General Thoracic Surgery (General Thoracic Surgery (Shields)) [2 VOLUME SET]

Editors: Shields, Thomas W.; LoCicero, Joseph; Ponn, Ronald B.; Rusch, Valerie W.

Title: General Thoracic Surgery, 6th Edition

Copyright 2005 Lippincott Williams & Wilkins

> Table of Contents > Volume I - The Lung, Pleura, Diaphragm, and Chest Wall > Section VII - Pulmonary Resections > Chapter 38 - Management of Perioperative Cardiac Events

Chapter 38

Management of Perioperative Cardiac Events

John C. Alexander Jr.

Donald P. Jones

Noncardiac thoracic surgery is relatively invasive in terms of its stress on a patient's cardiovascular system. The overall outcome of patients undergoing thoracic surgery can be dramatically affected by perioperative cardiac events that can result in significant morbidity and mortality despite successful thoracic surgery. Although respiratory problems are the most common postoperative complication of thoracic surgery, cardiac events are most frequently associated with severe morbidity and have the highest mortality of all complications occurring after thoracic surgery. This chapter addresses the identification and management of perioperative cardiac events following major thoracic surgery.

General thoracic surgical procedures often have more profound effects on the cardiopulmonary system than cardiac operations. A major lung resection decreases the pulmonary vascular bed and therefore may result in an acute increase in right ventricular and pulmonary artery pressure, leading to right ventricular failure. Other physiologic changes associated with thoracic surgery include a decrease in lung compliance and diffusing capacity, with a resultant increase in the work of breathing, which in turn increases myocardial workload and increases myocardial oxygen consumption, which may aggravate preexisting cardiac disease or lead to new-onset ischemia in the patient with stable coronary artery disease.

The management of cardiovascular complications following thoracic surgery is best begun prior to surgery with identification of cardiac risk and appropriate assessment and optimization. Cardiovascular events that can complicate thoracic surgery range from relatively benign atrial arrhythmias and systemic hypertension to pulmonary emboli, shock, myocardial infarction, and death. In general, the risk of cardiac complications increases with the patient's age and is more frequent in patients who undergo more extensive procedures such as pneumonectomy or esophageal resection. The most important morbid event following thoracic surgery is a perioperative myocardial infarction, which carries a mortality of nearly 50%. As we see a progressively older patient population, it is likely that we will begin to see more in the way of postoperative cardiovascular complications.

Thoracic surgery is also associated with an acute chest wall injury resulting in involuntary respiratory guarding and increased work of breathing and decreased efficiency of respiration. Chest wall effects of thoracic surgery are associated with an acute decrease in forced expiratory volume in 1 second (FEV₁) and vital capacity. In patients with diminished respiratory reserve, the acute ventilatory changes after surgery can lead to respiratory decompensation requiring prolonged mechanical ventilation and setting the stage for pneumonia and respiratory failure. Minimally invasive thoracic surgical approaches have, in some cases, reduced the importance of acute chest wall related problems; however, even in patients with the most minimal incisions, demonstrable changes in ventilatory mechanics are present and may lead to significant complications, as emphasized by Hazelrigg and associates (1991). Thoracic surgery by design results in a planned reduction in physiologic reserve of the lungs for a variety of reasons, whereas in contrast, cardiac surgery usually improves the physiologic reserve of the heart. In addition, sternotomy causes less derangement of chest wall mechanics than does posterolateral thoracotomy.

For these reasons, thoracic surgical procedures and upper abdominal vascular surgical procedures have the highest incidence of perioperative arrhythmias, myocardial infarction, and heart failure when compared with other general surgical procedures, as noted by Detsky (1986), Goldman (1977), and Steen (1978) and their associates.

EVALUATION OF CARDIAC RISK FACTORS

Operative risk is defined as the probability of morbidity or mortality after an operation because of the patient's preoperative condition, anesthesia, the surgical procedure itself, or the circumstances of the required postoperative convalescence. The decision to proceed with any operation must be made by weighing the potential risks against the

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The greatest cardiac risk factor for a patient undergoing a thoracotomy is the presence of known coronary artery disease. Based on the extensive data of Leppo (1995) as well as Freeman (1989), Lee (1999), Steen (1978), and Tarhan (1972) and their associates, who studied more than 50,000 patients, the likelihood of a perioperative myocardial infarction was observed to be only 0.15% in patients without prior evidence of clinical heart disease. In patients with a documented prior infarction, however, the incidence of reinfarction during a major noncardiac procedure ranged from 2.8% to 17.7%, with a mean of approximately 6%. The mortality for perioperative myocardial infarction is high and averages approximately 50% despite aggressive treatment.

The risk of perioperative infarction is inversely related to the time interval between the original myocardial infarction and the surgical procedure. This risk follows a curvilinear, rather than a linear, relation. Major noncardiac surgical procedures performed within 3 months of an acute myocardial infarction have been associated with a reinfarction rate of approximately 30%, whereas at 3 to 6 months after an infarction, the corresponding rate of reinfarction is approximately 14% and falls to 4% after 6 months. The institution of aggressive and comprehensive perioperative management guided by invasive hemodynamic monitoring, introduced by Rao and colleagues (1983), has produced a decrease in reinfarction rates; however, when the postoperative period is complicated by an infarction, it is still associated with high mortality.

