Guidelines for the Evaluation and Management of Heart Failure

Abstract

HomeCirculationVol. 92, No. 9Guidelines for the Evaluation and Management of Heart Failure Free AccessResearch ArticleDownload EPUBAboutView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticleDownload EPUBGuidelines for the Evaluation and Management of Heart Failure Report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on Evaluation and Management of Heart Failure) COMMITTEE MEMBERS, JOHN F. WILLIAMSJr, MICHAEL R. BRISTOW, MICHAEL B. FOWLER, GARY S. FRANCIS, ARTHUR GARSONJr, BERNARD J. GERSH, DONALD F. HAMMER, MARK A. HLATKY, CARL V. LEIER, MILTON PACKER, BERTRAM PITT, DANIEL J. ULLYOT, LAURA F. WEXLER and WILLIAM L. WINTERSJr TASK FORCE MEMBERS, JAMES L. RITCHIE, MELVIN D. CHEITLIN, KIM A. EAGLE, TIMOTHY J. GARDNER, ARTHUR GARSONJr, RAYMOND J. GIBBONS, RICHARD P. LEWIS, ROBERT A. O'ROURKE and THOMAS J. RYAN COMMITTEE MEMBERS COMMITTEE MEMBERS , JOHN F. WILLIAMSJrJOHN F. WILLIAMSJr , MICHAEL R. BRISTOWMICHAEL R. BRISTOW , MICHAEL B. FOWLERMICHAEL B. FOWLER , GARY S. FRANCISGARY S. FRANCIS , ARTHUR GARSONJrARTHUR GARSONJr , BERNARD J. GERSHBERNARD J. GERSH , DONALD F. HAMMERDONALD F. HAMMER , MARK A. HLATKYMARK A. HLATKY , CARL V. LEIERCARL V. LEIER , MILTON PACKERMILTON PACKER , BERTRAM PITTBERTRAM PITT , DANIEL J. ULLYOTDANIEL J. ULLYOT , LAURA F. WEXLERLAURA F. WEXLER and WILLIAM L. WINTERSJrWILLIAM L. WINTERSJr TASK FORCE MEMBERS TASK FORCE MEMBERS , JAMES L. RITCHIEJAMES L. RITCHIE , MELVIN D. CHEITLINMELVIN D. CHEITLIN , KIM A. EAGLEKIM A. EAGLE , TIMOTHY J. GARDNERTIMOTHY J. GARDNER , ARTHUR GARSONJrARTHUR GARSONJr , RAYMOND J. GIBBONSRAYMOND J. GIBBONS , RICHARD P. LEWISRICHARD P. LEWIS , ROBERT A. O'ROURKEROBERT A. O'ROURKE and THOMAS J. RYANTHOMAS J. RYAN Originally published1 Nov 1995https://doi.org/10.1161/01.CIR.92.9.2764Circulation. 1995;92:2764–2784Preamble It is becoming more apparent each day that despite a strong national commitment to excellence in health care, the resources and personnel are finite. It is, therefore, appropriate that the medical profession examine the impact of developing technology and new therapeutic modalities on the practice of cardiology. Such analysis, carefully conducted, could potentially have an impact on the cost of medical care without diminishing the effectiveness of that care. To this end, the American College of Cardiology and the American Heart Association in 1980 established a Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (now the ACC/AHA Task Force on Practice Guidelines) with the following charge: The task force of the American College of Cardiology and the American Heart Association shall develop guidelines relative to the role of new therapeutic approaches and of specific noninvasive and invasive procedures in the diagnosis and management of cardiovascular disease. The task force shall address, when appropriate, the contribution, uniqueness, sensitivity, specificity, indications, contraindications and cost-effectiveness of such diagnostic procedures and therapeutic modalities. The task force shall emphasize the role and values of the developed guidelines as an educational resource. The task force shall include a chair and eight members, four representatives from the American Heart Association and four representatives from the American College of Cardiology. The task force may select ad hoc members as needed upon the approval of the presidents of both organizations. Recommendations of the Task Force are forwarded to the President of each organization. The members of the task force are Melvin D. Cheitlin, MD, Kim A. Eagle, MD, Timothy J. Gardner, MD, Arthur Garson, Jr, MD, MPH, Raymond J. Gibbons, MD, Richard P. Lewis, MD, Robert A. O'Rourke, MD, Thomas J. Ryan, MD, and James L. Ritchie, MD, Chair. The Committee to Develop Guidelines on the Evaluation and Management of Heart Failure was chaired by John F. Williams, Jr, MD, and included the following members: Michael R. Bristow, MD, Michael B. Fowler, MB, MRCP, Gary S. Francis, MD, Arthur Garson, Jr, MD, MPH, Bernard J. Gersh, MB, ChB, DPhil, Donald F. Hammer, MD, Mark A. Hlatky, MD, Carl V. Leier, MD, Milton Packer, MD, Bertram Pitt, MD, Daniel J. Ullyot, MD, Laura F. Wexler, MD, and William L. Winters, Jr, MD. This document was reviewed by the officers and other responsible individuals of the American College of Cardiology and American Heart Association and received final approval in September 1995. It is being published simultaneously in Circulation and Journal of the American College of Cardiology. James L. Ritchie Chair, ACC/AHA Task Force on Practice Guidelines Introduction The American College of Cardiology and the American Heart Association (ACC/AHA) have long been involved in the joint development of practice guidelines designed to assist physicians in the management of selected cardiovascular disorders or in the selection of certain cardiovascular procedures. Selection