Acute heart failure

• Definition:
• Acute heart failure: rapid onset of new or worsening signs and symptoms of heart failure [1]
• Acute decompensated heart failure (ADHF): acute heart failure due to decompensation of preexisting disease/cardiomyopathy (most common) [1]
• De novo heart failure: acute heart failure occurring for the first time in a patient without known cardiomyopathy (∼15% of cases) [1][2]

Etiology:

Etiology of acute heart failure
Type of acute heart failure	Underlying etiology [1][3]
De novo heart failure	Acute myocardial dysfunction Cardiac ischemia due to acute coronary syndrome (ACS) Myocarditis Drug-induced cardiomyopathy  [4] Peripartum cardiomyopathy Thyroid storm Tachycardia-induced cardiomyopathy Takotsubo cardiomyopathy Acquired valvular pathology Acute mitral regurgitation after ACS  Bacterial endocarditis Nonbacterial thrombotic endocarditis Extracardiac pathologies that affect left ventricular output Pulmonary embolus Pericardial effusion causing tamponade Aortic dissection
ADHF	Uncontrolled and/or refractory hypertension (see “Hypertensive emergencies”) New/worsening cardiac ischemia Arrhythmias (e.g., atrial fibrillation with RVR, complete heart block) Serious infection/sepsis (e.g., pneumonia)  Drugs Nonadherence to heart failure medication  NSAID use Drugs with negative inotropic properties (e.g., nondihydropyridine CCBs) [2] Starting or uptitrating beta blockers  [5] Thiazolidinediones Recreational substance use, e.g., cocaine, alcohol, methamphetamines  Anemia Renal failure Volume overload, e.g., due to inappropriate fluid/salt intake or IV fluid therapy In 40–50% of cases, no trigger is found.

Pathophysiology:

Cardiac output, which is stroke volume times heart rate, is determined by three factors: preload, afterload, and ventricular contractility.

Underlying mechanism of reduced cardiac output 

• Heart failure with reduced ejection fraction (HFrEF)
  • Reduced contractility → systolic ventricular dysfunction → decreased left ventricular ejection fraction (LVEF) → decreased cardiac output
  • Causes include:
    • Damage and loss of myocytes (e.g., following myocardial infarction, coronary artery disease, dilated cardiomyopathy)
    • Cardiac arrhythmias
    • High-output conditions
• Heart failure with preserved ejection fraction (HFpEF)
  • Decreased ventricular compliance → diastolic ventricular dysfunction → reduced ventricular filling and increased diastolic pressure → decreased cardiac output (while the left ventricular ejection fraction remains normal) 
  • Causes include:
    • Increased stiffness of the ventricle (e.g., long-standing arterial hypertension with ventricular wall hypertrophy, restrictive cardiomyopathy)
    • Impaired relaxation of the ventricle (e.g., constrictive pericarditis, pericardial tamponade)
• Left-sided heart failure (HFrEF and/or HFpEF)
  • Increased left ventricular afterload: increased mean aortic pressure (e.g., arterial hypertension), outflow obstruction (e.g., aortic stenosis)
  • Increased left ventricular preload: left ventricular volume overload (e.g., backflow into the left ventricle caused by aortic insufficiency)
• Right-sided heart failure
• Increased right ventricular afterload: increase in pulmonary artery pressure (e.g., pulmonary hypertension)
• Increased right ventricular preload: right ventricular volume overload (e.g., tricuspid valve regurgitation, left-to-right shunt)

Clinical features:

Clinical features of acute heart failure are commonly classified according to perfusion and the presence of congestion at rest. [1][2][5]

Classification of acute heart failure [5][7]
	No evidence of congestion (∼5% of patients)	Evidence of congestion (∼95% of patients)
Adequate perfusion	Warm and dry	Warm and wet
Hypoperfusion	Cold and dry	Cold and wet