A thorough cardiovascular history is vital in the preoperative evaluation of thoracic surgical patients, and the findings must then be correlated with physical findings and laboratory testing. The factors associated with cardiac risk in thoracic surgical patients are summarized in Table 38-1. The presence of any of the risk factors noted in Table 38-1 should arouse suspicion of significant cardiac disease and, as suggested by Leppo (1995), should lead to a more comprehensive cardiac evaluation and possible presurgical cardiac intervention.

The clinical cardiac findings must be correlated with echocardiography and electrocardiography (ECG). The chronology and clinical course of prior myocardial infarction should be elucidated, and evidence of left ventricular dysfunction as manifested by symptoms of congestive heart failure should be sought carefully. Attention also should be paid to the presence, severity, and pattern of angina pectoris and to the efficacy and appropriateness of the current medical regimen.

Paul and Eagle (1995) note that interventional cardiology has added a dimension to the diagnosis and treatment of cardiac conditions that is important in the perioperative period. Patients who are at high risk for cardiac complications should be considered for stress testing before surgery. A patient with an early positive stress test should undergo further diagnostic testing and possibly interventions to correct cardiac problems (usually coronary artery disease) before elective thoracic surgery. The occasional patient may need angioplasty or stenting, or both, or even a coronary artery bypass before or in conjunction with thoracic surgery to reduce the probability of a postoperative cardiac event. Patients who have undergone noncardiac surgery after either coronary artery bypass graft or percutaneous transluminal coronary angioplasty (PTCA) have a lower rate of cardiac events than patients with similar medical histories in whom coronary revascularization has not been performed. It is presumed that aggressive cardiologic evaluation and treatment before surgery will lower the operative risk in this group of high-risk patients, as suggested by Mangano (1996), Gottlieb (1998), and Hassan (2001) and their colleagues.

Postoperative infarctions are significantly more lethal than infarctions in general, in part because the postoperative time frame is associated with an obligatory increased cardiac workload caused by the surgical stress of the procedure.

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In addition, acute changes in coagulation associated with the systemic inflammatory response to surgery make patients hypercoagulable in the early postoperative period. Deep venous thrombosis, pulmonary embolus, and coronary thrombosis are potentiated by the hypercoagulable state, which partially explains the high incidence of these problems in the postoperative period.

In patients who develop acute postoperative infarctions, aggressive interventional cardiology using PTCA and stents may be life saving. Lytic therapy is relatively contraindicated in most acute coronary artery emergencies that occur early after major surgery. Angiography and catheter-based interventions are the procedures of choice for unstable angina in these patients and should be used as soon as persistent ischemia is recognized, for it is very difficult to cool off angina in these patients.

Patients who are completely asymptomatic, have an active lifestyle, and have no significant risk factors for coronary artery disease, regardless of age, need not undergo further cardiac testing. Patients with symptomatic heart disease or baseline ECG or echocardiographic abnormalities suggestive of cardiac disease need further assessment. If symptoms of ischemic heart disease are present, stress testing should be considered before a major intrathoracic surgical procedure is recommended, particularly if the patient has a history of myocardial infarction, demonstrates symptomatic left ventricular dysfunction, or has hypertension or diabetes mellitus.

A variety of stress test methods have been used to evaluate cardiac reserve. Each has its own characteristics and is particularly useful for certain types of patients. The underlying principle, however, is the same independent of methodology: Stress testing can determine the cardiac reserve in a controlled manner before the patient is subjected to the uncontrolled stress associated with surgery and the postoperative period. Paul and Eagle (1995) believe that stress testing is the most useful screening procedure for patients during the planning phase of thoracic surgery if they have historical signs and symptoms suggestive of cardiac disease.

Transthoracic echocardiography and transesophageal echocardiography when indicated are useful noninvasive modalities to assess overall ventricular function and to detect any evidence of valvular pathology. Echocardiography is an excellent first-line screening examination in patients with any suggestive history or physical finding associated with heart failure or valvular heart disease.

Nonexercise stress testing [dobutamine echo or dipyridamole (Persantine) infusion] can be used if a physical limitation to exercise exists. Cardiac catheterization and coronary arteriography should be considered if the patient is unable to exercise to an adequate workload required for stress testing. The demonstration of significant anatomic coronary artery disease (left main or three-vessel involvement), significant physiologic ischemia, or valvular disease during noninvasive and invasive testing requires consideration of revascularization or valve surgery in certain instances when severe dysfunction is present.

