Evaluation of acute decompensated heart failure Authors Duane S Pinto, MD, MPH Stanley Lewis, MD Section Editor Wilson

S Colucci, MD Deputy Editor Susan B Yeon, MD, JD, FACC Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Apr 2012. |This topic last updated: Abr 1, 2011. INTRODUCTION Acute decompensated heart failure (ADHF) is a common and potentially fatal cause of acute respiratory distress. Heart failure may be new or an exacerbation of chronic disease. The clinical syndrome is characterized by the development of acute dyspnea associated with the rapid accumulation of fluid within the lung's interstitial and alveolar spaces, which is the result of elevated cardiac filling pressures (cardiogenic pulmonary edema) [1]. ADHF can also present as elevated left sided filling pressures and dyspnea without pulmonary edema. ADHF is most commonly due to left ventricular (LV) systolic or diastolic dysfunction, with or without additional cardiac pathology, such as coronary artery disease or valve abnormalities. However, a variety of conditions or events can cause cardiogenic pulmonary edema in the absence of heart disease, including primary fluid overload (eg, due to blood transfusion), severe hypertension, renal artery stenosis, and severe renal disease. Noncardiogenic pulmonary edema is a distinct clinical syndrome associated with diffuse filling of the alveolar spaces in the absence of elevated pulmonary capillary wedge pressure [1]. Focused history, physical examination, echocardiography, laboratory analysis and, in some cases, direct measurement of pulmonary capillary wedge pressure can be used to distinguish cardiogenic from noncardiogenic pulmonary edema, as well as from other causes of acute respiratory distress. (See "Noncardiogenic pulmonary edema".) Flash pulmonary edema is a term that is used to describe a particularly dramatic form of ADHF. In flash pulmonary edema the underlying pathophysiologic principles, etiologic triggers, and initial management strategies are similar to those of less severe ADHF, although there is a greater degree of urgency to the implementation of initial therapies and the search for triggering causes. (See 'Flash pulmonary edema' below.) General issues related to the diagnosis of ADHF will be reviewed here. The pathophysiology, etiology and treatment of ADHF and the evaluation of the clinically stable patient with suspected heart failure (HF) are presented separately. (See "Pathophysiology of acute decompensated heart failure" and "Treatment of acute decompensated heart failure: General considerations" and "Evaluation of the patient with suspected heart failure".) GENERAL APPROACH Acute decompensated HF is diagnosed using a constellation of clinical symptoms and signs. The diagnostic approach described here is in general agreement with the 2010 Heart Failure Society of America (HFSA) guidelines for ADHF [2], the 2009 focused update of the 2005 American College of Cardiology/American Heart Association (ACC/AHA) HF guidelines [3], the 2008 European Society of Cardiology (ESC) guidelines [4], and the 2006 Canadian Cardiovascular Society consensus conference recommendations [5]. Clinical signs and symptoms Patients with ADHF most commonly present with complaints of cough, dyspnea and fatigue, which rapidly become more severe, and which may or may not be associated with chest discomfort. Heart failure may be new or an exacerbation of chronic disease. Initial assessment should include a brief, focused, history and physical examination to evaluate signs and symptoms of HF as well as potential contributing factors and comorbidities. (See "Evaluation of the patient with suspected heart failure" and "Pathophysiology of acute decompensated heart failure".) Patients are typically tachypneic and may be using accessory muscles to breathe.

Chest examination usually reveals crackles indicative of interstitial pulmonary edema and some patients have wheezing (called cardiac asthma). Cardiac asthma is present in as many as one-third of elderly patients presenting with dyspnea due to heart failure and is associated with greater hypercapnia but similar mortality rates [6].

Patients may have a tachycardia and are often hypertensive. Adequacy of systemic perfusion should be assessed. Hypotension, if present, may indicate severe ventricular dysfunction and impending cardiogenic shock. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction".)

Examination of the heart may reveal the presence of an S3 or S4 or both (summation gallop) and a new or changed murmur. (See "Auscultation of cardiac murmurs" and "Auscultation of heart sounds".) Volume status should be evaluated. Elevated jugular venous pressure may reflect elevated right-sided filling pressures from right or left heart dysfunction. (See "Examination of the jugular venous pulse".) Examination of the extremities is usually normal, but may reveal evidence of peripheral edema if the patient has a history of chronic heart failure.