of the disorders or procedures for which to develop guidelines is based on several factors, including their importance to physicians and whether there is sufficient scientific data from which to derive accepted guidelines. The importance of congestive heart failure is underscored by the frequency with which the condition is encountered and its prognosis, for example, 4.7 million people (NHANES III data) in this country have congestive heart failure, and once failure develops, the 6-year mortality rate approaches 80% in men and 65% in women.1 Importantly, as our population ages, the incidence of heart failure and its mortality rate will continue to increase. Furthermore, recent advances in our understanding of the pathophysiology of heart failure and new developments in the therapy of this disorder have greatly expanded the information base on which to make decisions. However, the results of a number of ongoing clinical trials may require modification of the recommendations contained herein. These guidelines were developed by cardiovascular specialists and were based primarily on a comprehensive review of published reports. The references listed are not all inclusive but contain those which we believe are representative of the most convincing data. In cases where the data do not appear conclusive, recommendations are based on the consensus opinion of the group. We elected to limit our guidelines for adults to heart failure associated with left ventricular dysfunction, with the major focus on systolic dysfunction. This decision was based on the fact that the great majority of adults with heart failure in this country have left ventricular systolic dysfunction, and the greatest advances in our understanding and treatment of heart failure are associated with this disorder. The guidelines for adults are based on the manner in which patients present to physicians and encompass the extremes of presentation from acute pump failure with shock to asymptomatic left ventricular dysfunction. We have included patients in the latter category because proper treatment can delay or prevent the development of heart failure. Treatment strategies frequently depend on the etiology of the heart disease, and a major focus of these guidelines is the diagnostic approach to determine correctable etiologies and precipitating factors. However, our treatment strategies do not include specific therapies for correctable causes of heart failure, such as the surgical approach to valvular disease or the treatment of thyrotoxic heart disease. Our approach is to discuss the diagnostic studies and treatment necessary to stabilize the status of adult patient with acute heart failure and the evaluation and treatment of patients presenting with chronic left ventricular dysfunction or stabilized acute heart failure. In the pediatric population, the leading causes of heart failure are significantly different from those in the adult. Our therapeutic guidelines for the pediatric group therefore are directed more to specific causes of heart failure than for the adults. For both groups, we have followed the format of previous ACC/AHA guidelines for classifying indications for diagnostic procedures and therapeutic interventions. Class IUsually indicated, always acceptable Class IIAcceptable, but of uncertain efficacy and may be controversial Class IIIGenerally not indicated Because our goal was to develop guidelines for use by physicians, and our Task Force included only physicians, our guidelines do not include other aspects of care, such as nursing care, rehabilitation and the provision of social services. We recognize the importance of these areas in the overall management of patients with heart failure. The task force did not deal with issues relating to the diagnosis of heart failure, nor did we attempt to analyze the cost-effectiveness of our recommendations. We were acutely aware of cost implications of our recommendations, and these implications were considered in our deliberations. However, our primary goal was to develop guidelines to assist physicians in delivering the best care possible to those with heart failure. We emphasize that there are many factors, notably the wishes of informed patients, that ultimately determine the most appropriate therapy for an individual patient. Therefore, deviation from these guidelines may be appropriate in some circumstances. Furthermore, these guidelines are based on the assumption that the resources necessary to provide this care are readily available. Unquestionably, this is not true in all geographic areas, which further underscores our position that these are guidelines and not rigid requirements. Acute Heart Failure in Adults The clinical presentation of acute heart failure ranges from the sudden appearance of dyspnea to frank cardiogenic shock. The management of acute heart failure differs for the various patient groups residing within the clinical spectrum of this