25 Cardiovascular Disease

Chapter
25 CARDIOVASCULAR
DISEASE
Art Wallace
CORONARY ARTERY DISEASE ANEURYSMS OF THE AORTA

Patient History Management of Anesthesia
Electrocardiogram
CARDIOPULMONARY BYPASS
Risk Stratification versus Risk Reduction
Components of the Cardiopulmonary Bypass
Management of Anesthesia
Circuit
Postoperative Care
Monitoring During Cardiopulmonary Bypass
VALVULAR HEART DISEASE Myocardial Preservation
Mitral Stenosis Management of Anesthesia
Mitral Regurgitation Discontinuation of Cardiopulmonary Bypass
Aortic Stenosis Off-Pump Coronary Artery Bypass Graft Surgery
Aortic Regurgitation
QUESTIONS OF THE DAY
Mitral Valve Prolapse
DISTURBANCES OF CARDIAC CONDUCTION
AND RHYTHM
Heart Block
Sick Sinus Syndrome
Ventricular Premature Beats
Ventricular Tachycardia
Pre-Excitation Syndromes
Prolonged QT Interval Syndrome
ARTIFICIAL CARDIAC PACEMAKERS
ESSENTIAL HYPERTENSION
Preoperative Evaluation
Induction of Anesthesia
Maintenance of Anesthesia
Postoperative Management
CONGESTIVE HEART FAILURE
HYPERTROPHIC CARDIOMYOPATHY
PULMONARY HYPERTENSION AND COR
PULMONALE
CARDIAC TAMPONADE
383
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Section IV SPECIAL ANESTHETIC CONSIDERATIONS
C ardiovascular disease is the leading cause of death in

the United States, Canada, Europe, and Japan.1 Many
of the risk factors identified to predict perioperative death
new onset of angina, change in anginal pattern, unstable
angina, recent myocardial infarction, congestive heart
failure, or aortic stenosis, and presence of appropriate
are cardiac. Coronary artery disease, peripheral vascular medical therapy should determine whether patients are
disease, and risk for coronary artery disease increase in the best medical condition possible before elective
operative risk.2,3 Recent myocardial infarction, the pres- cardiac or noncardiac surgery.
ence of congestive heart failure, and aortic stenosis
are the most common major risk factors. Management
Patient History
of anesthesia for patients with cardiovascular disease
requires an understanding of the pathophysiology of the Important aspects of the history taken from patients with
disease process; appropriate preoperative testing; appli- coronary artery disease before noncardiac surgery include
cation of perioperative risk reduction strategies; careful cardiac reserve, characteristics of angina pectoris, the
selection of anesthetic, analgesic, neuromuscular, and presence of a prior myocardial infarction, and the medical,
autonomic blocking drugs; and use of monitors to match interventional cardiology, and cardiac surgical therapy for
the needs created by this disease. those conditions. Potential interactions of medications
used in the treatment of coronary artery disease with drugs
used to produce anesthesia must also be considered.
CORONARY ARTERY DISEASE Coexisting noncardiac diseases include hypertension,
peripheral vascular disease, chronic obstructive pulmo-
Coronary artery disease (ischemic heart disease), often nary disease from cigarette smoking, renal dysfunction
asymptomatic, is a common accompaniment of aging in associated with chronic hypertension, and diabetes
the American population. Of the adult patients who undergo mellitus. A thorough evaluation needs to recognize that
surgery annually in the United States, about 40% will either patients can remain asymptomatic despite 50% to 70%
have, or be at risk for, coronary artery disease.1 Patients stenosis of a major coronary artery.
who undergo anesthesia for noncardiac surgery have
increased rates of morbidity and mortality when coronary CARDIAC RESERVE
artery disease is present. History, physical examination with Limited exercise tolerance in the absence of significant
specific attention to cardiac and respiratory disease and pulmonary disease is the most striking evidence of
risks, and evaluation of exercise tolerance, cardiac symp- decreased cardiac reserve. Inability to lie flat, awakening
toms, and electrocardiogram (ECG) are important compo- from sleep with angina or shortness of breath, or angina
nents of the routine preoperative cardiac evaluation (also at rest or with minimal exertion are evidence of signi-
see Chapter 13).4 The most common symptoms of cardiac ficant cardiac disease. If a patient can climb two to
disease are shortness of breath with exercise in men and three flights of stairs without symptoms, cardiac reserve
fatigue in women. The presence of angina, angina at rest, is probably adequate.
orthopnea, paroxysmal nocturnal dyspnea, and dizziness
or fainting should also be evaluated. ANGINA PECTORIS
More specialized procedures, such as ambulatory ECG Angina pectoris is stable when no change has occurred
monitoring (Holter monitoring), exercise stress testing, for at least 60 days in precipitating factors, frequency,
transthoracic or transesophageal echocardiography, and duration. Chest pain or shortness of breath produced
radionuclide ventriculography (determination of ejection with less than normal activity or at rest, or lasting for
fraction), dipyridamole-thallium scintigraphy (mimics increasingly longer periods, is characteristic of unstable
the coronary vasodilator response but not the heart rate angina pectoris and may signal an impending myocardial
response associated with exercise), cardiac catheteriza- infarction. Dyspnea following the onset of angina pec-
tion, and angiography, are performed on selected toris probably indicates acute left ventricular dysfunction
patients. Invasive preoperative testing does not add due to myocardial ischemia. Angina pectoris due to
appreciably to the information provided by routine his- spasm of the coronary arteries (variant or Prinzmetal’s
tory and physical examination and electrocardiographic angina) differs from classic angina pectoris in that it
data for predicting adverse outcomes.1 For example, may occur at rest and then be absent during vigorous
echocardiographic determination of ejection fraction exertion. Silent myocardial ischemia does not evoke
does not improve upon the ability to predict the presence angina pectoris (asymptomatic) and usually occurs at a
of a preoperative myocardial infarction beyond that of a slower heart rate and lower systemic arterial blood pres-
careful preoperative clinical evaluation. Thallium scintig- sure than those present during exercise-induced myocar-
raphy, which evaluates adequacy of coronary blood flow, dial ischemia. About 70% of ischemic episodes are not
does not predict patients at risk for perioperative cardiac associated with angina pectoris and as many as 15% of
events.5,6 Ultimately, the history and physical examina- acute myocardial infarctions are silent. Women and
tion with specific attention to signs and symptoms of diabetics have a more frequent incidence of painless
384
Chapter 25 Cardiovascular Disease
myocardial ischemia and infarctions. The most common

Table 25-1 Incidence of Perioperative Myocardial
symptom in men is shortness of breath with exertion Infarction
and in women it is fatigue.
The heart rate or systolic blood pressure at which Reported Incidence
angina pectoris or evidence of myocardial ischemia is Time Elapsed Since
indicated on the ECG is useful preoperative information. Previous Myocardial Tarhan Steen Rao Shah
An increased heart rate is more likely than hypertension Infarction et al7 et al8 et al9 et al10
to produce signs of myocardial ischemia (Fig. 25-1). 0-3 months 37% 27% 5.7% 4.3%
Tachycardia increases myocardial oxygen requirements
while at the same time decreases the duration of diastole, 4 to 6 months 16% 11% 2.3% 0
thereby decreasing coronary blood flow and the delivery >6 months 5% 6% 5.7%
of oxygen to the left ventricle. Conversely, hypertension,
while increasing oxygen consumption, simultaneously
increases coronary perfusion despite the presence of
atherosclerotic coronary arteries. of a prior myocardial infarction. Most perioperative
myocardial reinfarctions occur in the first 48 to 72 hours
PRIOR MYOCARDIAL INFARCTION postoperatively. However, if ischemia is initiated by the
The incidence of myocardial reinfarction in the periopera- stress of surgery, the risk of myocardial infarction is
tive period is related to the time elapsed since the previous increased for several months after surgery.2,11
myocardial infarction (Table 25-1).7–10 The incidence Several factors influence the incidence of myocardial
of perioperative myocardial reinfarction does not stabilize infarction in the perioperative period. For example,
at 5% to 6% until 6 months after the prior myocardial the incidence of myocardial reinfarction is increased in
infarction. Thus, elective surgery, especially thoracic, upper patients undergoing intrathoracic or intra-abdominal
abdominal, or other major procedures are delayed for a operations lasting longer than 3 hours. Factors that do
period of 2 to 6 months after a myocardial infarction. Even not predispose to a myocardial reinfarction include the
after 6 months, the 5% to 6% incidence of myocardial (1) site of the previous myocardial infarction, (2) history
reinfarction is about 50 times more frequent than the of prior aortocoronary bypass graft surgery, (3) site of the
0.13% incidence of perioperative myocardial infarction in operative procedure if the duration of the surgery is shorter
patients undergoing similar operations but in the absence than 3 hours, and (4) techniques used to produce anesthe- IV
sia. Giving b-adrenergic blocking drugs 7 to 30 days prior
to surgery and continued for 30 days postoperatively
reduces the risk of cardiac morbidity (myocardial infarc-
tion or cardiac death) by 90% (also see Chapter 7 ).12,13
80 Giving b-adrenergic blocking drugs just prior to surgery
and continuing for 7 days reduces the mortality risk by
70 50%.14,15 Perioperative clonidine administration reduces
Patients with ischemia (%)
60 the 30-day and 2-year mortality risks.16 Statin therapy

with fluvastatin for 30 days before and after surgery, in
50 addition to b-blockade, reduces risk of myocardial infarc-
40 tion and death by an additional 50%.17 Intensive hemo-
dynamic monitoring using an intra-arterial catheter and
30 prompt pharmacologic intervention or fluid infusion to
20
treat physiologic hemodynamic alterations from the nor-
mal range may decrease the risk of perioperative cardiac
10 morbidity in high-risk patients (see Table 25-1).9
0
<70 70–89 90–109 ≥110
CURRENT MEDICATIONS
Drugs most likely taken by patients with coronary artery
Peak heart rate during anesthesia (beats/min)
disease are b-adrenergic antagonists, nitrates, calcium
channel blockers, angiotensin-converting enzyme inhibi-
Figure 25-1 The incidence of myocardial ischemia increases tors, drugs that decrease blood lipids, diuretics, antihy-
with heart rates with the greatest effect at heart rates above pertensives, and platelet inhibitors. Potential adverse
110 beats/min. (From Slogoff S, Keats AS. Does chronic interactions of these drugs with anesthetics is an important
treatment with calcium entry blocking drugs reduce preoperative consideration (see Chapters 7 to 9 and 22).
perioperative myocardial ischemia? Anesthesiology All patients with known coronary artery disease, known
1988;68:676-680, used with permission.) peripheral vascular disease, or with two risk factors for
385
coronary artery disease (e.g., being elderly, hypertension, related to digitalis therapy. Conversely, the block of con-
diabetes, significant smoking history, or hyperlipidemia) duction of cardiac impulses below the atrioventricular
should receive a perioperative b-adrenergic blocking drug node (right bundle branch block, left bundle branch
unless there is a specific contraindication.12–15 Even though block, or intraventricular conduction delay) most likely
chronic obstructive pulmonary disease (COPD) is not a con- reflects pathologic changes rather than drug effect.
traindication to perioperative b-adrenergic blockade,14,15
reactive asthma is. In patients who cannot tolerate
b-blockers, the a2-agonist clonidine may be used.16 Patients
Risk Stratification versus Risk Reduction
with coronary artery disease or vascular disease should
receive a statin unless there is a specific contraindication.17 One of the standard approaches to the perioperative care
Despite the potential for adverse drug interactions, of patients with cardiac disease is risk stratification.
cardiac medications being taken preoperatively should Risk stratification consists of a preoperative history and
be continued without interruption through the peri- physical examination followed by some series of tests
operative period. Discontinuation of b-adrenergic block- thought to predict perioperative cardiac morbidity and
ers,18 calcium channel blockers, nitrates, statins, or mortality risk. These tests may include persantine thal-
angiotensin-converting enzyme inhibitors in the periopera- lium, echocardiography, Holter monitoring, dobutamine
tive period increases perioperative morbidity and mortality stress echocardiography, and angiography, and may lead
rates and should be avoided. to angioplasty with or without an intracoronary stent or
coronary artery bypass surgery. As indicated previously,
preoperative risk stratification with invasive testing
Electrocardiogram (Also See Chapter 20)
adds little to a careful history and physical examina-
The preoperative ECG should be examined for evidence tion followed by prophylactic medical therapy.5,6,12–16
of (1) myocardial ischemia, (2) prior myocardial infarc- Furthermore, the risk of angiography and an intracoron-
tion, (3) cardiac hypertrophy, (4) abnormal cardiac ary stent or coronary artery bypass graft (CABG) surgery
rhythm or conduction disturbances, and (5) electrolyte prior to a surgical procedure does not reduce total
abnormalities. The exercise ECG simulates sympathetic risk.19,20 The combined risk of two procedures exceeds
nervous system stimulation as may accompany perioper- that of the original operation.19,21,22 Despite the lack of
ative events such as direct laryngoscopy, tracheal intuba- proven benefit of prophylactic invasive testing combined
tion, and surgical incision. The resting ECG in the with either CABG or coronary angioplasty with stenting
absence of angina pectoris may be normal despite exten- over medical therapy, the American College of Cardiol-
sive coronary artery disease. Nevertheless, an ECG ogy (ACC) and American Heart Association (AHA)
demonstrating ST-segment depression more than 1 mm, have developed a protocol entitled ACC/AHA Guideline
particularly during angina pectoris, confirms the pres- Perioperative Cardiovascular Evaluation for Noncardiac
ence of myocardial ischemia. Furthermore, the ECG lead Surgery.23–26 (See Figure 25-2). The use of this protocol
demonstrating changes of myocardial ischemia can is difficult to apply in practice with conflicting guidance
help determine the specific diseased coronary artery on indications for testing with physicians ordering more
(Table 25-2). Of particular importance is that a prior tests than suggested by the guidelines.27 Furthermore,
myocardial infarction, especially if subendocardial, may the ACC/AHA guidelines have not been shown to actually
not be accompanied by persistent changes on the ECG. reduce perioperative risk. Perioperative risk reduction
The preoperative presence of ventricular premature beats therapy with b-adrenergic blockers, clonidine, statins,
may signal their likely occurrence intraoperatively. A PR and aspirin may be superior to risk stratification with
interval on the ECG longer than 200 milliseconds may be invasive testing, angioplasty, and CABG.12–17,19–21
Table 25-2 Area of Myocardial Ischemia as Reflected by the Electrocardiogram

Coronary Artery Responsible Area of Myocardium That
Electrocardiogram Leads for Myocardial Ischemia May Be Involved
II, III, aVF Right coronary artery Right atrium
Sinus node
Atrioventricular node
Right ventricle
V3-V5 Left anterior descending coronary Anterolateral aspects of the left
artery ventricle
I, aVL Circumflex coronary artery Lateral aspects of the left ventricle
386
PERIOPERATIVE CARDIAC RISK REDUCTION THERAPY (PCRRT)
Patient scheduled for surgery with

β blockers:
• Atenolol 25 mg PO qd to start, if heart rate >60
and systolic blood pressure >120 mm Hg.
Coronary artery • Titrate dose to effect.
disease • Atenolol or Metoprolol IV on day of surgery.
• Atenolol or Metoprolol IV post op until taking
PO, then
Peripheral • Atenolol 100 mg PO qd for at least a week
vascular disease post op (hold for heart rate <55 or
systolic blood pressure <100 mm Hg).
• If known CAD or PVD, continue β blocker
Two risk factors: indefinitely.
Age ≥60
Hypertension
Diabetes If unable to take β blockers
Cholesterol >240 mg/dL
Smoking
If patient has a specific contraindication

(asthma not COPD) to β blockers:
• Clonidine 0.2 mg PO tablet night before
Aortic stenosis surgery.
Congestive heart failure • Clonidine TTS#2 Patch (0.2 mg/24 hr)
Unstable angina night before surgery.
New onset angina • Clonidine 0.2 mg PO tablet morning
Change in anginal pattern of surgery.
Angina without medical therapy • Hold for systolic blood pressure <120 mm Hg
Intracoronary stent on platelet
inhibitor
IV
Proceed with surgery
Refer to cardiology
Figure 25-2 Perioperative cardiac risk reduction therapy with beta-blockers and clonidine protocol. All patients with known coronary
artery disease, vascular disease, or two risk factors for coronary artery disease should be placed on prophylactic anti-ischemic agent
therapy with a long-acting b-blocker unless there is a specific contraindication. If there is a contraindication to b-blockade, then
prophylactic therapy with clonidine is an alternative.12–16 COPD, chronic obstructive pulmonary disease; PVD, peripheral vascular
disease. (From American College of Cardiology (ACC) and American Heart Association (AHA): ACC/AHA Guideline Perioperative
Cardiovascular Evaluation for Noncardiac Surgery. Anesth Analg 1994;5:1052-1064, used with permission.)
PERIOPERATIVE CARDIAC RISK REDUCTION THERAPY

