermia are present.
Since the initial dose of succinylcholine (2mg/kg) was appropriate, a repeat administration is not
indicated.
REFERENCES
1.
Ali SZ, Taguchi A, Rosenberg H. Malignant hyperthermia. Best Pract Res Clin Anaesthesiol.
2003; 17:519-533.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:23782379.
3.
MH muscle biopsy testing centers resource page. Malignant Hyperthermia Association of the
United States Web site. Available at http://www.mhaus.org. Accessed August 2006.
4
ITEM 5
Spinal cord stimulation (SCS), first introduced in the 1960s for the treatment of failed back surgery
syndrome, involves placement of stimulating electrodes in the epidural space. These electrodes are
connected to an implantable pulse generator that can be controlled via an external programmer (Figures 1
and 2). The goal of SCS is to relieve pain by providing enough stimulation to cause paresthesias in the
region that is painful. These paresthesias are often well tolerated and are eventually ignored by the
patient.
Figure 1. Implantable spinal cord stimulator generator with lead and external patient controlled
programmer. Image courtesy of Medtronic, Inc.
The most common indication in the United States for SCS remains failed back surgery syndrome.
Typically those patients with radicular pain, whether cervical or lumbar, respond better to SCS than those
with nociceptive or mechanical low back pain. However, with technology developments resulting in
multiple electrode arrays and complex programming, improvements in outcomes are also being seen in
patients with failed back surgery syndrome who have primarily axial pain.
The most common indication in Europe for SCS is treatment of pain arising from lower extremity
peripheral vascular disease. In addition to reduced ischemic pain, SCS has been documented to produce
improved lower extremity perfusion pressures, increased capillary density, and lower amputation rates in
some groups of patients with peripheral vascular disease.
5
Figure 2. Dual spinal cord stimulator leads placed in the epidural space showing stimulation electric
fields between electrodes on the same lead as well as stimulation between electrodes on separate leads.
Image courtesy of Medtronic, Inc.
Additional indications for SCS include intractable angina, peripheral neuropathies, complex regional pain
syndrome, postamputation pain syndrome, and pain from intractable spasticity. SCS has not been shown
to be as efficacious for myofascial pain, inflammatory pain, or pain resulting from burns.
REFERENCES
1.
Wallace MS, Staats PS. Pain Medicine and Management. Just the Facts. New York: McGrawHill; 2005:285-289.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:2774.
3.
Yu W, Maru F, Edner M, et al. Spinal cord stimulation for refractory angina pectoris: A
retrospective analysis of efficacy and cost-benefit. Coron Artery Dis. 2004; 15:31-37.
4.
Ubbink DT, Vermeulen H, Spincemaille GH, et al. Systematic review and meta-analysis of
controlled trials assessing spinal cord stimulation for inoperable critical leg ischaemia. Br J Surg.
2004; 91:948-955.
ITEM 6
As the general population ages, the surgical population will reflect an increasing incidence of
cardiovascular and cerebrovascular disease. Large randomized controlled trials have unequivocally found
that the use of platelet inhibitors significantly improves long-term outcome by reducing the incidence of
complications related to platelet aggregation (eg, stroke, transient ischemic attacks, coronary artery stent
thrombosis, and myocardial infarction). Clopidogrel is a member of a class of antiplatelet drugs that does
not act through the cyclooxygenase enzyme system but by irreversibly blocking ADP-induced platelet
aggregation via the P2Y12 portion of the glycoprotein IIb/IIIa (GP IIb/IIIa) receptor. It also acts to inhibit
6
platelet aggregation through other ADP agonists (eg, thromboxane, platelet-activating factor). Platelet
aggregation studies have found that most patients experience a 40%-60% inhibition of platelet
aggregation after approximately three to five days of therapy. Platelet mapping, an emerging laboratory
technique to measure inhibition of platelet aggregation, suggests a wide variation in patient response to
clopidogrel, with platelet inhibition ranging between 40% and 90%. Other drugs that block ADP-induced
platelet aggregation include:


intravenous agents (reversible GP IIb/IIIa receptor blockers)
o abciximab (Repro), monoclonal antibody to receptor
o eptifibatide (Integrilin)
o tirofiban (Aggrastat)
oral agents (the inopyridine derivatives with irreversible inhibition of ADP on P2Y12 receptor)
o ticlopidine (Ticlid)
o clopidogrel (Plavix, Sanofi)
Availability of the GP IIb/IIIa receptor allows fibrinogen to form a bridge between platelets, triggering
aggregation. GP IIb/IIIa receptor availability requires activation by ADP released during inflammation or
tissue injury. Irreversible binding to one of the three required receptors prevents platelet aggregation for
the life of the platelet (Figure 1).
Figure 1. Schematic representation of platelet receptors involved in platelet aggregation and the location
of inhibition by clopidogrel.
Aspirin is an irreversible nonselective cyclooxygenase (COX-1 and COX-2) enzyme inhibitor. The
COX-1 enzyme catalyzes the conversion of arachidonic acid to prostaglandins that safeguard gastric
mucosa, maintain renal perfusion, and platelet aggregation. The COX-2 enzyme catalyzes arachidonic
acid to produce prostaglandins that increase pain and tissue inflammation. Aspirin therapy, usually given
in doses of 100-350 mg daily, impairs platelet aggregation through a COX pathway and adds to the
clopidogrel-medicated inhibition of platelet adhesiveness.
While other drugs that alter plasminogen conversion to plasmin and clot lysis are available, clopidogrel
does not act by this mechanism.
7
Clopidogrel is a pro-drug and requires hepatic P450 metabolism to produce the active drug. Because
atorvastatin (Lipitor) is metabolized by the same route, patients taking atorvastatin may have lower serum
clopidogrel levels and thus reduced inhibition of aggregation. Clopidogrel is not hepatotoxic and will not
alter the hepatic production of coagulation factors.
REFERENCES
1.
Fleisher LA. Anesthesia and Uncommon Diseases. 5th ed. Philadelphia: Elsevier Saunders;
2006:369-373.
2.
Fleisher LA. Evidence-Based Practice of Anesthesiology. Philadelphia: Elsevier Saunders;
2004:277:282.
3.
Harder S, Klinkhardt U, Alvarez JM. Avoidance of bleeding during surgery in patients receiving
anticoagulant and/or antiplatelet therapy: Pharmacokinetic and pharmacodynamic considerations.
Clin Pharmacokinet. 2004; 43:963-981.
ITEM 7
Assessing the impact of antiplatelet drugs on surgical bleeding is increasingly important as patients
present for emergent or urgent surgery. To plan a course of treatment for patients on clopidogrel and/or
aspirin requires timely point-of-care platelet function assessment, something that is not available in all
hospitals. Of the currently accepted platelet function tests (Table 1), only thromboelastography (TEG) has
been shown to predict intraoperative bleeding. More complex testing using variations of the TEG
technology allows “platelet mapping,” an emerging technology that can more accurately assess point-ofcare platelet function. Platelet mapping is not routinely available.
8
Table 1. Currently accepted laboratory tests for platelet function.
Platelet Function Test
Aspects of Platelet
Function Measured
Advantages
Disadvantages
Bleeding time
In vivo screening test
Physiologic
Insensitive, invasive,
and poor reproducibility
Aggregometry—
turbidimetric methods
Responsiveness to panel
of agonists
Diagnostic
Labor intensive,
nonphysiologic
Aggregometry—
impedance methods
Responsiveness to panel
of agonists
Whole blood test
Insensitive
Aggregometry &
luminescence
Combined aggregation
and ADP release
More information
Semiquantitative
Adenine nucleotides
Stored and released
ADP
Sensitive
Specialized equipment
Thromboelastography
(TEG)
Global hemostasis
Predicts bleeding
Measures clot properties
only, insensitive to
aspirin
Glass filterometer
High shear platelet
function
Simple
Requires blood counter
Platelet function assay
Sensitive to platelet
function defects,
including drug-induced
Rapid, point-of-care
Specialized equipment
Platelet release markers
(eg, beta TG, PF4)
In vivo platelet
activation markers
Simple, systemic
measure of platelet
function
Prone to artifact
TEG is a whole blood point-of-care coagulation test that examines the functional interaction of platelets,
coagulation factors, and clot lysis (Figures 1, 2). The primary drawback of this test is the time necessary
to obtain a response and, for the average clinician, the complex nature of the test interpretation. To
mitigate this problem, many laboratories report the normal values of each measure with a general
interpretation of the significance of abnormal measurements. Fortunately, in many cases, pattern
recognition will allow a reasonable interpretation in emergency situations (Figure 2).
Figure 1 is a schematic representation of a normal TEG. The R value or clotting time is the time required
for initial fibrin formation; it is prolonged by anticoagulants like heparin. K time is a measure of clot
firmness or speed of clot strengthening and is prolonged with decreased fibrinogen, platelet inhibition,
and anticoagulants. The angle (alpha) to the shoulder of the trace is increased by increases in fibrinogen
9
or platelet adhesiveness and decreased by decreases in fibrinogen or platelet adhesiveness. Maximum
amplitude (MA) measures the maximum strength of the clot and is sensitive to early clot lysis or poor clot
formation. TEG has been established to be the most sensitive test for changes in ADP-induced platelet
aggregation.
Figure 1. Diagrammatic representation of a normal thromboelastogram (TEG). R value (clotting time):
time for initial fibrin clot formation; K time (clot kinetics): a measure of clot firmness or speed of clot
strengthening; α: measure of platelet adhesiveness; MA (maximum amplitude): maximum strength of the
clot. Used with permission, from Whitten CW, Greilich PE. Thromboelastography: Past, present, and
future. Anesthesiology. 2000; 92:1223-1224.
Figure 2. Characteristic TEG patterns and the associated coagulation defect. DIC, disseminated
intravascular coagulation. Used with permission, from Whitten CW, Greilich PE. Thromboelastography:
Past, present, and future. Anesthesiology. 2000; 92:1223-1224.
10
Bleeding time, once used as a standard measure of platelet function, has been discredited due to
inconsistent test results related to poor reproducibility and difficulty obtaining the test. Platelet
aggregometry uses changes in optical turbidity of a blood sample with and without a platelet agonist.
Platelet aggregometry, considered the “gold standard” in platelet function testing, is based on the concept
that turbidity will decrease as the size of platelet aggregates increase. Increased platelet adhesiveness will
increase the size of platelet aggregates. Unfortunately, the test is labor intensive, difficult to obtain,
semiquantitative, and has not reliably predicted surgical bleeding. It would not be the best test for platelet
function when rapid point-of-care assessment is required.
Activated partial thromboplastin time (aPTT) is the time needed for plasma to form a clot when calcium
and a phospholipids reagent are added to the sample. It is a measure of the intrinsic clotting system,
primary factors VIII, IX, and XII and to a lesser extent fibrinogen and factors II, V, and X. It is used to
monitor heparin anticoagulant activity and does not measure platelet function.
REFERENCES
1.
Fleisher LA. Anesthesia and Uncommon Diseases. 5th ed. Philadelphia: Elsevier Saunders;
2006:369-373.
2.
Spiess BD. Coagulation monitoring in the perioperative period. Int Anesthesiol Clin. 2004;
42(2):55-71.
3.
Harder S, Klinkhardt U, Alvarez JM. Avoidance of bleeding during surgery in patients receiving
anticoagulant and/or antiplatelet therapy: Pharmacokinetic and pharmacodynamic considerations.
Clin Pharmacokinet. 2004; 43:963-981.
4.
Srinivasa V, Gilbertson LI, Bhavani-Shankar K. Thromboelastography: Where is it and where is
it heading? Int Anesthesiol Clin. 2001; 39(1):35-49.
11
5.
Whitten CW, Greilich PE. Thromboelastography: Past, present, and future. Anesthesiology. 2000;
92:1223-1225.
ITEM 8
Clinical scenario: A 56-year-old man is undergoing an emergency craniotomy to drain a large acute
intraparenchymal hematoma. At the end of the procedure the neurosurgeon is unable to control the
bleeding. His coagulation test, platelet count, and platelet function test are normal.
Intracranial hemorrhage requiring emergency evacuation is most often encountered in the context of
traumatic injury or hypertensive hemorrhagic stroke. In the nonoperative setting, the six-month mortality
for intracranial hemorrhage is 30%-50% and of those who survive, only 20% return to normal life
activity. Prominent causes of intracranial hemorrhage include:











trauma
arteriovenous malformation
aneurysm
coagulopathy
hemorrhage into infarct
dural sinus thrombosis
neoplasm
cavernous angioma
dural ateriovenous fistula
venous angioma
cocaine/methamphetamine use
12

central nervous system vasculitis
In patients with normal systemic coagulation the initial size of the intracranial hemorrhage continues to
expand as much as 30% in the first three to six hours after the initial insult. The size of the hemorrhage is
directly related to increasing mortality and morbidity. Until recently, there has been no systemic treatment
that has reduced growth in intracranial hemorrhage volume and improved long-term outcome. In a large
multicenter study, administration of recombinant factor VIIa (rFVIIa) was found to significantly reduce
the volume of the intracranial hemorrhage if given within three hours of hemorrhage. Most importantly
the group who received rFVIIa had a markedly improved outcome at six months. This is the only therapy
that in randomized controlled trials improved long-term outcome.
Administration of rFVIIa increases factors Xa and IXa on the surface of the platelet with a subsequent
increase in thrombin. It significantly reduces localized clot lysis and reduces bleeding. The postulated
mechanism for localized intracranial hemorrhage is the release of local tissue plasminogen, which
produces localized clot lysis and can also produce the systemic disseminated intravascular coagulation
seen in severe brain injury. Thus use of rFVIIa for surgical intracranial bleeding would be the most
effective therapy available.
Randomized controlled trials, meta-analyses, and systematic reviews have demonstrated that in patients
with normal coagulation profiles blood component transfusions (fresh frozen plasma, platelets,
cryoprecipitate) are not effective in treating or reducing the size of intraoperative intracranial hemorrhage.
Administration of rFVIIa is not without risk. In the recent large randomized control trial that
demonstrated efficacy, there was an incidence of unintended thrombosis of about 7% in patients treated
with rFVIIa compared a 2% incidence of unintended thrombosis in control patients not treated with
rFVIIa.
The only use of rVIIa approved by the Food and Drug Administration remains treatment of hemophilia.
REFERENCES
1.
Srinivasa V, Gilbertson LI, Bhavani-Shankar K. Thromboelastography: Where is it and where is
it heading? Int Anesthesiol Clin; 2001; 39(1):35-49.
2.
Harder S, Klinkhardt U, Alvarez JM. Avoidance of bleeding during surgery in patients receiving
anticoagulant and/or antiplatelet therapy: Pharmacokinetic and pharmacodynamic considerations.
Clin Pharmacokinet. 2004; 43:963-981.
3.
Mayer SA, Rincon F. Treatment of intracerebral haemorrhage. Lancet Neurol. 2005; 4:662-672.
4.
Mayer SA, Brun NC, Begtrup K, et al; Recombinant Activated Factor VII Intracerebral
Hemorrhage Trial Investigators. Recombinant activated factor VII for acute intracerebral
hemorrhage. N Engl J Med. 2005; 352:777-785.
5.
Fleisher LA. Anesthesia and Uncommon Diseases. 5th ed. Philadelphia: Elsevier Saunders;
2006:370-374.
ITEM 9
13
Controversy exists concerning the advisability of performing outpatient surgery in patients with
obstructive sleep apnea (OSA). Ambulatory surgery is usually acceptable if the surgery is superficial or
involves an extremity, regional anesthesia is used, or complete and rapid recovery from general anesthesia
with full return to consciousness is accomplished.
In the recent practice guidelines adopted by the American Society of Anesthesiologists (ASA) for the
perioperative management of patients with OSA, specific recommendations for outpatient discharge
criteria were made. Clearly, discharge should occur when the patient meets specific clinical criteria rather
than after a designated duration of stay in the postanesthesia care unit. In addition, relying on the
discharge criteria used for patients without OSA is not adequate. Consultants involved in creating ASA
guidelines recommended the following criteria be met before discharge to home or any nonmonitored
setting:




Maintenance of baseline preoperative room air oxygen saturation when the patient is left
undisturbed.
Absence of new hypoxemia and airway obstruction when the patient is in an unstimulated
environment.
Monitoring before discharge for an extended period of time after the last episode of airway
obstruction or hypoxemia while breathing room air. The median recommendation by the
consultants was that this extended period be for an additional seven hours.
Monitoring before discharge for a longer period of time than patients who do not have OSA. The
median recommendation by the consultants was that this monitoring be for an additional three
hours.
REFERENCES
1.
Fleisher LA. Evidence-Based Practice of Anesthesiology. Philadelphia: Elsevier Saunders;
2004:255-256.
2.
Practice Guidelines for the Perioperative Management of Patients with Obstructive Sleep Apnea.
American Society of Anesthesiologists. Available at
http://www.asahq.org/publicationsAndServices/practiceparam.htm#apnea. Accessed August
2006.
ITEM 10
Commonly used carbon dioxide absorbents interact with volatile anesthetics to some extent. The classic
example is the interaction between trichloroethylene and soda lime to generate phosgene, a pulmonary
irritant capable of producing acute respiratory stress syndrome (ARDS).
Sevoflurane interacts with carbon dioxide absorbents to produce fluoromethyl-2,2-difluoro-1(trifluoromethyl)vinyl ether, also known as compound A. Factors associated with increased production of
compound A include:



low fresh gas flow rates
use of Baralyme as opposed to soda lime
higher sevoflurane concentrations
14

higher absorbent temperatures
Dehydration of absorbent increases production of compound A in the presence of Baralyme and decreases
production of compound A in the presence of soda lime.
The finding that high concentrations of compound A were capable of producing renal damage and death
in rats sparked a debate about the clinical relevance of compound A in humans. Conflicting data exist
regarding acute consequences of prolonged sevoflurane anesthesia at low fresh gas flow rates. Some
studies on patients with baseline normal renal function have failed to document any significant alterations
in blood urea nitrogen, creatinine, electrolyte concentrations, or other markers of renal function/integrity
such as creatinine clearance, renal excretion of protein, glucose, alanine aminopeptidase, γ-glutamyl
transpeptidase, β2-microglobulin, proximal tubular α-glutathione S-transferase (GST), distal tubular πGST, and N-acetyl-β-D-glucosaminidase (NAG). Other studies have reported transient (generally
resolved within four days) changes in renal excretion of glucose, albumin, α-GST, and 𝜋-GST. It should
be re-emphasized that all these studies were conducted in patients with normal renal function; the effect
of compound A on patients with impaired renal function remains controversial. Presumably these findings
contributed to recommendations to maintain higher fresh gas flow rates when using sevoflurane. There
are also concerns that the risk in pediatric patients may be increased because of their inability to handle
one of the major sevoflurane metabolites.
Perhaps because of these contradictory findings Saidman and Eger authored an editorial, “Safety of LowFlow Sevoflurane Anesthesia in Patients with Chronically Impaired Renal Function Is Not Proven,”
published in Anesthesiology in 2003.
Desflurane interacts with CO2 absorbents to produce carbon monoxide but does not produce compound
A. More carbon monoxide is produced when desflurane is used in conjunction with Baralyme than when
it is used in conjunction with soda lime.
REFERENCES
1.
Kharasch ED, Powers KM, Artru AA. Comparison of Amsorb, sodalime, and Baralyme
degradation of volatile anesthetics and formation of carbon monoxide and compound A in swine
in vivo. Anesthesiology. 2002; 96:173-182.
2.
Saidman LJ, Eger EI. Safety of low-flow sevoflurane anesthesia in patients with chronically
impaired renal function is not proven. Anesthesiology. 2003; 99:752.
3.
Kharasch ED, Conzen P, Michalowski P, et al. Safety of low-flow sevoflurane anesthesia in
patients with chronically impaired renal function is not proven: In reply. Anesthesiology. 2003;
99:752-754.
4.
Kobayashi S, Bito H, Obata Y, et al. Compound A concentration in the circle absorber system
during low-flow sevoflurane anesthesia: Comparison of Drägersorb Free, Amsorb, and Sodasorb
II. J Clin Anesth. 2003; 15:33-37.
5.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:251256.
15
ITEM 11
Infants have a larger blood volume per unit body weight (expressed as mL/kg) than adults; blood volume
gradually decreases with age. Newborns, especially premature neonates, have a larger blood volume than
infants or children. Table 1 presents the estimated blood volume for patients of different ages.
Table 1. Age-related blood volume estimates.
Age
Volume
Premature newborn
100-120 mL/kg
Term newborn
90 mL/kg
Infant 3-12 months old
80 mL/kg
Adult
70 mL/kg
Blood pressure in children is relatively resistant to hypovolemia. Some studies report that hypotension
does not reliably occur until a child has lost 25% of his or her estimated blood volume.
REFERENCES
1.
Nagano K, Kusaka T, Okubo K, et al. Estimation of circulating blood volume in infants using the
pulse dye densitometry method. Paediatr Anaesth. 2005; 15:125-130.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:2389.
ITEM 12
The electrodes of a blood gas machine measure samples at a constant temperature of 37°C. This means
that an arterial blood gas obtained from a patient at 28°C is warmed to 37°C, and the values obtained
represent the in vitro pH, PaCO2, and PaO2 at 37°C. When the sample is warmed, gases come out of
solution, and the measured gas values are higher and the measured pH is lower than the in vivo values.
For example, an in vitro arterial gas specimen measured at 37°C with a pH of 7.40 and PaCO2 of 40 mm
Hg represents in vivo values of pH 7.56 and PaCO2 of 26 mm Hg in a patient at 28°C.
Normally with hypothermia, both arterial pH and intracellular pH increase, keeping the transmembrane
pH gradient constant. This is important for maintaining normal enzyme system function, many of which
contain the imidazole moiety. The dissociation of this moiety, the alpha of imidazole, is kept constant
when the ratio of [OH-] and [H+] remain constant. This is the basis for alpha-stat management of arterial
blood gases. The blood gases are interpreted at 37°C, and the patient is managed according to those
16
values, not according to what the values would be at a lower temperature. Alpha-stat strategy maintains
the transmembrane pH gradient and is the strategy most often used for adult patients.
The pH-stat strategy attempts to maintain in vivo pH at 7.40 and PaCO2 at 40 mm Hg during hypothermia.
For a patient at 28°C to achieve in vitro pH of 7.40 and PaCO2 of 40 mm Hg, exogenous CO2 must be
added to the gas inflow of the cardiopulmonary bypass machine. The consequence of increasing PaCO2 is
cerebral vasodilation.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:14451446, 1599-1600.
2.
Hensley FA Jr, Martin DE, Gravlee GP. A Practical Approach to Cardiac Anesthesia. 3rd ed.
Philadelphia: Lippincott, Williams & Wilkins; 2003:595-597.
3.
Yao FS, Artusio JF. Anesthesiology: Problem-Oriented Patient Management. 3rd ed.
Philadelphia: JB Lippincott; 1993:155-156.
4.
Kiziltan HT, Baltali M, Bilen A, et al. Comparison of alpha-stat and pH-stat cardiopulmonary
bypass in relation to jugular venous oxygen saturation and cerebral glucose-oxygen utilization.
Anesth Analg. 2003; 96:644-650.
5.
Sakamoto T, Kurosawa H, Shin’oka T, et al. The influence of pH strategy on cerebral and
collateral circulation during hypothermic cardiopulmonary bypass in cyanotic patients with heart
disease: Results of a randomized trial and real-time monitoring. J Thorac Cardiovasc Surg. 2004;
127:12-19.
ITEM 13
Critical illness polyneuropathy is one cause of generalized neuromuscular weakness of patients in the
intensive care unit. Classified as a peripheral neuropathy that affects both sensory and motor neurons, it is
part of the multiorgan dysfunction of the systemic inflammatory response syndrome and may be present
in 50%-70% of patients with this condition. The systemic inflammatory response may involve damage to
the microcirculation of both central nervous system and peripheral nerves.
Critical illness polyneuropathy presents as generalized weakness that may involve the muscles of
respiration; it has been suggested as a cause of failure to wean a patient from mechanical ventilation due
to poor spontaneous tidal volumes. Other than physical rehabilitation, no specific treatment is available.
Patients who develop this condition have been found to manifest severely reduced quality of life and high
mortality rate (35%).
Retrospective studies have reported an association between hyperglycemia and the development of
critical illness polyneuropathy in both diabetic and nondiabetic patients. It has been suggested that
maintaining blood glucose at or below 110 mg/dL may reduce the risk of developing critical illness
polyneuropathy.
17
Electrophysiologic testing, including electromyography (EMG) and neurography, has been advocated for
establishing the diagnosis of critical illness polyneuropathy, but most studies report a high specificity
(> 90%) and a low sensitivity (< 50%) for these tests. EMG findings include prolonged latency and
spontaneous motor discharges.
As opposed to critical illness polyneuropathy, critical illness myopathy is a disease involving muscles and
may occur with normal nerve function. Critical illness myopathy is another cause of generalized muscle
weakness in patients in the intensive care unit and may coexist with critical illness polyneuropathy.
Critical illness myopathy involves muscle atrophy produced by prolonged immobility and has been
associated with sepsis and the use of corticosteroids and neuromuscular blocking agents. It presents as
flaccid weakness, including facial muscles and the diaphragm. Muscle biopsy may be used to differentiate
critical illness myopathy from other types of myopathy.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:531533.
2.
Bercker S, Weber-Carstens S, Deja M, et al. Critical illness polyneuropathy and myopathy in
patients with acute respiratory distress syndrome. Crit Care Med. 2005; 33:711-715.
3.
Pastores SM. Critical illness polyneuropathy and myopathy in acute respiratory distress
syndrome: More common than we realize!. Crit Care Med. 2005; 33:895-896.
ITEM 14
Dead space is that portion of the tidal volume that does not participate in gas exchange. Simplistically it
can be viewed as gas that does not reach functional lung units either because it remains in the conducting
airways or because the lung units it enters are ventilated but not perfused.
Under normal conditions dead space is frequently categorized as anatomical dead space (approximated by
the volume of the conducting airways), alveolar dead space (from lung units that are ventilated but not
perfused), and physiologic dead space (the sums of all forms of dead space). Under any conditions of
mechanical ventilation, apparatus dead space may also be present.
Several factors affect dead space (Table 1).
Table 1. Factors influencing dead space (VD).
Anatomical Dead Space
Alveolar Dead Space
Patient size: VD increased with increased body size
Cardiac output: VD increased with decreases in
cardiac output
Patient age: VD increased with increased age
Embolism: VD increased by venous embolism
18
Posture: VD decreased with supine
Posture: VD increased in lateral position
Position of jaw and neck: VD increased with neck
extension and jaw protrusion
Lung volume at end inspiration: VD increased with
increased lung volume
Artificial airway: VD decreased with tracheal tube,
laryngeal mask airway, tracheostomy
Bronchodilators: VD increased with bronchodilation
Tidal volume: VD decreased with low tidal volumes
Respiratory rate: VD decreased with low respiratory
rates
West Zone I (where alveolar pressure exceeds pulmonary artery pressure, PALV > PPA) represents dead
space (ventilation in the absence of perfusion). Since positive end-expiratory pressure (PEEP) produces
increases in PALV and decreases in transmural PPA, application of PEEP is associated with an increase in
dead space.
Decreased tidal volume is associated with decreased dead space. The conversion from turbulent flow to
laminar flow in the airways produces a cone-shaped front of gas flow that may result in inspired gas
reaching functioning lung units with tidal volumes as low as 60 mL.
Since dead space begins at the Y-piece in a normally functioning circle system, changing the length of
tubing will not affect dead space.
Insertion of an artificial airway device (tracheal tube, laryngeal mask airway, tracheostomy tube)
bypasses extrathoracic anatomical dead space, usually reducing total anatomical dead space by about
50%.
19
REFERENCES
1.
Belpomme V, Ricard-Hibon A, Devoir C, et al. Correlation of arterial PCO2 and PETCO2 in
prehospital controlled ventilation. Am J Emerg Med. 2005; 23:852-859.
2.
Lumb AB. Nunn’s Applied Respiratory Physiology. 6th ed. Philadelphia: Elsevier Butterworth
Heinemann; 2005:118-121.
ITEM 15
Poliomyelitis is caused by a single-stranded RNA enterovirus transmitted by the fecal-oral route.
Although the organism is extremely infectious, only 1%-2% of infected individuals develop paralytic
polio, most commonly manifested as an asymmetric flaccid paralysis. In addition to destruction of the
anterior horn motor neurons, autopsy studies demonstrate lesions in the motor nuclei of cranial nerves and
the reticular formation. Recovery generally begins in two to three weeks but is reported to plateau after 710 months.
Survivors of polio may experience a new onset of weakness and muscular atrophy, usually occurring 15
years or longer after the initial episode. Initially labeled postpoliomyelitis progressive muscular atrophy,
it has been shortened to postpolio syndrome. Specific diagnostic criteria include:




a history of paralytic polio with residual loss of motor neurons
a period of recovery and stable neurologic and functional status
new onset of fatigue, muscle weakness, or atrophy
exclusion of other conditions that could cause symptoms
Fatigue, either central (somnolence, difficulty concentrating) or peripheral (weakness), is the most
common symptom. Pain is reported by almost half of patients with postpolio syndrome and may result in
a referral to a pain clinic. Slow progressive muscular weakness, usually involving muscles affected by the
initial episode of polio, is commonly reported. Approximately 40% of patients with postpolio syndrome
report respiratory symptoms including decreased pulmonary function, sleep apnea (central or obstructive),
or respiratory failure. Obstructive sleep apnea (OSA) appears to be more common in patients with
postpolio syndrome, and OSA tends to occur at a lower body mass index in patients with postpolio
syndrome than in patients who have OSA without postpolio syndrome. Postpolio syndrome patients also
report cold intolerance (65%) and dysphagia (10%-20%).
REFERENCES
1.
Fleisher LA. Anesthesia and Uncommon Diseases. 5th ed. Philadelphia: Elsevier Saunders;
2006:583-585.
2.
Lambert DA, Giannouli E, Schmidt BJ. Postpolio syndrome and anesthesia. Anesthesiology.
2005; 103:638-644.
20
ITEM 16
In the United States the polio epidemic peaked in 1952-1953 with over 57,000 new cases reported.
Although most new cases of polio are restricted to Africa, Southeast Asia, and the Middle East, it was
estimated in 1987 that 640,000 people in the United States had postpolio syndrome, making it more
prevalent (1 in 390 people) than multiple sclerosis (1 in 1,000 people). These prevalence data are not
applicable to the current population of the United States; the aging of polio survivors has resulted in a
lower prevalence for the population as a whole. As polio survivors age some affected patients will present
for surgical procedures related to their initial problem.
Preoperative evaluation of polio survivors should specifically include asking questions about dysphagia
and other bulbar symptoms (which may be associated with an increased risk of aspiration), respiratory
problems, and the possibility of sleep apnea.
Because the literature contains no case series addressing management of patients with postpolio syndrome
and only a few isolated case reports, most recommendations regarding anesthetic management are based
on theoretic considerations. Two case reports, however, describe complications (one involving respiratory
failure and one cardiac arrest) in the early postoperative period. In conjunction with an apparent increased
prevalence of sleep apnea (central or obstructive) in patients with postpolio syndrome, current
recommendations include extended postoperative observation for these patients.
Many anesthesiologists are reluctant to use regional anesthesia in patients with progressive neuromuscular
disease. Animal studies document that under certain circumstances local anesthetics may be toxic to
neurons. Patients with postpolio syndrome have a decreased number of functional motor neurons and
some of those neurons are abnormal, establishing a theoretic basis for avoiding regional anesthesia in
these patients. At this time, however, there are no experimental data to indicate that these concerns are
applicable to patients with postpolio syndrome, and there are no reports in the literature describing
complications associated with regional anesthesia in these patients.
Patients with a history of polio, not just those with postpolio syndrome, have been described as having
increased sensitivity to nondepolarizing neuromuscular blocking drugs. The risk of a hyperkalemic
response to succinylcholine in any patient following polio is related to the degree of denervation of
muscle that is present.
There are several reasons to be concerned about the use of respiratory depressant medications in patients
with postpolio syndrome. In addition to the problems associated with sleep apnea, marginal ventilatory
status may predispose to postoperative respiratory insufficiency. There are also concerns about the effects
caused by lesions in the reticular activating system (the theoretic site of action of most general anesthetic
agents). In the absence of any documentation about the effect on patients of opioids or agents used for
induction or maintenance of general anesthesia, and in light of published case reports documenting
adverse outcomes in the early postoperative period, authors generally recommend cautious titration of
short-acting agents (induction agents, neuromuscular blocking drugs, opioids, general anesthetics).
Similarly, heavy reliance on nonsteroidal antiinflammatory drugs is advocated in an effort to reduce the
amounts of opioids required to control pain in the postoperative period. Ketorolac is not contraindicated
in patients with postpolio syndrome and may be especially effective in assisting with the management of
postoperative pain.
21
REFERENCES
1.
Fleisher LA. Anesthesia and Uncommon Diseases. 5th ed. Philadelphia: Elsevier Saunders;
2006:583-585.
2.
Lambert DA, Giannouli E, Schmidt BJ. Postpolio syndrome and anesthesia. Anesthesiology.
2005; 103:638-644.
ITEM 17
Pulmonary vascular resistance is lowest at normal functional residual capacity.
At low lung volumes (eg, residual volume) compression of larger pulmonary vessels results in an increase
in pulmonary vascular resistance.
At high lung volumes (eg, total lung capacity) pulmonary capillaries are compressed between adjacent
alveoli, resulting in an increase in pulmonary vascular resistance.
Vital capacity, the volume of gas that can be inspired from residual volume, is not a static volume. The
endpoint of a vital capacity breath is total lung capacity, which results in compression of pulmonary
capillaries and an increase in pulmonary vascular resistance.
Figure 1. Lung volume and pulmonary vascular resistance. Pulmonary vascular resistance (PVR) is
lowest at normal functional residual capacity.
REFERENCES
1.
Lumb AB. Nunn’s Applied Respiratory Physiology. 6th ed. Philadelphia: Elsevier Butterworth
Heinemann; 2005:118-121.
2.
Pinsky MR. Cardiovascular issues in respiratory care. Chest. 2005; 128(5 Suppl 2):592S-597S.
22
ITEM 18
Administration of sodium nitroprusside, a direct-acting peripheral vasodilator, produces relaxation of the
smooth muscle in arteries as well as veins in both the systemic and pulmonary circulations. Nitric oxide,
cyanide, and methemoglobin are produced by the interaction between nitroprusside and oxyhemoglobin.
Because this interaction is not enzymatic, the production of cyanide is not affected by temperature. Unlike
nitroglycerine, nitric oxide is generated by nitroprusside even in the absence of a thio-containing
compound.
Nitroprusside attenuates hypoxic pulmonary vasoconstriction, generally resulting in a decrease in the
partial pressure of oxygen in arterial blood. It has been postulated that the presence of some degree of
vascular obstruction is the reason why patients with chronic obstructive pulmonary disease demonstrate
less of an increase in shunt fraction than patients with healthy lungs.
Once mixed with 5% glucose in water, exposure of sodium nitroprusside to light results in conversion to
aquapentacyanoferrate and the release of hydrogen cyanide. Based on this, current recommendations are
that sodium nitroprusside be continuously protected from light by wrapping both the container and the
delivery tubing in foil. Studies have documented, however, that they cyanide concentration found in
sodium nitroprusside exposed to light for eight hours is unchanged from that found in sodium
nitroprusside afforded continuous protection from light.
REFERENCES
1.
Stoelting RK, Hillier SC. Pharmacology and Physiology in Anesthetic Practice. 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2006:355-361.
2.
Friederich JA, Butterworth JF 4th. Sodium nitroprusside: Twenty years and counting. Anesth
Analg. 1995; 81:152-162.
ITEM 19
Data may be described as being either categorical or interval. Categorical data, which may include such
things as demographic information, can be binary (only two choices, such as died/survived) or have
multiple categories (survived intact, survived with neurologic damage necessitating institutional care,
died). Interval data, which are numerical measurements, may be continuous (hemoglobin concentration)
or discrete (the number of coronary anastomoses performed). The statistical tests used for categorical data
are not appropriate for interval data and vice versa.
Measures of central tendency (mean, median, mode) are a form of descriptive statistics (as opposed to
inferential statistics) commonly used to give an indication of what is being presented. The mean is the
arithmetic average of the data (the sum of all values divided by the number of data points). The median is
the middle point of the data when all values are ranked from high to low (an equal number of points
above and below the value). The mean is more sensitive to extreme values (outliers) than the median. The
mode is the most frequently occurring value.
Measures of dispersion (standard deviation, standard error of the mean) are used to describe the
distribution of data. Standard deviation, the most commonly used measure of variability, is calculated by
23
determining the deviation of each value from the mean, squaring the deviations, totaling the deviations,
dividing by the number of measures, and determining the square root of the result. A small value for the
standard deviation indicates that the data are tightly grouped around the mean; a larger value indicates a
broader distribution of values. The standard error of the mean may be viewed as an attempt to estimate
the variability of the means of different samples compared to the true mean of the entire population.
Because the standard error of the mean is calculated by dividing the standard deviation by the square root
of N (the number of observations), the resulting value for the standard error of the mean will be less than
the standard deviation.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:882884.
2.
Guller U, DeLong ER. Interpreting statistics in medical literature: A vade mecum for surgeons. J
Am Coll Surg. 2004; 198:441-458.
ITEM 20
Risk of macroshock exists when an individual coming into contact with a “hot” electrical source
completes a circuit. This occurs because traditional power systems are grounded (connected to the earth)
and when an individual who also is in contact with the ground touches an area where current is flowing it
may now flow through them. To avoid this, operating rooms use an isolation transformer to convert
grounded power to an ungrounded or isolated power system. However, no power system is in total
isolation since small amounts of current leak to ground, leaving the system partially degraded. A line
isolation monitor (LIM) measures in milliamperes the total amount of current leakage present in an
isolated power system by continuously monitoring the integrity of the isolated power system. When a
piece of equipment with a damaged electrical circuit that allows leakage of current is connected to the
isolated power system, conversion to a grounded system may occur. The LIM alerts personnel when the
system is no longer isolated. Most LIMs are set to alarm at either 2 or 5 mA depending on the brand and
age of the monitor. The number on the LIM monitor is not a measure of actual current flowing but a
measure of the amount of current that would flow in the event of a first fault. If this number exceeds a
preset limit then an alarm will be triggered. If the LIM indicates a reading greater than 5 mA, a first fault
(a single power line is grounded) likely exists. Even in the event of a first fault this does not necessarily
indicate a dangerous situation unless a second fault occurs.
Equipment ground wires are essential to the proper function of the LIM; the LIM cannot detect broken
equipment ground wires and no alarm will be activated if this problem is present. If the ground wires are
not intact, a person coming into contact with faulty equipment can complete the circuit and is at risk for
macroshock.
If the LIM alarm is triggered during a case, the following are reasonable steps:



Check the reading, if greater than 5 mA, it is likely a faulty piece of equipment is in use
Unplug the most recently activated equipment if it is not essential
Unplug equipment until the alarm stops to identify faulty equipment
24


Remove faulty equipment that is not life-supporting
Do not connect additional electrical equipment until the faulty piece has been identified and
removed
One advantage to the LIM is that it alerts personnel to a first fault without stopping the electrical power.
Figure 1. (A) No electrical shock occurs when the power system is properly isolated from the ground. (B)
If a faulted secondary power line is touched, current may travel through a person to the ground
completing a circuit from point A to D and shock can occur. (C) A line isolation monitor alerts personnel
if isolated power system becomes grounded. Used with permission, from Miller RD. Miller’s Anesthesia.
6th ed.
REFERENCES
1.
Bernstein MS. Isolated power and line isolation monitors. Biomed Instrum Technol. 1990;
24:221-223.
2.
Nielsen R. Possible causes of alarming… Line isolation monitors. Biomed Instrum Technol.
2004; 38:288-289.
3.
Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006:157-162.
25
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:31423143.
4.
ITEM 21
Ulnar neuropathy is the most frequent type of postoperative nerve injury and accounts for one third of all
nerve injury claims in the American Society of Anesthesiologists Closed Claims Database. Prospective
studies estimate the incidence of postoperative ulnar neuropathy to be between 0.3%-0.5%. Ulnar
neuropathy has been well documented in surgical and nonsurgical patients. The main mechanism remains
unknown, however compression of the ulnar nerve within the cubital tunnel has been suggested as a
possible mechanism. Based on a multivariate analysis on over a million consecutive anesthetics during a
35-year period three factors were identified as being independent predictors for development of persistent
(> three months duration) ulnar neuropathy:



male gender
extremes (high or low) in body mass index (BMI)
prolonged hospital stay
The duration of anesthesia and intraoperative patient position were not associated with postoperative
ulnar neuropathy.
Lastly, it has been suggested that preexisting subclinical neuropathy may also play an important role,
which is supported by an increased incidence of contralateral nerve conduction problems and late
development of symptoms (two to seven days postprocedure) in affected patients.
REFERENCES
1.
Warner MA, Warner DO, Matsumoto JY, et al. Ulnar neuropathy in surgical patients.
Anesthesiology. 1999; 90:54-59.
2.
Warner MA, Warner ME, Martin JT. Ulnar neuropathy: Incidence, outcome, and risk factors in
sedated or anesthetized patients. Anesthesiology. 1994; 81:1332-1340.
3.
Caplan RA, Posner KL, Cheney FW. Perioperative ulnar neuropathy: Are we ready for shortcuts?
Anesthesiology. 1994; 81:1321-1323.
4.
Fleisher LA. Evidence-Based Practice of Anesthesiology. Philadelphia: Elsevier Saunders;
2004:228-229.
5.
Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006:651-652.
6.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:11541155.
26
ITEM 22
Although uncommon, perioperative alterations of vision and blindness have been well documented and
can be devastating. The process of establishing a diagnosis for a postoperative visual deficit can be
difficult. Potential causes include:





anterior and posterior ischemic optic neuropathy (ION)
central retinal artery occlusion
central retinal vein occlusion
cortical blindness
others (eg, glycine toxicity)
ION, the most commonly reported cause of postoperative visual deficit, is felt to develop secondary to
hypoperfusion or lack of perfusion to the anterior (classified at AION) or posterior (classified as PION)
portions of the optic nerve. Disrupting the blood supply to the optic nerve can result in ischemia, axonal
swelling, and eventually loss of function. ION typically presents as painless diminished visual acuity
and/or visual field deficits in one eye and often progresses to involve the other eye. Total blindness has
also been reported. Although ION may present immediately upon emergence from anesthesia, in many
circumstances the initial presentation does not occur until 24 hours or more after surgery. There is no
established treatment for ION; however approximately 43% of affected patients will show spontaneous
improvement. The etiology of perioperative ION is multifactorial. Associated factors include the
following:
Patient risk factors:
Intraoperative events:
 variable blood supply
 acute systemic hypotension
 small optic disc size
 venous obstruction
 age
 raised intraocular pressure
 hypertension
 lowered hematocrit
 diabetes
 increased blood viscosity
 vascular disease
ION has been established as a serious potential postoperative complication of cardiopulmonary bypass
and operative procedures involving the spine.
Cortical blindness is caused by damage to the occipital cortex or optic radiation and may result from
ischemia, trauma, emboli, or sustained hypotension from cardiac arrest. Cortical blindness has been
reported as a rare cause for postoperative blindness. Central retinal artery occlusion is a much less
common cause of postoperative blindness than ION. It is frequently caused by an embolism originating
from the carotid artery. It has been reported after spine and cardiac surgery. The mechanism is felt to be
extraocular pressure and hypotension leading to lack of flow in the retinal artery.
Although central retinal vein occlusion may occur as a result of pressure on the globe, presentation is
almost immediate. This problem is also commonly accompanied by extensive facial edema, especially if
the patient was in the head-down position. Central retinal vein occlusion is not the most common cause of
postoperative visual loss.
27
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:11571158, 3012-3014.
2.
Williams EL. Postoperative blindness. Anesthesiol Clin North America. 2002; 20:605-622.
3.
Buono LM, Foroozan R. Perioperative posterior ischemic optic neuropathy: Review of the
literature. Surv Ophthalmol. 2005; 50:15-26.
4.
Lee LA. ASA Postoperative Visual Loss Registry: Preliminary analysis of factors associated with
spine operations. ASA Newsl. 2003; 67(6):7-8. Available online at:
http://depts.washington.edu/asaccp/ASA/Newsletters/asa67_6_7_8.pdf. Accessed August 2006.
ITEM 23
Concern over what is perceived as an increase in the incidence of postoperative visual deficits led to the
formation of a Postoperative Visual Loss (POVL) Registry in 1999 by the American Society of
Anesthesiologists (ASA). Recently it was reported that of the 113 patients now in the POVL database,
63% were secondary to ischemic optic neuropathy (ION). The ASA also formed a task force on
perioperative blindness, which issued a practice advisory for perioperative visual loss associated with
spine surgery. Although few data support these recommendations, the consensus opinions of the task
force were as follows:








A subset of patients undergoing spine surgery while in the prone position and receiving general
anesthesia are at increased risk for the development of POVL.
Certain patients among these may be identified preoperatively as being at risk for prolonged
surgery, substantial blood loss, or both and can be considered high-risk.
High-risk patients should be informed that there is a small, unpredictable risk of POVL.
The use of deliberate hypotensive techniques during spine surgery has not been shown to be
associated with the development of POVL.
Colloids should be used along with crystalloids to maintain intravascular volume in patients who
have substantial blood loss.
At this time there is no apparent transfusion threshold that would eliminate the risk of POVL
related to anemia.
For a patient at high risk, the head should be positioned level with or higher than the heart when
possible. In addition, the head should be maintained in a neutral forward position (eg, without
significant neck flexion, extension, lateral flexion, or rotation) when possible.
Consideration should be given to the use of staged spine procedures in high-risk patients.
Ophthalmologic evaluation should be obtained as soon as possible for prompt diagnosis and potential
treatment.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:11571158.
28
2.
Lee LA. ASA Postoperative Visual Loss Registry: Preliminary analysis of factors associated with
spine operations. ASA Newsl. 2003; 67(6):7-8. Available online at:
http://depts.washington.edu/asaccp/ASA/Newsletters/asa67_6_7_8.pdf. Accessed August 2006.
3.
Lee LA, Roth S, Posner KL, et al. An analysis of 71 spine cases with ischemic optic neuropathy
from the ASA Postoperative Visual Loss Registry. Anesthesiology. 2005:103:A1. Available
online at: http://depts.washington.edu/asaccp/eye/providers/2005_103_A1.pdf. Accessed August
2006.
4.
Dunker S, Hsu HY, Sebag J, et al. Perioperative risk factors for posterior ischemic optic
neuropathy. J Am Coll Surg. 2002; 194:705-710.
5.
Practice Advisory for Perioperative Visual Loss Associated with Spine Surgery. A report of the
American Society of Anesthesiologist Task Force on Perioperative Blindness. Available online
at: http://www.asahq.org/publicationsAndServices/BlindnessAdvisoryFinal.pdf. Accessed August
2006.
ITEM 24
Reversal of nondepolarizing muscle relaxant by anticholinesterases, such as neostigmine, results mainly
from the increase in the acetylcholine concentration at the motor endplate. The resulting antagonism of
the nondepolarizing agents by acetylcholine is then time-dependent and directly affected by five factors:





depth of blockade at the time of reversal
antagonist administered
overall dose of antagonist
natural rate of spontaneous recovery from the nondepolarizing muscle relaxant
concentration of volatile agent present at reversal
In addition many other patient factors can adversely affect the adequacy of reversal including but not
limited to:






respiratory acidosis
metabolic alkalosis
electrolyte abnormalities
o hypocalcemia
o hypermagnesemia
o hypokalemia
hypothermia
coexisting disease (eg, myasthenia gravis)
drug interactions
o aminoglycosides
o calcium channel blockers
Respiratory acidosis inhibits antagonism. Hypoventilation to a PaCO2 above 50 mm Hg significantly
reduces the likelihood of being able to adequately reverse a nondepolarizing blockade. Therefore, the use
29
of opioids that result in decreased ventilation may lead to inadequate reversal. Metabolic alkalosis, as
opposed to acidosis, has been shown to inhibit reversal with neostigmine.
The use of calcium channel blockers such as verapamil, but not beta blockers, has been associated with
potentiation and impaired reversal of nondepolarizing neuromuscular blockade. Hypothermia, as opposed
to fever, may also interfere with the antagonism of nondepolarizing neuromuscular blockade.
Hypokalemia, not hyperkalemia, is associated with impaired reversal of nondepolarizing neuromuscular
blockade.
REFERENCES
1.
Bevan DR. Recovery from neuromuscular block and its assessment. Anesth Analg. 2000; 90(5
Suppl):S7-S13.
2.
Bevan DR, Donati F, Kopman AF. Reversal of neuromuscular blockade. Anesthesiology. 1992;
77:785-805.
3.
Barash, PG, Cullen, BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006:445-448.
4.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:519523.
ITEM 25
Plasma cholinesterase (also known as butyrylcholinesterase or pseudocholinesterase), an enzyme
produced in the liver, is responsible for the hydrolysis of succinylcholine and mivacurium. Efficient
hydrolysis by plasma cholinesterase results in only a fraction of the administered dose of the
neuromuscular blocking agent reaching the neuromuscular junction.
Prolonged neuromuscular blockade following administration of mivacurium or succinylcholine may occur
as a result of severely decreased plasma levels of normal plasma cholinesterase or normal levels of some
atypical forms of plasma cholinesterase.
Significantly decreased levels of plasma cholinesterase must be present to clinically produce prolongation
of neuromuscular blockade for patients with normal plasma cholinesterase. Decreased hepatic production
of plasma cholinesterase as a result of advanced liver disease can prolong neuromuscular blockade. The
administration of neostigmine, echothiophate, and metoclopramide all result in decreased plasma
cholinesterase activity and may produce clinically detectable prolongation of neuromuscular blockade
after succinylcholine or mivacurium administration.
Mivacurium is hydrolyzed by plasma cholinesterase. Administration of mivacurium to patients with
atypical plasma cholinesterase can result in prolonged neuromuscular blockade. An estimated
prolongation of neuromuscular blockade of 50%-100% greater than normal after a standard dose of
mivacurium would be expected for patients with an atypical homozygous plasma cholinesterase; this
would result in an estimated blockade time of 30-40 minutes.
30
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:487489.
2.
Stoelting RK, Hillier SC. Pharmacology and Physiology in Anesthetic Practice. 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2006:219-220.
3.
Hemadri M, Purva M, Traykova V. Unexpected prolonged neuromuscular block after
mivacurium: A case report. Med Princ Pract. 2002; 11:50-52.
ITEM 26
The oxyhemoglobin dissociation curve describes the relationship between the percentage of hemoglobin
that is saturated with oxygen for a given partial pressure of oxygen (see Figure 1). The dissociative
characteristics of adult human hemoglobin produce an oxygen partial pressure-saturation curve with rapid
changes of oxygen content in blood as partial pressure changes between 20 and 60 mm Hg. Minimal
changes in oxygen saturations occur for a partial pressure of oxygen less than 20 or greater than 100 mm
Hg.
Several factors affect the shifting of the oxyhemoglobin dissociation curve (see Table 1). Shifting of the
curve to the left (alkalosis, hypothermia, hemoglobin F) requires a lower partial pressure of oxygen before
oxygen is released to the tissues from hemoglobin. A shift of the curve to the right (acidosis,
hyperthermia, volatile agents) requires a higher partial pressure of oxygen to have the same oxygen
saturation when compared with a normal positioned curve. Volatile anesthetic agents may produce a
modest shift to the right of the oxyhemoglobin dissociation curve for unknown reasons.
Figure 1. The oxyhemoglobin dissociation curve.
31
Table 1. Conditions that shift the oxyhemoglobin dissociation curve.
Left shift
Right Shift
Alkalosis
Acidosis
Hypothermia
Hyperthermia
Hemoglobin F
Volatile agents
Carboxyhemoglobin
Exercise
Methemoglobin
Increased 2,3-DPG
Decreased 2,3-DPG
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:699701.
2.
Stoelting RK, Hillier SC. Pharmacology and Physiology in Anesthetic Practice. 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2006:788-790.
3.
Clerbaux T, Detry B, Geubel A, et al. The oxyhemoglobin dissociation curve in liver cirrhosis.
Chest. 2006;129:438-445.
ITEM 27
The matching of ventilation and perfusion is described by the ventilation-perfusion (V/Q) ratio. In healthy
young patients the V/Q ratio for most individual lung units is approximately 1 (Figure 1); in a
semirecumbent position, 95% of the lung has a V/Q ratio between 0.3 and 2.1.
If the V/Q ratio is high (> 1), the lung unit has ventilation in excess of perfusion; blood perfusing these
lung units should be fully oxygenated and will not contribute to hypoxemia. Ventilation in the absence of
perfusion is dead space.
When the V/Q ratio is low, perfusion is occurring in excess of ventilation. Unfortunately the terminology
regarding areas of low V/Q ratio is confusing. Although the term V/Q mismatch is commonly used to
describe lung units with a low but finite V/Q ratio, technically the phrase is also an accurate description of
lung units with a high V/Q ratio as well as of lung units with V/Q ratio = 0. To add to the confusion, the
term shunt may be used to describe either lung units with a low but finite V/Q ratio or lung units with
V/Q = 0.
The distinction between lung units with a low but finite V/Q ration and lung units with a V/Q ratio = 0
has some clinical significance; although both types of V/Q disturbances contribute to hypoxemia, the
administration of supplemental oxygen will increase the partial pressure of oxygen (PO2) in pulmonary
32
capillary blood draining lung units with low but finite V/Q ratios. Since blood perfusing lung units with
V/Q ratio = 0 is never exposed to alveolar gas, administration of supplemental oxygen has no impact on
the PO2 of pulmonary capillary (and therefore arterial) blood.
Figure 1. Normal V/Q ratio distribution. Used with permission, from Miller RD. Miller’s Anesthesia. 6th
ed. Philadelphia: Elsevier Churchill Livingstone; 2005:683.
REFERENCES
1.
West JB. Pulmonary Pathophysiology: The Essentials. 4th ed. Baltimore: Williams and Wilkins;
1992:20-33.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:701703.
3.
Payen DM. Inhaled nitric oxide and acute lung injury. Clin Chest Med. 2000; 21:519-529, ix.
ITEM 28
Anesthesiologists are familiar with the use of dantrolene to treat malignant hyperthermia in the acute
perioperative period. However, dantrolene is also used as a skeletal muscle relaxant for the treatment of
spasticity resulting from damage to upper motor neurons (eg, subarachnoid hemorrhage, spinal cord
injury, multiple sclerosis, cerebral palsy). The mechanism of action of dantrolene involves inhibition of
calcium release from the sarcoplasmic reticulum. Neuromuscular transmission is not altered by
dantrolene.
The most common manifestation from dantrolene is skeletal muscle weakness. Muscular weakness can be
severe enough to cause respiratory failure and aspiration pneumonia. Blurred vision, nausea, and diarrhea
can also occur following dantrolene administration. The liver metabolizes dantrolene, and hepatitis has
been reported in up to 0.5% of patients receiving dantrolene for more than 60 days. The hepatitis
associated with dantrolene has been fatal in 0.1%-0.2% of patients treated chronically with dantrolene.
33
Liver function testing is suggested for patients receiving chronic dantrolene treatment (longer than 30-45
days). Hepatitis is most common in women over 35 years of age and usually develops between the third
and twelfth month of therapy. Pleural effusion, pleural fibrosis, pericarditis, and sensorineural hearing
loss have all been associated with long-term dantrolene administration.
Hemolytic anemia, renal toxicity, and thrombocytopenia have not been associated with chronic dantrolene
administration.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:2221.
2.
Stoelting RK, Hillier SC. Pharmacology and Physiology in Anesthetic Practice. 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2006:596-597.
3.
Chan CH. Dantrolene sodium and hepatic injury. Neurology. 1990; 40:1427-1432.
4.
Physicians’ Desk Reference. 60th ed. Montvale, NJ: Thompson PDR; 2006:2690-2692.
ITEM 29
Lipid solubility, protein binding, degree of ionization, and tissue blood flow determine the distribution of
thiopental. It has been estimated that in normal patients the brain receives approximately 10% of the total
intravenous dose of thiopental within 30-40 seconds. In combination with high lipid solubility, this results
in very high concentrations of thiopental in the brain. Over the next several minutes, however, the lower
concentration of thiopental in plasma results in reversal of the concentration gradient and redistribution
from the brain. Over a period of five minutes, brain concentration of thiopental is reduced by
approximately 50%. This redistribution is the primary mechanism accounting for rapid awakening
following administration of a single induction dose of thiopental.
The combination of a high degree of protein binding and high lipid solubility minimizes the renal
excretion of thiopental. Less than 1% of an administered dose is excreted unchanged in the urine.
Although some extrahepatic metabolism may occur in the central nervous system and the kidneys, over
90% of thiopental metabolism takes places in the liver. Thiopental metabolism is manifested by a low
hepatic extraction ratio; following stabilization of plasma concentrations, only 10%-24% is metabolized
each hour.
Hoffman elimination, a spontaneous nonenzymatic degradation, occurs with atracurium but does not with
barbiturates.
REFERENCES
1.
Stoelting RK, Hillier SC. Pharmacology and Physiology in Anesthetic Practice. 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2006:129-131.
2.
Upton RN, Ludbrook GL, Grant C, et al. The effect of altered cerebral blood flow on cerebral
kinetics of thiopental and propofol in sheep. Anesthesiology. 2000; 93:1085-1094.
34
ITEM 30
The Bispectral Index (BIS®) is a commercial product that uses a mathematical algorithm to analyze the
frequency patterns found in electroencephalographic (EEG) signals to provide an arbitrarily assigned
scale between 100 (awake) to 0 (electrical silence). The company (Aspect Medical) has defined this
analysis as the Bispectral Index. The numbers obtained were then associated with various states of
consciousness as measured by several scales, with the most prominent being the Modified Observer’s
Assessment of Alertness/Sedation Scale (OAA/S), which is described in Table 1.
Table 1. Modified Observer’s Assessment of Alertness/Sedation Scale (OAA/S).
Expected Response
Score
Responds readily to name spoken in normal tone
5 (Alert)
Lethargic response to name spoken in normal tome
4
Responds only after name is called loudly and/or repeatedly
3
Responds only after mild prodding or shaking
2
Responds only after painful trapezius squeeze
1
Does not responds to painful trapezius squeeze
0
Early studies on the utility of the BIS index found that the type of anesthetic technique strongly
influenced the ability of the BIS score to predict or anticipate patient response. BIS analysis sought to
identify levels of consciousness or hypnosis, thus opioids alone had less effect on the “score” than a drug
like propofol, which is designed to effect consciousness. However, opioids will decrease the level of
arousal associated with a painful stimulus and thus affect the BIS value during surgical procedures. An
anesthetic technique using low to moderate opioid dose with hypnotic agent would be more likely to
provide a consistent “score” during various stimuli (incision, closure) than a high-dose opioid alone
where even sounds could cause arousal.
Aspect Medical suggests that loss of consciousness begins to occur at BIS values between 70 and 80. At
BIS values of 60 or less, the probability of consciousness is low. Generally at BIS values of 40-60, there
is adequate hypnotic effect for general anesthesia. At values below 40, the patient is in deep hypnosis.
The validity of BIS to predict level of consciousness in all patients is controversial. Clearly processing of
a two-lead EEG will reflect only the activity in that location and will not predict the complexity of
consciousness in all patients. Case reports document BIS values as low as 40 in volunteers who were
aware and responded to commands. Other studies have reported an unequivocal purposeful response to a
command in 13% of patients with BIS values of 60-70 and conscious recall in 25% of patients who
demonstrated purposeful responses (approximately 4% of the total).
35
There is little or no correlation between the BIS value and analgesia. Thus, a BIS value of 50 would not
necessarily indicate that the level of analgesia is adequate.
BIS values do not predict the spinal cord response of movement to painful stimuli. The BIS does report
decreasing EEG activity in the individual patient on a scale related to levels of consciousness and
responsiveness in the “average” patient.
REFERENCES
1.
Kerssens C, Klein J, Bonke B. Awareness: Monitoring versus remembering what happened.
Anesthesiology. 2003; 99:570-575.
2.
Johansen JW, Sebel PS. Development and clinical application of electroencephalographic
bispectrum monitoring. Anesthesiology. 2000; 93:1336-1344.
3.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:12501259.
4.
Vuyk J, Lichtenbelt BJ, Vieveen J, et al. Low bispectral index values in awake volunteers
receiving a combination of propofol and midazolam. Anesthesiology. 2004; 100:179-181.
ITEM 31
A mechanical assist device is a machine that provides blood flow by replacing the pumping action of a
failing left or right ventricle. Placement of a left ventricular assist device (LVAD) requires the placement
of a cannula inserted into the apex of the left ventricle to provide inflow to the device and placement of a
cannula into the aorta to provide perfusion to the patient’s systemic circulation.
In patients with aortic insufficiency, blood pumped from the device into the patient’s aorta may
regurgitate back into the left ventricle, decreasing forward flow into the systemic circulation and creating
a closed circuit from the left ventricle to the device and back again. This would increase flow through the
device as measured from the LVAD console by possibly up to 2L/min more than the patient’s cardiac
output as measured by thermodilution from the right ventricle. Even mild to moderate aortic insufficiency
can become severe after placement of an LVAD. Ventricular distention can ensue, resulting in
subendocardial ischemia. It is important to perform a complete transesophageal echocardiographic
examination prior to insertion of an LVAD to evaluate conditions that could impair proper functioning of
the device, such as aortic insufficiency, an intracardiac shunt (eg, atrial septal defect), or mitral stenosis.
Tricuspid insufficiency would not affect the flow through an LVAD. Right-sided heart failure, however,
is a potential complication following insertion of an LVAD due to the increased flow from the left side of
the heart, producing increased venous return. If right ventricular dysfunction occurs, tricuspid
insufficiency may worsen.
Aortic stenosis is not a contraindication to LVAD placement. Severe aortic stenosis would likely impair
weaning from the device and would compromise the patient’s forward flow if the device were to fail. The
aortic valve should not be open at all in a patient with a properly functioning LVAD.
36
Mitral insufficiency would not affect the flow through the LAD. If it is severe, mitral insufficiency may
impair future weaning from the device. Mitral stenosis, if severe, could impede flow into the device if the
inflow cannula is positioned in the left ventricle and should be corrected at time of device implant.
REFERENCES
1.
Patel H, Pagani FD. Extracorporeal mechanical circulatory assist. Cardiol Clin. 2003; 21:29-41.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:19911993.
37
ITEM 32
Clinical scenario: A patient with a pulsatile left ventricular assist device experiences a decrease in his
systolic blood pressure from 110 mm Hg to 75 mm Hg. Concurrently, outflow from the device decreases
from 4.5 L/m to 2 L/m. The patient’s heart rate is 75/min and central venous pressure is 6mm Hg.
A left ventricular assist device (LVAD) provides forward flow to the patient’s systemic circulation by
redirecting flow from the failing left ventricle into a mechanical pump and out to the patient’s ascending
aorta. The mechanical assist device provides the cardiac output for the systemic circulation. The left
ventricle becomes only a conduit for blood to pass through on its way to the LVAD. There is a continuous
monitor on the LVAD console that displays the device outflow in liters per minute. This value is
important to monitor whenever hemodynamic changes occur. If a decrease in the patient’s blood pressure
occurs concurrently with a decrease in outflow from the device, it suggests that inflow to the device is
compromised. The cannulae should be evaluated for kinks and intravenous fluid therapy should be used to
increase inflow to the device if the central venous pressure is not elevated.
Epinephrine, dopamine, and other sympathomimetic agents would stimulate the beta receptors on the
heart. As the left ventricle is not contributing significantly to the cardiac output in these patients, these
agents would not be effective in improving forward flow through the left ventricle. If right ventricular
dysfunction is suspected, beta-agonists may improve flow into the device by improving right-sided heart
function. The patient in question does not have an increased central venous pressure, thus right-sided
heart dysfunction is not suspected in this case.
Pacing would increase a patient’s heart rate and could increase right ventricular output, which is a
determinant of LVAD performance. In the setting of a low central venous pressure, external pacing is not
the best intervention.
REFERENCES
1.
Patel H, Pagani FD. Extracorporeal mechanical circulatory assist. Cardiol Clin. 2003; 21:29-41.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:19911993.
ITEM 33
The superior laryngeal nerve is a branch of the vagus nerve, not the glossopharyngeal nerve. The larynx is
innervated totally by two branches of the vagus nerve—the superior laryngeal nerve and the recurrent
laryngeal nerve. There is no laryngeal innervation by the glossopharyngeal nerve.
The superior laryngeal nerve is derived from the inferior ganglion of the vagus nerve. It divides into an
external and internal branch. The external branch provides the motor supply to the cricothyroid muscle
and inferior pharyngeal constrictors. The internal branch has upper and lower branches that together
supply sensory innervation to the lower pharynx, epiglottis, vallecula, and the laryngeal inlet above the
vocal cords. In addition, the internal branch is the motor supply to the arytenoid muscles.
38
The recurrent laryngeal nerve supplies sensory innervation to the larynx below the vocal cords including
the upper trachea. It also provides motor innervation to all the intrinsic laryngeal muscles except the
cricothyroid muscle.
Because it is more intimately related to the thyroid gland, the recurrent laryngeal nerve is more commonly
damaged than the superior laryngeal nerve during thyroid surgery. The external branch of the superior
laryngeal nerve is also at risk and may merit specific intraoperative identification as well.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:25372539.
2.
Hurtado-Lopez LM, Pacheco-Alvarez MI, Montes-Castillo Mde L, et al. Importance of the
intraoperative identification of the external branch of the superior laryngeal nerve during
thyroidectomy: Electromyographic evaluation. Thyroid. 2005; 15:449-454.
3.
Hartl DM, Travagli JP, Leboulleux S, et al. Clinical review: Current concepts in the management
of unilateral recurrent laryngeal nerve paralysis after thyroid surgery. J Clin Endocrinol Metab.
2005; 90:3084-3088.
ITEM 34
The strongest indications for lung isolation and single lung ventilation are those considered life saving or
absolutely indicated. The absolute indications for lung isolation techniques are to avoid contamination of
the contralateral lung (from blood or pus) and to control distribution of ventilation (eg, in the presence of
large air leaks). Table 1 summarizes specific examples of the absolute indications for lung isolation.
Table 1. Absolute indications for lung isolation.
To Minimize Contamination
To Distribute Ventilation
Infection
Major airway disruption (including surgery)
Lung abscess (including hydatid cyst)
Giant bulla
Bronchiectasis
Unilateral lung disease with severe hypoxemia
Severe hemoptysis
Bronchopleural fistula
Tumor
Infection (including tuberculosis and
fungus)
Arteriovenous malformation
Alveolar lavage (eg, alveolar proteinosis)
39
Lung isolation is most commonly achieved by means of a double-lumen tracheal tube or a bronchial
blocker. It is essential to confirm correct tube placement by means of fiberoptic bronchoscopy, especially
in the presence of an absolute indication for lung isolation.
Relative indications are not considered life saving but rather are related to optimal surgical exposure for
the planned surgical procedure. The most common procedures are descending thoracic aortic procedures,
lung resection and transplantation, esophageal resection, and thoracic spine procedures via an anterior
approach. These are summarized below:







descending thoracic aortic aneurysm
pneumonectomy and lung transplantation
upper lobectomy
thoracoscopy
middle/lower lobectomies
esophageal resection
thoracic spine procedures (anterior approach)
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:18731900.
2.
Lanken PN, Hanson CW, Manaker S. The Intensive Care Unit Manual. Philadelphia: WB
Saunders; 2001:847-856.
3.
Ulku R, Onen A, Onat S. Surgical treatment of pulmonary hydatid cysts in children: Report of 66
cases. Eur J Pediatr Surg. 2004; 14:255-259.
ITEM 35
Somatosensory evoked potential (SSEP) monitoring involves stimulation of a peripheral nerve (eg,
posterior tibial, common peroneal, ulnar, median) and subsequent measurement of the neural response.
The neural response ascends in the ipsilateral dorsal column to reach the thalamus via the lemniscal
pathways. Thereafter, it terminates in the cerebral cortex (see Figure 1). Thus, this neural traffic
represents the activity of the posterior spinal columns (proprioception and vibration) and not that of the
motor ventral spinal columns. Furthermore, this type of neuromonitoring can be used to assess neural
pathways not only in the spinal cord but also in the brainstem and cerebral cortex.
40
Figure 1. Overview of the somatosensory evoked potential neuroanatomical pathway and waveforms
generated.
To be effective, the stimulus must be applied below the area at risk and the measurement must occur
above the area at risk.
The most common application of SSEP monitoring is in spinal corrective surgery. Studies, including a
review of more than 51,000 scoliosis cases, have shown that it identifies neural complications. In fact, the
incidence of sensory deficit without SSEP changes was 0.63% (false negative rate). The Scoliosis
Research Society has developed a position statement endorsing the role of this type of neuromonitoring in
corrective spinal surgery. Motor deficits are not reliably detected by SSEP monitoring alone.
An important limitation of SSEPs is that the cortical responses are sensitive to inhalational anesthetics.
Intravenous anesthetic agents such as propofol have less effect and thus represent a technique of general
anesthesia that preserves SSEPs during major spinal surgery.
REFERENCES
1.
Sloan T. Clinical monitoring of the brain and spinal cord. Refresher Courses in Anesthesiology.
American Society of Anesthesiologists. 2005; 33:225-234.
2.
Meyer PR Jr, Colter HB, Gireesan GT. Operative neurological complications resulting from
thoracic and lumbar spine internal fixation. Clin Orthop Relat Res. 1988; 237:125-131.
3.
Nuwer MR, Dawson EG, Carlson LG, et al. Somatosensory evoked potential spinal cord
monitoring reduces neurologic deficits after scoliosis surgery: Results of a large multicenter
survey. Electroencephalogr Clin Neurophysiol. 1995; 96:6-11.
41
ITEM 36
Electroencephalographic (EEG) monitoring measures the spontaneous electrical activity of the brain,
specifically the pyramidal layer of the cerebral cortex. The EEG is measured from electrode pairs on the
scalp and represents cerebral activity in two regions immediately beneath the electrodes.
The EEG is able to detect cortical ischemia, which is manifested as a reduction in both amplitude and
frequency or as an asymmetric distribution of activity. Anesthetic depth affects the EEG symmetrically as
it alters general synaptic function. As anesthetic depth increases, four EEG changes are described:




reduction in variability
reduction in frequency progressing to burst suppression and ultimately isoelectric or flat EEG
an initial increase in amplitude followed by a reduction
shift of rhythmic activity to a frontal predominance
The EEG monitoring is often indicated during carotid endarterectomy to monitor for cerebral ischemia.
Although there are conflicting studies, EEG monitoring has been associated with a reduction in stroke
risk. This reduction is based, in part, on selective shunting in carotid endarterectomy when EEG changes
compatible with ischemia develop after carotid clamping. Nonetheless, a normal EEG does not rule out
stoke after carotid endarterectomy. Studies have documented intraoperative stoke occurring in up to 10%
of patients who had a normal intraoperative EEG. This may be due to many factors, such as intraoperative
emboli (air and atheroma) and/or postoperative carotid thrombus.
EEG monitoring is not reliably effective in detecting cerebral embolism. Transcranial Doppler, an
ultrasound technique focused on the internal carotid artery, allows detection of cerebral emboli.
REFERENCES
1.
Sloan T. Clinical monitoring of the brain and spinal cord. Refresher Courses in Anesthesiology.
American Society of Anesthesiologists. 2005; 33:225-234.
2.
Nuwer MR. Intraoperative electroencephalography. J Clin Neurophysiol. 1993; 10:437-444.
3.
Fleisher LA. Evidence-Based Practice of Anesthesiology. Philadelphia: Elsevier Saunders;
2004:339-341.
ITEM 37
Chemical dependence is a disease that is best understood by examining its three main components:
biological, psychological/behavioral, and social. Psychosocial factors have also been demonstrated to
participate prominently in the etiology of chemical dependence. Psychiatric disorders frequently coexist
with chemical dependence. Effective intervention must address both disease states.
Substance abuse is common amongst anesthesia providers, partly due to the ready access to addictive
medications. The measured prevalence at academic anesthesiology programs (1990-1997) was 1.6%
amongst anesthesia residents and 1.0% amongst attending anesthesiologists. The same study reported an
18% (30/167) prevalence of death or emergent resuscitation amongst affect individuals. In the most recent
42
survey of residency training programs (2005), the death rate related to substance abuse in residents reentering anesthesia training after treatment was reported as 14%.
Education programs mandated by the Accreditation Council for Graduate Medical Education and strict
federal policies relating to accounting of controlled substances have not produced a significant reduction
in the prevalence of substance abuse. Fentanyl and sufentanil remain the most commonly abused opioids
among anesthesia providers.
REFERENCES
1.
Berry AJ. Chemical dependence: Understanding the disease and its treatment. Refresher Courses
in Anesthesiology. American Society of Anesthesiologists. 2005; 33:13-20.
2.
Gallegos KV, Browne CH, Veit FW. Addiction in anesthesiologists: Drug access and patterns of
substance abuse. Qual Rev Bull. 1988; 14:116-122.
3.
Booth JV, Grossman D, Moore J, et al. Substance abuse among physicians: A survey of academic
anesthesiology programs. Anesth Analg. 2002; 95:1024-1030.
4.
Collins, GB, McAllister MS, Jensen M, et al. Chemical dependency treatment outcomes of
residents in anesthesiology: Results of a survey. Anesth Analg. 2005; 101:1457-1462.
ITEM 38
Clinical scenario: Placement of a femoral vein triple lumen catheter is planned in a 24-year-old man with
superior vena cava syndrome due to lymphoma.
The femoral vein is an optional site of placement of a central venous catheter. The location is less
desirable than either subclavian or jugular insertion sites in most circumstances because of the increased
risk of infection. However, in some cases, including superior vena caval obstruction, it is a reasonable
option.
Knowledge of the anatomy of the femoral canal is the key to successful placement of a femoral venous
catheter (Figure 1). The patient should be positioned in the supine position with the thigh in slight
abduction. The needle placement should be medial to the pulsation of the femoral artery at the junction of
the middle and distal thirds of the distance between the pubic tubercle and the anterior superior iliac
spine. The needle should be advanced towards the umbilicus at a 30 to 45 degree angle.
In addition to infection, complications of femoral venous cannulation include femoral or even iliac
arterial puncture (potentially causing life-threatening retroperitoneal bleeding) and thrombosis.
43
Figure 1. The anatomy of the femoral region. Used with permission, from Brown DL. Atlas of Regional
Anesthesia. 3rd ed. Philadelphia: Elsevier Saunders; 1999:106.
REFERENCES
1.
Merrer J, De Jonghe B, Golliot F, et al. Complications of femoral and subclavian venous
catheterization in critically ill patients. A randomized controlled trial. JAMA. 2001; 286:700-707.
2.
Fink MP, Abraham E, Vincent J-L. Textbook of Critical Care. 5th ed. Philadelphia: Elsevier
Saunders; 2005:1785-1790.
ITEM 39
Spinal hematoma after a neuraxial anesthetic technique is a rare but potentially catastrophic complication.
As many as 69% of patients with neuraxial hematoma have disordered coagulation (platelet and/or
coagulation proteins) at the time of neuraxial anesthetic administration. Needle placement in these cases
was reported as difficult in 25% of patients.
Muscle weakness was the first neurologic symptom in 46% of cases, while sensory deficit was the
presenting symptom in 14%.
44
This complication presents as a surgical emergency requiring urgent spinal cord imaging. Immediate
surgical decompression is indicated for spinal hematoma. Spinal cord ischemia tends to be reversible in
patients who undergo laminectomy within eight hours of onset of neurologic symptoms.
REFERENCES
1.
Broadman LM. Anticoagulation and regional anesthesia. Refresher Courses in Anesthesiology.
American Society of Anesthesiologists. 2005; 33:31-47.
2.
Vandermeulen EP, Van Aken H, Vermylen J. Anticoagulants and spinal-epidural anesthesia.
Anesth Analg. 1994; 79:1165-1177.
3.
Chestnut DH. Obstetric Anesthesia: Principles and Practice. 3rd ed. Philadelphia: Elsevier
Mosby; 2004:589-591.
4.
Horlocker TT, Wedel DJ, Benzon H, et al. Regional anesthesia in the anticoagulated patient:
Defining the risks (the second ASRA Consensus Conference on Neuraxial Anesthesia and
Anticoagulation). Reg Anesth Pain Med. 2003; 28:172-197.
ITEM 40
The femoral nerve divides into anterior and posterior divisions after emerging from under the inguinal
ligament. The anterior branch supplies the sartorius muscle on the medial aspect of the thigh. Its clinical
relevance is that the anterior branch is most commonly stimulated during a femoral nerve block, causing
medial thigh contraction. The posterior branch of the femoral nerve has many articular and muscular
branches; stimulation of this femoral division is identified by patella ascension due to contraction of the
quadriceps femoris on the anterolateral aspect of the thigh.
Indications for femoral nerve blockade include knee arthroscopy, femoral shaft fractures, major knee
ligament reconstructions, and total knee arthroplasty. Prospective randomized controlled trials have
documented that continuous femoral nerve blockade, compared to epidural analgesia, provides equivalent
analgesia with fewer side effects after total knee arthroplasty.
The three-in-one block is a technique of femoral nerve block with high volumes of local anesthetic with
the aim of blocking three nerves: the femoral, the lateral femoral cutaneous, and the obturator. The
femoral nerve is blocked up to 100% of the time, whereas block rates for the obturator nerve and the
lateral femoral cutaneous nerve are reported at 90% and 86%, respectively.
REFERENCES
1.
Pandin P, Vancutsem N, Salengros JC, et al. The anterior combined approach via a single skin
injection site allows lower limb anesthesia in supine patients. Can J Anaesth. 2003; 50:801-804.
2.
Vloka JD, Hadzic A, Drobnik L, et al. Anatomic landmarks for femoral nerve block: A
comparison of four needle insertion sites. Anesth Analg. 1999; 89:1467-1470.
45
3.
Capdevila X, Barthelet Y, Biboulet P, et al. Effects of perioperative analgesic technique on the
surgical outcome and duration of rehabilitation after major knee surgery. Anesthesiology. 1999;
91:8-15.
4.
Singelyn FJ, Deyaert M, Joris D, et al. Effects of intravenous patient-controlled analgesia with
morphine, continuous epidural analgesia and continuous three-in-one block on postoperative pain
and knee rehabilitation after unilateral total knee arthroplasty. Anesth Analg. 1998; 87:88-92.
5.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:17441745.
ITEM 41
Postpartum hemorrhage occurs in approximately 10% of deliveries. Uterine atony is the most common
cause of postpartum hemorrhage. Risk factors for uterine atony include:







grand multiparity
precipitous delivery
multiple gestation
macrosomia
chorioamnionitis
prolonged labor
tocolytic therapy
When uterine atony and postpartum hemorrhage occur, initial treatment includes uterine massage and
intravenous oxytocin. Because the number of uterine oxytocin receptors increases markedly near the end
of gestation, the drug is an especially effective agent for both prevention and treatment of postpartum
uterine atony. The majority of women who develop uterine atony are successfully treated with an
oxytocin infusion and require no additional treatment. Oxytocin does produce peripheral vasodilation.
Intravenous bolus doses as small as 5 U can cause hypotension. Therefore, oxytocin is administered as a
dilute intravenous infusion.
If uterine atony persists after treatment with uterine massage and intravenous oxytocin, other uterotonic
drugs are usually administered. The most common second-line drugs include methylergonovine and 15methylprostaglandin F2-alpha (Hemabate). Methylergonovine is an ergot alkaloid that produces a rapid
uterotonic effect after intramuscular injection and successfully treats uterine atony in most patients. It
likely produces myometrial contraction via alpha-adrenergic receptors. It also produces potent
vasoconstriction that can lead to severe hypertension, especially in patients with preexisting hypertension.
Therefore, it is relatively contraindicated in patients with preeclampsia or chronic hypertension.
Intravenous administration of methylergonovine has been associated with coronary artery vasospasm and
stroke. Therefore, it should only be administered intramuscularly.
The synthetic prostaglandin 15-methyl prostaglandin F2-alpha effectively increases uterine tone and is
frequently used to treat uterine atony unresponsive to oxytocin. Its uterotonic effect results from increases
in myometrial intracellular calcium concentrations and myosin light-chain kinase activity. It can be
administered intramuscularly or directly into the myometrium. It can also produce bronchospasm,
46
especially in patients with preexisting reactive airway disease. Therefore, it is relatively contraindicated in
asthmatic patients.
When uterine atony is unresponsive to pharmacologic therapy, invasive procedures must be performed to
prevent the postpartum hemorrhage from becoming life threatening. Surgical treatment, including
placement of a uterine compression stitch or hysterectomy, may need to be performed. Embolization of
the uterine arteries is another technique increasingly being used to treat refractory uterine atony. This
procedure requires the skill of an interventional radiologist, and the logistics of organizing this treatment
during an unanticipated postpartum hemorrhage can be difficult. However, an embolization procedure can
often prevent the need for hysterectomy and preserve fertility. Successful pregnancies have been reported
after embolization of the uterine arteries.
REFERENCES
1.
Chestnut DH. Obstetric Anesthesia: Principles and Practice. 3rd ed. Philadelphia: Elsevier
Mosby; 2004:668-671.
2.
El-Refaey H, Rodeck C. Post-partum haemorrhage: Definitions, medical and surgical
management. A time for change. Br Med Bull. 2003; 67:205-217.
ITEM 42
The increased metabolic demands experienced by a patient with a full thickness skin burn are
proportional to the size of the injury. Loss of skin integrity leads to increased fluid loss, heat loss, and
metabolic demands for tissue repair and the immune response. High endogenous catecholamine levels
also contribute to supranormal metabolism and protein catabolism. Current practice recommendations are
to begin enteral (postpyloric) feedings within 24 hours of injury.
Early enteral nutrition prevents protein catabolism and reduces the disruption of the gut barrier function.
Failure of the gut barrier allows intraluminal bacteria and endotoxins to enter the systemic circulation
leading to shock, sepsis, and death. High protein nutrition stimulates gastrointestinal blood flow, which
enhances gut viability and the function of critical immune tissue. Data in adults and children strongly
suggest that feeding within 24 hours of injury significantly improves nitrogen balance, increases serum
albumin concentrations, and maintains normal thyroid hormone levels when compared to delaying
feeding for 48 hours postinjury. Secretion of catecholamines (eg, epinephrine, dopamine, norepinephrine),
glucagon, cortisol, and insulin are reduced when enteral feeding is begun within 24 hours, making it
easier to attain appropriate glucose control. Hyperglycemia (glucose concentrations over 140 mg/dL) has
been shown to increase mortality in critically ill patients. Hyperglycemia even in nondiabetic patients
increases mortality. Providing adequate caloric intake using a parenteral route does not provide the
benefits of enteral nutrition. Mortality in patients with a greater than 50% burn is 63% with parenteral
nutrition versus 26% with enteral nutrition.
Burn care may require anesthesia as often as every 24 hours. Thus the standard eight-hour fast, which is
the ASA fasting guideline for oral nutrition containing protein and fat, is not feasible. The risk of sepsis,
delayed wound healing, and death is significantly increased when feeding is discontinued for long
periods. The benefits of feeding outweigh the risk of aspiration in most patients. For patients who come to
the operating room intubated, most major burn centers will continue enteral feeding during the surgical
47
procedure. The increase in gastric motility seen with burn patients as well as the technique of continuous
administration of a small volume of “food” has led most major burn units to withhold feeding only two to
four hours prior to surgery in patients who are not intubated. No large randomized trials have examined
the risk benefit ratio of this practice; it is an accepted approach developed in response to a significant
increase in mortality seen when nutrition is withheld.
REFERENCES
1.
Gottschlich MM, Jenkins ME, Mayes T, et al. The 2002 Clinical Research Award. An evaluation
of the safety of early vs delayed enteral support and effects on clinical, nutritional, and endocrine
outcomes after severe burns. J Burn Care Rehabil. 2002; 23:401-415.
2.
MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal injury. Anesthesiology.
1998; 89:749-770.
3.
Magnotti LJ, Deitch EA. Burns, bacterial translocation, gut barrier function, and failure. J Burn
Care Rehabil. 2005; 26(5):383-391.
4.
Fleisher LA. Anesthesia and Uncommon Diseases. 5th ed. Philadelphia: Elsevier Saunders;
2006:535-546.
ITEM 43
Treatment of burn patients is complicated by the physiologic changes that accompany a large fullthickness skin burn. Full-thickness skin injury is categorized as