condition; thus, this topic is approached by separately discussing the management of each of the major clinical groups. We assume that the physician has excluded noncardiac disorders whose clinical presentation can be similar in many respects to that of acute heart failure (eg, noncardiogenic pulmonary edema). Also, noncardiac support measures (eg, ventilator therapy) are not discussed in detail despite the fact that these measures are important in the overall management of these critically ill patients. Acute heart failure can be grouped clinically into acute cardiogenic pulmonary edema,cardiogenic shock, and acute decompensation of chronic left heart failure.With few exceptions, patients presenting with acute heart failure require hospital admission, particularly those with an initial episode of failure (see page 2778). Therapeutic interventions to produce hemodynamic improvement and stability must be undertaken expeditiously in these patients. In addition, it is imperative to obtain quickly those diagnostic tests necessary to detect causes of heart failure which are best treated by special therapeutic approaches. Myocardial injury/infarction, high degree atrioventricular (AV) block, ventricular tachycardia, pericardial tamponade and pulmonary embolism are examples of the latter causes of failure. Once etiologies of this type have been excluded, further diagnostic testing to determine the etiology of the heart disease generally can be deferred to a more appropriate time. Acute Cardiogenic Pulmonary Edema A brief medical history and directed physical examination are generally sufficient to initiate therapy. An intravenous catheter should be placed, blood obtained for essential laboratory studies and the patient placed on oxygen therapy. The sublingual administration of nitroglycerin (0.4 to 0.6 mg, repeated every 5 to 10 minutes four times as needed) is of value. Nitroglycerin is effective in patients with acute cardiogenic pulmonary edema due to both ischemic and nonischemic causes. If systemic blood pressure is acceptable (generally a systolic blood pressure ≥95 to 100 mm Hg), nitroglycerin can be administered intravenously (starting dose 0.3 to 0.5 μg/kg body weight per min) as well.2Sodium nitroprusside (starting dose 0.1 μg/kg per minute) may be selected for patients not immediately responsive to nitrate therapy and for those whose pulmonary edema is, in large part, attributable to severe mitral or aortic valvular regurgitation or marked, systemic hypertension.2 The dose is advanced as needed to improve the patient's overall clinical and hemodynamic status, using a systemic systolic pressure of 85 to 90 mm Hg as the usual lower limit for dose incrementation in patients previously normotensive and as long as adequate perfusion of vital organs is maintained.Furosemide (20 to 80 mg intravenously) should be given shortly after the diagnosis of acute pulmonary edema is established.Morphine sulfate (3 to 5 mg intravenously) is effective in ameliorating many of the symptoms of acute pulmonary edema and can be administered safely to most patients with this condition. However, morphine sulfate should be administered with caution to patients with chronic pulmonary insufficiency and those with respiratory or metabolic acidosis in whom suppression of ventilatory drive can cause a drastic lowering of systemic pH. Intubation and mechanical ventilation are of value in patients with severe hypoxia that does not respond rapidly to therapy and in those with respiratory acidosis. Patients with severe refractory pulmonary edema may benefit from intra-aortic balloon counterpulsation (see page 2769). This procedure is of particular value if the patient is to undergo urgent cardiac catheterization and definitive intervention. Intraaortic balloon counterpulsation should not be used in patients with significant aortic valvular insufficiency or aortic dissection. A rare patient presenting with severe refractory pulmonary edema and a correctable lesion may need to proceed directly to the operating room after prompt diagnosis (usually by clinical examination and echocardiography) of the precipitating lesion; examples include rupture of a papillary muscle with acute, marked mitral regurgitation and acute aortic dissection complicated by proximal coronary artery occlusion or marked aortic valvular insufficiency, or both. Patients who develop cardiogenic shock should be approached as discussed later. In most patients acute cardiogenic pulmonary edema can be stabilized with appropriate intervention and frequent, intermittent bedside evaluation without the routine introduction of indwelling pulmonary or systemic arterial catheters. Placement of a pulmonary artery balloon catheter should be considered in this setting if (1) the patient's clinical course is deteriorating; (2) recovery from the acute presentation is not proceeding as expected; (3) high dose nitroglycerin or nitroprusside is required