2. If a patient has an absolute contraindication to periop-
Recommendations for the administration of prophylactic
erative b-blockers, clonidine may be used as an alter-
medical therapy to stable patients with known coronary
native. Clonidine should be administered as follows:
artery disease or at risk for such disease have been
a. Clonidine 0.2 mg PO on the night before surgery as well
established (see Fig. 25-2). The protocol is as follows:
as a clonidine TTS#2 (0.2 mg/24 hours) patch. With-
1. All patients who have either coronary artery disease hold the tablet for systolic blood pressure less than
(CAD), peripheral vascular disease (PVD), or two risk fac- 120 mm Hg.
tors for coronary artery disease (age 60 years, cigarette b. Clonidine 0.2 mg PO on morning of surgery.
smoking, diabetes, hypertension, cholesterol 240 c. Leave the patch on for a week.
mg/dL) should receive perioperative b-adrenergic block- 3. b-Adrenergic blocking drugs should be given as soon as
ade unless they have a specific intolerance to b-blockers. the patient is identified as having CAD, PVD, or risk
Patients with renal failure or renal insufficiency may factors. If the surgeon identifies the patient as having
also benefit from therapy. risk, the surgeon should initiate the medication to the
387
patient. Likewise, if the anesthesia preoperative clinic 7. Additional attention should be given to patients with
identifies the patient, b-blockers should be started. If congestive heart failure (CHF), aortic stenosis, intracor-
the patient is not identified until the morning of sur- onary stents on platelet inhibitors, or renal failure.
gery, intravenous atenolol or metoprolol should be All patients who have CHF should be evaluated by a
used. If the drug is started prior to the day of surgery, cardiologist for the initiation of b-blocker therapy. Beta
atenolol 25 mg PO daily is an appropriate starting dose. blocker therapy reduces the risk of death from CHF.
4. b-Blockade should be continued until at least 30 days Many patients with CHF are profoundly improved
postoperatively, if not indefinitely, in patients with cor- by b-blockade, but the dose must be titrated slowly
onary artery disease or peripheral vascular disease. In and is usually supervised by a cardiologist. Patients
patients with only risk factors, 7 days may be sufficient. with aortic stenosis should be evaluated by cardiology,
5. The optimal time to start b-blockade is at the time of and b-adrenergic blockade initiated with a cardio-
identification of the risk. This process should be mul- logist’s supervision. Patients with intracoronary stents
titiered to avoid missing patients. The following on platelet inhibitors should be seen by a cardiologist.
approach should be used to provide the maximum Warning: Discontinuation of platelet inhibitors in
benefit at the minimum cost. patients with intracoronary stents can be lethal.20
a. The surgeon should give a b-blocker if patients 8. Patients with an indication for statin therapy and
have CAD, PVD, or two risk factors. Atenolol 25 mg especially those with known coronary artery disease
PO daily is an appropriate starting dose. or peripheral vascular disease should be considered
b. If a medical or cardiology consult is requested by sur- for statin therapy.17 Therapy should be started 30 days
gery, the most common advice is: start a b-blocker. prior to surgery and continued for at least 30 days
c. The anesthesia preoperative clinic checks to see after surgery,17 possibly indefinitely.
if the patients at risk are receiving a b-blocker. If
the patient is not getting adequate b-adrenergic
blockade, the dose is increased.
d. On the day of surgery, treatment with or increasing Anesthesia care for patients with known coronary artery
the dose of intravenous b-blockers should be consid- disease, known peripheral vascular disease, or two risk
ered. Intravenous metoprolol in 5-mg boluses is used. factors for coronary artery disease (age older than or equal
The standard dose is 10 mg IV (withhold for heart rate to 60 years, hypertension, diabetes, significant smoking his-
less than 50 beats/min or systolic blood pressure less tory, or hyperlipidemia) should begin as soon as the patient
than 100 mm Hg). Intraoperative doses are used as is identified as needing surgery.12–16 All patients with new-
needed. The patient should receive additional doses onset angina, a change in anginal pattern, unstable angina,
in the postanesthetic care unit as needed. angina without medical therapy, aortic stenosis, congestive
e. The patient receives the drug postoperatively for heart failure, or an intracoronary stent on a platelet inhibitor
30 days. If the patient is NPO, the patient receives should be referred to cardiology. Patients with recently
intravenous metoprolol (5 to 10 mg q6 hours) placed intracoronary stents on platelet inhibitors have a
unless systolic blood pressure is less than 100 mm high risk of intracoronary thrombosis and death when the
Hg or heart rate less than 50 beats/min. If the platelet inhibitors are discontinued for perioperative
patient is taking oral medications, the patient receives care.20,29,30 Patients with bare metal stents may require 3
atenolol 100 mg PO daily if the heart rate is more rapid or more months of antiplatelet therapy.29 Patients with
than 65 beats/min and the systolic blood pressure is drug-eluting intracoronary stents may require platelet inhi-
more than 100 mm Hg. If the heart rate is between 55 bitors for a year or more.30 Patients with stable coronary dis-
and 65 beats/min, the dose is 50 mg. There is a “hold ease on medical therapy with no evidence of congestive
order” for heart rate less than 50 beats/min or systolic heart failure or aortic stenosis should be started on an oral
blood pressure less than 100 mm Hg. b-blocker (atenolol 25 mg/day PO) and a statin drug.17
f. The patient receives the drug for at least 30 days Patients with congestive heart failure should have b-block-
postoperatively. ers initiated by cardiology over a prolonged period. The dose
g. Many patients should receive the drug for life (patients of b-blockers should be increased as tolerated. b-Blockers
with known CAD, known PVD, and hypertension). should be avoided in patients with a history of high-grade
6. Preoperative testing and revascularization22 should be atrioventricular (AV) block without a pacemaker, reactive
used only as needed for specific indications not pro- asthma, or an intolerance for b-blockers. Diabetes is an
phylaxis.28 If a patient is identified with new onset indication for perioperative b-blockade. For maximal effect,
angina, unstable angina, a change in the anginal pat- b-blockers should be started as soon as the patient is iden-
tern, or congestive failure, then further risk stratifica- tified as needing surgery (optimally 7 to 30 days before
tion is appropriate. If the patient is stable with known surgery).12 If a patient is identified the day of surgery, intra-
CAD, PVD, or two risk factors for CAD, the patient venous atenolol or metoprolol can be started in the preoper-
should receive a b-adrenergic blocker.12–16 ative area (atenolol or metoprolol 10 mg IV if heart rate is
388
more rapid than 55 beats/min or systolic blood pressure is

