PERIOPERATIVE CARDIAC COMPLICATIONS

POSTOPERATIVE MEDICAL COMPLICATIONS

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PERIOPERATIVE CARDIAC COMPLICATIONS Howard H. Weitz, MD

Although infrequent, perioperative cardiac complications are a source of major morbidity and mortality. As the population ages, the prevalence of cardiovascular disease is increasing. For physicians who refer patients for surgery as well as for clinicians directly involved in perioperative medical care, an understanding of perioperative cardiac complications, reduction of such complications, and treatment of complications are essential. This article summarizes the approach to perioperative hypertension, hypotension, myocardial ischemia, myocardial infarction (MI), and congestive heart failure (CHF). The reader is referred to the article by Sloan in this issue for a discussion of the approach to perioperative cardiac arrhythmias. PERIOPERATIVE HYPERTENSION Pathophysiology

Despite the extent of preoperative blood pressure control, perioperative hypertension or hypotension occurs in 25% of hypertensive patients who un48 Two preoperative predictors of perioperative hypertension are dergo previous hypertension, especially a diastolic blood pressure greater than 110 mm Hg, and the type of surgery. Hypertensive events occur most commonly with carotid surgery, abdominal aortic surgery, peripheral vascular procedures, and intraperitoneal or intrathoracic surgery.23 Data suggest that diastolic blood pressure of 110 mm Hg or greater is a preoperative marker of perioperative cardiac complications in patients with chronic hyperten~ion?~ In patients with chronic hypertension, as long as the

From the Department of Medicine, Jefferson Medical College; and Jefferson Heart Institute of Thomas Jefferson University Hospital, Philadelphia, Pennsylvania

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diastolic blood pressure is less than 110 mm Hg, hypertension in and of itself is not an indication to delay surgery. Data are conflicting regarding the role of preoperative hypertension as a cause of postoperative cardiac complications. In a multivariate analysis of risk factors for perioperative complications in men who underwent noncardiac surgery, the presence of preoperative hypertension increased the odds ratio for postoperative death to 3.8 times that of normoten~ives.~ In a case-controlled study of patients who died of a cardiac cause within 30 days of elective surgery, a preoperative history of hypertension was four times more likely than in an equal number of age-matched In contrast, a prospective, randomized multicenter study of more than 17,000 patients found that although preoperative hypertension was associated with perioperative bradycardia, tachycardia, and hypertension, it was not a predictor of myocardial infarction or cardiac death.17 The importance of systolic hypertension as a risk factor for surgery is unclear. In one retrospective study of patients who underwent carotid endarterectomy, a preoperative systolic blood pressure greater than 160 mm Hg was identified as a risk factor for postoperative hypertension (systolic blood pressure >220 mm Hg) with subsequent increased risk for stroke or death. 62 Incidence and Presentation

Perioperative hypertension tends to occur at four distinct time periods: (1) during laryngoscopy and induction of anesthesia, secondary to sympathetic stimulation with adrenergic mediated vasoconstriction; (2) intraoperatively secondary to acute pain-induced sympathetic stimulation leading to vasoconstriction; (3) in the early postanesthesia period, principally secondary to paininduced sympathetic stimulation, hypothermia (which decreases catecholamine reuptake and increases plasma catecholamine levels), hypoxia, or intravascular volume overload from excessive intraoperative fluid therapy; and (4) 24 to 48 hours after surgery as fluid is mobilized from the extravascular space. Also during this period, blood pressure elevation secondary to discontinuation of long-term antihypertensive medication may occur. An uncommon cause of perioperative hypertension that has received sigThis syndrome has nificant attention is the clonidine withdrawal been reported to occur 18 to 24 hours after abruptly stopping clonidine in patients who almost always were taking more than 1.0 mg/d. Clonidine withdrawal syndrome is of particular concern in the perioperative period because there is no rapidly acting, parenteral form of this drug for use in patients who are unable to take oral medications. Characterized by excessive sympathetic activity with rebound hypertension, this syndrome often resembles the hypertensive crisis of pheochromocytoma. Clonidine withdrawal syndrome may be aggravated by the simultaneous use of propranolol, which blocks peripheral vasodilatory p-receptors, leaving vasoconstricting a-receptors unopposed. The syndrome may be reversed by reinstitution of clonidine, which can be given intramuscularly, or by treatment with methyldopa or labetalol. Discontinuation syndromes manifested by hypertension may be provoked by withdrawal of pblockers, centrally acting antihypertensive agents (i.e., methyldopa), and other antihypertensive Treatment

The initial approach to treatment is prevention. Because many patients who develop postoperative hypertension do so as a result of withdrawal of their

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long-term antihypertensive regimen, this withdrawal should be minimized in the postoperative period. One preventive approach is to substitute long-acting preparations of the patient’s long-term antihypertensive regimen starting, if possible, several days before surgery and to be given in the morning of the day of surgery. There are no well-studied indications for acute control of hypertension in the perioperative period. The possible causes of the patient’s blood pressure elevation should be considered, and it should be decided if the hypertension is a hypertensive emergency or urgency. Hypertension that occurs in relation to tracheal intubation, surgical incision, and emergence from anesthesia often is due to increased sympathetic tone. It may be treated with short-acting P-blockers, short-acting narcotics, or, if needed, intravenous nitroprusside.hl Hypertensive emergencies are uncommon after noncardiac surgery. Hypertensive emergencies are characterized by severe elevation of blood pressure with associated target organ dysfunction. Examples include hypertensive encephalopathy, intracerebral hemorrhage, subarachnoid hemorrhage, and acute stroke; hypertension-induced acute renal dysfunction; and hypertension associated with unstable angina, acute MI, acute CHF, and acute aortic dissection. Other postoperative situations that may result in a hypertensive emergency include rebound hypertension after withdrawal of antihypertensive medications, hypertension resulting in bleeding from vascular surgery suture lines, hypertension associated with head trauma, and hypertension caused by acute catecholamine excess (i.e., pheochromocytoma).An initial approach is to reverse precipitating factors (pain, hypervolemia, hypoxia, hypercarbia, and hypothermia). In patients with a hypertensive emergency, it usually is necessary to treat with a parenteral antihypertensive agent (Table 1). In the acute setting, the treatment goal is to decrease blood pressure by no more than 25%. This goal decreases the likelihood of tooaggressive control, which may result in target organ hypoperfusion. Patients with chronic hypertension have cerebral and renal perfusion autoregulation shifted to a higher range. The brain and kidneys are particularly prone to hypoperfusion if blood pressure is lowered too rapidly. With the threat of organ injury diminished, attempts should be made to control blood pressure to baseline levels during 24 to 48 hours. A patient with postoperative hypertension without evidence of target organ damage can be approached similar to a patient with a hypertensive urgency. Precipitating factors (see earlier) should be reversed, and the patient’s preoperative antihypertensive medications should be restored. For patients who are unable to resume oral intake, parenteral alternative antihypertensive agents can be administered (Table 2). Sublingual nifedipine should be avoided in the treatment of perioperative hypertension. This agent can result in unpredictable severe h y p o t e n s i ~ n . ~ ~ PERIOPERATIVE HYPOTENSION Perioperative hypotension may result in myocardial ischemia and is a predictor of postoperative cardiac morbidity. Perioperative decrease of mean arterial blood pressure of more than 20 mm Hg has been shown to increase postoperative cardiac complications.ll The most common cause of perioperative hypotension is intravascular volume depletion or excessive vasodilation. Hypotension may be induced by anesthetic agents. Spinal anesthesia may result in hypotension secondary to vasodilation. Several inhalation anesthetic agents (e.g., isoflurane, desflurane, and sevoflurane) may cause hypotension by peripheral