for clinical stabilization; (4) dobutamine or dopamine are needed to augment systemic blood pressure and peripheral perfusion; or (5) uncertainty exists regarding the diagnosis of acute cardiogenic pulmonary edema (see page 2769). Early in the initial evaluation of patients with acute pulmonary edema, the physician must determine whether acute myocardial injury/infarction is present. At this stage, this determination is based on clinical assessment and the electrocardiogram (ECG). Evidence of acute myocardial injury/infarction should raise consideration of urgent myocardial reperfusion therapy. Cardiac catheterization and coronary arteriography followed by the most appropriate interventional procedure (if readily available), or thrombolytic therapy should be considered. The reader is referred to other ACC/AHA guidelines345 for additional, more specific information regarding the therapeutic approach to acute myocardial injury/infarction. Transthoracic Doppler–two-dimensional echocardiography is indicated in all patients who present with acute cardiogenic pulmonary edema, unless there are obvious precipitating factors and the patient's cardiac status had been adequately evaluated previously. Depending on the urgency for confirming or establishing a diagnosis, the procedure is performed as soon as possible after initial stabilization. Transesophageal echocardiography may be required to diagnose or more clearly define certain lesions (eg, ruptured chordae tendinea, aortic dissection). Initial Diagnostic Evaluation of Acute Pulmonary EdemaClass I1. Focused history/physical examination2. Twelve-lead ECG 3. Continuous ECG monitoring4. Blood–serum studies: complete blood count (CBC); electrolytes, blood urea nitrogen (BUN), creatinine and cardiac enzyme levels5. Digital pulse oximetry/arterial blood gases 6. Chest radiograph 7. Transthoracic Doppler–two-dimensional echocardiography 8. Cardiac catheterization/coronary arteriography for suspected coronary artery disease (1) if acute intervention for myocardial injury/infarction is anticipated; (2) to determine the cause(s) for refractory acute pulmonary edema Class II1. Indwelling arterial cannula 2. Transesophageal echocardiography 3. Tabulation of fluid volume intake and urine outputClass III Extensive evaluation (eg, cardiac catheterization and coronary arteriography) in a patient with a concomitant terminal illness or who would not be considered a candidate for the necessary major cardiovascular intervention. Therapeutic Management of Acute Pulmonary Edema Class I1. Oxygen therapy 2. Nitroglycerin, sublingually or intravenously 3. Intravenous administration of a diuretic (eg, furosemide) 4. Morphine sulfate 5. Administration of cardiovascular support drugs to attain and stabilize clinical–hemodynamic status (eg, intravenous infusion of nitroprusside, dobutamine, dopamine) 6. Thrombolytic therapy or urgent revascularization (angioplasty or coronary artery bypass surgery) for acute myocardial injury/infarction 7. Intubation and mechanical ventilation for severe hypoxia that does not respond rapidly to therapy and for respiratory acidosis8. Definitive correction of the underlying cause (eg, mitral valve replacement or repair of acute, severe mitral regurgitation) when indicated and clinically feasible Additional cardiovascular laboratory testing may be necessary to exclude correctable causes of heart failure once the patient's status is stabilized, as discussed in the section on chronic and stabilized acute heart failure. Without the detection and correction of a reversible cause or lesion, the long-term prognosis of patients who present with acute cardiogenic pulmonary edema is poor.6Cardiogenic Shock If cardiogenic shock is not caused by a reparable lesion, or if the lesion is not repaired in an efficient and effective manner, the mortality rate is ≥85%.78 Therefore, cardiogenic shock should be approached with diagnostic and therapeutic vigor in an attempt to identify a treatable lesion and to intervene in a definitive manner. Patients presenting with hypoperfusion but adequate blood pressure may be considered to be in near shock and should be approached in the same manner to prevent the progression to frank shock and death.The general principles of management are rapid recognition of the condition; rapid exclusion or treatment, or both, of readily reversible causes; and prompt stabilization of the clinical and hemodynamic status. As in most emergency situations, many of these activities are performed simultaneously without a routine or set sequence for all patients. An ECG should be obtained, continuous ECG monitoring instituted, an intravenous catheter inserted and an indwelling arterial cannula placed for continuous blood pressure monitoring. An indwelling pulmonary artery catheter should be inserted at an early stage of shock management, unless the patient responds rapidly to fluid infusion. The catheter should be inserted