Acute heart failure

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Key Recommendations

Initial management options include a combination of oxygen, diuretics, vasodilators, inotropes, and vasopressors.[1][2] Other possible therapies include extracorporeal ultrafiltration; ventilation (noninvasive and endotracheal intubation); and mechanical circulatory support (e.g., intra-aortic balloon pump, ventricular assist devices).[1]

Evidence supporting the use of intravenous morphine to treat dyspnea is lacking and data suggest there might be adverse effects.[64][65] Hence the current recommendation is that morphine should not be used routinely in patients with acute heart failure.[36] Morphine can be used for palliative care, and is helpful in individual patients because of its venodilator properties and because it decreases sympathetic drive; however, it should be used cautiously as it can cause respiratory depression, potentially increasing the chance of mechanical ventilation.

All patients should be admitted to the hospital. If the patient responds adequately to initial treatment and meets strict selection criteria, telemetry monitoring may be acceptable (e.g., hospital-at-home program).[66] Those who are hypotensive or fail to respond to initial therapy require admission to the intensive care unit and may need invasive monitoring if tissue perfusion is compromised.[67] If cardiogenic shock is present, invasive evaluation is required.

Patients with acute heart failure should undergo evaluation for potential precipitating factors, including myocardial ischemia, arrhythmias (commonly atrial fibrillation), underlying valvular disease, exacerbation of hypertension, anemia, thyroid disorders, and drug interactions. Other concomitant conditions, such as pneumonia and pulmonary embolism, may also be contributing factors.

Venous thromboembolism prophylaxis is recommended in all patients. See Venous thromboembolism (VTE) prophylaxis.

Patients with acute heart failure with reduced ejection fraction who are iron deficient should receive intravenous iron supplementation to reduce the risk of future heart failure hospitalizations.[68][69]

Maintenance of oxygen saturation

High-flow oxygen is recommended in patients with a capillary oxygen saturation <90% or PaO₂ <60 mmHg (8.0 kPa) to correct hypoxemia.[1]

Ventilation with noninvasive positive pressure ventilation or continuous positive airway pressure may be required if oxygen saturation cannot be maintained by oxygenation alone, and is associated with a decreased requirement for intubation and mechanical ventilation.[1]

Mechanical ventilation is only used when other treatments, including noninvasive ventilation methods, fail.

Tracheal intubation: animated demonstration

How to insert a tracheal tube in an adult using a laryngoscope.

Hemodynamically stable

Diuretics and vasodilators

Loop diuretics are the mainstay of treatment for patients who are hemodynamically stable and are effective in relieving symptoms.[1][2][73] Loop diuretics used for the treatment of acute heart failure and congestion include furosemide, bumetanide, and torsemide. The most commonly used agent appears to be furosemide, but some patients may respond more favorably to another loop diuretic.
Intravenous diuretics (bolus or continuous infusion) are indicated on initial hospitalization in patients with pulmonary congestion and volume overload.[1][2] All patients with symptoms and signs of congestion should receive diuretics, irrespective of the left ventricular ejection fraction. Patients already taking oral loop diuretics should be started on a higher dose intravenously (may require double their usual dose), with further titration as needed.[2][66] Diuretic response should be evaluated shortly after start of diuretic therapy, initially with hourly urine output measurement; ongoing monitoring should include careful measurement of 24-hour fluid intake and output, vital signs, and standing body weight measured at the same time each day.[1][2]
Nonloop diuretics may be added if there is an inadequate response to loop diuretics alone.[2] Evidence from randomized controlled trials supports the use of acetazolamide and hydrochlorothiazide as add-on diuretic therapy; other options include metolazone, or acute use of aldosterone antagonists such as spironolactone and eplerenone.[2][74][75]
- Acetazolamide added to loop diuretic therapy in patients with acute decompensated heart failure results in a greater incidence of successful decongestion.[75]
- Hydrochlorothiazide with intravenous furosemide results in greater diuresis and weight loss compared to furosemide alone, but with worsening renal function.[74]
Careful monitoring of renal function and electrolytes is essential when loop and nonloop diuretics are used in combination.[2] The minimum dose of diuretics should be used to relieve congestion, keep the patient asymptomatic, and maintain a dry weight (defined as when the patient is euvolemic).
In patients with reduced left ventricular ejection fraction, diuretics should be used only in combination with other medical therapies, such as an ACE inhibitor (or an angiotensin-II receptor antagonist or an angiotensin-II receptor antagonist/neprilysin inhibitor), a beta-blocker, and an aldosterone antagonist.[2]
In both acute heart failure and stable congestive heart failure, loop diuretics are the preferred agent for most patients. However, a thiazide diuretic may be considered for patients with hypertension and only mild fluid retention.[2]
Vasodilators (nitroglycerin, nitroprusside) are often used in acute heart failure to relieve symptoms of pulmonary congestion in patients without systemic hypotension; however, they do not improve long-term outcomes (i.e., reduction of mortality or rehospitalization).[1][2]
- Nitroglycerin is preferred in emergency settings.[34]
- Nitroprusside is usually given in the intensive care setting where enhanced monitoring is available (e.g., invasive hemodynamic blood pressure monitoring), due to its potential for marked hypotension and risk of cyanide toxicity.[2]

