AUTHOR: Theo E Meyer, MD, PhD

S E C T I O N E D I TO R : Wilson S Colucci, MD

D E P U T Y E D I TO R : Todd F Dardas, MD, MS

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Dec 2023.

This topic last updated: May 09, 2023.

INTRODUCTION

Acute decompensated heart failure (ADHF) is a clinical syndrome of new or worsening signs and
symptoms of HF that often lead to hospitalization or an emergency department visit. For the purposes
of this discussion, we use the term ADHF for all the acute HF syndromes.

The clinical manifestations and diagnosis of ADHF will be reviewed here. The pathophysiology, etiology,
and treatment of ADHF and the evaluation of the clinically stable patient with suspected HF are
presented separately. (See "Pathophysiology of cardiogenic pulmonary edema" and "Treatment of
acute decompensated heart failure: General considerations" and "Heart failure: Clinical manifestations
and diagnosis in adults".)

EPIDEMIOLOGY

Patients with ADHF represent a heterogeneous population with high postdischarge readmission rates
[1-12]. The onset and severity of symptoms of ADHF vary and depend on the nature of the underlying
cardiac disease and the rate at which the syndrome develops. The largest proportion of patients (70
percent) with ADHF are admitted due to worsening chronic HF, up to 15 to 20 percent of patients
present with HF for the first time, and approximately 5 percent are admitted for advanced or end-stage
HF. Low blood pressure (<8 percent) or shock (<3 percent) are complications of ADHF [1,2,11].

CAUSES AND PRECIPITATING FACTORS

Appropriate therapy for ADHF requires identification of the specific HF phenotype as well as the
potential causes and precipitants. Causes are the primary condition or disease process leading to the
development of HF. Precipitants are triggers or contributing factors for decompensation in patients
with established chronic heart disease.

The following are the major causes for new onset ADHF:

● Coronary artery disease:

• Acute coronary syndrome. (See "Initial evaluation and management of suspected acute
coronary syndrome (myocardial infarction, unstable angina) in the emergency department"
and "Diagnosis of acute myocardial infarction".)

- Myocardial infarction (MI)/ischemia.

- Ventricular septal rupture. (See "Acute myocardial infarction: Mechanical complications".)

● Arrhythmias:

• Atrial fibrillation and atrial flutter. (See "Overview of the acute management of
tachyarrhythmias", section on 'Narrow QRS complex tachyarrhythmias'.)

• Ventricular tachycardia, ventricular fibrillation, or high-frequency ventricular ectopy. (See

"Overview of the acute management of tachyarrhythmias", section on 'Wide QRS complex
tachyarrhythmias'.)

● Myocarditis. (See "Clinical manifestations and diagnosis of myocarditis in adults".)

● Acute valve syndromes:

• Acute mitral or aortic regurgitation secondary to infective endocarditis, ruptured chordae of a

degenerative mitral valve, ischemic papillary muscle rupture, or aortic dissection. (See "Acute
mitral regurgitation in adults" and "Acute aortic regurgitation in adults".)

• Thrombosed mechanical aortic or mitral valve. (See "Bioprosthetic valve thrombosis,

thromboembolism, and obstruction: Clinical manifestations and diagnosis".)

• Tear or perforation of a bioprosthetic aortic or mitral valve leaflet. (See "Clinical manifestations
and diagnosis of surgical aortic and mitral prosthetic valve regurgitation".)

● Progressive valve disease:

• Severe aortic or mitral valve stenosis, including left atrial myxoma. (See "Clinical manifestations
and diagnosis of aortic stenosis in adults" and "Rheumatic mitral stenosis: Clinical
manifestations and diagnosis".)

• Severe aortic or mitral regurgitation. (See "Clinical manifestations and diagnosis of chronic
aortic regurgitation in adults" and "Clinical manifestations and diagnosis of chronic mitral
regurgitation".)

● Cardiomyopathic states:

• Hypertrophic cardiomyopathy. (See "Hypertrophic cardiomyopathy: Clinical manifestations,

diagnosis, and evaluation".)

• Recent onset dilated cardiomyopathy. (See "Familial dilated cardiomyopathy: Prevalence,

diagnosis and treatment" and "Causes of dilated cardiomyopathy".)

• Tachycardia mediated cardiomyopathy. (See "Arrhythmia-induced cardiomyopathy".)

