Acute Decompensated Heart Failure
Cardiology
Illness script · Cardiology
Acute Decompensated Heart Failure
Sudden worsening of HF symptoms causing fluid overload and/or low cardiac output requiring urgent hospitalization.
This illness script for Acute Decompensated Heart Failure covers predisposing factors, classic presentation, mechanism, workup, management, and the clinical pivots that separate it from look-alikes—written for USMLE Step 1 and clerkship reasoning.
01
Predisposing factors
- Most common cause of hospitalization in adults >65 years
- Underlying HFrEF (EF <40%) or HFpEF (EF ≥50%, hypertension-driven)
- Key precipitants: medication/dietary nonadherence, ACS, AF, infection, uncontrolled HTN
- Other triggers: new nephrotoxins (NSAIDs), anemia, thyroid disease
- Risk factors: HTN, CAD, DM, obesity, prior HF, valvular disease
02
Presentation
- Acute dyspnea (orthopnea, PND) ± frothy pink sputum in flash pulmonary edema
- Bilateral crackles, S3 gallop, JVD, pitting edema — classic exam triad of overload
- Hepatojugular reflux positive; displaced PMI suggests dilated cardiomyopathy
- Weight gain >2 kg over days is a sensitive early sign
- Cold/clammy extremities + hypotension = cardiogenic shock (low-output state)
- Bendopnea (dyspnea bending forward) specific for elevated filling pressures
03
Pathophysiology
- ↑ ventricular filling pressures → pulmonary venous congestion → pulmonary edema
- Reduced CO activates RAAS and SNS → Na/water retention → worsening congestion
- Neurohormonal activation (↑ BNP, ↑ norepinephrine) is both marker and driver of decompensation
- Cardiorenal syndrome: ↓ renal perfusion compounds fluid retention
04
Diagnostics
- CXR first-line: pulmonary vascular congestion, Kerley B lines, cardiomegaly, pleural effusions
- BNP >400 pg/mL (NT-proBNP >1000) strongly supports HF vs. pulmonary cause of dyspnea
- BNP 100–400: intermediate — consider PE, cor pulmonale, renal failure
- Echo: confirms EF, wall motion, valvular pathology — defines HFrEF vs. HFpEF
- ECG + troponin to exclude ACS as precipitant; BMP for renal function/electrolytes
05
Management
- IV loop diuretics (furosemide) first-line: IV dose = 2.5× home oral dose if on chronic therapy
- IV nitroglycerin for afterload/preload reduction in hypertensive pulmonary edema
- Non-invasive ventilation (BiPAP/CPAP) for refractory hypoxia — reduces intubation rates
- Hold/down-titrate beta-blockers during acute decompensation; restart before discharge
- Cardiogenic shock: IV inotropes (dobutamine) ± vasopressors; consider IABP/LVAD
- Identify and treat precipitant (rate-control AF, revascularize if ACS, antibiotics if sepsis)
06
Clinical pivots
How to separate this script from the look-alikes that show up on exams and on the wards.
Pneumonia / ARDS
BNP normal/low; fever + productive cough; CXR infiltrates non-gravity-dependent; no JVD or S3
COPD/Asthma Exacerbation
Expiratory wheeze, barrel chest, no JVD; CXR hyperinflation; BNP normal; responds to bronchodilators
Pulmonary Embolism
Acute RV strain on ECG (S1Q3T3); BNP mildly elevated; CXR often clear; CT-PA diagnostic
Cardiac Tamponade
Beck's triad (hypotension, JVD, muffled hearts); pulsus paradoxus; echo shows pericardial effusion + RV collapse
Keep reading
Full library- Acute Compartment SyndromeElevated pressure within a closed fascial compartment compromises perfusion, causing ischemia and irreversible muscle/nerve damage if untreated.
- Acute Kidney InjuryAbrupt decline in renal function (↑Cr ≥0.3 mg/dL in 48h or ≥1.5× baseline in 7d) causing azotemia and fluid/electrolyte dysregulation.
Educational use only. This illness script is a study framework, not medical advice. Confirm decisions with current guidelines and your clinical supervisors.