In patients who do not respond to initial therapy, extracorporeal ultrafiltration is used to reduce volume overload.[76][77]

Hemodynamically unstable

Patients with hypotension (i.e., systolic blood pressure [BP] <90 mmHg) or shock should receive oxygen therapy if capillary oxygen saturation <90% or PaO₂ <60 mmHg (8.0 kPa), vasoactive drugs, and ventilation and mechanical circulatory support if needed.[1]

Cardiogenic shock is characterized by critical reduction in cardiac output and end-organ hypoperfusion in a patient with a systolic BP <90 mmHg.[2]

Short-term intravenous infusion of a vasoactive agent (vasopressor and/or inotrope) should be considered in patients with hypotension (systolic BP <90 mmHg) and/or signs or symptoms of hypoperfusion, despite adequate filling status.[1][2] Vasoactive agents may cause tachycardia, and induce arrhythmias and myocardial ischemia.[1][2]

Vasopressor therapy aims to reverse the mismatch between vessel tone and intravascular volume by inducing vasoconstriction. The preferred vasopressor is norepinephrine (noradrenaline).[1][2]

Inotropes (e.g., dobutamine, milrinone) can increase cardiac output and improve hemodynamics in patients with cardiogenic shock.[2] Inotropes should be used with caution because there is evidence that they result in increased mortality.[1][2][13] Inotropes should be discontinued if there are sustained arrhythmias or symptomatic coronary ischemia. Continuous monitoring of cardiac rhythm is recommended during infusion of inotropes. There is a lack of robust evidence to suggest a clear benefit of one inotropic agent over another in cardiogenic shock.[2][78]

Selection of appropriate vasoactive agents may vary according to clinician preference and local practice guidelines. Consult a specialist for guidance on suitable regimens.

Temporary mechanical circulatory support (MCS) devices (e.g., extracorporeal membrane oxygenation or intra-aortic balloon pump) should be considered in patients with persistent cardiogenic shock despite inotropic therapy.[1][2][79]

See Shock.

Specific treatment of underlying cause

Coronary artery disease

Intravenous nitroglycerin is first-line treatment.
The common adverse effect of nitroglycerin is headache and hypotension. The dose of nitrates should be reduced if systolic BP decreases below 90 to 100 mmHg, and discontinued permanently if BP drops further.
In cases of significant coronary artery disease causing acute heart failure, percutaneous revascularization or coronary artery bypass should be carried out. Aspirin, in combination with a P2Y12 inhibitor (e.g., clopidogrel, prasugrel, ticagrelor), is given to all patients with coronary ischemia and those undergoing revascularization.[80]
In the case of cardiogenic shock with acute myocardial infarction, revascularization is recommended. Thrombolysis in this setting is not effective.[81]
See Overview of acute coronary syndrome.

Hypertensive emergency

Use of intravenous nitroglycerin is recommended.
If additional medications are needed, nitroprusside is recommended in addition to other choices. Nitroprusside should be given in a setting where enhanced monitoring is available (e.g., invasive hemodynamic blood pressure monitoring).
See Hypertensive emergencies.