Table 25-4 Determinants of Myocardial Oxygen
higher than 100 mm Hg) and continued postoperatively.15 Requirements and Delivery
Perioperative b-blockers should be continued for at least
7 days postoperatively.15 In patients with more frequent risks Myocardial Oxygen Requirements
(those with known coronary artery disease or peripheral vas- Heart rate
Systolic blood pressure
cular disease) b-blockers should be continued at least 30 days
Myocardial contractility
if not indefinitely.12,13 In patients with cardiac risk (coronary Ventricular volume
disease, peripheral vascular disease, or two risk factors for
coronary disease) who cannot tolerate b-blockade, the a2- Myocardial Oxygen Delivery
agonist clonidine reduces the risk of 30-day and 2-year mor- Coronary blood flow
Oxygen content of arterial blood
tality.16 Clonidine (#2TTS ¼ 0.2 mg/day patch plus a 0.2-mg
tablet) is started the night before surgery. A second tablet
of clonidine 0.2 mg PO is given on the morning of surgery.
The patch takes 24 hours to achieve adequate blood Monitoring with an intra-arterial catheter facilitates the
levels, so the tablet plus patch makes an infusion and bolus ability to maintain stable systemic blood pressures.
of drug. The patch is discontinued after 7 days and autota- Nevertheless, about one half of all new perioperative
pers the drug. Esmolol boluses during surgery do not consti- ischemic episodes are not preceded by, or associated
tute perioperative b-blockade and are not adequate to with, significant changes in heart rate or systemic blood
reduce perioperative cardiac risk.16 Appropriate dosing of pressure.33 A single 1-minute episode of myocardial
b-blockers is appropriate to avoid hypotension, bradycardia, ischemia detected by 1-mm ST-segment elevation or
and possible sequelae.31 depression increases the risk of cardiac events tenfold
The intraoperative anesthetic management as well and the risk for death twofold.3,34 Tachycardia for
as postoperative pain management of patients with coro- 5 minutes above 120 beats/min in the postoperative
nary artery disease includes modulation of sympathetic period can increase the risk of death tenfold. The only
nervous system responses and rigorous control of hemo- clinically proven method to reduce the risk of perio-
dynamic variables.1 Management of anesthesia should be perative myocardial ischemia and associated death is
based on a preoperative evaluation of left ventricular perioperative b-blockade12–15 (atenolol or metoprolol)
function and should sustain a favorable balance between or a2-agonist therapy with clonidine.16
myocardial oxygen requirements and myocardial oxygen IV
delivery to prevent myocardial ischemia (Tables 25-3 MONITORING (Also See Chapter 20)
and 25-4). Persistent tachycardia, systolic hypertension, Anticipation of problems and avoidance of potential
arterial hypoxemia, or diastolic hypotension can adversely disasters is a key component in successful anesthetic
influence this delicate balance. management in patients with cardiovascular disease.
Persistent and excessive changes in heart rate and sys- Prophylactic therapy and more extensive monitoring
temic blood pressure should be minimized (Fig. 25-1).32 reduce risk. Continuous intra-arterial pressure monitor-
Maintaining heart rate and systemic blood pressure within ing can reduce the risk of hemodynamic events by early
20% of the awake values is commonly recommended. identification of problems. Continuous ECG monitoring
rapidly identifies arrhythmias, tachycardia, and myocar-
dial ischemia. Monitoring should be continuous if possi-
ble. Rapid changes in hemodynamics can quickly lead to
Table 25-3 Evaluation of Left Ventricular Function
cardiac arrest; monitoring can quickly identify those
Assessment Impaired changes and permits prompt therapy prior to further
Feature Good Function Function complications. When operations are completed, monitor-
Previous myocardial No Yes ing should be continued into the recovery room or inten-
infarction sive care unit (ICU). When patients are transferred from
the operating room table to the gurney or ICU bed, or
Evidence of No Yes
congestive heart
are turned from supine to prone or back to supine, moni-
failure toring should be as continuous as possible. Unconscious
patients with cardiac disease may have rapid hemody-
Ejection fraction >0.55 <0.4 namic collapse with transfers from the operating room
Left ventricular end- <12 mm Hg >18 mm Hg table to the gurney or ICU bed or when turned over
diastolic pressure and should be monitored during transfers. If arterial
Cardiac index >2.5 L/min/m2 <2 L/min/m2 blood pressure, ECG, and saturation are monitored, the
problem can be quickly identified and corrected prior to
Areas of ventricular No Yes serious sequelae. Intravascular volume, vasoconstrictors,
dyskinesia
b-agonists, b-blockers, anticholinergics, and vasodilator
389
drugs should be immediately available. Loss of a pulse catheter to monitor blood pressure allows rapid pharma-
oximeter signal or desaturation can imply hypoxia or cologic manipulations and a very stable induction of
inadequate arterial blood pressure or cardiac output and anesthesia. An infusion of phenylephrine (0.2 to 0.4 mg/
should signal an immediate search for a cause and cor- kg/min) started prophylactically stabilizes arterial blood
rective action. The pulse oximeter is a monitor both of pressure and can eliminate most hemodynamic changes
oxygen saturation and perfusion. If the pulse oximeter with induction. Etomidate is a popular anesthetic to
loses a signal, adequacy of perfusion should be assessed. induce anesthesia because of its limited inhibition of
Loss of the pulse oximeter signal may be the first warn- the sympathetic nervous system and limited hemody-
ing of impending hemodynamic collapse. Continuous namic effects38 (also see Chapter 9). The lack of inhibition
monitoring and prophylactic therapy can reduce the risk of autonomic reflexes by etomidate may lead to hyper-
in patients with cardiovascular disease. tension with laryngoscopy and endotracheal intubation.
The intensity of monitoring in the perioperative period Propofol is popular secondary to its antiemetic effects
is influenced by the complexity of the operative proce- and rapid recovery, but the dose should be reduced to
dure and the severity of the coronary artery disease. avoid hypotension with induction. Fentanyl and midazo-
The five-lead ECG serves as a noninvasive monitor of lam in combination with an infusion of phenylephrine
the balance between myocardial oxygen requirements and a nondepolarizing muscle relaxant cause minimal
and myocardial oxygen delivery in unconscious patients changes in arterial blood pressure or heart rate.
(see Chapter 20). When this balance is unfavorably Ketamine is not often used to induce anesthesia for
altered, myocardial ischemia occurs, as evidenced on patients with coronary disease because of the associated
the ECG by at least a 1-mm downsloping of the ST seg- increase in heart rate and systemic blood pressure, which
ment from baseline. A precordial V5 lead is a useful may increase myocardial oxygen requirements. When
selection for detecting ST-segment changes characteristic giving desflurane, the inspired concentration should be
of ischemia of the left ventricle during anesthesia. Intra- slowly increased because of sympathetic stimulation
arterial pressure monitoring can speed the identification and associated tachycardia, pulmonary hypertension,
and treatment of hemodynamic changes. Monitoring myocardial ischemia, and bronchospasm.39 Tracheal
should be continuous if possible. Ventricular wall motion intubation is facilitated by the administration of succi-
abnormalities observed by transesophageal echocardiog- nylcholine or a nondepolarizing neuromuscular blocking
raphy may be the most sensitive indicator of myocardial drug (also see Chapter 12).
ischemia, but this monitor is expensive, invasive, and Myocardial ischemia may accompany the tachycardia
requires additional training before use. Intraoperative and hypertension that results from the stimulation of
monitoring of pulmonary artery pressures or use of direct laryngoscopy as necessary for tracheal intubation.
transesophageal echocardiography should be reserved Adequate anesthesia and a brief duration of direct laryn-
for selected high-risk patients (cardiac surgery, recent goscopy is important in minimizing the magnitude of
myocardial infarction, current congestive heart failure, these circulatory changes. When the duration of direct
unstable angina).1 Continuous cardiac output monitoring laryngoscopy is not likely to be brief, or when hyperten-
may improve intravascular fluid management.35 sion coexists, the addition of other drugs to minimize the
pressor response produced by tracheal intubation should
INDUCTION OF ANESTHESIA be considered. For example, laryngotracheal lidocaine
Preoperative anxiety can lead to preoperative myocardial (2 mg/kg) administered just before placing the tube in
ischemia.36 Myocardial ischemia predisposes to sub- the trachea produces rapid topical anesthesia of the tra-
sequent myocardial ischemia. Preoperative b-blocker cheal mucosa and minimizes the magnitude and duration
therapy or clonidine reduces the incidence of myocardial of the systemic blood pressure increase. Alternatively,
ischemia.36,37 Patients should receive their routine medi- lidocaine (1.5 mg/kg IV), administered just before initiat-
cations except for oral hypoglycemic drugs. Preoperative ing direct laryngoscopy, is efficacious.
sedative medication is intended to produce sedation and Opioids (fentanyl, sufentanil, alfentanil, or remifenta-
reduce anxiety, which if unopposed, could lead to secre- nil) before initiating direct laryngoscopy reduce the stim-
tion of catecholamines and an increase in myocardial ulation produced by tracheal intubation. b-Adrenergic
oxygen requirements because of an increase in heart rate blockers are effective in attenuating heart rate increases
and systemic blood pressure. Oral administration of associated with tracheal intubation. Tachycardia should
benzodiazepines (diazepam PO) is an effective phar- be avoided in all patients with coronary disease, vascular
macologic approach frequently selected to allay anxiety. disease, or risk factors for coronary disease.
Supplemental oxygen may be needed if narcotics are
combined with benzodiazepines for sedation. MAINTENANCE OF ANESTHESIA
Induction of anesthesia is acceptably accomplished The choice of anesthesia is often based on left ventricular
with the intravenous administration of rapidly acting function (see Table 25-3). For example, patients with cor-
drugs. Preinduction placement of an intra-arterial onary artery disease but normal left ventricular function
390
may develop tachycardia and hypertension in response to Patients with impaired left ventricular function, as
intense stimulation. Controlled myocardial depression associated with a prior myocardial infarction, may not
produced by a volatile anesthetic with or without nitrous tolerate direct myocardial depression produced by vola-
oxide may be appropriate if the primary goal is to pre- tile anesthetics. In these patients, the use of short-acting
vent increased myocardial oxygen requirements. Equally opioids with nitrous oxide may be a more acceptable
acceptable for the maintenance of anesthesia is the use of selection. Nitrous oxide, when administered to patients
a nitrous oxide–opioid technique with the addition of a who have received opioids for anesthesia, may produce
volatile anesthetic as necessary to treat acute increases undesirable decreases in systemic blood pressure and car-
in systemic blood pressure as produced by a change in diac output. High-dose fentanyl (50 to 100 mg/kg IV) or
the level of surgical stimulation. When hypertension is equivalent doses of sufentanil or alfentanil as the pri-
treated with a volatile anesthetic (isoflurane, desflurane, mary anesthetic with benzodiazepines added to ensure
sevoflurane), the drug-induced decrease in systemic vas- amnesia may be useful for patients who cannot tolerate
cular resistance is more responsible for decreases in sys- the myocardial depression from even low concentrations
temic blood pressure than is drug-induced myocardial of anesthetics. Yet, this technique is not clearly better
depression. The ability to rapidly increase the alveolar than moderate dose narcotics with an inhaled volatile
concentration of sevoflurane makes this drug uniquely or intravenous anesthetic.46
efficacious for treating sudden increases in systemic A regional anesthetic is an excellent technique in
blood pressure. Abrupt and large increases in the deliv- patients with coronary artery disease (also see Chapters
ered concentrations of desflurane, may be accompanied 17 and 18). Regional anesthesia for peripheral surgery
by stimulation of the sympathetic nervous system and (orthopedic, podiatric, peripheral vascular) and lower
transient increases in systemic blood pressure, heart rate, abdominal surgery (gynecologic and urologic) is a very
pulmonary hypertension, and myocardial ischemia (see safe technique for patients with cardiac risk. However, flow
Chapter 8).39 through critically narrowed coronary arteries is pressure-
Volatile anesthetics are vasodilators. Under unusual dependent. Therefore, decreases in systemic blood pressure
clinical circumstances, potent coronary vasodilators associated with a regional anesthetic that are more than
could divert blood flow from ischemic areas of myocar- 20% of the preblock value probably should be treated
dium (blood vessels already fully dilated) to nonischemic with an intravenous infusion of crystalloid solutions or a
areas of myocardium supplied by vessels capable of vasoconstrictor such as phenylephrine. Phenylephrine
vasodilation. Regional myocardial ischemia associated improves coronary perfusion pressure but at the expense IV
with drug-induced vasodilation is known as coronary of increasing afterload and myocardial oxygen require-
artery steal. There are reports that the incidence of myo- ments. Nevertheless, the increase in coronary perfusion
cardial ischemia is either unchanged or increased in pressure is likely to more than offset any increase in myo-
patients with coronary artery disease and anesthetized cardial oxygen requirements. Perioperative b-blockers or
with isoflurane compared with those receiving a different clonidine should be used in patients with cardiac risk
volatile anesthetic or an opioid-based anesthetic.40–42 undergoing surgery using regional anesthesia.
Volatile anesthetics to varying degrees (halothane, iso-
flurane, sevoflurane, and desflurane) induce ischemic NEUROMUSCULAR BLOCKING DRUGS (Also See
preconditioning and may protect the myocardium from Chapter 12)
subsequent ischemia.43,44 All facts considered, volatile The choice of nondepolarizing neuromuscular blocking
anesthetics may be either beneficial in patients with cor- drug during maintenance of anesthesia for patients
onary artery disease because they decrease myocardial with coronary artery disease may be influenced by the
oxygen requirements and induce ischemic precondition- circulatory effects of these drugs. Vecuronium, rocuro-
ing, or detrimental because they decrease systemic blood nium, and cisatracurium do not evoke histamine release
pressure and coronary perfusion pressure or produce and associated decreases in systemic blood pressure,
coronary artery steal (isoflurane) or tachycardia (desflur- even with the rapid intravenous administration of large
ane).45 A large clinical trial in patients undergoing doses. Likewise, the systemic blood pressure lowering
cardiac surgery failed to demonstrate a difference effects of atracurium and mivacurium, are usually
between halothane, enflurane, isoflurane, and narcotic- modest, especially if the drug is injected over 30 to
based anesthetics.46 Avoiding tachycardia with the use 45 seconds to minimize the likelihood of drug-induced
of long-acting (metoprolol or atenolol) b-blockers is histamine release. None of these neuromuscular block-
more important than anesthetic choice.12–16,18,46 Intra- ing drugs will adversely alter myocardial oxygen
operative bolus doses of short-acting b-blockers (esmo- requirements. Pancuronium increases heart rate and
lol) have not been shown to be effective in reducing systemic blood pressure, but these changes are usually
perioperative cardiac risk. Prophylactic perioperative less than 15% above predrug values, making this
administration of long-acting b-blockers (metoprolol or drug a possible choice for administration to patients
atenolol) is needed to reduce perioperative risk.16 with coronary artery disease. Furthermore, circulatory
391
changes produced by pancuronium can be used to offset need for monitoring, right atrial pressure is more likely to
negative inotropic or chronotropic effects of drugs correlate with pulmonary artery occlusion pressure in
being used for anesthesia. In contrast to pancuronium, patients with coronary artery disease when the ejection
the other nondepolarizing neuromuscular blocking fraction is larger than 0.5 and when there is no evidence
drugs would not be expected to offset decreases in sys- of left ventricular dysfunction.47,48 Abrupt increases in
temic blood pressure or heart rate as associated with the pulmonary artery pressure may also reflect acute
the administration of large doses of opioids. Use of pan- myocardial ischemia; however, when compared with
curonium has decreased with the increased use of more transesophageal echocardiography monitoring (TEE),
selective neuromuscular blocking drugs (vecuronium, monitoring with a pulmonary artery catheter is not a
rocuronium, and cisatracurium). highly sensitive approach for detecting myocardial ische-
Nondepolarizing neuromuscular blockade in patients mia. TEE also provides an assessment of regional wall
with coronary artery disease can be safely antagonized with motion, global ventricular function, valvular function,
anticholinesterase drugs combined with an anticholinergic intravascular fluid volume, and associated ventricular fill-
drug. Glycopyrrolate has more titratable chronotropic ing. TEE is more expensive than pulmonary artery
effects than atropine. Tachycardia after reversal of nonde- catheterization but the information is more accurate and
polarizing muscle relaxants can still occur. One of the com- useful than pulmonary artery catheter data.
mon causes of postoperative myocardial ischemia and Decreases in body temperature that occur intra-
infarction is tachycardia after emergence, which may be operatively may predispose to shivering on awakening,
the result of the combination of emergence, surgical pain, leading to abrupt increases in myocardial oxygen require-
and reversal of nondepolarizing muscle relaxants. The addi- ments. Attempts to minimize decreases in body tem-
tion of long-acting intravenous b-blockers should be used perature and provision of supplemental oxygen are of
to avoid tachycardia, which may lead to myocardial ische- obvious importance. Postoperative pain relief is important
mia in this period. The use of sugammadex should eliminate as pain-induced activation of the sympathetic nervous
these cardiovascular problems with reversal of neuromus- system can increase myocardial oxygen requirements.
cular blockade.
Postoperative Care (Also See Chapter 39)
TREATMENT OF MYOCARDIAL ISCHEMIA
The appearance of signs of myocardial ischemia on the Postoperative care of the patient with coronary artery
ECG supports the aggressive treatment of adverse disease is based on provision of perioperative anti-
changes in heart rate or systemic blood pressure. Only ischemic agents (b-blockers or clonidine, statins),
5% of perioperative myocardial ischemia found on Holter analgesia, and if needed, sedation to blunt excessive sym-
ECG is identified by clinicians. Prophylactic therapy pathetic nervous system activity and facilitate rigorous
with long-acting b-blockers or clonidine is essential control of hemodynamic variables. Intensive and continu-
to reduce perioperative risk.12–16 Tachycardia is treated ous postoperative monitoring is useful for detecting myo-
with the administration of atenolol, metoprolol, propran- cardial ischemia, which is often asymptomatic. In addition
olol, or esmolol. Excessive increases in systemic blood to detecting it, the occurrence of myocardial ischemia
pressure respond to narcotics, increases in inhaled should be prevented. Episodes of myocardial ischemia lead
agents, b-blockers, or continuous intravenous infusion to increased risk and increasingly frequent episodes.2,37,49
of nitroprusside. Nitroglycerin is a more appropriate Reducing the incidence of episodes of myocardial ischemia
choice than nitroprusside when myocardial ischemia is with b-blockers or clonidine reduces 30-day and 2-year
associated with a normal systemic blood pressure. Hypo- mortality rates.36,37 All patients with known coronary
tension should be treated with a phenylephrine infusion artery disease, known peripheral vascular disease, or two
to rapidly restore pressure-dependent perfusion through risk factors for coronary artery disease (including the
atherosclerotic coronary arteries. In addition to drugs, elderly, hypertension, diabetes, significant smoking
the intravenous infusion of fluids to restore systemic history, or hyperlipidemia) should receive a perioperative
blood pressure helps myocardial oxygen requirements. b-blocker unless there is a specific contraindication.12–15
A disadvantage of this approach is the time necessary They should receive b-blockers as soon as they are identi-
for intravenous fluid treatment to be effective. fied as being at risk for cardiac complications.12,13 Patients
The use of pulmonary artery catheters, in selected with lower risk should take the drug for at least 7 days post-
patients, may be helpful for monitoring responses to intraoperatively.14,15 Patients with known coronary disease or
venous fluid replacement and the therapeutic effects of vascular disease should take the drug for at least 30 days,
drugs on left ventricular function. Right atrial (central if not permanently.12,13 Chronic obstructive pulmonary
venous) pressure may not reliably reflect left-sided heart disease (COPD) is not a contraindication to perioperative
filling pressure in the presence of left ventricular dysfunc- b-blockade, but reactive asthma is. Diabetes is not a
tion due to coronary artery disease if the ejection fraction contraindication for perioperative b-blockade; it is an
is less than 50%. In healthy patients who have a reduced indication. In patients who cannot tolerate b-blockers,
392
the a2-agonist clonidine may be used.16 All medications The obstruction produces an increase in left atrial and
have a therapeutic index and b-blockers are no exception. pulmonary venous pressure. Increased pulmonary vascu-
The dose of perioperative b-blockers should follow lar resistance is likely when the left atrial pressure is
standard manufacturer guidelines to avoid hypotension, chronically higher than 25 mm Hg. Distention of the left
bradycardia, morbidity, and death.31 atrium predisposes to atrial fibrillation, which can result
The major determinant of pulmonary complications in stasis of blood, the formation of thrombi, and systemic
(atelectasis, pneumonia) after cardiac surgery is poor car- emboli. Chronic anticoagulation or antiplatelet therapy
diac function. Early mobilization and pain control are (or both) of patients with atrial fibrillation can reduce
likely to minimize the incidence of clinically significant the risk of systemic embolic events. Mitral stenosis is
pulmonary complications. commonly due to the fusion of the mitral valve leaflets
during the healing process of acute rheumatic carditis.
Symptoms of mitral stenosis do not usually develop until
VALVULAR HEART DISEASE about 20 years after the initial episode of rheumatic
(Also See Chapter 26) fever. A sudden increase in the demand for cardiac
output as produced by pregnancy or sepsis, however,
The most frequently encountered forms of valvular may unmask previously asymptomatic mitral stenosis.
heart disease produce pressure overload (mitral stenosis, Patients with mitral stenosis who are being chron-
aortic stenosis) or volume overload (mitral regurgitation, ically treated with digitalis for the control of heart rate
aortic regurgitation).50 The net effect of valvular heart should continue to take this drug throughout the periop-
disease is interference with forward flow of blood from erative period. Adequate digitalis effect for heart rate
the heart into the systemic circulation. Transesophageal control is generally reflected by a ventricular rate less
echocardiography has revolutionized the evaluation and than 80 beats/min. Because diuretic therapy is common
intraoperative management of valvular heart disease in these patients, the serum potassium concentration
(Table 25-5). Selection of anesthetic drugs and neuromus- should be measured preoperatively. Other common anti-
cular blocking drugs for patients with valvular heart dis- arrhythmic drugs such as b-blockers should also be
ease is often based on the likely effects of drug-induced continued. The discontinuation of anticoagulant or anti-
changes in cardiac rhythm, heart rate, systemic blood pres- platelet therapy should be discussed with the surgeon
sure, systemic vascular resistance, and pulmonary vascular and cardiologist. Patients should be switched from warfa-
resistance relative to maintenance of cardiac output in
these patients. Although no specific general anesthetic is
rin (Coumadin) therapy to heparin therapy prior to sur- IV
gery depending on the type of case. Also, patients with
superior, when cardiac reserve is minimal, an anesthetic mitral stenosis can be more susceptible than normal indi-
combination of opioids, an amnestic benzodiazepine, and viduals to the ventilatory depressant effects of sedative
an inhaled anesthetic is common. Dexmedetomidine drugs used for preoperative medication. If patients are
infusions may be extremely useful in combination with given sedative drugs, supplemental oxygen may increase
other drugs. Patients with valvular heart disease should the margin of safety. Most medications that patients are
receive appropriate antibiotics in the perioperative period taking, except anticoagulants, antiplatelet agents, and
for protection against infective endocarditis. Monitoring oral hypoglycemic agents, should be continued through-
intra-arterial pressure is helpful in patients with clinically out the preoperative period. Patients with diabetes
significant valvular heart disease. may benefit from an intravenous insulin infusion with
frequent glucose monitoring.51
Mitral Stenosis
Mitral stenosis is characterized by mechanical obstruc- MANAGEMENT OF ANESTHESIA
tion of left ventricular diastolic filling secondary to a Preinduction of anesthesia placement of intra-arterial
progressive decrease in the orifice of the mitral valve. pressure monitoring can speed the identification and
treatment of hemodynamic changes in patients with clin-
ically significant valvular disease. Induction of anesthe-
Table 25-5 Diagnosis: Echocardiography and Valvular sia in the presence of mitral stenosis can be achieved
Heart Disease with intravenous drugs, with the possible exception of
▪ Determine significance of cardiac murmurs (most ketamine, which may be avoided because of its propen-
sity to increase the heart rate. Tracheal intubation is
often aortic stenosis).
▪ Identify hemodynamic abnormalities associated with facilitated by the administration of a neuromuscular
blocking drug. Neuromuscular blocking drugs with mini-
physical findings (most often mitral regurgitation).
▪ Determine transvalvular pressure gradient. mal effect on heart rate are commonly chosen. Drugs
▪ Determine cardiac valve regurgitation. used for maintenance of anesthesia should cause minimal
▪ Evaluate prosthetic valve function. changes in heart rate and in systemic and pulmonary
vascular resistance. Furthermore, these drugs should not
393
greatly decrease myocardial contractility. No one anes- position may not be well tolerated because the pulmo-
thetic has been proved to be superior. These goals can nary blood volume is already increased.
be achieved with combinations of an opioid and low con- Monitoring intra-arterial pressure and possibly right
centrations of a volatile anesthetic or intravenous anes- atrial pressure is a helpful guide to the adequacy of intra-
thetics such as propofol or dexmedetomidine. Although vascular fluid replacement. An increase in right atrial
nitrous oxide can increase pulmonary vascular resis- pressure could also reflect pulmonary vasoconstriction,
tance, this increase is not sufficiently great to justify suggesting the need to check for causes, which may
avoiding this drug in all patients with mitral stenosis.52 include nitrous oxide, desflurane, acidosis, hypoxia,
The effect of nitrous oxide on pulmonary vascular resis- increased mitral regurgitation, or light anesthesia.
tance, however, seems to be accentuated when coexisting Postoperatively, patients with mitral stenosis are at high
pulmonary hypertension is severe. Avoiding the use of risk for developing pulmonary edema and right-sided heart
nitrous oxide allows higher inspired oxygen concentra- failure. Mechanical support of ventilation of the lungs may
tions and may reduce pulmonary vasoconstriction. Rapid be necessary, particularly after major thoracic or abdominal
increases in the concentration of desflurane may cause surgery. The shift from positive-pressure ventilation to
tachycardia, bronchospasm, and pulmonary hypertension spontaneous ventilation with weaning and extubation
and should be avoided. Control of arterial blood pressure may lead to increased venous return and increased central
with a prophylactic intravenous infusion of the vasocon- venous pressures with worsening of heart failure.
strictors phenylephrine can reduce hemodynamic
changes with induction of anesthesia.
Mitral Regurgitation
Nondepolarizing neuromuscular blocking drugs with
minimal circulatory effects are useful in patients with Mitral regurgitation is characterized by left atrial volume
mitral stenosis. Pancuronium is less appropriate because overload and decreased left ventricular forward stroke
of its ability to increase the speed of transmission of car- volume due to the backflow of part of each stroke volume
diac impulses through the atrioventricular node, which through the incompetent mitral valve back into the left
could lead to excessive increases in heart rate. Such atrium. This regurgitant flow is responsible for the char-
increases may be problematic in the presence of atrial acteristic V waves seen on the recording of the pulmo-
fibrillation because the ventricular response to atrial nary artery occlusion pressure.53 Mitral regurgitation
impulses is determined by the degree of atrioventricular secondary to rheumatic fever usually has a component
conduction. The adverse effects of drug-induced tachy- of mitral stenosis. Dilated cardiomyopathy, which may
cardia in response to drug-assisted antagonism of nonde- be from ischemia, multiple myocardial infarctions, viral
polarizing neuromuscular blocking drugs should be or parasitic infections, or other causes, may cause mitral
avoided (Table 25-6). Sugammadex, which can replace regurgitation. Isolated mitral regurgitation may be acute,
neostigmine, does not cause cardiovascular changes. If reflecting papillary muscle dysfunction after a myocar-
cases are prolonged and neuromuscular blockade is not dial infarction or rupture of chordae tendineae secondary
required for the conduct of the case, allowing the nonde- to infective endocarditis.
polarizing neuromuscular blockade to be eliminated
through metabolism may reduce the risk of tachycardia MANAGEMENT OF ANESTHESIA
with drug-assisted antagonism. Intraoperative intrave- Management of anesthesia in patients with mitral regur-
nous fluid therapy must be carefully titrated because gitation should avoid decreases in the forward left ven-
these patients are susceptible to intravascular volume tricular stroke volume. Conversely, cardiac output can
overload and to the development of left ventricular be improved by mild increases in heart rate and mild
failure and pulmonary edema. Likewise, the head-down decreases in systemic vascular resistance (Table 25-7).
Preinduction placement of intra-arterial pressure moni-
toring can speed the identification and treatment of
Table 25-6 Anesthetic Considerations in the Patients hemodynamic changes in patients with clinically signifi-
with Mitral Stenosis cant valvular disease.
▪ Avoid sinus tachycardia or rapid ventricular response
rate during atrial fibrillation.
▪ Avoid marked increases in central blood volume Table 25-7 Anesthetic Considerations in Patients with
Mitral Regurgitation
associated with overtransfusion or head-down position.
▪ Avoid drug-induced decreases in systemic vascular ▪ Avoid sudden decreases in heart rate.
resistance. ▪ Avoid sudden decreases in systemic vascular resistance.
▪ Avoid events such as arterial hypoxemia or ▪ Minimize drug-induced myocardial depression.
hypoventilation that may exacerbate pulmonary ▪ Monitor the magnitude of the V wave as a reflection of
hypertension and evoke right ventricular failure. mitral regurgitant flow.
394
A general anesthetic is the usual choice for patients increased myocardial oxygen demand because of the
with mitral regurgitation. Although decreases in systemic increased amounts of ventricular muscle associated with
vascular resistance are theoretically beneficial, the rapid myocardial hypertrophy in combination with higher
onset and uncontrolled nature of this response with a spi- intraventricular pressures. There is a decrease in oxygen
nal anesthetic may detract from the use of this technique. delivery secondary to the aortic valve pressure gradient
Local or regional anesthesia may be used safely for sur- in combination with an increase in oxygen requirements
gery on peripheral body sites. Additional monitoring from the increase in left ventricular pressure and
with continuous intra-arterial pressure monitoring can stroke work.
improve the identification of hypotension and improve Isolated nonrheumatic aortic stenosis usually results
the margin of safety. Continuous spinal anesthetics may from progressive calcification and stenosis of a congeni-
allow a slow titration of the regional block and can be tally abnormal (usually bicuspid) valve. Aortic stenosis
a good choice of anesthetic. Maintenance of general due to rheumatic fever almost always occurs in associa-
anesthesia can be provided with volatile anesthetic, with tion with mitral valve disease. Likewise, aortic stenosis
or without nitrous oxide, or a continuous infusion of is usually accompanied by some degree of aortic regur-
intravenous anesthetic. The concentration of volatile gitation. Regardless of the etiology of aortic stenosis,
anesthetic can be adjusted to attenuate undesirable the natural history of the disease includes a long latent
increases in systemic blood pressure and systemic vascu- period, often 30 years or more, before symptoms occur.
lar resistance that can accompany surgical stimulation. Because aortic stenosis may be asymptomatic, it is
Avoiding the use of nitrous oxide allows higher inspired important to listen for this cardiac murmur (systolic
oxygen concentrations and may reduce pulmonary murmur in the second right intercostal space that may
vasoconstriction. Rapid increases in the concentration radiate to the right carotid) in patients scheduled for
of desflurane may cause tachycardia, bronchospasm, surgery. The incidence of sudden death is increased in
and pulmonary hypertension and should be avoided. patients with aortic stenosis.
Control of blood pressure with a prophylactic intrave-
nous infusion of the vasoconstrictor phenylephrine can MANAGEMENT OF ANESTHESIA
reduce hemodynamic changes with induction. Nondepo- Goals during management of anesthesia in patients with
larizing neuromuscular blocking drugs that lack signi- aortic stenosis are maintenance of normal sinus rhythm
ficant circulatory effects are useful. Intravascular fluid and avoidance of extreme and prolonged alterations in
volume must be maintained by prompt replacement of heart rate, systemic vascular resistance, and intravascular IV
blood loss to ensure adequate venous return and ejection fluid volume (Table 25-8). Preservation of normal sinus
of an optimal forward left ventricular stroke volume. rhythm is critical because the left ventricle is dependent
on properly timed atrial contractions to ensure optimal
left ventricular filling and stroke volume. Marked
Aortic Stenosis
increases in heart rate (higher than 100 beats/min)
Aortic stenosis is characterized by increased left ventric- decrease the time for left ventricular filling and ejection,
ular systolic pressure to maintain the forward stroke and decrease coronary blood flow while increasing myo-
volume through a narrowed aortic valve. The magnitude cardial oxygen consumption. Coronary blood flow to the
of the pressure gradient across the valve serves as an left ventricle occurs during diastolic and changes in heart
estimate of the severity of valvular stenosis. Hemody- rate primarily effect diastolic time. Bradycardia (lower
namically significant aortic stenosis is associated with than 50 beats/min) can lead to acute overdistention of
pressure gradients less than 50 mm Hg or valve areas less the left ventricle. Tachycardia may lead to myocardial
than 1.2 cm2. A peak systolic gradient exceeding 50 mm ischemia and ventricular dysfunction. In view of the
Hg in the presence of normal cardiac output or an effec-
tive aortic orifice less than about 0.75 cm2 in an average-
sized adult (i.e., 0.4 cm2/m2 of body surface area or less Table 25-8 Anesthetic Considerations in Patients
than approximately one fourth of the normal orifice) with Aortic Stenosis
is generally considered to represent critical aortic steno- Intra-arterial pressure monitoring
sis. The combination of symptoms (angina, congestive Rapid availability or prophylactic administration of
failure, or fainting), signs (serious left ventricular dys- intravenous vasoconstrictors (phenylephrine)
function and progressive cardiomegaly), and a reduced
Maintenance of normal sinus rhythm
valve area also may make the diagnosis of critical aortic
stenosis requiring surgical replacement. Increased intra- Avoidance of extreme bradycardia or tachycardia
ventricular pressures are accompanied by compensatory Avoidance of sudden decreases in systemic vascular
increases in the thickness of the left ventricular wall. resistance
Angina pectoris occurs often in these patients in the
Optimization of intravascular fluid volume
absence of coronary artery disease, reflecting an
395
obstruction to left ventricular ejection, decreases in sys- with the increase in left ventricular diastolic pressure
temic vascular resistance may be associated with large substantially decreases the coronary perfusion pressure
decreases in systemic blood pressure and coronary blood gradient. Acute aortic regurgitation is most often due to
flow and myocardial ischemia. Intra-arterial pressure infective endocarditis, trauma, or dissection of a thoracic
monitoring is essential and can speed identification and aortic aneurysm. Chronic aortic regurgitation is usually
treatment of hemodynamic changes. Prophylactic infu- due to prior rheumatic fever. In contrast to aortic steno-
sions of vasoconstrictors, such as phenylephrine, may sis, the occurrence of sudden death in patients with aortic
reduce hemodynamic changes. regurgitation is rare.
A general anesthetic may be preferred to a regional
anesthetic because sympathetic nervous system blockade MANAGEMENT OF ANESTHESIA
can lead to undesirable decreases in systemic vascular Management of anesthesia for noncardiac surgery in
resistance. If surgery is peripheral, a regional anesthetic patients with aortic regurgitation is as described for
with careful intra-arterial pressure monitoring can be patients with mitral regurgitation (see Table 25-7).
equally successful. Maintenance of general anesthesia Preinduction intra-arterial pressure monitoring can
can be achieved with both intravenous and inhaled speed the identification and treatment of hemodynamic
anesthetics. A potential disadvantage of volatile inhaled changes and should be used for patients with significant
anesthetics is depression of sinus node automaticity, aortic regurgitation. Anesthetics with minimal effects on
which may lead to junctional rhythm and decreased left systemic vascular resistance or cardiac function should
ventricular filling due to loss of properly timed atrial be selected.
contractions. Techniques with peripheral vasodilation
should be used carefully. A prophylactic intravenous
Mitral Valve Prolapse
infusion of phenylephrine can be started prior to induc-
tion to reduce hemodynamic changes. The most impor- Mitral valve prolapse (click-murmur syndrome, Barlow
tant technique for the management of patients with syndrome) is characterized by an abnormality of the
aortic stenosis is intra-arterial pressure monitoring mitral valve support structure that permits prolapse of
with careful avoidance of hypotension. the valve into the left atrium during contraction of the
Intravascular fluid volume must be maintained by left ventricle.54 Previous estimates that mitral valve
prompt replacement of blood loss and liberal administration prolapse was present in 5% to 15% of individuals are
of intravenous fluids. If a pulmonary artery catheter is most likely erroneously high.55 Transesophageal or trans-
placed, it should be remembered that the occlusion pressure thoracic echocardiography can confirm the diagnosis of
may overestimate the left ventricular end-diastolic volume mitral valve prolapse, particularly in the absence of the
because of the decreased compliance of the left ventricle characteristic systolic murmur. The incidence of mitral
that accompanies chronic aortic stenosis. A cardiac defibril- valve prolapse in patients probably increases with mus-
lator should be promptly available when anesthesia is culoskeletal abnormalities, including Marfan syndrome,
administered to patients with aortic stenosis since external pectus excavatum, and kyphoscoliosis.
cardiac compressions are unlikely to generate an adequate Despite the prevalence of mitral valve prolapse, most
stroke volume across a stenosed aortic valve. patients are asymptomatic, emphasizing the usually
benign course of this abnormality. Nevertheless, serious
complications may accompany mitral valve prolapse
Aortic Regurgitation
(Table 25-9). For example, mitral valve prolapse is prob-
Aortic regurgitation is characterized by decreased for- ably the most common cause of pure mitral regur-
ward left ventricular stroke volume due to regurgitation gitation, which may progress to the need for surgical
of part of the ejected stroke volume from the aorta back intervention. Infective endocarditis is a potential compli-
into the left ventricle through an incompetent aortic cation, and transient ischemic attacks in patients younger
valve. A gradual onset of aortic regurgitation results in than 45 years of age are often associated with mitral
marked left ventricular hypertrophy and eventually
dilation. Increased myocardial oxygen requirements sec-
ondary to left ventricular hypertrophy, plus a character- Table 25-9 Complications Associated with Mitral Valve
istic decrease in aortic diastolic pressure that decreases Prolapse
coronary blood flow, can manifest as angina pectoris in Mitral regurgitation
the absence of coronary artery disease. Coronary blood Infective endocarditis
flow to the left ventricle occurs during diastole. In severe
or acute aortic regurgitation with low diastolic pressures Transient ischemic events
and elevated end-diastolic ventricular pressures, coronary Cardiac dysrhythmias
blood flow can be severely compromised. The combina-
Sudden death (extremely rare)
tion of a low diastolic pressure from aortic regurgitation
396
valve prolapse. Sudden death is an extremely rare 1. What is the heart rate?
complication of mitral valve prolapse, which may be 2. Are P waves present, and what is their relationship to
due to a ventricular cardiac dysrhythmia. the QRS complexes?
3. What is the duration of the PR interval (normal 120 to
MANAGEMENT OF ANESTHESIA 200 msec)?
Management of anesthesia for patients with mitral valve 4. What is the duration of the QRS complex (normal 50
prolapse should avoid events that can increase cardiac to 120 msec)?
emptying, which can accentuate prolapse of the mitral 5. Is the ventricular rhythm regular?
valve into the left atrium.56 Perioperative events that 6. Are there early cardiac beats or abnormal pauses after
can increase cardiac emptying include (1) sympathetic a preceding QRS complex?
nervous system stimulation, (2) decreased systemic 7. Is there evidence of prior myocardial infarction or
vascular resistance, and (3) performance of surgery with ventricular hypertrophy?
patients in the head-up or sitting position. Adequate 8. Is there evidence of myocardial ischemia?
intravascular fluid volume is of prime importance in the 9. Is there a conduction disturbance such as left bundle
preoperative period. Although intravenous anesthetics branch block, right bundle branch block, or intraven-
can be used to induce anesthesia, a sudden prolonged tricular conduction delay?
decrease in systemic vascular resistance must be avoided.
Also, intra-arterial pressure monitoring can facilitate
Heart Block
recognition and treatment of hemodynamic changes dur-
ing induction of anesthesia. Prophylactic infusions of Disturbances of conduction of cardiac impulses can be
phenylephrine can reduce systemic vasodilation with classified according to the site of the conduction block
induction of anesthesia. Ketamine and pancuronium are relative to the atrioventricular node (Table 25-10).
not recommended because of their ability to increase Heart block occurring above the atrioventricular node is
cardiac contractility and heart rate. Yet, these drugs usually benign and transient. Heart block occurring
are probably given to patients with undiagnosed and below the atrioventricular node tends to be progressive
asymptomatic mitral valve prolapse without problems. and permanent.
Addition of a narcotic to the anesthetic can minimize A theoretical concern in patients with bifascicular
sympathetic nervous system activation due to noxious heart block is that perioperative events, such as altera-
intraoperative stimulation. Volatile anesthetics should be tions in systemic blood pressure, arterial oxygenation, IV
titrated to avoid excessive decreases in systemic vascular or electrolyte concentrations, might compromise conduc-
resistance. Regional anesthetic can be used so long as tion in the one remaining intact fascicle, leading to the
undesirable decreases in systemic vascular resistance are acute onset intraoperatively of third-degree atrioventric-
avoided, which dictates appropriate monitoring. Prompt ular heart block. However, surgery performed during a
replacement of blood loss and generous administration general or regional anesthetic has not been shown to
of intravenous fluids will contribute to maintenance of
an optimal intravascular fluid volume and decrease the
potential adverse effects of positive-pressure ventilation. Table 25-10 Classification of Heart Block
Lidocaine, amiodarone, metoprolol, and esmolol should First-degree atrioventricular heart block
be available to treat cardiac dysrhythmias. If a vasocon-
Second-degree atrioventricular heart block
striction is needed to treat hypotension, an a-agonist,
such as phenylephrine, should probably be used. Mobitz type I (Wenckebach)
Mobitz type II
DISTURBANCES OF CARDIAC CONDUCTION Unifascicular heart block

