Sections

Presentation

History

In evaluating patients with heart failure, the clinician should ask about the following comorbidities and/or risk factors:

Myopathy
Previous myocardial infarction
Valvular heart disease, familial heart disease
Alcohol use
Hypertension
Diabetes
Dyslipidemia
Coronary/peripheral vascular disease
Sleep-disordered breathing
Collagen vascular disease, rheumatic fever
Pheochromocytoma
Thyroid disease
Substance abuse (previous/current history)
History of chemotherapy/radiation to the chest

The New York Heart Association (NYHA) classification of heart failure is widely used in practice and in clinical studies to quantify clinical assessment of heart failure (see Heart Failure Criteria, Classification, and Staging). Breathlessness, a cardinal symptom of left ventricular (LV) failure, may manifest with progressively increasing severity as the following:

Exertional dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Dyspnea at rest
Acute pulmonary edema

Other cardiac symptoms of heart failure include chest pain/pressure and palpitations. Common noncardiac signs and symptoms of heart failure include anorexia, nausea, weight loss, bloating, fatigue, weakness, oliguria, nocturia, and cerebral symptoms of varying severity, ranging from anxiety to memory impairment and confusion. Findings from the Framingham Heart Study suggested that subclinical cardiac dysfunction and noncardiac comorbidities are associated with increased incidence of heart failure, supporting the idea that heart failure is a progressive syndrome and that noncardiac factors are extremely important.^{[31, 32, 57]}

Older patients with heart failure frequently have preserved ejection fraction and an atypical and/or delayed presentation.^[58]

Exertional dyspnea

The principal difference between exertional dyspnea in patients who are healthy and exertional dyspnea in patients with heart failure is the degree of activity necessary to induce the symptom. As heart failure first develops, exertional dyspnea may simply appear to be an aggravation of the breathlessness that occurs in healthy persons during activity, but as LV failure advances, the intensity of exercise resulting in breathlessness progressively declines; however, subjective exercise capacity and objective measures of LV performance at rest in patients with heart failure are not closely correlated. Exertional dyspnea, in fact, may be absent in sedentary patients.

Orthopnea

Orthopnea is an early symptom of heart failure and may be defined as dyspnea that develops in the recumbent position and is relieved with elevation of the head with pillows. As in the case of exertional dyspnea, the change in the number of pillows required is important. In the recumbent position, decreased pooling of blood in the lower extremities and abdomen occurs. Blood is displaced from the extrathoracic compartment to the thoracic compartment. The failing LV, operating on the flat portion of the Frank-Starling curve, cannot accept and pump out the extra volume of blood delivered to it without dilating. As a result, pulmonary venous and capillary pressures rise further, causing interstitial pulmonary edema, reduced pulmonary compliance, increased airway resistance, and dyspnea.

Orthopnea occurs rapidly, often within a minute or two of recumbency, and develops when the patient is awake. Orthopnea may occur in any condition in which the vital capacity is low. Marked ascites, regardless of its etiology, is an important cause of orthopnea. In advanced LV failure, orthopnea may be so severe that the patient cannot lie down and must sleep sitting up in a chair or slumped over a table.

Cough, particularly during recumbency, may be an "orthopnea equivalent." This nonproductive cough may be caused by pulmonary congestion and is relieved by the treatment of heart failure.

Paroxysmal nocturnal dyspnea

Paroxysmal nocturnal dyspnea usually occurs at night and is defined as the sudden awakening of the patient, after a couple of hours of sleep, with a feeling of severe anxiety, breathlessness, and suffocation. The patient may bolt upright in bed and gasp for breath. Bronchospasm increases ventilatory difficulty and the work of breathing and is a common complicating factor of paroxysmal nocturnal dyspnea. On chest auscultation, the bronchospasm associated with a heart failure exacerbation can be difficult to distinguish from an acute asthma exacerbation, although other clues from the cardiovascular examination should lead the examiner to the correct diagnosis. Both types of bronchospasm can be present in a single individual.

In contrast to orthopnea, which may be relieved by immediately sitting up in bed, paroxysmal nocturnal dyspnea may require 30 minutes or longer in this position for relief. Episodes may be so frightening that the patient may be afraid to resume sleeping, even after the symptoms have subsided.

Dyspnea at rest

Dyspnea at rest in heart failure is the result of the following mechanisms:

Decreased pulmonary function secondary to decreased compliance and increased airway resistance
Increased ventilatory drive secondary to hypoxemia due to increased pulmonary capillary wedge pressure (PCWP); ventilation/perfusion (V/Q) mismatching due to increased PCWP and low cardiac output; and increased carbon dioxide production
Respiratory muscle dysfunction, with decreased respiratory muscle strength, decreased endurance, and ischemia

Pulmonary edema

Acute pulmonary edema is defined as the sudden increase in PCWP (usually >25 mm Hg) as a result of acute and fulminant LV failure. It is a medical emergency and has a very dramatic clinical presentation. The patient appears extremely ill, poorly perfused, restless, sweaty, tachypneic, tachycardic, hypoxic, and coughing, with an increased work of breathing and using respiratory accessory muscles and with frothy sputum that on occasion is blood tinged.