Third degree: destruction of the epidermis and the dermis
Fourth degree: destruction or damage to fascia, muscle, or bone
Mortality and morbidity are related to the size and thickness of the burn, age of the patient, presence of an
inhalational burn, and presence of other injuries. Increased mortality rates are associated with age over 60
years or under 12.
A 10-fold increase in endogenous circulating catecholamines coupled with increased secretion of
glucagon and cortisol result in insulin resistance. Amino acids become the systemic energy source. Amino
acid catabolism leads to loss of muscle mass and decreased serum proteins including albumin. Albumin is
also lost through the burned area. Decreased serum albumin has a significant effect on the availability of
commonly used anesthetic drugs. Low serum albumin increases the free fraction of acidic drugs; thus,
drugs like thiopental and benzodiazepines require a lower dose for the same physiologic effect (ie, serum
free fraction). In contrast, basic drugs such as lidocaine and many beta-blockers have decreased serum
availability; a larger mg/kg drug dose of basic drugs is necessary to realize the same physiologic effect.
For example, the amount of lidocaine administered during tissue infiltration for systemic toxicity (eg,
seizure, cardiac depression) is increased.
A burn injury also leads to a proliferation of acetylcholine receptors throughout the muscle in the area
under the burn. When a burn exceeds 30%, the characteristic response to all nondepolarizing muscle
relaxants changes. Additional factors such as increased renal excretion and altered serum protein binding
cause a change in nondepolarizing muscle relaxant drug action. These pharmacologic changes include:
48



increased time to onset
reduced depression of neuromuscular function at a given mg/kg does
reduced duration of action
These effects usually develop one week after the injury and last five to six weeks depending on the
severity of the burn and other comorbid conditions. Succinylcholine will produce severe hyperkalemia
and cannot be administered beginning 24 hours after a burn and continuing through at least six months
after the burn. The duration of the hyperkalemic effect is not clear and it is probably prudent to choose a
nondepolarizing muscle relaxant even after this six-month interval.
Most burn patients experience rapid tolerance to opioids. The most effective opioid is methadone because
it has N-methyl-D-aspartate receptor antagonistic activity. The NMDA antagonism helps prevent central
sensitization, hyperalgesia, and neuropathic pain. Most patients do not develop rapid tolerance to
methadone. Fentanyl, a drug commonly used as a continuous infusion in the burn unit, is associated with
rapid tolerance, making it a less effective analgesic. Morphine administration has been reported to reduce
the frequency of posttraumatic stress disorder. Tolerance does develop, so it needs to be titrated “to
effect.”
REFERENCES
1.
Ryan CM, Schoenfeld DA, Thorpe WP, et al. Objective estimates of the probability of death from
burn injuries. N Engl J Med. 1998; 338:362-366.
2.
Woodenson LC, Sherwood ER, Morvant EM, et al. Anesthesia for burned patients. In: Herndon
DN. Total Burn Care. 2nd ed. Philadelphia: WB Saunders; 2002:183-206.
3.
Fleisher LA. Anesthesia and Uncommon Diseases. 5th ed. Philadelphia: Elsevier Saunders;
2006:535-546.
ITEM 44
Succinylcholine is an invaluable drug for anesthesiologists. It is the muscle relaxant of choice for rapid
sequence induction and also is useful for short surgical procedures. One disadvantage of the drug,
especially in healthy surgical outpatients, is a high incidence of postoperative myalgias. For decades,
anesthesiologists have used pretreatment with a variety of drugs to prevent both fasciculations and
myalgias. Of patients who do not receive any form of pretreatment, approximately 50% experience
postoperative myalgias after receiving succinylcholine.
A recent meta-analysis investigated drugs specifically administered for myalgia prevention as well as
drugs administered for anesthesia induction for their effects on succinylcholine-induced fasciculations
and myalgias. Many of the results confirmed the beliefs of anesthesiologists concerning the efficacy of
certain drugs, but some results challenged widely held opinions concerning the prevention of
fasciculations and myalgias. The authors did not find a clear correlation between the prevention of
fasciculations and the prevention of postoperative myalgias. Some drugs effectively reduced
fasciculations but not myalgias and the opposite occurred with other drugs.
The effects on fasciculation and myalgia prevention of various drugs used for induction of general
anesthesia are shown in Table 1. A higher dose of succinylcholine was associated with a lower incidence
49
of myalgias (63% with 1.0 mg/kg vs 45% with 1.5 mg/kg). Opioids had no effect on the incidence of
myalgias. Induction with propofol compared to thiopental appeared to increase the risk of developing
myalgias (65% with propofol vs 49% with thiopental),
Table 1. Impact of induction agent, opioids, and different succinylcholine doses on myalgia and
fasciculation. Used with permission, from Schreiber J, Lysakowski C, Fuchs-Buder T, et al. Prevention of
succinylcholine-induced fasciculation and myalgia. Anesthesiology. 2005; 103:877-884.
The effects of drugs that were administered specifically to prevent succinylcholine-induced myalgias are
depicted in Figure 1. NSAIDs were most effective in reducing myalgias although they did not prevent
fasciculations. Sodium channel blockers, including lidocaine, were also quite effective in decreasing the
incidence of postoperative myalgias. Small doses of nondepolarizing muscle relaxants are probably most
commonly used to prevent both fasciculations and myalgias. They are effective for both purposes.
However, when deciding whether to use one of these muscle relaxants or another agent, such as lidocaine
or an NSAID, to prevent myalgias, the anesthesiologist should consider that adverse effects related to
drug administration occurred more frequently with the nondepolarizing muscle relaxants. Some of these
adverse events were minor, including blurred vision and heavy eyelids, but others were more significant,
such as difficulty breathing and swallowing.
50
Figure 1. Prevention of succinylcholine-related myalgia at 24 hours. For each intervention that was tested
in at least three trials, a meta-analysis was performed (# = number of analyzed trials). Symbol sizes are
proportional to the number of analyzed patients. CI = confidence interval; NNT = number needed to treat;
NSAID = nonsteroidal antiinflammatory drug (aspirin, diclofenac); benzodiazepine (diazepam,
midazolam); sodium channel blocker (lidocaine, phenytoin); RB = relative benefit. Used with permission,
from Schreiber J, Lysakowski C, Fuchs-Buder T, et al. Prevention of succinylcholine-induced
fasciculation and myalgia. Anesthesiology. 2005; 103:877-884.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:491.
2.
Schreiber J, Lysakowski C, Fuchs-Buder T, et al. Prevention of succinylcholine-induced
fasciculation and myalgia. Anesthesiology. 2005; 103:877-884.
ITEM 45
The use of alternative medicine techniques, including acupuncture, is gaining wider acceptance by both
patients and health care professionals. In one study, more than 40% of patients expressed interest in
incorporating acupuncture into their perianesthetic care. An increasing number of insurance companies
now provide coverage for acupuncture treatment. Successful acupuncture therapy requires a trained
professional because the treatment is quite complex. The practitioner must know the precise acupuncture
point or points that must be stimulated to produce the desired therapeutic effect. In addition, the mode of
stimulation (eg, manual, electrical, or acupressure) also affects results.
Acupuncture has been proposed as a treatment for several conditions encountered in the perioperative
period, including preoperative anxiety, postoperative pain, and postoperative nausea and vomiting
(PONV). Currently the data are most promising for the use of acupuncture in reducing preoperative
anxiety and PONV. Randomized double-blinded studies that included patients who received sham
acupuncture found that the use of preoperative auricular acupuncture reduces preoperative anxiety and the
51
need for anxiolytic drugs. The relaxation produced by the acupuncture can last as long as 48 hours
postoperatively.
Acupuncture might also play a role in the treatment of postoperative pain although conflicting results
from different studies still make this treatment controversial. Investigators have determined that
acupuncture does stimulate the release of endogenous opioids and activates structures in the descending
antinociceptive pathway. In addition, some well-designed studies have demonstrated a significant
analgesic effect for acupuncture in the management of postoperative pain. However, other studies have
not found acupuncture to significantly reduce postoperative analgesic requirements. It has been suggested
that the conflicting results may have been due to differing skill levels among the acupuncturists,
especially since appropriate point selection and mode of stimulation are crucial in the success of
acupuncture when used to provide pain relief. Likely, acupuncture can provide effective analgesia but
requires a very high level of practitioner expertise that is not often available.
The use of acupuncture in the perioperative setting has gained widest acceptance in the prevention of
PONV. Many studies have documented the effectiveness of P6 point stimulation in reducing the
incidence of PONV. In fact, several investigations have found that acupuncture at the P6 point is as
effective as pharmacologic treatment with ondansetron for PONV prophylaxis. It has been shown,
however, that acupuncture is effective in reducing PONV only if it is initiated before the induction of
general anesthesia. Several modes of acupuncture stimulation have been used to prevent PONV, including
manual needle stimulation, electrical stimulation, and acupressure. Clearly, noninvasive techniques, such
as acupressure, require less practitioner skill and are better tolerated by patients. However, some data
suggest this method of acupuncture is not as effective in preventing PONV as the invasive techniques.
The use of intraoperative acupuncture to augment general anesthesia has also been investigated. However,
acupuncture does not reduce volatile anesthetic requirements during surgery.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:491.
2.
Chernyak GV, Sessler DI. Perioperative acupuncture and related techniques. Anesthesiology.
2005; 102:1031-1049.
ITEM 46
Hypothyroidism is commonly encountered by anesthesiologists since it occurs in approximately 5% of
the adult population. In adequately treated patients, anesthetic morbidity is not increased. However, when
caring for patients with hypothyroidism who have not been receiving treatment, the anesthesiologist
should be aware of the pathophysiologic processes and the anesthetic considerations they pose.
Cardiovascular consequences of hypothyroidism include:





bradycardia
decreased stroke volume and cardiac output
increased systemic vascular resistance
narrow pulse pressure
increased circulating catecholamine concentrations
52
Adverse responses that may occur in the overtly hypothyroid patient during the perioperative period will
affect decisions concerning anesthetic management. Effects to consider include:








increased sensitivity to sedative and opioid drugs
myocardial depression
slow drug metabolism
diminished responsiveness to baroreceptor reflexes
depressed ventilatory response to hypoxemia and hypercarbia
hyponatremia
impaired temperature regulation
adrenal insufficiency
It is advisable either to avoid preoperative sedative drugs or use them with caution in patients with
untreated hypothyroidism since they may have an increased sensitivity to the drugs and depressed
ventilatory responses to hypoxemia and hypercarbia. To avoid myocardial depression, the use of ketamine
for the induction of general anesthesia is sometimes recommended, although other induction agents have
been used successfully. Hypothyroidism does not significantly decrease the minimum alveolar
concentration of volatile anesthetics.
Prevention of hypothermia is a major goal in the anesthetic management of patients with inadequate
thyroid function. All modalities to maintain body temperature, including the use of forced-air warming
blankets and intravenous fluid warmers, should be used. Temperature monitoring should be utilized.
The inappropriate secretion of antidiuretic hormone that is associated with hypothyroidism leads to
impaired clearance of free water, which places these patients at increased risk for developing
hyponatremia. Therefore, hypotonic intravenous fluids should not be administered.
Patients with hypothyroidism have an increased incidence of adrenal insufficiency as well as a reduce
adrenocorticotropic hormone response to stress. Therefore, many endocrinologists recommend that these
patients receive stress doses of steroids in the perioperative period.
REFERENCES
1.
Stoelting RK, Dierdorf SF. Anesthesia and Co-Existing Disease. 4th ed. New York: Churchill
Livingstone; 2002:417-420.
2.
Farling PA. Thyroid disease. Br J Anaesth. 2000; 85:15-28.
ITEM 47
Modulation of the renin-angiotensin-aldosterone system (RAAS), a physiologic system that regulates
blood pressure and water salt homeostasis, has become increasingly common treatment for a wide variety
of comorbid conditions. There are two angiotensin II receptor subtypes. Stimulation of the angiotensin II
type 1 (AT1) receptor acts to increase blood pressure by direct vasoconstriction and by increasing the
sympathetic nervous system activity. Renal effects of AT1 activation are sodium and water reabsorption,
potassium excretion, aldosterone release, and vasoconstriction of the afferent glomerular arterioles. Longterm cardiac effects include vascular and cardiac muscle hypertrophy progressing to fibrosis and
endothelium dysfunction. Endothelium dysfunction increases plasminogen activator inhibition, increases
53
intravascular thrombosis, and activates inflammatory cytokines. AT2 receptor activation antagonizes and
reduces the effect of AT1 receptors.
REFERENCES
1.
Park KW. Angiotensin-converting enzyme inhibitors, AG receptor blockers, and aldosterone
receptor antagonists. Int Anesthesiol Clin. 2005; 43(2):23-37.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:627628, 659, 792-793, 796, 1486.
ITEM 48
With better understanding of the complex actions of the renin-angiotensin-aldosterone system (RAAS),
drug modulation of the system has increased. Three categories of RAAS drugs are available: angiotensinconverting enzyme (ACE) inhibitors (eg, ramipril, captopril, lisinopril), ACE receptor blockers or ARBs
(eg, losartan, irbesartan), and angiotensin receptor antagonists or ARAs (eg, spironolactone, which is
nonspecific, and eplerenone, which is specific for kidney, brain, and blood vessels). Drugs modulating the
RAAS have been generally found to have beneficial systemic effects at doses that do not affect blood
pressure. Consequently, an increasing number of hypertensive patients as well as nonhypertensive
patients with chronic diseases like diabetes, renal disease, or cerebrovascular disease will arrive for
surgery taking RAAS medications. Recent international randomized control trials have demonstrated
large relative-risk reductions in mortality, morbidity, and disease regression for patients taking RAAS
drugs; thus, careful consideration must be given to the risks of discontinuing these drugs versus the
benefit of reducing possible anesthetic drug interaction.
When compared to placebo controls, beneficial effects of ACE inhibitors and ARBs include relative risk
reductions of up to 39% in cardiac mortality and morbidity in patients with





myocardial infarction (MI)
congestive heart failure (CHF)
myocardial dysfunction
hypertension
stroke
ARAs, primarily spironolactone and eplerenone, have only been found to reduce symptoms and
hospitalizations for CHF.
In a patient with cerebrovascular disease, the risk of stroke is reduced with diuretics, calcium channel
blockers, and ARBs.
RAAS activity can lead to nephropathy characterized by proteinuria and loss of functioning glomeruli.
Administration of ACE inhibitors and ARBs has been shown to slow the progression of renal failure,
particularly in diabetic patients. Some large randomized controlled trials (RCTs) have reported regression
of renal disease.
Obesity is associated with diabetes, hypertension, stroke, and renal disease, all chronic diseases that may
be treated with RAAS-modifying drugs. Adiponectin, a hormone produced by adipocytes to regulate
energy metabolism, is downregulated in obese individuals. This reduction leads to decreased insulin
54
sensitivity and increased atherosclerosis. Leptin, another hormone produced by adipocytes, acts to insulin
sensitivity and increases adiponectin. Leptin, another hormone produced by adipocytes, acts to increases
renin, angiotensin, and aldosterone levels. Administration of ACE inhibitors and ARBs increases insulin
sensitivity and increases adiponectin. Use of ACE inhibitors for treatment of hypertension in insulindependent diabetic patients has been found to reduce serum glucose. In large RCTs, obese hypertensive
patients when treated with ACE inhibitors were significantly less likely to develop diabetes than patients
treated with diuretics or beta-blockers.
A large body of research supports increased use of RAAS-modifying drugs for common chronic diseases.
This class of drugs has been associated with significant systemic hypotension with the induction of
anesthesia, in some cases refractory hypotension. Modification of anesthetic technique by reducing drug
doses and increasing fluid administration has been advocated. Treatment of refractory hypotension with
drugs that act directly by stimulation of sympathetic nervous system receptors (eg, norepinephrine,
epinephrine) or vasopressin (eg, arginine vasopressin) has been reported to be effective. To date there has
been little research into this area. Single intraoperative doses of ACE inhibitors have been shown in small
studies to reduce myocardial injury and improve postoperative renal function following coronary artery
bypass graft surgery or infrarenal aortic surgery. RAAS drugs may become important perioperative
management tools for anesthesiologists.
REFERENCES
1.
Park KW. Angiotensin-converting enzyme inhibitors, AG receptor blockers, and aldosterone
receptor antagonists. Int Anesthesiol Clin. 2005; 43(2):23-37.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:627628, 659, 792-793, 796, 1486.
ITEM 49
Heparin is a naturally occurring mucopolysaccharide that binds with antithrombin III (AT III) forming a
complex. Thrombin is an enzyme in the coagulation cascade that converts fibrinogen to fibrin, induces
platelet aggregation, and activates coagulation factors V, VIII, and XIII. Heparin also binds to factors
IXa, Xa, XIa, and XIIa but not fibrin.
The AT III/thrombin complex is rapidly removed from the circulation. Heparin therapy can reduce
plasma AT III to 60% of normal within 24 hours. Adequate levels of AT III are necessary for heparin
activity. The presence of AT III deficiency will attenuate heparin response and may produce
circumstances where anticoagulation may be inadequate; for instance, prior to instituting
cardiopulmonary bypass. AT III levels can be supplemented by infusion of AT III concentrate or fresh
frozen plasma.
Heparin-induced thrombocytopenia is increasingly recognized as a serious clinical occurrence that can
result in acute ischemia from arterial thrombosis. The frequency ranges from 1% to 5% in different
surgical populations. Thrombocytopenia alone is found in approximately 20% of intensive care patients.
Unfortunately, the currently available diagnostic tests (serotonin release assay and heparin-platelet factor
4 enzyme linked immunosorbent assay) used to distinguish thrombocytopenia from the more serious
condition of heparin-induced thrombocytopenia are nonspecific and expensive.
Arterial thrombosis in heparin-induced thrombocytopenia may be treated with the direct thrombin
inhibitors agratroban and lepirudin. Both are approved for use in patients in whom there is a suspicion or
diagnosis of heparin-induced thrombocytopenia.
55
Protamine is the only commercially available compound to reverse heparin. Protamine binds free heparin
in the circulation by a simple acid-base neutralization (heparin is an acid, protamine a base). Protamine
has a shorter half-life than heparin, which may sometimes result in a “rebound” heparin effect when
sequestered heparin reenters the systemic circulation and is no longer subject to protamine neutralization.
Protamine itself has significant unwanted clinical side effects. It may cause systemic hypotension,
pulmonary hypotension, and anaphylaxis.
Pharmacologic preparations of heparin are derived from porcine intestines and bovine lung, with a large
variation in individual heparin molecular weight ranging from 10,000 to 30,000 Daltons. Standardization
attempts by the US Pharmacopoeia notwithstanding, the heterogeneous nature of commercially prepared
heparin results in variable pharmacologic effects. Thus, measurement of anticoagulant activity is
necessary.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:1116.
2.
Hoppensteadt D, Walenga JM, Fareed J, et al. Heparin, low-molecular-weight heparins, and
heparin pentasaccharide: Basic and clinical differentiation. Hematol Oncol Clin North Am. 2003;
17(1):313-341.
3.
Hassell K. The management of patients with heparin-induced thrombocytopenia who require
anticoagulant therapy. Chest. 2005; 127(2 Suppl):1S-8S.
4.
Kaplan JA, Reich DL, Konstadt SN. Cardiac Anesthesia. 5th ed. Philadelphia: Elsevier Saunders;
2006:813-815.
ITEM 50
Clinical scenario: Following abdominal surgery for a ruptured gallbladder, a 67-year-old male develops
sepsis and severe disseminated intravascular coagulation (DIC).
Disseminated intravascular coagulation (DIC) is caused by a variety of clinical disorders, most of which
are associated with inflammatory activation. DIC can lead to massive systemic activation of coagulation,
intravascular deposition of fibrin in the microvasculature, and simultaneous consumption of coagulation
factors and platelets. Widespread microvascular thrombosis as well as profuse bleeding from various sites
can occur.
In recent years, the mechanisms involved in pathological microvascular fibrin deposition in DIC have
become increasingly clear. Various clinical disorders trigger the release of pro-inflammatory cytokines
such as interleukin-6 (IL-6), tissue necrosis factor-α (TNF-α), and IL-1, which leads to the following:



Tissue-factor-mediated activation of coagulation
Inhibition of physiologic anticoagulation pathways
Depression of fibrinolysis due to high levels of plasminogen activator inhibitor type 1 (PAI-1)
These in turn lead to enhanced fibrin formation and impaired fibrin degradation, ultimately resulting in
microvascular thrombosis. Microvascular thrombosis can then lead to end-organ injury and failure.
56
Platelets and coagulation factors are generally consumed in DIC; thrombocytopenia is common in these
patients.
Figure 1. Pro-inflammatory cytokine pathways in DIC. Modified, from Levi M, de Jonge E, van der Poll
T. New treatment strategies for disseminated intravascular coagulation based on current understanding of
the pathophysiology. Ann Med. 2004; 36:41-49.
REFERENCES
1.
Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006:237-238.
2.
Levi M, de Jonge E, van der Poll T. New treatment strategies for disseminated intravascular
coagulation based on current understanding of the pathophysiology. Ann Med. 2004; 36:41-49.
3.
Franchini M, Manzato F. Update on the treatment of disseminated intravascular coagulation.
Hematology. 2004; 9:81-85.
4.
Levi M, de Jonge E, van der Poll T. Therapeutic intervention in disseminated intravascular
coagulation: Have we made any progress in the last millennium? Blood Rev. 2002; 16(suppl
I):S29-S34.
5.
Stoelting RK, Dierdorf SF. Anesthesia and Co-Existing Disease. 4th ed. New York: Churchill
Livingstone; 2002:496-497.
ITEM 51
Pneumoperitoneum, patient position, hypercarbia, and anesthesia all combine to cause the cardiovascular
responses observed during laparoscopy. The pertubations generally include decreased cardiac
output/cardiac index, increased systemic and pulmonary blood pressures, and increased systemic and
57
pulmonary vascular resistances. The change in cardiac output/index is initially proportional to increasing
the intraabdominal pressure but improves gradually over the course of the procedure. It is postulated that
surgical stress associated with increase in serum concentrations of catecholamines, angiotensin-renin, and
vasopressin contributes to the improved cardiac output/index and increased vascular resistance. Serum
concentrations of endogenous vasopressin correlate with changes in vascular resistance. Release of
vasopressin and catecholamines may also be related to increases in intrathroacic pressure and mechanical
stimulation of peritoneal stretch receptors. The initial reduction in cardiac output/index is usually
attributed to venal caval compression causing decreased venous return, increased venous vascular
resistance, and pooling of blood in the legs, especially when patients are in reverse Trendelenburg
position. A fluid bolus of 500 mL prior to insufflation increases intravascular volume and ameliorates the
decrease in cardiac index. This improvement in cardiovascular parameters augments perfusion and
potentially reduces complications in patients with severe cardiac disease. The decreased venous return
associated with peritoneal insufflation is attenuated in the Trendelenburg position.
The basic pattern of cardiovascular change is similar in healthy adults and patients with significant
cardiovascular disease but the quantitative effects and the physiologic consequences are greater and less
predictable in the cardiac patient. Management is more difficult since standard measures of cardiovascular
function (eg, ejection fraction as measured by echocardiography, cardiac filling pressures as measured by
pulmonary artery catheter) are not reliable during laparoscopy. Postoperative congestive heart failure
from fluid overload has been reported to occur due to the difficulty in estimating intravascular volume
while administering fluids and vasopressors to maintain adequate cardiac output.
Cardiac dysrhythmias are not common during an uncomplicated laparoscopy. If a dysrhythmia occurs, it
is more likely to be a bradydysrhythmia due to stretching of the peritoneum. Intense vagal stimulation,
especially in a beta-blocked patient, has been reported to result in asystole. Rapid deflation of the
abdomen and atropine are effective treatments. Complications such as venous gas embolism can also
cause a severe bradycardia and cardiac arrest.
REFERENCES
1.
Joris JL, Noirot DP, Legrand MJ, et al. Hemodynamic changes during laparoscopic
cholecystectomy. Anesth Analg. 1993; 76:1067-1071.
2.
Giebler RM, Behrends M, Steffens T, et al. Intraperitoneal and retroperitoneal carbon dioxide
insufflation evoke different effects on caval vein pressure gradients in humans: Evidence for the
Starling resistor concept of abdominal venous return. Anesthesiology. 2000; 92:1568-1580.
3.
Hirvonen EA, Poikolainen EO, Paakkonen ME, et al. The adverse hemodynamic effects of
anesthesia, head-up tilt, and carbon dioxide pneumoperitoneum during laparoscopic
cholecystotomy. Surg Endosc. 2000; 14:272-277.
4.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:22902293.
ITEM 52
Severe acute respiratory syndrome (SARS) is a prototypical highly contagious respiratory disease in
which the infectious agent is transmitted by close contact. Examples of circumstances believed to be
associated with transmission of SARS include:
58


direct contact with expiratory secretions or bodily fluids (sharing eating/drinking utensils, talking
within three feet, direct body contact)
exposure to large droplets (generated by talking, coughing, sneezing, singing) or bodily fluids
Tracheal intubation is classified as an “aerosol-generating procedure” and is associated with an especially
high risk of transmission of SARS to the health care worker.
Isolation should include placing the patient in a negative pressure isolation room (where pressure in the
room is less than pressure in the adjacent hallways) to minimize contamination of the surrounding
environment. A surgical mask should be placed over the nose and mouth of the patient to trap large
particles. All personnel entering the room should use full barrier precautions (disposable gown, gloves,
and goggles). Care givers should wear a disposable, fit-tested mask conforming to the N95 standard of the
National Institute for Occupational Safety and Health. Masks conforming to this standard maintain a 95%
efficiency in removing organisms from the air. Placement of a surgical mask under the N-95 mask will
allow unfiltered air to enter beneath the mask, defeating the purpose of the device. Handwashing should
occur regardless of contact with the patient and even if gloves have been worn on entering the room.
Information about the transmission of SARS and recommended isolation precautions may be found at
Web sites for the Centers for Disease Control and Prevention (www.cdc.gov), the World Health
Organization (www.who.int/en/), and the International Society of Infectious Diseases (www.isid.org/).
REFERENCES
1.
Stackhouse RA. Severe acute respiratory syndrome and tuberculosis. Anesthesiol Clin North
America. 2004; 22:437-455.
2.
Goldman L, Ausiello DA. Cecil Textbook of Medicine. 22nd ed. Philadelphia: WB Saunders;
2004:552-554.
3.
Fink MP, Abraham E, Vincent J-L, et al. Textbook of Critical Care. 5th ed. Philadelphia: Elsevier
Saunders; 2005:656.
ITEM 53
A 74-year-old male remains on mechanical ventilation two weeks after undergoing an exploratory
laparotomy for ischemic bowel. To maintain adequate oxygenation and ventilation, he is receiving
mechanical ventilation with the following settings: FIO2 0.4, synchronized intermittent mandatory
ventilation (SIMV) rate of 6/min, tidal volume 700 mL, pressure support 10 cm H2O, positive endexpiratory pressure (PEEP) 5 cm H2O. He is in respiratory distress with a total respiratory rate of 36
breaths/min; spontaneous tidal volumes are less than 150 mL. His SPO2 is 94%.
Assuming the patient’s respiratory rate is being driven by a normal carbon dioxide response, ventilatory
maneuvers that augment minute ventilation will decrease the patient’s spontaneous respiratory rate. This
objective could be achieved by


increasing the ventilator (SIMV) rate and/or
increasing the pressure support, which would result in increased spontaneous tidal volumes.
59
Decreasing the delivered mechanical ventilator breaths to 4/min would decrease the patient’s minute
ventilation and would be more likely to result in an increased respiratory rate.
Increasing the FIO2 from to 0.4 to 0.6 may increase the patient’s PaO2 but would not be likely to decrease
the patient’s respiratory rate unless his respirations were being driven by hypoxemia, which is unlikely
when SPO2 is 94%. Increasing PEEP from 5 to 10 cm H2O would have this same effect.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:28202828.
2.
Calfee CS, Matthay MA. Recent advances in mechanical ventilation. Am J Med. 2005; 118:584591.
3.
Prinianakis G, Kondili E, Georgeopolous D. Patient-Ventilator Interactions. An overview. Resp
Care Clin N Am. 2005; 11:201-224.
ITEM 54
Elderly patients of similar chronological age present with a wide range of physiologic responses to a
similar illness or injury. The elderly have been subdivided into three groups depending on their biologic
age in an attempt to categorize expected responses to life stresses.