AND RHYTHM (Also See Chapter 20) Left anterior hemiblock
Left posterior hemiblock
The ECG is a valuable tool for diagnosing disturbances
of cardiac conduction and rhythm. Ambulatory ECG mon- Right bundle branch block
itoring (Holter monitoring) is useful in documenting the Left bundle branch block
occurrence of life-threatening cardiac dysrhythmias and
Bifascicular heart block
assessing the efficacy of antidysrhythmic drug therapy.
The incidence of intraoperative cardiac dysrhythmias Right bundle branch block plus anterior hemiblock
depends on the definition (benign versus life-threatening), Right bundle branch block plus posterior hemiblock
patient characteristics, and the type of surgery (frequent
Third-degree (trifascicular, complete) atrioventricular heart
incidence during cardiothoracic surgery).56 The following
block
questions should be asked when interpreting the ECG:
397
predispose to the development of third-degree atrioven- with the intravenous administration of amiodarone,
tricular heart block in patients with coexisting bifascicu- lidocaine, or procainamide. Torsade-de-point responds
lar block. Therefore, placement of a prophylactic artificial to magnesium. Symptomatic ventricular tachycardia is
cardiac pacemaker is not required before anesthesia and best treated with external electrical cardioversion. The
surgery, but it should be available. presence of ventricular tachycardia should elicit an
Third-degree atrioventricular heart block is treated immediate search for a cause such as myocardial ische-
by placement of an artificial cardiac pacemaker. An arti- mia, hypoxia, electrolyte abnormalities, or myocardial
ficial cardiac pacemaker can be inserted intravenously stimulation by the surgeons.
(endocardial lead) or by the subcostal approach (epicardial
or myocardial lead). An alternative to emergency trans-
Pre-Excitation Syndromes
venous artificial cardiac pacemaker placement is non-
invasive transcutaneous or temporary esophageal cardiac Pre-excitation syndromes are characterized by activation
pacing. A continuous intravenous infusion of isoprotere- of a portion of the ventricles by cardiac impulses that
nol acting as a pharmacologic cardiac pacemaker may be travel from the atria via accessory (anomalous) conduc-
necessary to maintain an adequate heart rate until artificial tion pathways. These pathways bypass the atrioventricu-
electrical cardiac pacing can be established. lar node such that activation of the ventricles occurs
earlier than it would if impulses reached the ventricles
by normal pathways.
Sick Sinus Syndrome
Sick sinus syndrome is characterized by inappropriate
WOLFF-PARKINSON-WHITE SYNDROME
sinus bradycardia associated with degenerative changes
The Wolff-Parkinson-White syndrome is the most com-
in the sinoatrial node. Frequently, bradycardia due to
mon pre-excitation syndrome, with an incidence of
this syndrome is complicated by episodes of supra-
approximately 0.3% of the general population. The lack
ventricular tachycardia. Artificial cardiac pacemakers
of physiologic delay in transmission of cardiac impulses
may be indicated when therapeutic plasma concentra-
along the Kent fibers results in the characteristic short PR
tions of drugs necessary to control tachycardia result
interval (less than 120 msec) on the ECG. The wide QRS
in bradycardia. The increased incidence of pulmonary
complex and delta wave on the ECG reflect the composite
embolism in these patients may be a reason to initiate
of cardiac impulses conducted by normal and accessory
anticoagulation.
pathways. Paroxysmal atrial tachycardia is the most
frequent cardiac dysrhythmia. More patients with Wolff-
Ventricular Premature Beats Parkinson-White syndrome are frequently treated by cath-
eter ablation of accessory pathways as identified by
Ventricular premature beats (VPCs) are recognized on the
electrophysiologic mapping. Supraventricular tachy-
ECG by (1) premature occurrence, (2) the absence of a
cardias such as atrial fibrillation or atrial flutter with
P wave preceding the QRS complex, (3) a wide and often
one-to-one conduction may lead to hemodynamic col-
bizarre QRS complex, (4) an inverted T wave, and (5) a
lapse in patients with Wolff-Parkinson-White syndrome.
compensatory pause that follows the premature beat.
The primary goal with VPCs should be to identify any
underlying cause (myocardial ischemia, arterial hypox- MANAGEMENT OF ANESTHESIA
emia, hypercarbia, hypertension, hypokalemia, mechani- The goal during management of anesthesia in the presence
cal irritation of the ventricles) if possible and correct it. of a pre-excitation syndrome is to avoid events (anxiety) or
Ventricular premature beats can be treated with lidocaine drugs (anticholinergics, ketamine, pancuronium) that
(1 to 2 mg/kg IV) when they (1) are frequent (more than might increase sympathetic nervous system activity and
6 premature beats/min), (2) are multifocal, (3) occur predispose to tachydysrhythmias.56 All cardiac antidysr-
in salvos of 3 or more, or (4) take place during the hythmic drugs should be continued throughout the peri-
ascending limb of the T wave (R on T phenomenon) that operative period. Anesthesia can be induced with
corresponds to the relative refractory period of the intravenous anesthetic, with the possible exception of
ventricle. ketamine. Tracheal intubation should be performed only
after a sufficient concentration or dose of anesthetic has
been given to reliably blunt sympathetic nervous system
Ventricular Tachycardia
stimulation evoked by instrumentation of the upper
Ventricular tachycardia is defined as the appearance of at airway. Intravenous b-adrenergic blockers (atenolol, met-
least three consecutive wide QRS complexes (longer than oprolol, propranolol, or esmolol) can be used to avoid
120 msec) on the ECG occurring at an effective heart tachycardia during induction of anesthesia. Neuromus-
rate more rapid than 120 beats/min. Ventricular tachy- cular blocking drugs with minimal effects on heart rate
cardia not associated with hypotension is initially treated should be used.
398
The onset of paroxysmal atrial tachycardia or fibrilla- cardiac pacemaker placed for third-degree heart block,
tion in the perioperative period can be treated with the appropriate experts regarding the continuous operation
intravenous administration of drugs that abruptly pro- of that device and monitoring of its operation need to be
long the refractory period of the atrioventricular node immediately available. If a pacemaker implanted for
(adenosine) or lengthen the refractory period of accessory third-degree heart block is to be disconnected to change
pathways (procainamide). b-Adrenergic blockers may be the stimulator, transvenous pacing may be needed. If the
used to control heart rate. Digitalis and verapamil may device is an automatic defibrillator, it will need to be inac-
decrease the refractory period of accessory pathways tivated during electrical-surgical cautery to avoid the
responsible for atrial fibrillation, resulting in an increase device erroneously detecting ventricular dysrhythmias
in ventricular response rate during this dysrhythmia and and defibrillating, which would waste battery life and pos-
should be avoided. Electrical cardioversion is indicated sibly cause R on T phenomena (see electrocardiogram) and
when tachydysrhythmias are life-threatening. ventricular fibrillation. The device should be reactivated
after the surgical procedure and interrogated for proper
function. The magnet mode of many implanted devices
Prolonged QT Interval Syndrome
is now programmable. The magnet mode cannot automat-
A prolonged QT interval (longer than 440 msec on the ically be assumed to be “safe.” The specific magnet mode
ECG) syndrome is associated with ventricular dysrhyth- for a patient’s device should be identified as some magnet
mias, syncope, and sudden death. Treatment probably modes change with device state or are programmable.
should include b-adrenergic antagonists or left stellate Magnet mode for many pacemakers is asynchronous at
ganglion block. The effectiveness of a left stellate gan- 99 beats/min. If the patient has a spontaneous heart rate
glion block supports the hypothesis that this syndrome of 60 to 80 beats/min, the asynchronous mode at
results from a congenital imbalance of autonomic inner- 99 beats/min would be safe. However, in some devices,
vation to the heart produced by decreases in right cardiac the magnet mode shifts to asynchronous at 50 beats/min
sympathetic nerve activity. Management of anesthesia at the end of battery life. Asynchronous pacing at
includes avoidance of events or drugs that are likely to 50 beats/min may lead to R on T phenomena if the patient
activate the sympathetic nervous system and availability has a spontaneous heart rate above 50 beats/min. The spe-
of b-antagonists (metoprolol, atenolol, propranolol, or cific magnet mode should be identified and used only
esmolol) or electrical cardioversion to treat life-threatening when needed given the circumstances of the case.
ventricular dysrhythmias.56 Inhaled and intravenous Intraoperative monitoring of patients with artificial IV
anesthetics can prolong the QT interval on the ECG in cardiac pacemakers includes the ECG and possible intra-
normal patients. Fortunately, these anesthetics do not arterial pressure monitoring so as to detect the appear-
produce additional prolonged QT interval in those patients ance of asystole promptly. Atropine, isoproterenol, and
with this syndrome in a predictable manner.57 Many an external pacemaker should be available if the artificial
medications have the potential to prolong the QT interval cardiac pacemaker ceases to function. If electrocautery
(droperidrol)58,59 and should be avoided if possible, in interferes with the ECG, monitoring intra-arterial pres-
patients with prolonged QT syndrome. sure, or arterial oxygenation, auscultation through an
esophageal stethoscope or a palpable pulse confirms
continued cardiac activity. Monitoring systemic blood
ARTIFICIAL CARDIAC PACEMAKERS pressure with an intra-arterial catheter provides immedi-
ate evidence of loss of pacemaker function and should be
Preoperative evaluation of the patient with an artificial considered in patients with third-degree heart block.
cardiac pacemaker in place includes determination of Inhibition of pulse generator activity by electromagnetic
the reason for placing the pacemaker, assessment of its interference most commonly from electrosurgical cau-
present function, as well as the brand, model, magnet tery, which is interpreted as spontaneous cardiac activity
mode, and availability of a programmer for this specific by the artificial cardiac pacemaker, is most likely when
device and a person who knows how to operate the the ground plate for electrocautery is placed too near
programmer.60 Many implanted electrical devices can the pulse generator or unipolar cautery is used. For this
be used. A device under the skin may not be a pacemaker. reason, the ground plate should be placed as far as possi-
Implanted devices include deep brain stimulators, auto- ble from the pulse generator. Bipolar electrocautery may
matic implantable cardiac defibrillators, intravenous also reduce interference between electrosurgical cautery
pumps, spinal stimulators for chronic pain, bladder and the pacemaker. If surface pads are placed for external
stimulators for neurogenic bladder, gastric stimulators pacing or defibrillation, they should be placed away from
for the treatment of obesity, intravenous ports, and vagal the implanted device to reduce current passing down the
stimulators for sleep. pacing lead and hyperpolarizing a small segment of myo-
Special considerations are necessary for devices where cardium, which could interfere with pacemaker capture
the patient’s life depends on the device. If a device is a after defibrillation. Automatic implantable cardioversion
399
devices sense ventricular fibrillation or ventricular peripheral vascular disease should be recognized, as all
tachycardia. They provide a cardioversion shock through patients with peripheral vascular disease have coronary
implanted cardiac leads. Electrocautery signals can be artery disease. About 50% of patients with evidence of
misinterpreted as ventricular dysrhythmias, thus trigger- peripheral vascular disease will have more than 50% ste-
ing unnecessary shocks and decreasing battery life. These nosis of one or more coronary arteries even in the absence
devices should be reprogrammed to the standby mode of angina pectoris and the presence of a normal resting
prior to elective surgery and returned postoperatively to ECG. Additional monitoring, including intra-arterial cath-
full function with interrogation of proper operation. eter monitoring, is justified for significant operations.
Selection of drugs or techniques for anesthesia is Patients with increased pulse pressure have increased
not influenced by the presence of artificial cardiac pace- perioperative and long-term complications.63 Essential
makers as there is no evidence that the threshold and sub- hypertension is associated with a shift to the right of the
sequent response of these devices is altered by drugs curve for the autoregulation of cerebral blood flow,
administered in the perioperative period. However, patients emphasizing that these patients are more vulnerable to
with artificial cardiac pacemakers or implanted cardio- cerebral ischemia should perfusion pressures decrease.
version devices have a frequent incidence of coexisting Detection of renal dysfunction due to chronic hyperten-
cardiac disease and should be monitored carefully and sion may influence the selection of drugs, particularly if
anesthetized with care. Patients with defibrillators fre- elimination from the plasma depends on renal clearance
quently have poor ventricular function. Insertion of a pulmo- or metabolites of the drugs are known potential nephro-
nary artery catheter will not disturb epicardial electrodes toxins (fluoride from metabolism of sevoflurane).
but might dislodge recently placed (within 2 weeks) trans- Hypertension should be treated preoperatively because
venous endocardial electrodes.61 Pulmonary artery catheters the incidence of hypotension and evidence of myocardial
are not necessary for cases with minimal fluid shifts. ischemia on the ECG during the maintenance of anesthesia
is increased in patients who remain hypertensive before
the induction of anesthesia.62 Perioperative therapy with
ESSENTIAL HYPERTENSION b-adrenergic blockers for at least 7 days and continued for
30 days postoperatively reduces the risk of cardiac morbid-
Essential hypertension is arbitrarily defined as sustained ity and death 90% for patients at risk.12–15 Perioperative
increases in systemic blood pressure (systolic blood pres- therapy with clonidine started the night before surgery
sure higher than 160 mm Hg or a diastolic blood pressure and continued for 4 days reduces the 30-day and 2-year
higher than 90 mm Hg) independent of any known cause. mortality rates.16 Administration of intravenous b-blockers
Treatment of essential hypertension with appropriate drug just prior to surgery and continued for 7 days reduces the
therapy decreases the incidence of stroke and congestive risk of death 50%.14,15 Prophylactic cardiac risk reduction
heart failure. Hypertension is a risk factor for coronary therapy with b-blockers or clonidine of patients with coro-
artery disease, and the longer the patient has hypertension nary artery disease, peripheral vascular disease, or two risk
the higher the risk of end organ damage. Patients with two factors (age greater than or equal to 60, hypertension,
risk factors (hypertension, smoking, diabetes, elevated cholesterol higher than 240 mg/dL, diabetes, or smoking)
cholesterol, or the elderly) for coronary artery disease reduces risk of perioperative death.12–16 Appropriate dosing
should be treated as if they have coronary artery disease. of b-adrenergic blockers is important to avoid sequelae.31
Management of anesthesia for patients with essential Despite therapy, systemic blood pressure increases during
hypertension includes preoperative evaluation of drug the intraoperative period are more likely to occur in patients
therapy and extent of the disease plus a consideration of with a history of essential hypertension regardless of the
the implications of exaggerated systemic blood pressure degree of pharmacologic control of systemic blood pressure
responses elicited by painful intraoperative stimulation.62 established preoperatively. Furthermore, the incidence of
postoperative cardiac complications is not increased when
hypertensive patients undergo elective operations as long
Preoperative Evaluation (Also See Chapter 13)
as the preoperative diastolic blood pressure is not more than
Preoperative evaluation of patients with essential hyper- 110 mm Hg and heart rate is controlled. Pretreatment with a
tension begins with a determination of the adequacy of b-blocker or the a2-agonist, such as clonidine, may be useful
systemic blood pressure control and a review of the phar- in blunting exaggerated sympathetic nervous system
macology of the antihypertensive drugs being used for responses and reduces perioperative mortality rate.14–16
therapy (see Chapter 7). Antihypertensive drugs should be
continued throughout the perioperative period. Evidence
Induction of Anesthesia
of major organ dysfunction (congestive heart failure, cor-
onary artery disease, cerebral ischemia, renal dysfunction) Induction of anesthesia with intravenous drugs is accept-
must be sought. Patients with essential hypertension have able, remembering that an exaggerated decrease in
an increased risk of coronary artery disease. Evidence of systemic blood pressure may occur, particularly if
400
hypertension is present preoperatively. Sodium thiopental,

