None of the individuals in control of the content for this article (a continuing medical education activity) reported relevant financial relationships with commercial interests.
Acute heart failure is the rapid onset or worsening of heart failure symptoms, and it is a common cause of hospitalization in older patients. Multiple triggers can cause an acute decompensation of preexisting heart failure (ADHF) but the condition may also occur suddenly in patients with no previous history of the condition (de novo heart failure). Diagnosis is based on typical clinical features (e.g., dyspnea), laboratory findings (e.g., elevated BNP), and imaging findings (e.g., pulmonary edema). Management is often challenging because of comorbidities; most patients require admission for treatment with IV diuretics, vasodilators, adjustment of their chronic heart failure medications, respiratory support, and careful monitoring.
- Acute heart failure: rapid onset of new or worsening signs and symptoms of heart failure 
- Acute decompensated heart failure (ADHF): acute heart failure due to decompensation of preexisting disease/cardiomyopathy (most common) 
- De novo heart failure: acute heart failure occurring for the first time in a patient without known cardiomyopathy (∼15% of cases) 
|Etiology of acute heart failure|
|Type of acute heart failure||Underlying etiology |
|De novo heart failure|| |
|Classification of acute heart failure |
|No evidence of congestion (∼5% of patients)||Evidence of congestion (∼95% of patients)|
|Adequate perfusion|| || |
|Hypoperfusion|| || |
Congestion (most common) 
- Acute dyspnea and orthopnea (i.e., worse when supine)
- Flash pulmonary edema: rapid, life-threatening accumulation of fluid associated with the risk of acute respiratory distress
- Signs of increased work of breathing (WOB)
- Cough (occasionally with frothy, blood-tinged sputum)
- Coarse crackles/rales (and occasionally wheezing) on auscultation
- Severe cases: central cyanosis
- edema : peripheral
Diagnosis of acute heart failure consists of a combination of clinical features, laboratory markers (e.g., BNP), and supportive imaging findings. It is important to evaluate for the underlying cause and rule out life-threatening comorbidities (e.g., ACS).
↑ BNP (or NT-proBNP): Measure in every patient suspected of having acute heart failure.
- Should always be interpreted in comparison to the patient's baseline and in the context of history, examination, and imaging.
- High diagnostic utility in patients with unclear diagnosis 
|Natriuretic peptide levels in the diagnosis of heart failure |
|Heart failure unlikely||Heart failure likely|
|BNP (in pg/mL)|| |
< 100 
> 400 
|NT-proBNP (in pg/mL)|| |
< 300 
- To evaluate for underlying cause/severity
Indicated in all patients to exclude ACS. Findings are variable and may include: 
- Acute ischemic changes due to ACS (see “Diagnosis of myocardial infarction”)
- Atrial fibrillation
- Left ventricular hypertrophy
- Bundle branch block
- Non-specific ST-segment changes
- Low voltage QRS 
- ECG findings may be normal.
X-ray findings in pulmonary congestion
- Septal lines/Kerley B lines: visible horizontal interlobular septa caused by pulmonary edema
- Prominent pulmonary vessels and perihilar alveolar edema (the hilar shadow has a butterfly or “bat wing” appearance)
- Basilar interstitial edema
- Bilateral pleural effusions 
- Cephalization: increased prominence of pulmonary vessels in the upper lobes of the lungs due to venous congestion 
- Peribronchial cuffing
Transthoracic echocardiogram (TTE) 
- Indications: all patients with suspected acute heart failure (imaging modality of choice) 
- Characteristic findings
- Specific findings related to underlying etiology
POCUS in acute heart failure
- Description: bedside ultrasound of the lung fields, IVC, and heart
Characteristic findings 
- Lung fields
- IVC: diameter ≥ 2 cm, collapsibility of < 50% 
If more detailed information about myocardial viability and/or perfusion is needed (e.g., procedural planning, myocardial ischemia is suspected), further imaging modalities may be necessary after the patient is stabilized. Both MRI and CT require the patient to lie flat for sustained periods and are less accurate at higher heart rates.
- Cardiac MRI (CMR) 
- Cardiac CT: assessment of coronary arteries (e.g., in suspected ischemic heart disease) and structural defects 
- Stress imaging 
See also “Differential diagnoses of dyspnea.”
- Acute coronary syndrome
- COPD, asthma
- Noncardiogenic pulmonary edema (e.g., ARDS)
- Pulmonary embolism
- Transfusion-related acute lung injury
- High altitude
The differential diagnoses listed here are not exhaustive.
- Assess patients for signs of cardiogenic shock or respiratory failure.
- Stable patients: Use clinical features to guide treatment (see “Classification of acute heart failure”).
- All patients: Identify and treat the underlying cause.
Hemodynamically unstable patients (i.e., cardiogenic shock) 
See “cardiogenic shock refractory to the following interventions.” for details on therapeutic targets and monitoring. See “ ” for management of patients with
Dry and cold
- Assess : consider small then reevaluate . 