Chest pain/pressure and palpitations

Chest pain/pressure may occur as a result of either primary myocardial ischemia from coronary disease or secondary myocardial ischemia from increased filling pressure, poor cardiac output (and, therefore, poor coronary diastolic filling), or hypotension and hypoxemia.

Palpitations are the sensation a patient has when the heart is racing. It can be secondary to sinus tachycardia due to decompensated heart failure, or more commonly, it is due to atrial or ventricular tachyarrhythmias.

Fatigue and weakness

Fatigue and weakness are often accompanied by a feeling of heaviness in the limbs and are generally related to poor perfusion of the skeletal muscles in patients with a lowered cardiac output. Although they are generally a constant feature of advanced heart failure, episodic fatigue and weakness are also common in earlier stages.

Nocturia and oliguria

Nocturia may occur relatively early in the course of heart failure. Recumbency reduces the deficit in cardiac output in relation to oxygen demand, renal vasoconstriction diminishes, and urine formation increases. Nocturia may be troublesome for patients with heart failure because it may prevent them from obtaining much-needed rest. Oliguria is a late finding in heart failure, and it is found in patients with markedly reduced cardiac output from severely reduced LV function.

Cerebral symptoms

The following may occur in elderly patients with advanced heart failure, particularly in those with cerebrovascular atherosclerosis:

Confusion
Memory impairment
Anxiety
Headaches
Insomnia
Bad dreams or nightmares
Rarely, psychosis with disorientation, delirium, or hallucinations

Physical Examination

Patients with mild heart failure appear to be in no distress after a few minutes of rest, but they may be obviously dyspneic during and immediately after moderate activity. Patients with left ventricular (LV) failure may be dyspneic when lying flat without elevation of the head for more than a few minutes. Those with severe heart failure appear anxious and may exhibit signs of air hunger in this position.

Patients with a recent onset of heart failure are generally well nourished, but those with chronic severe heart failure are often malnourished and sometimes even cachectic. Chronic marked elevation of the systemic venous pressure may produce exophthalmos and severe tricuspid regurgitation, and it may lead to visible pulsation of the eyes and of the neck veins. Central cyanosis, icterus, and malar flush may be evident in patients with severe heart failure.

In mild or moderate heart failure, stroke volume is normal at rest; in severe heart failure, it is reduced, as reflected by a diminished pulse pressure and a dusky discoloration of the skin. With very severe heart failure, particularly if cardiac output has declined acutely, systolic arterial pressure may be reduced. The pulse may be weak, rapid, and thready; the proportional pulse pressure (pulse pressure/systolic pressure) may be markedly reduced. The proportional pulse pressure correlates reasonably well with cardiac output. In one study, when pulse pressure was less than 25%, it usually reflected a cardiac index of less than 2.2 L/min/m².^[59]

Ascites occurs in patients with increased pressure in the hepatic veins and in the veins draining into the peritoneum; it usually reflects long-standing systemic venous hypertension. Fever may be present in severe decompensated heart failure because of cutaneous vasoconstriction and impairment of heat loss.

Increased adrenergic activity is manifested by tachycardia, diaphoresis, pallor, peripheral cyanosis with pallor and coldness of the extremities, and obvious distention of the peripheral veins secondary to venoconstriction. Diastolic arterial pressure may be slightly elevated.

Rales heard over the lung bases are characteristic of heart failure that is of at least moderate severity. With acute pulmonary edema, rales are frequently accompanied by wheezing and expectoration of frothy, blood-tinged sputum. The absence of rales does not exclude elevation of pulmonary capillary pressure due to LV failure.

Systemic venous hypertension is manifested by jugular venous distention. Normally, jugular venous pressure declines with respiration; however, it increases in patients with heart failure, a finding known as the Kussmaul sign (also found in constrictive pericarditis). This reflects an increase in right atrial pressure and, therefore, right-sided heart failure. In general, elevated jugular venous pressure is the most reliable indicator of fluid volume overload in older patients, and thorough evaluation is needed.^[58]

The hepatojugular reflux is the distention of the jugular vein induced by applying manual pressure over the liver; the patient's torso should be positioned at a 45° angle. The hepatojugular reflux occurs in patients with elevated left-sided filling pressures and reflects elevated capillary wedge pressure and left-sided heart failure.

