CHAPTER 7 DAVID A. FULLERTON, M.D. ALDEN H. HARKEN, M.D. KEITH A. HORVATH, M.

Cardiac Insufficiency
Assessment of cardiac risk and determination of the level of risk that is acceptable are crucial components of preoperative evaluation. A patient and a physician might be willing to accept substantive operative risks to relieve incapacitating pain or claudication. Conversely, the indication for operation of a pulmonary nodule or an asymptomatic carotid bruit is prolongation of the patients life. Ultimately, the natural history of the patients disease must be evaluated and measured against the risk of surgical morbidity and mortality. Actuarial data on risk-benefit assessment have been developed with persuasive precision by insurance companies for large populations of patients. However, risk analysis in an individual patient is much less a precise science than an art. In 1996, in an effort to clarify some of the issues surrounding assessment of cardiac risk in general surgical patients and vascular surgical patients, the American College of Cardiology and the American Heart Association collaborated with the aim of developing guidelines for perioperative cardiovascular evaluation for noncardiac surgery.1 In what follows, we outline a stepwise approach that takes these guidelines into account. Absolute Necessity of Operation versus Indications for Cardiovascular Evaluation

To a patient, an operation is rarely pleasant and almost never risk-free. Accordingly, surgical therapy is proposed only when the anticipated benefits to the patient outweigh the physiologic, psychological, social, and economic risks. Many, if not most, surgeons find it easier to summarize the anticipated benefits of surgery than to rigorously assess the various risks that may militate against operation. Our purpose in this chapter is to examine the tools currently available for analysis of cardiac risk in surgical patients. An issue that must be addressed early on is the question of whether preoperative cardiac evaluation is indicated at all. Certainly, there are some conditions, such as a perforated viscus or an infected gangrenous foot, that simply obligate surgical intervention even in the face of considerable cardiac risk. When faced with such a condition, one

should simply assume that cardiovascular disease is present and then proceed with the operation using invasive monitoring. In the absence of any such absolute indications for operation, however, one should not make this assumption and should address the issue of cardiac risk, beginning with a history and a physical examination. History and Physical Examination

The most direct method of determining whether a patient has heart disease is by direct questioning. In the absence of a positive history, men are considered at risk for coronary artery disease at age 35 and older, whereas women are considered at risk beginning at age 40.2,3 Younger men and women who have no history of cardiovascular problems may proceed to operation, on the presumption that there is no unusual cardiac risk. Although the Multiple Risk Factor Intervention Trial was not designed to examine single risk factors, regression analysis revealed that both elevated plasma cholesterol levels and a history of cigarette smoking were significant predictors of coronary disease. These findings may be used to increase the sensitivity of preoperative historical screening. VALVULAR HEART DISEASE During preoperative assessment, it is important for the surgeon to ascertain whether valvular heart disease is present and, if it is, to gauge its severity. The surgeon should be concerned primarily with diseases of the aortic valve. In an asymptomatic patient, aortic stenosis is the only valvular lesion that must be excluded. Significant valvular disease should be suspected if there is a history of dyspnea, congestive heart failure, angina, or syncope. The foundation for diagnosis of significant valvular disease is the physical examination. Electrocardiography will demonstrate evidence of left ventricular hypertrophy. Chest x-ray may or may not show evidence of congestive heart failure or calcification of the aortic valve, and left ventricular hypertrophy or dilatation may be visible. If the history and physical examination suggest significant aortic stenosis, its severity should be quantified by echocardiography and, if necessary, cardiac catheterization. CONGESTIVE HEART FAILURE The preoperative history and physical examination must assess the possibility of congestive heart failure. In the three most frequently referenced indices of cardiac risk,2,4,5 the dominant predictors of perioperative cardiac complications are all accessible via the history and the physical examination: (1) myocardial infarction within six months, (2) cardiac rhythm other than sinus, (3) age greater than 70 years, and (4) evidence of congestive failure (S3 gallop or jugular venous distention). There is also the stair test, which has resurfaced as the Duke activity status index.6 Thus, using inexpensive means, one can accurately identify both high-risk and low-risk patients. For these patients, subsequent steps are relatively clear-cut: if cardiac risk is low, one may proceed directly to elective surgery, whereas if it is high, one reevaluates the need for the surgical procedure and then, if the need still exists, proceeds directly to coronary angiography. For intermediate-risk patients, however, subsequent steps are less clear-cut, and various tests may be indicated. DYSRHYTHMIAS In the preoperative period, the patient should be asked if he or she has experienced symptoms of dysrhythmia, such as palpitations or syncope. In the physical examination, attention should be directed to the patients heart rate and rhythm for evidence of irregularity. In addition to these steps, the preoperative electrocardiogram and rhythm strip should be studied for evidence of dysrhythmia. If the history and physical examination suggest the presence of a dysrhythmia that either was not diagnosed by the electrocardiogram or is severe enough to necessitate further evaluation, the patient should be evaluated by means of continuous ambulatory electrocardiographic monitoring over a 12-hour to 24-hour period. Dysrhythmias must be well controlled preoperatively. The ventricular response in the patient with atrial fibrillation should be controlled with digoxin. There is no uniformity of opinion regarding the treatment of premature ventricular contraction, but in an otherwise healthy individual, such contractions do not call for preoperative therapy. However, significant dysrhythmias that probably should be treated include