• Stress (takotsubo) cardiomyopathy. (See "Clinical manifestations and diagnosis of stress

(takotsubo) cardiomyopathy".)

● Poorly controlled hypertension:

• Bilateral renal artery stenosis. (See "Chronic kidney disease resulting from atherosclerotic renal
artery stenosis", section on 'Clinical manifestations'.)

ADHF due to decompensation of chronic HF can occur without known precipitant factors but more
often occurs with one or more factors, such as infection, uncontrolled hypertension, rhythm
disturbances, and nonadherence with drugs and diet. Moreover, the in-hospital course is determined
by the interplay between precipitants, underlying structural heart disease, and comorbidities. These
factors are listed in the table ( table 1).

CLINICAL MANIFESTATIONS

Patients present with a myriad of chief complaints, symptoms, and physical examination findings. Such
heterogeneity prompts an initially broad differential diagnosis, thus securing the correct diagnosis can
be challenging. For practical purposes, it is helpful to view the presentation of ADHF according to the
predominant clinical characteristics on admission. As noted above, most patients presenting with ADHF
have known chronic HF and may or may not have had a prior episode of decompensation. In many
patients with chronic HF, symptoms have gradually worsened over the preceding days and weeks but
have not been sufficient for the patient to seek medical attention. In a minority of patients, an episode
of ADHF may be the first presentation of HF.

Approximately 50 percent of patients hospitalized for HF have HF with preserved ejection fraction
(HFpEF; left ventricular ejection fraction [LVEF] >50 percent); the remainder of patients have HF with
reduced ejection fraction (HFrEF; LVEF ≤40 percent) or HF with mid-range ejection fraction (LVEF 41 to
50 percent). (See "Epidemiology of heart failure", section on 'Magnitude of the problem'.)

The following five clinical and hemodynamic profiles are modified from those described in the 2021
European Society of Cardiology guidelines for the diagnosis and treatment of ADHF [12]:

● ADHF without pulmonary edema

● ADHF with severe pulmonary edema
● Cardiogenic shock
● High-output HF
● Right HF

The above clinical groups are not mutually exclusive (eg, a patient with hypertensive crisis or
cardiogenic shock may develop severe pulmonary edema).

ADHF — This syndrome is seen in patients with new-onset HF or acute decompensation of chronic HF
who develop signs or symptoms of decompensation; in this setting, there is no cardiogenic shock or
hypertensive crisis. There may be no, or mild, pulmonary congestion. This scenario accounts for 50 to
70 percent of all HF admissions [13-16]. In contrast to the other phenotypes, this presentation is
characterized by more gradual onset, and the primary alteration is progressive fluid retention and
systemic congestion. New-onset HF is seen much less frequently (less than one-third of HF admissions)
than decompensation of chronic HF but may present with the same phenotype.

Usual symptoms:

● Progressive dyspnea is the most common complaint of patients presenting with ADHF.

● Symptoms of abdominal and peripheral congestion – Patients may report ankle swelling and
epigastric tenderness or a sensation of abdominal fullness. Abdominal tenderness is often due to
hepatic congestion and distention of the hepatic capsule. With severe hepatic congestion, the
patient may also complain of nausea and anorexia.

● Other symptoms include nocturia and neurologic symptoms such as confusion, headaches,
insomnia, anxiety, disorientation, and impaired memory.

Physical signs:

● Vary according to the severity of fluid overload HF.

● Signs of congestion – An elevated jugular venous pressure, positive hepatojugular reflux test, and
a tender, enlarged liver are frequent findings in these patients.

Diminished air entry at the lung bases is usually caused by a pleural effusion, which is often more
frequent in the right pleural cavity than in the left. Rales (crackles) and wheezing may or may not
accompany signs of pleural effusion. An absence of rales does not imply lack of pulmonary venous
pressure elevation.

Leg edema is frequently evident in both legs, particularly in the pretibial region and ankles in
ambulatory patients. Sacral and upper thigh edema can be detected in patients who are
bedridden.

● Cardiac examination – This may be entirely normal in patients with HF secondary to diastolic
dysfunction, whereas many patients with advanced systolic dysfunction exhibit a third heart
sound and a laterally displaced apex beat. A murmur of mitral regurgitation is often audible when
the left ventricle (LV) is markedly enlarged, or a tricuspid regurgitation murmur is present when
the right ventricle is volume or pressure overloaded.

