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Rapid Review·Cardiovascular

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Heart Failure

T2High yield

Acute Decompensated Heart Failure

Focus on

Acute worsening of known or new heart failure, usually triggered by missed medication. Decide stability first (respiratory failure gets positive-pressure ventilation, shock gets inotropes), decongest with an intravenous loop diuretic, add nitroglycerin when the diuretic is not enough or the patient is hypertensive, and find the trigger with an ECG, troponin and echo.

Key takeaways

What it is and what triggers it

Acute decompensated heart failure (ADHF)

acute worsening of new or pre-existing heart failure.

Medication non-adherence

the most common cause of hospitalization; dietary indiscretion is the other everyday trigger.

Other precipitants

infection, trauma or surgery, ischemia, and arrhythmias.

Drugs

non-steroidal anti-inflammatory drugs (NSAIDs), negative inotropes such as non-dihydropyridine calcium-channel blockers, thiazolidinediones, and cocaine, alcohol or methamphetamine.

Clinical features

Symptoms

acute dyspnea, orthopnea and paroxysmal nocturnal dyspnea, with progressive exercise intolerance and weight gain.

Signs of distress

accessory muscle use, tachycardia, tachypnea, diffuse crackles, and sometimes wheeze (cardiac asthma).

Signs of congestion

an S3, jugular venous distension and peripheral edema.

Blood pressure

hypertension is common; hypotension means severe disease.

Diagnosis

The diagnosis is clinical

dyspnea plus the examination, supported by tests.

B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP)

separates a heart failure exacerbation from other causes of dyspnea; a BNP over 400 makes heart failure likely.
Cardiogenic pulmonary edema on a frontal chest film: an enlarged heart shadow, prominent pulmonary vessels and hazy perihilar alveolar edema spreading out from both hila (the bat-wing pattern), with basal interstitial edema.
What this shows
Cardiogenic pulmonary edema on a frontal chest film: an enlarged heart shadow, prominent pulmonary vessels and hazy perihilar alveolar edema spreading out from both hila (the bat-wing pattern), with basal interstitial edema.

Chest radiograph in cardiogenic pulmonary edema

the classic film.
  • Cardiomegaly or an enlarged heart shadow.
  • Prominent pulmonary vessels with perihilar "bat wing" alveolar edema.
  • Basal interstitial edema, Kerley B (septal) lines, and pleural effusions.
  • Slowly progressive decompensation may show little or no pulmonary edema.

After stabilization

a transthoracic echocardiogram evaluates ventricular and valvular function when the cause is unclear.
  • Significant systolic dysfunction then gets a stress test or coronary angiography for ischemic cardiomyopathy.

Management: stability first

Initial management of acute decompensated heart failure, three tracks in parallel. Evaluate clinical stability (respiratory failure: supplemental oxygen, NIPPV, intubation; cardiogenic shock: inotropes such as dobutamine or milrinone). Improve symptoms by reducing preload (IV diuretics such as furosemide, with or without a vasodilator such as nitroglycerin; a balanced vasodilator such as nitroprusside if afterload reduction is also needed). Investigate the precipitating factors (ECG and troponin for ischemia or arrhythmia, bedside echo for valve dysfunction). Stabilize oxygenation and perfusion, remove congestion, and identify the precipitating problem in parallel.
What this shows
Initial management of acute decompensated heart failure, three tracks in parallel. Evaluate clinical stability (respiratory failure: supplemental oxygen, NIPPV, intubation; cardiogenic shock: inotropes such as dobutamine or milrinone). Improve symptoms by reducing preload (IV diuretics such as furosemide, with or without a vasodilator such as nitroglycerin; a balanced vasodilator such as nitroprusside if afterload reduction is also needed). Investigate the precipitating factors (ECG and troponin for ischemia or arrhythmia, bedside echo for valve dysfunction). Stabilize oxygenation and perfusion, remove congestion, and identify the precipitating problem in parallel.

