Evaluation of acute decompensated heart failure2

11/5/13 Evaluation of acute decompensated heart failure
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Official reprint from UpToDate®
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Authors
Duane S Pinto, MD, MPH
Robb D Kociol, MD
Section Editor
Wilson S Colucci, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC
Evaluation of acute decompensated heart failure
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2013. | This topic last updated: Aug 6, 2013.
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. Less commonly, ADHF manifests as a low cardiac output state, characterized by fatigue, marked exercise intolerance, anorexia, and
cognitive impairment.
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 cardiogenic pulmonary edema" and "Treatment of acute decompensated heart failure: General
considerations" and "Evaluation of the patient with suspected heart failure".)
GENERAL APPROACH — Acute decompensated heart failure (ADHF) 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) [2], the 2013 American College of Cardiology Foundation/American Heart Association (ACCF/AHA)
[3], and the 2008 European Society of Cardiology (ESC) guidelines [4].
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 cardiogenic pulmonary edema".)
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 [5]. The
absence of rales does not rule out ADHF, as many patients with chronic heart failure have increased pulmonary lymphatic drainage of alveolar edema.
Patients may have a tachycardia and hypertension.
Adequacy of systemic perfusion should be assessed. Hypotension, if present, may indicate severe ventricular dysfunction and impending cardiogenic shock. However,
normotensive patients may still suffer inadequate systemic perfusion in the presence of increased system vascular resistance. (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. Elevated jugular
venous pressure is also the most sensitive and specific sign of elevated left-sided filling pressures, yet one-third of patients with elevated left-sided filling pressures will have
a normal jugular venous pressure. (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. Cool extremities or
mottled extremities may represent low cardiac output and inadequate systemic perfusion.
Identification of precipitating factors — We recommend that patients admitted with ADHF undergo evaluation for potential precipitating factors including the following:
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 [6]. 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 cardiogenic pulmonary edema", section on 'Renovascular hypertension').
Renal failure. (See "Diagnostic approach to the patient with acute kidney injury (acute renal failure) 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 "Acute mitral regurgitation in adults" 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. [7] It has been
named the Pickering syndrome [8] and is an indication for renal artery revascularization. (See "Pathophysiology of cardiogenic pulmonary edema".)
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 (waveform 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 [9]. 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
(image 1A-D). The presence of bilateral perihilar alveolar edema may give the typical "butterfly" appearance [10]. Unilateral cardiogenic pulmonary edema is infrequent (2 percent of
cardiogenic pulmonary edema cases in one study) and is chiefly caused by eccentric mitral regurgitation [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. Troponin is often elevated in ADHF as a result
of subendocardial ischemia, myocyte apoptosis, inflammatory mediator activation, and increased myocardial oxygen demand in the setting of fixed coronary disease.
Therefore, troponin elevation in acute HF does not necessarily indicate the presence of an acute coronary syndrome. (See "Troponins and creatine kinase as biomarkers of
cardiac injury" and "Biomarkers suggesting 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 [14]. (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
[2,4,14,15]. 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 cardiogenic pulmonary edema".)
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 Heart Failure Society of America or 2013 American College of Cardiology/American Heart Association (ACCF/AHA) guidelines [2,14]. However, the
ACCF/AHA guideline recommends invasive hemodynamic monitoring in patients with acute HF with persistent symptoms and/or when hemodynamics are uncertain [14].
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:
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
2013 ACCF/AHA HF guideline, coronary arteriography is reasonable when ischemia may be contributing to HF [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 acute decompensated heart failure (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 [16]. (See "Indications for antithrombotic therapy 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".)
Noncardiogenic pulmonary edema — Causes of noncardiogenic pulmonary include permeability pulmonary edema due to adult respiratory distress syndrome (ARDS) and
other causes such as pulmonary embolism, reperfusion, re-expansion, high altitude, neurogenic, opiate overdose, salicylate toxicity, viral infections, and veno-occlusive
disease. (See "Noncardiogenic pulmonary edema".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are
written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best
for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more
detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education
articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
Basics topics (see "Patient information: When your lungs fill with fluid (The Basics)")
SUMMARY AND RECOMMENDATIONS
Acute decompensated heart failure (ADHF) is characterized by the development of acute dyspnea associated with elevated intracardiac 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.)
ACKNOWLEDGMENT — The UpToDate editorial staff would like to thank Dr. Stanley Lewis for his contributions as an author to previous versions of this topic review.
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. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure: Executive Summary: A Report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 128:1810.
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. Jorge S, Becquemin MH, Delerme S, et al. Cardiac asthma in elderly patients: incidence, clinical presentation and outcome. BMC Cardiovasc Disord 2007; 7:16.
6. 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.
7. Pickering TG, Herman L, Devereux RB, et al. Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical
revascularisation. Lancet 1988; 2:551.
8. Messerli FH, Bangalore S, Makani H, et al. Flash pulmonary oedema and bilateral renal artery stenosis: the Pickering syndrome. Eur Heart J 2011; 32:2231.
9. Littmann L. Large T wave inversion and QT prolongation associated with pulmonary edema: a report of nine cases. J Am Coll Cardiol 1999; 34:1106.
10. Neville, RA. Squire's Fundamentals of Radiology, Harvard University Press, 1997.
11. Attias D, Mansencal N, Auvert B, et al. Prevalence, characteristics, and outcomes of patients presenting with cardiogenic unilateral pulmonary edema. Circulation 2010;
122:1109.
12. Collins SP, Lindsell CJ, Storrow AB, et al. Prevalence of negative chest radiography results in the emergency department patient with decompensated heart failure. Ann
Emerg Med 2006; 47:13.
13. Weintraub NL, Collins SP, Pang PS, et al. Acute heart failure syndromes: emergency department presentation, treatment, and disposition: current approaches and future
aims: a scientific statement from the American Heart Association. Circulation 2010; 122:1975.
14. 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.
15. 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.
16. Darze ES, Latado AL, Guimarães AG, et al. Acute pulmonary embolism is an independent predictor of adverse events in severe decompensated heart failure patients. Chest
2007; 131:1838.
Topic 3497 Version 10.0