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Table 1. DRUGS FOR TREATMENT OF PERIOPERATIVE HYPERTENSION Drug

Administration

Nitroprusside

IV

Nitroglycerin

IV

Nicardipine

IV

Fenoldopam Enalaprilat

IV N

Labetalol

IV

Esmolol

IV

Methyldopa

IV

IV = Intravenous; ACE

Dose Range

Comments

0.5-10 pg/kg/min

Requires invasive blood pressure monitoring. Onset 2-4 minutes with brief duration of action. Use when urgent control of blood pressure required 20-400 pg/min Useful with coexistent myocardial ischemia Initiate at 5-15 mg/h; Useful for patients maintenance, 0.5-2.2 mg/h receiving long-term calcium channel blockers 0.1-0.3 mg/kg/min 0.625-1.25 mg q 6 h Useful for patients receiving long-term ACE inhibitors, angiotensin receptor blockers 20-80 mg as IV bolus every Contraindicated in patient with excessive 10 min; up to 2 mg/min as IV infusion bradycardia or CHF 25-100 pg/kg/min. May increase infusion rate to 300 pg/kg/min 250-500 mg q 6 h Onset of action 4 h

=

angiotensin-converting enzyme; CHF

=

congestive heart failure.

Table 2. PARENTERAL SUBSTITUTION OF LONG-TERM ORAL ANTIHYPERTENSIVE THERAPY Drug

P-Blockers Propranolol Labetalol Esmolol Diuretics Furosemide Central agent Methyldopa Clonidine

Dosage

0.5-2.0 mg q 4 4 h IV 20-80 mg as IV bolus every 10 min; up to 2 mg/min as N infusion 25-100 pg/kg/min IV. May increase infusion rate to 300 pg/kg/min 20-60 mg IV 250-500 mg q 6 h IV Transdermal patch (must be placed 48 hours before desired effect)

Calcium channel antagonists Nicardipine

0.5-2.2 mg/h IV

Angiotensin-converting enzyme inhibitors, angiotensin receptor blocker Enalaprilat

0.625-1.25 mg q 6 h IV

IV = Intravenous.

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vasodilation as well as by myocardial depression. Other causes of perioperative hypotension include MI, pulmonary embolus, and sepsis. Hypotension caused by volume depletion or vasodilation is treated best by volume expansion. When clinically significant vasodilation-induced hypotension does not respond to this approach, a peripheral vasoconstrictor (phenylephrine) should be considered. Hypotension resulting from direct myocardial depression may be treated with inotropic agents, such as dopamine, dobutamine, and milrinone.

MYOCARDIAL ISCHEMIA AND MYOCARDIAL INFARCTION Pathophysiology

A variety of factors in the perioperative period may produce myocardial ischemia, which if prolonged or intense may lead to MI5*,53; factors include increases in myocardial oxygen demand and decreased myocardial oxygen supply. The normal physiologic response to surgery is an increase in circulating catecholamines. This response causes an increase in heart rate, myocardial contractility, and peripheral vascular resistance, all of which increase myocardial oxygen demand. In the patient with significant coronary artery disease, myocardial oxygen supply may be unable to meet this increased demand, resulting in myocardial ischemia. Hypotension and tachycardia may decrease myocardial oxygen supply by decreasing effective coronary artery perfusion. Coronary artery perfusion pressure is the difference between aortic diastolic pressure and left ventricular diastolic pressure. Coronary artery perfusion pressure is lowered when there is diastolic hypotension, and in the presence of diminished coronary artery blood flow, distal myocardial perfusion is impaired. In a related fashion, when heart rate is increased, diastolic filling time is decreased, which may result in decreased myocardial perfusion. Other causes of decreased myocardial oxygen delivery are anemia and hypoxia. Evidence also suggests that perioperative activation of hemostasis with activation of platelets, increased production of fibrinogen, and a temporary shutdown of fibrinolysis during the early postoperative period may contribute to an increased risk of perioperative thrombotic events?' Atherosclerotic coronary artery disease may predispose to perioperative myocardial ischemia and MI. In an autopsy study of 42 patients who sustained fatal MI intraoperatively or within 30 days of surgery, 19% were found to have greater than 50% stenosis of the left main coronary artery, and significant triplevessel coronary disease was present in 59%. In more than half of the cases, the pathophysiology leading to the fatal MI was disruption of an atherosclerotic plaque leading to coronary thrombosis and coronary artery obstruction. These findings were similar to a matched group of patients whose fatal MIS were not related to noncardiac ~urgery.'~ In a retrospective analysis of patients who had coronary angiography during the 6 months before major vascular surgery at the Cleveland Clinic and sustained a fatal or nonfatal MI related to the surgery, the infarcted myocardium was found in most cases to be supplied by occluded coronaries that were collateralized inadequately or by coronaries with nonobstructive lesions.16These studies suggest that a commonly held belief that a critical fixed coronary stenosis is the common denominator for perioperative MI may not be true.