● Chest radiograph in this setting may show cardiomegaly. Some patients have evidence of pleural
effusion and redistribution of blood flow from bases to the upper lobes. There may or may not be
evidence of interstitial edema. (See 'Chest radiograph' below.)

ADHF with severe pulmonary edema — Pulmonary edema has been observed in 15 percent or more
of patients admitted with ADHF [13], but severe pulmonary edema is seen in less than 3 percent of
these patients [1]. This phenotype is characterized by the rapid onset of symptoms or signs of HF,
frequently presenting with a systolic blood pressure >180 mmHg [17]. Patients with this condition
frequently have a history of poorly controlled hypertension [18]. There is usually predominant
pulmonary rather than systemic congestion, as is manifest by minimal weight gain prior to admission.

Clinical findings:

● Patients typically experience a sudden and overwhelming sensation of suffocation and air hunger;
this is invariably accompanied by extreme anxiety, cough, expectoration of a pink frothy liquid,
and a sensation of drowning.

● The patient sits bolt upright, is unable to speak in full sentences, and may thrash about. The
respiratory rate is increased, the alae nasi are dilated, and there is inspiratory retraction of the
intercostal spaces and supraclavicular fossae.

● Respiration is often noisy, and there may be audible inspiratory and expiratory gurgling sounds.
An ominous sign is obtundation, which may be a sign of severe hypoxemia. Sweating is profuse,
and the skin tends to be cool, ashen, and cyanotic, reflecting increased sympathetic outflow.

● The pulse rate is most often elevated secondary to an increased adrenergic drive. When the blood
pressure is found to be markedly elevated, it is more likely to be the cause of, or an important
contributing factor to, pulmonary edema rather than the consequence of the condition.

● The oxygen saturation is usually less than 90 percent of room air before treatment. Auscultation
of the lungs usually reveals coarse airway sounds bilaterally with rhonchi, wheezes, and moist fine
crepitant rales that are detected first at the lung bases but then extend upward to the apices as
the lung edema worsens.

● Cardiac auscultation may be difficult in the acute situation, but third and fourth heart sounds may
be present. When valvular abnormalities and/or mechanical complications after MI result in ADHF,
the murmurs of mitral and aortic regurgitation and ischemic ventricular septal defect are often
audible, but detection requires a careful and skillful auscultator. (See "Auscultation of cardiac
murmurs in adults".)

● The chest radiograph may show cardiomegaly, upper zone redistribution of blood flow, interstitial
edema (with ill-defined vessels, peribronchial cuffing, and interlobular septal thickening), and
alveolar edema (with perihilar and lower-lobe airspace filling, with the periphery generally spared
in the mid and upper lung zones) [19]. (See 'Chest radiograph' below.)

Cardiogenic shock — In one study of patients who presented with acutely decompensated HF, at least
one sign of cardiogenic shock (eg, blood pressure <90 mmHg, cutaneous pallor, mental confusion) was
present in 3.6 percent of patients [20].

● Low-output HF is characterized by symptoms and signs that are related to decreased end-organ
perfusion. A typical patient with this clinical syndrome has severely impaired LV function and
usually presents with symptoms of fatigue, altered mental status, or signs of organ hypoperfusion
such as prerenal azotemia or abnormal hepatic enzymes.

● The patient may present with tachypnea at rest, tachycardia, and a cold and cyanotic periphery
with poor capillary refill. The degree of peripheral hypoperfusion may be so advanced that the
skin over the lower extremities is mottled, cool, or diaphoretic.

● A diminished pulse pressure, consistent with a reduced stroke volume, is often found in patients
with this syndrome. Occasionally, the clinician may detect pulsus alternans: when a strong or
normal pulse alternates with a weak pulse during normal sinus rhythm. This physical finding is
rare but, when present, is a sign of severe LV dysfunction. (See "Examination of the arterial pulse"
and "Examination of the arterial pulse", section on 'Pulsus alternans'.)

● A subset of patients with decompensated end-stage HF present with occult shock and may be
difficult to distinguish from patients with mildly decompensated chronic HF and stable HF [21].
The only parameter differentiating occult shock patients from nonshock patients is a significantly
elevated lactic acid level. Therefore, we suggest checking a lactic acid level in patients who present
with marked weakness and/or uncertain peripheral perfusion. (See 'Laboratory data' below.)

