Acute heart failure

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.

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][6]
	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]
  • Clinical features of left heart failure
    • 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
  • Clinical features of right heart failure: 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.”

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).

Laboratory studies ^[7]

• ↑ 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 ^[7]
  • See “Diagnostics” in “Congestive heart failure.”
• To evaluate for underlying cause/severity
  • Troponin: to rule out ACS ^[5]
  • BMP and serum electrolytes
  • CBC ^[8]
  • Consider also: liver function tests, thyroid function tests ^[5][7]

Measuring BNP (or NT-proBNP) is especially helpful in patients with unclear diagnosis. BNP has a high diagnostic value when combined with physical examination and imaging.

ECG

Indicated in all patients to exclude ACS. Findings are variable and may include: ^[5][6]

• 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 ^[9][10]
• ECG findings may be normal.

Initial imaging

All patients with suspected acute heart failure should have a CXR and echocardiography performed.

CXR ^[5][11]

• X-ray findings in pulmonary congestion
  • Cardiomegaly
  • 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 ^[12]
  • Cephalization: increased prominence of pulmonary vessels in the upper lobes of the lungs due to venous congestion ^[13]
  • Peribronchial cuffing

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

Transthoracic echocardiogram (TTE) ^[5][14]

• Indications: all patients with suspected acute heart failure (imaging modality of choice) ^[15]
• Characteristic findings
  • Reduced or normal LVEF ^[16]
  • Diastolic dysfunction
  • Left atrial dilation, valvular disorders ^[14]
  • 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 ^[15]
  • 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, 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 ^[17]
• Characteristic findings ^{[18][19][20][21]}
  • Lung fields
    • Pleural effusions
    • ≥ 3 B lines in ≥ 2 bilateral lung zones suggest pulmonary edema.
  • IVC: diameter ≥ 2 cm, collapsibility of < 50% ^[20]
  • Heart
    • Reduced global systolic function
    • Other: pericardial effusion, features suggestive of an underlying etiology (e.g., cardiac tamponade, right ventricular dilation in PE) ^[21]

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 ^[15]
  • For suspected ischemic etiology or valvular pathology
  • Findings may include: wall motion abnormalities, reduced coronary flow, myocardial deformation, interstitial fluid

Approach ^[6]

• Assess patients for signs of cardiogenic shock or respiratory failure.
  • Cardiogenic shock: usually require inotropic and/or vasopressor support (see “Management of cardiogenic shock”).
  • Respiratory failure: supplemental oxygen and ventilatory support (see “Respiratory support in acute heart failure”)
• Stable patients: Use clinical features to guide treatment (see “Classification of acute heart failure”).
  • Patients classified as dry may require judicious intravenous fluid therapy.
  • Patients classified as wet will need diuretics for volume overload and, depending on symptoms, vasodilator therapy.
• All patients: Identify and treat the underlying cause.

Hemodynamically unstable patients (i.e., cardiogenic shock)

Management of cardiogenic shock [22][6]
	Treatment
Dry and cold	Consider an initial small fluid bolus (250–500 mL) [23][22] Assess fluid responsiveness; consider additional bolus if fluid responsive. [24] Reassess for volume overload If shock persists, start a vasopressor, ideally, norepinephrine. [22][6][25] Administer inotropic support if hypoperfusion persists despite fluids and vasopressors [5] Dobutamine [5] Dopamine [5] Milrinone [5]
Wet and cold	Administer inotropic support. If shock persists, start a vasopressor (ideally, norepinephrine ) [22][6][25] Once systolic BP is > 90 mm Hg, start diuretics (see “Diuretic therapy in acute heart failure”). If symptoms persist, see the section on “Refractory acute heart failure.”

Avoid inotropes in patients with left ventricular outflow tract obstruction (e.g., hypertrophic cardiomyopathy, aortic stenosis). ^[26]

Hemodynamically stable patients

Management of hemodynamically stable patients with acute heart failure [6]
	Treatment
Dry and warm	Optimize oral therapy.
Wet and warm	Start diuretics for volume overload (see “Diuretic therapy in acute heart failure”). Consider a vasodilator (see “Vasodilator therapy in acute heart failure”). If symptoms persist, see the section on “Refractory acute heart failure.”
Wet and cold (if SBP is > 90 mm Hg)

Respiratory support in acute heart failure ^[6]

• Positioning: : Ensure the patient is sitting upright. ^[27]
• 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. ^{[28][29][30][31]}
• NIPPV: for patients with respiratory distress despite supplemental oxygen ^[6]
  • BiPAP is preferred over CPAP.
  • Avoid in patients with isolated RV failure , severe hypotension ^[32]
• 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. ^[6]
    • 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.

