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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 (CHF) 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|| |
- See “Pathophysiology” in “Congestive 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) 
- hypertension, pulmonary congestion, and minimal peripheral edema : Typically manifests with
- Blood pressure: may be low, normal, or elevated and should be interpreted in relation to the patient's baseline blood pressure
Assess for clinical features that are suggestive of hypoperfusion (e.g., narrow pulse pressure, cool extremities, peripheral cyanosis, altered mental status, below baseline blood pressure) to identify patients with or at risk of cardiogenic shock. 
Diagnosis of AHF is primarily clinical; obtain natriuretic peptide if the diagnosis is uncertain.
- Evaluate clinically for possible triggers (e.g., missed medications, clinical features of ACS, infections).
- Obtain CXR and/or lung ultrasound to confirm and evaluate pulmonary congestion.
- Order ECG and laboratory studies (e.g., troponin, BMP, CBC) to investigate underlying conditions (e.g., ACS) and/or differential diagnoses.
- Arrange early TTE for ADHF with a suspected decline in cardiac function OR any de novo heart failure.
BNP (or NT-proBNP): useful for diagnostic confirmation and prognostication; can be measured serially to guide therapy 
- 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 an unclear diagnosis 
|Natriuretic peptide levels in the diagnosis of heart failure |
|Heart failure unlikely ||Heart failure likely |
|BNP (pg/mL)|| |
< 100 
|NT-proBNP (pg/mL)|| |
< 300 
> 1000 
- Additional blood tests
- ECG findings in acute heart failure are variable and may include: 
Chest x-ray 
X-ray findings in pulmonary congestion
- Enlarged heart shadow due to cardiomegaly and/or pericardial effusion 
- Kerley B lines (also known as septal lines)
- 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 echocardiographic findings of AHF
- Specific findings related to underlying etiology
POCUS in acute heart failure
- Description: bedside ultrasound of the lung fields, inferior vena cava (IVC), and heart
Characteristic findings 
- Lung fields
- ≥ 2–2.5 cm, reduced IVC collapsibility  : diameter
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 
- Coronary angiography: to evaluate for ischemic cardiomyopathy 
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
Wheezing can be heard in both acute heart failure and (e.g., , ). 
The differential diagnoses listed here are not exhaustive.
Initial management 
- Perform a rapid ABCDE survey to assess hemodynamic stability.
- Identify and treat any acute underlying cause of AHF for all patients (e.g., consider PCI for patients with ACS).
Hemodynamically stable patients
- Clinical presentation: SBP > 90 mm Hg AND no ; respiratory distress can be present.
- Management: depends on the
- Clinical improvement
- Adjust CHF medications and begin supportive care (See “Ongoing hospital management.”)
- Consider the need for hospital admission vs. discharge home in patients presenting to the emergency department (see “Disposition”).
- Clinical deterioration: See “Hemodynamically unstable patients.”
- Clinical improvement
Hemodynamically unstable patients 
Early specialist consultation (e.g., critical care, cardiology) and admission to hospital is recommended.
- Clinical presentation: can vary
Management: depends on the (See also “ “ ” and .”)
- Evidence of congestion with shock (wet and cold)
- Shock without evidence of congestion (dry and cold): Consider ; add vasopressors and inotropes for shock refractory to fluids.
- with (wet and warm)
- Next steps
Patient with a wet and cold clinical presentation have a high risk of rapid deterioration and require close hemodynamic monitoring regardless of their blood pressure. 
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) and underlying triggers.
- VTE prophylaxis 
- For large volume ascites, consider therapeutic paracentesis. 
Optimizing chronic therapy for CHF 
- Administer beta blockers cautiously in beta-blocker-naive patients.
- Initiate, adjust, or continue
- Patients already on a stable dose of beta blockers: Continue the same dosage. 
- Significant decline in renal function: Consider reducing or stopping ACEIs, ARBs, aldosterone antagonists, and digoxin.
- Hypotension: Consider discontinuing hydralazine/isosorbide dinitrate, ACEIs, ARBs, and beta blockers.
- Bradycardia: Consider reducing or discontinuing beta blockers and digoxin.
- Optimize blood pressure control (see “Hypertension”).
For patients not previously on beta blockers, use cautiously and only once the patient has been stabilized.
- Daily weights, intake/output monitoring
- Check renal function and electrolytes every 12–24 hours (see “Diuretic therapy in acute heart failure”)
- Consider serial BNP or NT-proBNP measurement. 
- Consider .
- POCUS can be used to monitor volume overload. 
Treatment of refractory acute heart failure 
Consider the following if AHF persists despite maximal respiratory and hemodynamic support.
- Ultrafiltration (e.g., hemodialysis): indicated in congestion with no response to medical therapy 
- heart failure  : indicated in reversible refractory acute
- Management of effusions: Consider therapeutic thoracentesis or pericardiocentesis as needed.
Management depends on the Management of cardiogenic shock” for details on therapeutic targets and monitoring.. See “
Dry and cold AHF 
- Assess : consider small then reevaluate . 
- If shock refractory to fluids: Start vasopressor (ideally norepinephrine ). 
- If hypoperfusion persists despite fluids and vasopressor administration: Add inotropic support (e.g., dobutamine ). 
Wet and cold AHF 
- Begin with inotropic support (e.g., dobutamine , dopamine , OR milrinone ). 