Elderly
Aged
Very old
65-74 years
75-84 years
85+ years
The best predictor to and recovery from a new life stress, such as a surgical procedure, is not
chronological age but instead the pre-event level of life functioning. Cognitive function plays an
important role in recovery. At 65 years of age, 6%-8% of patients will have clinically detectable
dementia. Any cognitive impairment decreases a patient’s ability to report illness, leading to greater
severity prior to diagnosis, and decreases his or her ability to actively participate in rehabilitation efforts.
Postoperative dementia and quality of life outcome are predicted by preoperative mental status. Results of
the Mini-Mental State Exam (found at www.fpnotebook.com/NEU75.htm) may help the anesthesiologist
prepare the family for changes in cognitive function and prevent the assumption that a change in cognitive
function is solely related to anesthetic management. A Mini-Mental State Exam may also help establish if
the patient can comprehend and grant informed consent.
The most significant independent risk factor for perioperative morbidity and mortality is emergency
surgery. With elective surgery, medical management of preexisting comorbidities can be optimized, thus
significantly improving outcome. All major systemic diseases (eg, cardiac, renal, pulmonary), poor
nutritional status, and living in a care facility are associated with increased perioperative morbidity.
Surgical procedure is also an independent predictor of outcome and has been divided by the American
College of Cardiology/American Heart Association into risk categories for cardiac events or death from
cardiac events (Table 1).
60
Table 1. Categories of perioperative risk based on surgical procedures.
Category
Risk of death or MI
Surgical procedure/event
High
> 5%
Emergency, all vascular surgery,
procedures with large fluid shifts
(eg, Whipple)
Intermediate
5%-1%
Moderately invasive (eg, carotid
endarterectomy, radical neck,
short thoracic, or abdominal
procedures, transurethral
resection, orthopedic procedures)
Low
< 1%
Noninvasive procedures (eg,
endoscopy, sigmoidoscopy,
cataracts, mastectomy)
MI, myocardial infarction
Involuntary weight loss of greater than 10 pounds over the previous six months is associated with poor
outcome. In the elderly malnutrition occurs in approximately 17% of women and 11% of men living
independently in the community and in 15%-26% of patients in nursing homes. Malnutrition is defined by
some of the following signs: hypoalbuminemia, involuntary weight loss, hypcholesterolemia, vitamin
deficiency, and abnormal (high or low) body mass index. It is important to remember that obese patients
may have substantial nutritional deficiency.
REFERENCES
1.
John AD, Sieber FE. Age associated issues: Geriatrics. Anesthesiol Clin North America. 2004;
22:45-58.
2.
Eagle KA, Brundage BH, Chaitman BR, et al. Guidelines for perioperative cardiovascular
evaluation for noncardiac surgery. Report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines. Committee on Perioperative
Cardiovascular Evaluation for Noncardiac Surgery. Circulation. 1996; 93:1278-1317.
3.
Eagle KA, Berger PB, Calkins H, et al. ACC/AHA guideline update for perioperative
cardiovascular evaluation for noncardiac surgery—executive summary. A report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines.
Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for
Noncardiac Surgery. Circulation. 2002; 105:1257-1267. This report is also available online at:
http://www.americanheart.org/presenter.jhtml?identifier=3000370. Accessed August 2006.
4.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:2440,
2444.
61
ITEM 55
A history of complaints by more than one family member of weakness and muscle stiffness (myotonia)
following exertion is suggestive of familial hyperkalemic periodic paralysis. It is an autosomal dominant
disorder characterized by muscle weakness several hours after vigorous exercise or with hypoglycemia.
The paralysis rarely lasts more than several minutes to hours and never involves the respiratory muscles.
Some patients also complain of mild myotonia (sustained muscle contraction) after exercise. High
potassium intake can also precipitate the syndrome: consequently, avoiding drugs such as potassium salts
of common antibiotics or intravenous fluids that contain potassium is important. Respiratory acidosis
during spontaneous ventilation at the end of an anesthetic can also increase potassium sufficiently to
initiate the symptoms of hyperkalemic periodic paralysis. Succinylcholine increases serum potassium,
making its administration contraindicated. There is no information regarding the administration of
nondepolarizing muscle relaxants. Based on common sense rather than evidence, textbooks recommend
caution when administering nondepolarizing muscle relaxants and careful neuromuscular blockade
monitoring in part because the actual cause of postoperative hyperkalemia or paralysis may be unclear.
Standard volatile anesthetics, sedatives, and induction drugs have not been reported to trigger
hyperkalemic periodic paralysis. Shivering in these patients can initiate hyperkalemia, so care to maintain
normothermia and prophylactic treatment of shivering is advised. Serum glucose should be maintained
above 100 mg/dL.
REFERENCES
1.
Levitt J, Cochran P, Jant Jankowlak J. Attacks of immobility cause by diet or exercise? The
mystery of periodic paralysis. Neurology. 2004; 63:E17-E18. Available online at
www.neurology.org. Accessed August 2006.
2.
Fontaine B, Vale-Santos J, Jurkat-Rott K, et al. Mapping of the hypokalemic periodic paralysis
(HypoPP) locus to chromosome 1q31-32 in three European families. Nat Genet. 1994; 6:267-272.
3.
Naguib M, Flood P, McArdle JJ, et al. Advances in neurobiology of the neuromuscular junction:
Implications for the anesthesiologist. Anesthesiology. 2002; 96:202-231.
4.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:538,
543-546, 1098-1099.
ITEM 56
Cigarette smoking is one of the few preexisting conditions that can be modified in the preoperative
period, leading to a decrease in the incidence of postoperative pulmonary complications. Smoking
cessation the evening prior to surgery does not improve outcome. However, for high-risk patients
requiring elective surgery, time-related smoking cessation leads to stepwise improvement in pulmonary
function and reductions in postoperative pulmonary complications (Table 1).
It has been long recognized that to be effective smoking cessation must occur at least eight weeks prior to
elective surgery. Patients who discontinue smoking eight or more weeks before surgery have a reduced
likelihood of developing postoperative respiratory complications (eg, pneumonia, hypoxia, postoperative
ventilation). Shorter time periods have an effect on short-term measures, but there is no improvement in
62
long-term outcome. Smoking cessation for 48 hours is associated with a decrease in carboxyhemoglobin
concentration and an increase in ciliary activity. Smoking cessation for one to two weeks is associated
with a decrease in sputum production. Patients who abstain from smoking four to six weeks have
improved pulmonary function tests, a reduction in previous smoking symptoms (eg, chronic cough) and
an improved sense of well being. Smoking cessation for more than two months does not further decrease
postoperative respiratory risk but does eventually improve general health and long-term survival.
Table 1. Effect of smoking cessation on pulmonary physiology and the development of postoperative
pulmonary complications in a patient with 20 plus years of smoking history.
Smoking Cessation Interval
Physiologic Effect
Risk Reduction
< 24 hours
Nicotine withdrawal symptoms
None reported
48 hours
Decreased cardiovascular
stimulant effect
None reported
Carboxyhemoglobin normal
Improved ciliary activity
1-2 weeks
Decreased sputum
None reported
4-6 weeks
Improved pulmonary symptoms
None reported
Improved pulmonary function
tests
> 8 weeks
No further change
Decreased incidence of
postoperative pulmonary
complications
REFERENCES
1.
Rock P, Rich PB. Postoperative pulmonary complications. Current Opinion in Anaesthesiology.
2003; 16:123-131.
2.
Bluman LG, Mosca L, Newman N, et al. Preoperative smoking habits and postoperative
pulmonary complications. Chest. 1998; 113:883-889.
3.
Warner MA, Offord KP, Warner ME, et al. Role of preoperative cessation of smoking and other
factors in postoperative pulmonary complications: A blinded prospective study of coronary artery
bypass patients. Mayo Clin Proc. 189; 64:609-616.
63
4.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:10851089.
5.
Fleisher LA. Evidence-Based Practice of Anesthesiology. Philadelphia: Elsevier Saunders;
2004:57-61.
ITEM 57
Mean values for heart rate in normal children are presented in Table 1. The mean heart rate for a 24-hourold neonate is approximately 120 beats/min; the mean heart rate for a 30-day-old infant is approximately
160 beats/min.
Table 1. Normal heart rate for children up to 1 year of age.
Age
Mean Heart Rate (beats/min)
< 24 hours
120
1-7 days
135
1 week-1 month
160
3-12 months
140
Normal cardiac output for a neonate is approximately three times that of an adult and ranges from 200 to
325 mL∙kg-1∙min-1.
Normal blood pressure (50th percentile) for a 1-month-old is approximately 85/50 mm Hg. Even at the
25th percentile, normal blood pressure should be approximately 80/50 mm Hg.
The fact that the pulmonary artery pressure exceeds the aortic pressure in utero results in right ventricular
predominance with a consequent right-sided QRS axis. After birth gradual hypertrophy of the left
ventricle results in a shift of the QRS axis. Although T waves are upright across the precordium at birth,
they become isoelectric within a few hours. By 1 week of age, T wave inversion from V1 to V4 is normal.
REFERENCES
1.
Coté CJ, Todres ID, Goudsouzian NG, et al. A Practice of Anesthesia for Infants and Children.
3rd ed. Philadelphia: WB Saunders; 2001:15-16.
2.
Kay JD, Sinaiko AR, Daniels SR. Pediatric hypertension. Am Heart J. 2001; 142:422-432.
ITEM 58
Duchenne dystrophy, a sex-linked recessive trait, occurs in 1 in 3,500 live births and is the most common
form of muscular dystrophy. A child with Duchenne dystrophy generally presents with proximal muscle
weakness, most commonly initially manifested as frequent falls, difficulty climbing stairs, and an
abnormal gait; the ability to ambulate is usually lost before 12 years of age. Involvement of muscles of
64
the trunk leads to thoracolumbar scoliosis; contractures occur with unequal involvement of different
muscle groups. Virtually all muscles, including the myocardium, are involved. The diagnosis is usually
not established until 5 years of age.
Deep tendon reflexes are depressed in patients with Duchenne dystrophy; by 10 years of age almost half
of these children will have lost the deep tendon reflexes of proximal muscles.
Up to 70% of patients with muscular dystrophy will have some cardiac abnormality. Involvement of the
myocardium results in a dilated cardiomyopathy; scarring of the left ventricle, especially the posterobasal
portion, may also occur and present as tall R waves in the right precordium with deep Q waves on the left
as well as decreased left ventricular ejection fraction. Involvement of the papillary muscle may lead to
mitral regurgitation. The aortic valve is usually not involved in patients with Duchenne dystrophy.
Although compromise of respiratory muscle function can often be documented by age 10, diaphragmatic
function is initially adequate. Weakness of the respiratory muscles results in an increased incidence of
pneumonia by the third decade of life.
Gastric emptying time is reported as prolonged in patients with Duchenne dystrophy, placing them at risk
for possible regurgitation and aspiration.
REFERENCES
1.
Fleisher LA. Anesthesia and Uncommon Diseases. 5th ed. Philadelphia: Elsevier Saunders;
2006:304-306.
2.
Bosser G, Lucron H, Lethor JP, et al. Evidence of early impairments in both right and left
ventricular inotropic reserves in children with Duchenne’s muscular dystrophy. Am J Cardiol.
2004; 93:724-727.
3.
Bahler RC, Mohyuddin T, Finkelhor RS, et al. Contribution of Doppler tissue imaging and
myocardial performance index to assessment of left ventricular function in patients with
Duchenne’s muscular dystrophy. J Am Soc Echocardiogr. 2005; 18:666-673.
ITEM 59
It has been estimated that over 400,000 patients have a lower extremity total joint replacement annually;
some form of cement, commonly methylmethacrylate, is used in the majority of these procedures.
Hemodynamic complications associated with total joint replacement may occur as a result of
embolization of fat or cement. Animal studies have documented profound vasodilation with intravenous
administration of methylmethacrylate. Laboratory studies have also demonstrated a significant decrease in
contractility in cardiac muscle exposed to this compound. Other possible causes of hypotension (eg,
release of complement or prostaglandins) also occur in a clinical setting. Adequate volume loading seems
to have resulted in a decreased incidence of hypotension occurring in association with cementing of
prostheses. The fact that patients undergoing hip prosthesis surgery using cement have a higher incidence
of hypotension than patients in whom cement is not used suggests that methylmethacrylate presents a
significant risk independent of other factors. Studies evaluating patients undergoing total joint
65
replacement report decreased systemic vascular resistance, decreased cardiac output, and decreased
cardiac preload (attributed to venodilation) occurring with use of cement.
Embolization, presumably of cement as well as fat, occurs in most patients undergoing total arthroplasty
of the hip or knee. Some authors have documented the occurrence of embolization during total knee
replacement even while a tourniquet remains inflated. Embolization to the lungs, whether of fat or
cement, decreases the cross-sectional area of the pulmonary circulation producing an increase in
pulmonary vascular resistance. Decreased oxygenation is a common finding during the procedure and in
the postoperative period—up to 28% of patients undergoing total hip arthroplasty are reported to
experience a clinically significant increase in shunt fraction. The etiology of the hypoxemia (embolism of
air, fat, or cement vs. atelectasis) has been the subject of debate.
REFERENCES
1.
Kim KJ, Chen da G, Chung N, et al. Direct myocardial depressant effect of methylmethacrylate
monomer: Mechanical and electrophysiologic actions in vitro. Anesthesiology. 2003; 98:11861194.
2.
Kato N, Nakanishi K, Yoshino S, et al. Abnormal echogenic findings detected by transesophageal
echocardiography and cardiorespiratory impairment during total knee arthroplasty with
tourniquet. Anesthesiology. 2002; 97:1123-1128.
3.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:2417.
ITEM 60
Ketamine, a derivative of phencyclidine, produces amnesia and profound analgesia in what has been
termed “dissociative anesthesia,” where the patient’s eyes may remain open, sometimes with a slow
nystagmus, but the patient remains noncommunicative. Although generally available as a racemic
mixture, S(+)-ketamine has the following advantages over either R(-)-ketamine or the racemic mixture:




superior analgesia
faster recovery
decreased salivation
lower incidence of emergence delirium
Ketamine’s primary site of action is on the N-methyl-D-aspartate (NMDA) receptors. Ketamine may also
have effects at opioid receptors, muscarinic receptors, and sodium channels. Ketamine’s effect on
GABAA receptors is weak.
Ketamine undergoes extensive hepatic metabolism, primarily via the cytochrome P-450 enzymes, with a
high rate of hepatic clearance (1 L/min). Norketamine, the metabolic product of this process, has some
activity (up to one third that of the parent compound) and has been theorized to be the etiology of
prolonged analgesia following ketamine administration. Less than 5% of an intravenous dose of ketamine
is excreted unchanged by the kidneys.
66
The rapid onset of action of ketamine is due in part to the relatively small amount of protein binding,
including binding to albumin. High lipid solubility and distribution to highly perfused tissues contribute
to the fact that concentrations in the brain may be four to five times greater than concentrations in the
plasma. Increased cerebral blood flow resulting from ketamine may also contribute to the high levels that
occur in the brain.
Increased rate of metabolism, with associated tolerance, has been reported to follow as little as two
exposures to ketamine within a short period of time.
REFERENCES
1.
Stoelting RK, Hillier SC. Pharmacology and Physiology in Anesthetic Practice. 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2006:167-169.
2.
Tobias JD. Tolerance, withdrawal, and physical dependency after long-term sedation and
analgesia of children in the pediatric intensive care unit. Crit Care Med. 2000; 28:2122-2132.
3.
Swenson JD, Davis JJ, Johnson KB. Postoperative care of the chronic opioid-consuming patient.
Anesthesiol Clin North America. 2005; 23:37-48.
ITEM 61
Although infrequent, entrapment of the suprascapular nerve may occur when an anesthetized patient is in
the lateral decubitus position. Ventral shift of a patient in the lateral position may shift the dependent arm
into a more ventromedial position with resulting displacement of the scapula. If the nondependent arm is
not allowed to rotate freely with the patient (eg, supported with pillows or on an armrest attached to the
bed) but is instead supported in a manner that results in the nondependent arm being in a relatively fixed
position (eg, attached to a bar supporting the anesthesia screen), dorsal shift of the patient may also result
in ventromedial rotation of the arm. Either circumstance may result in entrapment of the suprascapular
nerve under the transverse scapular ligament at the suprascapular notch. Involvement of sensory fibers to
the glenoacromial and acromioclavicular joints result in complaints of pain at the superior border of the
scapula, sometimes described as radiating into the shoulder. Movement of the shoulder, especially
adduction of the arm, may exacerbate pain. Physical examination may reveal tenderness at the point of
entrapment and weakness during abduction and external rotation of the shoulder.
Patients with repetitive motions of the shoulder (eg, baseball pitchers, volleyball players, weight lifters)
have a relatively high incidence of entrapment of the suprascapular nerve at the spinoglenoid notch.
Because the sensory fibers of the suprascapular nerve exit before the nerve reaches this location,
entrapment at the spinoglenoid notch results in weakness of the infraspinatus muscle without complaints
of pain.
Although stretch injuries are the most common cause of brachial plexus trauma during anesthesia, in the
lateral decubitus position the brachial plexus on the dependent side is more vulnerable than the
nondependent side to compression injuries. Injury to the musculocutaneous nerve would be expected to
produce loss of flexion at the elbow and a sensory deficit over the radial aspect of the forearm. Injury to
the axillary nerve would be expected to produce loss of arm abduction and sensory deficits of the lateral
67
shoulder. Injury to the long thoracic nerve produces paralysis of the serratus anterior muscle, which
results in restriction of abduction and inability to flex the arm above the level of the shoulder.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:1156.
2.
Shapiro BE, Preston DC. Entrapment and compressive neuropathies. Med Clin North Am. 2003;
87:663-696.
ITEM 62
The prevalence of asthma has increased dramatically; it is estimated that during the last 20 years the
prevalence of asthma in children has doubled and that between 15% and 30% of children in “developed”
countries have this disease. The primary pathophysiology associated with asthma is decreased air flow
during exhalation. Airway inflammation or contraction of bronchial smooth muscle may result in gas
trapping and hyperinflation, which manifest as chest “tightness” and wheezing.
Tracheal intubation may precipitate bronchospasm, especially if the patient is lightly anesthetized.
Ventilatory strategies that permit increased expiratory time facilitate exhalation. Decreasing respiratory
rate increases expiratory time and, if tidal volume is kept constant, is associated with a decrease in
hyperinflation. Decreasing tidal volume means that less gas must be exhaled after each breath and, if
respiratory rate is kept constant, is associated with a decrease in hyperinflation. A combination of
decreased tidal volume and decreased respiratory rate with resultant hypercapnia may be necessary to
prevent air trapping and the associated risk of volutrauma. Decreased inspiratory time may result in
increased peak airway pressures but should allow more time for exhalation and thus decrease
hyperinflation. Decreased expiratory time will result in increased lung hyperinflation and worsening of
wheezing.
REFERENCES
1.
Mason RJ, Broaddus VC, Murray JF, et al. Murray & Nadel’s Textbook of Respiratory Medicine.
4th ed. Philadelphia: Elsevier Saunders; 2005:1198.
2.
Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006:808-809.
3.
Rodrigo GJ, Rodrigo C, Hall JB. Acute asthma in adults: A review. Chest. 2004; 125:1081-1102.
ITEM 63
In 1987 a committee of the North American Society of Pacing and Electrophysiology (now known as the
Heart Rhythm Society) and the British Pacing and Electrophysiology Group developed a standard
nomenclature consisting of five letters to describe the function of pacemakers. The initial
recommendations were revised in 2002. The significance of each position and the possible designations
are presented in Table 1. Currently the designation of most pacemakers is generally abbreviated to include
the first three positions.
68
Table 1. Five-letter code as recommended by the North American Society of Pacing and
Electrophysiology and the British Pacing and Electrophysiology Group.
1st Letter:
Chamber Paced
2nd Letter:
Chamber Sensed
3rd Letter:
Response to
Sensing
4th Letter:
Programmable
Features
5th Letter:
Multisite Pacing
A = atrium
A = atrium
T = triggered
O = not
programmable
A = atrium
V = ventricle
V = ventricle
I = inhibited
R = rate modulated V = ventricle
D = dual
D = dual
D = dual
D = dual
O = none
O = none
O = none
O = none
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:1084.
2.
Stone KR, McPherson CA. Assessment and management of patients with pacemakers and
implantable cardioverter defibrillators. Crit Care Med. 2004; 32(4 Suppl):S155-S165.
3.
Chan TC, Cardall TY. Electronic pacemakers. Emerg Med Clin North Am. 2006; 24:179-194, vii.
4.
Practice advisory for the perioperative management of patients with cardiac rhythm management
devices: Pacemakers and implantable cardioverter-defibrillators. A report by the American
Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac
Rhythm Management Devices. Anesthesiology. 2005; 103:186-198. Available online at:
http://www.asahq.org/publicationsAndServices/CRMDAdvisory.pdf. Accessed August 2006.
ITEM 64
The superior hypogastric plexus is the most inferior of the large sympathetic plexuses. The pelvic visceral
afferents and sympathetic efferents from the aortic plexus and L2 and L3 splanchnic nerves form the
plexus. There are also contributions from the parasympathetic fibers from S2-4. The plexus does not
include any somatic fiber contributions. The superior hypogastric plexus is a retroperitoneal structure
positioned at the sacral promontory between L5 and S1 close to the bifurcation of the common iliac
vessels.
The introduction of the superior hypogastric block has provided pain specialists an important tool to treat
pelvic pain. It has been used with neurolytic agents primarily for the palliation of intractable pelvic pain
secondary to cancer, with patients often experiencing significant reductions in pain. Neurolysis of the
superior hypogastric plexus has been used to successfully treat pain in the descending and sigmoid colon,
rectum, vaginal fundus, bladder, prostate, testes, prostatic urethra, seminal vesicles, uterus, and ovaries.
69
Recently superior hypogastric block has been performed with local anesthetics on patients with chronic
nonmalignant pelvic pain, with observational and anecdotal reports suggesting favorable outcomes.
The ascending colon, gallbladder, and pancreas are innervated by the celiac plexus.
REFERENCES
1.
Waldman SD. Interventional Pain Management. 2nd ed. Philadelphia: WB Saunders; 2001:528534.
2.
Plancarte R, Amescua C, Patt RB, et al. Superior hypogastric plexus block for pelvic cancer pain.
Anesthesiology. 1990; 73:236-239.
3.
Michalek P, Dutka J. Computed tomography-guided anterior approach to the superior hypogastric
plexus for noncancer pelvic pain: A report of two cases. Clin J Pain. 2005; 21:553-556.
4.
Cousins MJ, Bridenbaugh PO. Neural Blockade in Clinical Anesthesia and Management of Pain.
3rd ed. Philadelphia: Lippincott-Raven; 1998:468-472.
ITEM 65
Many agents have become available to treat postherpetic neuralgia over the last several years, and a large
number of randomized controlled trials have demonstrated the treatment efficacy of antidepressants,
anticonvulsants, topical analgesics, opioids, and other therapies.
Tricyclic antidepressants (TCAs) have typically been one of the first-line agents for the treatment of
postherpetic neuralgia. Amitriptyline is the prototypical TCA used. There are multiple controlled trials
demonstrating the efficacy of TCAs, however the side effect profile has limited widespread acceptance of
this treatment. These side effects include anticholinergic effect, sedation, weight gain, and postural
hypotension, all of which can be particularly troublesome in the elderly population. Nortriptyline and
desipramine appear to be at least as effective as amitriptyline but with less severe side effects. The
selective serotonin reuptake inhibitors (SSRIs) are a potential alternative, however they have not
demonstrated significant efficacy in several trials. The newer selective serotonin and norepinephrine
reuptake inhibitors (SSNRIs) such as duloxetine and venlafaxine may be a potential alternative to the
TCAs but with fewer side effects.
Anticonvulsants have been shown to be very effective in the treatment of postherpetic neuralgia. Multiple
clinical trials of gabapentin have shown significant superiority in pain relief compared with placebo.
Furthermore, it is an agent thought to have a more benign side effect profile compared to TCAs. A
version of gabapentin, pregabalin, has recently been released; it has an improved pharmacokinetic profile
and has also demonstrated benefit in treating postherpetic neuralgia. There are many additional
anticonvulsants available for the treatment of postherpetic neuralgia including carbamazepine,
oxcarbazepine, lamotrigine, topiramate, levetiracetam, and others. Only gabapentin and pregabalin are
currently approved by the Food and Drug Administration for the treatment of postherpetic neuralgia.
Until recently, the use of opioids for neuropathic pain has been limited due to the belief that they lacked
efficacy and concerns about addiction and tolerance. More recently, well-designed studies have
demonstrated significant clinical improvement with the use of sustained-release oxycodone in patients
70
with postherpetic neuralgia. While not a front-line agent, long-acting opioids are becoming more accepted
for the treatment of refractory postherpetic neuralgia.
Sympathetic blocks have not been shown to be as effective for postherpetic neuralgia as during the acute
phase of shingles. Typically they provide pain relief only for the duration of the local anesthetic. In those
situations in which they provide demonstrable sustainable benefit, they can be considered part of the
treatment algorithm.
Nonsteroidal antiinflammatory drugs have not been found to be particularly useful in the management of
postherpetic neuralgia.
REFERENCES
1.
Dworkin RH, Schmader KE. Treatment and prevention of postherpetic neuralgia. Clin Infect Dis.
2003; 36:877-882.
2.
Jung BF, Johnson RW, Griffin DR, et al. Risk factors for postherpetic neuralgia in patients with
herpes zoster. Neurology. 2004; 62:1545-1551.
3.
Baron R. Post-herpetic neuralgia case study: Optimizing pain control. Eur J Neurol. 2004;
11(Suppl 1):3-11.
4.
Dworkin RH, Schmader KE. The epidemiology and natural history of herpes zoster and
postherpetic neuralgia. In: Watson CPN, Gershon AA, eds. Herpes Zoster and Postherpetic
Neuralgia. 2nd ed. New York: Elsevier; 2001:39-64.
5.
Rowbotham M, Harden N, Stacey B, et al. Gabapentin for the treatment of postherpetic neuralgia:
A randomized controlled trial. JAMA. 1998; 280:1837-1842.
ITEM 66
Neuropathic pain results from injury to or dysfunction of the peripheral or central nervous system.
Gabapentin, an antiepileptic drug, has been found to be effective in reducing neuropathic pain associated
with diabetes mellitus, postherpetic neuralgia, cancer, and a variety of other pain syndromes. A recent
meta-analysis of randomized controlled trials of gabapentin yielded a number needed to treat (NNT) of
4.3—comparable to other antiepileptic agents for the treatment of neuropathic pain. It has become a frontline agent for many neuropathic conditions due to its low rate of intolerable side effects and ease of
administration, with no need for blood or serum monitoring. The drug is not metabolized and there are no
known drug-drug interactions.
Although “gaba” is part of its name, gabapentin has not been shown to directly impact GABA production.
Furthermore, antagonism at the GABA receptor would be expected to increase pain. While gabapentin
was originally developed as an analog of the inhibitory neurotransmitter gamma-aminobutyric acid
(GABA), no evidence exists demonstrating a direct interaction with the GABA receptor or any other key
receptors in nociceptive transmission. While there are some preliminary investigations suggesting that
gabapentin interacts with a subtype of the presynaptic GABAa receptor on excitatory neurons, it works as
an agonist, not an antagonist. Gabapentin has not been demonstrated to have any activity with the sodium
channels. On the other hand, it has been found to interact with a specific alpha2delta subunit of voltage71
gated Ca2+ channels. This subunit is up-regulated after nerve injury, and its activation leads to increased
Ca2+ influx with resultant increase in excitatory neurotransmission. Gabapentin does not directly interact
with the N-methyl-D-aspartate (NMDA) receptor.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:2771.
2.
Baillie JK, Power I. The mechanism of action of gabapentin in neuropathic pain. Curr Opin
Investig Drugs. 2006; 7:33-39.
3.
Loeser JD, Butler SH, Chapman CR, et al. Bonica’s Management of Pain. 3rd ed. Philadelphia:
Lippincott, Williams & Wilkins; 2001:106.
4.
Backonja M, Beydoun A, Edwards KR, et al. Gabapentin for the symptomatic treatment of
painful neuropathy in patients with diabetes mellitus: A randomized controlled trial. JAMA. 1998;
280:1831-1836.
ITEM 67
Pain has been defined by the International Association for the Study of Pain as an “unpleasant sensory or
emotional experience associated with actual or potential tissue damage, or described in terms of such
damage.” This defines pain as a subjective experience for which there is no objective measure, unlike
many diseases (eg, hypertension or diabetes). Pain is often confused with the concept of nociception—the
neural signals generated and transmitted to the spinal cord and brain in the face of stimuli that are
potentially or actually tissue damaging. Pain, in contrast, requires a functioning brain to process these
nociceptive signals and translate them into a subjective experience.
Nociceptive signals are transmitted along two nerve fiber types: A-delta and C fibers. Each has its own
characteristics. A-delta fibers are thinly myelinated, transmit at 5-30 m/s and are responsible for the
“first” pain that is felt immediately after stimulus. The sensation generated is easily localizable, sharp, and
pricking. A-delta fibers respond to heat, mechanical, and chemical stimuli. In contrast, C fibers are
unmyelinated and conduct nociceptive signals more slowly, typically 0.5-2.0 m/s. As a consequence of
the slow conduction velocity, it takes approximately one second for these signals to converge on the brain
to represent the “second” pain. This pain is typically deep, aching, throbbing, and burning in nature and
tends to be much poorly localized than the information provided from A-delta fibers.
A-gamma efferent neurons innervate intrafusal muscle fibers found within the muscle spindle and are
rapidly conducting (15-40 m/s). B fibers are autonomic fibers; they do not conduct pain sensations.
REFERENCES
1.
Wallace MS, Staats PS. Pain Medicine and Management. Just the Facts. New York: McGrawHill; 2005:7-9.
2.
Kandel ER, Schwartz JH, Jessell TM. Principles of Neural Science. 4th ed. New York: McGrawHill; 2000:472-475.
72
ITEM 68
The brachial plexus is composed of the nerve roots C5-T1 that combine to form the superior, middle, and
inferior trunks. These trunks further divide to form the lateral, medial, and posterior cords, which then
branch off into the peripheral nerves of the upper extremity (Table 1).
Table 1. Peripheral innervation of the upper extremity.
Nerve
Motor
Sensation
Musculocutaneous
Arm flexion
Lateral forearm
Median
Lateral deviation of wrist and
grip of thumb, index, and middle
fingers
Medial aspect of palm including
thumb, index, and middle fingers
Ulnar
Medial deviation of wrist and
grip of 4th and 5th fingers
Medial forearm and lateral aspect
of hand including 4th and 5th
fingers
Radial
Arm and wrist extension
Extensor surfaces of arm and
hand
Interscalene Block: The interscalene block is performed predominantly for shoulder surgery. Interscalene
blocks generally do not provide adequate coverage of the arm due to only partially blocking the median
nerve and essentially not blocking the ulnar nerve.
Supraclavicular and Infraclavicular Blocks: Performed at the level of the cords of the brachial plexus,
these blocks are excellent for surgeries distal to the mid-humeral level.
Axillary Block: The axillary block is frequently performed for surgeries distal to the elbow.
REFERENCES
1.
Wallace MS, Staats PS. Pain Medicine and Management. Just the Facts. New York: McGrawHill; 2005:102-103.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:16861692.
3.
Shinaman RC, Mackey S. Continuous peripheral nerve blocks. Curr Pain Headache Rep. 2005;
9:24-29.
ITEM 69
Compliance of the respiratory system (CT) is a measure of the pressure necessary to overcome the elastic
resistance of the lung and chest wall. Compliance of the respiratory system is determined by the equation:
73
CT (L/cm H2O) = ΔV (L)/ΔP (cm H2O), where
ΔV = change in volume, and
ΔP = change in pressure
Under normal situations the compliance of the lung (CL) and chest wall (CCW) are approximately equal at
0.2L/cm H2O. The relationship of each factor to CT is described by the equation:
1/CT = 1/CL + 1/CCW
Obesity is a classic example of a condition that produces a decrease in chest wall compliance. The
additional weight of the fat on the thorax and in the abdomen necessitates greater than normal changes in
pressure to produce a change in lung volume. Although there is a general trend for the degree of obesity
to correlate with the decrease in chest wall compliance, patients with obesity hypoventilation syndrome
appear to have a greater decrease in chest wall compliance than would be predicted based on their weight
alone. Other examples of conditions that produce a decrease in chest wall compliance include:






pregnancy
kyphoscoliosis
neuromuscular disease
burn scarring on the thorax
hemothorax/pneumothorax/pleural effusion
ankylosing spondylitis
Pneumonia and atelectasis produce decreases in compliance of the lung itself; they have no effect on chest
wall compliance. Interstitial pulmonary edema, although primarily producing a decrease in lung
compliance, is also associated with a decrease in chest wall compliance. It is hypothesized that this is due
to abdominal distention from ascites, edema of the chest wall, and pleural effusion.
Retained secretions in the airway result in an increase in airway resistance but have no effect on chest
wall compliance.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:989990.
2.
Mason RJ, Broaddus VC, Murray JF, et al. Murray & Nadel’s Textbook of Respiratory Medicine.
4th ed. Philadelpha: Eelsevier Saunders; 2005:2327.
3.
Gibson GJ. Lung volumes and elasticity. Clin Chest Med. 2001; 22:623-635, vii.
ITEM 70
Pressure in the anesthesia circuit is transmitted to the vaporizer and anesthesia machine. This “back
pressure” may cause a variation in the concentration of volatile anesthetic agent delivered by a vaporizer.
Vaporizer output may be increased (“pumping effect”) or decreased (“pressurizing effect”) by the back
74
pressure. In most clinical circumstances the pumping effect produces greater changes than the
pressurizing effect.
Vaporizers may be classified as either concentration-calibrated (also described as variable bypass,
automatic plenum, etc.) or measured-flow (as exemplified by the classic “copper kettle”) vaporizers.
Since current US standards required concentration-calibrated vaporizers on all anesthesia machines, only
this type of vaporizer is described in the subsequent discussion.
Pumping Effect: Back pressure from the circuit prevents outflow of gases from both the vaporizing
chamber and the vaporizer bypass, resulting in compression of gas in both areas. Since the volume of the
vaporizing chamber is greater than the volume of the bypass, more gas enters the vaporizing chamber,
with the net result that more anesthetic agent is vaporized due to the increased gas in the vaporizing
chamber. The alteration of the normal ratio between gas in the vaporizing chamber and bypass produces
an increased concentration of volatile anesthetic agent from the vaporizer. Factors associated with an
increase in the output of a vaporizer occurring as a result of intermittent back pressure include:





low levels of agent in the vaporizer chamber
low fresh gas flow rate
frequent fluctuations in airway pressure
increased magnitude of fluctuations in airway pressure
low dial setting on the vaporizer
Pressurizing Effect: Some vaporizers may manifest a decrease in the concentration of volatile anesthetic
when intermittent back pressure occurs. In this situation intermittent back pressure to the vaporizer
compresses the carrier gas but the number of molecules of anesthetic agent in the vaporizing chamber
remains unchanged because the amount of agent vaporized depends on the saturated vapor pressure of the
drug and not the pressure in the chamber. The net result is a decrease in the concentration of the volatile
anesthetic agent from the vaporizer. Factors associated with a decrease in the output of a vaporizer
occurring as a result of intermittent back pressure include:



high fresh gas flows
increased magnitude of fluctuations in airway pressure
low dial setting on the vaporizer.
REFERENCES
1.
Dorsch JA, Dorsch SE. Understanding Anesthesia Equipment. 4th ed. Baltimore: Williams &
Wilkins; 1999:131-134.
2.
Odin I, Feiss P. Low flow and economics of inhalational anesthesia. Best Pract Res Clin
Anaesthesiol. 2005; 19:399-413.
3.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:286288.
75
ITEM 71
The administration of sevoflurane affects many respiratory parameters including tidal volume, respiratory
rate, bronchomotor tone, and the ventilatory response to hypoxemia.
Sevoflurane causes a dose-dependent decrease in tidal volume. Even though an increase in respiratory
rate is present, an overall decrease in minute ventilation will occur.
Sevoflurane also causes a dose-dependent increase in the respiratory rate. This is not true for isoflurane;
isoflurane will increase the respiratory rate up to a dose of 1 minimum alveolar concentration (MAC).
Sevoflurane is a potent direct-acting bronchodilator. Bronchodilation occurs through a variety of
mechanisms, including decreased intracellular calcium concentrations, alterations in acetylcholine release,
etc.
All volatile agents, including sevoflurane, attenuate the ventilatory response to hypoxemia. This effect is
mediated at the peripheral chemoreceptors located in the carotid bodies. The carotid bodies regulate the
ventilatory response to hypoxemia by sensing oxygen tension. The ventilatory response to hypoxemia can
be attenuated up to 70% at very low anesthetic concentrations (0.1 MAC) and continues to be inhibited in
a dose-dependent manner, with 100% depression occurring at approximately 1 MAC. The clinical
implication of inhibiting the ventilatory response to hypoxemia could be significant, especially for
patients with the need to maintain a hypoxic drive to breathe (eg, patients with chronic obstructive
pulmonary disease).
REFERENCES
1.
Tobin WR, Kaiser HE, Groeger AM, et al. The effects of volatile anesthetic agents on pulmonary
surfactant function. In Vivo. 2000; 14:157-163.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:155181.
ITEM 72
Clinical scenario: A 48-year-old man develops new-onset bilateral pulmonary infiltrates after an
esophagectomy. His PaO2 is 67 mm Hg while being mechanically ventilated with an FIO2 of 0.8. A
transthoracic echocardiogram shows normal left ventricular function and no evidence of volume overload.
This patient has the acute respiratory distress syndrome (ARDS), which is characterized by the acute
development of bilateral pulmonary infiltrates of noncardiogenic origin and a PaO2 to FIO2 (P/F) ratio of
200 or less. The P/F ratio of this patient is 84 (PaO2 / FIO2 = 67/.8 = 84). A less severe form, acute lung
injury (ALI) is defined by similar criteria but the P/F ratio is between 200 and 300. ARDS is a lifethreatening inflammatory condition with a mortality rate of 25%-40%. The syndrome may develop as a
result of a direct injury to the lung such as after aspiration of gastric contents or may occur in the setting
of a more generalized insult such as in association with septic shock.
Therapy for ARDS is supportive. One of the difficulties in treating ARDS is that therapeutic interventions
that improve oxygenation in the short term have not been shown to improve overall outcome. While the
76
use of inhaled nitric oxide, inhaled prostaglandins, and the prone position all improve oxygenation as
assessed by the P/F ratio, multiple studies have failed to show a decrease in mortality rate.
Ventilator-induced lung injury has been recognized for at least two decades. In 2000 a National Institutes
of Health-sponsored multicenter trial performed by the ARDS Network showed that the use of a low tidal
volume strategy conferred a significant survival benefit over the use of “conventional” mechanical
ventilation. The low tidal volume strategy for management of patients with ARDS aims to limit
overdistention, volutrauma, and barotrauma by using tidal volumes of 6 mL/kg of predicted body weight.
Predicted body weight is based on the height and the gender of the patient but not on his or her measured
weight.
Ventilatory strategies that are part of the low tidal volume protocol advocated for the management of
ARDS include




limitation of plateau pressures to 30 cm H2O or less
use of positive end-expiratory pressure (PEEP) to recruit lung units and keep the lungs “open”
avoidance (if possible) of inspired oxygen greater than 60%
use of low tidal volumes
Patients ventilated using this protocol typically need deep sedation and occasionally also require
administration of muscle relaxants.
Inhaled nitric oxide (NO) is a selective pulmonary vasodilator, which is approved by the Food and Drug
Administration for the treatment of persistent pulmonary hypertension of the newborn. In ARDS, inhaled
NO selectively dilates the blood vessels in those air spaces to which it gains access (ie, ventilated air
spaces). Thus it improves ventilation/perfusion matching. Unfortunately, in multiple studies, the shortterm physiologic benefit of an improvement in oxygenation has not been translated into increased
survival.
Inhaled prostaglandins act in a manner similar to inhaled nitric oxide. Oxygenation improves as selective
vasodilation occurs in aerated lung units. Despite the physiologic benefit, a survival advantage has not
been demonstrated.
Dependent areas of the lungs tend to collapse in patients with ARDS. The use of the prone position
redistributes areas of collapse and consolidation, improves dorsal lung ventilation, and increases
functional residual capacity. Oxygenation improves in some but not all patients. Even in those in whom
oxygenation improves, randomized trials have not shown increased survival.
REFERENCES
1.
Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med. 2000; 342:13341339.
2.
Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung
injury and the acute respiratory stress syndrome. The Acute Respiratory Distress Syndrome
Network. N Engl J Med. 2000; 342:1301-1308.
77
3.
Fan E, Needham DM, Stewart TE. Ventilatory management of acute lung injury and acute
respiratory stress syndrome. JAMA. 2005; 294:2889-2896.
4.
Gattinoni L, Tognoni G, Pesenti A, et al. Effect of prone positioning on the survival of patients
with acute respiratory failure. N Engl J Med. 2001; 345:568-573.
5.
Jain R, DalNogare A. Pharmacological therapy for acute respiratory distress syndrome. Mayo
Clinic Proc. 2006; 81:205-212.
6.
Murray MJ, Coursin DB, Pearl RG, et al. Critical Care Medicine: Perioperative Management. 2nd
ed. Philadelphia: Lippincott Williams & Wilkins; 2002:408-416.
ITEM 73
End-stage liver disease due to cirrhosis becomes a multisystem disease with potential cardiac, pulmonary,
renal, neurologic, and other organ system issues. The treatment of choice for end-stage liver disease is
orthotopic liver transplantation. The Child-Turcotte-Pugh score has been used for many years to quantify
the severity of liver dysfunction, and this classification was one of the criteria used to prioritize patients
for liver transplantation.
Table 1. Child-Turcotte-Pugh classification.
1 Point
2 Points
3 Points
None
1, 2
3, 4
Absent
Slight
Moderate
1-2
2-3
>3
Albumin level (g/dL)
> 3.5
2.8-3.5
< 2.8
Prothrombin time
(seconds prolonged)
<4
4-6
>6
Encephalopathy grade
Ascites
Bilirubin (mg/dL)
Class A = 1-6 points, Class B = 7-9 points, Class C = 10-15 points
It has been recognized that the Child-Turcotte-Pugh score was a suboptimal measure of liver dysfunction.
For example, a patient with a bilirubin of 40 mg/dL received the same number of points as a patient with
a bilirubin of 4 mg/dL. In addition, some of the Child-Turcotte-Pugh criteria were subjective (eg, degree
of encephalopathy) or open to institutional differences (eg, prothrombin time). Accordingly, a new system
for determining the severity of liver dysfunction was required. Hence, the Model for End-stage Liver
Disease was introduced and validated.
The MELD score is based solely on the patient’s serum bilirubin, serum creatinine, and international
normalized ratio (INR). The higher a patient’s MELD the more likely he or she is to die within three
months. In February 2002 the United Network for Organ Sharing (UNOS), the donor organ allocation
body in the United States, adopted the MELD score as the criterion for determination of priority for liver
transplantation.
78
Both the MELD score and the Child-Turcotte-Pugh classification were originally developed to predict the
outcome of patients after transjugular intrahepatic portosystemic shunts. MELD was derived from
prospective data, whereas the Child-Turcotte-Pugh classification was derived from empiric data. The
variables in the MELD score are objective, not subject to interinstitutional differences, and lack the
ceiling effect of the Child-Turcotte-Pugh classification.
Neither weight nor age is part of the MELD score. The MELD score may be calculated whether or not a
patient has been listed for liver transplantation. One of the reasons for the use of MELD in donor organ
allocation for liver transplantation is to minimize the importance of waiting time on prioritization for
transplant.
REFERENCES
1.
Keegan MT, Plevak DJ. Pre-operative assessment of the patient with liver disease. Am J
Gastroenterol. 2005; 100:2116-2127.
2.
Stoelting RK, Dierdorf SF. Anesthesia and Co-Existing Disease. 4th ed. New York: Churchill
Livingstone; 2002:299-324.
3.
Wiesner RH, McDiarmid SV, Kamath PS, et al. MELD and PELD: Application of survival
models to liver allocation. Liver Transpl. 2001; 7:567-580.
ITEM 74
Clinical scenario: The following hemodynamic pattern is seen in a patient who has cirrhosis with portal
hypertension and end-stage liver disease:
Pulmonary artery occlusion pressure
Cardiac output
Mean pulmonary artery pressure
Pulmonary vascular resistance
Decreased
Normal
Increased
Increased
End-stage liver disease may cause significant pulmonary dysfunction. Hypoxemia may occur because of
hepatic hydrothorax, atelectasis, or aspiration. Of even more concern is that patients may develop
portopulmonary hypertension. This must be distinguished from hepatopulmonary syndrome.
The diagnosis of portopulmonary hypertension requires the presence of portal hypertension due to
cirrhosis, a mean pulmonary artery pressure (PAP) greater than 25 mm Hg, pulmonary vascular resistance
greater than 120 dynes·sec/cm5, and a pulmonary artery occlusion pressure (PAOP) less than 15 mm Hg.
Portopulmonary hypertension is a vasoconstrictive and thrombotic process most likely caused by
circulating factors that are usually cleared by the liver. The condition may be classified as mild (mean
PAP < 35 mm Hg), moderate (mean PAP 35-50 mm Hg), or severe (mean PAP > 50 mm Hg). Patients
with severe portopulmonary hypertension tend to do poorly after liver transplantation, so efforts are made
to treat their pulmonary hypertension prior to transplantation. This may take weeks or months and usually
involves medications such as intravenous prostaglandins (administered by continuous infusion), oral
endothelin antagonists (such as bosentan), or phosphodiesterase 5 inhibitors (such as slidenafil).
79
Hepatopulmonary syndrome is different. It is caused by right to left shunting at the pulmonary level
because of microvascular or (less commonly) macrovascular dilatations in the pulmonary vessels. The
supine position may be useful in patients with hepatopulmonary syndrome who tend to have increased
shunting and worsening hypoxemia when they are upright (a condition known as orthodeoxia). Diagnosis
of hepatopulmonary syndrome is by contrast echocardiography, looking for delayed right to left shunting,
or by radio-labeled albumin scan. The response to administered oxygen will determine the suitability for
liver transplantation, which is the best treatment. Pulmonary angiogram with coiling of macrovascular
shunts is a treatment for some patients with hepatopulmonary syndrome.
The patient’s decreased pulmonary artery occlusion pressure suggests that fluid overload is not the
problem.
REFERENCES
1.
Hoeper MM, Krowka MJ, Strassburg CP. Portopulmonary hypertension and hepatopulmonary
syndrome. Lancet. 2004; 363:1461-1468.
2.
Yao FSF. Yao and Artusio’s Anesthesiology: Problem-Oriented Patient Management. 5th ed.
Philadelphia: Lippincott Williams & Wilkins; 2003:485-509.
ITEM 75
Intraabdominal pressure may be measured by transducing the pressure in an indwelling bladder catheter.
Pressures above 20 cm H2O are cause for concern. Above this pressure, the abdominal cavity is on the
steep part of the pressure-volume curve and small increases in intraabdominal volume may cause large
increases in pressure.
Abdominal compartment syndrome may raise intracranial pressure and cause cardiac, renal, and
respiratory failure. A decrease in splanchnic blood flow may result in bowel ischemia.
Cardiac filling pressures may be elevated despite an underfilled heart. Cardiac index is decreased because
the intraabdominal pressure impedes venous return to the heart. Cardiac failure with increased pulmonary
artery occlusion pressure, increased systemic vascular resistance, and decreased cardiac index is a typical
finding in profound intraabdominal hypertension.
Pressure from the abdominal contents is transferred to the diaphragm and to the thoracic cavity. High
peak airway pressures may prevent an adequate tidal volume from being delivered as the ventilator flow
stops when the high airway pressure alarm limit is reached.
The urine output is usually decreased in abdominal compartment syndrome. Oliguria and anuria despite
aggressive fluid resuscitation is a typical sign.
The treatment of abdominal compartment syndrome is usually emergent laparotomy, and the abdomen is
generally packed open thereafter. In the operating room, the tamponade effect of the abdominal pressure
on a bleeding vessel may be lost when the abdomen is opened. This may lead to further bleeding and
hemodynamic instability. However, once the abdomen is opened, oxygenation and ventilation will usually
become easier, venous return will improve with subsequent improvement in cardiac index, and renal
function will usually improve because of increased cardiac output and renal blood flow.
80
REFERENCES
1.
Sugrue M. Abdominal compartment syndrome. Curr Opin Crit Care. 2005; 11:333-338.
2.
Fink MP, Abraham E, Vincent J-L. Textbook of Critical Care. 5th ed. Philadelphia: Elsevier
Saunders; 2005:2031-2038.
ITEM 76
Clinical scenario: A 27-year-old woman is transferred from the neuroscience intensive care unit to the
operating room for emergency laparotomy to repair a perforated duodenal ulcer. The patient has been
hospitalized for a number of weeks undergoing investigations for a progressive degenerative neurological
disorder. After administration of propofol and succinylcholine, the following sequence of
electrocardiographic changes are seen and the patient becomes pulseless.
When succinylcholine depolarizes muscle that has been traumatized (eg, crush injury) or denervated (eg,
upper motor neuron lesion), severe hyperkalemia may result. The susceptibility to hyperkalemia is
thought to be caused by proliferation of junctional and extrajunctional cholinergic receptors. The receptor
up-regulation provides more postjunctional sites at which succinylcholine may interact, and this causes an
increased release of potassium. Prolonged immobility during this particular patient’s hospital stay,
coupled with the neurologic disorder, has the potential to increase the risk of succinylcholine-induced
hyperkalemia.
The electrocardiographic manifestations of progressive hyperkalemia (eg, in renal failure) follow a
predictable pattern. In the case of a rapid increase of potassium (as in the patient under discussion) the
ECG may change dramatically and rapidly.
Treatment of acute hyperkalemia after succinylcholine administration includes
81





multiple boluses of intravenous calcium
beta-agonists
hyperventilation
consideration of sodium bicarbonate administration
consideration of insulin administration, with or without dextrose
Full cardiopulmonary resuscitation may be required.
Magnesium is especially useful in the treatment of torsades de pointes (polymorphic ventricular
tachycardia that occurs in association with a prolonged QT interval). The tracings do not reflect this
scenario, however.
Lidocaine is being used less and less for the treatment of ventricular dysrhythmias and is not the initial
drug of choice for treatment of ventricular dysrhythmias associated with hyperkalemia.
REFERENCES
1.
Christopherson TJ. Succinylcholine side effects. In: Faust RJ. Anesthesiology Review. 3rd ed. New
York: Churchill Livingstone; 2002:134-136.
2.
Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states:
Etiologic factors and molecular mechanisms. Anesthesiology. 2006; 104:158-169.
3.
Weiner KL. Cardiac dysrhythmias. In: Duke J, Rosenburg SG. Anesthesia Secrets. Philadelphia:
Hanley and Belfus; 1996:214-216.
ITEM 77
The serotonin syndrome is a potentially life-threatening complication of administration of certain drugs or
drug combinations. It is a predictable consequence of excess serotonin at central and peripheral receptors.
Many drugs are proserotoninergic. Monoamine oxidase inhibitors (MAOIs) and the selective serotonin
reuptake inhibitors (SSRIs) have enhancement of serotonin activity as their main pharmacodynamic
mechanism. However, many commonly used drugs can activate the serotonin system including opioids,
lithium and other antidepressants (tricyclics, trazodone, buspirone, venlafaxine), antiemetics
(ondansetron, metoclopramide), antimicrobials (linezolid, ritonavir), and even dextromethorphan, a
component of over-the-counter cold remedies.
There is a spectrum of severity, but manifestations usually include agitation, delirium, tremor, akathisia,
and hyperreflexia. Progression to clonus, muscular hypertonicity, and autonomic instability with
hyperthermia, tachycardia, and hypertension may occur.
82
Figure 1. Spectrum of clinical findings. Manifestations of the serotonin syndrome range from mild to
life-threatening. The vertical arrows suggest the approximate point at which clinical findings initially
appear in the spectrum of the disease, but all findings may not be consistently present in a single patient
with the serotonin syndrome. Severe signs may mask other clinical findings. For example, muscular
hypertonicity can overwhelm tremor and hyperreflexia. Used with permission, from Boyer EW, Shannon
M. The serotonin syndrome. N Engl J Med. 2006; 352:1112-1120.
REFERENCES
1.
Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2006; 352:1112-1120.
2.
Ford MD, Delany KA, Ling LJ, et al. Clinical Toxicology. Philadelphia: WB Saunders; 2001:240.
ITEM 78
Anesthesiologists may be asked to assist with tests for the determination of brain death of patients in the
intensive care unit or may be asked to care for brain-dead individuals undergoing organ harvesting in the
operating room. Strict criteria need to be applied to determine brain death, and it is important that each
test is performed properly. A neurologist or neurosurgeon will usually (though not necessarily) perform
the tests, and those clinicians determining brain death should be independent of any transplant teams that
may eventually harvest organs. In addition to other tests, the cough and corneal reflexes are tested.
Absence of a cough in response to tracheal suctioning is a prerequisite for the declaration of brain death.
The presence of a corneal reflex indicates function of at least part of the fifth and seventh cranial nerves
and brain death cannot be declared in this circumstance.
Before a clinical examination for the determination of brain death is performed, medical conditions that
may confound the clinical assessment (eg, severe electrolyte, acid-base, or endocrine disturbances) must
be ruled out, the patient’s core temperature must be greater than 32°C, and the patient must not be
hypotensive. In addition, the cause of coma should be known, and the presence of neuromuscular
blocking agents or drugs capable of altering consciousness or mental status should be excluded.
After the absence of brain stem reflexes has been documented, apnea must be formally demonstrated by
the apnea test. After preoxygenation and documentation of a normal PaCO2, the ventilator is disconnected
83
and evidence of breathing is sought. (Note that the “normal” PaCO2 must take into consideration the
patient’s preexisting pulmonary status. For example, a patient with chronic obstructive pulmonary disease
may have a baseline PaCO2 of 55 mm Hg.) Oxygen is continuously insufflated into the trachea. Serial
blood gases are drawn. If the PaCO2 increases to 60 mm Hg (or 20 mm Hg greater than the patient’s
baseline CO2) without evidence of respiratory efforts, then the patient’s respiratory center has failed.
Hypotension or hypoxemia may prompt discontinuation of the apnea test, though this is unusual if
properly performed. Brain death cannot be diagnosed if the patient makes any respiratory efforts; such
efforts represent at least partial preservation of the medullary respiratory center.
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.
REFERENCES
1.
Wijdicks EFM. The diagnosis of brain death. N Engl J Med. 2001; 344:1215-1221.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:29552968.
ITEM 79
Modern defibrillators can be classified as monophasic or biphasic based on their waveforms. Currently
most defibrillators being manufactured produce biphasic waveforms, but many monophasic defibrillators
are still in use. Monophasic waveform defibrillators, which were introduced first, deliver current in one
direction of flow (polarity). Impedance-compensated low-energy biphasic waveforms were first
introduced as part of automated external defibrillator technology and are now available in manual
defibrillators. Biphasic waveform defibrillators deliver energy in two directions, allowing a measure of
impedance. Compensation can then be made by adjusting the waveform based on impedance and
delivering a more effective current at lower energy levels:
Current (amperes) = {Energy (joules) / [Resistance (ohms) x Duration (seconds)]}1/2.
It has been demonstrated in several randomized studies that the use of biphasic waveforms of relatively
low energy (≤ 200 J) is safe and has equivalent or higher efficacy at terminating ventricular fibrillation
when compared with monophasic waveform shocks. The three “stacked” shock sequence with escalating
energy levels (200 J, 300 J, 360 J) was based on monophasic defibrillation. Repeated shocks were
necessary with monophasic waveforms because the first shock often failed to eliminate ventricular
fibrillation. Three shocks were recommended because current increased and transthoracic impedance
decreased with subsequent shocks. The first-shock success rate for terminating ventricular fibrillation is
higher with modern biphasic defibrillators. However, neither waveform has been shown to provide a
consistently higher rate of survival to hospital discharge or higher rate of return to spontaneous circulation
when compared with the other. Biphasic defibrillators are effective at a lower energy level and therefore
theoretically have a lower risk of causing myocardial damage during defibrillation.
Guidelines for the use on monophasic defibrillators now recommend using a single dose of 360 J for the
initial and all subsequent shocks. This was done to simplify the algorithm for sudden cardiac arrest and
because the initial lower dose was often ineffective at terminating ventricular fibrillation. The risk of
84
myocardial damage at a higher energy level was weighed against the benefit of eliminating ventricular
fibrillation on the first shock. Every biphasic defibrillator uses one of two waveforms that have proven to
be effective at eliminating ventricular fibrillation over certain energy levels. The two waveforms are:


biphasic truncated exponential at 150-200 J
rectilinear biphasic waveform at 120 J
It is recommended to start at these energy levels for the first shock and use the same or higher energy
levels for subsequent shocks. It is unclear whether increasing biphasic energy level increases the
incidence of successful defibrillation. If the recommended energy levels for a specific biphasic machine
are unknown, starting at 200 J has been suggested.
REFERENCES
1.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. Management of Cardiac Arrest. Circulation. 2005; 112(24); Part 7.2:IV58—IV-67. Available at: http://circ.ahajournals.org/content/vol112/24_suppl/. Accessed August
2006.
2.
American Heart Association. Currents in Emergency Cardiovascular Care. Winter 2005-2006;
16(4):1-28. Available at:
www.americanheart.org/downloadable/heart/1132621842912Winter2005.pdf. Accessed August
2006.
3.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:29352940.
4.
Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006:1501-1508.
ITEM 80
Patient simulation training offers a useful tool for practicing various technical aspects of anesthesia and
evaluating performance during clinical scenarios. Experience in other industries and the results of various
studies offer compelling evidence that simulation training has the potential to improve task performance.
Simulation training has many potential advantages for anesthesia training. Some of these include the
ability to:









practice technical skills and procedures without potential risk to patients
repeat routine procedures until comfortable
practice treatment of uncommon events and crisis management
learn to use complex equipment or devices
evaluate individual or group performance
compare performance between individuals for a certain scenario
allow errors to occur for learning purposes without patient risk
stop a clinical scenario to teach or demonstrate an alternative therapy
record, replay, and critique performance
85
However, there are a variety of issues that need to be resolved before the effectiveness of simulation
training and assessment can be truly validated. The biggest question to be answered is whether
simulation-based training is cost-effective. It is clear that most educators believe substantial benefits can
come from simulation training, but the costs of a complete “hands-on” simulator can be substantial,
ranging from $45,000 to more than $200,000 depending on the type. This cost does not take into account
space, clinical equipment, and staffing costs. This cost/benefit ratio will be debated for some time. There
has been substantial work done and progress made in the validation of various performance measures to
assess the effectiveness of simulation. Currently however there is no accepted methodology for measuring
performance in anesthesia. A well-accepted standard for performance evaluation is need. Correlating the
effects of simulation training with actual patient outcomes would be extremely difficult and expensive. It
is not felt to be feasible by most experts at this time. One of the biggest hurdles in attempts to evaluate the
ability of simulation to improve performance has been the potential for bias. Chopra and colleagues
evaluated simulation training to improve treatment of malignant hyperthermia (MH). They found that
practice led to significant improvements in treatment when this group was examined four months later.
Only half the study subjects received simulation training on the treatment of MH, but all the subjects had
experience in the use of simulation. These authors therefore significantly reduced this bias toward better
simulation performance. However, it is extremely difficult to remove all such bias when evaluating
performance via simulation. As different criteria and methodologies for evaluation of simulation-based
performance are developed, there is no doubt they will become powerful tools for education and
evaluation in anesthesia.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:30733099.
2.
Chopra V, Gesink BJ, de Long J, et al. Does training on an anesthesia simulator lead to I
mprovement in performance? Br J Anaesth. 1994; 73:293-297.
3.
Byrne AJ, Greaves JD. Assessment instruments used during anaesthetic simulation: Review of
published studies. Br J Anaesth. 2001; 86:445-450.
4.
Schwid HA, Rooke GA, Michalowski P, et al. Screen-based anesthesia simulation with debriefing
improves performance in a mannequin-based anesthesia simulator. Teach Learn Med. 2001;
13:92-96.
ITEM 81
Perioperative hypothermia, defined as a body temperature less than 36°C, has many potential risks as well
as benefits in patients. Major outcome studies have shown that mild hypothermia (a decrease of 1°-2°C)
can significantly increase the risk of the following:




surgical blood loss and need for transfusion
surgical site infection
prolonged hospital stay (by 20%)
morbid cardiac outcomes
86
Hypothermia impairs platelet function and directly inhibits the enzymes in the coagulation cascade.
Importantly, impairment may not be seen on routine laboratory tests performed at 37°C. Randomized
clinical trials have shown that mild hypothermia can substantially increase blood loss during hip surgery
as well as increase the need for transfusion. Hypothermia also impairs the immune system, and via
vasoconstriction, decreases oxygen delivery to tissue. These factors can contribute to increased risk of
wound infection. Animal models have demonstrated that mild hypothermia impairs resistance to both
Escherichia coli and Staphylococcus aureus dermal infections. In patients undergoing colon surgery, a
prospective randomized trial indicated that mild hypothermia tripled the incidence of surgical site
infection.
Animal models have shown that just 1°-3°C of hypothermia can provide significant protection from
cerebral ischemia and hypoxia. Human studies on therapeutic hypothermia have been less conclusive.
Hypothermia in brain trauma initially appeared beneficial, but further analysis and randomized studies
indicated no overall benefit to patients. A nonrandomized study recently demonstrated a benefit in brain
trauma patients with increased intracranial pressure refractory to other treatments. The International
Hypothermia in Aneurysm Trial completed in 2003 found no alteration in outcomes for patients who
underwent intraoperative cooling prior to aneurysm clipping. Conversely, one situation where randomized
trials have been able to conclusively demonstrate improved outcomes from therapeutic hypothermia is
during recovery from cardiac arrest. These controlled randomized studies and the consensus statements
that followed support the use of mild hypothermia in comatose patients after resuscitation from
ventricular fibrillation cardiac arrest. They also suggest it may be effective following other causes of
cardiac arrest.
At first, protection was felt to be secondary to a decrease in metabolic rate (8%/°C), but other treatments
that significantly reduce metabolic rate do not provide comparable protection. Other factors, such as
decreased release of excitatory amino acids, probably play a role in the protective effect of hypothermia.
The current evidence indicates that the majority of benefit from hypothermia occurs in the first few
degrees of reduction in temperature (and would not require a temperature < 30°C).
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:15711583.
2.
Clifton GL, Miller ER, Choi SC, et al. Lack of effect of induction of hypothermia after acute
brain injury. N Engl J Med. 2001; 344:556-563.
3.
Polderman KH, Tjong Tjin Joe R, Peerdeman SM, et al. Effects of therapeutic hypothermia on
intracranial pressure and outcome in patients with severe head injury. Intensive Care Med. 2002;
28:1563-1573.
4.
Tood MM, Hindman BJ, Clarke WR, et al. Intraoperative Hypothermia for Aneurysm Surgery
Trial (IHAST) Investigators. Mild intraoperative hypothermia during surgery for intracranial
aneurysm. N Engl J Med. 2005; 352:135-145.
5.
Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital
cardiac arrest with induced hypothermia. N Engl J Med. 2002; 346:549-556.
87
7.
Nolan JP, Morley PT, Vanden Hoek TL, et al; Advancement Life Support Task Force of the
International Liaison Committee on Resuscitation. Therapeutic hypothermia after cardiac arrest.
An advisory statement by the Advancement Life Support Task Force of the International Liaison
Committee on Resuscitation. Resuscitation. 2003; 57:231-235.
8.
Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of surgicalwound infection and shorten hospitalization. Study of Wound Infection and Temperature Group.
N Engl J Med. 1996; 334:1209-1215.
ITEM 82
Etomidate is a water-insoluble agent and unstable at physiologic pH in aqueous solution. Therefore it is
formulated in a 35% propylene glycol solution, which contributes to the unpleasant side effect of burning
on injection. Recently a new lipid formulation has been adopted in Europe (Etomidate-Lipuro) that has a
much lower risk of this side effect. Metabolism of etomidate takes place primarily by ester hydrolysis in
the liver. It is converted into a mainly inactive metabolite and excreted. An induction dose of etomidate
decreases both cerebral blood flow and cerebral metabolic rate but does not alter mean arterial pressure.
Cerebral perfusion pressure is therefore maintained or increased, and overall the oxygen supply-demand
ratio is improved. The exact mechanism of the hypnotic action of etomidate is not known, but it is
thought that it may exert its effect at the GABAA receptor beta2 and beta3 subunits. Its mechanism of
action may be similar to that of propofol. Etomidate has very little effect on ventilatory drive but will
decrease the response to carbon dioxide. An induction dose of etomidate produces a brief period of
hyperventilation followed by a brief period of apnea. It is not very effective at blunting the airway
reflexes that can result in coughing or hiccupping in response to laryngoscopy. Etomidate has minimal
effects on cardiovascular function with minimal changes in heart rate, blood pressure, pulmonary artery
pressure, or stroke volume. Adverse effects of etomidate include rare cases of adrenal suppression after
prolonged infusion, myoclonus, and postoperative nausea and vomiting.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:353355.
2.
Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006:157-162.
3.
Gries A, Weis S, Herr A, et al. Etomidate and thiopental inhibit platelet function in patients
undergoing infrainguinal vascular surgery. Acta Anaesthesiol Scand. 2001; 45:449-457.
4.
Franks NP. Molecular targets underlying general anaesthesia. Br J Pharmacol. 2006; 147(Suppl
1):S72-S81.
ITEM 83
Persistent, severe metabolic acidosis can profoundly decrease ventricular function manifested by global
hypokinesis. Also in this setting, the response to catecholamines and vasopressors may be blunted,
manifested by hypotension resistant to increasing doses of these medications. The patient with refractory
88
hypotension, global ventricular dysfunction, and metabolic acidosis should be evaluated for anion gap and
lactic academia. Mesenteric ischemia, sepsis, chronic renal failure, and other causes of increased anion
gap acidosis can produce this clinical scenario.
Hyperthermia would produce increased heart rate but not decreased global ventricular dysfunction itself.
It is accompanied by sepsis and metabolic acidosis, depressed ventricular function could occur in the
hyperthermic patient. Severe hypothermia (eg, induced hypothermia for giant cerebral aneurysm clipping)
can produce severe global ventricular hypokinesis. Intraoperative echocardiography is useful in these
patients to monitor ventricular function; they are also susceptible to cardiac dysrhythmias, including
ventricular fibrillation.
Pericardial tamponade is a form of restrictive cardiac disease where cardiac filling is impeded through
compression of cardiac chambers by pericardial fluid or clot. It does not cause decreased ventricular
function.
Hypokalemia may cause dysrhythmias but is not likely to cause severely decreased global ventricular
function.
REFERENCES
1.
Lafrance JP, Leblanc M. Metabolic, electrolytes, and nutritional concerns in critical illness. Crit
Care Clin. 2005; 21:305-327.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:353355.
ITEM 84
Hypercalcemia can affect the neurologic, gastrointestinal, and cardiac systems, requiring emergent
treatment when serum calcium values exceed 15mg/dL (normal 8.5-10.5) or when symptoms arise.
Neurologic symptoms include depression, somnolence, and lethargy. Cardiac manifestations include
hypertension and electrocardiogram changes including prolonged PR interval, short QT interval, and
widened QRS complex. Gastrointestinal symptoms include anorexia, nausea, vomiting, constipation, and
peptic ulcer disease. These symptoms vary depending on the magnitude of hypercalcemia and the acuity
of onset.
The most common causes of hypercalcemia are malignancy and hyperparathyroidism. Breast, lung, and
prostate cancers can metastasize to the bone, resulting in hypercalcemia from osteolytic lesions, however
bone metastases are not required for hypercalcemia to occur.
Hypocalcemia can occur after parathyroidectomy or, transiently, during massive blood transfusion of
citrated blood. It can manifest with neuromuscular changes that include muscle cramps, perioral and distal
extremity numbness, tetany, stridor, and laryngospasm. Electrocardiographic changes include prolonged
QT interval and atrioventricular block.
Hypermagnesemia occurs most commonly from iatrogenic causes or excessive use of laxatives.
Electrocardiographic changes include widened QRS complex and prolonged PR interval. Neuromuscular
symptoms may include sedation, decreased deep tendon reflexes, and muscle weakness.
89
Hypomagnesemia may occur in patients who are critically ill, in hypermetabolic states (eg, pregnancy), or
who are receiving chronic diuretic therapy; it can also result from chronic alcohol abuse. Neuromuscular
symptoms include hyperreflexia, skeletal muscle spasm, and seizures. Cardiac dysrhythmias, including
ventricular fibrillation, may occur.
REFERENCES
1.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:17701776.
2.
Wald DA. ECG manifestations of selected metabolic and endocrine disorders. Emerg Med Clin
North Am. 2006; 24:145-157.
ITEM 85
The gradient across a valve is determined by the velocity of blood flow across the valve according to the
simplified Bernoulli equation as follows:
Pmax = 4 vmax2
Where Pmax = peak pressure gradient and vmax = the maximal blood velocity across the valve as
measured by Doppler echocardiography. Blood flow velocity across a valve is affected by ventricular
function, valve area, and stroke volume.
Left ventricular function is a determinant for the velocity of blood flow. Patients with depressed
ventricular function will have decreased flow velocities and thus lower transvalvular gradients, even in
the presence of critical aortic stenosis.
Valve area is also a determinant of blood flow velocity across the aortic valve. The more narrow the
orifice, the faster the velocities will be for a given flow rate.
Stroke volume is also a determinant of blood flow velocity since the velocities will be lower, even in the
presence of critical aortic stenosis, if the volume of blood flowing through the valve is decreased. For
example, a patient with left ventricular hypertrophy and an underfilled left ventricle with normal function
may have a small stroke volume and lower velocities. Conversely, patients with coexisting aortic
regurgitation have higher transvalvular stroke volumes and higher velocities, even if the degree of aortic
stenosis is not as severe.
A technical limitation to Doppler flow velocity measurements is the need for parallel alignment to the
blood flow to obtain the highest flow velocities. If the Doppler signal is not parallel to the flow, the
measured velocities will be lower than the actual velocities.
REFERENCES
1.
Otto CM. Textbook of Clinical Echocardiography. 3rd ed. Philadelphia: WB Saunders; 2004:5460, 277-293.
90
2.
Giorgi D, Di Bello V, Talini E, et al. Myocardial function in severe aortic stenosis before and
after aortic valve replacement: A Doppler tissue imaging study. J Am Soc Echocardiogr. 2005;
18:8-14.
ITEM 86
Clinical scenario: An 18-month-old boy is scheduled for an inguinal hernia repair. The anesthetic plan
includes intravenous fentanyl, sevoflurane, and a bupivacaine field block for postoperative analgesia.
The Food and Drug Administration (FDA) acts to protect the public from drugs with the potential for
harm and assure the public of drug effectiveness. Approval of drug uses depends on evidence from both
the drug company and high-quality published scientific literature evaluating both drug efficacy and safety.
While the FDA has often been criticized for its strict criteria and evaluation process, it has been effective
in preventing approval of drugs that elsewhere caused great harm.
Off-label use is defined as any deviation from the specific FDA-labeled indications for dosing, patient
population, or route of administration (eg, intrathecal, transnasal). A classic example of this is the
universal use of volatile anesthetics and most opioids in children. Until recently the FDA did not require
specific studies that documented safe and effective use in children or that required specific dosage
guidelines in major subgroups (eg, gender, ethnicity, and age) of the population. Rapacuronium is an
example of a drug that was allowed to enter the market without adequate evaluation in children, causing
an age-related catastrophic complication. Several months after formal release by the FDA, it was
withdrawn from the market secondary to life-threatening, in some cases lethal, bronchospasm seen
primarily in patients with respiratory comorbid conditions. It was especially injurious to children at risk
for bronchospasm. The FDA and the company were aware of but did not thoroughly publicize the fact
that rapacuronium use in the adult population resulted in mild bronchoconstriction, which was seen as a
fairly brief and mild increase in ventilatory pressure after intubation. When this drug was used off-label in
children, however, the incidence of severe bronchospasm necessitated its immediate voluntary withdrawal
from the US market. Thus, off-label use of an unfamiliar drug can result in unexpected and severe
complications. Thalidomide administered to pregnant women for morning sickness, an off-label use,
resulted in many children being born with limb deformities. However, off-label use is an accepted
anesthesia practice and only on rare occasions has this practice proven to be detrimental to patients.
Furthermore, significant harm would come to adult and especially pediatric patients if clinicians could not
prescribe or administer volatile anesthetics, sedatives, many opioids, and most other drugs for off-label
uses. Table 1 lists common drugs frequently administered off-label.
91
Table 1. Common anesthetic drugs and their accepted off-label uses.
Drug
Off-label Use
Sufentanil
Intrathecal administration
Fentanyl
Intrathecal and epidural administration
Use in children under 2 years
Propofol
Infusion faster than 40 mg/10second in adults and children
Infusion faster than 20 mg/10 seconds in patients over 65, debilitated, or ASA
physical class III or IV
Ketamine
Obstetric patients
Children under 16 years
Bupivacaine
Children under 12 years
Lorazepam
All pediatric patients
Volatile Anesthetics
All pediatric patients
So accepted has the off-label use of many drugs become that failure to administer some drugs in an offlabel manner would be considered poor practice and in some instances as possible malpractice. Generally
accepted off-label uses are often caused by financial considerations. The cost of funding and reporting of
new studies for an off-label use to the FDA is high and the financial gain for a drug company is usually
quite small. This is most common in drugs no longer under patent protection where new uses will not
produce any significant increase in income. For other drugs, like dexmedetomidine, the manufacture
supports research into off-label uses such as sedation in the operating room and prolonged sedation in the
intensive care unit (ICU). The manufacturer depends on the FDA’s position that it does not regulate the
practice of medicine and thus does not restrict the discretionary use of any drug approved for use in the
US. When off-label use occurs, it is at the physician’s discretion and risk. It is important to remember that
the risk-benefit ratio of this practice remains unknown because rigorous studies establishing safety and
efficacy are lacking. Even prolonged familiarity with a drug in an off-label use does not mean rare
catastrophic complications cannot occur. Propofol infusion in the pediatric ICU, an off-label use, resulted
in fatal metabolic acidosis in some children and is no longer used for prolonged sedation in the ICU.
Thus, in this scenario, an accepted anesthesia plan is not only composed of off-label use of all the drugs
administered but remains the best current practice available.
REFERENCES
1.
Goudsouzian NG. Rapacuronium and bronchospasm. Anesthesiology: 2001; 94:727-728.
92
2.
Chang NS, Simone AF, Schultheis LW. From the FDA: What’s in a Label? A guide for the
anesthesia practitioner. Anesthesiology. 2005; 103:179-185.
3.
Steinbrook R. Commercial support and continuing medical education. N Engl J Med. 2005;
352:534-535.
4.
Stossel TP. Regulating academic-industrial research relationships—solving problems or stifling
progress? N Engl J Med. 2005; 353:1060-1065.
5.
Steinbrook R. Financial conflicts of interest and the Food and Drug Administrations’ Advisory
Committees. N Engl J Med. 2005; 353:116-118.
ITEM 87
Terbutaline is a beta-adrenergic agonist used as a tocolytic agent in the management of premature labor. It
is effective in delaying delivery for at least 24-48 hours, thus allowing the administration of
corticosteroids for fetal lung maturation. However, studies have not found beta-adrenergic drugs to be
effective in prolonging pregnancy for significantly longer periods. In addition, perinatal outcome—
including perinatal mortality, proportion of low birth weight infants, and incidence of delivery before 37
weeks gestation—has not been shown to be improved by the administration of beta-adrenergic tocolytic
drugs.
Because tocolytic therapy commonly fails, the anesthesiologist often cares for parturients who have
recently received terbutaline. Significant maternal side effects are associated with this drug. It is relatively
selective for beta2 receptors. As a result, vasodilation occurs, which can lead to hypotension. Other
cardiovascular side effects associated with terbutaline include tachycardia, cardiac dysrhythmias, and
pulmonary edema. Although the mechanism of pulmonary edema in parturients receiving tocolytic
therapy is not well understood, it is most likely noncardiogenic.
Metabolic abnormalities also may occur with the administration of terbutaline. Hyperglycemia ensues
soon after the initiation of therapy. In nondiabetic parturients, though, glucose levels return to normal
within 24 hours and insulin therapy is not required because beta-adrenergic stimulation of the pancreas
leads to increased release of insulin. When terbutaline is administered to diabetic parturients, meticulous
glucose control is required, sometimes by means of intravenous insulin infusion. Hypokalemia also is
associated with terbutaline therapy. It probably results from the increased release of insulin, which leads
to transport of potassium into the intracellular space. However, total body potassium is not decreased, so
replacement therapy is not required. In fact, rebound hyperkalemia has been reported after discontinuation
of beta-adrenergic therapy in parturients who receive potassium supplementation for treatment of
hypokalemia.
Terbutaline rapidly crosses the placenta, and fetal side effects can occur. The direct beta-adrenergic
stimulation of the fetal heart may lead to fetal tachycardia. If delivery occurs soon after the administration
of terbutaline, maternal hyperglycemia and fetal hyperinsulinemia can lead to neonatal hypoglycemia.
However, long-term adverse effects on the fetus or neonate seem unlikely.
93
REFERENCES
1.
Chestnut DH. Obstetric Anesthesia: Principles and Practice. 3rd ed. Philadelphia: Elsevier
Mosby; 2004:614-616.
2.
Anotayanonth S, Subhedar NV, Garner P, et al. Betamimetics for inhibiting preterm labour.
Cochrane Database Syst Rev. 2004 Oct 18; (4):CD004352.
ITEM 88
Intraoperative awareness during general anesthesia is a rare event with an estimated incidence of 0.1%0.2%. However, the psychological consequences for patients who do experience awareness can be severe.
Therefore, the American Society of Anesthesiologists recently published a practice advisory to assist
anesthesiologists in identifying risk factors for intraoperative awareness and developing strategies to
decrease its frequency.
An important component of the preanesthetic evaluation is the identification of risk factors for
intraoperative awareness. These include both patient and surgical factors. Patient characteristics that
potentially place a patient at increase risk are:






limited hemodynamic reserve
substance abuse
chronic pain treatment with large doses of opioids
anticipated difficult intubation
history of intraoperative awareness
ASA physical status IV or V
Certain surgical procedures may also place a patient at increased risk for experiencing intraoperative
awareness. These include:




cesarean delivery
cardiac surgery
trauma surgery
emergency surgery
Consultants involved in the development of the ASA practice advisory did not believe that informing
patients preoperatively about possible intraoperative awareness increases the risk of experiencing
awareness. However, the advisory does not recommend that this complication be discussed with all
patients during the preanesthetic evaluation. Instead, it is recommended that high-risk patients be
informed that intraoperative awareness could occur.
Although some anesthesiologists may advocate the use of brain function monitoring as a technique to
prevent intraoperative awareness, the current scientific data does not support the statement that brain
function monitoring reliably prevents intraoperative awareness. One randomized controlled study did
report a decreased risk of explicit recall in high-risk patients when a Bispectral Index (BIS®) monitor was
used. However, other data have shown that a specific index value generated from a brain function monitor
does not correlate with a specific depth of anesthesia and does not have uniform sensitivity among
94
different categories of patients and anesthetic agents. Therefore the ASA practice advisory indicated the
evidence is insufficient to justify the routine use of brain function monitoring in all patients undergoing
general anesthesia. In addition, the task force did not recommend the use of brain function monitoring in
all patients considered to be at high-risk for intraoperative awareness, including those undergoing
emergency surgery. Rather, they recommended that the decision to use a brain function monitor in these
patients be made on a case-by-case basis.
REFERNCES
1.
Practice Advisory for Intraoperative Awareness and Brain Function Monitoring: A Report by the
American Society of Anesthesiologists Task Force on Intraoperative Awareness. Anesthesiology.
2006; 104:847-864. Available online at http://www2.asahq.org/publications/pc-109-4-practiceadvisory-for-intraoperative-awareness-and-brain-function-monitoring.aspx. Accessed August
2006.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:12581259.
ITEM 89
Due to the respiratory changes of pregnancy, by 12 weeks gestation a normal arterial blood gas in a
parturient differs from that of a nonpregnant woman. Minute ventilation increases by 40%-50%, due
primarily to an increase in tidal volume. The increased ventilation results from the respiratory stimulant
effect of increasing progesterone levels and begins during the first trimester. As a result, the normal PaCO2
for a parturient is decreased from 40 to 30 mm Hg. Despite this marked increase in minute ventilation, the
increase in arterial blood pH is much smaller due to a partial metabolic compensation. The normal serum
bicarbonate concentration decreases from approximately 24 mEq/L in a nonpregnant woman to 20 mEq/L
in a parturient at term gestation. As a result, arterial pH only increases to 7.44. However, hyperventilation
during labor, which most commonly occurs in women who do not receive adequate analgesia, can lead to
increases in minute ventilation that are 70%-200% greater than pre-pregnant values and produces a
significant respiratory alkalosis. Decreases in uterine blood flow can result from this alkalosis.
Due to a reduce arteriovenous oxygen difference in pregnancy, the normal PaO2 for an upright parturient
at 37 weeks gestation is slightly increased to 103 mm Hg. However, by the third trimester of pregnancy,
PaO2 is less than 100 mm Hg in many women when they assume the supine position. This occurs because
the functional residual capacity becomes less than closing capacity when assuming the supine position,
leading to closure of some small airways during normal tidal breathing.
REFERENCES
1.
Chestnut DH. Obstetric Anesthesia: Principles and Practice. 3rd ed. Philadelphia: Elsevier
Mosby; 2004:16-17.
2.
Wise RA, Polito AJ, Krishnan V. Respiratory physiologic changes in pregnancy. Immunol
Allergy Clin North Am. 2006; 26:1-12.
95
ITEM 90
Multiple sclerosis is a disease that usually presents in early adulthood. Therefore anesthesiologists should
expect to encounter this disorder in obstetric patients. When deciding on labor analgesia for these
parturients, providers must consider the possible consequences of both pregnancy and anesthetic
technique on disease progression. The risk of exacerbation of multiple sclerosis is slightly decreased
during pregnancy but increased in the first six months postpartum. Although the data are limited, the
stress and fatigue associated with the presence of an infant is probably a significant contributing factor to
this increased risk of exacerbation.
Because multiple sclerosis is a disease characterized by demyelination of the central nervous system and
women are at increased risk for relapse in the postpartum period, some anesthesiologists have considered
the use of neuraxial labor analgesia in these patients controversial. However, the use of systemic opioids,
such as intravenous patient-controlled analgesia (IV-PCA) with fentanyl, provides inferior analgesia. In a
parturient with severe preeclampsia, epidural analgesia also achieves additional benefits, including
improvement in uteroplacental perfusion. While few studies have addressed the use of neuraxial analgesia
in the parturient with multiple sclerosis, there is no suggestion that this anesthetic technique is a
significant factor in postpartum relapses nor do the available data support withholding this technique
when other patient factors favor its use. One study found that the risk of relapse in the first three
postpartum months was similar for parturients who received epidural anesthesia, general anesthesia, or
local anesthesia infiltration.
When epidural anesthesia is utilized in the parturient with multiple sclerosis, it is advisable to use the
lowest concentration of local anesthetic that provides adequate analgesia. In the study mentioned above,
all patients who experienced an exacerbation after receiving epidural anesthesia had received a high
concentration of local anesthetic, such as 0.5% bupivacaine. Excellent labor analgesia is achieved in most
parturients with 0.125% bupivacaine or 0.2% ropivacaine.
Some have argued that spinal anesthesia theoretically may be more likely than epidural anesthesia to have
an adverse effect on the progression of multiple sclerosis because demyelinated areas of the spinal cord
could be exposed to higher concentrations of anesthetic agents with injection into the subarachnoid space.
Nonetheless, spinal anesthesia has been used safely in parturients with multiple sclerosis and no study has
compared the two techniques. In a patient with severe preeclampsia, moreover, other factors would favor
the administration of epidural analgesia over combined spinal epidural (CSE) analgesia. Patients with
severe preeclampsia are at increased risk for requiring emergency cesarean delivery, and the risks of
general anesthesia are significant in these patients. When a CSE technique is used to provide labor
analgesia, the epidural catheter remains untested until the initial intrathecal medication has resolved. An
epidural technique allows the effectiveness of the epidural catheter to be determined immediately after
placement. Therefore, epidural labor analgesia is preferred over CSE analgesia in parturients considered
at high risk for cesarean delivery.
REFERENCES
1.
Chestnut DH. Obstetric Anesthesia: Principles and Practice. 3rd ed. Philadelphia: Elsevier
Mosby; 2004:872-874.
96
2.
Perlas A, Chan VWS. Neuraxial anesthesia and multiple sclerosis. Can J Anaesth. 2005; 52:454458.
3.
Bader AM, Hunt CO, Datta S, et al. Anesthesia for the obstetric patient with multiple sclerosis. J
Clin Anesth. 1998; 1:21-24.
ITEM 91
Local anesthetic agents differ in certain chemical properties that affect each drug’s activity and produce
significantly different clinical effects. Lipid solubility is a primary determinant of a local anesthetic’s
potency. The more lipophilic a drug is, the more easily it can cross the lipid membrane of the nerve. As a
result, the most lipid-soluble local anesthetics, such as bupivacaine and tetracaine, are more potent than
less lipid-soluble local anesthetics, such as lidocaine.
pKa is the pH at which the uncharged case form and the positively charged cationic form of a drug exist
in equal concentrations. This property is a determinant of a local anesthetic’s onset time. A drug with a
pKa close to physiologic pH has a greater number of molecules in the uncharged base form than a drug
with a higher pKa. Because uncharged molecules readily diffuse across the nerve membrane while
ionized molecules do not, local anesthetic agents with a lower pKa close to physiologic pH generally have
a more rapid onset time than drugs with a high pKa. This is not the only determinant of onset time,
however, For instance, chloroprocaine has a high pKa but a rapid onset of action. This likely occurs
because the drug is administered in such a high concentration (3%) that the number of uncharged
molecules reaching the nerve membrane is increased despite the low percentage of drug present in the
base form.
Determinants of a local anesthetic’s duration of action include the degree of protein binding and intrinsic
vasodilation. Once local anesthetics reach a nerve cell, they bind to protein receptor sites. Those drugs
that possess a high degree of protein binding will bind to those sites with a greater affinity than less
protein-bound drugs, leading to a longer duration of action. A drug’s intrinsic vasodilation, however,
affects the amount of drug that reaches the nerve membrane. Local anesthetic agents that produce
relatively more vasodilation undergo greater systemic absorption, leaving less drug available to exert its
conduction blocking effect within the nerve.
REFERENCES
1.
Covino BG. Pharmacology of local anesthetic agents. Br J Anaesth. 1986; 58:701-716.
2.
Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006:457-458.
ITEM 92
The American Society of Anesthesiologists (ASA) has developed several practice guidelines and
advisories that provide recommendations concerning the clinical care of patients undergoing anesthesia.
These practice parameters significantly impact the clinical practice of all anesthesiologists. It is important,
therefore, to understand the evidence-based process used to develop practice parameters and the
differences between guidelines and advisories.
97
A task force composed of experts in the area being considered for guideline development first devises
evidence linkage statements that describe relationships between anesthetic interventions and clinical
outcomes. Many of these statements compare outcomes between two possible interventions (eg, “Epidural
local anesthetics versus intravenous opioids improves postoperative analgesia after abdominal surgery.”).
Evidence to support or refute these statements is then collected. An extensive literature search is initiated
to identify any original reports that address the topic under review. Although prospective, randomized
controlled studies will provide the strongest evidence, data from other sources within the scientific
literature are also considered by the task force when developing a practice parameter. These sources
include nonrandomized prospective studies, observational studies, retrospective studies, and case reports.
Statisticians who are members of the task force assist with evaluation of research design and statistical
methods for the studies being reviewed.
Although evidence from the scientific literature plays a major role in the development of practice
guidelines and advisories, the task force also utilizes consensus opinion from other experts and
practitioners when devising its recommendations. Approximately 75-150 consultants are identified by the
task force as experts in the subject matter being studied. They are asked to complete surveys addressing
the evidence linkage statements and provide comments on the initial draft document written by the task
force. To gain even wider consensus-based information, members of the ASA are also asked to complete
an opinion survey. Data from these surveys undergo statistical analysis and are an important source of
evidence used by the task force. Once a draft report has been written, additional consensus opinion is
obtained via open discussions of the proposed recommendations at one or more public forums held at
national meetings. The draft document is also posted on the ASA website, and members can submit their
comments.
This process is followed for both practice guidelines and practice advisories that are issued by the ASA.
The difference between a guideline and an advisory is based on the amount of evidence available from
controlled studies addressing the topic. When there are not enough data to support a meta-analysis, an
advisory rather than a guideline is issued. The required components for both types of documents are
summarized in Table 1.
Table 1. Components of practice guidelines and practice advisories.
Component
Practice
Guideline
Practice
Advisory
Review and evaluation of published scientific literature
yes
yes
Meta-analysis of controlled studies
yes
no
Statistical analysis of opinion surveys
yes
yes
Evaluation of opinions obtained from public commentary
yes
yes
98
REFERENCES
1.
Fleisher LA. Evidence-Based Practice of Anesthesiology. Philadelphia: Elsevier Saunders;
2004:3-6.
2.
American Society of Anesthesiologists: Policy statement on practice parameters. Approved by the
House of Delegates on October 13, 1993, and last amended on October 27, 2004. Available
online at www.asahq.org/publicationsAndServices/standards/01.pdf. Accessed August 2006.
ITEM 93
Clinical scenario: A 19-year-old woman at 33 weeks gestation presents to the labor and delivery unit
complaining of vaginal bleeding and abdominal pain. Uterine activity monitoring indicates she is having
tetanic uterine contractions.
Placenta previa and abruptio placenta are the most common serious etiologies of antepartum vaginal
bleeding. Placenta previa typically presents as painless vaginal bleeding during the second or third
trimester. It is not associated with increased uterine tone, including tetanic contractions. Diagnosis of
placenta previa is confirmed with ultrasonography.
Unlike placenta previa, vaginal bleeding resulting from abruptio placentae is generally associated with
abdominal pain. In addition, uterine tone is often increased. Most parturients who present with vaginal
bleeding and tetanic uterine contractions are diagnosed with placental abruption. Because placental
separation decreases the surface area available for transport of oxygen to the fetus, fetal distress is also
more likely to occur with abruptio placentae than with placenta previa.
Uterine rupture is another serious but less common etiology of antepartum hemorrhage. Abdominal pain
may be associated with uterine rupture but it occurs in only approximately 10% of women who develop
this complication. The most common sign of uterine rupture is fetal bradycardia, which occurs in nearly
70% of cases. Loss of contractions and recession of the presenting part, rather than the presence of tetanic
contractions, is consistent with uterine rupture.
Placenta accreta is an abnormal placentation in which the placenta is adherent to the myometrium.
Although the diagnosis of placenta accreta may be suspected antepartum based on risk factors (eg,
combination of placenta previa and previous cesarean delivery) and the presence of abnormalities on
ultrasound or magnetic resonance imaging, the diagnosis is generally not established until after delivery
of the infant when difficulty is encountered separating the placenta from the uterus. Antepartum signs of
vaginal bleeding, abdominal pain, and increased uterine tone are not associated with placenta accreta.
REFERENCES
1.
Chestnut DH. Obstetric Anesthesia: Principles and Practice. 3rd ed. Philadelphia: Elsevier
Mosby; 2004:662-667, 673.
2.
Crochetiere C. Obstetric emergencies. Anesthesiol Clin North America. 2003; 21:111-125.
99
ITEM 94
Clinical scenario: A 19-year-old woman at 33 weeks gestation presents to the labor and delivery unit
complaining of vaginal bleeding and abdominal pain. Uterine activity monitoring indicates she is having
tetanic uterine contractions.
The patient is admitted to the labor and delivery unit, and within a few minutes recurrent late fetal
decelerations are noted. The obstetrician decides to proceed with cesarean delivery. Estimated vaginal
blood loss since admission is 400 mL. The patient’s blood pressure is 110/60 mm Hg and her heart rate is
100/min. Results of laboratory tests sent at admission are not yet available.
Providing anesthesia for emergency cesarean delivery in the setting of placental abruption is quite
challenging. Because significant bleeding can be concealed within a retroplacental hematoma,
anesthesiologists are more likely to underestimate the degree of hypovolemia in these patients compared
to other etiologies of antepartum hemorrhage, especially since otherwise healthy parturients may have
relatively normal vital signs in the setting of significant blood loss. Therefore, it is essential that largebore venous access be established and blood for transfusion be available when undertaking cesarean
delivery for abruptio placentae intraoperatively, increased blood loss may also occur because these
patients are at increased risk for disseminated intravascular coagulation (DIC) and uterine atony.
Approximately 10% of patients with placental abruption develop DIC and the incidence is even greater in
patients with a severe abruption that leads to fetal distress or fetal demise.
The choice anesthetic technique when performing cesarean delivery for abruptio placentae will be based
on a variety of factors including fetal condition, maternal hemodynamic status, and coagulation status. In
the scenario described, recurrent late decelerations indicate compromised fetal status, which requires
expeditious delivery. The presence of fetal distress also indicates that the patient likely has a severe
placental abruption, which increases the likelihood of DIC and significant hypovolemia. Therefore,
epidural and spinal anesthesia would not be advisable. Induction of neuraxial anesthesia with its
associated sympathectomy could precipitate severe hypotension, leading to further maternal and fetal
compromise. In addition, because the patient is at increased risk of DIC and coagulation values are not yet
available, avoidance of a neuraxial technique may be prudent, even if the patient is assessed to be
hemodynamically stable.
Induction of general anesthesia, using a rapid sequence technique, would allow a more rapid delivery of
the compromised fetus than initiation of a neuraxial technique. However, the choice of induction agent
must be given careful consideration. Because the patient is likely hypovolemic, induction of general
anesthesia with thiopental could precipitate severe hypotension. Ketamine in large doses has been shown
to increase uterine tone. The patient is already experiencing tetanic contractions. Additional increases in
uterine tone could further compromise uteroplacental perfusion. Therefore, despite concerns about
maternal hypovolemia, ketamine is likely not the best choice for induction of general anesthesia.
Etomidate does not affect uterine tone, causes minimal cardiac depression, and would, therefore, be a
good drug choice for induction of anesthesia in the setting of emergency cesarean delivery for placental
abruption. Although the use of etomidate does not guarantee the prevention of hypotension during
induction of anesthesia in a hypovolemic patient, it is less likely to produce severe hypotension than
thiopental. It may be advisable to reduce the dose of etomidate when severe hemorrhage is suspected.
REFERENCES
1.
Chestnut DH. Obstetric Anesthesia: Principles and Practice. 3rd ed. Philadelphia: Elsevier
Mosby; 2004:665-667.
2.
Crochetiere C. Obstetric emergencies. Anesthesiol Clin North America. 2003; 21:111-125.
100
ITEM 95
Clinical scenario: The following capnograph was recorded after induction of anesthesia in a 30-year-old
female undergoing knee arthroscopy. The patient has no relevant past medical history and her vital signs
are stable.
The capnograph is a monitor used with most general anesthetics and is typically used to assist with
tracheal tube confirmation, identification of adverse intraoperative events, and control of ventilation. The
American Society of Anesthesiologists in the 2005 Standards for Basic Anesthetic Monitoring requires
monitoring of expired carbon dioxide, preferably by a continuous monitor such as capnography, for all
patients receiving general anesthesia unless “invalidated by the nature of the patient, procedure, or
equipment.”
The capnograph monitors exhaled CO2 over time and displays it as a waveform. The normal capnograph
waveform (see Figure 1) can be divided into four phases:




Phase I: exhalation; anatomical dead space
Phase II: exhalation; mixed anatomical dead space and alveolar dead space
Phase III: exhalation; alveolar plateau
Phase IV: inhalation
Figure 1. The normal capnograph waveform depicting phase I to IV. The y axis is the PCO2; the x axis is
time. Modified from: Duarte AG, Lick S, Bidani A. Capnography in a double-lung transplant recipient.
Respiratory Care, 1999; 44:1099-1207.
An increased baseline of the capnograph waveform is a sign of rebreathing (see Figure 2). Causes of
rebreathing with an increased baseline of PCO2 include exhausted carbon dioxide (CO2) absorbent and a
faulty expiratory check valve.
101
Figure 2. The capnograph waveform with an increased PCO2 baseline.
The capnograph waveform depicted in Figure 3 is a tracing of obstructive lung disease. Not the prolonged
phase II and an increasing slope of phase III in the waveform.
Figure 3. The capnograph waveform is obstructive lung disease.
The capnograph waveform in Figure 4 has a “curare cleft,” which is characterized by a downward
deflection in phase III. This phenomenon occurs when the patient attempts to initiate a spontaneous
inspiration while being mechanically ventilated.
Figure 4. The capnograph waveform with a curare cleft.
Seen with low tidal volumes or respiratory rates, cardiogenic oscillations appear on the capnograph
waveform due to the changes in lung volume precipitated by the beating of the heart. Increased
pulmonary blood volume occurring as a result of right ventricular systole results in flow of a small
102
volume of gas from the lung; the decrease in pulmonary blood volume occurring during diastole results in
flow of a small volume of gas into the lung (see Figure 5). These oscillations correlate with the heart rate
and occur in phase III of the waveform.
Figure 5. The capnograph waveform with cardiogenic oscillations.
REFERENCES
1.
Pond D, Jaffe RA, Brock-Utne JG. Failure to detect CO2-absorbent exhaustion: Seeing and
believing. Anesthesiology. 2000; 92:1196-1198.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:14581461.
3.
Gravenstein JS, Jaffe MB, Paulus DA. Capnography: Clinical Aspects: Carbon Dioxide Over
Time and Volume. Cambridge, UK: Cambridge University Press; 2004: 361-363.
4.
Gravenstein JS, Paulus DA, Hayes TJ. Capnography in Clinical Practice. Boston: Butterworth;
1989:27.
ITEM 96
Clinical scenario: The following capnograph was recorded after induction of anesthesia in a 30-year-old
female undergoing knee arthroscopy. The patient has no relevant past medical history and her vital signs
are stable.
103
The increased PCO2 baseline is due to rebreathing of CO2, the causes of which include exhaustion or
absence of CO2 absorbent and a fault expiratory check valve. An increased concentration of expired CO2
is also present. Treatment options for rebreathing in this clinical setting include:


Replacement of the CO2 absorbent; this is challenging during the intraoperative course because of
the potential risks of anesthesia machine failure and ventilation delays during changing of the
absorbent.
Increase the fresh gas flow to greater than the minute ventilation; this creates a condition of a
semi-open system and eliminates rebreathing. The efficacy of this maneuver can be evaluated by
observing a decrease of the exhaled PCO2 on the capnograph waveform and elimination of
inspired CO2.
The capnogram is not consistent with a “curare cleft,” which could be eliminated by complete muscle
relaxation. Although additional relaxant may eliminate a curare cleft, it is generally more appropriate to
treat the underlying stimulus (pain, hypercarbia, acidosis).
The patient is already hypercarbic; decreasing tidal volume will exacerbate that problem.
Albuterol is indicated for bronchoconstriction not for rebreathing of CO2.
REFERENCES
1.
Pond D, Jaffe RA, Brock-Utne JG. Failure to detect CO2-absorbent exhaustion: Seeing and
believing. Anesthesiology. 2000; 92:1196-1198.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:14581461.
ITEM 97
Clinical scenario: The following arterial blood gas and laboratory results were obtained in a patient
scheduled for thoracic surgery.


pH 7.32, PaCO2 38 mm Hg, PaO2 100 mm Hg, bicarbonate 15 mEq/L, BE (base excess) -9
sodium 135 mEq/L, potassium 5.0 mEq/L, chloride 112 mEq/L, total CO2 18 mEq/L
Acid-base disorders are common in the perioperative period. A systematic approach to evaluation of
arterial blood gas results can simplify the classification of acid-base disorders. One approach to evaluate
an arterial blood gas is:
Check the pH:



< 7.35 = academia
> 7.45 = alkalemia
7.35-7.45 = normal or compensated disturbance
Check the PaCO2:



< 35 mm Hg = respiratory alkalosis (primary or compensation for metabolic acidosis)
35-45 mm Hg = normal
> 45 mm Hg = respiratory acidosis (primary or compensation for metabolic alkalosis)
104
Check the base excess (BE):



< -5 = metabolic acidosis
-5 to +5 = normal
> +5 = metabolic alkalosis
For this patient:



pH 7.32 = acidemia
PaCO2 = 38 (normal)
BE -9 = metabolic acidosis
Metabolic acidosis may be categorized based on the magnitude of the serum anion gap—a calculation
based on the difference between the routinely measured cations and anions. The concept of anion gap
has the potential to be confusing for two reasons. First, there is no actual difference between the
concentrations of cations and anions in the serum; the calculated “gap” exists because of the failure to
measure all cations and anions. Second, two formulas are widely accepted for calculating the anion
gap:
Anion Gap = (Na + K) – (Cl + HCO3)
or
Anion Gap = Na – (Cl + HCO3)
The value of the “normal” gap obviously depends on which formula is being used. The normal value
for the anion gap is 12 ± 4 if K is included in the formula; if K is not included, the normal range is 8 ±
4. (Older references may present slightly higher values for the normal anion gap, but improvements in
the ability to measure Cl concentrations have resulted in a decrease in the normal values for this
calculation). Despite these limitations, calculation of the anion gap is still widely advocated to
facilitate the development of a differential diagnosis for a patient with a metabolic acidosis.
For this patient:
Anion Gap = (Na + K) – (Cl + HCO3)
(135 + 5) – (112 + 18) = 140 -130 = 10 = normal
Or:
Anion Gap = Na – (Cl + HCO3)
(135) – (112 + 18) = 5 = normal
Based on the above calculations, this patient has a non-anion-gap metabolic acidosis.
REFERENCES
1. Casaletto JJ. Differential diagnosis of metabolic acidosis. Emerg Med Clin North Am. 2005;
23:771-787.
2. Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:16021614.
105
ITEM 98
Clinical scenario: The following arterial blood gas and laboratory results were obtained in a patient
scheduled for thoracic surgery.


pH 7.32, PaCO2 38 mm Hg, PaO2 100 mm Hg, bicarbonate 15 mEq/L, BE (base excess) -9
sodium 135 mEq/L, potassium 5.0 mEq/L, chloride 112 mEq/L, total CO2 18 mEq/L
Metabolic acidosis can result from several etiologies. One common way to narrow the differential
diagnosis of the metabolic acidosis is to determine if an anion gap is present. Having a positive anion-gap
metabolic acidosis implies the presence of an unmeasured anion while a non-anion-gap metabolic
acidosis implies either a net increase of a predominantly measured anion (Cl-) or a net loss of a
predominantly measured cation (Na+).
Etiologies of a non-anion-gap metabolic acidosis include:





renal tubular acidosis
severe diarrhea
excessive normal saline administration
mannitol administration
carbonic anhydrase inhibitor administration
Etiologies of an anion-gap metabolic acidosis include:








lactic acidosis
ketoacidosis (diabetic, alcoholic, starvation)
methanol poisoning
ethylene glycol poisoning
isopropyl alcohol poisoning
ethanol poisoning
acute renal failure (uremia)
salicylate poisoning
This patient has a non-anion-gap metabolic acidosis; of the choices listed, the most likely etiology would
be renal tubular acidosis. Renal tubular acidosis occurs due to increased cation loss (Na+) with a relative
inability to excrete the anion (Cl-); this results in a hyperchloremic metabolic acidosis with no anion gap.
REFERENCES
1.
Casaletto JJ. Differential diagnosis of metabolic acidosis. Emerg Med Clin North Am. 2005;
23:771-787.
2.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:16021614.
106
ITEM 99
Clinical scenario: A 58-year-old male recovering from minor surgery in the postanesthesia care unit is
noted to be unresponsive and the monitor indicates ventricular fibrillation. The nurse leaves the bedside to
get the defibrillator.
The most critical component of advanced cardiac life support is good basic life support, and this is
emphasized in the 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation.
Immediate and adequate bystander cardiopulmonary resuscitation (CPR) is critical to improve survival.
This, along with defibrillation as soon as possible for ventricular fibrillation and pulseless ventricular
tachycardia, is a Class I recommendation (supported by high-level prospective studies indicating the
benefits far outweigh the risks).
Several studies have examined the effects of bystander CPR and time to defibrillation on survival from
cardiac arrest. If no CPR is provided, survival rates from witnessed ventricular fibrillation decrease 7%10% for every minute between collapse and defibrillation versus 3%-4% when CPR is provided.
Administration of adequate CPR can change the characteristics of ventricular fibrillation, making it more
likely to be amendable to defibrillation (Figure 1). Rescue breathing and chest compressions are both
important during CPR, but during the first few minutes of ventricular fibrillation oxygen delivery is felt to
be limited more by blood flow than by oxygen content. Adequate chest compressions produce blood flow.
Therefore the advanced provider should limit interruptions in chest compressions for attempts to insert an
advanced airway, including a tracheal tube. The 2005 American Heart Association guidelines emphasize
the following points about chest compressions during CPR:



In order to give adequate chest compressions, all rescuers need to “push hard and push fast.”
Compress the chest at a rate of about 100 compressions per minute for all victims (except
newborns).
Allow adequate chest recoil (return to normal position) after each compression, and compression
to relaxation times should be approximately equal.
Limit interruptions in chest compressions as much as possible. Blood flow stops whenever
compressions are stopped.
Basic life support in the adult is properly provided in cycles of two rescue breaths each over one second
followed by chest compressions at 100 compressions/min. Adequate chest compressions should be
performed at the lower half of the sternum, between the nipples, with a compression depth of 1.5 to 2
inches. The 2005 recommendations state that the compression to ventilation ratio should be 30:2 for
scenarios with either one or two rescuers. The use of an advanced airway device, administration of
intravenous epinephrine, and use of central venous access are all potentially useful in the treatment of
sudden cardiac arrest from ventricular fibrillation but would not be the most critical intervention prior to
the arrival of a defibrillator.
107
Figure 1. Changes in ventricular fibrillation waveform from coarse to fine without CPR and back to
coarse after CPR is administered. Used with permission, from Berg RA, Hilwig RW, Ewy GA, et al.
Precountershock cardiopulmonary resuscitation improves initial response to defibrillation from prolonged
ventricular fibrillation: A randomized, controlled swine study. Crit Care Med. 2004; 32:1352-1357.
REFERENCES
1.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. Management of Cardiac Arrest. Circulation. 2005; 112(24); Part 7.2:IV58—IV-67. Available online at: http://circ.ahajournals.org/content/vol112/24_suppl/. Accessed
August 2006.
2.
American Heart Association. Currents in Emergency Cardiovascular Care. Winter 2005-2006;
16(4):1-28. Available online at:
www.americanheart.org/downloadable/heart/1132621842912Winter2005.pdf. Accessed August
2006.
3.
Berg RA, Hilwig RW, Ewy GA, et al. Precountershock cardiopulmonary resuscitation improves
initial response to defibrillation from prolonged ventricular fibrillation: A randomized, controlled
swine study. Crit Care Med. 2004; 32:1352-1357.
4.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:29352940.
5.
Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006:1501-1515.
ITEM 100
The 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency
Cardiovascular care state that when attempting to defibrillate a person in sudden cardiac arrest all rescuers
should deliver one shock followed by immediate cardiopulmonary resuscitation (CPR), beginning with
chest compressions. All rescuers should check the victim’s rhythm after giving about five cycles
(approximately two minutes) of CPR. This is a change from the 2000 guidelines that advised rescuers to
deliver up to three shocks without CPR between shocks as well as checking the rhythm before and after
each shock. This change in the guidelines was based on three new findings:
108




Rhythm analysis after each shock (particularly with automated external defibrillators) resulted in
long interruptions in compressions, which can be harmful.
Modern defibrillators eliminate ventricular fibrillation in more than 85% of the cases with the
first shock. If the first shock fails, continuing CPR is of greater value than a repeat shock and may
increase the chances of a successful second defibrillation.
Even if a shock eliminates ventricular fibrillation, the heart is stunned and does not resume
normal function/rhythm for some time. Chest compressions can deliver oxygen, energy, and
eliminate waste products from the heart by effectively perfusing it. This increases the chances
that normal rhythm and function will return.
There is no evidence that chest compressions after a successful defibrillation result in any harm.
It is anticipated by the American Heart Association that automated external defibrillator manufacturers
will reprogram their products to support the new changes instituted in the guidelines.
Administration of atropine intravenously is not part of the American Heart Association algorithm for
treatment of sudden cardiac arrest from ventricular fibrillation.
REFERENCES
1.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. Management of Cardiac Arrest. Circulation. 2005; 112(24); Part 7.2:IV58—IV-67. Available online at: http://circ.ahajournals.org/content/vol112/24_suppl/. Accessed
August 2006.
2.
American Heart Association. Currents in Emergency Cardiovascular Care. Winter 2005-2006;
16(4):1-28. Available online at:
www.americanheart.org/downloadable/heart/1132621842912Winter2005.pdf. Accessed August
2006.
3.
Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:29352940.
4.
Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006:1501-1508.
109
IN-TRAINING TAXONOMY
The Joint Council on In-Training Examinations of the American Board of Anesthesiology and the
American Society of Anesthesiologists have prepared a Content Outline; this was last revised in 2003 and
available online at http:www.asahq.org/publicationsAndServices/audio.htm#training. It is used by the
joint council to code the questions of the In-Training Examination for subject area. Using this Content
Outline, the Editorial Board of the Anesthesiology Continuing Education Program provides one or more
codes relating to the theme(s) of each question of the ACE Program. These codes will be tallied and
printed in each volume. This index of Content Outline Codes may be of some use in identifying specific
content areas within the ACE Program.
Item
Code
Item
Code
Item
Code
1
III.D.3.b
19
I.C.2
37
V.D.3.
2
IV.I.
20
I.B.14.b.
38
I.A.1.d.
3
I.D.1.e.1
21
II.A.6.a.5.
39
III.C.4.a.4.
4
I.D.1.e.1.
IV.B.3.c.
22
II.A.6.a.5.
40
IV.A.2.b.3.
5
IV.A..2.b.5.
23
II.A.6.a.5.
41
IV.C.3.b.7.
6
III.B.3.
III.G.1.a.1
24
I.D.5.g.
I.D.5.h.
42
II.A.1.d.
7
III.G.1.a.4.
25
I.D.5.b.
43
I.D.1.a.
8
III.G.2.a.2.
26
III.A.1.a.5.a
44
I.D.5.e.
9
III.A.4.a.1.a.
27
III.A.1.a.3.c.
45
II.A.8.e.1.
10
I.B.7.c.5.I.D.2.j.
28
I.D.1.e.1.
46
III.F.3.b.2.
11
IV.B.4.
29
I.D.3.b.2.
47
III.B.3.g.
12
III.B.4.f.1.
30
I.B.8.c.
48
III.B.3.g.
13
III.C.4.a.5.
31
III.B.4.f.3.
49
III.B.4.f.1.e.
14
III.A.1.a.1.b.
32
III.B.4.f.3.
50
III.G.2.a.1.
15
III.C.4.a.5.
33
III.A.2.c.1.
51
IV.F
16
III.C.4.a.5.
34
III.A.4.a.3.b.2.c.
52
III.A.4.a.2.c.
17
III.A.1.a.
35
III.C.1.a.4.b.
53
III.A.4.a.3.c.2.b.
18
III.B.3.f.
36
III.C.1.a.3.a.
54
IV.K.2.
110
Item
Code
Item
Code
Item
Code
55
III.C.4.a.5
70
I.B.5.
86
IV.B.
56
III.A.4.a.1.c.
III.A.4.a.3.a.
71
I.D.2.e.
87
IV.C.2.a.3.
57
IV.B.6.b.
72
III.A.4.a.3.c.1.
88
II.A.3.a.
58
III.C.4.a.5.
IV.B.9.b.
73
III.D.3.b.1.
89
IV.C.1.b.
IV.H
74
III.B.4.d.4.b.
III.D.3.b.
90
II.A.2.b.1.
IV.C.3.a.10
59
60
I.D.3.
75
III.A.4.a.2.e.
91
I.D.4.a.
61
II.A.6.a.
76
I.D.5.e.
III.B.4.c.3
92
V.D.
62
III.A.4.a.1.c.
III.A.4.a.3.b.2.c.
77
III.C.4.a.3.
93
IV.C.3.b.6.
63
I.B.13.c.
78
III.C.1.a.3.b.
94
IV.C.3.b.6.
64
IV.A.2.
79
I.B.12.
III.B.4.k.2.
95
I.B.8.f.
64
IV.A.2.
80
V.D.5.
96
I.B.7.c.4.I.B.8.f.
65
IV.A.2.b.
81
II.A.6.c.
97
III.A.3.a.
III.A.4.a.3.a
66
III.C.3.a.4.
IV.A.2.
82
I.D.3.d.
98
III.A.3.a.
III.A.4.a.3.a
67
III.C.1.f.1.
83
III.B.4.d.3.a.
99
III.B.4.k.2.
68
II.A.2.c.2.
84
III.B.3.h.
100
II.B.4.k.2.
69
III.A.1.a.2.a.
III.A.4.a.2.c.
85
III.B.4.b.
111
ALPHANUMERICAL LIST OF CONTENT OUTLINE CODES IN-TRAINING TAXONOMY
(item numbers in bold)
I.
BASIC SCIENCES
A. Anatomy: 38
B. Physics, Monitoring, and Anesthesia Delivery Devices: 10, 20, 30, 63, 70, 79, 95, 96
C. Mathematics: 19
D. Pharmacology: 3, 4, 10, 24, 25, 28, 29, 43, 44, 60, 71, 76, 82, 91
II.
CLINICAL SCIENCES
A. Anesthesia Procedures Methods, and Techniques: 21, 22, 23, 42, 45, 61, 68, 81, 88, 96
III.
ORGAN-BASED BASIC AND CLINICAL SCIENCES
A. Respiratory System: 9, 14, 17, 26, 27, 33, 34, 52, 53, 56, 62, 69, 72, 75, 97, 98
B. Cardiovascular System: 6, 12, 18, 31, 32, 47, 48, 49, 74, 76, 79, 83, 84, 85, 99, 100
C. Central and Peripheral Nervous Systems: 13, 15, 16, 35, 36, 39, 55, 58, 66, 67, 73, 74, 77, 78
D. Gastrointestinal/Hepatic: 1
E. Renal Urinary:
F. Endocrine/Metabolic: 46
G. Hematology: 6, 7, 8, 50
IV.
CLINICAL SUBSPECIALTIES
A. Painful Disease States: 5, 40, 64, 65, 66
B. Pediatric Anesthesia: 4, 11, 57, 58, 86
C. Obstetrical Anesthesia: 41, 87, 89, 90, 93, 94
D. Otolaryngology (ENT) Anesthesia; Airway Endoscopy; Microlaryngeal Surgery; Laser
Surgery; Hazards, Complications; Jet Ventilation:
E. Anesthesia for Plastic Surgery, Liposuction:
F. Anesthesia for Laparoscopic Surgery; Cholecystecomy; Gynecologic Surgery; Gastric
Stapling; Hiatus Hernia Repair; Anesthetic Management; Complications: 51
G. Ophthalmologic Anesthesia, Retrobulbar and Peribulbar Blocks; Open Eye Injuries:
H. Orthopedic Anesthesia; Tourniquet Management, Complications, Regional vs General
Anesthesia: 59
I. Trauma, Burn Management, Mass Casualty, Biological/Chemical Warfare: 2
J. Ambulatory Anesthesia:
K. Geriatric Anesthesia/Aging: 54
V.
SPECIAL PROBLEMS OR ISSUES
A. Electroconvulsive Therapy:
B. Organ Donors:
C. Radiologic Procedures; CT Scan; MRI:
D. Ethics, Practice Management, Medicolegal Issues: 37, 80, 92
112