Although edema is a cardinal manifestation of heart failure, it does not correlate well with the level of systemic venous pressure. In patients with chronic LV failure and low cardiac output, extracellular fluid volume may be sufficiently expanded to cause edema in the presence of only slight elevations in systemic venous pressure. Usually, a substantial gain of extracellular fluid volume (ie, a minimum of 5 L in adults) must occur before peripheral edema develops. Edema in the absence of dyspnea or other signs of LV or right ventricular (RV) failure is not solely indicative of heart failure and can be observed in many other conditions, including chronic venous insufficiency, nephrotic syndrome, or other syndromes of hypoproteinemia or osmotic imbalance.

Hepatomegaly is prominent in patients with chronic right-sided heart failure, but it may occur rapidly in acute heart failure. When hepatomegaly occurs acutely, the liver is usually tender. In patients with considerable tricuspid regurgitation, a prominent systolic pulsation of the liver, attributable to an enlarged right atrial V wave, is often noted. A presystolic pulsation of the liver, attributable to an enlarged right atrial A wave, can occur in tricuspid stenosis, constrictive pericarditis, restrictive cardiomyopathy involving the right ventricle, and pulmonary hypertension (primary or secondary).

Hydrothorax is most commonly observed in patients with hypertension involving both the systemic and pulmonary circulation. It is usually bilateral, although when unilateral, it is usually confined to the right side of the chest. When hydrothorax develops, dyspnea usually intensifies because of further reductions in vital capacity.

Cardiac findings

Protodiastolic (S₃) gallop is the earliest cardiac physical finding in decompensated heart failure in the absence of severe mitral or tricuspid regurgitation or left-to-right shunts. The presence of an S₃ gallop in adults is important, pathologic, and often the most apparent finding on cardiac auscultation in patients with significant heart failure.

Cardiomegaly is a nonspecific finding that nonetheless occurs in most patients with chronic heart failure. Notable exceptions include heart failure from acute myocardial infarction, constrictive pericarditis, restrictive cardiomyopathy, valve or chordae tendineae rupture, or heart failure due to tachyarrhythmias or bradyarrhythmias.

Pulsus alternans (during pulse palpation, this is the alternation of one strong and one weak beat without a change in the cycle length) occurs most commonly in heart failure due to increased resistance to LV ejection, as occurs in hypertension, aortic stenosis, coronary atherosclerosis, and dilated cardiomyopathy. Pulsus alternans is usually associated with an S₃ gallop, signifies advanced myocardial disease, and often disappears with treatment of heart failure.

Accentuation of the P₂ heart sound is a cardinal sign of increased pulmonary artery pressure; it disappears or improves after treatment of heart failure. Mitral and tricuspid regurgitation murmurs are often present in patients with decompensated heart failure because of ventricular dilatatation. These murmurs often disappear or diminish when compensation is restored. Note that the correlation is poor between the intensity of the murmur of mitral regurgitation and its significance in patients with heart failure. Severe mitral regurgitation may be accompanied by an unimpressively soft murmur.

Cardiac cachexia is found in long-standing heart failure, particularly of the RV, because of anorexia from hepatic and intestinal congestion and sometimes because of digitalis toxicity. Occasionally, impaired intestinal absorption of fat occurs and, rarely, protein-losing enteropathy occurs. Patients with heart failure may also exhibit increased total metabolism secondary to augmentation of myocardial oxygen consumption, excessive work of breathing, low-grade fever, and elevated levels of circulating tumor necrosis factor (TNF).

Predominant Right-Sided Heart Failure

Ascites, congestive hepatomegaly, and anasarca due to elevated right-sided heart pressures transmitted backward into the portal vein circulation may result in increased abdominal girth and epigastric and right upper quadrant (RUQ) abdominal pain. Other gastrointestinal symptoms, caused by congestion of the hepatic and gastrointestinal venous circulation, include anorexia, bloating, nausea, and constipation. In preterminal heart failure, inadequate bowel perfusion can cause abdominal pain, distention, and bloody stools. Distinguishing right-sided heart failure from hepatic failure is often clinically difficult.

Dyspnea, prominent in left ventricular failure, becomes less prominent in isolated right-sided heart failure because of the absence of pulmonary congestion. However, when cardiac output becomes markedly reduced in patients with terminal right-sided heart failure (as may occur in isolated right ventricular infarction and in the late stages of primary pulmonary hypertension and pulmonary thromboembolic disease), severe dyspnea may occur as a consequence of the reduced cardiac output, poor perfusion of respiratory muscles, hypoxemia, and metabolic acidosis.

Heart Failure in Children

In children, manifestations of heart failure vary with age.^[60]Signs of pulmonary venous congestion in an infant generally include tachypnea, respiratory distress (retractions), grunting, and difficulty with feeding. Often, children with heart failure have diaphoresis during feedings, which is possibly related to a catecholamine surge that occurs when they are challenged with eating while in respiratory distress.