Cardiac arrhythmias

Either rapid arrhythmias or severe bradycardia/conduction disturbance can precipitate acute heart failure.
Patients presenting acutely with atrial fibrillation or atrial flutter require anticoagulation, rate control, and rhythm control when indicated (e.g., urgent DC cardioversion for patients with hemodynamic instability).[82]
Severe bradycardia may require temporary pacing or drug interventions; patients with non-reversible causes may require an implantable pacemaker with or without a defibrillator.[83]
See Evaluation of tachycardia and Bradycardia.

Valvular heart disease

In cases of severe aortic stenosis with heart failure, nitroprusside can be used with careful monitoring, provided the patient is not hypotensive.[1][84]
The definitive treatment for aortic stenosis or mitral stenosis is valve replacement, but in resistant heart failure a percutaneous valvotomy may be used as temporary measure until definitive valve replacement is carried out. In mitral stenosis, percutaneous valvuloplasty may be done if no thrombus is present on transesophageal echocardiogram.
Similarly in heart failure associated with mitral regurgitation or aortic regurgitation, a vasodilating drug such as nitroprusside may be used.[2] A decrease in the peripheral arterial resistance results in an increase in the cardiac output and a decrease in regurgitant volume, which, in turn, is associated with a reduction in left ventricular end-diastolic volume and an augmentation of the ejection fraction.
See Aortic stenosis, Aortic regurgitation, Mitral stenosis, and Mitral regurgitation.

Acute right heart failure

Therapy is centered around treatment of the underlying pathology; e.g., pulmonary embolism (anticoagulation, thrombolytics, catheterization, or surgically directed thrombectomy), right ventricular infarction (percutaneous coronary intervention or thrombolytics), and chronic thromboembolic pulmonary hypertension (thromboendarterectomy).[85]
See Pulmonary embolism.

Acute myocarditis

Myocarditis caused by autoimmune disease (clinical or endomyocardial biopsy evidence of autoimmune disease) including giant cell myocarditis is treated with single or combination immunosuppressant therapy which may include corticosteroids, azathioprine, and cyclosporine.[1][86]
Treatment of other forms of myocarditis is limited to supportive care, alongside standard heart failure therapy for at least 6 months.[1]
See Myocarditis.

Resistance to maximal medical therapy

In cases of advanced heart failure resistant and refractory to maximal medical therapy, a durable mechanical circulatory support (MCS) device (e.g., a left ventricular assist device [LVAD]) is recommended for select patients (e.g., patients dependent on continuous intravenous inotropes).[2][87]

There are several accepted indications for implantation of a durable LVAD, including bridge to transplantation and destination therapy (permanent pump implantation in patients not eligible for cardiac transplantation).[1][88] Some of the absolute contraindications for providing durable mechanical support include irreversible hepatic, renal, and neurologic disease; medical nonadherence; and severe psychosocial limitations.[89]

In some cases of nonischemic cardiomyopathy, sustained reversal of severe heart failure is seen with implantation of an LVAD.[90] The use of LVADs has evolved significantly over the past 25 years and various types of LVAD now exist.

Use of temporary devices can help stabilize patients and allow time for decisions about the appropriateness of transitions to definitive management (bridge to decision), such as durable MCS or cardiac transplantation.[2] Extracorporeal devices, the most common of which are the extracorporeal membrane oxygenators, require full heparinization and are typically used for days or weeks as a bridge for patients who are expected to recover within days. Percutaneous short-term devices (e.g., Tandem Heart) are inserted through the femoral artery and advanced into the left ventricle. Longer-term assist devices are divided into first-generation (e.g., Heart Mate I), second-generation (e.g., Heart Mate II), and third-generation (e.g., HVAD and Dura Heart) devices.

Ongoing therapy

Once the patient is stabilized, definitive medical therapy for heart failure should be commenced.

Recommended therapies include:[1][2]

Renin-angiotensin system inhibitors (i.e., angiotensin-II receptor antagonist/neprilysin inhibitor, ACE inhibitor, or an angiotensin-II receptor antagonist)
Beta-blockers
Aldosterone antagonists
Sodium-glucose cotransporter 2 (SGLT2) inhibitors.