by an operator skilled in this technique in a suitable environment (eg, procedure room of the emergency department, intensive care unit or catheterization laboratory), with assistance from experienced staff. If arrhythmias are present, their contribution to the hemodynamic state and need for rapid cardioversion or pacing must be determined. In patients presenting with cardiogenic shock, a relative or absolute reduction in left ventricular filling pressure as the cause of hypotension must be excluded. Because of prior diuretic therapy or acute interspace volume shifts, it is estimated that 10% to 15% of patients with an acute myocardial infarction may be significantly volume depleted.79 Right ventricular infarction, pericardial tamponade and certain instances of pulmonary embolization are other common examples of acute heart failure that fall into this category. Unless there are signs of left heart volume overload (eg, S3 gallop, moist pulmonary rales, vascular or pulmonary congestion on chest radiograph), normal saline solution should be administered intravenously at a reasonably fast rate (≥500-mL bolus, followed by 500 mL/h). Jugular venous pressure is not a consistently reliable indicator of left heart filling pressure,10 and, thus, elevation of jugular pressure does not obviate the need for fluid administration in a number of clinical situations (eg, pericardial tamponade, right ventricular myocardial infarction). In patients with an acute inferior infarction with shock, a right ventricular infarction should be suspected, resulting in right ventricular failure and inadequate filling of the left heart system. Right-sided precordial ECG leads in addition to the standard leads should be used in these patients. An injury pattern is often but not uniformly observed on the right precordial lead tracings (V3R, V4R) in patients with a right ventricular infarction. The diagnosis of right ventricular infarction frequently can be made on the basis of clinical findings such as an increase in jugular venous pressure during inspiration. An echocardiogram or the insertion of a pulmonary artery balloon catheter, or both, are helpful in patients in whom the diagnosis is unclear. Right-sided cardiac pressure recordings generally show mean right atrial and right ventricular filling pressures equaling or exceeding pulmonary artery occlusive (wedge) pressure with normal or low pulmonary artery pressures.111213 Echocardiography can be used to establish or confirm the presence of right heart involvement, assess tricuspid valve competence, evaluate the extent of left heart damage and left ventricular function and exclude pericardial tamponade (which can have a similar clinical presentation). As an alternative, radionuclide angiography can be used to detect right ventricular infarction by demonstrating right ventricular enlargement and dysfunction. Fluid volume administration is a major component of therapy for patients with right ventricular infarction to maintain the elevated right-sided filling pressure necessary to maintain cardiac output. Fluid administration initially may be guided by clinical variables (eg, systemic blood pressure, peripheral perfusion, urine output, ventricular gallop sounds), but hemodynamic monitoring by a pulmonary artery catheter is generally required to optimize volume administration. Failure of fluid volume administration to achieve clinical and hemodynamic improvement and stabilization in these patients requires additional therapeutic approaches (eg, dobutamine, intra-aortic balloon counterpulsation or interventional procedures). The use of diuretic drugs or vasodilator agents in patients with a right ventricular infarction can result in severe hypotension. Occasionally, vasodilator agents and diuretic drugs produce hypotension in patients with an acute myocardial infarction and pulmonary edema because the translocation of fluid into the lung reduces intravascular volume. These patients should be treated as described later. Severe hypotension (systolic blood pressure ≤70 mm Hg) or clinical shock, or both, occurring in the presence of volume overload or persisting after bolus saline administration should be approached with moderate (4 to 5 μg/kg body weight per minute), then, if necessary, increasing doses of dopamine.1415If hypotension or clinical shock or near shock persists at dopamine doses ≥15 μg/kg per minute, institution of intra-aortic balloon counterpulsation should be considered for patients with a potentially reversible condition or as a bridge to transplantation. If intra-aortic balloon counterpulsation is not available, norepinephrine can be added to increase systemic blood pressure to acceptable levels (systolic pressure ≥80 mm Hg) and the patient transferred on an emergency basis to a more comprehensive medical facility. Patients with volume overload (or after adequate volume loading) in near shock or with a lesser degree of systemic hypotension often respond favorably to dobutamine (2 to 3 μg/kg per minute initially) or low to moderate doses of dopamine (2 to 5 μg/kg per minute initially).1415During treatment, attention should remain focused on (1) the status of the patient's intravascular volume; (2) the condition of the patient's ventricular function; (3) the presence of myocardial injury/infarction, and (4) whether correctable, mechanical lesions are present. 