the following [see I Emergency Care, 3 Cardiac Dysrhythmias]: 1. Multifocal premature ventricular contractions or nonsustained ventricular tachycardia. These rhythm problems bespeak a diffusely hyperexcitable ventricle. The five most common causes of hyperexcitability are regional ischemia, hypokalemia, hypercalcemia, exogenous (or endogenous) catecholamines, and drug toxicity (typically related to digitalis). Each of these problems is readily diagnosed and treated. 2. Supraventricular tachycardias. These dysrhythmias are runs of narrowQRS complex rhythms with a ventricular response greater than 100 beats/min. A narrow-complex tachycardia indicates a supraventricular origin. When the tachycardia is generated from a supranodal site, the surgeon may block the node in the short term with adenosine or over the long term with digitalis. ANGINA PECTORIS The diagnosis of angina pectoris can usually be made on the basis of the patients history. The surgeon must be especially alert to the possible presence of variant (Prinzmetals) angina or the more worrisome unstable angina. Variant angina is characterized by anginal pain at rest, frequently in the early hours of the morning. The patient may, however, experience exertional angina as well. Unstable angina is defined as (1) crescendo angina superimposed on relatively stable angina, (2) angina with minimal exertion and at rest, or (3) angina of new onset (change in a stable anginal pattern during the past six weeks) that is elicited by minimal exertion.1,2 The significance of unstable angina is that it may be the harbinger of myocardial infarction; the surgeon must therefore be certain of the absence of unstable angina before proceeding with an operation. Diagnostic Testing

Noninvasive cardiac testing should be reserved for patients who are at moderate risk.7 Testing of low-risk patients loses its predictive value because of the high incidence of false negative and false positive indicators. RESTING ELECTROCARDIOGRAM Most organs do not exhibit dysfunction until stressed. However, for practical and economic purposes, physicians continue to screen patients with a resting ECG. A previous myocardial infarction is accepted as evidence of coronary artery disease. A previous infarction is indicated by the presence of a Q wave 0.04 sec or wider in any of the 12 ECG leads.1,2 However, the absence of pathological Q waves does not necessarily denote a healthy heart.8 Although perioperative risk increases with left ventricular hypertrophy or a nonsinus rhythm (which is easily detected by palpating a pulse) and three to four percent of adults exhibit a previously undiagnosed myocardial infarction, the resting ECG is not a powerful predictor of cardiac complications. The ability to extract information from a communicative patient is extremely important. The patients willingness or ability to communicate is perhaps the weakest link in the entire algorithm. If a patient denies exertional angina, fatigue, shortness of breath, or syncope and if the resting ECG reveals no evidence of coronary artery disease, the surgeon may proceed with elective surgery. If there is any doubt as to the presence of coronary artery disease, an exercise ECG should be obtained. AMBULATORY ELECTROCARDIOGRAM Studies examining the ambulatory ECG indicate that more than 75 percent of patients with diagnosed coronary artery disease exhibit silent (asymptomatic) ischemia.8 Ambulatory monitoring has determined that silent ischemia occurs in

almost all (70 to 100 percent) patients with chronic stable angina. However, in patients without diagnosed coronary artery disease, the ambulatory ECG has both low sensitivity and low specificity for the detection of ischemic heart disease.8 If the surgeon uncovers angina that had not been previously diagnosed or a history of chest pain of uncertain etiology, it is appropriate to perform 12-lead exercise testing to confirm the diagnosis and to help evaluate the severity of the disease.