Table 25-11 Management of Anesthesia for Patients
propofol, midazolam, synthetic opioids (fentanyl, sufenta- with Essential Hypertension
nil, alfentanil, remifentanil), and etomidate all have been
used to induce anesthesia. Any anesthetic is acceptable Preoperative Evaluation
if used with appropriate dosing and careful monitoring. ▪ Determine the adequacy of systemic blood pressure
Etomidate or combinations of midazolam and fentanyl control.
are frequently used because of their limited hemodynamic ▪ Review the pharmacology of antihypertensive drugs.
effects. Ketamine is rarely selected for induction of anes- ▪ Evaluate associated organ dysfunction (cardiac, central
thesia in patients with essential hypertension because it nervous system, renal).
can increase systemic blood pressure and cause tachy- ▪ Consider the administration of prophylactic anti-
cardia, which may lead to myocardial ischemia. Placement ischemic therapy (perioperative b-blockade or
of an intra-arterial pressure monitor prior to induction clonidine).
of anesthesia and prophylactic infusions of the vaso- ▪ Choose appropriate monitors and consider intra-arterial
constrictor phenylephrine can reduce hemodynamic per- pressure monitoring.
turbations with induction of anesthesia. Hemodynamic Induction of Anesthesia and Tracheal Intubation
changes with induction most likely reflect unmasking ▪ Anticipate exaggerated systemic blood pressure
of decreased intravascular fluid volume due to chronic changes.
hypertension combined with a stiffening of the arterial ▪ Consider initiation of prophylactic infusion of
vasculature. phenylephrine to reduce hemodynamic perturbation
Hypertension can occur during direct laryngoscopy with induction.
for tracheal intubation in patients with essential hyper- ▪ Minimize the pressor response during tracheal
tension but may be attenuated with administration of intubation by limiting the duration of direct
opioids and b-adrenergic blockers. Tachycardia may lead laryngoscopy to <15 seconds.
to episodes of myocardial ischemia. A single 1-minute
episode of myocardial ischemia increases the risk of peri-
operative cardiac morbidity tenfold and death twofold. ▪ Use a volatile anesthetic and vasoconstrictors to
control systemic arterial blood pressure.
The risk of myocardial ischemia can be reduced by
prophylactic therapy with b-blockers or clonidine.14–16 ▪ Monitor the electrocardiogram for evidence of
Maximal attenuation of sympathetic nervous system
myocardial ischemia (avoidance is better than
detection).
IV
responses should be attempted during direct laryngoscopy
by administering anesthetics, intravenous opioids, and ▪ Anticipate excessive increases in systemic blood
pressure with emergence.
b-blockers before attempting tracheal intubation. Careful
attention to the airway is critical in all anesthetics, and Postoperative Management
the risks are even more intense in patients with cardiac ▪ Ensure effective pain control.
disease. If the patient has a recognized difficult airway ▪ Patient’s blood pressure will return to preoperative level
precluding direct laryngoscopy, heart rate control is of or greater after emergence from anesthesia, be ready to
prime importance, including possibly selecting alternative treat as needed.
approaches such as fiberoptic intubation. Hypoxia, tachy- ▪ Continue perioperative anti-ischemic therapy for at
cardia, hypotension, hypertension, and myocardial ische- least a week in low-risk patients, 30 days in those at
mia must be avoided. Yet, an excessive concentration or higher risk, and permanently in patients with known
dose of anesthetic drugs can produce hypotension, which coronary artery disease or vascular disease.
is as undesirable as hypertension. An important concept
for limiting pressor responses elicited by tracheal intu-
bation is to limit the duration of direct laryngoscopy to less
than 15 seconds if possible. In addition, the administration or without nitrous oxide and a narcotic are commonly
of laryngotracheal lidocaine immediately before place- used. Changes in the concentration of volatile anesthetics
ment of the tube in the trachea will minimize any addi- allow rapid adjustments in the depth of anesthesia in
tional pressor response. response to increases or decreases in arterial blood pres-
sure. Changes in surgical stimulation may lead to
changes in blood pressure and heart rate. Additional
doses of narcotics, b-blockers, and changes in the dose
The goal during maintenance of anesthesia is to adjust of volatile anesthetic can be used to control hemodynam-
the concentrations of anesthetics so tachycardia and wide ics. Heart rate control is the most critical element for
fluctuations in systemic blood pressure can be avoided preventing cardiac morbidity and death. Heart rates
(Table 25-11). No anesthetic technique has been shown above 120 beats/min increase mortality rate. Volatile
to be superior. Combinations of volatile anesthetics with anesthetics are useful for attenuating activity of the
401
sympathetic nervous system, which is responsible for ischemia in the days prior to surgery. The night before
these pressor responses. The ability to rapidly increase surgery is stressful and prophylactic b-blockade or cloni-
the alveolar concentration of sevoflurane (because of its dine can reduce the risk of sympathetic stimulation
low blood solubilities) makes this volatile anesthetic resulting in tachycardia and subsequent myocardial
uniquely efficacious for treating sudden increases in ischemia. There is the erroneous belief that minor surgery
systemic blood pressure (see the discussion under “Coro- causes minor stress. Patients scheduled for ophthalmic
nary Artery Disease,” at “Maintenance of Anesthesia”). surgery, a minor outpatient procedure, commonly have
Rapid changes in desflurane concentration may lead to sympathetic stimulation resulting in preoperative hyper-
tachycardia, hypertension, pulmonary hypertension, and tension. Prophylactic therapy with b-blockers or clonidine
myocardial ischemia and should be avoided. A positive can reduce the preoperative hypertensive episodes and
feedback situation can occur with desflurane anesthetics myocardial ischemia. Appropriate dosing of all medica-
whereby a surgical stimulus can raise blood pressure, tions is essential and inappropriate dosing may lead to
the anesthetist raises the desflurane concentration, which hypotension, bradycardia, and increased morbidity and
stimulates the sympathetic system causing the blood mortality rates.31 All medications have a therapeutic
pressure to increase, which causes the anesthetist to index. Withholding antihypertensive medications may
further increase the desflurane concentration, which lead to withdrawal phenomena and increase the morbidity
further raises the blood pressure. and mortality rates.
Both intravenous and inhaled anesthetics can be used.
For example, a nitrous oxide–opioid technique is accept-
Postoperative Management
able for the maintenance of anesthesia, but the addition
of a volatile anesthetic is often necessary to prevent Hypertension in the early postoperative period is a fre-
hypertension, particularly during periods of maximal quent occurrence in patients with a preoperative diagno-
surgical stimulation. Total intravenous anesthesia (com- sis of essential hypertension. Prophylactic or therapeutic
binations of dexmedetomidine, propofol, narcotics, and administration of b-blockers or clonidine can reduce
benzodiazepines) can also be used. Continuous intrave- these episodes of hypertension and reduce risk of periop-
nous infusions of phenylephrine, nitroprusside, nitrogly- erative ischemia and death. If hypertension persists
cerine, carvedilol, or esmolol can be used to maintain despite b-blockers and adequate analgesia, it may be
normotension during the intraoperative period. Hypo- necessary to pharmacologically decrease systemic blood
tension that occurs during maintenance of anesthesia pressure utilizing a continuous intravenous infusion of
is often treated by decreasing the concentrations of nitroprusside, nitroglycerin, or intermittent injections of
volatile anesthetic while infusing fluids intravenously to hydralazine (5 to 20 mg IV) or labetalol (0.1 to 0.5 mg/
increase intravascular fluid volume. Sympathomimetics, kg IV). Tachycardia in the postoperative period must be
such as ephedrine, or vasoconstrictors such as phenyl- actively avoided as it increases morbidity and mortality
ephrine may be necessary to restore perfusion pressures rates. A heart rate of 120 beats/min raises the risk of
until the underlying cause of the hypotension can be postoperative death. Clearly the arterial blood pressure
corrected. needs to be controlled during the entire perioperative
The choice of intraoperative monitors for patients period. The patient needs preoperative, intraoperative,
with coexisting essential hypertension is influenced by and postoperative hemodynamic and autonomic control
the complexity of the surgery. The ECG is monitored with to prevent associated cardiac morbidity and death. Anes-
the goal of recognizing changes suggestive of myocardial thesia care for patients with cardiac disease truly needs to
ischemia. Invasive monitoring with an intra-arterial be perioperative for optimal outcomes. If a patient needs
pressure monitor is commonly used. Pulmonary artery a medication to control blood pressure and heart rate
catheters may be considered if major surgery is planned while at home, he will likely need it during surgery
and there is evidence preoperatively of left ventricular and postoperative care. Withdrawal of antihypertensive
dysfunction, although there is no evidence that demon- and anti-ischemic medications in the perioperative
strates improved outcomes with pulmonary artery period increases cardiac risk.23,25,26
catheter monitoring. Monitoring with transesophageal
echocardiography is an alternative to placement of a
pulmonary artery catheter. CONGESTIVE HEART FAILURE
A regional anesthetic is an excellent choice in patients
with multiple medical conditions scheduled for peri- Elective surgery should not be performed on patients
pheral surgery. Whatever the choice of anesthetic, b- with congestive heart failure unless optimally treated.
adrenergic blockers, a2-agonist clonidine, and sedatives The preoperative presence of congestive heart failure is
can be used to reduce sympathetic nervous system stim- associated with significant postoperative morbidity or
ulation. Patients with cardiac disease who are scheduled mortality rates. Cardiology consultation is frequently
for elective surgery can have episodes of myocardial helpful in patients with congestive failure as consideration
402
of surgical or interventional revascularization and im-