• Congestion (most common)  [1][5][7]
  • Clinical features of left heart failure
    • Acute dyspnea and orthopnea (i.e., worse when supine) 
    • Signs of increased work of breathing (WOB)
    • Cough (occasionally with frothy, blood-tinged sputum)
    • Coarse crackles/rales (and occasionally wheezing) on lung auscultation 
    • S3 gallop on heart auscultation
    • Severe cases: central cyanosis 
  • Clinical features of right heart failure
    • Jugular venous distention
    • Hepatojugular reflux
    • Peripheral edema
    • Ascites
  • Flash pulmonary edema: Typically manifests with hypertension, pulmonary congestion, and minimal peripheral edema 
• Hypoperfusion
  • Weakness, fatigue, altered mental status
  • Signs of poor peripheral perfusion (e.g., cold, clammy skin, peripheral cyanosis, skin mottling)
  • See also “Cardiogenic shock.”
• Blood pressure: may be low, normal, or elevated and should be interpreted in relation to the patient's baseline blood pressure

Diagnosis:

Approach

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.

Laboratory studies [9]

• BNP (or NT-proBNP): useful for diagnostic confirmation and prognostication; can be measured serially to guide therapy [10][11]
• 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  [9]

Natriuretic peptide levels in the diagnosis of heart failure  [12][7][13]
	Heart failure unlikely  [14]	Heart failure likely  [14]
BNP (pg/mL)	< 100  [12]	> 500
NT-proBNP (pg/mL)	< 300  [15]	> 1000  [13]

• Additional blood tests
  • Troponin: to rule out ACS  [16]
  • BMP  [5]
  • CBC  [17]
  • Liver chemistries  [18]
  • Consider thyroid function tests.  [5][9]

ECG

An ECG is indicated in all patients to assess for ACS, arrhythmias, and conduction abnormalities.

• ECG findings in acute heart failure are variable and may include: [5][7]
  • Acute ischemic changes due to ACS (see “Diagnosis of myocardial infarction”) 
  • Atrial fibrillation
  • Left ventricular hypertrophy
  • Bundle branch block
  • Nonspecific ST segment changes
  • Low voltage QRS  [19][20]
  • ECG findings may be normal.

Initial imaging

All patients with suspected acute heart failure should have a chest x-ray and echocardiography performed. 

Chest x-ray  [5][21]

• X-ray findings in pulmonary congestion
  • Enlarged heart shadow due to cardiomegaly and/or pericardial effusion [22]
  • 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  [23]
  • Cephalization: increased prominence of pulmonary vessels in the upper lobes of the lungs due to venous congestion [24]
  • Peribronchial cuffing

ABCDE: Alveolar edema (bat wings), Kerley B lines (interstitial edema), Cardiomegaly, Dilated prominent pulmonary vessels, and Effusions

Transthoracic echocardiogram (TTE) [5][25]

• Indications: all patients with suspected acute heart failure (imaging modality of choice)  [26]
• Characteristic echocardiographic findings of AHF
  • Reduced or normal LVEF  [27]
  • Diastolic dysfunction
  • Left atrial dilation, valvular disorders [25]
  • Pericardial effusion 
  • Right ventricular systolic dysfunction, increase in right ventricular systolic pressure
• Specific findings related to underlying etiology
  • Acute myocardial ischemia: regional wall motion abnormalities, papillary muscle rupture, mitral valve regurgitation, septal or ventricular free wall rupture [26]
  • Endocarditis: vegetation on the valve
  • See “Diagnostics” in “Pulmonary embolism.”
  • See “Diagnostics” in “Takotsubo cardiomyopathy.”