EXERCISE ELECTROCARDIOGRAM An operative procedure is a stressful hemodynamic insult. If a patient has a history of coronary artery disease, myocardial infarction, typical exercise- or emotion-induced angina, or a positive resting ECG, then it is appropriate to proceed to exercise electrocardiography. Patients with a positive exercise ECG have a significantly higher risk of ischemic heart disease than patients with a negative exercise ECG.9 One study evaluated thousands of healthy individuals and patients, using data collected by the Seattle Heart Watch.10,11 These investigations carefully related exercise level to (1) heart rate, (2) heart rate multiplied by systolic blood pressure (rate pressure product), and (3) calculated total-body oxygen uptake. Four indications of ischemic heart disease were observed: 1. Depression of ST segment ( 2 mm). 2. Exercise-induced hypotension ( 10 mm Hg fall in systolic blood pressure). 3. Complex ventricular ectopy ( 3 consecutive premature ventricular depolarizations). 4. Symptomatic chest pain. This test is quite specific.12 In one series,13 37 percent of vascular surgical patients with a positive test result experienced a perioperative myocardial infarction, compared with only 1.5 percent of patients with a negative test result. Unfortunately, many vascular surgical patients are unable even to get on the treadmill, and in 40 percent of cases, exercise tolerance testing is nondiagnostic. RADIOISOTOPE IMAGING Radioisotope imaging can be valuable in diagnosing coronary artery disease. Currently, thallium-201 is the isotope most frequently used for cardiac imaging. Thallium is concentrated in perfused and viable myocardial cells by the membrane-bound Na+, K+-ATPase pumps. Thallium is almost completely extracted from coronary arterial blood by healthy myocardial cells in a single pass. Thus, thallium uptake reflects zones of perfused and viable heart. Decreased or absent thallium uptake indicates myocardial hypoperfusion. A thallium defect (absence of thallium uptake during exercise that fills in at rest) depicts myocardial ischemia. An exercise thallium scan is accomplished by having the patient perform a standard Bruce protocol exercise test. During exercise, a 2 mCi dose of thallium-201 is administered intravenously for a period of several minutes. Eight-minute thallium cardiac images are obtained during exercise. Three hours later, delayed images are obtained to assess redistribution (filling in) or reperfusion. Again, absence of thallium uptake during exercise delineates regions of nonperfused myocardium. At the three-hour resting scan, regions that fill in are interpreted as having been ischemic during exercise. Zones that do not fill in during the three-hour resting scan are presumed to be dead, nonviable scar tissue.14 Many surgical patients who have vascular disease or orthopedic problems cannot exercise hard enough to meet the demands of an exercise study. In addition, patients with conduction defects (e.g., aberrant ventricular conduction, bundle branch block, or accessory atrioventricular bypass tracts [Wolff-Parkinson-White syndrome]) have ECGs that do not permit the analysis of ischemia with or without exercise. For patients who cannot exercise, the adenosine- or dipyridamole-thallium scan has been developed.15 Adenosine is a potent natural coronary vasodilator. Dipyridamole, also a potent coronary vasodilator, is injected intravenously in a dosage of 0.5 mg/kg over a period of four minutes. After maximal pharmacological coronary vasodilation, thallium-201 is injected, and immediate and three-hour delayed images are obtained.