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Incidence and Presentation

In a study of men who had coronary artery disease or were at risk for it, Mangano et a140 found that preoperative myocardial ischemia, detected by electrocardiographic monitoring, was common. It occurred in 27% of patients, equally divided between patients with known coronary artery disease and patients at risk for it. Intraoperative myocardial ischemia was similar in incidence and severity to preoperative ischemia, suggesting that surgery is not as stressful as previously believed. The incidence and severity of perioperative myocardial ischemia were found to be greatest during the first 48 hours after surgery. The cause of this postoperative phenomenon is not known and may be multifactorial. Mangano et aI4Onoted a significant increase in heart rate in the postoperative period that may have increased myocardial oxygen demand. Other investigators detected no link between increased postoperative heart rate and myocardial ischemia.34 Early studies indicated that most perioperative MIS occur during the 5 days after surgery with the peak incidence at about 48 to 72 hours postoperaA study by Badner et a16found that the peak incidence of perioperative MI was during the first 24 hours after surgery, with most MIS occurring on the first postoperative night. This study of 323 patients with ischemic heart disease followed for 7 days after surgery is the first perioperative MI surveillance study to use troponin T as a marker of myocardial injury. The diagnosis of perioperative MI is difficult. Perioperative myocardial ischemia and MI often are ~ i l e n tIn . ~Mangano’s study of postoperative myocardial ischemia,4O 94% of ischemic episodes were not associated with anginal pain. Badner’s study6 of patients with known ischemic heart disease found that only 17% of patients experienced chest pain at the time of MI. Other investigators found that MI occurring after noncardiac surgery is not associated with chest pain in 20% to 70% of cases. Possible reasons for the absence of chest pain include a residual effect of anesthetics and analgesics, altered pain perception resulting from competing somatic stimuli (e.g., incisional pain), and increased pain tolerance as has been noted in nonsurgical patients with silent myocardial ischemia.21,35 When present, features of perioperative MI may include arrhythmias, CHF, hypotension, excessive hyperglycemia in diabetics, and impaired mental status, particularly in the elderly. The patient at risk for perioperative MI should be placed under increased surveillance for at least 48 hours after surgery and in selected cases for 5 days. The American College of Cardiology/American Heart Association guideline for evaluation and care of patients with cardiovascular disease who are to undergo noncardiac surgery states that for the patient at risk for perioperative MI an electrocardiogram (ECG) be obtained before surgery, immediately after surgery, and for the first 2 postoperative days.I4 Many perioperative MIS are not associated with the development of Q waves (non-Q wave MI, non-ST segment elevation MI).6The ECG may be normal or reveal only subtle changes of the ST and T waves. In patients in whom perioperative MI is suspected, serum markers of myocardial injury may be helpful in establishing the diagnosis. Creatine kinase-MB activity rises within 4 to 8 hours of MI and remains elevated for 48 to 72 hours. Although it has been a relatively reliable aid to MI diagnosis not related to surgery, current studies indicate that serial measurements of creatine kinase-MB isoenzymes after surgery are associated with a relatively high falsepositive rate. Cardiac-specifictroponins begin to rise by 3 hours after myocardial injury. Troponin I elevations persist for 7 to 10 days, and troponin T elevations persist for 10 to 14 days after MI. Elevated troponin I levels ( > L O ng/mL) are

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more specific for perioperative MI or ischemia than are elevations of creatine kinase-MB isoenzymes.' It has been recommended that cardiac enzyme levels should not be checked postoperatively in all patients who undergo noncardiac surgery but that they be restricted to patients who are deemed to be at high risk for MI.22 Studies have found that the mortality of perioperative MI is high (17% to 41%).6f20, 55 Perioperative myocardial ischemia and MI indicate the potential for adverse cardiac events long after surgery. Mangano et a P found that patients with postoperative myocardial ischemia had a 2.2-fold increase in the rate of adverse cardiac outcome during the first 2 years after surgery. Patients who sustained postoperative MIS had a 20-fold increased risk for subsequent cardiac complications, particularly during the first 6 months after surgery.

Prevention There is solid evidence to support the use of P-blockers to decrease the incidence of myocardial ischemia and MI related to noncardiac surgery. Mangano et a1,4I in a study of 200 patients with coronary artery disease or coronary disease risk factors, found a long-term benefit of atenolol when given before and for several days after surgery. In this study, myocardial ischemia was reduced by 50% in the atenolol-treated group during the first 48 hours after surgery. There was no difference between groups in terms of nonfatal or fatal MI during the first week after surgery; however, during the 2-year follow-up period, the mortality rate was 10% in patients given atenolol and 21% in 6o Based on this study, the American College of Physicians guideline on preoperative evaluation recommends the use of atenolol for patients with known coronary artery disease or significant coronary artery disease risk factorsMRaby et al,49in a small pilot study, showed that strict perioperative heart rate control with P-blockers, when tailored to an individual's ischemic threshold (determined by preoperative continuous ambulatory ischemia monitoring) was associated with a reduction of postoperative myocardial ischemia during the 48 hours after surgery. In a trial of high-risk (presence of risk factors as well as demonstrable myocardial ischemia on a preoperative dobutamine echocardiography stress test) vascular surgery patients, Poldermans et a147showed that perioperative administration of the P-blocker bisoprolol (5 to 10 mg daily begun 1 week before surgery and continued for 30 days after surgery) was associated with a marked reduction of nonfatal and fatal MI (i.e., a 34% incidence of cardiac death or nonfatal MI in the standard treatment group compared with 3.4% in patients treated with bisoprolol). On the basis of these results, Poldermans et a147recommended that high-risk surgical patients receive P-blockers for 1 to 2 weeks before surgery with therapy continuing for at least 2 weeks after surgery. These investigators suggested that P-blockers be titrated to reduce heart rate to less than 70 beats/min during the surgical procedure and to less than 80 beats/ min in the immediate postoperative period. There is no evidence that intraoperative nitrates or calcium channel antagonists are of benefit to prevent intraoperative myocardial ischemia.54, 58 Prophylactic nitrates may be harmful if they lead to excessive preload reduction with subsequent hypotension. a,-Adrenoceptor agonists (e.g., clonidine, dexmedetomidine, mivazerol) have been studied to assess whether their effect by reducing central sympathetic activity decreases perioperative myocardial ischemia. There is no evidence to support their use; however, a study in a small group of patients suggested that