The preoperative cardiac evaluation of thoracic surgical patients requires making important and reasonable decisions in a responsible and cost-effective manner. Some authors suggest that all patients older than a certain age undergo an extensive noninvasive, and possibly even invasive, evaluation to determine the presence of coexistent coronary artery disease. The intent is to electively revascularize those patients in whom significant disease is identified. This approach, as noted by Abraham and Eagle (1994), is gaining support because evidence is accumulating that prophylactic revascularization by any technique provides greater protection from ischemic events after surgery and is more successful than intensive medical therapy during the postsurgical period. However, the predictive accuracy of some of these investigations remains unclear.

Clinical Cardiac Risk Assessment

The purpose of cardiac risk assessment is to stratify patients into low, intermediate, or high risk categories based on preoperative factors. A number of clinical risk indices have been developed in an effort to identify patients at high risk for cardiac morbidity after noncardiac surgery, including the systems reported by Palda and Detsky (1997) and by Mangano and Goldman (1995).

Initial noninvasive evaluation includes history, physical examination, and ECG. Further noninvasive testing available for subsequent risk stratification includes echocardiogram, radionuclide angiography (left ventricular function assessment), exercise or pharmacologic stress testing, and ambulatory ECG monitoring (cardiac ischemia) and dobutamine stress echocardiography (ischemia and ventricular function).

Clinical Utility

It is important not only to identify the presence or absence of heart disease but also to determine and define its severity and previous treatment, and cardiac stability. Successful surgical management of these patients depends on teamwork and close cooperation and communication among the patient's thoracic surgeon, anesthesiologist, cardiologist, and primary care physician. Table 38-1 represents a composite comprehensive clinical risk stratification plan for patients undergoing elective noncardiac thoracic surgery. It serves as a clinical framework for cardiac risk assessment.

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Patients who have major clinical predictors require careful and complete investigation including ECG, stress testing, echocardiography with or without dobutamine, and, depending on the results, possibly radionuclide angiography and coronary catheterization. The indications for coronary angiography are the same as for patients not undergoing thoracic surgery and should be carefully tailored to each individual patient.

Patients with intermediate risk predictors should be further stratified with respect to functional capacity. Those with poor functional capacity [<4 metabolic equivalents (METS)] should undergo noninvasive testing by ECG stress test and echocardiography and possibly radionuclide angiography. Further studies (coronary angiography) may indicate a need for PTCA or stenting or for surgical revascularization prior to the planned thoracic procedure.

In general, patients with only minor clinical risk predictors should be assessed with respect to functional capacity. If such assessment indicates poor (<4 METS) or moderate (4 to 7 METS) functional capacity, these patients should be assessed like the intermediate risk group.

Those patients with minor clinical risk predictors whose exercise capacity is excellent (>7 METS) can usually undergo the planned thoracic procedure without further cardiac investigation. In summary, each patient must be considered individually and clinical judgment exercised, as emphasized by Fleisher and Eagle (2001).

Pulmonary Hypertension

Thoracic surgical patients should be evaluated clinically for the presence of pulmonary hypertension, a problem that may be aggravated by pulmonary resection. Shortness of breath with minimal exertion or signs of right-sided heart failure should alert the clinician to possible pulmonary hypertension. Reactive pulmonary vasoconstriction leading to acute right ventricular failure is a very morbid complication. Persons thought to have pulmonary hypertension may require further noninvasive testing or a right-sided catheterization to evaluate the degree of pulmonary vascular disease. Echocardiography is a useful noninvasive method for estimating right ventricular performance and pulmonary artery pressures. Acute pulmonary hypertension is very difficult to treat. Nitrous oxide and prostaglandin have been used with success, but the long-term outlook is poor.

MANAGEMENT OF SURGICAL PATIENTS WITH CARDIOVASCULAR DISEASE

Since the 1970s, there has been a substantial overall decrease in premature mortality from cardiovascular diseases. Some authors have suggested that modifications in dietary habits and an increased awareness of physical fitness are primarily responsible for improvements in cardiovascular health. Good evidence also exists that shows that the use of modern drug therapy to control hypertension and reduce cholesterol levels has played an important role in lowering premature cardiovascular disease morbidity and mortality. Consequently, many patients are surviving or avoiding the early complications of cardiovascular disease, only to be seen by surgeons later in their lives for noncardiac problems of all types that require surgical treatment. Consequently, one can expect to be faced with patients who bring an ever-increasing set of cardiovascular problems with them to the operating room. Because of their older age and multiple associated illnesses, these patients present risks that must be carefully considered in the design of their surgical management plan.

The cardiovascular diseases that are most frequently encountered in the thoracic surgical patient fall into four general categories: ischemic heart disease (which was dealt with in the first section of this chapter), hypertension, chronic congestive heart failure, and arrhythmias. Considerable overlap, however, exists between these categories.

Hypertension

Hypertension is a common finding in surgical patients. The number of patients diagnosed with this disorder has increased substantially since the 1970s. In approximately 95% of hypertensive patients, no single cause for the elevation in blood pressure can be identified. Although many theories exist to explain the increased peripheral vascular resistance seen in hypertension, the possibility that a single etiology is responsible for all essential hypertension is unlikely.