POCUS in acute heart failure

• Description: bedside ultrasound of the lung fields, inferior vena cava (IVC), and heart 
  • Can be used to assess volume status prior to and during treatment
  • Higher diagnostic accuracy than chest x-ray combined with NT-proBNP [28]
• Characteristic findings [29][30][31][32]
  • Lung fields
    • Pleural effusions 
    • ≥ 3 B lines in ≥ 2 bilateral lung zones suggest pulmonary edema   [33]
  • IVC ultrasound: diameter ≥ 2–2.5 cm, reduced IVC collapsibility   [31]
  • Heart 
    • Reduced systolic function in patients with HFrEF
    • Other: pericardial effusion, features suggestive of an underlying etiology (e.g., cardiac tamponade, right ventricular dilation in PE) [32]

Advanced imaging

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) [5]
  • May show evidence of fibrosis, cardiomyopathy, or perfusion defects
  • Can be used to assess LVEF
• Cardiac CT: assessment of coronary arteries (e.g., in suspected ischemic heart disease) and structural defects [5]
• Stress imaging  [26]
  • For suspected ischemic etiology or valvular pathology
  • Findings may include: wall motion abnormalities, reduced coronary flow, myocardial deformation, interstitial fluid
• Coronary angiography: to evaluate for ischemic cardiomyopathy [5]

Differential diagnoses:

• Acute coronary syndrome
• Pneumonia
• COPD, asthma
• Noncardiogenic pulmonary edema (e.g., ARDS)
• Pulmonary embolism
• Transfusion-related acute lung injury
• High altitude
• 
  

Management:

Initial management [7]

• 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 signs of end-organ hypoperfusion; respiratory distress can be present.
• Management: depends on the classification of AHF
  • No evidence of congestion (dry and warm): Optimize oral therapy.
  • Evidence of congestion (wet and warm)
    • Start initial measures for respiratory support in AHF (e.g., positioning, supplemental O2) as needed.
    • Start diuretic therapy for AHF if there is volume overload.
    • Consider vasodilators for AHF, e.g., nitrates.
  • Morphine is no longer routinely recommended.  [7][35]
• Next steps
  • 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.”

To remember the management of ADHF, think of “LMNOP”: Loop diuretics (furosemide), Modify medications, Nitrates, Oxygen if hypoxic, Position (with elevated upper body). [7][35]

For patients with ACS complicated by acute heart failure, consult cardiology for consideration of urgent coronary catheterization.

Hemodynamically unstable patients [36]

Early specialist consultation (e.g., critical care, cardiology) and admission to hospital is recommended.

• Clinical presentation: can vary
  • Cardiogenic shock: SBP < 90 mm Hg OR signs of end-organ hypoperfusion 
  • Hypertensive emergency: hypertension (e.g., SBP > 180 mm Hg) PLUS flash pulmonary edema and hypoxemic respiratory failure
• Management: depends on the classification of AHF (See also “Hemodynamic support for AHF” and “Management of cardiogenic shock.”)
  • Evidence of congestion with shock (wet and cold)
    • Prioritize respiratory support for AHF.
    • Consider inotropic support (e.g., dobutamine, norepinephrine).
  • Shock without evidence of congestion (dry and cold): Consider fluid challenge; add vasopressors and inotropes for shock refractory to fluids.
  • Hypertensive emergency with flash pulmonary edema (wet and warm)
    • Begin NIPPV and vasodilators for AHF.  [35][37][38]
    • Identify and treat the underlying trigger: e.g., poorly controlled hypertension, arrhythmias, acute coronary syndrome, valvular heart disease. [39][40]
• Next steps
  • Clinical improvement: Once stabilized, start diuretics for AHF, adjust CHF medication, and begin supportive care (see “Ongoing hospital management”).
  • Clinical deterioration: See “Treatment of refractory heart failure.”

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. [7]

If atrial fibrillation is thought to be causing hemodynamic or respiratory instability, consider immediate electric cardioversion.

