Acute Heart Failure

Background

• Patients with acute heart failure have newly diagnosed heart failure or decompensation of chronic heart failure.
• Acute heart failure may be due to a wide variety of causes such as:
  • left ventricular dysfunction due to arrhythmias
  • volume overload
  • complications of myocardial infarction (such as free wall rupture, ventricular septal defect, or acute mitral regurgitation due to papillary muscle rupture)
  • medication-related (such as excess beta blockade)
• Three major types of heart failure are heart failure with reduced ejection fraction, heart failure with preserved ejection fraction, and heart failure with mildly reduced ejection fraction.
• Symptoms are due to hemodynamic abnormalities resulting in congestion (most common presentation) and/or low cardiac output.
• Complications of heart failure, particularly acute heart failure, include respiratory and/or renal failure.

Evaluation

• Suspect acute heart failure in patients with symptoms including dyspnea and/or fatigue, and findings on exam including jugular venous distension, hypotension, S3 heart sound, rales, and/or edema, leading to unscheduled medical care or hospital admission.
• Identify potential precipitating factors for acute heart failure including new or worsened left ventricular dysfunction, noncompliance with medications and/or diet, volume overload, drug exposure, arrhythmia, valvular disease, and/or uncontrolled hypertension (Strong recommendation).
• Obtain initial testing including complete blood count, serum chemistries, lipid profile, liver function tests, iron studies, thyroid-stimulating hormone, and urinalysis to identify precipitating and complicating factors and to guide treatment (Strong recommendation).
• Obtain B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) level, especially if diagnosis is uncertain (Strong recommendation); higher levels increase the likelihood of a diagnosis of heart failure but may be elevated due to other causes.
• Obtain 12-lead electrocardiogram (ECG) to optimize management (Strong recommendation) and to evaluate for possible acute coronary syndrome as a potential cause of heart failure or other causes of heart failure such as arrhythmia.
• Obtain a chest x-ray to evaluate for presence of pulmonary edema, to evaluate heart size, and to detect underlying lung disease as a possible noncardiac cause of symptoms (Strong recommendation).
• Use transthoracic echocardiography during initial evaluation to assess cardiac function and structure (Strong recommendation) including assessment of left and right ventricular function, chamber size, wall motion, valve function, left atrial size, markers of diastolic function, and to identify other structural abnormalities (such as left ventricular hypertrophy).
  • Perform other imaging such as cardiac magnetic resonance (CMR), radionuclide imaging, or cardiac computed tomography (CT) to assess left ventricular ejection fraction in patients for whom echocardiography is insufficient (Strong recommendation).
• Consider coronary arteriography for patients eligible for revascularization when ischemia may be contributing to heart failure.
• Differential diagnosis includes other causes of dyspnea such as asthma, COPD, pulmonary infections, and pulmonary embolism.

Management

• For those with
  • ischemia which may be contributing to heart failure, see Diagnostic Cardiac Catheterization and Coronary Angiography and Revascularization for Acute Coronary Syndromes.
  • cardiogenic shock: see Cardiogenic Shock.
  • refractory heart failure: see End-stage (Refractory) Heart Failure.
• Administer oxygen in patients with oxygen saturation by pulse oximetry < 90% or partial pressure of oxygen in arterial blood (PaO₂) < 60 mm Hg (8 kilopascals [kPa]) (Strong recommendation).
• Administer IV loop diuretics (such as furosemide 40 mg IV over 1-2 minutes initially; initial IV dose should be about twice usual daily dose) to treat symptoms of fluid overload (Strong recommendation).
• Check serum electrolytes and renal function at baseline; recheck blood chemistry (especially potassium, blood urea nitrogen [BUN], and serum creatinine) 1-2 weeks after initiation and dose changes of diuretics and/or renin-angiotensin system (RAS) inhibitors.
• Consider invasive hemodynamic monitoring with pulmonary artery catheter to guide therapy in heart failure patients with persistent or worsening diagnostic parameters, symptoms, signs, and in whom hemodynamics are uncertain (Weak recommendation).
• For patients requiring additional measures to promote diuresis
  • Consider intensification of diuresis using higher doses of IV loop diuretics or addition of second diuretic (Weak recommendation).
  • Reserve addition of thiazide diuretic (such as metolazone) to those not responding to moderate or high-dose loop diuretics to reduce electrolyte abnormalities (Strong recommendation).
  • Consider vasodilators (IV nitroglycerin or nitroprusside) as adjunct to diuretics to relieve dyspnea in absence of systemic hypotension (Weak recommendation).
  • Consider ultrafiltration in patients with refractory volume overload not responsive to diuretic treatment (Weak recommendation), though comparisons with diuresis have inconsistent results including increased risk for serious adverse events.
  • Vasopressin antagonists (also called vaptans) are typically reserved for acute management of volume overload to reduce congestion in patients with hyponatremia if other measures such as reversal of underlying causes and free water restriction are not effective.
• For patients who have significant dyspnea despite supplemental oxygen and aggressive diuresis
  • Consider noninvasive positive pressure ventilation in patients with respiratory distress (respiratory rate > 25 breaths per minute, oxygen saturation by pulse oximetry < 90%) as soon as possible to decrease respiratory distress and reduce rate of mechanical endotracheal intubation (Weak recommendation).
• Inotropic support
  • Consider inotropes in patients with systolic blood pressure < 90 mm Hg and evidence of hypoperfusion not responding to standard treatment (including fluid challenge) to maintain end-organ function and improve peripheral perfusion (Weak recommendation).
  • Consider inotropes and/or vasopressors in patients with low cardiac output and evidence of hypoperfused organs as bridge to mechanical circulatory support (MCS) or heart transplantation (Weak recommendation).
  • See cardiogenic shock for management of patients who require inotropic support due to persistent hypotension and/or reduced cardiac output.
• Give venous thromboembolism prophylaxis (for example, using low-molecular-weight heparin) in hospitalized patients not already anticoagulated and without contraindication to anticoagulation to prevent deep venous thrombosis and pulmonary embolism (Strong recommendation).
• Treatment considerations after initial stabilization of acute heart failure in selected patients may include
  • starting (or continuing) oral beta blockers proven to reduce mortality (carvedilol, metoprolol succinate extended-release, or bisoprolol) to reduce mortality and hospitalizations in patients with heart failure with reduced ejection fraction (HFrEF) with current or previous symptoms (Strong recommendation).
  • starting (or continuing) a renin-angiotensin system inhibitor such as angiotensin receptor-neprilysin inhibitor (ARNI [preferred]), angiotensin-converting enzyme (ACE) inhibitor, or angiotensin receptor blocker (ARB [least preferred]) in patients with HFrEF (Strong recommendation).
  • starting or continuing other guideline-directed medical therapy in appropriate patients, including mineralocorticoid receptor antagonists (MRAs) and sodium-glucose cotransporter 2 (SGLT2) inhibitors.