Acute Heart Failure

Rapid onset or worsening of heart failure symptoms/signs requiring urgent evaluation and treatment, resulting from acute cardiac dysfunction (systolic or diastolic) causing inadequate cardiac output and/or congestion. May represent de novo heart failure or acute decompensation of chronic heart failure (more common).

Classified by hemodynamic profile (perfusion and congestion status):

• Warm-wet (most common): adequately perfused, congested, pulmonary edema, peripheral edema
• Cold-wet: poorly perfused AND congested, cardiogenic shock with congestion, high mortality
• Warm-dry: adequately perfused, not congested, compensated
• Cold-dry: poorly perfused, not congested, hypoperfusion without overload

Common precipitants: medication/dietary non-adherence, acute MI/ischemia, arrhythmia (especially new-onset AF), infection, uncontrolled hypertension, valvular deterioration, renal failure, NSAID use, anemia, thyrotoxicosis, pulmonary embolism.

• Dyspnea (exertional progressing to at rest), orthopnea, paroxysmal nocturnal dyspnea
• Fatigue, reduced exercise tolerance
• Peripheral edema (ankles, sacral), abdominal distension/discomfort (hepatic congestion, ascites)
• Examination: raised JVP, bibasal crackles, S3 gallop, peripheral edema, tachycardia, tachypnea, cool peripheries if poor perfusion, hepatomegaly, displaced apex beat
• Signs of poor perfusion (cardiogenic shock spectrum): hypotension, cold/clammy extremities, prolonged capillary refill, reduced urine output, altered mental status, narrow pulse pressure
• Acute pulmonary edema presentation: severe breathlessness, frothy pink sputum, anxiety/agitation, use of accessory muscles, unable to lie flat

• Natriuretic peptides (BNP/NT-proBNP): elevated supports diagnosis (high negative predictive value if normal/low, helps exclude HF as cause of dyspnea); interpret with caution in renal impairment (falsely elevated) and obesity (falsely low)
• CXR: cardiomegaly, upper lobe diversion, Kerley B lines, bilateral perihilar/interstitial infiltrates, pleural effusion
• ECG: assess for precipitating ischemia, arrhythmia (especially new AF), evidence of prior MI, LVH
• Echocardiography: assess LV/RV function (ejection fraction (distinguishes HFrEF from HFpEF), valvular pathology, wall motion abnormalities) should be performed promptly (within 48h) in new presentations
• Bloods: FBC, U&E/creatinine (renal function, guides diuretic dosing), LFTs, troponin (exclude ACS as precipitant), TSH, glucose
• Lung ultrasound: B-lines indicate pulmonary congestion, rapid and repeatable at bedside

Differentials: COPD/asthma exacerbation (can coexist), pneumonia, pulmonary embolism, ARDS from other cause, renal failure with fluid overload.

Immediate (acute pulmonary edema/severe presentation):

• Sit patient upright (reduces preload, improves ventilation mechanics)
• Oxygen: titrate to SpO2 94-98% (88-92% if COPD/CO2 retention risk)
• Non-invasive ventilation (CPAP): for respiratory distress not responding to initial medical therapy, reduces preload/afterload, improves oxygenation, reduces need for intubation
• IV diuretics: furosemide 40-80mg IV bolus (higher dose if already on chronic diuretic therapy, typically 2.5x usual oral dose IV, or continuous infusion for refractory cases), reassess response within 1-2 hours
• IV vasodilators (if SBP >90-100mmHg): GTN infusion, titrate to symptom relief and BP tolerance, particularly beneficial in hypertensive acute heart failure
• Avoid routine opioids: associated with worse outcomes and respiratory depression risk
• Treat precipitant concurrently

If hypotensive/cardiogenic shock (cold profile):

• Avoid vasodilators/high-dose diuretics until perfusion addressed
• Inotropic support: dobutamine infusion, or milrinone (if on beta-blocker)
• Vasopressor (noradrenaline) if concurrent hypotension with hypoperfusion
• Consider mechanical circulatory support (IABP, ECMO, Impella) for refractory cardiogenic shock
• Urgent cardiology involvement: identify reversible cause

Arrhythmia-driven decompensation:

• New-onset AF with rapid ventricular response: rate control (digoxin preferred if hemodynamically compromised; amiodarone if rhythm control needed), synchronized cardioversion if unstable
• Bradyarrhythmia causing decompensation: atropine, temporary pacing if needed

Once stabilized, optimize guideline-directed medical therapy (HFrEF):

• ACE inhibitor/ARB or ARNI (sacubitril-valsartan), beta-blocker (start low once euvolemic and stable, do not initiate during acute decompensation), mineralocorticoid receptor antagonist, SGLT2 inhibitor, the "four pillars", sequenced/overlapped per current guidelines
• Fluid/sodium restriction, daily weight monitoring, diuretic dose titration for discharge

Discharge planning: ensure euvolemic, stable on oral diuretics, medication optimization initiated, weight/symptom monitoring education, early follow-up within 1-2 weeks, heart failure specialist nurse/clinic referral.

Referral: cardiology for all new-onset heart failure, cardiogenic shock (ICU + cardiology), device therapy assessment (ICD/CRT) once optimized and EF reassessed at 3 months.