It is well recognized from therapeutic trials that many of the cardiovascular complications resulting from hypertension can be ameliorated by pharmacologic intervention, a finding that has led to the widespread use of antihypertensive agents. Some of these agents may have a profound influence on a patient's ability to respond to the stresses associated with surgery, including reduced ability to develop tachycardia in response to blood loss and to vasoconstrict in response to hypovolemia. The different classes of antihypertensive agents will be considered separately.

Diuretics

Diuretics, including the thiazides and furosemide, are the recommended first-line agents in the treatment of mild or moderate hypertension. These drugs increase urinary excretion of salt and water, and relative hypovolemia may result. Hypovolemia may result in hypotension with the administration of general anesthesia. Hypovolemia may interfere with the ability of reflex tachycardia, a normal homeostatic response, to increase cardiac output and maintain blood pressure. As a result, relatively minor blood loss may result in profound hypotension and a severe decrease in cardiac output if preexisting volume deficits are present because of prolonged diuretic administration. Obtaining a full history

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Loop diuretics work by increasing the delivery of sodium to the distal renal tubule. Sodium potassium exchange occurs in the kidney, resulting in a net potassium loss and resultant hypokalemia following prolonged administration of most diuretic agents. In the presence of hypokalemia, the arrhythmogenic effects of digoxin, anesthetic agents, and the stress of surgery may result in cardiac arrhythmias that can lead to ventricular irritability and premature ventricular contractions or fibrillation. Repletion of diminished total body potassium stores before surgery is essential to reduce the incidence of cardiac rhythm disturbances.

Adrenergic Blockers

A second major category of agents used to treat hypertension is the adrenergic inhibitors. These drugs inhibit the function of the sympathetic nervous system and are classified according to the site at which they inhibit the sympathetic reflex arc. Each class of drug exhibits different patterns of potential toxicity that may produce problems in surgical patients.

The peripherally acting agents, such as reserpine and guanethidine, which are not commonly used today, produce profound sympathoplegia by either blocking or inhibiting biogenic amine functions in both peripheral and central neurons. The problems of depressed cardiac output and hypotension from blunted sympathetic responses in the presence of volume depletion or exposure to anesthetic agents are often seen in surgical patients who have received these agents before surgery. It is advisable to discontinue peripherally acting adrenergic blocking agents before any elective surgical procedure. Substitution of a more rapidly acting and easily managed agent, such as a -blocker or calcium channel antagonist, is recommended.

The centrally acting adrenergic inhibitors, such as clonidine and methyldopa, reduce sympathetic outflow from vasopressor centers in the brainstem. These agents are also seldom used today. Because these agents allow the brain to retain its sensitivity to baroreceptor input, these drugs do not depress normal cardiovascular reflexes and thus do not depress cardiac output or produce the orthostatic hypotension seen with peripherally acting agents. Abrupt withdrawal of clonidine may result in a hypertensive crisis or other evidence of profound sympathetic overactivity. This drug should therefore be continued throughout the perioperative period or gradually withdrawn while other antihypertensive therapy is substituted.

-Blockers

Although beta-blocking agents were used initially to treat angina pectoris, it soon became apparent that they were extremely effective agents for the treatment of hypertension and a variety of other disorders, such as thyrotoxicosis, migraine headaches, arrhythmias, glaucoma, and essential tremor. Currently, many treatment regimens in patients with mild or moderately severe hypertension include a -blocker. -blockers are well tolerated in surgical patients and appear to offer a significant degree of protection from postoperative rhythm disturbances in addition to blood pressure control if continued without interruption throughout the postoperative period. Bronchospasm may be a problem with -blockers in thoracic surgery patients, but usually patients can be managed with these agents in the postoperative period. Abrupt withdrawal of -blockers has been associated with the onset of atrial arrhythmias and even acute myocardial infarction, and should be avoided. Recently, the risk of perioperative ischemic cardiac events has been shown to be significantly reduced by the use of -blockers in the perioperative period, as reported by Auerbach and Goldman (2002). Not only should these agents be continued preoperatively, but consideration should be given to instituting -blockers preoperatively in patients at increased risk of cardiac events or undergoing major operations.

Vasodilators

Peripheral vasodilators, initially used in the management of hypertension only if a diuretic and adrenergic blocker did not control the blood pressure, are being used more frequently. Hydralazine is the only drug routinely used as an oral agent. Intravenous nitroprusside (a potent vasodilator) is a common choice for the control of acute hypertension in the operating room or during the early postoperative period, since it is rapid acting and easily titrated under conditions of proper monitoring to achieve expeditious control of the patient's blood pressure.