● It is imperative to rapidly identify the cardiac causes of shock. After an acute coronary syndrome
has been excluded, echocardiography should be done as soon as possible to exclude cardiac
tamponade and further characterize left and right ventricular function and the integrity of the left-
sided valves.

High-output heart failure — This phenotype is an uncommon cause of ADHF and generally presents
with warm extremities, pulmonary congestion, tachycardia, and a wide pulse pressure. Underlying
conditions include anemia, obesity, thyrotoxicosis, advanced liver failure, and skeletal conditions such
as Paget disease. (See "Causes and pathophysiology of high-output heart failure".)

Right-sided heart failure — This syndrome of predominantly right-sided HF occurs commonly in

patients with severe isolated tricuspid regurgitation, right ventricular dysfunction, and chronic lung
disease, such as those with chronic obstructive lung disease, interstitial lung disease, or long-standing
pulmonary hypertension. These patients are often oxygen dependent and present with signs and
symptoms of right-sided volume overload. Pulmonary embolism as an acute cause of dyspnea and
right HF should be excluded. (See 'Differential diagnosis' below.)

DIAGNOSTIC EVALUATION

Initial assessment of ADHF should include a brief, focused history and a physical examination to
evaluate signs and symptoms of HF as well as potential causes and precipitants. The diagnostic workup
should occur in parallel with steps to characterize the patient's cardiopulmonary status and to initiate
appropriate management to stabilize patients in a timely manner ( table 2). Several steps are
necessary to comprehensively evaluate a patient with ADHF ( table 2).

The diagnostic approach described here is in general agreement with the 2010 Heart Failure Society of
America [22], the 2013 American College of Cardiology Foundation/American Heart Association [23],
and the 2021 European Society of Cardiology guidelines [12].

Initial evaluation for cardiopulmonary instability — The goal of the initial evaluation of patients with
ADHF is to determine the patient’s cardiopulmonary status, including the severity of dyspnea,
hemodynamic status (evidence of hypoperfusion including hypotension), and heart rate and rhythm.

ADHF is a heterogeneous condition, and successful management often relies on identifying the cause
of decompensation. The search for specific causes is an essential first step in the evaluation of these
patients. These include acute coronary syndrome (ACS), hypertensive emergency, rapid arrhythmias or
severe bradycardia/conduction disturbance, acute mechanical causes such as acute valve regurgitation
or acute pulmonary embolism, infection, including myocarditis, and tamponade. The acronym
CHAMPIT (ACS, Hypertension, Arrhythmia, Mechanical causes, Pulmonary embolus, Infection, and
Tamponade) was suggested as a useful reminder of the etiologic considerations by the European
Society of Cardiology [12].

Symptoms of ACS (eg, chest pain) are assessed and an electrocardiogram (ECG) is obtained and
assessed for evidence of ischemia. (See "Initial evaluation and management of suspected acute
coronary syndrome (myocardial infarction, unstable angina) in the emergency department".)

Patients with respiratory failure and/or shock — Patients with respiratory distress and/or
hypotension require immediate treatment, as discussed separately, followed by an expedited
diagnostic evaluation ( table 2). (See "Treatment of acute decompensated heart failure: Specific
therapies", section on 'Supplemental oxygen and assisted ventilation' and "Treatment of acute
decompensated heart failure: Specific therapies", section on 'Management of hypotensive patients'.)

Patients with acute coronary syndrome — Patients with ADHF with suspected ACS should be
promptly identified by ECG and cardiac troponin testing and referred for consideration of cardiac
catheterization with coronary angiography and hemodynamic evaluation as appropriate for the
condition and prognosis of the patient. The evaluation and management of patients with symptoms
and signs of ACS are discussed separately ( table 3). (See "Initial evaluation and management of
suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency
department" and "Treatment of acute decompensated heart failure in acute coronary syndromes".)

If myocardial ischemia or MI is suspected, cardiac enzymes should be measured to evaluate potential

myocardial injury. Of note, troponin is often mildly elevated in ADHF as a result of myocardial injury,
myocyte apoptosis, inflammatory mediator activation, and increased myocardial oxygen demand in the
setting of fixed coronary disease. Therefore, troponin elevation in ADHF does not necessarily indicate
the presence of an ACS. (See "Troponin testing: Clinical use" and "Use of creatine kinase to detect
myocardial injury".)