1. Status of intravascular volume. The best means of assessing and monitoring intravascular volume in these patients is by hemodynamic measurements through the pulmonary artery catheter. However, in the presence of left ventricular dysfunction, the usual pressure criteria used to assess intravascular volume do not apply. The optimal left ventricular diastolic filling pressure, as estimated by the pulmonary artery occlusive (wedge) pressure (or pulmonary artery diastolic pressure when comparable), for most patients with shock or near shock secondary to acute myocardial infarction residesbetween 14 to 18 mm Hg.162. Status of patient's ventricular function. Transthoracic Doppler–two-dimensional echocardiography is helpful in assessing the status of ventricular function and guiding additional studies and interventions. The finding of segmental hypokinesia or akinesia suggests the presence of occlusive coronary artery disease, although similar findings may occur in some patients with acute myocarditis or idiopathic dilated cardiomyopathy. Global left ventricular enlargement and dysfunction generally indicate a more diffuse or chronic process. The thermodilution pulmonary artery catheter can provide diagnostic information and a general functional assessment of ventricular and overall cardiovascular performance. Depressed stroke volume in the setting of elevated pulmonary artery occlusive (wedge) pressure generally indicates a significant reduction in left ventricular function. Elevated V (systolic) waves in the wedge position suggest the presence of mitral regurgitation, although the absence of elevated V waves does not exclude mitral regurgitation. Significant oxygen desaturation in mixed venous blood drawn from the pulmonary artery indicates depressed systemic oxygen delivery. 3. Existence of myocardial injury/infarction. Emergency cardiac catheterization and selective coronary arteriography should be considered in the patient with cardiogenic shock or near shock and ECG evidence of acute myocardial injury/infarction.3171819 Reperfusion of the injured/infarcted region of the acutely occluded coronary artery in patients with shock not responding to fluid administration has been reported20 to reduce the mortality rate from <85% to ≤60%. Ideally, the patient is transferred to the catheterization laboratory shortly after initial stabilization. In patients in near shock/shock who do not respond to fluid administration and cannot undergo catheterization–intervention expeditiously, thrombolytic therapy should be considered. Admittedly the effect of thrombolytic therapy on mortality under these conditions is unclear. 4. Are correctable, mechanical lesions present? Clinical evaluation and transthoracic Doppler–two-dimensional echocardiography are the primary methods to diagnose or exclude most of these lesions initially. The most commonly encountered potentially reversible defects in this clinical setting are pericardial tamponade; massive pulmonary embolism; rupture of chordae tendinae, papillary muscle or ventricular septum; critical valvular stenosis or acute regurgitation; aortic dissection with complicating lesions (eg, acute coronary occlusion, acute aortic valvular regurgitation); acute obstruction or incompetency of a prosthetic heart valve; and cardiac tumors. Additional diagnostic testing, such as transesophageal echocardiography and cardiac catheterization may be necessary to more precisely define the lesion(s) and disease process before definitive surgical intervention. Initial Diagnostic Evaluation of Cardiogenic Shock/Near ShockClass I 1. Focused history–physical examination2. Twelve-lead ECG (plus occasional right-sided leads)3. Continuous ECG monitoring 4. Blood–serum studies: complete blood count, platelet count, clotting studies, electrolytes, BUN, creatinine, glucose and cardiac and liver enzymes 5. Arterial blood gases and lactate concentration6. Chest radiograph 7. Transthoracic Doppler–two-dimensional echocardiography 8. Indwelling arterial cannula for continuous monitoring of systemic blood pressure and for arterial blood gas sampling 9. Tabulation of fluid volume intake, urine output and other fluid volume loss 10. Cardiac catheterization/coronary arteriography if acute revascularization for acute myocardial injury/infarction is anticipated Class II Transesophageal echocardiography Class III Extensive evaluation in a patient with a concomitant terminal illness or who is not a candidate for cardiovascular intervention Therapeutic Managem