Right-sided venous congestion is characterized by hepatosplenomegaly and, less frequently, with edema or ascites. Jugular venous distention is not a reliable indicator of systemic venous congestion in infants, because the jugular veins are difficult to observe. Also, the distance from the right atrium to the angle of the jaw may be no more than 8-10 cm, even when the infant is sitting upright. Uncompensated heart failure in an infant primarily manifests as a failure to thrive. In severe cases, failure to thrive may be followed by signs of renal and hepatic failure.

In older children, left-sided venous congestion causes tachypnea, respiratory distress, and wheezing (cardiac asthma). Right-sided congestion may result in hepatosplenomegaly, jugular venous distention, edema, ascites, and/or pleural effusions. Uncompensated heart failure in older children may cause fatigue or lower-than-usual energy levels. Patients may complain of cool extremities, exercise intolerance, dizziness, or syncope.

For more information, see the Medscape Drugs & Diseases article Pediatric Congestive Heart Failure.

Framingham system for diagnosis of heart failure

In the Framingham system, the diagnosis of heart failure requires that either two major criteria or one major and two minor criteria be present concurrently, as shown in Table 1 below.^[1]Minor criteria are accepted only if they cannot be attributed to another medical condition.

Table 1. Framingham Diagnostic Criteria for Heart Failure (Open Table in a new window)

Major Criteria	Minor Criteria
Paroxysmal nocturnal dyspnea	Nocturnal cough
Weight loss of 4.5 kg in 5 days in response to treatment	Dyspnea on ordinary exertion
Neck vein distention	A decrease in vital capacity by one third the maximal value recorded
Rales	Pleural effusion
Acute pulmonary edema	Tachycardia (rate of 120 bpm)
Hepatojugular reflux	Hepatomegaly
S₃ gallop	Bilateral ankle edema
Central venous pressure >16 cm water
Circulation time of ≥25 seconds
Radiographic cardiomegaly
Pulmonary edema, visceral congestion, or cardiomegaly at autopsy
Source: Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol.

Stage A

American College of Cardiology/American Heart Association (ACC/AHA) stage A patients are at high risk for heart failure; thus, this stage is now also known as "at risk for heart failure."^{[4, 5, 6, 7]} Patients in this stage do not have structural heart disease or symptoms of heart failure. Thus, management in these cases focuses on prevention, through reduction of risk factors. Measures include the following^[3]:

Treat hypertension (optimal blood pressure: < 130/80 mm Hg ^[61])
Encourage smoking cessation
Treat lipid disorders
Encourage regular exercise
Discourage alcohol intake and illicit drug use

Patients who have a family history of dilated cardiomyopathy should be screened with a comprehensive history and physical examination together with echocardiography and transthoracic echocardiography every 2-5 years.^[8]

Stage B

ACC/AHA stage B patients are now also designated as "pre-heart failure..^{[4, 5, 6, 7]} These individuals are asymptomatic, with left ventricular (LV) dysfunction from previous myocardial infarction (MI), LV remodeling from LV hypertrophy (LVH), and asymptomatic valvular dysfunction, which includes patients with New York Heart Association (NYHA) class I heart failure (see Heart Failure Criteria, Classification, and Staging for a description of NYHA classes).^[3]In addition to the heart failure education and aggressive risk factor modification used for stage A, treatment with an angiotensin-converting enzyme inhibitor/angiotensin-receptor blocker (ACEI/ARB) and/or beta-blockade is indicated.

Evaluation for coronary revascularization either percutaneously or surgically, as well as correction of valvular abnormalities, may be indicated.^[3]Treatment with an implantable cardioverter-defibrillator (ICD) for primary prevention of sudden death in patients with an LV ejection fraction (LVEF) below 30% that is more than 40 days post-MI is reasonable if the expected survival is more than 1 year.

There is less evidence for implantation of an ICD in patients with nonischemic cardiomyopathy, an LVEF less than 30%, and no heart failure symptoms. There is no evidence for use of digoxin in these populations.^[62]Aldosterone receptor blockade with eplerenone is indicated for post-MI LV dysfunction.

Stage C

ACC/AHA stage C patients have structural heart disease and current or previous symptoms of heart failure; they are therefore designated as having "symptomatic heart failure."^{[4, 5, 6, 7]} ACC/AHA stage C corresponds with NYHA class I-IV heart failure. The preventive measures used for stage A disease are indicated, as is dietary sodium restriction.