Diagnostic approach — ADHF is diagnosed based upon finding a constellation of clinical symptoms
and signs.

● Initial assessment should include a brief, focused history and a physical examination to evaluate
signs and symptoms of HF as well as potential contributing factors and comorbidities. (See "Heart
failure: Clinical manifestations and diagnosis in adults" and "Pathophysiology of cardiogenic
pulmonary edema".)

● The diagnosis of ADHF is based primarily on signs and symptoms and supported by appropriate
investigations, such as ECG, chest radiograph, biomarkers (B-type natriuretic peptide [BNP] or N-
terminal proBNP [NT-proBNP]), and Doppler echocardiography [12,24]. (See 'How to diagnose
ADHF' below.)

• The diagnosis of decompensated chronic HF is generally straightforward, especially when a

patient presents with fluid retention and exertional dyspnea. It is essential to rule out alternate
causes of the patient's symptoms and signs. (See 'Differential diagnosis' below.)

• A BNP or NT-proBNP level is obtained when the diagnosis of HF is uncertain. (See 'Initial tests'
below.)

• An echocardiogram is generally recommended, particularly if this is a first presentation of HF

or if there has been abrupt deterioration in the patient’s condition. (See 'Echocardiography'
below.)

● Swan-Ganz catheterization is not generally required but is helpful when the diagnosis is uncertain
and for management of patients with persistent symptoms despite treatment of HF. (See 'Swan-
Ganz catheter' below.)

How to diagnose ADHF — ADHF is a clinical diagnosis based upon the presence of a constellation of
symptoms and signs of HF. While test results (eg, natriuretic peptide level, chest radiograph,
echocardiogram) are often supportive, the diagnosis cannot be based on a single symptom or sign [25]
or test result [26]. The simplest approach is to categorize patients with suspected ADHF into three
categories:

High probability — ADHF can be diagnosed with high probability in patients with or without prior
history of HF:

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prior history of HF – When a patient with prior history of HF presents with exertional
dyspnea and evidence of fluid retention (ie, elevated jugular venous pressure [JVP] and/or
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evidence of pulmonary edema and/or peripheral edema), there is a high probability of ADHF [26].
Approach to diagnosis and evaluation of acute decompensated heart failure in adults
● Patients with no prior history of HF – When a patient with no prior history of HF presents with new
Topic Graphics (11)
onset orthopnea, elevated JVP, typical chest radiograph findings of pulmonary edema (see 'Chest
radiograph' below), and no fever, there is a high probability of ADHF [26].

Intermediate probability — For patients presenting with symptoms of dyspnea who have no prior
history of HF but have known cardiac disease, cardiac risk factors (eg, known coronary artery disease,
valve disease, diabetes mellitus, or hypertension), or have ECG abnormalities (atrial fibrillation,
evidence of left ventricular hypertrophy, or ischemia), and have uncertain JVP and no evidence of
pulmonary edema, there is an intermediate probability of ADHF. In this group of patients, testing of
serum natriuretic peptide levels (BNP or NT-proBNP) [26], and in some cases also echocardiography,
may be helpful. (See 'Natriuretic peptide levels' below.)

Low probability — There is low probability of ADHF in patients who present with dyspnea who lack
evidence of cardiac disease (including a normal ECG) and who have another explanation for dyspnea
such as chronic lung disease or pneumonia. Other causes of dyspnea should be evaluated and treated.
If uncertainty regarding a possible diagnosis of ADHF persists, further testing (eg, natriuretic peptide
level) may be indicated.

Clinical categories — Clinical presentations of ADHF can be categorized according to adequacy of

peripheral perfusion ("warm" versus "cold") and the presence of congestion ("dry" or "wet") ( figure 1)
[7,27]. Such categorization predicts prognosis and facilitates attention to specific therapies.

● The most common combination of peripheral perfusion and congestion (more than 70 percent of
patients with ADHF) is the "warm and wet" clinical profile [1,2]. This group of patients typically
presents with either normal or markedly elevated systolic blood pressure.

• The group with normal blood pressure presents largely with significant volume overload with
pulmonary and peripheral congestion (cardiac type).