With initial vasodilation by dipyridamole, the entire myocardium should fill in, thereby leaving no opportunity for assessment of redistribution and reperfusion on three-hour resting scan. Thallium images, however, always provide comparisons of uptake in one region with that in an adjacent region. Dipyridamole leads to hyperperfusion of normal zones and therefore to relative hypoperfusion of regions fed by diseased vessels. The three-hour resting image should exhibit redistribution of thallium into these areas of potentially ischemic but viable tissue. CARDIAC CATHETERIZATION AND CORONARY ANGIOGRAPHY After initial assessment, if the exercise thallium scan is positive, the 12-lead exercise ECG is positive, or valvular and left ventricular disease appears to be present, then invasive cardiac evaluation is indicated. Not all patients undergoing cardiac catheterization will require cardiac operative intervention. The purpose of the evaluation is to balance the medically controlled cardiac disease against the primary surgical problem. If after cardiac catheterization an operable cardiac problem is identified and this problem is greater than the original or primary surgical problem, then the patient should proceed to cardiac surgical repair. After cardiac operation, the patients primary surgical problem should be reevaluated. If after cardiac catheterization the patients identified cardiac disease is less significant or less urgent than the primary surgical problem, the operation for the latter problem should be performed with invasive monitoring.16 The High-Risk Patient Once the preoperative cardiac assessment of a patient at high cardiac risk has been completed and the decision has been made to proceed with operation, the inherent risk of the procedure may be minimized with invasive hemodynamic monitoring and aggressive pharmacological management. INVASIVE MONITORING

When general anesthesia is planned for a patient with presumed or documented cardiopulmonary dysfunction, techniques should be employed for continuous hemodynamic monitoring: 1. An arterial catheter serves as a means of monitoring systemic pressure and assessing arterial oxygenation (blood gases). Acid-base status may be effectively monitored simply by assessing mixed venous blood gas values. 2. A Foley catheter permits continuous assessment of peripheral organ perfusion. With progressive hemodynamic compromise, peripheral vasoconstriction redistributes the limited blood flow preferentially to the

coronary and carotid circulations. Measurement of extremity temperature and urine output may permit estimation of the adequacy of cardiac output. 3. Central venous catheterization permits recognition of right-sided heart filling pressure. In the young trauma victim, this pressure is a valuable assay of total volume status. In the elderly patient with depressed cardiovascular function, the left not the rightside of the heart is characteristically limiting. Florid pulmonary edema is possible even in the presence of a normal central venous pressure. 4. A pulmonary arterial catheter permits measurement of left ventricular filling pressure, cardiac output, and mixed venous blood gases. A patient normally compensates for decreased systemic oxygen delivery by increasing tissue oxygen extraction. Mixed venous acid-base status relates to arterial acid-base status with clinically relevant precision.17 To obtain values for arterial carbon dioxide tension (PCo2) from values for mixed venous PCO2, one subtracts 5 mm Hg. To obtain

arterial pH values from mixed venous pH values, one adds 0.05. The pulmonary arterial catheter has been subjected to a certain amount of high-profile criticism.18 Although no robust link between surgical outcome and data obtained via the pulmonary arterial catheter has been established,19 it still appears to be easier to manage high-risk patients with the help of invasive monitoring. 5. ECG monitoring using a single lead can assess heart rate, atrioventricular synchrony, and ventricular ectopy. Continuous 12-lead monitoring is impractical for this purpose. To optimize the search for ST segment abnormalities, the simultaneous and continuous assessment of anterior (V1), lateral (V5), and inferior (II or aVF) leads is recommended. 6. Transesophageal echocardiographic monitoring may permit continuous assessment of ventricular function and regional wall motion abnormalities or ischemia.20,21 ADJUSTMENT OF MEDICATIONS As a rule, all medications should be administered until the time of operation. Moreover, if beta blockers, nitrates, or calcium channel blockers are required for control of heart rate and blood pressure before operation, these medications should be continued throughout the preoperative period. Intravenous propranolol (0.25 to 0.50 mg) or continuous nitroglycerin infusion should be used liberally in the perioperative period to control blood pressure and heart rate. A reluctance to initiate vasoactive medications, such as nitroglycerin or dobutamine, immediately before or during operation has been noted. This hesitancy is not warranted, because once infusion of these medications has begun, it is easy to change the dose. It is important to assume aggressive hemodynamic control continuously before, during, and after operation. Policies for utilization of hospital beds now place extraordinary pressures on the surgeon to prepare and manage cardiovascular abnormalities outside the hospital. When a patient presents on the morning of an operative procedure with inadequately controlled hypertension (i.e., with a diastolic pressure > 120 mm Hg), it is wise to postpone the operation. Conversely, one study has demonstrated that in the