Ongoing hospital management [7]

Supportive care

• Fluid restriction: 1.5–2 L/day [5]
• Sodium restriction: < 3 g/day [5]
• Discontinue/avoid any cardiotoxic medications (e.g., NSAIDs, morphine) [7][35]
• Identify and treat comorbidities (e.g., atrial fibrillation, pneumonia, COPD) and underlying triggers.
• VTE prophylaxis  [5][41]
• For large volume ascites, consider therapeutic paracentesis.  [7]

Optimizing chronic therapy for CHF [2][5][7]

• Administer beta blockers cautiously in beta-blocker-naive patients.
  • Start at a low dose (see “Medical treatment of heart failure for dosages”).
  • Administer only after stabilization (e.g., after volume status has been optimized and IV diuretics, vasodilators, and inotropic agents have been discontinued)  [7][35]
• Initiate, adjust, or continue medical treatment of heart failure as needed.
  • Patients already on a stable dose of beta blockers: Continue the same dosage.  [2]
  • 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.

Monitoring [2][5]

• 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.  [5][7][42]
• Consider invasive hemodynamic monitoring.
• POCUS can be used to monitor volume overload. [43]

Treatment of refractory acute heart failure [7]

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 [5]
• Mechanical circulatory support: indicated in reversible refractory acute heart failure [36][44]
  • ECMO is the most widely used form of mechanical support in acute heart failure.
  • Intra-aortic balloon pump and left ventricular assist device may be useful in certain etiologies, e.g., mitral regurgitation.
• Management of effusions: Consider therapeutic thoracentesis or pericardiocentesis as needed.

Haemodynamic support

Management depends on the classification of AHF. See “Management of cardiogenic shock” for details on therapeutic targets and monitoring.

Dry and cold AHF

• Assess fluid responsiveness: consider small fluid challenge  then reevaluate volume status. [35][36]
  • If fluid responsive: Consider repeating fluid challenge.
  • If signs of volume overload: Avoid fluids and optimize respiratory support for acute heart failure.
• If shock refractory to fluids: Start vasopressor (ideally norepinephrine). [7][36][45]
• If hypoperfusion persists despite fluids and vasopressor administration: Add inotropic support (e.g., dobutamine). [5][7]

Wet and cold AHF

• Begin with inotropic support (e.g., dobutamine, dopamine OR milrinone). [5]
• If shock refractory to inotropes: Add a vasopressor (ideally norepinephrine). [7][36][45]

Avoid inotropes in patients with left ventricular outflow tract obstruction (e.g., hypertrophic cardiomyopathy, aortic stenosis). [46]

Respiratory support

The cornerstones of respiratory support in acute heart failure are oxygen therapy and positive pressure ventilation, typically starting with the least invasive modality and escalating as needed. [7]

Initial measures

• Positioning: Ensure the patient is sitting upright.  [47]
• Supplemental oxygen: indicated for patients with an SpO2 < 90% or PaO2 < 60 mm Hg (see “Oxygen therapy”). 

Respiratory failure

• High-flow nasal cannula (HFNC): Consider in patients with an SpO2 < 90% non-responsive to basic oxygen delivery systems.  [48][49][50][51]
• NIPPV: for patients with respiratory distress despite supplemental oxygen [7]
  • BiPAP is preferred over CPAP.
  • Avoid in patients with isolated RV failure , severe hypotension  [52]
• Invasive mechanical ventilation
  • Indications
    • Hypoxemic respiratory failure unresponsive to NIPPV
    • Refractory hypoxemia (PaO2 < 60 mm Hg)
    • Hypercapnia (PaCO2 > 50 mm Hg)
    • Acidosis (pH < 7.35)
  • Intubation and mechanical ventilation in patients with acute heart failure can be challenging.  [7]
  • See “High-risk indications for mechanical ventilation” and “Hemodynamic compromise in mechanically ventilated patients.”

EPAP and/or PEEP should be used with caution in patients with hemodynamic compromise.