provement of medical therapy can improve cardiac func- HYPERTROPHIC CARDIOMYOPATHY
tion. Preoperative initiation of b-blockers and vasodilator
therapy with angiotensin-converting enzyme inhibitors Hypertrophic cardiomyopathy (idiopathic hypertrophic
can improve ventricular function and reduce operative subaortic stenosis) is characterized by obstruction to left
risk. These drugs should be started by physicians with ventricular outflow produced by asymmetrical hypertro-
expertise in treating congestive failure and the doses phy of the intraventricular septal muscle.64 Associated
increased slowly as tolerated over 3 to 6 months as the left ventricular hypertrophy in an attempt to overcome
heart function recovers. the obstruction may be so massive that the volume of
the left ventricular chamber is decreased. Despite these
adverse changes, the stroke volume remains normal or
Management of Anesthesia increased owing to the hypercontractile state of the myo-
When surgery cannot be delayed, however, the drugs cardium. This disease is often hereditary, and the genetic
and techniques chosen to provide anesthesia must be defect seems to be an increased density of calcium
selected with the goal of minimizing detrimental channels manifesting as myocardial hypertrophy.
effects on cardiac output. Optimal cardiac output can
be obtained when the impedance of the vasculature
(preload and afterload) match the impedance of the Management of Anesthesia
heart and can be achieved by careful preload and The goal during management of anesthesia for patients
afterload management. with hypertrophic cardiomyopathy is to decrease the
Etomidate may be useful for the induction of anesthe- pressure gradient across the left ventricular outflow
sia in the presence of congestive heart failure because of obstruction (Table 25-12). Decreases in myocardial con-
its limited effect on the sympathetic nervous system. tractility and increases in preload (ventricular volume)
Small concentrations of volatile anesthetics can maintain and afterload will decrease the magnitude of left ventric-
anesthesia, but cardiac depression should be avoided if ular outflow obstruction. Volatile anesthetics are useful
possible. In the presence of severe congestive heart fail- for maintenance of anesthesia, providing mild depression
ure, the use of opioids in large doses as the primary anes- of myocardial contractility. Theoretically, isoflurane, des-
thetic in combination with amnestic benzodiazepines flurane, and sevoflurane would be less ideal choices than
(midazolam) may be justified, although no evidence sup- halothane because these drugs decrease systemic vascular IV
ports this approach over the use of a primary volatile resistance more than does halothane. Rapid increases in
anesthetic combined with narcotics.46 Positive-pressure desflurane may cause sympathetic stimulation with
ventilation of the lungs may be beneficial by decreasing tachycardia, hypertension, bronchospasm, and pulmo-
pulmonary congestion, improving arterial oxygenation, nary hypertension and should be avoided. Primary opioid
and eliminating the work of breathing. The resumption anesthetics may not be optimal as they do not produce
of negative intrathoracic pressures with spontaneous myocardial depression and can decrease systemic vascu-
ventilation following extubation can lead to increased lar resistance. High potency opioids stimulate the vagus
filling pressures and worsening heart failure. Invasive nerve, lower heart rate, and can decrease sympathetic
monitoring of intra-arterial blood pressure is helpful. stimulation improving hemodynamics. Combinations of
Use of pulmonary arterial catheters can be helpful in volatile agents (sevoflurane or isoflurane) with an opioid
hemodynamic management but no evidence exists that are commonly selected.
they reduce operative risk or improve outcome. Main-
tenance of blood pressure with vasoconstrictors (phen-
ylephrine) should precede increasing myocardial
contractility with continuous intravenous infusions of Table 25-12 Events that Decrease Left Ventricular
inotropic drugs such as epinephrine, dopamine, and Outflow Obstruction in the Presence of Hypertrophic
dobutamine. The use of b-adrenergic agonists in patients Cardiomyopathy
with congestive heart failure may decrease chance of sur- Decreased Myocardial Contractility
vival and should only be used when necessary. b-Adrenergic blockade (atenolol, metoprolol, propranolol,
Regional anesthesia should be considered for patients esmolol)
with congestive heart failure requiring peripheral or Volatile anesthetic (sevoflurane or isoflurane)
minor surgery. Anesthetics with minimal hemodynamic Increased Preload
effects are optimal. If the surgery precludes such a choice, Increased intravascular fluid volume
general anesthesia with careful hemodynamic control Bradycardia (fentanyl or sufentanil)
with intra-arterial pressure monitoring, infusions of
Increased Afterload
vasoconstrictors, and possibly inotropic drugs, with the a-Adrenergic stimulation (phenylephrine infusions)
careful avoidance of tachycardia, should be used.
403
Intraoperative hypotension is generally treated with right ventricular failure, combinations of b-agonists and
intravenous fluids or an a-agonist such as phenylephrine. phosphodiesterase inhibitors (amrinone or milrinone)
Drugs with b-agonist activity are not likely to be used can provide synergistic improvements in ventricular
to treat hypotension because any increase in cardiac function and vasodilation, thus improving cardiac
contractility or heart rate could increase left ventricular output.
outflow obstruction. When hypertension occurs, an
increased delivered concentration of isoflurane or sevo-
flurane can be used. Vasodilators, such as nitroprusside CARDIAC TAMPONADE
or nitroglycerin, should be used with caution because
decreases in systemic vascular resistance can increase left Cardiac tamponade is characterized by (1) decreases in
ventricular outflow obstruction. diastolic filling of the ventricles, (2) decreases in stroke
volume, and (3) decreases in systemic blood pressure due
to increased intrapericardial pressure from accumulation
of fluid in the pericardial space (Table 25-13). Decreased
PULMONARY HYPERTENSION AND COR
stroke volume from inadequate ventricular filling results
PULMONALE
in activation of the sympathetic nervous system (tachycar-
dia, vasoconstriction) in attempts to maintain the cardiac
Cor pulmonale is the designation for right ventricular
output. Cardiac output and systemic blood pressure are
hypertrophy and eventual cardiac dysfunction that
maintained only as long as the pressure in the central
occurs secondary to chronic pulmonary hypertension.
veins exceeds the right ventricular end-diastolic pressure.
Elective operations in patients with cor pulmonale should
Institution of general anesthesia and positive-pressure
not be performed until any reversible component of the
ventilation of the lungs in the presence of cardiac tampo-
coexisting pulmonary vascular disease has been treated.
nade can lead to profound hypotension or death, reflecting
anesthetic-induced peripheral vasodilation, direct myo-
cardial depression, and decreased venous return. When
percutaneous pericardiocentesis cannot be performed
Goals during management of anesthesia in patients with using local anesthesia, the induction and maintenance of
cor pulmonale are to avoid events or drugs that could general anesthesia are extremely dangerous but may be
increase pulmonary vascular resistance. Volatile anes- achieved while carefully maintaining spontaneous respi-
thetics are useful for relaxing vascular smooth muscle ration. Potential adverse effects of increased intrathoracic
and attenuating airway responsiveness to stimuli pressure from controlled respiration on venous return
produced by a tracheal tube. Pulmonary vasodilation must be taken seriously. If possible, positive-pressure
with prostaglandins (epoprostenol, treprostinil, iloprost, ventilation of the lungs should be avoided until drainage
beraprost), endothelin receptor antagonists (bosentan, of the pericardial space is imminent. With this in mind,
sitaxsentan, ambrisentan), inhaled nitric oxide, inhaled tracheal intubation with topical anesthesia has been
milrinone, type 5 phosphodiesterase inhibitors (sildenafil, suggested.
vardenafil), or soluble guanylate cyclase activators (cina-
ciguat, riociguat) have been tried with variable success.
Patients with pulmonary hypertension have significant
increased risk and should be treated with extreme care.
Table 25-13 Manifestations of Cardiac Tamponade
Nitrous oxide may increase pulmonary vascular resis-
tance and should probably be avoided.52 Another disad- Primary diastolic dysfunction from increased pericardial
vantage of nitrous oxide is the associated decrease in pressure
the inspired concentration of oxygen necessitated by Hypotension
the administration of this drug.
Tachycardia
Intra-arterial pressure monitoring is very helpful for
hemodynamic management. Monitoring of pulmonary Increased systemic vascular resistance
arterial or right atrial pressure (or both) may be helpful Low cardiac output
to detect any adverse effect on pulmonary vasculature.
TEE monitoring can be very helpful in blood volume Equalization of left and right diastolic filling pressures
management. In severe cor pulmonale, inotropic support Exaggeration of blood pressure variation with respiration
with b-agonists can improve cardiac function. Therapy Fixed and reduced stroke volume (cardiac output and
should be chosen based on the hemodynamic problem systemic blood pressure dependent on heart rate)
(volume, systemic vascular resistance, chronotropy, ino-
tropy, and pulmonary hypertension). b-Agonists must Failure to respond to volume and multiple inotropes with
cardiogenic shock
be used carefully to avoid myocardial ischemia. In severe
404
Management of Anesthesia Starting b-blockers on the day of surgery and continuing

for 7 days reduces mortality rate 50%.15 Clonidine reduces
Prior to the induction of general anesthesia in patients
30-day and 2-year mortality rates16 and may be used in
with significant cardiac tamponade, the patient should
patients with specific contraindications (reactive asthma
be positioned on the operating room table. Intra-arterial
or atrioventricular block or allergy) to b-blockade. Periop-
monitoring is helpful if time permits. The chest and
erative statin use reduces risk of mortality an additional
abdomen should be prepped and draped for surgery.
50% over the benefits of b-blockers and should be started
The surgeons should be scrubbed, gowned, gloved, and
30 days preoperatively and continued at least 30 days
at the operating room table ready for incision prior to
postoperatively, if not indefinitely.17
anesthetic induction. It is optimal if anesthetic induction,
The surgical approach certainly influences the anes-
intubation, incision, and drainage of the pericardial tam-
thetic. Endovascular aneurysm repair is less invasive
ponade can occur in extremely rapid succession (less
and may require only regional anesthesia, although in
than 60 seconds). Although continuous intravenous infu-
prolonged cases general anesthesia is preferred. Open
sions of catecholamines (epinephrine, norepinephrine,
procedures for aortic aneurysm surgery are major proce-
dopamine, dobutamine, or isoproterenol) and vasocon-
dures and require general anesthesia. All patients under-
strictors may be necessary to maintain cardiac output
going anesthesia for resection of an abdominal aortic
and blood pressure, the primary therapy is pericardial
aneurysm should have monitoring of intra-arterial
drainage. A common sign of cardiac tamponade is
pressures. The use of pulmonary arterial pressure moni-
hemodynamic collapse and cardiogenic shock unrespon-
toring is controversial.47,48 Patients with coexisting coro-
sive to fluids and inotropes. Systolic ventricular function
nary artery disease are likely to develop increases in
is not the problem; diastolic dysfunction from increased
the pulmonary artery occlusion pressure and evidence
pericardial pressure is the primary problem. Once the
of myocardial ischemia during cross-clamping of the
pericardium is drained, venous return can enter the heart
abdominal aorta. Transesophageal echocardiography
and hemodynamics will rapidly normalize.
may be useful in evaluating the adequacy of intravascu-
lar volume replacement and in the recognition of cardiac
wall motion abnormalities associated with myocardial
ischemia, although no data support its use as a risk
ANEURYSMS OF THE AORTA
reduction strategy. Intraoperatively, myocardial ischemia
Aneurysms of the aorta most often involve the abdomi-
is treated by decreasing heart rate with b-blockers and IV
maintaining systemic blood pressure and filling pressures
nal aorta but may involve any part including thoracic
to acceptable levels by pharmacologic interventions,
or abdominal. Most patients are hypertensive, and many
which may include continuous intravenous infusion of
have associated atherosclerosis. A dissecting aneurysm
phenylephrine (for hypotension), nitroprusside, or nitro-
denotes a tear in the intima of the aorta that allows blood
glycerine (for hypertension). Preoperative hydration with
to enter and penetrate between the walls of the vessel,
a balanced salt solution and prompt intraoperative
producing a false lumen. Ultimately, the dissection may
replacement of blood loss as guided by data obtained
reenter the lumen through another tear in the intima or
from the pulmonary artery catheter, echocardiography,
rupture through the adventitia.
or continuous cardiac output devices are considered
Elective repair of an abdominal aneurysm is often
useful for maintaining intravascular fluid volume and
recommended when the estimated diameter of the aneu-
thus renal function. Diuresis is often facilitated by intra-
rysm is more than 5 cm. The incidence of spontaneous
operative administration of a diuretic (mannitol, furo-
rupture increases dramatically when the size of the aneu-
semide, or both) with or without dopamine. Despite
rysm exceeds this diameter. Extension of the abdominal
these interventions, glomerular filtration rate and renal
aneurysm to include the renal arteries occurs in about
blood flow are not predictably improved.65
5% of patients.
Hypotension can accompany unclamping of the
abdominal aorta, presumably reflecting sudden increases
in vascular resistance and venous compliance with reper-
fusion. Systemic blood pressure decreases can be mini-
All surgery patients with vascular disease should be con- mized by infusing intravenous fluids to maintain the
sidered for prophylactic b-blocker and statin therapy. pulmonary artery occlusion pressure between 10 and
Perioperative administration of b-blockers reduces periop- 20 mm Hg before removal of the aortic cross-clamp.
erative mortality rate 50% to 90%. b-Blockers should be Gradual removal of the aortic cross-clamp minimizes
started as soon as patients are identified as needing sur- decreases in systemic blood pressure by allowing time
gery. Starting b-blockers 7 to 30 days preoperatively and for return of pooled venous blood to the circulation.
continuing for at least 30 days postoperatively is most The exact cause of hypotension and vasodilation follow-
effective, with a 90% reduction in mortality rate.12,13 ing removal of the aorta is unclear.
405
CARDIOPULMONARY BYPASS cava into a reservoir, followed by its pumping through

(Also See Chapter 26) a heat exchanger, oxygenator, and filter, followed by its
return to the arterial system, usually the ascending aorta,
Cardiopulmonary bypass (extracorporeal circulation) by means of a centrifugal or roller pump (Fig. 25-3).66
support is used to stabilize the myocardium reducing In the presence of a competent aortic valve, the heart is
motion during coronary artery bypass surgery and allow excluded from the patient’s circulation by either a single
ascending aortic and intraventricular procedures (valve venous cannula inserted into the right atrium (see
repair or replacement). Cardiopulmonary bypass is char- Fig. 25-3) and advanced into the inferior vena cava, or
acterized by gravity drainage of blood from the vena by dual catheters placed into the superior and inferior
Arterial inflow
Aorta cross clamp

Pulmonary artery
SVC
Antegrade
Aorta cardioplegia
Venous return line

LV vent
RA LA
LV
RV
SVO2
IVC
Retrograde coronary sinus catheter

Reservoir
Cardioplegia
KCl pump
Bubble
detector
Cardioplegia
Centrifugal heat exchanger
pump
Flow Filter
Motor Heat
meter
exchanger Oxygenator
Figure 25-3 Schematic diagram of a cardiopulmonary bypass circuit. Blood from cannulas placed through the right atrium and into the
inferior vena cava drains by gravity into a reservoir and then is pumped by a centrifugal pump through a heat exchanger, oxygenator,
and filter prior to return to the ascending aorta. Blood mixed with cardioplegia solution is pumped alternatively into the proximal
ascending aorta or into the coronary sinus. Venting can be from a cannula placed through the right superior pulmonary vein into the left
ventricle, or from the ascending aorta antegrade cardioplegia cannula, or the pulmonary artery.
406
venae cavae so that all returning blood enters the large checklist of required items. Checklists are effective in
cannulas in these vessels. If the aortic valve is not com- improving anesthetic care. The checklist prior to going
petent, venting of the left ventricle may be necessary on cardiopulmonary bypass follows the acronym
(1) through a drain placed from the right superior pulmo- HADDSUE, pronounced HAD TO SUE, making it easy to
nary vein into the left ventricle, (2) by aspirating from the remember (Table 25-14).
antegrade cardioplegia line placed in the proximal ascend-
ing aorta, or (3) via a pulmonary venous drain. Otherwise,
Components of the Cardiopulmonary Bypass
retrograde blood flow through the incompetent aortic
Circuit
valve could cause distention of the left ventricle and dam-
age ventricular function. Venting of blood returning via The bypass pump produces nonpulsatile flow into the
the thebesian or bronchial veins may also be necessary. patient’s aorta by either a centrifugal or roller pump. The
An aortic cross-clamp is placed between the antegrade centrifugal pump has three disks rotating at 3000 to 4000
cardioplegia catheter and the arterial inflow catheter to rpm that use blood viscosity to pump blood. Centrifugal
separate the heart from the circulation and allow cardio- pumps are superior to roller pumps because they are less
plegic arrest. The ventricle should not be overdistended traumatic to blood cells, do not pump air bubbles secondary
in any situation in which it is not pumping. If the aortic to air being less dense than blood, and are afterload-depen-
cross-clamp is removed and ventricular contraction has dent, avoiding the risk of line rupture with clamping of the
not returned, the ventricle may become overdistended in arterial inflow circuit. Roller pumps compress the fluid-
situations with aortic valve insufficiency. When the heart filled tubing between the roller and curved metal back
is isolated from the circulation, total cardiopulmonary plate and are able to pump air and can have tube rupture
bypass is present, and ventilation of the lungs is no longer with arterial inflow clamping. The necessary cardiac index
necessary to maintain oxygenation. However, in any situ- delivered by the bypass pump is determined by the
ation in which there is a pulsatile pulmonary pressure patient’s body temperature and oxygen consumption. For
detected by pulmonary arterial catheter measurement, normothermia or mild hypothermia, a cardiac index of
there is partial pulmonary bypass, and the lungs should 2 to 4 L/min/m2 is satisfactory, although flows of about half
be ventilated to avoid pumping desaturated blood sys- these levels have been used successfully. Low flows have the
temically. Gravity-dependent venous drainage to the car- advantage of less blood trauma and less noncoronary collat-
diopulmonary bypass machine can be improved by raising eral blood flow, which might result in better myocardial
the level of the operating table or placing a small negative protection. Blood is oxygenated by a membrane or IV
pressure on the cardiotomy reservoir. bubble oxygenator. Membrane oxygenators use a blood-
The use of extracorporeal circulatory support is dan- membrane-gas interface rather than a blood-gas interface
gerous and requires special precautions. Prior to going and produce less trauma to the blood compared with bubble
on cardiopulmonary bypass it is important to review a oxygenators. Because membrane oxygenators cause less
Table 25-14 Protocol to Initiate Cardiopulmonary Bypass: HADDSUE