moderately controlled hypertensive patient with a diastolic blood pressure below 120 mm Hg, elective surgery may proceed without increased risk.22 Indeed, subjective assessment of surgical risk (expressed as a score) with appropriate therapeutic intervention by an experienced anesthesiologist23 may constitute optimal evaluation, and use of Goldmans cardiac risk index may not enhance evaluation significantly.2,22 It is essential to maintain hormonal supplementation during the operation. One half of the usual daily dose of regular insulin may be given before operation and may be augmented intravenously during the procedure. Thyroid hormone is provided in routine doses. Patients on long-term adrenal corticosteroid therapy should receive supplemental doses the evening before and immediately before operation as well as intraoperatively. The only exception to the rule that patients preoperative drug regimens should not be changed during operation applies to patients receiving antidepressants. Administration of these agents should be routinely discontinued before operation. Monoamine oxidase (MAO) inhibitors alter intrinsic catecholamine uptake, with a resultant profound influence on myocardial excitability.24 Therefore, MAO inhibitors should be discontinued, if possible, two weeks before elective surgery. Similarly, tricyclic antidepressants may have a chronotropic and arrhythmogenic influence in association with halothane and pancuronium.25 Some safe antidepressant alternatives are available.25 PACEMAKERS The pacemaker-dependent patient presents an important but easily solvable problem. Virtually all surgeons employ electrocautery devices. All currently

implanted pacemakers are essentially of the demand type, which are likely to sense the electrocautery signal (which is much like the signal emitted by a microwave oven) and turn off when they sense it. As soon as electrocautery is discontinued, however, the demand pacemaker will resume its normal pacing function. Thus, the electrocautery causes a problem only when it must be in use for protracted, continuous periods. To prevent this intermittent problem, a sterile magnet may be placed over the pacer battery to convert the pacemaker to a fixed-rate mode, or the pacemaker may be reprogrammed to the fixed-rate mode. While the pacemaker is in this fixed-rate mode, it will emit impulses and pace the heart regardless of extraneous electrocautery (or ventricular) activity. Spontaneous ventricular activity with a superimposed paced impulse (R on T phenomenon) is possible but unlikely. Continuous electrocardiographic monitoring is essential while the pacemaker is in the fixed-rate mode. Identification and management of pacemaker malfunctions are discussed elsewhere [see I Emergency Care, 3 Cardiac Dysrhythmias]. Discussion Of the 27 million patients who undergo surgical procedures annually in the United States, probably about one third have coexisting coronary artery diseaseseemingly a good argument for preoperative evaluation of cardiac risk. For preoperative

assessment of anything to be worthwhile, however, a problem must be common, the tools to identify it must be available, and, ultimately, a constructive response must be possible. As of this writing, each of these conditions has been met. It has been argued that a little testing begets more testing at rapidly escalating cost and that surgeons should therefore simply treat all patients as if they had coronary artery disease. Our view, however, is that preoperative cardiovascular assessment can be highly useful if pursued in a practical, cost-effective manner. The importance of cardiac-related mortality in surgical patients is underscored by the findings of various studies [see Table 1]. A multifactorial cardiac risk index system (CRIS) has been developed for cardiac risk assessment in patients undergoing noncardiac operation [see Table 2]. The CRIS reflects the high risk of perioperative cardiac complications in patients with evidence of congestive heart failure or recent myocardial infarction. According to the CRIS, any elective operation is contraindicated in patients 70 years of age or older with a third heart sound and evidence of a recent myocardial infarction.2 The Framingham Study demonstrated that only five percent of patients who presented with intermittent claudication underwent amputation for gangrene within five years.26 In contrast, 23 percent experienced symptoms of coronary artery disease within five years, and of this latter group, 13 percent suffered cerebrovascular accidents and 20 percent died. One third of patients who undergo operation for lower extremity vascular disease die of heart disease or stroke within five years. To subject some high-risk patients to noncardiac operation to prolong life may be misdirected. In the past, some centers performed routine preoperative coronary angiography followed by selective myocardial revascularization in high-risk patients to reduce the risk of cardiovascular complications.27 A retrospective study of 60 patients who underwent myocardial revascularization and who subsequently underwent 77 operative procedures found that no intraoperative or perioperative mortality occurred in relation to the general operation.27 Similarly, at the Cleveland Clinic, all patients who presented with abdominal aortic aneurysms or peripheral vascular disease were advised to undergo routine coronary angiography.28 Forty-one of 68 patients with abdominal aortic aneurysms and 26 of 71 patients with aortoiliac occlusive disease had clinical evidence of ischemic heart disease before angiography. Six patients from both groups underwent elective aortic reconstruction after myocardial revascularization; one of these six patients died. Although this strategy has been associated with a reduction in postoperative mortality, routine coronary angiography is impractical and expensive and does involve a certain degree of risk. Indeed,