• By contrast, patients with the hypertensive profile manifest with fluid redistribution to the
lungs and minimal peripheral fluid accumulation (vascular type). This profile of ADHF is often
seen in older adult females with labile hypertension and a preserved left ventricular ejection
fraction (LVEF). (See 'ADHF with severe pulmonary edema' above.)

● A minority of patients with ADHF (less than 20 percent) present with a "cold and wet" clinical
profile. This includes most patients with cardiogenic shock and low-output syndrome. Patients in
this category are at increased risk of death and cardiac transplantation at one year compared with
patients with HF with reduced EF with a "wet and warm" profile [7]. (See 'Cardiogenic shock'
above.)

● Less than 10 percent of patients with ADHF present with a "warm and dry" or "cold and dry"
profile.

Initial tests — Initial testing in patients with ADHF includes a 12-lead ECG, chest radiograph, and
laboratory tests.

Electrocardiogram — A 12-lead ECG is performed soon after the patient presents with ADHF to assess
for evidence of ACS (myocardial ischemia or MI) and arrhythmias (eg, atrial fibrillation). The ECG may
also identify other predisposing or precipitating conditions for HF such as left ventricular hypertrophy
or left atrial abnormalities ( waveform 1).

Additional ECG abnormalities may be seen in a patient during an episode of ADHF. These include
nonspecific ST and T wave abnormalities. Transient giant negative T waves, global T wave inversions,
and marked QT interval prolongation have also been reported [28]. These changes may represent
subendocardial ischemia (which can be the cause or the result of the pulmonary edema), increase in
cardiac sympathetic tone, or metabolic changes. They can also be seen in patients with pulmonary
edema due to noncoronary events such as cerebrovascular disease. (See "Neurogenic pulmonary
edema".)

Chest radiograph — Radiographic findings in ADHF can range from mild pulmonary vascular
redistribution to marked cardiomegaly and extensive bilateral interstitial markings ( image 1 and
image 2 and image 3 and image 4). The presence of bilateral perihilar alveolar edema may give
the typical "butterfly" appearance [29]. Unilateral cardiogenic pulmonary edema is infrequent (2
percent of cardiogenic pulmonary edema cases in one study) and is chiefly caused by eccentric mitral
regurgitation [30]. Pleural effusions are often absent in patients with de novo ADHF but are frequently
present in patients with acute decompensation of chronic HF. Up to 20 percent of patients with ADHF
may have normal chest radiographs [31].

Lung ultrasound — In experienced centers, LUS is an adjunctive diagnostic modality that may be
helpful in the evaluation of patients with dyspnea with suspected ADHF [32,33]; it should not replace
standard clinical assessment (including chest radiograph and selective natriuretic peptide level testing).
(See 'Chest radiograph' above and 'Natriuretic peptide levels' below.)

The presence of multiple B-lines (generally three or more) per intercostal space on point-of-care
ultrasound (LUS) is a sign of lung interstitial syndrome; causes of multiple diffuse bilateral B-lines
include pulmonary edema as well as interstitial pneumonia or pneumonitis or diffuse parenchymal
lung disease (pulmonary fibrosis) [34]. B-lines are laser-like (also described as comet-like), vertical,
hyperechoic artifacts that arise from the pleural line, extend to the bottom of the screen without fading,
and move synchronously with lung sliding, as defined by the 2012 International evidence-based
recommendations for point-of-care lung ultrasound [34]. (See "Indications for bedside ultrasonography
in the critically ill adult patient", section on 'Thoracic ultrasonography'.)

Limitations of this modality include technique-dependence and limited specificity [32,34]. While the
presence of bilateral B-lines is not specific for pulmonary edema, associated sonographic findings may
help distinguish pulmonary edema from other causes. Sonographic findings indicative of diffuse
parenchymal lung disease (pulmonary fibrosis) include pleural line abnormalities (irregular,
fragmented), subpleural abnormalities (small echo-poor areas), and a nonhomogeneous distribution of
B-lines [34]. Repeated examination may also be helpful since B-lines caused by pulmonary edema vary
with volume changes and position (sitting versus supine) [32]. Sonographic findings indicative of acute
respiratory distress syndrome include anterior subpleural consolidation, absence or reduction of lung
sliding, spared areas of normal parenchyma, pleural line abnormalities (irregular, fragmented), and
nonhomogenous distribution of B-lines [34]. (See "Indications for bedside ultrasonography in the
critically ill adult patient", section on 'Thoracic ultrasonography'.)