Drugs routinely used in these patients include ACEI/ARBs, beta-blockers, or angiotensin receptor–neprilysin inhibitors (ARNIs), in conjunction with evidence-based beta-blockers, and loop diuretics for fluid retention.^{[3, 61, 63]}For selected patients, therapeutic measures include aldosterone receptor blockers, hydralazine and nitrates in combination, and cardiac resynchronization with or without an ICD (see Electrophysiologic Intervention).^{[3, 61, 63]}

A meta-analysis performed by Badve et al suggested that the survival benefit of treatment with beta-blockers extends to patients with chronic kidney disease and systolic heart failure (risk ratio 0.72).^[64]

The 2016 and 2017 ACC/AHA focused updates to the 2013 guidelines added a class IIa recommendation for ivabradine, a sinoatrial node modulator, in patients with stage C heart failure.^{[61, 63]} They indicate that ivabradine may reduce hospitalization for patients with symptomatic (NYHA class II-III) stable chronic heart failure with reduced ejection fraction (LVEF ≤35%) who are receiving recommended therapy, including a beta blocker at the maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 bpm or greater at rest.^{[61, 63]}

Stage D

ACC/AHA stage D patients have refractory heart failure (NYHA class IV) that requires specialized interventions; they are in "advanced heart failure."^{[4, 5, 6, 7]}Therapy includes all the measures used in stages A, B, and C. Treatment considerations include heart transplantation or placement of an LV assist device in eligible patients; pulmonary catheterization; and options for end-of-life care.^[3]For palliation of symptoms, continuous intravenous infusion of a positive inotrope may be considered.