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mivazerol may be of benefit.42Pending results of large-scale trials, these agents cannot be recommended to decrease myocardial ischemia and MI in the perioperative period. In a study of 300 patients with known coronary artery disease or high risk for coronary artery disease who underwent abdominal, thoracic, or vascular surgery, maintenance of perioperative normothermia led to a decreased incidence of perioperative morbidity (unstable angina, cardiac arrest, MI). There was a 6.3% incidence of morbid events in the hypothermic group versus 1.4% in the normothermic group. The normothermic group experienced a decrease in episodes of ventricular tachycardia as well.I9 No well-designed, prospective, randomized study has been done to evaluate the impact of invasive hemodynamic monitoring on the incidence of cardiovascular complications in the perioperative period. It is unlikely that such a study ever will be done. Intuitive indications for invasive hemodynamic monitoring would be anticipation of fluid shifts in patients with left ventricular dysfunction or fixed cardiac output, major vascular surgery in patients with left ventricular dysfunction, and surgery in patients with recent MI or unstable angina? No prospective, randomized studies have been conducted to evaluate the efficacy of preoperative coronary artery revascularization in reducing perioperative risk. A protective effect of previous coronary artery bypass graft (CABG) surgery has been suggested. Pooled data from studies that used historical control subjects reveal that of 2000 patients who underwent noncardiac surgery, the rate of postoperative infarction was significantly lower in patients who underwent previous CABG surgery (0% to 1.2%) than in patients who did not (1.lY0 to 6'70).~~ In addition to the perioperative benefit, Hertzer et alZ7noted a late benefit that they attributed to perioperative coronary revascularization. In a group of patients who underwent CABG surgery before aortic aneurysm repair, survival 5 years after aneurysm surgery was similar to that of patients with trivial coronary disease.27 In other studies, the overall benefit of preoperative myocardial revascularization has been less clear. Data from the Coronary Artery Surgery Study (CASS) revealed higher perioperative mortality in nonrandomized patients who underwent noncardiac surgery without preceding coronary surgery (2.4%) than in patients who had preceding coronary surgery (0.9%). The operative mortality for CABG surgery was 1.4%. The combination of coronary surgery followed by noncardiac surgery was no less risky than was noncardiac surgery alone in medically treated patients.I8 In a subsequent analysis of the CASS registry database, Eagle et all5found that in patients with known coronary artery disease, noncardiac surgery involving the thorax, abdomen, vasculature, or head and neck was associated with increased risk of perioperative cardiac complication, which was reduced in patients with prior CABG surgery. It also was shown that this protection afforded by CABG surgery was sustained for at least 6 years after the coronary revascularization pr~cedure.'~ The American College of Cardiology/American Heart Association consensus-based guidelines for preoperative cardiovascular evaluation before noncardiac surgery recommend that the individual patient's perioperative and long-term risk be considered when deciding whether or not to perform CABG surgery before noncardiac surgery. The American College of Cardiology/American Heart Association advocate that CABG surgery be performed before noncardiac surgery in patients who meet established criteria for CABG surgery (i.e., left main coronary stenosis, three-vessel coronary artery disease in conjunction with left ventricular dysfunction, twovessel coronary disease when one of the vessels is the left anterior descending coronary artery with a severe proximal stenosis, and myocardial ischemia de-

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spite a maximal medical regimen). The guidelines highlight that CABG surgery should be performed in the above-mentioned patients before high-risk or intermediate-risk noncardiac surgery when long-term outcome would be improved by the coronary surgery.14 It has been suggested that percutaneous transluminal coronary angioplasty reduces perioperative cardiac morbidity when it is performed to alleviate myocardial ischemia before noncardiac surgery. The few studies that have assessed this technique were nonrandomized, however, and based on historical cont r o l ~ .Because ~ , ~ ~ there may be elastic recoil and plaque disruption at the site of the coronary angioplasty, it has been recommended, based on theoretic grounds, to delay elective noncardiac surgery for several days to allow for stabilization of the coronary endothe1i~m.I~ The patient who has had coronary stenting accompanying coronary angioplasty in the period immediately before noncardiac surgery presents a unique challenge in the perioperative period. In a retrospective observational analysis of 40 patients who underwent noncardiac surgery less than 6 weeks after coronary stenting, there were 7 perioperative MIS, 11 major bleeding episodes, and 8 deaths. All deaths and MIS as well as most of the bleeding episodes occurred in patients who underwent noncardiac surgery less than 14 days after coronary stent placement. The authors of this study suggest that elective noncardiac surgery should be postponed for 2 to 4 weeks after coronary artery stenting to allow completion of the mandatory antiplatelet regimen. This approach reduces the risk of stent thrombosis in patients whose antiplatelet agents would be discontinued prematurely and bleeding in patients who would undergo surgery while still receiving their antiplatelet regimen.33 For patients with chronic stable angina, it is important to continue antianginal therapy in the perioperative period. P-Blockers are continued to the time of surgery. For prolonged effect, a long-acting preparation (i.e., nadolol or atenolol) may be given on the morning of surgery. If patients are unable to resume oral intake 24 hours after surgery, @-blockersmay be given intravenously (e.g., propranolol, 0.5 to 2 mg every 1 to 6 hours). Parenteral metoprolol or esmolol also may be used. Oral P-blocker therapy is resumed as soon as possible after surgery. Patients who are receiving long-term antianginal treatment with calcium channel antagonists usually are given a long-acting oral preparation on the morning of surgery. If patients are unable to resume oral intake 24 hours after surgery, intravenous or topical nitrates can be added to the regimen. The only calcium channel antagonists available for intravenous use are verapamil and diltiazem. Because the effect of verapamil and diltiazem is primarily antiarrhythmic when they are given intravenously, these agents should not be used as primary anti-ischemic therapy for patients who are unable to take oral medications. Treatment of Perioperative Myocardial Infarction

The immediate goals for treatment of perioperative MI are the same as those for treatment of MI in the nonsurgical setting. These goals include reperfusion of ischemic myocardium supplied by the culprit coronary artery, antithrombotic therapy to prevent rethrombosis of a subtotal coronary stenosis, adjunctive measures to decrease ongoing myocardial oxygen demand, and prevention of MI-related left ventricular remodeling. Thrombolytic therapy is indicated for many patients with acute MI but