- If shock refractory to fluids: Start vasopressor (ideally norepinephrine ). 
- If shock refractory to fluids AND vasopressors: Administer inotropic support (e.g., Dobutamine ). 
- Wet and cold
Hemodynamically stable patients
|Management of hemodynamically stable patients with acute heart failure |
|Dry and warm|| |
|Wet and warm|
|Wet and cold (if SBP is > 90 mm Hg)|
Respiratory support in acute heart failure 
- Positioning: : Ensure the patient is sitting upright. 
- Supplemental oxygen: indicated for patients with an SpO2 < 90% or PaO2 < 60 mm Hg (see “Oxygen therapy”).
- High-flow nasal cannula (HFNC): Consider in patients with an SpO2 < 90% non-responsive to basic oxygen delivery system. 
- NIPPV: for patients with respiratory distress despite supplemental oxygen 
Invasive mechanical ventilation
- Intubation and mechanical ventilation in patients with acute heart failure can be challenging. 
Diuretic therapy in acute heart failure
- Initial treatment: Diuretics should be administered intravenously (if possible).
Assess the effect of diuretics (e.g., urine output, symptoms) every 6 hours. 
- If urinary output is < 100 mL/hour : Consider doubling the diuretic dose.
- If urinary output is > 100–150 mL/hour :
- Options for refractory congestion despite high doses of loop diuretics:
- Assess the effect of diuretics (e.g., urine output, symptoms) every 6 hours. 
- Transition to oral diuretic: Once the patient is euvolemic/at their baseline. 
Vasodilator therapy in acute heart failure 
- Treatment options
Treatment of refractory acute heart failure
- Ultrafiltration (e.g., hemodialysis): indicated in congestion with no response to medical therapy 
- Mechanical circulatory support: indicated in reversible refractory acute heart failure 
- Management of effusions: Consider therapeutic thoracentesis or pericardiocentesis as needed.
Ongoing hospital management
- Fluid restriction: 1.5–2 L/day 
- Sodium restriction: < 3 g/day 
- Discontinue/avoid any cardiotoxic medications (e.g., NSAIDs, morphine) 
- Identify and treat comorbidities (e.g., atrial fibrillation, pneumonia, COPD)
- VTE prophylaxis 
- For large volume ascites, consider therapeutic paracentesis. 
Optimization of medical therapy for chronic heart failure 
- Patients previously on a stable dose of beta blockers should continue them. 
- Patients not previously on beta blockers: start beta blockers cautiously at a low dose after stabilization (e.g., after volume status has been optimized and IV diuretics, vasodilators, and inotropic agents have been discontinued) 
- Patients should continue all other heart failure medications, unless there is:
- Blood pressure control should be optimized.
For patients not previously on beta blockers, use cautiously and only once the patient has been stabilized.
Management of common comorbidities and complications
Atrial fibrillation with rapid ventricular response 
- Management is complex; consult early with cardiology.
- Rate control is typically preferred strategy in the acute setting
- If refractory to other measures, consider pharmacologic cardioversion with, e.g., amiodarone (see “Cardioversion”).
- Cardiorenal syndrome: management is complex; consult early with nephrology (see “Cardiorenal syndrome”)
- ABCDE approach
- Provide respiratory support.
- Check BNP/NT-proBNP, BMP, electrolytes, CXR, TTE, ECG.
- Consider further workup to identify underlying cause (e.g., cardiac ischemia, hypertensive crisis, infection).
Hemodynamically unstable patients (i.e., cardiogenic shock)
- Immediate cardiology consult for consideration of urgent coronary vascularization
- Treat hypoperfusion with small fluid bolus and/or inotrope/vasopressor support (see “Management of cardiogenic shock”).
- ICU/CCU transfer
- Consider invasive blood pressure monitoring.
- Continuous telemetry and pulse oximetry
Hemodynamically stable patients
- Start IV diuretics (see “Diuretic therapy in acute heart failure”).
- Consider vasodilator if pulmonary edema is present and/or the patient is hypertensive.
- Continue home beta blockers and ACE inhibitor/ARB for patients already on therapy.
- Refractory to standard therapy or complex comorbidities: Consult cardiology, nephrology and consider ultrafiltration.
- Supportive care: fluid restriction, sodium restriction, VTE prophylaxis, discontinue/avoid any cardiotoxic medications
- Monitoring: daily weights, strict intake/output, serial electrolytes, renal function
- Consider continuous telemetry while undergoing diuresis
- Continuous pulse oximetry if the patient has hypoxia
- Identify and treat comorbidities/complications (e.g., atrial fibrillation with RVR, hyponatremia).
- One-Minute Telegram 15-2020-4/4: Early IV nitrate treatment for acute heart failure: should we or shouldn’t we?
Interested in the newest medical research, distilled down to just one minute? Sign up for the One-Minute Telegram in “Tips and links” below.