Identification of precipitating factors The 2010 Heart Failure Society of America (HFSA) guidelines and the 2009 ACC/AHA focused update recommended that patients admitted with ADHF undergo evaluation for potential precipitating factors including the following [2,3]: Adherence and process of care issues: Dietary indiscretion Nonadherence to medications Iatrogenic volume overload Significant drug interactions and side effects such as recent addition of negative inotropic drugs (eg, verapamil, nifedipine, diltiazem, beta blockers) or nonsteroidal anti-inflammatory agents (see "Drugs that should be avoided or used with caution in patients with heart failure"). Cardiac Myocardial infarction and myocardial ischemia. Patients with ADHF commonly have coronary artery disease with or without an acute coronary syndrome [7]. Patients should be monitored for signs and symptoms of ongoing ischemia. If acute coronary syndrome is suspected, serial ECGs and measurements of cardiac enzymes should be performed and urgent coronary angiography should be considered. (See "Criteria for the diagnosis of acute myocardial infarction" and 'Coronary angiography' below.) Valvular disease (eg, acute or progressive mitral regurgitation) Atrial fibrillation and other arrhythmias (sinus tachycardia, atrial flutter, other supraventricular tachycardias, ventricular tachycardia). (See "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm".) Progression of underlying cardiac dysfunction. Stress-induced (takotsubo) cardiomyopathy (See "Stress-induced (takotsubo) cardiomyopathy".) Cardiotoxic agents such as alcohol, cocaine, and certain chemotherapy drugs. Right ventricular pacing, which produces dyssynchrony. Noncardiac

Severe hypertension, which is common in patients with ADHF (see "Epidemiology and causes of heart failure" and "Treatment of hypertension in patients with heart failure" and "Pathophysiology of acute decompensated heart failure", section on 'Renovascular hypertension').

Renal failure. (See "Diagnostic approach to the patient with acute or chronic kidney disease".) Miscellaneous factors such as anemia, hypo- or hyperthyroidism, fever, infection (eg, pneumonia), and uncontrolled diabetes. Pulmonary emboli. (See "Diagnosis of acute pulmonary embolism".)

Flash pulmonary edema Flash pulmonary edema is a dramatic form of ADHF in which acute increases in left ventricular diastolic pressure, often associated with chronic elevation of diastolic filling pressures, cause rapid fluid accumulation in the pulmonary interstitium and alveolar spaces. Flash pulmonary edema may develop in some patients with myocardial ischemia with or without myocardial infarction, acute severe mitral regurgitation, hypertensive crisis, acute aortic regurgitation and stress-induced (takotsubo) cardiomyopathy. (See "Treatment of acute decompensated heart failure in acute coronary syndromes" and "Pathophysiology, clinical features, evaluation, and management of acute mitral regurgitation" and "Treatment of specific hypertensive emergencies", section on 'Acute pulmonary edema' and "Acute aortic regurgitation in adults" and "Stress-induced (takotsubo) cardiomyopathy".) Patients with bilateral renal artery stenosis are at increased risk for developing flash pulmonary edema; this association was first described by Pickering et al. [8] It has been named the Pickering syndrome [9] and is an indication for renal artery revascularization. (See "Pathophysiology of acute decompensated heart failure".) TESTS Electrocardiogram The ECG may identify underlying predisposing or precipitating conditions for heart failure such as left ventricular hypertrophy, left atrial abnormalities, myocardial ischemia or infarction, or the presence of atrial fibrillation (figure 1). Acute coronary syndrome precipitating ADHF should be promptly identified by electrocardiogram and cardiac troponin testing and treated as appropriate for the condition and prognosis of the patient with consideration of coronary angiography. (See "Electrocardiographic diagnosis of left ventricular hypertrophy" and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" and 'Coronary angiography' below.) Additional ECG abnormalities may be seen in a patient during an episode of ADHF. These include giant negative T waves, global T wave inversions, and marked QT interval prolongation. These changes may represent ischemia, which can be the cause or the result of the pulmonary edema. They can also be seen in patients with pulmonary edema due to noncoronary events, such as cerebrovascular disease. (See "Neurogenic pulmonary edema".) One report described nine patients with cardiogenic but nonischemic pulmonary edema who developed large inverted T waves with marked QT interval prolongation within 24 hours of treatment and stabilization [10]. These repolarization abnormalities resolved within one week and were not associated with any in-hospital mortality. The causes of these ECG changes may include: Subendocardial ischemia due to increased wall stress, high end-diastolic pressure, or decreased coronary artery flow An acute increase in cardiac sympathetic tone An increase in electrical heterogeneity due to underlying myocardial damage or hypertrophy and exacerbated by ischemia, metabolic changes, or catecholamines. Chest radiography Radiographic findings in ADHF can range from mild pulmonary vascular redistribution to marked cardiomegaly and extensive bilateral interstitial markings (picture 1A-D). The presence of bilateral perihilar alveolar edema may give the typical "butterfly" appearance [11]. Pleural effusions are often absent given the acute nature of the accumulation of pulmonary edema. A normal chest radiograph does not exclude ADHF [12].