GRAPHICS
Electrocardiogram in a patient with flash pulmonary edema
The ECG tracing reveals left ventricular hypertrophy (LVH) assoicated
with ST segment depression and T wave inversions; these ST-T wave
changes (arrows) may also represent subendocardial ischemia, which
along with the LVH may be responsible for the episode of flash
pulmonary edema.

Pulmonary edema
This plain frontal chest radiograph of a 55-year-old male with
known coronary artery disease demonstrates characteristic
radiographic features of heart failure with interstitial pulmonary
edema, bilateral perihilar alveolar edema producing a characteristic
butterfly pattern and bilateral pleural effusions.
Photo courtesy of Jonathan Kruskal, MD.
Normal chest radiograph
Posteroanterior view of a normal chest radiograph.
Courtesy of Carol M Black, MD.

Heart failure
This chest radiograph of a 65-year-old male with dyspnea and
orthopnea demonstrates mild pulmonary vascular congestion,
septal lymphatic distention (white arrow), interstitial veiling, and
enlarged hilar shadows (black arrow), indicative of left ventricular
decompensation.
Courtesy of Jonathan Kruskal, MD.

Severe heart failure
This chest radiography shows severe heart failure with
cardiomegaly, pulmonary vascular congestion with infiltrates in
the mid lung fields (white arrow), and a small pleural effusion
(black arrow).
Courtesy of Jonathan Kruskal, MD.

Acute left ventricular failure
This plain frontal radiograph of the chest of a 30-year-old male
demonstrates bilateral perihilar alveolar edema, giving a typical
butterfly appearance, with bilateral interstitial edema and
pulmonary venous redistribution to the upper lobes. The acute
nature of this condition is manifest by the absence of pleural
effusions or an enlarged cardiac silhouette.
Photo courtesy of Jonathan Kruskal, MD.

www.uptodate.com/contents/evaluation-of-acute-decompensated-heart-failure?topicKey=CARD%2F3497&elapsedTimeMs=3&source=see_link&view=pri… 10/10
Differential diagnosis of heart failure with preserved left ventricular ejection fraction
Diastolic heart failure
Hypertensive heart disease
Restrictive cardiomyopathy
Infiltrative cardiomyopathies
Hypertrophic cardiomyopathy
Noncompaction cardiomyopathy
Coronary heart disease
Miscellaneous factors: diabetes mellitus, chronic kidney disease, aging
Valvular heart disease
Valvular stenosis
Valvular regurgitation
Right heart failure
Pulmonary hypertension
Right ventricular infarction
Arrhythmogenic right ventricular cardiomyopathy
Pericardial disease
Cardiac tamponade
Constrictive pericarditis
Effusive-constrictive pericardial disease
Intracardiac mass
Atrial myxoma
Congenital heart disease
High-output heart failure
Episodic or reversible LV systolic dysfunction
Pulmonary vein stenosis
Adapted from: Oh JK, Hatle L, Tajik AJ, Little WC. Diastolic heart failure can be diagnosed by comprehensive two-dimensional and Doppler echocardiography. J Am
Coll Cardiol 2006; 47:500.

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