The role of LUS as an adjunct to other evaluation is supported by the following studies [35,36]:

A meta-analysis including six studies with a total of 1827 patients compared the diagnostic accuracies
of LUS and chest radiography (CXR) for ADHF in patients presenting with dyspnea (to an emergency
department or inpatient internal medicine ward) [35]. For LUS, the pooled estimates were 0.88 (95% CI
0.75-0.95) for sensitivity and 0.90 (95% CI 0.88-0.92) for specificity. For CXR, the pooled estimates were
0.73 (95% CI 0.70-0.76) for sensitivity and 0.90 (95% CI 0.75-0.97) for specificity. Thus, the findings
suggest that LUS has greater sensitivity and similar specificity compared to CXR for diagnosis of ADHF
in this patient population.

A potential diagnostic advantage of LUS as compared to a combination of CXR plus measurement of N-

terminal pro-B-type natriuretic peptide (NT-proBNP) was suggested by a randomized trial [36]. A total of
518 patients presenting to an emergency department with acute dyspnea underwent initial clinical
assessment followed by randomized assignment to initial testing with either LUS or CXR/NT-proBNP. A
diagnosis was recorded based upon the initial clinical evaluation plus initial testing. Patients who
initially received a LUS later received CXR/NT-proBNP testing and patients who initially received CXR/NT-
proBNP testing received LUS at the discretion of the treating physician. Adjudication of ADHF was
performed after hospital discharge or death by two expert intensivists/emergency medicine physicians,
blinded to LUS results and initial diagnostic group assignment, based upon review of the complete
medical record. Initial testing with LUS improved diagnostic accuracy (AUC 0.95) compared with initial
clinical assessment alone (AUC 0.88). In contrast, initial testing with CXR/NT-proBNP did not significantly
improve diagnostic accuracy compared with initial clinical assessment (AUC 0.87 and 0.85, respectively).

Further study is needed to define the role of LUS in the diagnosis of ADHF.

Laboratory data — Initial laboratory data are obtained when feasible but are generally not needed to
make the diagnosis or guide initial therapy; treatment should NOT be delayed while waiting for the
results of laboratory tests.

● Pulse oximetry is often used for initial identification of hypoxia. Arterial blood gas analysis is
recommended in all patients with hypoxia and/or severe respiratory distress to assess ventilatory
and acid-base status [37].

● Routine chemistries including serum electrolytes, bicarbonate, blood urea nitrogen (BUN), and
serum creatinine are helpful in guiding electrolyte (eg, potassium and magnesium) repletion
during diuresis and in assessing and monitoring renal function. A decline in renal function is
commonly found in patients with advanced HF (cardiorenal syndrome). This may be due in part to
a low-output state and elevated central venous pressures. Increased BUN and serum creatinine
may also reflect underlying renal disease and, in some cases, may reflect bilateral renal artery
stenosis.

● We suggest checking a lactic acid level in patients in shock as well as in those with marked
weakness and/or uncertain peripheral perfusion. (See 'Cardiogenic shock' above and "Approach to
the adult with metabolic acidosis".)

● Serum troponin (T or I) levels are obtained in any patient with possible ACS. For patients with
criteria for ST elevation MI, reperfusion therapy (percutaneous coronary intervention or
thrombolysis) should not be delayed to wait for the results of troponin measurements ( table 3).
(See "Troponin testing: Clinical use" and "Initial evaluation and management of suspected acute
coronary syndrome (myocardial infarction, unstable angina) in the emergency department" and
"Overview of the acute management of ST-elevation myocardial infarction".)

● A complete blood count may help identify the presence of infection or anemia that may have
precipitated the event. (See "Evaluation and management of anemia and iron deficiency in adults
with heart failure".)

Natriuretic peptide levels — If the diagnosis of HF is uncertain in a patient with dyspnea and other
signs and symptoms suggestive of ADHF, plasma BNP or NT-proBNP concentration should be
measured. Decision analysis suggests that BNP or NT-proBNP testing is generally most useful in
patients who have an intermediate probability of HF [38]. The natriuretic peptide concentration should
not be interpreted in isolation but in the context of all available clinical data bearing on the diagnosis of
ADHF. (See 'How to diagnose ADHF' above.)