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should not be used in most patients who have undergone recent surgery. Although it is not known exactly how soon after surgery it is safe to use thrombolytic agents, any operation within the previous 2 weeks that could be a source of uncontrollable bleeding with thrombolytic therapy is an absolute contraindication to its use. Recent surgery more than 2 weeks before thrombolytic therapy has been suggested as a relative contraindication to its use, and the choice must be made on an individual basis.50 Urgent cardiac catheterization with percutaneous coronary angioplasty should be considered in perioperative patients with evolving acute MIS. In the absence of contraindications, aspirin, 160 to 325 mg, is administered during the acute phase of MI. Use of aspirin has been shown to decrease early mortality from MI by 21%.32If patients are unable to tolerate oral medications in the perioperative period, aspirin, 325 mg, may be given by rectal suppository. For patients allergic to aspirin, clopidogrel has been recommended in a consensus guideline of the American College of Chest Physicians.8 Heparin has been shown to reduce morbidity and mortality in the peri-MI period for patients who have not received thrombolytic therapy50If there are no contraindications and hemostasis is stable, heparin is used in the initial care of patients with perioperative MI. There is evidence that subcutaneous low-molecular-weight heparin (e.g., enoxaparin, 1 mg/kg every 12 hours) is more effective than continuously administered unfractionated heparin, but this has been determined in nonsurgical patients5 Pending study in perioperative patients, either heparin preparation probably is an acceptable choice. Heparin and antiplatelet agents, although of benefit post-MI, may increase bleeding after noncardiac surgery. The benefit and risk of these agents must be considered before their use in the perioperative period. P-Blockers given to patients with acute MIS decrease excessive reflex activation of the sympathetic nervous system, which may increase myocardial ischemia, platelet aggregation, and arrhythmia. These agents reduce post-MI morbidity and mortality.63 In the absence of contraindications, p-blockers can be administered to all patients with acute MI. Intravenous P-blockers (propranolol, metoprolol, esmolol) are administered to patients who are unable to tolerate oral P-blockers. The dose is titrated to decrease the heart rate to less than 70 beats/ min. Contraindications to the use of P-blockers in the perioperative period include significant bradycardia or hypotension, severe left ventricular dysfunction, heart block, and severe bronchospastic lung disease. Nitroglycerin is effective in decreasing the pain of acute ongoing myocardial ischemia. Nitroglycerin is beneficial when MI is complicated by CHF or pulmonary edema. There is no evidence that prophylactic nitrates decrease mortality after acute MI. The typical starting dose for nitroglycerin is 5 to 10 &min intravenously for most patients with perioperative MIS. The dose is increased by 5 to 10 &min every 5 to 10 minutes. During titration, continuous monitoring of vital signs is essential. Although titration endpoints for nitroglycerin vary among patients, guidelines suggest the following: (1)control of symptoms or a decrease in mean arterial blood pressure of 10% in patients with normal blood pressure or 30% in patients with hypertension (never a systolic blood pressure of <90 mm Hg); (2) a maximum increase in heart rate of more than 10 beats/min, but usually not greater than 110 beats/min; and (3) a decrease in pulmonary artery end-diastolic pressure of 10% to 30%. For most patients, the final nitrate dose is less than 200 kg/min. Evidence indicates that angiotensin-converting enzyme (ACE) inhibitors given early after MI have been shown to increase survival, especially for patients with anterior infarctions or patients with left ventricular ejection fraction less

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than 40%. The Heart Outcomes Prevention Evaluation (HOPE) trial suggested that all patients who have sustained MIS might benefit from long-term ACE inhibitor therapyz6,50 It is essential that the patient who sustains a perioperative MI be treated after the acute phase in a manner similar to the treatment of MI in the nonsurgical setting. This treatment includes assessment of myocardium at risk with a post-MI stress test in patients with uncomplicated MI; assessment of cardiac risk factors, including determination of lipid status and initiation of lipid-lowering therapy if indicated and smoking cessation counseling; and a plan for cardiac rehabilitation. PERIOPERATIVE CONGESTIVE HEART FAILURE

CHF is a syndrome in which cardiac output is insufficient for the body's needs. CHF is the only major cardiovascular disorder that is increasing in incidence, prevalence, and overall mortality. CHF currently affects 2% of the US. population, with a prevalence of 6% to 10% in individuals older than age 65.28As the population of the United States ages, the incidence of chronic CHF in patients who undergo noncardiac surgery is likely to increase. The many possible causes include myocardial dysfunction related to ischemia, infarction, hypertension, valvular and pericardial disease, and cardiomyopathy. CHF may be precipitated by noncardiac causes that increase the demand for cardiac output; common examples that occur in the perioperative period include anemia, fever, and hypoxia. Pathophysiology

When valvular lesions, pericardial disease, and noncardiac conditions that increase the demand for cardiac output are ruled out, a primary myocardial abnormality is usually the cause of CHF. About 70% of cases are related to left ventricular systolic dysfunction, and the remaining 30% are related to left ventricular diastolic dysfunction. Impaired left ventricular contractility is the cause of left ventricular systolic dysfunction. This impairment is associated with a decreased left ventricular ejection fraction. Preload and cardiac volume subsequently increase as compensatory responses to increase cardiac output, but as left ventricular function deteriorates, cardiac output cannot increase. Increasing cardiac volume and ventricular pressure result in elevation of the left atrial pressure with subsequent pulmonary venous congestion. Decreased left ventricular contractility leads to decreased cardiac output. In patients with primary left ventricular diastolic dysfunction, the main abnormality is reduced ventricular compliance. These patients usually have normal or enhanced left ventricular contractile function. The ventricular myocardium is less compliant than normal; increases in preload result in marked elevation of left ventricular end-diastolic pressure with a subsequent rise in pulmonary venous pressure and pulmonary venous hypertension. Left ventricular diastolic dysfunction is characterized by marked sensitivity to changes in intravascular volume. Patients are at risk for marked elevation of ventricular filling pressure in the setting of intravascular volume overload and for hypotension as a consequence of decreased ventricular pressure when intravascular volume is depleted. If patients subsequently develop ventricular systolic dys-

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function, these responses become more dramatic. The most common cause of ventricular diastolic dysfunction is left ventricular hypertrophy resulting from hypertension. Other less common causes include myocardial infiltrative processes, such as amyloidosis and restrictive cardi~myopathy.~~ Risk for the Development of Perioperative Congestive Heart Failure