Diuretic therapy in acute heart failure

• Initial treatment: Diuretics should administered intravenously (if possible).
  • Diuretic-naive patients: IV furosemide or bumetanide ^[33]
  • Patients already taking diuretics: Administer 1–2.5 times the patient's usual oral dose intravenously as a bolus or continuous infusion. ^[23][33]
• Continuing treatment
  • Assess the effect of diuretics (e.g., urine output, symptoms) every 6 hours. ^[34][35]
    • 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 duiretic at current dose.
      • For patients with no residual congestion: Consider less frequent dosing or transition to oral diuretic.
  • Options for refractory congestion despite high doses of loop diuretics:
    • Combination therapy with a thiazide diuretic, e.g., metolazone , hydrochlorothiazide , chlorothiazide ^[5][34]
    • Addition of a vasodilator (see below) ^[5]
    • Low-dose dopamine infusion (see “Management of cardiogenic shock”) ^[5]
• Monitoring
  • Monitor and replete serum electrolytes (potassium, magnesium, sodium) every 12–24 hours (see “Electrolye repletion”).
  • Monitor urine function (creatinine) at least daily. ^[5]
  • Consider continuous cardiac monitoring.
• Transition to oral diuretic: Once the patient is euvolemic/at their baseline. ^[3]

Vasodilator therapy in acute heart failure ^[5][6]

• Indications
  • Acute heart failure caused by hypertensive emergency (see “Treatment of hypertensive crises”) ^[36][6]
  • Flash pulmonary edema
  • Adjuvant to diuretics for symptomatic relief of dyspnea ^[5]
• Treatment options
  • IV nitroglycerin ^[5]
  • Sodium nitroprusside
  • If there are contraindications to nitroglycerin, consider nesiritide. ^[23]
• Cautions
  • Do not use vasodilators if SBP is < 90 mm Hg
  • Doses should be carefully titrated to prevent large drops in blood pressure. ^[37]
  • Use with caution in patients with mitral or aortic stenosis. ^[38]

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

Treatment of refractory acute heart failure

• Ultrafiltration (e.g., hemodialysis): indicated in congestion with no response to medical therapy ^[5]
• Mechanical circulatory support: indicated in reversible refractory acute heart failure ^[22][39]
  • 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.

To remember the management of ADHF, think of “LMNOP”: Loop diuretics (furosemide), Modify medications, Nitrates, Oxygen if hypoxic, Position (with elevated upper body). ^[23][6]

Ongoing hospital management

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) ^[23][6]
• Identify and treat comorbidities (e.g., atrial fibrillation, pneumonia, COPD)
• VTE prophylaxis ^[5][40]
• For large volume ascites, consider therapeutic paracentesis. ^[6]

Optimization of medical therapy for chronic heart failure ^[5][2][6]

• Beta blockers
  • Patients previously on a stable dose of beta blockers should continue them. ^[2]
  • 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) ^[23][6]
    • Metoprolol ^[5]
    • Carvedilol ^[5]
    • Bisoprolol ^[5]
• Other medications
  • Patients should continue all other heart failure medications, unless there is:
    • 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.
  • 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

• Hyponatremia
  • Fluid restriction
  • Consider vasopressin antagonists (e.g., conivaptan, tolvaptan)
  • See also “Hyponatremia.”
• Atrial fibrillation with rapid ventricular response ^[41]
  • Management is complex; consult early with cardiology.
  • Rate control is typically preferred strategy in the acute setting
    • Target heart rate < 120/minute
    • Digoxin is considered first-line ^[23][42]
    • Consider cautious addition of beta blocker (e.g., metoprolol ) ^[41]
    • Avoid calcium channel blockers unless systolic function is preserved (e.g., HFpEF)
  • 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”)
  • Patients with reduced eGFR may require higher initial doses of diuretic therapy. ^[34]
  • Ultrafiltration may be necessary. ^[43]

Monitoring ^[5][2]

• Daily weights, intake/output monitoring
• Renal function, electrolyte monitoring every 12–24 hours (see “Diuretic therapy in acute heart failure”)
• Consider serial BNP or NT-proBNP measurement. ^[5][6][44]
• POCUS can be used to monitor volume overload. ^[45]