Heparin Was heparin administered? If the surgeon is placing sutures in the aorta for aortic cannulation, ask about heparin.
Do not allow a surgeon to initiate cardiopulmonary bypass without heparin administration or alternative profound
anticoagulant, the results will immediately be fatal.
ACT Did the heparin increase the ACT to 450 seconds or greater? Were antifibrinolytics given?
Drugs Were additional nondepolarizing muscle relaxants and/or anesthetics administered to prevent inspiration during
venous cannula placement, which could result in gas emboli?
Drips Did you discuss any infusions with the perfusionist that may interfere with hemodynamic management during
bypass? Blood pressure on cardiopulmonary bypass depends on flow and resistance. Drugs that affect resistance
will affect blood pressure. Drugs that affect venous capacity will reduce venous return to the reservoir and force a
reduction in pump flow.
Swan Pull back the pulmonary arterial catheter 5 cm to avoid pulmonary arterial injury or pulmonary infarction during
bypass.
Urine Measure the total urine output so that the urine produced during bypass can be tabulated. Urine output can be
quite variable during bypass depending on the extracorporeal circulatory prime, volume administered, intrinsic
hormonal response to cardiopulmonary bypass, and renal function.
Emboli Check the aortic cannula visually to detect any emboli.
ACT, activated clotting time.
407
trauma to blood components than bubble oxygenators, viscosity during hypothermia. It is mandatory that all air
membrane-based oxygenator systems are the norm. Bubble be cleared from the arterial side of the circuit before
oxygenators consisted of an oxygenator column, a defoam- institution of cardiopulmonary bypass. Indeed, pumping
ing section to remove air bubbles, and an arterial reservoir. of air into the patient by the cardiopulmonary bypass
They are not commonly used today. With either form of machine is an ever-present hazard. Carbon dioxide flush-
oxygenator PaO2 is maintained by adjusting the concentra- ing prior to priming and continuous flushing of the peri-
tion of oxygen into the oxygenator. Air-oxygen mixing cardium reduce gas emboli risk. Patients who suffer gas
may be used to avoid hyperoxia. Carbon dioxide levels are emboli can be treated with hyperbaric oxygen with
controlled between 35 and 45 mm Hg by controlling the improvements in neurologic function even 24 hours after
sweep (the total free gas flow through the oxygenator). In embolization.68 Early treatment may have better results.
the past carbon dioxide was added to maintain PaCO2 and Heparin-induced anticoagulation of the patient is
pH at levels considered normal for 37 C. Carbon dioxide mandatory before placement of the venous and aortic
is no longer added to cardiopulmonary bypass circuits to cannulas used for cardiopulmonary bypass. The usual
maintain blood gases. Bypass circuits are flushed with car- initial dose of heparin administered intravenously is
bon dioxide prior to priming to speed priming and reduce 300 to 400 units/kg. The adequacy of anticoagulation is
gas emboli in the circuit. Carbon dioxide is also continu- subsequently confirmed by determination of the acti-
ously flushed into the pericardial cavity to replace air during vated coagulation time, which is typically maintained at
bypass in an effort to reduce the significance of gas emboli greater than 450 seconds during cardiopulmonary bypass
during bypass. Carbon dioxide is more easily absorbed than (when baseline normal is 90 to 120 seconds).66
the nitrogen in air reducing the duration that gas emboli
take be resorbed.
Monitoring During Cardiopulmonary Bypass
Heat exchangers are incorporated into bypass circuits
to control the patient’s body temperature by heating or Institution of cardiopulmonary bypass is often associated
cooling blood as it circulates. Hot or cold water entering with decreases in mean arterial pressure, presumably
the unit at one end with blood entering at the other pro- reflecting the dramatic decreases in viscosity that result
vides an efficient countercurrent flow system. Metabolic from infusion of prime solutions and activation of sys-
requirements are decreased about 8% for every degree temic inflammatory response. In addition, peripheral
Celsius decrease in body temperature below 37 C. The vasodilation may accompany decreased oxygen delivery
optimal temperature management for cardiopulmonary that occurs in the early period of hemodilution. Adminis-
bypass is not entirely clear. Eighteen degrees (18 C) is tration of an a-agonist, such as phenylephrine, to
used prior to circulatory arrest and 28 C is common increase perfusion pressures to higher than 40 mm Hg
during aortic cross-clamping with rewarming to 37 C in the early period after institution of cardiopulmonary
prior to weaning from bypass. Newer protocols maintain bypass may be recommended on the assumption that per-
temperature between 31 C and 33 C. Normothermic fusion pressure is important for maintenance of cerebral
(37 C) bypass is associated with an increase in cerebro- blood flow. The correct blood pressure during bypass is
vascular accidents.67 debatable. Lower pressures may reduce cerebral blood
Blood from the pericardial cavity and the opened heart, flow and reduce emboli load to the brain. Higher pres-
as during a valve replacement, is returned to a cardiotomy sures may improve cerebral blood flow and reduce water-
reservoir, where it is filtered, defoamed, and pumped to the shed infarction but higher pressures come from higher
oxygenator for recirculation. The cardiotomy suction may flows and more emboli per unit time. Pressures less than
be a major cause of hemolysis and emboli during car- 40 mm Hg are avoided if possible in adults. Pressures
diopulmonary bypass. Filters are incorporated in the cardi- higher than 60 mm Hg are used during rewarming. Pres-
otomy reservoir and the arterial circuit to act as traps for sures up to 80 to 90 mm Hg may be used in patients with
particulate debris (blood clot, latex, talc, fat, Silastic, cerebral vascular disease. Evidence to support these
polyethylene, etc.) that could act as systemic emboli. recommendations is limited.
The tubing used for the cardiopulmonary bypass sys- After the initial decrease, mean arterial pressure dur-
tem is flushed with carbon dioxide, then filled (primed) ing cardiopulmonary bypass often begins to increase
with crystalloid. Additives to the circuit may include spontaneously, perhaps reflecting activation of the
albumin, hetastarch, blood, bicarbonate, heparin, and renin-angiotensin system or sympathetic nervous system.
antibiotics. The goal is a predetermined solution that is Mean arterial pressures higher than 100 mm Hg can lead
calculated to produce a specific hematocrit with institu- to impairment of tissue perfusion as well as the risk of
tion of total cardiopulmonary bypass. Because whole intracranial hemorrhage. Furthermore, noncoronary col-
body hypothermia (18 C to 28 C) may be utilized, the lateral blood flow is likely to be increased as mean arte-
pump prime often contains little or no blood, such that rial pressure increases, resulting in perfusion of the
the hematocrit of blood during cardiopulmonary bypass heart with blood at higher temperatures than desired for
is 20% to 30%. Hemodilution is important for decreasing optimal cellular protection. Hypertension is often treated
408
by decreasing systemic vascular resistance with volatile

Myocardial Preservation
agents administered through the oxygenator or the con-
tinuous intravenous administration of nitroprusside. The goal of myocardial preservation is to decrease myo-
Nitroglycerine has reduced effect on cardiopulmonary cardial damage introduced by the period of ischemia
bypass because its action is predominantly venodilation associated with cardiopulmonary bypass. This goal is
and arterial pressures during bypass are primarily depen- achieved by decreasing myocardial oxygen consumption
dent on systemic vascular resistance. by infusing cardioplegia solutions containing potassium
An increasing central venous pressure with or without into the aortic root, which in the presence of a distally
facial edema (eyelids and scleras) may reflect improper cross-clamped aorta and competent aortic valve ensures
placement of the vena cava cannula resulting in obstruc- diversion of the solution into the coronary arteries. Alter-
tion to venous drainage. For example, insertion of a can- natively, the cardioplegia solution may be administered
nula too far into the superior vena cava can obstruct the in retrograde fashion through a cannula placed into the
right innominate vein, leading to an increase of cerebral coronary sinus. Monitoring of coronary sinus pressures
venous pressure with associated cerebral edema. Place- during retrograde administration is used to assess cathe-
ment of a cannula too far into the inferior vena cava ter placement. If the pressure at the distal tip of the coro-
results in abdominal distention. Confirmatory evidence nary sinus catheter during cardioplegia administration at
of misplacement of a vena cava cannula is inadequate 200 mL/min is equal to central venous pressure, the cath-
venous return from the patient to the cardiopulmonary eter is not in the coronary sinus but is most likely in the
bypass machine. Prompt withdrawal of the vena cava right atrium. If the pressure is very high (>100 mm Hg)
cannula to a more proximal position should immediately the coronary sinus catheter is up against a vascular wall.
improve venous drainage. If the pressure in the coronary sinus catheter is 40 to
A pulmonary artery catheter detects increases in 60 mm Hg during a 200 mL/min infusion, the catheter
pulmonary artery pressures caused by malfunction of is correctly positioned. Positioning of the coronary sinus
the left ventricular vent and the associated inadequate catheter should be checked with transesophageal echo-
decompression of the left ventricle. Persistent left ven- cardiography and manual feel by the surgeon. If the
tricular distention can result in damage to the contractile catheter is in too deep, cardioplegia to the right ventricle
elements of the myocardium. will be compromised, resulting in poor right ventricular
Blood gases and pH are monitored frequently during protection. An additional route for infusion of cardiople-
cardiopulmonary bypass. A mixed venous PO2 lower than gia solutions is directly into newly placed bypass grafts. IV
30 mm Hg associated with metabolic acidosis suggests Potassium in the cardioplegia solution blocks the initial
inadequate tissue perfusion. Temperature correction of phase of myocardial depolarization, resulting in cessation
PaCO2 and pH is probably not necessary (see Chapter 17). of electrical and mechanical activity. The cold solution
Urine output may serve as a guide to the adequacy of produces selective hypothermia of the cardiac muscle. At
renal perfusion, with an output of 1 mL/kg/hour being 30 C, the normally contracting heart muscle consumes
a common expectation. oxygen at a rate of 8 to 10 mL/100 g/min. Oxygen consump-
During total cardiopulmonary bypass, the lungs are tion in the fibrillating ventricle at 22 C is 2 mL/100 g/min.
left quiescent with or without moderate continuous posi- The electromechanically quiet heart at 22 C consumes
tive airway pressure. The best composition of gases in the oxygen at a rate of 0.3 mL/100 g/min. The effectiveness of
lungs during this period is unsettled. Continued ventila- cold cardioplegia is monitored by measuring heart tempera-
tion of the lungs with oxygen may be appropriate when ture with a temperature probe placed into the left ventricular
there is some pulmonary blood flow, as evidenced by a muscle plus the absence of any visible electrical activity on
pulsatile pulmonary artery trace. If there is a pulsatile the ECG. Cold cardioplegia infusions are supplemented by
pulmonary arterial pressure or systemic arterial pressure, total-body hypothermia and localized epicardial surface
the lungs should be ventilated because there is only cooling using ice or cold irrigation solutions placed in the
partial cardiopulmonary bypass. pericardial space. Cardioplegia solutions may also contain
Esophageal, rectal, bladder, and blood temperatures many additives, including blood, insulin, glucose, aspartate,
are monitored routinely. Rapid rewarming caused by a glutamate, calcium, magnesium, nitroglycerine, supero-
high blood-to-body temperature gradient is avoided to xide dismutase, at the discretion of the surgeon. None of
avoid gas emboli. Drug-induced vasodilation as produced these additives are definitively better than cold blood
by a volatile anesthetic or nitroprusside may speed the cardioplegia with a short cross-clamp time. Adequate
rewarming process, as reflected by a more rapid approach myocardial preservation is suggested by good myocardial
of the rectal (core) to esophageal (blood) temperature, but contractility without the need for inotropic drugs at the con-
should be used carefully. Measurement of urinary bladder clusion of cardiopulmonary bypass.
temperature may be a superior alternative to monitoring A side effect of cardioplegia solutions is an increased
rectal temperature, as bladder temperature may reflect incidence of atrioventricular heart block due to intra-
core temperatures better than rectal. myocardial hyperkalemia. This heart block usually
409
resolves in 1 to 2 hours and can be treated temporarily by