Follow the pathway

stabilize, decongest, and find the cause in parallel.
Non-invasive positive-pressure ventilation through a tight full-face mask: it pushes fluid out of the alveoli and lowers preload and afterload, which is why it treats acute pulmonary edema rather than only supporting breathing.
What this shows
Non-invasive positive-pressure ventilation through a tight full-face mask: it pushes fluid out of the alveoli and lowers preload and afterload, which is why it treats acute pulmonary edema rather than only supporting breathing.

Respiratory failure

supplemental oxygen with non-invasive positive-pressure ventilation (NIPPV) first.
  • Intubate if the patient worsens on it or is unconscious.
  • Positive-pressure ventilation is a treatment in its own right for acute pulmonary edema, not just support.

Cardiogenic shock

systolic blood pressure under 90 mm Hg or end-organ hypoperfusion.
  • Wet and cold: respiratory support plus an inotrope (dobutamine or milrinone, norepinephrine if needed).
  • Dry and cold: a fluid challenge first, then vasopressors and inotropes if refractory.

Management: relieve congestion, then the admission

First line is an intravenous (IV) loop diuretic

furosemide at about 2.5 times the home oral dose.
  • Monitor potassium, creatinine and blood pressure.

Add IV nitroglycerin

a venodilator that lowers preload and filling pressures, when the response to the diuretic is inadequate.

Avoid vasodilators in a hypotensive patient

and reserve inotropes for cardiogenic shock.

Investigate the cause

electrocardiogram (ECG) and troponin for ischemia or arrhythmia, then echocardiography.

Start or continue a sodium-glucose cotransporter-2 (SGLT2) inhibitor

in every hemodynamically stable patient.

Restart the beta blocker only after stabilization

at a low dose.
A patient with known heart failure arrives with a blood pressure of 210/120, severe dyspnea and diffuse crackles after missing medications for a week. What is the first drug, and what supports breathing?

Flash pulmonary edema from a hypertensive emergency, so IV nitroglycerin comes first (before or instead of the loop diuretic), with NIPPV for respiratory failure; positive pressure itself treats the pulmonary edema. Missed medication is the most common trigger.

How it's tested

A man with known heart failure stops his furosemide, and arrives with orthopnea, crackles and a BNP of 900: acute decompensated heart failure from non-adherence; IV furosemide, then find out why he stopped.

Blood pressure 210/120, sudden respiratory distress and pink frothy sputum: flash pulmonary edema in a hypertensive emergency; non-invasive ventilation and IV nitroglycerin come first, with the diuretic.

Cool extremities, blood pressure 78/50, oliguria and pulmonary congestion: wet and cold cardiogenic shock; respiratory support and an inotrope (dobutamine or milrinone), not a vasodilator.

Decompensated patient on carvedilol asks when it restarts: after stabilization, at a low dose.

Go deeper

Related Step 2 pages: Heart Failure, Cardiogenic Shock

High-yield images3
Initial management of acute decompensated heart failure, three tracks in parallel. Evaluate clinical stability (respiratory failure: supplemental oxygen, NIPPV, intubation; cardiogenic shock: inotropes such as dobutamine or milrinone). Improve symptoms by reducing preload (IV diuretics such as furosemide, with or without a vasodilator such as nitroglycerin; a balanced vasodilator such as nitroprusside if afterload reduction is also needed). Investigate the precipitating factors (ECG and troponin for ischemia or arrhythmia, bedside echo for valve dysfunction). Stabilize oxygenation and perfusion, remove congestion, and identify the precipitating problem in parallel.
Cardiogenic pulmonary edema on a frontal chest film: an enlarged heart shadow, prominent pulmonary vessels and hazy perihilar alveolar edema spreading out from both hila (the bat-wing pattern), with basal interstitial edema.
Non-invasive positive-pressure ventilation through a tight full-face mask: it pushes fluid out of the alveoli and lowers preload and afterload, which is why it treats acute pulmonary edema rather than only supporting breathing.
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