Preparatory Mindset
Heart failure is a clinical syndrome in which the heart cannot pump enough blood to meet metabolic demands — not a single diagnosis but a final common pathway of cardiac disease (most commonly CAD → MI → systolic HF). It affects millions worldwide with a poor prognosis (~50% 5-year mortality). The exam approach: (1) classify by ejection fraction (HFrEF vs HFmrEF vs HFpEF) and by side (left vs right), (2) recognise the compensatory mechanisms (Frank-Starling, sympathetic, RAAS) that initially help but ultimately harm, and (3) master GDMT (neurohormonal blockade: ACEi/ARB/ARNi + β-blocker + MRA + SGLT2i) for HFrEF, plus device therapy (ICD/CRT) and acute decompensation management. LMCHK candidates must also know the HKHA Handbook's LVEF classification cut-offs, natriuretic-peptide rule-out values, and the acute pulmonary oedema treatment algorithm.
Core Concepts
Classification by ejection fraction
| Category | LVEF | Characteristics |
|---|---|---|
| HFrEF (reduced) | ≤40% | Systolic dysfunction, dilated LV (post-MI classic) |
| HFmrEF (mildly reduced) | 41–49% | Borderline |
| HFpEF (preserved) | ≥50% | Diastolic dysfunction, stiff LV (hypertension, ageing, obesity) |
| HFimpEF (improved) | Previous ≤40%, now >40% | Recovered function |
Clinical presentation (left vs right)
- Left-sided HF → pulmonary congestion: dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea (PND), fatigue, pulmonary oedema, crackles, displaced PMI, S3 gallop.
- Right-sided HF → systemic congestion: JVD, peripheral/pedal oedema, ascites, hepatomegaly, hepatojugular reflux.
- NYHA class: I (no limitation) → IV (symptoms at rest) — functional classification for symptom severity (complements EF-based classification).
Compensatory mechanisms (initially helpful, eventually harmful)
- Frank-Starling: ↑ preload → ↑ contractility → eventually pulmonary congestion.
- Sympathetic activation: ↑ HR, ↑ contractility → ↑ O₂ demand, arrhythmias.
- RAAS activation: ↑ volume, ↑ vasoconstriction → ↑ afterload, fibrosis (remodelling).
- This is why neurohormonal blockade (not inotropes) is the cornerstone of chronic therapy.
Investigations
- Bloods: CBC, LFT, RFT, clotting, TFT, cardiac biomarkers (troponin, CK), iron profile.
- Natriuretic peptides (BNP/NT-proBNP): BNP <35 pg/mL or NT-proBNP <125 pg/mL → HF unlikely (rule-out).
- ECG, CXR (cardiomegaly, pulmonary congestion), echocardiography (EF — the single most important prognostic marker).
- Selected: CMR (infiltrative/cardiomyopathy), CTCA/stress imaging (CAD), cardiopulmonary exercise test (transplant/MCS evaluation), right heart catheterisation, endomyocardial biopsy (rapidly progressive HF of unknown cause), coronary angiography, genetic testing.
Pharmacotherapy (chronic HFrEF — GDMT)
| Drug class | Mechanism | Outcome benefit |
|---|---|---|
| ACEi / ARB / ARNi | Block RAAS (ARNi = sacubitril-valsartan; needs ≥36 h washout after ACEi to avoid angioedema) | ↓ Mortality, ↓ Hospitalisation |
| β-blocker (bisoprolol, carvedilol, metoprolol succinate) | ↓ Sympathetic tone | ↓ Mortality, ↓ Sudden death |
| MRA (spironolactone/eplerenone) | Block aldosterone | ↓ Mortality in HFrEF |
| SGLT2i (dapagliflozin, empagliflozin) | ↓ Glucose reabsorption (benefit independent of diabetes) | ↓ HF hospitalisation, ↓ Mortality |
| Loop diuretics (furosemide) | ↓ Volume overload | Symptom relief (no mortality benefit) |
| Digoxin | ↑ Inotropy | ↓ Hospitalisation (no mortality benefit) |
Additional therapies once GDMT optimised: ivabradine (NYHA II-III, sinus rhythm, HR ≥70 on max β-blocker), vericiguat (NYHA II-IV, LVEF <45%, recent HF hospitalisation), ferric carboxymaltose (iron deficiency), AF ablation (tachycardia-induced cardiomyopathy).
Device therapy
- ICD: primary prevention — ischemic/non-ischemic cardiomyopathy, LVEF ≤35%, NYHA I-III, expected survival >1 year.