Angiotensin-Converting Enzyme Inhibitors

Captopril was the first orally effective inhibitor of angiotensin-converting enzyme (ACE), the enzyme responsible for conversion of inactive angiotensin I to the pressor peptide angiotensin II. Many new ACE inhibitor drugs are now available. The ACE inhibitors are potent and specific antihypertensive agents that lower total peripheral resistance while causing little change in cardiac output, heart rate, or pulmonary artery wedge pressure. They are particularly effective in hypertensive patients with elevated renin levels. They do not appear to interfere with normal cardiovascular homeostatic responses even when administered simultaneously with a diuretic. If significant volume depletion occurs as a result of a concomitantly administered diuretic, however, hypotension may develop. Abrupt withdrawal of ACE inhibitors may result in hypertension that is difficult to manage. These drugs should be continued throughout the perioperative period.

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Acute Perioperative Hypertension

Uncontrolled hypertension in any postoperative surgical patient is a serious problem. It is essential to formulate a plan for the management and control of blood pressure in the operating room and postoperatively before discontinuing any form of antihypertensive therapy. This planning should include the surgeon, anesthesiologist, and cardiologist/internist. Rapidly acting agents, such as intravenous nitroprusside, a potent vasodilator, or esmolol or other ultrashort-acting intravenous -blockers, are the agents of choice for sudden-onset severe hypertension and tachycardia during the intraoperative or immediate postoperative period, as noted by Schwartz and associates (1988). These agents should be administered only under carefully monitored conditions because of their ability to rapidly produce profound bradycardic hypotension. After passing the period of hemodynamic instability surrounding the immediate operative period, the patient's normal antihypertensive regimen should be reinstituted. In the past, it was frequent to discontinue antihypertensive medicines prior to surgery. This approach is much less frequent today. Patients can usually be managed with little interruption in their antihypertensive medicines, particularly in thoracic surgery.

Congestive Heart Failure

Traditional treatment for patients with cardiac failure consisted of salt restriction, diuretics, and the administration of a digitalis preparation for its inotropic effect. Cohn (1981) and Cohn and associates (1986) recognized that an increase in impedance to left ventricular ejection (afterload) was an important factor in producing the left ventricular dysfunction found in congestive heart failure. Increased impediment to ejection or afterload is the result of a complex series of peripheral vascular events produced by increased activity of the sympathetic system and the renin-angiotensin system. The final result of this abnormal activity is diffuse narrowing of the arterioles, decreased arterial compliance, and a reduction in venous compliance. An important change occurred in the treatment of heart failure based on this pathophysiologic concept. Instead of vigorously stimulating the failing heart with inotropic agents, attempts are now made to reduce afterload by the use of peripheral vasodilators. The concept of afterload reduction by pharmacologic means is well established in the treatment of hypertension and has been extended to other disease states that produce severe congestive heart failure, such as aortic or mitral valve incompetence, ischemic heart disease, and cardiomyopathy.

Drugs that produce vasodilatation can favorably affect the performance of the heart in two ways, according to Chatterjee and Parmley (1983) and Ribner and colleagues (1982). First, by decreasing peripheral vascular resistance through the mechanism of arteriolar relaxation, the ventricular ejection fraction increases, stroke volume improves, and end-systolic volume decreases. Second, the relaxation of venous smooth muscle shifts blood from the central circulation into the peripheral venous capacitance bed, thereby decreasing the preload and end-diastolic volume, which results in a reduction in myocardial wall stress and consequent lowering of myocardial oxygen requirements and a decrease in left ventricular end-diastolic pressure and pulmonary venous pressure with relief of pulmonary congestion. Improved diastolic coronary perfusion of the myocardium as a result of lowering the transmyocardial pressure gradient between epicardial and endocardial blood vessels improves coronary perfusion and ventricular performance.

The surgical management of patients with preexistent congestive heart failure has been improved with the addition of vasodilator drugs to their medical regimen. This improvement has been particularly evident in elective cardiac and thoracic surgical patients, who can be optimized preoperatively and brought to the operating room in a more stable and optimal state than was previously possible.

Any patient with heart disease severe enough to produce symptoms or signs of congestive heart failure presents a substantial risk for any thoracic surgical operation. A comprehensive evaluation of the patient's underlying cardiac pathology and the institution or continuation of appropriate therapy, coupled with the judicious use of perioperative monitoring of cardiac function, are important to reduce surgical risk to an acceptable level. In almost all instances, drugs that have successfully controlled symptoms of cardiac failure before surgery should be continued throughout the preoperative, operative, and postoperative periods.

Arrhythmias

Bailey and Betts (1943) and Currens and associates (1943) first called attention to the increased incidence of both supraventricular and ventricular arrhythmias after thoracotomy for pulmonary and esophageal disease. Krosnick and Wasserman (1955) first drew attention to an association between the occurrence of postoperative arrhythmias and postoperative mortality. This argument was strengthened by Shields and Ujiki (1968) when they reported a series of 125 patients undergoing thoracotomy. The findings of their nonrandomized study suggested that prophylactic digitalization reduced mortality related to arrhythmias. Since that time, considerable controversy regarding the incidence, importance, etiology, methods of treatment, and usefulness of prophylaxis for these arrhythmias has existed in the thoracic surgical literature. Ferguson (1992) carefully reviewed and documented the relation between cardiac arrhythmias and thoracic surgery and concluded that the