Differential Diagnoses

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Media Gallery

Heart Failure. This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases, signs of acute heart failure.
Heart Failure. Cardiac cirrhosis. Congestive hepatopathy with large renal vein.
Heart Failure. Cardiac cirrhosis. Congestive hepatopathy with large inferior vena cava.
Heart Failure. This electrocardiogram (ECG) is from a 32-year-old female with recent-onset congestive heart failure and syncope. The ECG demonstrates a tachycardia with a 1:1 atrial:ventricular relationship. It is not clear from this tracing whether the atria are driving the ventricles (sinus tachycardia) or the ventricles are driving the atria (ventricular tachycardia [VT]). At first glance, sinus tachycardia in this ECG might be considered with severe conduction disease manifesting as marked first-degree atrioventricular block with left bundle branch block. On closer examination, the ECG morphology gives clues to the actual diagnosis of VT. These clues include the absence of RS complexes in the precordial leads, a QS pattern in V6, and an R wave in aVR. The patient proved to have an incessant VT associated with dilated cardiomyopathy.
Heart Failure. This is a posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. The earliest activation is recorded in red; late activation displays as blue to magenta. Fragmented low-amplitude diastolic local electrocardiograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
Heart Failure. A 28-year-old woman presented with acute heart failure secondary to chronic hypertension. The enlarged cardiac silhouette on this anteroposterior (AP) radiograph is caused by acute heart failure due to the effects of chronic high blood pressure on the left ventricle. The heart then becomes enlarged, and fluid accumulates in the lungs (ie, pulmonary congestion).
Heart Failure. Epsilon wave on an electrocardiogram in a patient with arrhythmogenic right ventricular dysplasia (ARVD). ARVD is a congenital cardiomyopathy that is characterized by infiltration of adipose and fibrous tissue into the RV wall and loss of myocardial cells. Primary injuries usually are at the free wall of the RV and right atria, resulting in ventricular and supraventricular arrhythmias. The most significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias.
Heart Failure. Electrocardiogram depicting ventricular fibrillation in a patient with a left ventricular assist device (LVAD). Ventricular fibrillation is often due to ischemic heart disease and can lead to myocardial infarction and/or sudden death.
Heart Failure. The rhythm on this electrocardiogram (ECG) is sinus with borderline PR prolongation. There is evidence of an acute/evolving anterior ischemia/myocardial infarction (MI) superimposed on the left bundle branch block (LBBB)–like pattern. Note the primary T-wave inversions in leads V2-V4, rather than the expected discordant (upright) T waves in the leads with a negative QRS. Although this finding is not particularly sensitive for ischemia/MI with LBBB, such primary T-wave changes are relatively specific. The prominent voltage with left atrial abnormality and leftward axis in concert with the left ventricular intraventricular conduction delay (IVCD) are consistent with underlying left ventricular hypertrophy. This ECG is an example of "bundle branch block plus." Image courtesy of http://ecg.bidmc.harvard.edu.
Heart Failure. This electrocardiogram (ECG) shows evidence of severe left ventricular hypertrophy (LVH) with prominent precordial voltage, left atrial abnormality, lateral ST-T abnormalities, and a somewhat leftward QRS axis (–15º). The patient had malignant hypertension with acute heart failure, accounting also for the sinus tachycardia (blood pressure initially 280/180 mmHg). The ST-T changes seen here are nonspecific and could be due to, for example, LVH alone or coronary artery disease. However, the ECG is not consistent with extensive inferolateral myocardial infarction. Image courtesy of http://ecg.bidmc.harvard.edu.
Heart Failure. The rhythm on this electrocardiogram is atrial tachycardia (rate, 154 beats/min) with a 2:1 atrioventricular (AV) block. Note the partially hidden, nonconducted P waves on the ST segments (eg, leads I and aVL). The QRS is very wide with an atypical intraventricular conduction defect (IVCD) pattern. The rSR' type complex in the lateral leads (I, aVL) is not due to a right bundle branch block (RBBB) but to an atypical left ventricular conduction defect. These unexpected rSR' complexes in the lateral leads (El-Sherif sign) correlate with underlying extensive myocardial infarction (MI) and, occasionally, ventricular aneurysm. (El-Sherif. Br Heart J. 1970;32:440-8.) The notching on the upstroke of the S waves in lead V4 with a left bundle branch block-type pattern also suggests underlying MI (Cabrera sign). This patient had severe cardiomyopathy secondary to coronary artery disease, with extensive left ventricular wall motion abnormalities. Image courtesy of http://ecg.bidmc.harvard.edu.
Heart Failure. On this electrocardiogram, baseline artifact is present, simulating atrial fibrillation. Such artifact may be caused by a variety of factors, including poor electrode contact, muscle tremor, and electrical interference. A single premature ventricular complex (PVC) is present with a compensatory pause such that the RR interval surrounding the PVC is twice as long as the preceding sinus RR interval. Evidence of a previous anterior myocardial infarction is present with pathologic Q waves in leads V1-V3. Borderline-low precordial voltage is a nonspecific finding. Cardiac catheterization showed a 90% stenosis in the patient's proximal portion the left anterior descending coronary artery, which was treated with angioplasty and stenting. Broad P waves in lead V1 with a prominent negative component is consistent with a left atrial abnormality. Image courtesy of http://ecg.bidmc.harvard.edu.
Heart Failure. This electrocardiogram (ECG) is from a patient who underwent urgent cardiac catheterization, which revealed diffuse severe coronary spasm (most marked in the left circumflex system) without any fixed obstructive lesions. Severe left ventricular wall motion abnormalities were present, involving the anterior and inferior segments. A question of so-called takotsubo cardiomyopathy (left ventricular apical ballooning syndrome) is also raised (see Bybee et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Int Med 2004:141:858-65). The latter is most often reported in postmenopausal, middle-aged to elderly women in the context of acute emotional stress and may cause ST elevations acutely with subsequent T-wave inversions. A cocaine-induced cardiomyopathy (possibly related to coronary vasospasm) is a consideration but was excluded here. Myocarditis may also be associated with this type of ECG and the cardiomyopathic findings shown here. No fixed obstructive epicardial coronary lesions were detected by coronary arteriography. The findings in this ECG include low-amplitude QRS complexes in the limb leads (with an indeterminate QRS axis), loss of normal precordial R-wave progression (leads V1-V3), and prominent anterior/lateral T-wave inversions. Image courtesy of http://ecg.bidmc.harvard.edu.
Heart Failure. This electrocardiogram shows an extensive acute/evolving anterolateral myocardial infarction pattern, with ST-T changes most apparent in leads V2-V6, I, and aVL. Slow R-wave progression is also present in leads V1-V3. The rhythm is borderline sinus tachycardia with a single premature atrial complex (PAC) (fourth beat). Note also the low limb-lead voltage and probable left atrial abnormality. Left ventriculography showed diffuse hypokinesis as well as akinesis of the anterolateral and apical walls, with an ejection fraction estimated at 33%. Image courtesy of http://ecg.bidmc.harvard.edu.
Heart Failure. This electrocardiogram shows a patient is having an evolving anteroseptal myocardial infarction secondary to cocaine. There are Q waves in leads V2-V3 with ST-segment elevation in leads V2-V5 associated with T-wave inversion. Also noted are biphasic T waves in the inferior leads. These multiple abnormalities suggest occlusion of a large left anterior descending artery that wraps around the apex of the heart (or multivessel coronary artery disease). Image courtesy of http://ecg.bidmc.harvard.edu.
Heart Failure. A color-enhanced angiogram of the left heart shows a plaque-induced obstruction (top center) in a major artery, which can lead to myocardial infarction (MI). MIs can precipitate heart failure.
Heart Failure. Emphysema is included in the differential diagnosis of heart failure. In this radiograph, emphysema bubbles are noted in the left lung; these can severely impede breathing capacity.
Heart Failure. Cervicocephalic fibromuscular dysplasia (FMD) can lead to complications such as hypertension and chronic kidney failure, which can lead to heart failure. In this color Doppler and spectral Doppler ultrasonographic examination of the left internal carotid artery (ICA) in a patient with cervicocephalic FMD, stenoses of about 70% is seen in the ICA.
Heart Failure. Cervicocephalic fibromuscular dysplasia (FMD) can lead to complications such as hypertension and chronic kidney failure, which, in turn, can lead to heart failure. Nodularity in an artery is known as the "string-of-beads sign," and it can be seen this color Doppler ultrasonographic image from a 51-year-old patient with low-grade stenosing FMD of the internal carotid artery (ICA).
Heart Failure. Electrocardiogram from a 46-year-old man with long-standing hypertension. Note the left atrial abnormality and left ventricular hypertrophy with strain.
Heart Failure. Electrocardiogram from a 46-year-old man with long-standing hypertension. Left atrial abnormality and left ventricular hypertrophy with strain is revealed.
Heart Failure. Apical four-chamber echocardiogram in a 37-year-old man with arrhythmogenic right ventricular dysplasia (ARVD), a congenital cardiomyopathy. Note the prominent trabeculae and abnormal wall motion of the dilated RV. ARVD can result in ventricular and supraventricular arrhythmias. The most significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias.
Heart Failure. Cardiac magnetic resonance image (CMRI), short-axis view. This image shows right ventricular (RV) dilatation, trabucular derangement, aneurysm formation, and dyskinetic free wall in a patient with arrhythmogenic RV dysplasia.
Heart Failure. This transthoracic echocardiogram demonstrates severe mitral regurgitation with a heavily calcified mitral valve and prolapse of the posterior leaflet into the left atrium.
Heart Failure. Echocardiogram of a patient with severe pulmonic stenosis. This image shows a parasternal short-axis view of a thickened pulmonary valve. Pulmonic stenosis can lead to pulmonary hypertension, which can result in hepatic congestion and in right-sided heart failure.
Heart Failure. Echocardiogram of a patient with severe pulmonic stenosis. This image shows a Doppler scan of the peak velocity (5.2 m/s) and gradients (peak 109 mmHg, mean 65 mmHg) across the valve.
Heart Failure. Echocardiogram of a patient with severe pulmonic stenosis. This image shows moderately severe pulmonary insufficiency (orange color flow) is also present.
Heart Failure. This video is an echocardiogram of a patient with severe pulmonic stenosis. The first segment shows the parasternal short-axis view of the thickened pulmonary valve. The second segment shows the presence of moderate pulmonary insufficiency (orange color flow). AV = aortic valve, PA = pulmonary artery, PI = pulmonary insufficiency, PV = pulmonary valve.
Heart Failure. Transesophageal echocardiogram with continuous wave Doppler interrogation across the mitral valve. An increased mean gradient of 16 mmHg is revealed, consistent with severe mitral stenosis.