Laboratory data Initial laboratory data can be obtained but is usually not needed to make the diagnosis or guide initial therapy; treatment should NOT be delayed while waiting for the results of laboratory tests. An arterial blood specimen or pulse oximetry can quantify the level of hypoxia if oxygen saturation is low. Arterial blood gas analysis is recommended in all patients with severe respiratory distress for information on ventilatory and acid-base status [4]. A complete blood count may help identify the presence of infection or anemia that may have precipitated the event. Routine chemistries may identify renal dysfunction. This may be due in part to a low output state, a setting in which the blood urea nitrogen (BUN) and serum creatinine concentrations can be used as a marker of cardiac output, or to underlying renal disease, particularly bilateral renal artery stenosis. If ongoing myocardial ischemia is suspected, cardiac enzymes should be measured to evaluate potential myocardial injury. (See "Troponins and creatine kinase as biomarkers of cardiac injury" and "Biomarkers of cardiac injury other than troponins and creatine kinase".) Diagnostic utility of BNP and NT-proBNP B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) assays can supplement clinical judgment when the cause of a patient's dyspnea is uncertain, particularly among patients with an intermediate probability of HF [2,13]. Results should be interpreted in the context of all available clinical data [3]. (See "Evaluation of the patient with suspected heart failure" and "Natriuretic peptide measurement in heart failure".) Echocardiography and other imaging modalities Major society guidelines recommend Doppler echocardiography to aid in the diagnosis and classification of heart failure [2-5]. Assessment of ventricular function by echocardiography or other method (eg, radionuclide, CMR, CT, or contrast ventriculography) is helpful in characterizing the type (systolic versus diastolic), severity, and potential cause of ventricular dysfunction. When reduced LVEF (<40 percent) is found, the cause of heart failure may be ascribed to systolic dysfunction (with or without other causes such as diastolic dysfunction or valvular disease) [4]. When preserved left ventricular systolic function is found, the cause of heart failure may be diastolic dysfunction, transient systolic dysfunction, other cause of heart failure with preserved ejection fraction (table 1), or diagnostic error (no heart failure with symptoms/signs due to another cause). Two-dimensional and Doppler echocardiography enables evaluation of ventricular size, global and regional systolic function, diastolic function, valvular disease, and pericardial disease. Echocardiography also enables estimation of right atrial pressure, pulmonary artery pressures and pulmonary capillary wedge pressure. (See "Evaluation of the patient with suspected heart failure", section on 'Echocardiography' and "Pathophysiology of acute decompensated heart failure".) In patients with STEMI and pulmonary congestion, echocardiography should be performed urgently to estimate LV and RV function and to exclude a mechanical complication. (See "Mechanical complications of acute myocardial infarction".) Swan-Ganz catheter Available evidence on flow-directed pulmonary artery (Swan-Ganz) catheters in patients with ADHF does not support their routine use. (See "Management of refractory heart failure", section on 'Hemodynamic monitoring'.) Thus, routine use of invasive hemodynamic monitoring in patients with ADHF is NOT recommended by the 2010 HFSA or 2009 ACC/AHA guidelines [2,3]. However, the ACC/AHA guidelines recommend invasive hemodynamic monitoring in patients who are in respiratory distress or have clinical evidence of hypoperfusion in whom the excess or adequacy of intracardiac filling pressure cannot be determined by clinical assessment [3]. In addition, invasive monitoring can be useful in carefully selected patients with persistent symptoms despite empiric adjustment of standard therapies and one of the following conditions [3]:

Volume status, perfusion or systemic or pulmonary vascular resistances are uncertain. Systolic pressure remains low, or is associated with symptoms, despite initial therapy. Renal function is worsening with therapy. Parenteral vasoactive agents are required, OR Consideration of advanced device therapy or cardiac transplantation may be required.