- If shock refractory to inotropes: Add a vasopressor (ideally norepinephrine ). 
Initial measures 
- 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 systems. 
- 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. 
- See “High-risk indications for mechanical ventilation” and “Hemodynamic compromise in mechanically ventilated patients.”
Diuretic therapy in acute heart failure
- Administer diuretics intravenously, if possible.
- Diuretic-naive patients: IV furosemide OR bumetanide 
- Patients already taking diuretics: Administer 1–2.5 times the patient's usual oral dose intravenously as a bolus or continuous infusion. 
Dosage adjustment: 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 :
- Refractory AHF (despite high doses of loop diuretics): Consider any of the following.
- Transition to oral diuretic: once the patient is euvolemic/at their baseline 
Use diuretics judiciously and assess volume status, electrolytes, and creatinine levels regularly to avoid overaggressive diuresis, as this may lead to hypotension, electrolyte imbalances, and/or a deterioration in renal function. 
- Monitor and (e.g., potassium, magnesium, sodium) every 12–24 hours.
- Monitor renal function (creatinine levels) at least once daily.
- Consider continuous cardiac monitoring.
Vasodilator therapy in acute heart failure
- Acute heart failure caused by hypertensive emergency (see “Treatment of hypertensive crises”) 
- Flash pulmonary edema
- Adjuvant to diuretics for symptomatic relief of dyspnea 
Treatment options 
- IV nitroglycerin 
- Sodium nitroprusside 
- If there are contraindications to nitroglycerin, consider nesiritide. 
For patients with hypertensive acute heart failure with pulmonary edema in the emergency department or prehospital setting, consider a single dose of sublingual nitroglycerine (i.e., nitroglycerine 0.4 mg sublingual once) while obtaining IV access and setting up an infusion. 
- Do not use vasodilators if SBP is < 90 mm Hg.
- Doses should be carefully titrated to prevent large drops in blood pressure. 
- Use with caution in patients with mitral or aortic stenosis. 
Complications and comorbidities
- Fluid restriction
- Diuretics, if signs of fluid overload are present
- Consider vasopressin antagonists (e.g., conivaptan, tolvaptan) in consultation with a specialist.
- See also “Hyponatremia.”
Consult cardiology early, as management can be complex.
- Patients with intractable ischemia or hemodynamic instability require immediate electrical cardioversion, see “Unstable tachycardia with pulse.” 
- If A-fib is thought to cause AHF : strategy (e.g., with amiodarone, anticoagulation, and elective cardioversion) is preferred.
- If A-fib is detected, but not thought to cause AHF : Either or strategy may be pursued.
- The majority of patients will require anticoagulation.
Patients presenting with acute heart failure are usually initially managed in the emergency department; most require subsequent hospitalization.
Hospital admission criteria 
Consider admission for patients with any of the following:
- De novo heart failure: for further evaluation and management
- Significant respiratory distress: i.e., dyspnea and/or tachypnea at rest
- Features of decreased cardiac output: e.g., altered mental status, renal impairment, hypotension
- Hemodynamically significant arrhythmia
- Acute coronary syndrome
- Comorbid conditions requiring treatment: e.g., persistent electrolyte abnormalities
- Weight gain of > 2.25 kg (> 5 lbs)
Discharge from the emergency department 
Discharge may be considered in selected patients with known CHF who have returned to their baseline status of health after initial management.
All patients 
- Perform ABCDE survey
- Provide supplemental O2 for hypoxia and consider upright positioning.
- Start continuous cardiac monitoring and pulse oximetry.
- Establish IV access and order laboratory studies (BNP/NT-proBNP, BMP, troponin, CBC).
- Obtain CXR or perform lung ultrasound.
- Obtain ECG.
- Arrange early TTE.
- Begin acute therapy for AHF according to hemodynamic stability.
- Identify and treat the underlying cause (e.g., ACS, hypertensive crisis, infection).
- Provide supportive care: e.g., fluid restriction, sodium restriction, VTE prophylaxis, discontinue/avoid any cardiotoxic medications
- Optimize once stable.
- Monitor daily weights, strict intake/output, serial electrolytes, renal function
- Identify and treat comorbidities/complications (e.g., A-fib with RVR, hyponatremia).
- Consult cardiology and nephrology for AHF refractory to standard therapy (e.g., for ultrafiltration)
Hemodynamically stable patients 
- Start furosemide) if there is pulmonary congestion. (e.g,
- Consider nitrates) (e.g.,
- Consider hospital admission.
Hemodynamically unstable patients 
- Urgently consult cardiology and critical care.
- Consider more aggressive respiratory support (e.g., HFNC, NIPPV, intubation and mechanical ventilation) for respiratory failure.
- Consider small fluid challenge for shock without pulmonary congestion
- Consider inotropic support (e.g., dobutamine) for shock with pulmonary congestion and/or shock refractory to fluids.
- Treat hypertensive crisis (flash pulmonary edema) with NIPPV and (e.g., nitrates).
- Consider invasive blood pressure monitoring.
- Consider urgent PCI.
- Admit to ICU/CCU.
- One-Minute Telegram 31-2021-3/3: Benefits to rehabilitation programs for older patients with heart failure?
- One-Minute Telegram 15-2020-4/4: Early IV nitrate treatment for acute heart failure: should we or shouldn’t we?
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