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The perioperative management of patients with cardiac arrhythmias and conduction disturbances is an important part of the care of thoracic surgical patients. Knowledge of the preoperative medication history, electrocardiography, echocardiography, and the patient's cardiovascular history should be combined with an understanding of the intraoperative and postoperative factors that facilitate the occurrence of cardiac rhythm disturbances. A number of factors may be identified perioperatively that predispose to the development of arrhythmias, including ventilatory problems that produce hypoxemia or respiratory acidosis, hypokalemia and other electrolyte abnormalities, hypotension, hypertension, reduced cardiac output, anemia, myocardial infarction, vagal stimulation, and direct atrial trauma. An important perioperative factor appears to be an increase in circulatory catecholamines associated with surgery and postthoracotomy pain that accompanies thoracic surgical procedures. The most important clinical predictor of postoperative arrhythmias is a history of preoperative arrhythmias. These predisposing factors must be considered in the evaluation of a surgical patient with cardiac rhythm disturbance, and initial treatment should always be directed toward correction of these abnormalities, which will reduce the driving force behind the arrhythmias.

The aim of antiarrhythmic therapy is to reduce ectopic pacemaker activity. The indications for the use of antiarrhythmic drugs in surgical patients are based on a knowledge of the natural history of the rhythm disturbance and whether it is of physiologic significance in the overall management of the patient. Careful documentation and precise diagnosis of the type of rhythm disturbance are essential. Harrison (1985) suggested a limited role for the prophylactic use of drug therapy in an attempt to prevent the development of arrhythmias. Most antiarrhythmic drugs have proarrhythmic effects and therefore may actually precipitate a rhythm disturbance. In general, all cardiac rhythm disturbances that are potentially life threatening, that cause hemodynamic compromise, or that result in significant symptoms should be diagnosed precisely and treated specifically.

Patients with no known structural heart disease usually do not require specific drug therapy for benign rhythm disturbances such as sinus tachycardia, premature atrial beats, or unifocal premature ventricular beats. The most prudent approach in these patients may be to define and treat underlying contributory factors, such as fever, hypoxemia, pain, or anxiety. In some patients, the presence of structural heart disease may complicate the use of antiarrhythmic therapy. Heart failure and conduction system disease are the most serious problems. Most antiarrhythmic drugs depress left ventricular function to a variable and dose-related degree. Patients with left ventricular dysfunction may tolerate these agents poorly. Drug therapy for patients with atrioventricular nodal disease or with conduction blocks below the atrioventricular node should be monitored carefully because of the potential for profound depression of cardiac conduction with resultant heart block leading to marked bradycardia, hypotension, and ventricular fibrillation, as noted by Amar (1997).

Bradyarrhythmias

Sinus bradycardia is usually caused by increased vagal tone related to direct stimulation of the carotid sinus or the vagus nerves or to pain-induced increases in vagal tone. Myocardial ischemia should always be considered as a cause for sudden cardiac slowing.

Sinus bradycardia is best treated by administering atropine intravenously in 0.50-mg boluses, giving up to 2.0 mg over a 30-minute period. If atropine therapy is unsuccessful, a continuous infusion of dopamine or dobutamine may be administered and titrated to achieve the desired heart rate responses. If pharmacologic therapy is unsuccessful, a temporary transvenous pacemaker should be placed. The need for pacing is very rare in the absence of ischemia.

Ventricular Arrhythmias

Ventricular arrhythmias are a complex and changing subject that is not easily simplified. The criteria for instituting therapy are not clear. Patients with episodes of prolonged ventricular tachycardia and those with symptomatic or hemodynamically compromising ventricular dysrhythmias require expeditious treatment, particularly when there is depressed left ventricular function.

Intraoperative or postoperative ventricular ectopy is often precipitated by hypoxemia, hypercarbia, hypokalemia, anxiety, pain, or fever, and correction of these problems often leads to cessation of the ectopy without resorting to specific drug therapy. Ventricular ectopic activity that occurs in the absence of clinical heart disease is generally benign and well tolerated.

In patients with a history of ischemic heart disease or with electrocardiographic or clinical evidence of perioperative ischemia or infarction in whom ventricular ectopic activity in the form of frequent multifocal ventricular beats or ventricular couplets develops, intravenous amiodarone therapy appears to be highly effective, as shown by Desai and colleagues (1997).

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Supraventricular Tachyarrhythmias

Development of supraventricular tachyarrhythmias in the thoracic surgical patient is frequently associated with identifiable risk factors such as myocardial infarction or ischemia, congestive heart failure, electrolyte derangements, hypoxemia, pulmonary embolism, administration of arrhythmogenic drugs such as catecholamines or bronchodilators, or fever. Correction of these problems obviates the need for specific drug therapy in approximately one-third of patients.