A pulmonary capillary wedge pressure 18 mmHg favors cardiogenic pulmonary edema. (See "Pulmonary artery catheterization: Indications and complications" and "Pulmonary artery catheterization: Interpretation of tracings".) However, it is important to appreciate that pulmonary artery catheterization measurements can be misleading in certain settings. Most important, myocardial ischemia can cause severe but transient left ventricular dysfunction. If the wedge pressure is first measured after the ischemia has resolved (and if left ventricular function has improved), a relatively normal value may be obtained, leading to the erroneous conclusion that the respiratory distress was caused by noncardiogenic mechanisms. On the other hand, an elevated wedge pressure does not exclude the possibility of noncardiogenic pulmonary edema. It is estimated that as many as 20 percent of patients with pulmonary edema due to acute respiratory distress syndrome (ARDS) have concomitant left ventricular dysfunction. The contribution of ARDS to the pulmonary edema requires monitoring the wedge pressure response to treatment. Noncardiogenic factors are probable if the pulmonary infiltrates and hypoxemia do not improve appreciably within 24 to 48 hours after normalization of the wedge pressure. (See "Noncardiogenic pulmonary edema".) In patients with adequate acoustic windows, echocardiography may provide a noninvasive means of estimating filling pressures. (See "Tissue Doppler echocardiography", section on 'Estimation of LV filling pressures'.) Coronary angiography Urgent or early coronary angiography and intervention is indicated in patients with ADHF and an acute coronary syndrome. As recommended in the 2009 focused update of the 2005 ACC/AHA HF guidelines, urgent cardiac catheterization and revascularization is reasonable when it is likely to prolong meaningful survival in patients with acute HF and known or suspected acute myocardial ischemia due to occlusive coronary disease, especially when there are signs and symptoms of systemic hypoperfusion [3]. (See "Treatment of acute decompensated heart failure in acute coronary syndromes" and "Overview of the acute management of ST elevation myocardial infarction" and "Coronary arteriography and revascularization for unstable angina or non-ST elevation acute myocardial infarction".) DIFFERENTIAL DIAGNOSIS Since ADHF frequently presents with the sudden onset of respiratory distress that may or may not be associated with chest discomfort or a previous history of heart disease, other medical conditions must be excluded: Pulmonary embolism The sudden onset of dyspnea, pleuritic chest pain, and cough may reflect a pulmonary embolism (PE). Establishing the diagnosis may depend upon the characteristics of the ECG and the difference in appearance of typical chest x-ray findings in the two conditions. (See "Diagnosis of acute pulmonary embolism".) In addition to being part of the differential diagnosis, venous thromboembolism is more common in patients with heart failure and, in patients with ADHF, is associated with a worse prognosis [14]. (See "Indications for anticoagulation in heart failure".) Pneumonia Pneumonia can present with acute shortness of breath, hypoxemia, and an inconclusive pulmonary examination. Chest x-ray findings may be similar to HF in cases of bibasilar pneumonia or unilateral pulmonary edema. (See "Diagnostic approach to community-acquired pneumonia in adults".)

Asthma Reactive airways disease can cause acute shortness of breath, cough, and fatigue. In addition, patients with ADHF may present with wheezing that can simulate asthma. (See "Diagnosis of asthma in adolescents and adults".)

SUMMARY AND RECOMMENDATIONS Acute decompensated heart failure (ADHF) is characterized by the development of acute dyspnea associated with elevated left sided filling pressures with or without pulmonary edema. Heart failure may be new or an exacerbation of chronic disease. (See 'Clinical signs and symptoms' above.) Initial assessment should include a brief, focused history and physical examination to evaluate signs and symptoms of HF as well as potential contributing factors and comorbidities. (See 'Clinical signs and symptoms' above.) Precipitating factors for ADHF include adherence and process of care issues, cardiac and noncardiac disorders. (See 'Identification of precipitating factors' above.) Flash pulmonary edema is a dramatic form of ADHF in which acute increases in left ventricular diastolic pressure cause rapid fluid accumulation in the pulmonary interstitium and alveolar spaces. (See 'Flash pulmonary edema' above.) Acute coronary syndrome precipitating ADHF should be promptly identified by electrocardiogram and cardiac troponin testing and treated as appropriate for the condition and prognosis of the patient with consideration of coronary angiography. (See 'Electrocardiogram' above.) B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) assays can supplement clinical judgment when the cause of a patient's dyspnea is uncertain, particularly among patients with an intermediate probability of HF. (See 'Diagnostic utility of BNP and NT-proBNP' above.) Routine use of invasive hemodynamic monitoring in patients with ADHF is not recommended. However, invasive hemodynamic monitoring is indicated in patients who are in respiratory distress or have clinical evidence of hypoperfusion in whom clinical assessment cannot adequately determine intracardiac filling pressures. (See 'Swan-Ganz catheter' above.) Urgent or early coronary angiography and intervention is indicated in patients with ADHF and an acute coronary syndrome. (See 'Coronary angiography' above.) The differential diagnosis of ADHF includes other causes of acute respiratory distress such as pulmonary embolism, pneumonia, and asthma. (See 'Differential diagnosis' above.) Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES 1. Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. N Engl J Med 2005; 353:2788. 2. Heart Failure Society of America, Lindenfeld J, Albert NM, et al. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail 2010; 16:e1. 3. Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2009; 119:e391. 4. Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur Heart J 2008; 29:2388. 5. Arnold JM, Liu P, Demers C, et al. Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006: diagnosis and management. Can J Cardiol 2006; 22:23. 6. Jorge S, Becquemin MH, Delerme S, et al. Cardiac asthma in elderly patients: incidence, clinical presentation and outcome. BMC Cardiovasc Disord 2007; 7:16. 7. Flaherty JD, Bax JJ, De Luca L, et al. Acute heart failure syndromes in patients with coronary artery disease early assessment and treatment. J Am Coll Cardiol 2009; 53:254.