Goldman et alZ4found the preoperative presence of symptoms and signs of CHF to be the best predictor of the development of perioperative CHF. A history of CHF, which was absent in most of the patients who did develop heart failure, was a less powerful predictor. In a study of patients at higher risk (i.e., patients with hypertension or diabetes), Charlson et all0found that the risk for postoperative CHF was limited to patients with preoperative symptomatic cardiac disease (e.g., previous MI, valvular disease, or CHF). Patients with diabetes were at greatest risk, particularly if they had overt cardiac disease. Intraoperative fluctuations of the mean arterial blood pressure (increases or decreases of >40 mm Hg) were related to increased rates of postoperative heart failure. In the study by Mangano et a139described earlier, postoperative myocardial ischemia, a history of cardiac arrhythmia, and diabetes were found to predict the development of postoperative CHF. When Perioperative Congestive Heart Failure Occurs

In a review of cases of perioperative CHF that occurred during the 1950s and 1960s, Cooperman and Price1*noted that most cases developed within 1 hour of the cessation of anesthesia (most during the first 30 minutes). In a highrisk population of patients with diabetes or hypertension, most patients who developed perioperative CHF did so on the day of surgery or on the second postoperative day.I0 The risk for postoperative CHF is greatest during two periods. The risk is significantly increased immediately after surgery, probably as a result of hypertension or hypotension, myocardial ischemia, intraoperative fluid administration, sympathetic stimulation, cessation of positive-pressure ventilation, and hypoxia. The second peak occurs 24 to 48 hours after surgery and may be related to the reabsorption of interstitial fluid, myocardial ischemia, and, in some patielits, the effects of withdrawal from long-term oral CHF medications. Diagnosis

In the perioperative period, appropriate CHF therapy is facilitated by determining whether CHF is caused by systolic ventricular dysfunction, diastolic ventricular dysfunction, or a combination of both. Although a cardiac imaging study (e.g., echocardiogram, radionuclide ventriculogram, or standard left ventricular angiogram) is necessary to diagnose definitively the presence of left ventricular systolic dysfunction, many clues to the diagnosis of CHF can be found in patients’ histories, physical examinations, chest radiographs, and ECGs. CHF in patients with history of MI, cardiomegaly, or third heart sound (S3) strongly suggests the presence of left ventricular systolic dysfunction. In contrast, CHF in patients with hypertension, S4,normal heart size on chest radiograph, left ventricular hypertrophy on ECG, and no history of MI is suggestive of left

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ventricular diastolic dysfunction. Considerable overlap occurs, however, because patients with CHF may have systolic and diastolic components to myocardial dysfunction. Interstitial pulmonary edema may be found in both varieties and does not aid in discrimination. Although the absence of left ventricular systolic dysfunction in patients with CHF suggests that diastolic dysfunction is the cause, a diagnosis of left ventricular diastolic dysfunction ideally requires invasive documentation of increased pulmonary capillary wedge pressure or elevated left ventricular end-diastolic pressure. Approach to Patients With Compensated Chronic Congestive Heart Failure Who Require Noncardiac Surgery

In patients with compensated chronic CHF, effort is directed at identifying destabilizing factors (e.g., fluid overload, anemia, fever) that may occur in the perioperative period, preventing them if possible, and rendering immediate treatment if they occur. The need for invasive hemodynamic monitoring must be assessed. Patients’ CHF medical regimens must be converted to appropriate parenteral regimens for use until oral intake can be resumed. Perioperative cardiac mortality depends most on patients’ clinical status at the time of surgery. The risk of CHF is greatest if signs of CHF are present at the time of surgery or during the week before the surgical procedure. Patients with chronic CHF are evaluated to determine whether the condition is compensated. If patients are thought to be decompensated, surgery is delayed if possible, and attempts are made to achieve medical stabilization. Because the risk imposed by CHF is greatest in patients who have pulmonary edema within 7 days of surgery, elective surgery can be delayed for at least 1 week after CHF stabilization. Although no large-scale, randomized, controlled clinical trials have been performed to assess the impact of perioperative invasive hemodynamic monitoring in patients with histories of CHF who undergo noncardiac surgery, invasive monitoring provides important hemodynamic data (e.g., cardiac output, pulmonary capillary wedge pressure, systemic vascular resistance) that is helpful in the perioperative period. Invasive hemodynamic monitoring with a pulmonary artery catheter should be considered in the following clinical situations: recent CHF, significant left ventricular dysfunction, critical aortic stenosis, unstable angina, recent MI in a patient undergoing a surgical procedure associated with significant intravascular volume shifts, substantial changes in preload or afterload, and risk of perioperative myocardial ischemia? For patients with decompensated CHF who require emergent or semiemergent surgery, invasive hemodynamic monitoring may aid in further preoperative cardiac stabilization. Because the risk of postoperative CHF extends beyond the immediate surgical period, invasive hemodynamic monitoring usually is continued for 48 to 72 hours after surgery. Use of Long-Term Congestive Heart Failure Medications in the Perioperative Period

Several medications used to treat chronic CHF may cause electrolyte or metabolic abnormalities in the perioperative period. Diuretics may induce intravascular volume depletion, which can predispose patients to hypotension if they are given vasodilator anesthetic agents or spinal anesthesia. Orthostatic changes