For patients with heart failure with reduced ejection fraction (HFrEF), a combination of drugs from all four of these medication classes should be commenced, increased rapidly to maximum recommended and tolerated doses, and continued long term.[2][68][91] Patients who have persistent signs of fluid overload will need ongoing diuretics.

Usually an angiotensin-II receptor antagonist/neprilysin inhibitor (e.g., sacubitril/valsartan) or an ACE inhibitor (or an angiotensin-II receptor antagonist if ACE inhibitors are not tolerated and use of an angiotensin-II receptor antagonist/neprilysin inhibitor is not feasible) is started first, followed by the addition of beta-blockers. [ ] An angiotensin-II receptor antagonist/neprilysin inhibitor is recommended both as a first-line treatment for patients newly diagnosed with acute heart failure, and to replace ACE inhibitor (or angiotensin-II receptor antagonist) therapy in patients with chronic heart failure with reduced ejection fraction that remains symptomatic despite existing therapy.[2] The dose of these agents should be increased to the maximum tolerated dose depending upon BP and heart rate. Typically, beta-blockers are started only after patients have stabilized, but should continue long term to reduce the risk of major cardiovascular events even if symptoms do not improve.[2]

Patients with ongoing symptoms despite this therapy should be treated as having chronic heart failure. In patients with reduced left ventricular ejection fraction (LVEF), an aldosterone antagonist (e.g., spironolactone, eplerenone) should be prescribed.[2] Aldosterone antagonists require careful monitoring of potassium, renal function, and diuretic dosing to minimize risk of hyperkalemia and renal insufficiency.[2] There is also evidence to support the long-term use of a SGLT2 inhibitor (e.g., dapagliflozin, empagliflozin, sotagliflozin) in patients with reduced LVEF regardless of whether they have type 2 diabetes mellitus.[1][2][66][92][93] Patients with diabetes taking SGLT2 inhibitors are at increased risk of developing diabetic ketoacidosis (including euglycemic ketoacidosis).[30]

For black patients with low LVEF, a combination of hydralazine and isosorbide dinitrate can be particularly beneficial, and can be considered for other patients unable to take first-line agents.[2]

Patients with heart failure with mildly reduced ejection fraction (HFmrEF, LVEF 41% to 49%) should have repeat evaluation of LVEF to determine the trajectory of their disease process.[2] For patients with HFmrEF and heart failure with preserved ejection fraction (HFpEF, LVEF ≥50%), good control of BP and other comorbidities (e.g., arrhythmias and underlying ischemia) is essential.[94] There is increasing evidence that therapies usually recommended for patients with reduced ejection fraction also benefit patients with HFmrF and HFpEF (LVEF >40%); in particular, SGLT2 inhibitors reduce future heart failure admissions regardless of ejection fraction and should be started in patients with heart failure before discharge when possible.[1][2][66][68][92][94][95][96][97] If needed, diuretics may be prescribed to reduce congestion and improve symptoms.[2]

Treatment with ivabradine in stable patients with chronic heart failure (i.e., LVEF <35%) and a resting heart rate of >70 bpm - on a background of guideline-based heart failure therapy - is associated with reducing the risk of hospitalization for worsening heart failure.[2][98] In one randomized, double-blind, placebo-controlled trial, addition of ivabradine to standard background therapy did not improve the outcome in patients with stable coronary artery disease without clinical heart failure (no evidence of left ventricular systolic dysfunction, in the overall study population mean ejection fraction was 56.4%). In the subgroup analysis of the study, ivabradine was associated with an increase in the incidence of the primary end point (death from cardiovascular causes or nonfatal myocardial infarction) among patients who had angina of Canadian Cardiovascular Society class II or higher but not among patients without angina or those who had angina of class I. Ivabradine was associated with an increased incidence of bradycardia, QT prolongation, and atrial fibrillation.[99]

Digoxin significantly reduces the risk of composite end point of mortality or hospitalization in ambulatory chronic heart failure patients with NYHA class 3 or 4 symptoms, LVEF <25%, or cardiothoracic ratio of >55%, and should be considered in these patients.[100] In patients with heart failure who are in sinus rhythm, use of digoxin has no effect on mortality but is associated with a lower rate of hospitalization and clinical deterioration.[101]

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