- CRT-D: NYHA II-III, LVEF ≤35%, sinus rhythm with QRS ≥150 ms (or LBBB 130–149 ms).
- Advanced HF: heart transplantation, mechanical circulatory support (MCS).
HFmrEF / HFpEF management
- Diuretics for volume overload + SGLT2i; consider ACEi/ARB/ARNi, MRA; treat underlying aetiologies (hypertension, ischaemia, obesity, AF).
Acute decompensation / Acute pulmonary oedema (APO)
- General: bed rest/prop-up, high-flow O₂, low-salt diet + fluid restriction (NPO if very ill), identify and treat precipitants (arrhythmia, IHD, uncontrolled hypertension, chest infection).
- If BP stable: frusemide (Lasix) 40–120 mg IV, IV nitrate (GTN 1 μg/kg/min), morphine 2–5 mg slow IV (cautious).
- If refractory: inotropes — dopamine 2.5–10 μg/kg/min, dobutamine 2.5–15 μg/kg/min; monitor BP/P, I/O, SaO₂, CVP, RR every 30–60 min.
- Ventilatory support for desaturation/exhaustion/cardiogenic shock: NIV (BIPAP/CPAP) or intubation + mechanical ventilation.
- If still unstable: mechanical circulatory support, PCI for ischaemic cause, intervention for significant valvular lesion.
HKHA Handbook (LMCHK) — Key Points
- LVEF classification (HA standard): HFrEF ≤40%; HFimpEF (previous ≤40% → >40%); HFmrEF 41–49%; HFpEF ≥50% + evidence of raised LV filling pressures (elevated natriuretic peptide or haemodynamic measurement).
- Natriuretic-peptide rule-out: BNP <35 pg/mL or NT-proBNP <125 pg/mL → HF unlikely.
- HFrEF GDMT (HA): ACEi/ARB/ARNi + β-blocker (bisoprolol/carvedilol/metoprolol succinate) + MRA + SGLT2i, titrated to target dose as tolerated — with the ARNi 36-hour ACEi washout warning.
- Post-GDMT add-ons: ivabradine (HR ≥70 sinus rhythm), vericiguat (LVEF <45%, recent HF hospitalisation), digoxin (symptomatic), ferric carboxymaltose (iron deficiency), AF ablation.
- Devices (HA criteria): ICD — LVEF ≤35%, NYHA I-III, >1-yr survival; CRT-D — LVEF ≤35%, sinus rhythm, QRS ≥150 ms (or LBBB 130–149 ms).
- HFpEF/HFmrEF: diuretics + SGLT2i; consider ACEi/ARB/ARNi/MRA; treat underlying causes.
- APO acute management (HA algorithm): frusemide 40–120 mg IV + IV GTN 1 μg/kg/min + morphine 2–5 mg slow IV (BP stable); inotropes (dopamine/dobutamine) if not stabilised; NIV (BIPAP/CPAP) or intubation for respiratory failure; MCS/PCI for refractory ischaemic cause.
High-Yield Points
- EF cut-offs: HFrEF ≤40%, HFmrEF 41–49%, HFpEF ≥50%.
- Left HF → pulmonary congestion; Right HF → systemic congestion.
- Compensatory mechanisms (Frank-Starling, sympathetic, RAAS) eventually harm → treat with neurohormonal blockade.
- GDMT = ACEi/ARB/ARNi + β-blocker + MRA + SGLT2i; diuretics for symptoms only; digoxin no mortality benefit.
- ICD: EF ≤35%; CRT: QRS ≥150 ms (LBBB 130–149) + EF ≤35%.
- BNP <35 / NT-proBNP <125 pg/mL rules out HF.
- APO: O₂ + frusemide 40–120 mg IV + IV GTN + morphine (cautious); NIV if respiratory failure.
- EF is the single most important prognostic marker.
Topic Summary
Heart failure is a syndrome of inadequate cardiac output with two orthogonal classifications: by EF (HFrEF ≤40 / HFmrEF 41–49 / HFpEF ≥50) and by side (left → pulmonary, right → systemic congestion). Compensatory neurohormonal activation (Frank-Starling, sympathetic, RAAS) maintains output initially but drives progression, which is why GDMT (ACEi/ARB/ARNi + β-blocker + MRA + SGLT2i) is the cornerstone of HFrEF therapy, with ICD/CRT devices for selected patients and diuretics for symptom control. Acute decompensation (APO) is managed with O₂, IV frusemide, IV nitrates and cautious morphine, escalating to inotropes, NIV and MCS as needed — the HKHA algorithm being an LMCHK priority.