several groups23,29 have concluded that neither noninvasive nor invasive tests add much to an end-of-the-bed evaluation performed by a seasoned clinical surgeon. When coronary artery bypass grafting and coronary angioplasty are indicated, it is exclusively on the basis of the patients cardiac symptoms and coronary anatomy, not as measures for enhancing the safety of a planned noncardiac surgical procedure.29 The most complete studies of perioperative cardiac mortality have been conducted at the Mayo Clinic. During the late 1960s, the records of more than 32,000 patients who underwent general anesthesia for noncardiac operations were examined.30

Patients with a history of myocardial infarction who suffered a perioperative myocardial reinfarction exhibited a 54 percent mortality, with 80 percent of the deaths occurring within 48 hours of operation. A decade later, when this study was reevaluated and updated to include new patient records, the incidence of myocardial reinfarction was slightly lower, but the mortality in patients with perioperative reinfarction was 69 percent.31 The guiding principle of medical therapy for cardiac ischemia is aggressive reduction of myocardial oxygen demand. During unrecognized intraoperative myocardial ischemia, the unsuspecting surgeon violates this principle and stresses the heart, with poor results. Two questions then arise. First, can surgeons identify intraoperative myocardial ischemia and hemodynamic instability? Second, if they can identify these conditions, can they influence perioperative cardiac mortality by means of invasive monitoring and aggressive pharmacological control of hemodynamic status? Virtually all patients with significant coronary artery disease experience both angina and silent myocardial ischemia during daily life. Insufficient coronary blood flow is to be expected in many of these patients during the stress of operation. It is essential that the surgeon watch for this induced myocardial ischemia during operation and take action to minimize its effects. Predictably, any hypotension that occurs during anesthesia and operation may result in inadequate blood flow across coronary arterial obstructive lesions. Cardiac pressure work, as opposed to flow work, expends much energy and oxygen. Thus, the combination of tachycardia and hypertension, such as occurs with stress, is dangerous. The importance of invasive monitoring and pharmacological control in patients undergoing general anesthesia is underscored by the results of a classic comparison of two groups of surgical patients who received different degrees of operative support. In the mid-1970s, 364 patients undergoing general anesthesia (group I) were evaluated retrospectively.32 This control group was managed without aggressive monitoring or aggressive pharmacological support. From 1977 to 1982, 733 patients (group II) were managed prospectively with frequent invasive monitoring, and aggressive use was made of vasodilators, inotropic agents, vasopressors, beta blockers, and antiarrhythmic agents. The two groups were compared with respect to the incidence of intraoperative hemodynamic aberration and myocardial reinfarction [see Table 3]. All preoperative medications were continued before and during operation. ECG monitors and radial arterial, pulmonary arterial, and urinary catheters were used for all patients considered at risk for cardiac disease. Monitoring was minimized if the procedure was expected to last less than 30 minutes. Monitoring was particularly aggressive for any patient who had had a myocardial infarction during the prior 18 months. Baseline hemodynamic measurements were obtained, and nitroglycerin, dopamine, and phenylephrine infusions were immediately available to maintain systolic pressure, pulmonary arterial pressures, heart rate, cardiac output, and systemic vascular resistance within 20 percent of the preinduction values during the entire procedure. Arterial blood gases, potassium, and blood glucose were corrected frequently; the hematocrit was kept above 30 percent; and urine output was