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Table 1. Framingham Diagnostic Criteria for Heart Failure

Major Criteria	Minor Criteria
Paroxysmal nocturnal dyspnea	Nocturnal cough
Weight loss of 4.5 kg in 5 days in response to treatment	Dyspnea on ordinary exertion
Neck vein distention	A decrease in vital capacity by one third the maximal value recorded
Rales	Pleural effusion
Acute pulmonary edema	Tachycardia (rate of 120 bpm)
Hepatojugular reflux	Hepatomegaly
S₃ gallop	Bilateral ankle edema
Central venous pressure >16 cm water
Circulation time of ≥25 seconds
Radiographic cardiomegaly
Pulmonary edema, visceral congestion, or cardiomegaly at autopsy
Source: Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol.

Table 2. Evidence-Based BNP and NT-proBNP Cutoff Values for Diagnosing HF

Criterion		BNP, pg/mL		NT-proBNP, pg/mL
Criterion		HF Unlikely (LR-Negative)	HF Likely (LR-Positive)	HF Unlikely (LR-Negative)	HF Likely (LR-Positive)
Age, y	>17	< 100 (0.13)^*	>500 (8.1)^*	-	-
	>21	-	-	< 300 (0.02)^†	-
	21-50	-	-	-	>450 (14)^†
	50-75	-	-	-	>900 (5.0)^†
	>75	-	-	-	>1800 (3.1)^†
Estimated GFR, < 60 mL/min		< 200 (0.13)^‡	>500 (9.3)^‡	-	-
BNP = B-type natriuretic peptide; GRF = glomerular filtration rate; HF = heart failure; LR = likelihood ratio; NPV = negative predictive value; NT-pro-BNP = N-terminal proBNP; PPV = positive predictive value; – = not specifically defined. ^* Derived from Breathing Not Properly data (1586 emergency department [ED] patients, prevalence of HF = 47%).^[65] ^† Derived from PRIDE data (1256 ED patients, prevalence of HF = 57%).^{[66, 75]} ^‡ Derived from subset of Breathing Not Properly data (452 ED patients, prevalence of HF = 49%).^[74]

Table 3. 2013 American College of Cardiology Foundation/American Heart Association (ACCF/AHA) Heart Failure Staging System