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in blood pressure and pulse should be monitored for during the preoperative physical examination in all patients who receive diuretics. If orthostatic changes are documented, it is important that intravascular volume be replenished before surgery. A similar approach is followed for patients who are being treated with vasodilators. Preoperative serum potassium levels are obtained in all patients who are receiving diuretics and are corrected before surgery if necessary. Although hypokalemia may cause ventricular ectopy, acute potassium loss is probably more arrhythmogenic than is chronic potassium loss. Hypokalemia that does not resolve with potassium supplementation suggests the presence of hypomagnesemia, which also must be corrected before surgery is undertaken. The hyperkalemia that sometimes accompanies the use of potassium-sparing diuretics may cause heart block and other abnormalities of cardiac conduction. Another potential cause of hyperkalemia in the perioperative period is aldosterone antagonists. Use of aldosterone antagonists has increased in the heart failure patient since they have been shown to decrease mortality when used long term in patients with New York Heart Association class I11 or IV heart For patients who receive digoxin, serial blood levels are measured if renal function declines, and the dose is adjusted accordingly. Clinical trials have documented that although digoxin does not decrease mortality, it does decrease CHF symptoms and increases exercise tolerance.57There is evidence that withdrawal of digoxin may result in clinical deterioration. In a small study, Uretsky et a159found the full effect of digoxin withdrawal on exercise tolerance 12 weeks after digoxin discontinuation. An initial decline in exercise tolerance was found at 2 weeks. Although this study was not designed to assess functional capacity less than 2 weeks after digoxin withdrawal, it may be a good practice to avoid discontinuation of digoxin in the perioperative period. Digoxin is continued in patients who have been receiving long-term oral digoxin therapy and is given intravenously when oral intake is suspended. Cardiovascular drugs that may increase digoxin levels in the perioperative period include quinidine, verapamil, and amiodarone. For patients who are maintained on ACE inhibitors, these medications can be administered until the time of surgery; then oral agents can be given again as soon as possible in the postoperative period. Patients’ left ventricular function, degree of compensation, dependence on ACE inhibitors, and risk for perioperative CHF determine the need for parenteral ACE inihibitors after surgery until oral intake can be resumed. Patients with moderate-to-severe ventricular dysfunction who are at high risk for perioperative CHF are given intravenous ACE inhibitors (enalaprilat, 0.625 to 1.25 mg every 6 hours) until oral ACE inhibitors can be resumed. Many patients, particularly those who cannot tolerate ACE inhibitors, take the combination of nitrates and hydralazine as vasodilator therapy for CHF. During the time that patients are unable to take oral medications, topical or intravenous nitrates are given. Because of its short duration of action and risk for hypotension, parenteral hydralazine should not be used as a substitute for oral hydralazine. If CHF decompensates while patients being maintained on nitrates and hydralazine are unable to take oral medications, the nitrates can be discontinued and intravenous nitroprusside used for its preload-reducing and afterload-reducing properties. In some cases, if the contraindication to ACE inhibitors is not well defined, intravenous enalaprilat can be administered. In patients who are unable to receive ACE inhibitors, perioperative CHF therapy is centered on diuretics; preload reduction with nitrates; preload and afterload

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reduction with nitroprusside; digoxin if indicated; and intravenous inotropic agents such as dopamine, dobutamine, and milrinone. P-Blockers decrease symptoms and mortality in patients with New York Heart Association class I1 and I11 heart failure secondary to left ventricular systolic dysfunction and have become a standard therapy in this patient 43 P-Blockers are initiated when the patient has been clinically compensated for at least 2 to 4 weeks. Use of P-blockers in patients whose CHF is not compensated can provoke further decompensation. Although there are no established guidelines regarding their use in the perioperative period, one approach is to continue P-blockers if possible. If noncardiac surgery necessitates interruption of p-blockers, the practice guidelines of the Heart Failure Society of America can be followed, which suggest that if P-blockers are interrupted for a period greater than 72 hours they be reinitiated at 50% of their previous dose if the patient still is deemed a candidate for their use. The dose is increased cautiously generally no sooner than at 2-week intevals.2 Treatment of Acute Congestive Heart Failure in the Perioperative Period

Numerous factors may lead to the new onset of CHF or the decompensation of otherwise stable CHF in the perioperative period. Myocardial ischemia or MI, perioperative volume overload, hypertension with a subsequent increase in afterload, occult valvular heart disease (e.g., aortic stenosis, mitral regurgitation), renal failure, anemia, sepsis, pulmonary embolus, pneumonia, and the new onset of atrial fibrillation or flutter with decreased cardiac output may provoke perioperative CHF. The stress of surgery in a patient receiving an inadequate medical regimen for CHF may precipitate acute CHF in patients with otherwise stable chronic CHF in the nonoperative setting. Medical regimens may be inadequate because of inappropriate medication or inability to substitute orally administered drugs taken on a long-term basis with intravenous equivalents. Treatment is directed at the primary cause of the acute episode of CHF. If volume overload is present, diuretics are administered. If patients are found to have left ventricular systolic dysfunction, inotropic agents are given to increase myocardial contractility and cardiac output. Intravenous inotropic agents, such as dobutamine and dopamine, are effective in the short-term but must be used cautiously in patients with acute myocardial ischemia or MI because they may increase myocardial oxygen demand and exacerbate myocardial ischemia. Digoxin is less helpful in the treatment of acute CHF in patients with left ventricular systolic dysfunction but may be beneficial for patients whose CHF is provoked by atrial fibrillation. Digoxin slows the atrial fibrillation ventricular response, prolonging ventricular filling time and decreasing myocardial oxygen demand. Vasodilator medical therapy may be used in the perioperative period. Intravenous nitroprusside is the agent of choice for immediate blood pressure control and reduction of afterload in patients with CHF who exhibit hypertension or increased systemic vascular resistance. Intravenous nitroprusside is of benefit when acute perioperative CHF is associated with aortic or mitral regurgitation. It decreases afterload and serves to decrease the regurgitant fraction in patients with these valvular lesions. Use of intravenous nitroprusside is limited by the need for continuous blood pressure monitoring and the risk of cyanate toxicity when it is administered for more than a short period. For patients who require long-term parenteral vasodilator therapy, enalapri-