maintained with volume and diuretics. Ventricular ectopy was suppressed with lidocaine and procainamide. Patients were not extubated at the completion of the procedure unless they were awake and alert and had adequate measured tidal volume and vital capacity. Comparison of the two groups revealed that there was a substantially lower incidence of hemodynamic aberrations in group II, and even though this group had twice as many patients, one half as many reinfarctions were reported (14 in group II versus 28 in group I). Operation remains a predictable hemodynamic insult. Surgeons can identify patients at increased cardiac risk with clinically useful precision. If these patients are carefully observed for myocardial ischemia and treated aggressively by maintaining blood pressure and heart rate within tight bounds, surgeons can minimize perioperative cardiac morbidity and mortality.

References 1. American College of Cardiology/American Heart Association Task Force Report: Guidelines for perioperative cardiovascular evaluation for non-cardiac surgery. Circulation 93:1278, 1996 2. Mangano DT, Goldman L: Pre-operative assessment of patients with known or suspected coronary disease. N Engl J Med 333:1750, 1995 3. Multiple Risk Factor Intervention Trial Research Group: Coronary heart disease death, nonfatal acute myocardial infarction and other clinical outcomes in the Multiple Risk Factor Intervention Trial. Am J Cardiol 58:1, 1986 4. Detsky AS, Abrams HB, McLaughlin JR, et al: Predicting cardiac complications in patients undergoing non-cardiac surgery. J Gen Intern Med 1:209, 1986 5. Larsen SF, Olesen KH, Jacobsen E, et al: Prediction of cardiac risk in non-cardiac surgery. Eur Heart J 8:179, 1987 6. Nelson CL, Herndon JE, Mark DB, et al: Relation of clinical and angiographic factors to functional capacity as measured by the Duke Activity Status Index. Am J Cardiol 68:973, 1991 7. Fleisher LA, Eagle KA: Screening for cardiac disease in patients having non-cardiac surgery. Ann Intern Med 124:767, 1996 8. Kawanishi DT, Rahimtoola SH: Silent myocardial ischemia. Curr Probl Cardiol 12:509, 1987 9. Bartels C, Bechtel JF, Hossmann V, et al: Cardiac risk stratification for high risk vascular surgery. Circulation 95:2473, 1997 10. Bruce RA: Exercise testing for evaluation of ventricular function. N Engl J Med 296:671, 1977 11. Bruce RA, Hornstein TR: Exercise stress testing in evaluation of patients with ischemic heart disease. Prog Cardiovasc Dis 11:371, 1969 12. Paul SD, Eagle KA: A stepwise strategy for coronary risk assessment for non-cardiac surgery. Med Clin North Am 79:1241, 1995 13. Cutler BS, Wheeler HB, Paraskos JA, et al: Applicability and interpretation of exercise stress testing in patients with peripheral vascular disease. Am J Surg 141:501, 1981 14. Refsnyder T, Bandyk DF, Lanza D, et al: Use of stress thallium imaging to stratify cardiac risk in patients undergoing vascular surgery. J Surg Res 52: 147, 1992 15. Mumtaz H, Bomanji JB, Guptka NK, et al: Myocardial perfusion scintography in patients undergoing major non-vascular abdominal surgery. Ann R Coll Surg (Engl) 78:420, 1996 16. Mason JJ, Owens DK, Harris RA, et al: The role of coronary angiography and coronary revascularization before non-cardiac vascular surgery. JAMA 273:1919, 1995 17. Steinberg JJ, Harken AH: Central venous catheter in the assay of acid-base status. Surg Gynecol Obstet 152:221, 1981 18. Dalen JE, Bone RC: Is it time to pull the pulmonary artery catheter? JAMA 276:916, 1996 19. Tuman KJ, Roizen MF: Outcome assessment and pulmonary artery catheterization: why does the debate continue? Anesth Analg 84:1, 1997 20. Practice guidelines for perioperative transesophageal echocardiography. Anesthesiology 84:986, 1996