Atrial fibrillation is the most common supraventricular arrhythmia observed in thoracic surgical patients. When atrial fibrillation occurs, the first goal of treatment is to control the ventricular response rate, which usually is done best by administering -blockers or calcium channel blockers. Occasionally, digoxin can be used, but the onset of action of digoxin is unpredictable and often prolonged. In patients with a rapid ventricular response to atrial fibrillation and no evidence of depressed ventricular function, diltiazem should be given intravenously. For severe cardiac compromise because of tachycardia, synchronized cardioversion remains the treatment of choice, but is seldom necessary.

Treatment of the underlying medical conditions that precipitate atrial fibrillation and rate control of the ventricular response to atrial fibrillation usually result in spontaneous conversion to normal sinus rhythm relatively quickly. If the patient remains in atrial fibrillation for 48 hours despite adequate rate control, a specific antiarrhythmic drug should be considered in an attempt to achieve conversion to sinus rhythm.

Control of the ventricular rate in patients with atrial flutter is often more difficult than in those with atrial fibrillation. Although the treatment approach has traditionally been to administer digoxin, good clinical evidence suggests that diltiazem as the first drug may be more efficacious. Also, it is well known that atrial flutter is uniquely treatable by cardioversion, which should be used in any patient with evidence of hemodynamic compromise secondary to atrial flutter.

Other forms of supraventricular tachyarrhythmia, including atrioventricular nodal reentry tachycardia, sinus node reentry tachycardia, intraatrial tachycardia, automatic junctional tachycardia, or a reentrant conduction pathway, may occur in surgical patients and require pharmacologic treatment. In some instances, these arrhythmias may be terminated by vagotonic maneuvers, but if this effort is unsuccessful, intravenous administration of diltiazem in the same dosage recommended for atrial fibrillation is the therapy of choice and should be successful in approximately 80% of cases.

Esmolol is an ultrashort-acting cardioselective -blocker. Esmolol is rapidly converted to inactive metabolites by blood esterases, and full recovery from -blockade occurs rapidly, usually in less than 30 minutes in patients with a normal cardiovascular system. The indications for esmolol are situations in which a rapid -blockade onset and termination are desired, such as in supraventricular tachycardia, perioperative tachycardia, or perioperative hypertension. Esmolol is an excellent drug for the acute management of supraventricular tachycardia, as shown by Amar (2002) and by Bayliff (1999) and Amar (1997) and their associates.

Low Cardiac Output Syndrome

Low cardiac output syndrome in surgical patients must be recognized and treated promptly before severe cellular and end-organ damage occurs. The syndrome is secondary to inadequate perfusion at the tissue level, which may occur for a variety of reasons. The clinical picture is characterized by evidence of decreased organ perfusion reflected as decreasing urinary output and an altered mental state in the awake patient. Acidosis ultimately results because of decreased tissue perfusion. In the postsurgical state, the body is hypermetabolic and lacks the ability to efficiently reduce metabolic demand, leading to progressive metabolic acidosis. Compromised cardiac output that cannot keep pace with metabolic demand can quickly result in death.

Low cardiac output in a surgical patient is best evaluated by a methodic physiologic analysis. Careful clinical observation and serial monitoring of hemodynamic parameters, such as heart rate, arterial blood pressure, cardiac filling pressures, and cardiac output, are mandatory. The metabolic status of the patient should be followed by serial arterial blood gas measurements and mixed venous oxygen content analysis. Electrolyte abnormalities should be sought and corrected as required. Monitoring with a Swan-Ganz catheter is important in these critically ill patients. Debate over the value of Swan-Ganz catheters has cast doubt on the necessity for their use, but the authors believe that the information gained is valuable.

Hypovolemic Shock

The most common cause of the low cardiac output state in surgical patients is hypovolemia because of unreplaced blood or fluid losses that occur as a result of the basic underlying disease process, losses incurred at the time of the surgical procedure, and importantly, unmeasurable third space fluid loss. The typical feature in these patients is reduced cardiac filling pressures as reflected by low pulmonary artery diastolic pressure and pulmonary capillary wedge pressure, reflecting low left ventricular end-diastolic filling pressures. Decrease in urine output and concentrated urine are present. Because of sympathetic compensatory reflexes, the peripheral circulation is profoundly vasoconstricted,

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Management of the low cardiac output state associated with hypovolemia begins with recognition of blood and fluid loss. It is treated by judiciously replacing deficits with the appropriate IV solution, blood products, or both. Therapy is best guided by Swan-Ganz catheter measurements of left-sided filling pressures and repeated determinations of cardiac output and calculation of peripheral vascular resistance.

Cardiogenic Shock

A second and more ominous cause of low cardiac output is primary myocardial dysfunction or cardiogenic shock. The most frequent cause of cardiogenic shock in thoracic surgical patients is myocardial ischemia or infarction. This type of dysfunction may be related to preexisting cardiac disease or acute myocardial infarction. Regardless of the etiology, the principles of diagnosis and the approach to management of this entity are the same. The left-sided filling pressures must be carefully optimized to take maximal advantage of the Frank-Starling mechanism without causing pulmonary edema. Cardiac rate and synchrony between atrium and ventricle are important factors in the maintenance of optimal cardiac pump function, and every attempt should be made to return them to normal, including the use of a pacemaker or cardioversion if needed in patients with significantly compromised cardiac output.