Table 25-15 Checklist for Weaning from
use of an artificial cardiac pacemaker. Intramyocardial Cardiopulmonary Bypass: WRMVP
hyperkalemia also produces decreased myocardial contrac-
tility. Systemic hyperkalemia can occur when coronary Warm Body temperature (37 C) is likely to
sinus blood containing cardioplegia solution is returned decrease rapidly after cardiopulmonary
bypass if patient is not adequately
to the oxygenator for subsequent circulation. Decreased
rewarmed, with resultant metabolic
renal function during cardiopulmonary bypass will also acidosis and poor myocardial contractility.
contribute to hyperkalemia. If hyperkalemia persists at
the conclusion of cardiopulmonary bypass, regular insulin Rhythm Confirm that the patient has a stable
(10 to 20 units IV) can be given in combination with glu- cardiac rhythm.
cose (25 to 50 mg IV) in an attempt to shift potassium into Monitors Confirm that the monitors are turned on;
the cells. Alternatively, furosemide can be used. The per- pulse oximeter is essential for arterial
fusionist can also add crystalloid solutions to the bypass oxygen saturation and cardiac output.
circuit and then use a hemoconcentrator to ultrafiltrate Ventilator Confirm that it is turned on.
the blood and thereby eliminate potassium.
Perfusion Confirm heart beating, presence of
vasodilation.
Drugs selected for maintenance of anesthesia in patients
undergoing cardiopulmonary bypass are influenced by
Wide Receiver Most Valuable Player (a wide receiver is
the patient’s cardiac disease. Patients with diabetes or
a football position for our non–United States readers):
those who develop glucose intolerance during surgery
should have infusions of insulin with a target of glucose 1. Warm: Is the patient at 37 C?
between 120 and 150 mg/dL. Avoidance of hypoglycemia 2. Rhythm: Does the patient have a stable cardiac rhythm?
is essential to avoid neurologic injury. Hyperglycemia 3. Monitors: Are the monitors turned back on? How about
may lead to increased risk of infections and neurologic the pulse oximeter? The pulse oximeter is essential post-
sequelae. Infusions of dexmedetomidine are associated operatively both as a monitor of arterial oxygen satu-
with reduced risk of delirium.69 Institution of cardiopul- ration and cardiac output. If the pulse oximeter is not
monary bypass may produce a sudden dilution of circulat- working, it may be that perfusion is inadequate. The
ing drug concentrations. For this reason, supplemental pulse oximeter is an excellent low cardiac output alarm.
anesthetics, such as benzodiazepines or opioids, may be 4. Ventilator: Is the ventilator back on? It is easy to for-
needed. An additional dose of nondepolarizing muscle get this and rapid desaturation after bypass detected
relaxant should be administered just prior to placement from the pulse oximeter should be quickly identified.
of the venous cannula to avoid inspiratory efforts entrain- 5. Perfusion: Is the heart beating? Is the vasculature ap-
ing air. Anesthetic depth can also be increased by volatile propriate for the cardiac function? Very few hearts foll-
anesthetics from vaporizers incorporated into the cardio- lowing cardiopulmonary bypass are adequate to
pulmonary bypass circuit. The effect of hemodilution maintain blood pressure in the face of profound systemic
on drug concentrations is likely to be offset by a decreased vasodilation. The systemic vascular resistance should be
need for drugs during hypothermia. Anesthetic require- normal (not profoundly vasodilated or constricted).
ments seem to be minimal following rewarming to a
Cardiopulmonary bypass is discontinued when the patient
normal body temperature at the conclusion of cardiopul-
is hemodynamically stable and normothermia has been
monary bypass. Therefore, additional anesthesia is not
reestablished. In the absence of adequate rewarming
routinely required during rewarming or the early period
before discontinuation of cardiopulmonary bypass, body
after the conclusion of cardiopulmonary bypass. However,
temperature is likely to decrease rapidly in the postcar-
additional anesthetic will be needed to maintain tracheal
diopulmonary bypass period, resulting in metabolic aci-
intubation for transfer and postoperative ventilation in
dosis and poor myocardial contractility. When the left
the intensive care unit. An intravenous anesthetic (propo-
side of the heart has been opened, as during valve
fol or dexmedetomidine) with minimal hemodynamic
replacement surgery, it is mandatory to remove all air
effects can be given in the procedure and continued into
from the cardiac chambers and pulmonary veins before
the ICU. Dexmedetomidine-induced sedation may reduce
permitting the heart to eject blood into the aorta. Other-
the risk of postoperative delirium after cardiac surgery.69
wise, systemic air emboli can occur with disastrous car-
Discontinuation of Cardiopulmonary Bypass diac and central nervous system effects. The presence of
air can be checked with transesophageal echocardiogra-
Optimal anesthetic care can be achieved with checklists. phy. Unrecognized air in the coronary arteries may be a
The checklist for weaning from cardiopulmonary bypass cause of sudden onset of poor myocardial contractility
consists of the mnemonic WRMVP (Table 25-15), as in after discontinuation of cardiopulmonary bypass. Air
410
embolization with neurologic defects can be treated with or milrinone) with an intra-aortic balloon pump or left
hyperbaric oxygen even 24 hours after surgery with ventricular assist device is necessary to maintain optimal
improvements in neurologic outcome.68 Measurement of cardiac output. The use of combinations of b-agonists
cardiac filling pressures, determination of thermodilution and phosphodiesterase inhibitors produce synergistic
cardiac outputs, and calculation of systemic and pulmo- increases in cardiac function. The vasoconstriction of
nary vascular resistance are helpful for guiding intra- epinephrine or norepinephrine is counterbalanced by
venous fluid replacement and the appropriate selection the vasodilation of the phosphodiesterase inhibitor.
of drugs in the early postcardiopulmonary bypass period Careful measurement of systemic vascular resistance
(Table 25-16). Alternatively, transesophageal echocardi- and supplementation with a vasoconstrictor such as
ography can be used to estimate the adequacy of intra- phenylephrine is frequently needed to maintain a normal
vascular fluid volume and myocardial contractility. systemic vascular resistance. If b-agonists are needed,
Transesophageal echocardiography is also useful for frequent attention must be given to measurement and
evaluating cardiac valve function and intracardiac blood control of potassium, glucose, calcium, pH, and the pres-
flow patterns, particularly following surgical repair or ence of arrhythmias. Gas emboli to the coronaries may
replacement. suddenly and profoundly reduce ventricular function.
The most common hemodynamic abnormality after Posterior papillary muscle dysfunction at the conclusion
cardiopulmonary bypass is low systemic vascular resis- of cardiopulmonary bypass may result in mitral regurgi-
tance (SVR). It is very difficult to wean from cardiopul- tation as evidenced by the presence of prominent
monary bypass with a systemic vascular resistance that V waves on the pulmonary artery occlusion pressure
is low. SVR can be calculated from the following: tracing. This dysfunction may reflect less than optimal
cardioplegic protection of the posterior myocardium,
Mean arterial pressure ðmm HgÞ which is most vulnerable to warming effects from blood
central venous pressure ðmm HgÞ= in the adjacent descending aorta, as well as perfusion
pump flow ðL=minÞ 80 with warm blood representing noncoronary collateral
circulation. Acute mitral regurgitation can also occur
Systemic vascular resistance should be between 1200 and with volume overload from excessive fluid admini-
1400 prior to weaning from bypass. The units of SVR are stration; it can be managed simply by the use of the
dynes seconds/centimeters5 (dyns/cm5). Systemic vas- reverse Trendelenburg position to reduce venous return
cular resistance can be normalized with a vasoconstrictor to the heart. IV
prior to weaning from cardiopulmonary bypass. The goal A mechanical complement to inotropic support of
should be to match the vascular input impedance to the cardiac output is the intra-aortic balloon pump. The
cardiac output impedance to optimize energy transfer. It intra-aortic balloon pump (a 25-cm long balloon
is much easier to adjust the vasculature to match the mounted on a 90-cm stiff plastic catheter) is typically
heart, than force the heart to tolerate a dilated vascula- inserted percutaneously through the femoral artery and
ture. On occasion, an inotropic drug, such as epinephrine, advanced so that the tip is just distal to the left subcla-
norepinephrine, dopamine, or dobutamine, is needed. In vian artery. The balloon is timed to inflate during diastole
cases of severe ventricular dysfunction, a combination to augment diastolic blood pressure and increase the
of drugs (epinephrine or norepinephrine and amrinone gradient for coronary perfusion improving coronary
Table 25-16 Diagnosis and Treatment of Cardiovascular Dysfunction after Cardiopulmonary Bypass
Systemic Blood Pressure Atrial Pressure Cardiac Output Diagnosis Therapy
Decreased Decreased Decreased Hypovolemia Administer volume
Decreased Decreased Increased Vasodilation Vasoconstrictor
Low blood viscosity Erythrocyte transfusion
Decreased Increased Decreased Left ventricular dysfunction Inotrope
Inodilator
Vasodilator
Mechanical assistance
Increased Increased Decreased Vasoconstriction Vasodilator
Left ventricular dysfunction Inotrope
Increased Decreased Increased Hyperdynamic Volatile anesthetic
b-Antagonist
411
blood flow. The balloon deflates immediately before sys- intubation is common after leaving the operating room.
tole, thus decreasing afterload and lowering oxygen Once the PaO2 with an FIO2 of 0.40 is above 80 mm Hg,
requirements. Coronary blood flow is increased, with the bleeding is controlled, the patient is awake, and neu-
little or no increase in cardiac work, which may result romuscular function has recovered, extubation can be
in improvements in cardiac output. Aortic insufficiency considered. There is no benefit from prolonged postoper-
may be worsened by intra-aortic balloon inflation. Rapid ative ventilation in cardiac surgery. The blood and fluid
heart rates and cardiac dysrhythmias interfere with that remain in the cardiopulmonary bypass circuit are
proper balloon timing and optimal augmentation of washed and collected into sterile plastic bags as packed
cardiac output. Temporary ventricular assist can also be cells for possible reinfusion to the patient. High resis-
provided by catheters with impellers that rely on the tance to blood flow in the arm induced by vasoconstric-
Archimedes screw technology. The impeller device comes tion may result in a falsely low systemic blood pressure
in two sizes capable of 2.5 or 5.0 L/min flow. reading from the radial artery in the early period after
When an adequate systemic blood pressure and cardiac cardiopulmonary bypass. If there is a question of inade-
output have been maintained for several minutes, the quate arterial blood pressure, direct pressure measure-
vena caval cannula is removed and protamine admin- ment from the ascending aorta can be instantly
istration is begun to reverse heparin anticoagulation. obtained. Placement of a femoral arterial catheter is
Protamine administration is dangerous and frequently is needed if there is a gradient between central and radial
associated with hypotension from release of histamine. pressure. Any gradient between central aortic and radial
Occasionally there is severe pulmonary hypertension or artery blood pressure usually disappears within 60
even anaphylaxis from protamine administration. Prot- minutes.
amine should be administered after a test dose slowly to The large financial cost of cardiac surgery is due in
avoid catastrophic hemodynamic collapse. Administra- part to the duration of intensive care required for these
tion of the vasoconstrictor phenylephrine can be used patients. Improvements in anesthetic, surgical, and perfu-
to maintain blood pressure. In cases of hemodynamic sion techniques serve to decrease the need for prolonged
collapse even epinephrine boluses will be inadequate, care of these patients in an ICU. The concept known
and return to cardiopulmonary bypass after emergency as “fast track” as applied to cardiac surgical patients
reheparinization can be life-saving. NPH insulin is made includes early postoperative awakening and tracheal
with protamine. Diabetics who use NPH insulin may be at extubation.71
increased risk for protamine reactions. Protamine allergic
reactions may be reduced with a combination of hista-
Off-Pump Coronary Artery Bypass Graft
mine blockade (H1 [diphenhydramine] and H2 blocker
Surgery
[cimetidine]) and a steroid (hydrocortisone). The aortic
cannula is removed after protamine administration is In an effort to minimize postoperative morbidity, coro-
safely concluded. Pharmacologic measures to decrease nary artery bypass graft (CABG) surgery may be accom-
bleeding include administration of antifibrinolytics (ami- plished in selected patients without institution of
nocaproic acid, tranexamic acid, and formerly aprotinin) cardiopulmonary bypass and in the presence of a spon-
and desmopressin (improves platelet function in patients taneously beating heart and normothermia. Cardio-
with von Willibrand’s disease). Blood loss throughout pulmonary bypass using extracorporeal circulatory
the procedure as well as the blood in the bypass tubing support was developed because it is difficult to safely
can be salvaged, washed, and retransfused using “cell produce a high-quality anastomosis between a vessel
saver” devices. and a coronary artery while the heart is beating. Off-
Administration of nitrous oxide after cardiopulmo- pump CABG was developed to reduce the sequelae of
nary bypass is not recommended because this gas could extracorporeal circulatory support, which may include
unmask the presence of air in the heart or coronary arte- stroke, global encephalopathy, renal failure, pulmonary
ries. For this reason, anesthesia is most often supplemen- injury, and death. Off-pump CABG surgery is limited
ted, when necessary, by the intravenous administration by several considerations including the quality of the
of propofol, dexmedetomidine, opioids, benzodiazepines, distal anastomosis and long-term graft patency is of
or alternatively with low inhaled concentrations of vola- primary concern. There are several problems with off-
tile anesthetics. Intravenous anesthetics such as propofol pump CABG or “beating heart” surgery. The first is
infusions,70 dexmedetomidine infusions,69 or opioids motion of the coronary artery making suture placement
and benzodiazepines are continued after bypass and for the anastomosis difficult. Anticoagulation with hep-
continued into the ICU to provide sedation prior to extu- arin is achieved and the activated clotting time (ACT) is
bation. Dexmedetomidine sedation may reduce post- measured. There is some debate on the appropriate ACT
operative delirium after cardiac surgery.69 The time to levels of an off-pump CABG with some surgeons using
tracheal extubation is shortening after cardiopulmonary standard doses appropriate for cardiopulmonary bypass
bypass but some period of time of postoperative (300 to 400 units/kg ACT > 450 seconds) and others
412
using lower dose heparin (200 unit/kg). Antifibrinolytics preconditioning may reduce ischemic injury at the cost
(aprotinin, aminocaproic acid, or transexemic acid) are of a longer operative time.
not used if the patient is not going on extracorporeal Anastomosis of the left internal mammary artery
circulatory support. The ability to immediately go on (LIMA) to the left anterior descending (LAD) coronary
extracorporeal circulatory support must be available artery was the first off-pump bypass and is technically
during the conduct of off-pump CABG should the simplest and most important for reducing myocardial
patient have circulatory collapse or cardiac arrest. Blood ischemia. The LIMA to LAD anastomosis is usually con-
flow in the target coronary artery is usually stopped by ducted first, which improves coronary blood flow to the
placement of a proximal and distal latex suture, which LAD circulation. Saphenous vein grafts (SVG) are then
is lifted up, consequently arresting flow. Alternatively, placed to the obtuse marginal (OM) branches off the cir-
a silicon stent can be placed in the target coronary cumflex artery and finally to the posterior descending
artery during production of the anastomosis to maintain artery (PDA), which usually branches from the right coro-
coronary flow. The silicon stent is removed just prior nary artery. Placement of the lateral wall grafts to the
to tightening the suture. Stopping the coronary blood obtuse marginal branches requires shifting the heart to
flow in the target coronary artery may cause myocar- the right, which may be better tolerated by opening the
dial ischemia, ventricular arrhythmias, ventricular dys- right pleural space and placing lifting-stay sutures into
function, heart block, hemodynamic collapse, and the inferior pericardium. Steep Trendelenburg with right
cardiac arrest. When flow is resumed in the coronary tilt will improve hemodynamics. Intravascular administra-
artery reperfusion arrhythmias may occur. Prophylactic tion of colloid and vasoconstriction with phenylephrine
antiarrhythmic therapy should be administered prior to should be used to maintain arterial blood pressure. The
off-pump CABG. Magnesium (2 g IV slowly) combined ECG amplitude may diminish dramatically making ST
with lidocaine (100 mg bolus followed by 2 mg/min) segments difficult to observe secondary to myocardial
infusion works well. Intravenous amiodarone should positioning. Transesophageal echocardiography of the
be used in patients who demonstrate a tendency toward ventricle may be impossible secondary to lifting of the
ventricular tachycardia or fibrillation. ventricle off the esophagus. Anastomosis to the posterior
The technology for the off-pump CABG was devel- descending coronary artery can be produced with steep
oped in the 1990s and initially stabilized the heart with Trendelenburg, volume loading, and vasoconstriction with
a retractor that simply pushed on the myocardium while phenylephrine. Low cardiac outputs can be tolerated for
it was lifted into the retractor with stay sutures. This the brief period of the distal anastomosis. Completion of IV
system was difficult to use because ventricular diastolic the proximal aortic anastomosis for the saphenous vein
filling was compromised by external pressure on the grafts requires placement of a side biter clamp on the
heart. The development of a retractor that used a vacuum ascending aorta. Devices that staple the proximal anasto-
foot (Octopus) to stabilize the heart eliminated the exter- mosis are available and may reduce the use of side biter
nal pressure on the myocardium and improved ventricu- clamps with less aortic trauma. Arterial blood pressure can
lar diastolic function during the distal anastomosis. be decreased to assist placement of this clamp with increas-
Coronary grafts to the inferior and lateral circulation ing inspired concentrations of volatile anesthetics or cardiac
were difficult to perform because retraction of the heart manipulation to reduce venous return. Once the distal and
reduced diastolic filling and caused hemodynamic col- proximal anastomoses are complete any air in the saphe-
lapse. The use of suction retractors (Starfish and Urchin) nous vein graft must be removed to avoid coronary gas
for lateral and anterior displacement of the heart during emboli. Removal of the aortic side biter should only be done
production of the lateral and inferior anastomosis in once any remaining air is removed from the saphenous vein
combination with steep Trendelenburg positioning grafts to avoid systemic gas emboli. Heparin anticoagula-
greatly stabilized hemodynamics. Careful cooperation tion should then be carefully reversed with protamine. Prot-
between the cardiac surgeon and cardiac anesthesiologist amine reactions, which include hypotension, pulmonary
is essential for off-pump CABG. Surgical positioning hypertension, and anaphylaxis, are more difficult to treat
must be performed in conjunction with anesthesia. The in off-pump CABG because rapid return to extracorporeal
surgeon must not open the coronary artery for a distal circulatory support will require full reheparinization,
anastomosis without ensuring that the patient will hemo- bypass circuit priming, followed by proximal aortic cannula
dynamically tolerate the 10- to 15-minute anastomosis. and right atrial venous cannula placement. If hypotension
Communication between the cardiac surgeon and cardiac occurs following protamine administration, rapid treatment
anesthesiologist is especially critical during this process. with the vasoconstrictor phenylephrine is frequently
Some surgeons use a 5-minute period of ischemic needed. Severe reactions to protamine may be treated with
preconditioning prior to a 5-minute recovery period fol- intravenous epinephrine, diphenhydramine, H2 blockade,
lowed by the anastomosis. The 5-minute preconditioning steroids, intravascular fluid administration, and if necessary
period can be used to optimize hemodynamics and test to reheparinization, and initiation of extracorporeal circula-
see if the patient will tolerate the anastomosis. Ischemic tory support. The use of off-pump CABG is becoming less
413
frequent after the publication of the ROOBY trial which the possible rapid sequelae of complications. Maintenance
showed a reduction in graft patency and poorer outcomes of anesthesia is usually with a volatile agent (isoflurane or
in the off-pump group.72 sevoflurane) in combination with an opioid (fentanyl or
sufentanil). Nitrous oxide should be avoided secondary to
MANAGEMENT OF ANESTHESIA reduction in FIO2, potential for pulmonary vasoconstric-
Anesthesia for off-pump CABG is very similar to anesthe- tion, and potential to increase the volume of gas emboli.
sia for on-pump CABG with a few notable exceptions. Maintenance infusions of propofol, dexmedetomidine, or
Patients for off-pump CABG have similar medical condi- remifentanil are also commonly used. If remifentanil is
tions, medical therapies, and requirements for care as chosen, inadvertent discontinuation of the infusion should
those receiving on-pump CABG. All preoperative medica- be avoided because the metabolism is rapid. Cardiac
tions with the exception of oral hypoglycemic agents depression may be more with remifentanil than fentanyl
should be continued in the perioperative period. Patients or sufentanil, making its use more difficult in patients with
with diabetes should be managed with intravenous insulin limited cardiac reserve. Prophylactic antiarrhythmic ther-
infusions and frequent blood glucose determinations. apy (lidocaine and magnesium or amiodarone) is appropri-
Coumadin (warfarin) should be stopped at least 7 days ate to avoid arrhythmias from manual manipulation of the
prior to an operation. Platelet inhibitors, with the excep- heart, from ischemia during the distal anastomosis, and
tion of aspirin, should be discontinued preoperatively upon reperfusion after completion of the anastomosis.
depending on clearance. Preoperative heparin infusions Anticoagulation is achieved with heparin and monitored
can be continued into the operating room and discontin- with ACT (activated clotting time) or heparin assay.
ued after full heparinization. Preoperative sedation with Hemodynamic stability during the distal anastomosis is
a benzodiazepine (diazepam 10 mg PO) and nasal cannula achieved with careful surgical manipulation and retraction
oxygen is effective at reducing sympathetic stimulation. of the heart, table positioning, infusions of vasoconstric-
Induction of anesthesia should have the goal to maintain tors, and volume. Inotropic stimulation with b-agonists
arterial blood pressure within 10% to 20% of baseline. has the potential to raise the heart rate, making comple-
Baseline measurements of heart rate, blood pressure, pul- tion of the distal anastomosis more difficult and lowering
monary artery pressures, central venous pressures, and the threshold for ventricular arrhythmias. If b-agonists are
cardiac output can be obtained using intra-arterial and needed to support cardiac output during conduct of the
pulmonary arterial catheters allowing preinduction opti- distal anastomosis, use of extracorporeal circulatory sup-
mization of hemodynamics. If severe pulmonary hyperten- port should be considered. Heparin anticoagulation is
sion or low cardiac output is identified, a discussion of the reversed with protamine after completion of the proximal
case with the cardiac surgeon is warranted. An infusion of and distal anastomosis and is confirmed by measurement
the vasoconstrictor phenylephrine may be started prior to of an ACT near baseline (120 to 140 seconds). The period
induction of anesthesia and then titrated to maintain and requirements for postoperative ventilation and seda-
blood pressure. Any intravenous anesthetic can be used tion may be reduced in off-pump CABG and extubation
to induce anesthesia, but benzodiazepines (midazolam) should be performed once hemodynamics are stable,
and narcotics (fentanyl) are common. Sufentanil decreases bleeding is controlled, oxygen requirements are reduced
heart rate more than fentanyl, which may or may not be (FIO2 ¼ 0.40 with PO2 more than 80 mm Hg), neuromuscu-
advantageous. Dexmedetomidine can be used to supple- lar blockade has been reversed, and the patient is awake
ment other agents and may reduce stress response and and breathing spontaneously with the help of continuous
postoperative delirium.69 Etomidate, propofol, and thio- positive-pressure ventilation. Postoperative b-blockade
pental are also effective for induction of anesthesia, but may reduce the incidence of atrial fibrillation and
doses should be reduced in patients at risk for hypoten- myocardial ischemia and should be started as soon as
sion. Once anesthetic induction is complete, a muscle hemodynamics will tolerate. Aspirin therapy should be
relaxant can be given. Bradycardia (heart rates between resumed once bleeding is controlled. Discontinuation of
45 and 60 beats/min) is helpful during conduct of the dis- anti-ischemic and vasodilator agents (b-blockers, calcium
tal anastomosis, so use of pancuronium may be avoided. If channel blockers, nitrates, and angiotensin inhibitors)
reflux is a concern, a modified rapid sequence induction should be avoided because withdrawal phenomena may
with cricoid pressure is warranted. If the patient is thought lead to increased morbidity and mortality rates.
to have a difficult airway, the standard difficult airway Cardiac surgery is continually advancing with hybrid
protocols should be used with special attention to avoid operations, off-pump CABG, minimal access, surgical ven-
tachycardia and sympathetic stimulation. Intubation of tricular restoration, left ventricular assist devices, artificial
cardiac surgery patients should follow the standard proto- hearts, and robotic mitral and coronary artery bypass
cols for airway management, the only difference being surgery. Vigilance, cooperation, team work, and a very
that the tolerance for tachycardia, hypotension, or hyper- clear understanding of the surgical plans and hemody-
tension is greatly reduced and myocardial ischemia, namic consequences of procedures are essential to reduce
ventricular arrhythmias, and hemodynamic collapse are the morbidity and mortality rates of these operations.
414
4. What is the “magnet mode” of a programmable car-

QUESTIONS OF THE DAY diac pacemaker? Why should the specific magnet
mode be known during the perioperative period?
1. What factors influence the risk of perioperative myo- 5. What factors reduce left ventricular outflow obstruc-
cardial infarction? tion in a patient with hypertrophic cardiomyopathy?
2. Which patients are most likely to benefit from periop- 6. What are the clinical manifestations of cardiac tampo-
erative b-blockade? nade? What are the most important aspects of anes-
3. What are the hemodynamic goals for management of thesia management for a patient with cardiac
patients with aortic stenosis who are undergoing tamponade who requires a pericardial window?
anesthesia?
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Chapter

CORONARY ARTERY DISEASE ANEURYSMS OF THE AORTA

C ardiovascular disease is the leading cause of death in

myocardial ischemia and infarctions. The most common

60 the 30-day and 2-year mortality risks.16 Statin therapy

Table 25-2 Area of Myocardial Ischemia as Reflected by the Electrocardiogram

PERIOPERATIVE CARDIAC RISK REDUCTION THERAPY (PCRRT)

Patient scheduled for surgery with

If patient has a specific contraindication

PERIOPERATIVE CARDIAC RISK REDUCTION THERAPY

more rapid than 55 beats/min or systolic blood pressure is

DISTURBANCES OF CARDIAC CONDUCTION Unifascicular heart block

hypertension is present preoperatively. Sodium thiopental,

of surgical or interventional revascularization and im-

Management of Anesthesia Starting b-blockers on the day of surgery and continuing

CARDIOPULMONARY BYPASS cava into a reservoir, followed by its pumping through

Aorta cross clamp

Venous return line

Retrograde coronary sinus catheter

Table 25-14 Protocol to Initiate Cardiopulmonary Bypass: HADDSUE

ACT, activated clotting time.

by decreasing systemic vascular resistance with volatile

resolves in 1 to 2 hours and can be treated temporarily by

4. What is the “magnet mode” of a programmable car-

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