21. London MJ: Ventricular function and myocardi-al ischemia: is transesophageal echocardiography a good monitor? Controversies in Intraoperative Echocardiography. Kaplan JA, Ed. WB Saunders Co, Philadelphia, 1997, p 61 22. Goldman L, Caldera DL: Risks of general anesthesia and elective operation in the hypertensive patient. Anesthesiology 50:285, 1979 23. Prause G, Offner A, Ratzenhofer-Komenda B, et al: Comparison of two pre-operative indices to predict perioperative mortality in non-cardiac thoracic surgery. Eur J Cardiothorac Surg 11:670, 1997 24. Wells PH, Kaplan JA: Optimal management of patients with ischemic heart disease for non-cardiac surgery by complementary anesthesiologist and cardiologist interaction. Am Heart J 102:1029, 1981 25. Edwards RP, Miller RD: Cardiac responses to imipramine and pancuronium during anesthesia with halothane or enflurane. Anesthesiology 50: 421, 1979 26. Peabody CN, Kannel WB, McNamara PM: Intermittent claudication: surgical significance. Arch Surg

109:693, 1974 27. McCollum CH, Garcia-Rinaldi R, Graham JM, et al: Myocardial revascularization prior to subsequent major surgery in patients with coronary artery disease. Surgery 81:302, 1977 28. Hertzer NR, Beven EG, Young JR: Coronary artery disease in peripheral vascular patients: a classification of 1000 coronary angiograms and results of surgical management. Ann Surg 199:223, 1984 29. Krupski WC, Bensard DD: Pre-operative cardiac risk management. Surg Clin North Am 75:647, 1995 30. Tarham S, Moffitt EA, Taylor WF, et al: Myocardial infarction after general anesthesia. JAMA 220:1451, 1972 31. Steen PA, Tinker JH, Tarhan S: Myocardial reinfarction after anesthesia and surgery. JAMA 239: 2566, 1978 32. Rao TLK, Jacobs KH, El-Etr AA: Reinfarction following anesthesia in patients with myocardial infarction. Anesthesiology 59:499, 1983 33. Goldman L: Assessment of perioperative cardiac risk. N Engl J Med 330:707, 1994 34. Cooperman M, Pflug B, Martin EW Jr, et al: Cardiovascular risk factors in patients with peripheral vascular disease. Surgery 84:505, 1978 35. Carliner NH, Fisher ML, Plotnick GD, et al: Routine preoperative exercise testing in patients undergoing major noncardiac surgery. Am J Cardiol 56:51, 1985 36. Arous EJ, Baum PL, Cutler BS: The ischemic exercise test in patients with peripheral vascular disease: implications for management. Arch Surg 119:780, 1984 37. Gerson MC, Hurst JM, Hertzberg VS, et al: Cardiac prognosis in noncardiac geriatric surgery. Ann Intern Med 103:832, 1985 38. Pasternack PF, Imparato AM, Riles TS, et al: The value of radionuclide angiogram in the prediction of perioperative myocardial infarction in patients undergoing lower extremity revascularization procedures. Circulation 72:1113, 1985 Acknowledgments Table 2 Data from Multifactorial Index of Cardiac Risk in Noncardiac Surgical Procedures, by L. Goldman, D. L. Caldera, S. R. Nussbaum, et al, in New England Journal of Medicine 297:845, 1977, and Preoperative Assessment of Patients with Known or Suspected Coronary Disease, by D. T. Mangano and L. Goldman, in New England Journal of Medicine 333:1750, 1995. Table 3 From Reinfarction following Anesthesia in Patients with Myocardial Infarction, by T. L. K. Rao, K. H. Jacobs, and A. A. El-Etr, in Anesthesiology 59:499, 1983, and Reduction in Mortality from Cardiac Causes in Goldman Class IV Patients, by K. Shah, B. Leomman, T. Rao, et al, in Journal of Cardiothoracic Anesthesia 2:789, 1988.

Winter 1998

Special Problems in Perioperative Care