An impaired myocardium functions best when the afterload is reduced. Afterload reduction is best achieved by the use of short-acting peripheral vasodilators such as nitroprusside administered intravenously under carefully monitored and controlled loading conditions and titrated to maintain a systemic vascular resistance in the low normal range. Additional support of the failing myocardium can be achieved by the use of an inotropic agent that improves cardiac contractility without producing a pronounced increase in cardiac rate or significant increases in peripheral vascular resistance. The inotropic agents that appear to achieve these goals most ably are dobutamine, milrinone, and dopamine, used either alone or in combination. If pharmacologic and fluid therapy are unsuccessful in restoring myocardial function, revascularization using catheter techniques or mechanical support with an intraaortic balloon pump, or both, should be considered, but the prognosis in this subgroup is guarded. If ongoing ischemia is present, patients should be catheterized to diagnose and treat ischemia with catheter intervention. Unstable angina in postoperative patients is very hard to stabilize without intervention. Patients with ongoing ischemia should be treated very aggressively.

Septic Shock

A third cause of the low cardiac output syndrome in thoracic surgical patients is systemic sepsis. A wide range of microbial agents can cause profound cardiovascular alterations leading to septic shock and death. The treatment of septic shock is more controversial than either hypovolemic or cardiogenic shock, and the mortality rate remains greater than 50% in almost all reported series.

The most important aspect of the management of a surgical patient who is septic is prompt recognition of the problem and careful monitoring and optimization of the hemodynamic status while beginning a thorough search for the source of the sepsis. Surgical drainage of sources of infection and the institution of antibiotics are crucial. In most instances, intravascular volume deficits are present and should be corrected. The hemodynamic interventions instituted in septic shock should augment cardiac output because demands for increased perfusion exist. In nonsurvivors, it is common for cardiac output to be high but ineffective at the tissue level because of peripheral shunting. In patients with ongoing sepsis in whom cardiac output begins to fall despite therapy, prognosis is extremely grave, as noted by Anderson and Visner (1990).

When tissue perfusion cannot be adequately improved by increasing intravascular volume and preload, afterload reduction should be considered. In some forms of septic shock, the primary hemodynamic alteration appears to be intense peripheral vasoconstriction that eventually leads to irreversible tissue and organ damage. In this setting, the use of a vasodilator, such as nitroprusside, may be indicated under careful monitoring. Blood pressure commonly decreases when these agents are used, despite an increase in cardiac output. Some degree of hypotension is usually well tolerated by younger patients without preexisting coronary artery or cerebrovascular disease, but the fixed and stenotic lesions often present in the coronary and cerebral circulation of older patients place them at substantial risk for myocardial infarction or stroke. The prognosis of these patients is extremely grave.

When afterload reduction fails to improve cardiac output and tissue perfusion, the use of inotropic agents should be considered. The sympathomimetic agents dopamine, dobutamine, and milrinone can provide inotropic support in association with the dose-related peripheral vascular effects previously discussed. The objective is to increase cardiac output enough to achieve adequate tissue perfusion.

Septic shock is a unique problem that presents a dilemma in management. Cardiac output is usually more than sufficient initially to meet the theoretical peripheral metabolic demands of the body for oxygen and substrate. Inadequate tissue perfusion, on the other hand, persists because sepsis induces peripheral shunting of blood away from capillary tissue beds. Cardiac output and venous oxygen

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Acute Congestive Heart Failure and Pulmonary Edema

Acute pulmonary edema in the thoracic surgical patient is often the result of fluid overload in the presence of chronically compromised cardiac function or the occurrence of a recent myocardial infarction. Therapy with oxygen and an intravenous diuretic such as furosemide is indicated. Morphine possesses both venodilatory and vasodilatory properties and may also alleviate the anxiety often seen in these patients. In some situations, it may be necessary to aid the failing ventricle by the use of intravenous vasodilators, such as nitroprusside or nitroglycerin, and to treat the patient with inotropic agents. Acute pulmonary edema in pneumonectomy patients is an emergency and must be treated aggressively (see Chapter 37). Intubation should be avoided if possible, but may be necessary.

In the event that a rapid diuresis occurs, aggressive replacement of potassium is necessary to prevent hypokalemia. For patients who develop acute pulmonary edema in association with preexistent or acute renal insufficiency, aggressive therapy with ultrafiltration or dialysis may be needed.

Right Ventricular Failure

Thoracic surgical patients are uniquely susceptible to acute right ventricular failure because of sudden right ventricular pressure overload secondary to pulmonary artery hypertension, exacerbated by intraoperative pulmonary manipulation or resection of sufficient pulmonary tissue that limits the pulmonary vascular bed. This problem is best addressed by anticipating and avoiding it; however, acute pharmacologic treatment with oxygen, nitroprusside, prostaglandins, and inhaled nitric oxide may be required.

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