Pharmacotherapy

Diuretic therapy in acute heart failure

Initial treatment

• Administer diuretics intravenously, if possible.
• Diuretic-naive patients: IV furosemide OR bumetanide [53]
• Patients already taking diuretics: Administer 1–2.5 times the patient's usual oral dose intravenously as a bolus or continuous infusion.  [35][53]

Continuing treatment

• Dosage adjustment: Assess the effect of diuretics (e.g., urine output, symptoms) every 6 hours.  [54][55]
  • If urinary output is < 100 mL/hour : Consider doubling the diuretic dose. 
  • If urinary output is > 100–150 mL/hour :
    • For patients with continued congestion (e.g., pulmonary edema): Continue scheduled diuretic at the current dose.
    • For patients with no residual congestion: Consider less frequent dosing or transition to an oral diuretic.
• Refractory AHF (despite high doses of loop diuretics): Consider any of the following. 
  • Combination therapy with a thiazide diuretic, e.g., metolazone, hydrochlorothiazide, chlorothiazide [5][54]
  • Addition of a vasodilator for AHF [5]
  • Low-dose dopamine infusion  [5][56]
• Transition to oral diuretic: once the patient is euvolemic/at their baseline  [3]

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. [5][14]

Monitoring

• Monitor and replete serum electrolytes (e.g., potassium, magnesium, sodium) every 12–24 hours. 
• Monitor renal function (creatinine levels) at least once daily.
• Consider continuous cardiac monitoring.

Elevated creatinine is not a contraindication to diuretic therapy in patients with acute heart failure, as renal function typically improves with effective diuresis in cardiorenal syndrome. [5]

Vasodilator therapy in acute heart failure

Indications  [5][7]

• Acute heart failure caused by hypertensive emergency (see “Treatment of hypertensive crises”)  [7][57]
• Flash pulmonary edema 
• Adjuvant to diuretics for symptomatic relief of dyspnea [5]

Treatment options  [5]

• IV nitroglycerin [5]
• Sodium nitroprusside [5]
• If there are contraindications to nitroglycerin, consider nesiritide.[35]

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. [35]

Cautions

• Do not use vasodilators if SBP is < 90 mm Hg.
• Doses should be carefully titrated to prevent large drops in blood pressure. [58]
• Use with caution in patients with mitral or aortic stenosis. [59]

Avoid the use of vasodilators in patients with acute heart failure and hypotension.

Complications and comorbidities

Hyponatremia

• 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.”

Atrial fibrillation with RVR [60]

Consult cardiology early, as management can be complex.

• Patients with intractable ischemia or hemodynamic instability require immediate electrical cardioversion, see “Unstable tachycardia with pulse.”  [61]
• If A-fib is thought to cause AHF : Rhythm control strategy (e.g., with amiodarone, anticoagulation, and elective cardioversion) is preferred.
• If A-fib is detected, but not thought to cause AHF : Either rate control or rhythm control strategy may be pursued.
  • Rate control target heart rate < 120/minute
  • Digoxin is considered first-line. [35][62]
  • Consider cautious addition of a beta blocker (e.g., metoprolol). [60]
  • Avoid calcium channel blockers unless systolic function is preserved (e.g., HFpEF).
• The majority of patients will require anticoagulation.

Cardiorenal syndrome

Cardiorenal syndrome causes prerenal acute kidney injury with hypervolemia. Management is complex and involves early nephrology input, fluid restriction, and diuretics (see “Hemodynamic support in patients with AKI”).

• Patients with reduced eGFR may require higher initial doses of diuretic therapy. [54]
• Ultrafiltration may be necessary.  [63]

Disposition

Patients presenting with acute heart failure are usually initially managed in the emergency department; most require subsequent hospitalization.

Hospital admission criteria [2][8][35]

Consider admission for patients with any of the following:

• De novo heart failure: for further evaluation and management
• ADHF with:
  • 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)

Consider ICU admission for patients at high risk of deterioration, and/or patients with hemodynamic instability and/or respiratory failure requiring aggressive support. [8]

Discharge from the emergency department [2][8][35]

Discharge may be considered in selected patients with known CHF who have returned to their baseline status of health after initial management.

• Optimize medical therapy for chronic heart failure.
• Ensure close outpatient follow-up (typically within 1 week).
• Educate patients on medication adherence, fluid and salt restriction, self-monitoring, and symptom recognition (see “General measures” in “Treatment of heart failure”).

Summary:

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.

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Acknowledgement: AMBOSS