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lat, an ACE inhibitor that is administered intravenously, is effective in reducing preload and afterload. When patients resume oral intake, oral ACE inhibitors may be substituted. Nitrates are beneficial in the treatment of perioperative CHF when myocardial ischemia is contributing to the condition or when reduction in preload is desired. P-Blockers and calcium channel antagonists should not be given to patients with acute perioperative CHF caused by left ventricular systolic dysfunction but may prove helpful in patients with left ventricular diastolic dysfunction by promoting left ventricular relaxation and increased compliance. When patients who have perioperative CHF in the absence of acute myocardial ischemia do not respond to the alleviation of precipitating factors and provision of medical therapy directed at normalizing intravascular volume and cardiac output, the presence of acute pulmonary embolism, sepsis, or other noncardiac causes must be considered. References 1. Adams JE, Sicard GA, Allen BT, et al: Diagnosis of perioperative myocardial infarction with measurement of cardiac troponin I. N Engl J Med 330:670474, 1994 2. Adams KF, Baughman KL, Dec WG, et a1 HFSA guidelines for management of patients with heart failure caused by left ventricular systolic dysfunction-pharmacological approaches. J Card Fail 5:357-382, 1999 3. Allen J, Helling T, Hartzler G: Operative procedures not involving the heart after percutaneous transluminal coronary angioplasty. Surg Gynecol Obstet 173:285-288, 1991 4. American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization: Practice guidelines for pulmonary artery catheterization. Anesthesiology 78:380394, 1993 5. Antman EM, Cohen M, Radley D, et a1 Assessment of the treatment effect of enoxaparin for unstable angina/non-Q wave myocardial infarction. TIM1 IIB-ESSENCE meta-analysis. Circulation 100:1602-1608, 1999 6. Badner NH, Knill RL, Brown JE, et a1 Myocardial infarction after noncardiac surgery. Anesthesiology 88:572-578, 1998 7. Browner WS, Mangano D: In-hospital and long-term mortality in male veterans following noncardiac surgery. The Study of Perioperative Ischemia Research Group. JAMA 268:22&232, 1992 8. Cairns JA, Theroux P, Lewis HD, et al: Antithrombotic agents in coronary artery disease. Fifth ACCP Conference on Antithrombotic Therapy. Chest 114:611%33S, 1998 9. Charlson ME, MacKenzie CR, Ales KL, et a1 The post-operative electrocardiogram and creatine kinase: Implications for diagnosis of myocardial infarction after noncardiac surgery. J Clin Epidemiol42:25-34, 1989 10. Charlson ME, MacKenzie CR, Gold J, et al: Risks for postoperative congestive heart failure. Surg Gynecol Obstet 17295-104, 1991 11. Charlson ME, MacKenzie R, Gold J, et al: Intraoperative blood pressure: What patterns identify patients at risk for postoperative complications? Ann Surg 50:567-580, 1990 12. Cooperman LH, Price HL: Risk for postoperative congestive heart failure: A review of 40 cases. Ann Surg 172:833-891, 1970 13. Dawood M, Gutpa DK, Southern J, et al: Pathology of fatal perioperative myocardial infarction: Implications regarding pathophysiology and prevention. Int J Cardiol573744, 1996 14. Eagle KA, Brundage BH, Chaitman BR, et al: Guidelines for perioperative cardiovascular evaluation for noncardiac surgery. J Am Coll Cardiol27910-948, 1996 15. Eagle KA, Charanjit SR, Mickel MC, et al: Cardiac risk of noncardiac surgery: Influence of coronary disease and type of surgery in 3368 operations. Circulation 96:1882-1887, 1997

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16. Ellis SG, Hertzer NR, Young JR, et al: Angiographic correlates of cardiac death and myocardial infarction complicating major nonthoracic vascular surgery. Am J Cardiol 771126-1128, 1996 17. Forrest JB, Rehder K, Cahalan MK, et al: Multicenter study of general anesthesia: 111. Predictors of severe perioperative adverse outcomes [published erratum appears in Anesthesiology 1992 Ju1;77222]. Anesthesiology 76:3-15, 1992 18. Foster E, Davis K, Carpenter J: Risk of noncardiac operation in patients with defined coronary artery disease: The Coronary Artery Surgery Study (CASS) Registry experience. Ann Thorac Surg 41:42, 1986 19. Frank S, Fleisher L, Breslow M, et al: Perioperative maintenance of normothermia reduces the incidence of morbid events. JAMA 227:1127-1134, 1997 20. Gedebou TM, Barr ST, Hunter G, et al: Risk factors in patients undergoing major nonvascular abdominal operations that predict perioperative myocardial infarction. Am J Surg 174:755-758, 1997 21. Glazier JJ, Chierchia S, Brown MJ, et al: Importance of generalized defective perception of painful stimuli as a cause of silent myocardial ischemia in chronic stable angina pectoris. Am J Cardiol 58:667-672, 1986 22. Goldman L Assessment of perioperative risk. N Engl J Med 330:707-709, 1994 23. Goldman L, Caldera DL: Risks of general anesthesia and elective operation in the hypertensive patient. Anesthesiology 50:285, 1979 24. Goldman L, Caldera DL, Nussbaum SR, et al: Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 297845, 1978 25. Grossman E, Messerli F, Grodzicki T, et al: Should a moratorium be placed on sublingual nifedipine? JAMA 276:1328, 1996 26. Heart Outcomes Prevention Evaluation Study Investigators: Effect of an angiotensinconverting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med 342145-153, 2000 27. Hertzer NR, Young JR, Beven E, et al: Late results of coronary bypass in patients with infrarenal aortic aneurysms: The Cleveland Clinic experience. Ann Surg 205:360-367, 1987 28. Ho K, Pinsky JL, Kannel WB, et al: The epidemiology of heart failure: The Framingham Study. J Am Coll Cardiol 22:6A-l3A, 1993 29. Houston MC: Abrupt cessation of treatment in hypertension: Consideration of clinical features, mechanisms, prevention, and management of the discontinuation syndrome. Am Heart J 102415, 1981 30. Howell SJ, Sear YM, Yeates D, et al: Hypertension, admission blood pressure and perioperative cardiovascular risk. Anaesthesia 51:lOOO-1004, 1996 31. Huber K, Evans M, Bresnahan J, et al: Outcome of noncardiac operations in patients with severe coronary artery disease successfully treated preoperatively with coronary angioplasty. Mayo Clin Proc 6715-21, 1992 32. ISIS-2 Collaborative Group: Randomized trial of intravenous streptokinase, oral aspirin, both or neither among 17,187 cases of suspected acute myocardial infarction. Lancet 2:349-360, 1988 33. Kaluza GL, Joseph J, Lee JR, et al: Catastrophic outcomes of noncardiac surgery soon after coronary stenting. J Am Coll Cardiol 35:1288-1294, 2000 34. Landesberg G, Luria M, Cotev S, et al: Importance of long-duration postoperative STsegment depression in cardiac morbidity after vascular surgery. Lancet 341:715-719, 1993 35. Langer A, OConnor P: Central modulation of pain perception in patients with silent myocardial ischemia. Am J Cardiol 74:182-184, 1994 36. Lechat P, Packer M, Chalon S, et al: Clinical effects of beta adrenergic blockade in chronic heart failure: A meta analysis of double-blind, placebo-controlled, randomized trials. Circulation 9831184-1191, 1998 37. Mangano DT Perioperative cardiac morbidity. Anesthesiology 72:153-184, 1990 38. Mangano DT, Browner WS, Hollenberg M, et al: Long-term cardiac prognosis following noncardiac surgery. JAMA 268:233-239, 1992 39. Mangano DT, Browner WS, Hollenberg M, et al: Association of perioperative myocar-

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Address reprint requests to Howard H. Weitz, MD Division of Cardiology Jefferson Medical College Thomas Jefferson University 1025 Walnut Street, 403 College Philadelphia, PA 19107 e-mail: [email protected]