Stage	Description	Examples	Notes
A	At high risk for heart failure but without structural heart disease or symptoms of heart failure	Patients with coronary artery disease, hypertension, or diabetes mellitus without impaired left ventricular (LV) function, LV hypertrophy (LVH), or geometric chamber distortion	Patients with predisposing risk factors for developing heart failure No corresponding New York Heart Association (NYHA) functional classification
B	Structural heart disease but without signs/symptoms of heart failure	Patients who are asymptomatic but who have LVH and/or impaired LV function	Corresponds with patients with NYHA class I
C	Structural heart disease with current or past symptoms of heart failure	Patients with known structural heart disease and shortness of breath and fatigue, as well as reduced exercise tolerance	The majority of patients with heart failure are in this stage Corresponds with NYHA classes I, II, III and IV
D	Refractory heart failure requiring specialized interventions	Patients who have marked symptoms at rest despite maximal medical therapy	Patients in this stage may be eligible to receive mechanical circulatory support, receive continuous inotropic infusions, undergo procedures to facilitate fluid removal, or undergo heart transplantation or other procedures Corresponds with patients with NYHA class IV

Table 4. 2022 ACC/AHA/Heart Failure Society of America (HFSA) Heart Failure Staging System

Proposed Terminology	Stage	Definition and Criteria
At risk for HF	A	At risk of HF; asymptomatic, no structural heart disease nor cardiac biomarkers of stretch injury (eg, patients with hypertension, atherosclerotic cardiovascular disease, diabetes, metabolic syndrome and obesity, exposure to cardiotoxic agents, genetic variant for cardiomyopathy, or positive family history of cardiomyopathy)
Pre-HF	B	No signs/symptoms of HF and evidence of one of the following: Structural heart disease Reduced left or right ventricular systolic function Reduced ejection fraction, reduced strain Ventricular hypertrophy Enlarged chamber Wall motion anomalies Valvular heart disease Evidence for raised filling pressures by invasive hemodynamic measurements or by noninvasive imaging that suggests elevated filling pressures (eg, Doppler echocardiography) Patients with risk factors and raised levels of B-type natriuretic peptides or persistently elevated cardiac troponin in the absence of competing diagnoses that result in such biomarker elevations (eg, acute coronary syndrome, chronic kidney disease, pulmonary embolus, or myopericarditis)
Symptomatic HF	C	Structural heart disease with current or previous symptoms of HF
Advanced HF	D	Marked HF symptoms that interfere with daily life and with repeated hospitalizations despite attempts to optimize guideline-directed medical therapy
HF = heart failure

Table 5. 2022 ACC/AHA/HFSA Classification of Heart Failure (HF) by Left Ventricular Ejection Fraction (LVEF)

HF Type by LVEF

Criteria

HF with reduced EF

(HFrEF)

LVEF ≤40%

HF with improved EF

(HFimpEF)

Previous LVEF ≤40% and a followup LVEF >40%

HF with mildly reduced EF

(HFmrEF)

LVEF of 41%-49%

Evidence of spontaneous/provokable increased LV filling pressures (eg, elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement)

HF with preserved EF

(HFpEF)

LVEF ≥50%

Evidence of spontaneous/provokable increased LV filling pressures (eg, elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement)

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Author

Ioana Dumitru, MD Associate Professor of Medicine, Division of Cardiology, Founder and Medical Director, Heart Failure and Cardiac Transplant Program, University of Nebraska Medical Center; Associate Professor of Medicine, Division of Cardiology, Veterans Affairs Medical Center

Ioana Dumitru, MD is a member of the following medical societies: American College of Cardiology, Heart Failure Society of America, International Society for Heart and Lung Transplantation

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Yasmine S Ali, MD, MSCI, FACC, FACP Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine; President, LastSky Writing, LLC

Yasmine S Ali, MD, MSCI, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Medical Writers Association, National Lipid Association, Tennessee Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: LastSky Writing;Philips Healthcare;M Health;Athena Health;PeerView Institute;Verywell Health; HealthCentral;MedEdicus;Pharmaceutical Training Institute;Elsevier;MedStudy;North American Thrombosis Forum;WellnessVerge;Prose Media; AKH, Inc.<br/>Serve(d) as a speaker or a member of a speakers bureau for: North American Thrombosis Forum.

Chief Editor

Gyanendra K Sharma, MD, FACC, FASE Professor of Medicine and Radiology, Director, Adult Echocardiography Laboratory, Section of Cardiology, Medical College of Georgia at Augusta University

Gyanendra K Sharma, MD, FACC, FASE is a member of the following medical societies: American Association of Cardiologists of Indian Origin, American Association of Physicians of Indian Origin, American College of Cardiology, American Society of Echocardiography, Society for Cardiovascular Magnetic Resonance, Society of Cardiovascular Computed Tomography

Disclosure: Nothing to disclose.

Additional Contributors

Mathue M Baker, MD Cardiologist, BryanLGH Heart Institute and Saint Elizabeth Regional Medical Center

Mathue M Baker, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.

Mariclaire Cloutier Freelance editor, Medscape Drugs & Diseases

Disclosure: Nothing to disclose.

Acknowledgements

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York AcademyofSciences,and Society for Academic Emergency Medicine