Most dyspneic patients with HF have plasma BNP values above 400 pg/mL. For patients <50, 50 to 75,
and >75 years of age, the optimal plasma NT-proBNP cutoffs for diagnosing HF are 450, 900, and
1800 pg/mL, respectively. (See "Natriuretic peptide measurement in heart failure".)

There is considerable overlap in BNP and NT-proBNP levels in patients with and without HF, which
makes the test less robust in an individual patient with intermediate levels of BNP (approximately 200
to 400 pg/mL). Since many conditions increase natriuretic peptide levels, low values of BNP (<100
pg/mL) or NT-proBNP (<300 pg/mL) are most useful because the diagnosis of ADHF is very unlikely as
an explanation for dyspnea [39]. However, unexpectedly low natriuretic peptide levels are occasionally
found in some patients with end-stage HF, acute pulmonary edema, and right-sided HF [12].

Results of BNP or NT-proBNP testing must be interpreted with caution, and such testing must support
rather than override careful clinical judgment. (See "Natriuretic peptide measurement in heart failure"
and "Natriuretic peptide measurement in heart failure", section on 'BNP and the diagnosis of HF in the
patient with dyspnea' and "Natriuretic peptide measurement in heart failure", section on 'Acute
decompensated HF'.)

Echocardiography — Echocardiography is recommended for patients with new HF and for patients
with prior history of HF with suspected change in cardiac function. The urgency of echocardiography
varies with the acuity of presentation. This imaging modality should be utilized early on during the
evaluation of patients with cardiogenic shock or low-output syndrome. This imaging modality is also
critical in the evaluation of patients with known or suspected valvular heart disease. In patients with ST
elevation MI and pulmonary congestion, echocardiography should be performed urgently to estimate
left and right ventricular function and to exclude a mechanical complication. (See "Acute myocardial
infarction: Mechanical complications".)

Doppler echocardiography aids in the diagnosis and classification of HF, as recommended in major
society guidelines [22,37,40,41]. 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 "Heart failure: Clinical manifestations and
diagnosis in adults", section on 'Echocardiography' and "Pathophysiology of cardiogenic pulmonary
edema".)

Assessment of ventricular function by echocardiography or other methods (eg, radionuclide,

cardiovascular magnetic resonance imaging, computed tomography, 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 HF may be ascribed to systolic
dysfunction (with or without other causes such as diastolic dysfunction or valvular disease) [37]. When
preserved LV systolic function is found, the cause of HF may be diastolic dysfunction, transient systolic
dysfunction, other causes of HF with preserved EF including valvular heart disease ( table 4), or
diagnostic error (no HF with symptoms/signs due to another cause).

Additional tests

Swan-Ganz catheter — Routine use of invasive hemodynamic monitoring in patients with ADHF is
NOT recommended [22,40]. 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 with reduced ejection fraction", section on 'Use of pulmonary artery catheter'.)

However, invasive hemodynamic monitoring is recommended for patients with ADHF with persistent
symptoms and/or when hemodynamics are uncertain [40]. In addition, invasive monitoring can be
useful in carefully selected patients with persistent symptoms despite empiric adjustment of standard
therapies and one or more of the following conditions:

● Renal function is worsening with therapy

● Parenteral vasoactive agents are required
● Advanced device therapy or cardiac transplantation may be required

A pulmonary capillary wedge pressure or its equivalent, pulmonary artery occlusion pressure, of ≥18
mmHg favors cardiogenic pulmonary edema. (See "Pulmonary artery catheterization: Indications,
contraindications, and complications in adults" and "Pulmonary artery catheterization: Interpretation of
hemodynamic values and waveforms in adults".)

However, it is important to appreciate that pulmonary artery catheterization measurements can be

misleading in certain settings. Most importantly, intermittent myocardial ischemia can cause severe but
transient reduction in LV compliance, accompanied by an elevation in the LV filling pressure. Because of
the change in ventricular compliance, this elevation in pressure may or may not be accompanied by an
elevation in the LV volume. Furthermore, if the pulmonary capillary wedge pressure is first measured
after the ischemia has resolved (and if LV 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 LV 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".)