IM1.1-7 | Heart Failure Foundations and Aetiology — Summary & Reflection

KEY TAKEAWAYS

Heart failure is a clinical syndrome of inadequate cardiac output and/or elevated filling pressures, arising from structural or functional cardiac disease.

Classification:
- LVEF-based: HFrEF ≤40%, HFmrEF 41–49%, HFpEF ≥50% (know exact cut-offs)
- NYHA Class I–IV (symptom severity; fluctuates with treatment)
- ACC/AHA Stages A–D (structural progression; unidirectional)

Left vs Right failure: LHF → pulmonary congestion (dyspnoea, orthopnoea, PND); RHF → systemic venous congestion (JVP, oedema, hepatomegaly). Most clinical HF is biventricular. Systolic failure = impaired contraction (↓LVEF, eccentric hypertrophy, HFrEF causes: IHD, DCM). Diastolic failure = impaired relaxation (preserved LVEF, concentric hypertrophy, HFpEF causes: hypertension, HCM, amyloid).

Compensatory mechanisms (all maladaptive chronically): Frank-Starling (dilation → ↑SV at cost of ↑LVEDP); SNS activation (tachycardia, vasoconstriction, catecholamine toxicity); RAAS (Ang II → vasoconstriction + aldosterone → fluid retention + fibrosis); natriuretic peptides (BNP/ANP) as counter-regulation; ventricular remodelling (eccentric = HFrEF, concentric = HFpEF).

Exacerbating factors: Ischaemia/MI, arrhythmias (especially AF), anaemia, thyrotoxicosis, infections, dietary sodium excess, medication non-compliance, NSAIDs/CCBs, renal failure, PE.

Arrhythmias: AF (30–50% of HF; atrial fibrosis + reentry + sympathetic activation; use CHA₂DS₂-VASc ≥2 in men/≥3 in women → DOAC for non-valvular AF); VT/VF (scar-border reentry in ischaemic HF; EADs + QT prolongation + hypokalaemia in non-ischaemic); sudden cardiac death in 40–50% of HFrEF deaths.

Key investigations: BNP/NT-proBNP (confirm diagnosis, grade severity), ECG, CXR (cardiomegaly, upper lobe diversion, Kerley B), TTE (LVEF, wall motion, diastolic function, valvular pathology), coronary angiography (exclude ischaemic aetiology).

Management (HFrEF 4 pillars): ACE-I/ARNI + beta-blocker + MRA + SGLT2-I. Diuretics for symptom relief. ICD for LVEF ≤35% primary SCD prevention. CRT for LBBB + QRS ≥150 ms + LVEF ≤35%. Acute decompensation: IV furosemide, oxygen, nitrates (if hypertensive), CPAP/BiPAP.

REFLECT

Return to the man in the opening hook — the 58-year-old with hypertension, diabetes, an LVEF of 32%, and four-pillow orthopnoea. You now have the framework to place him precisely: HFrEF (LVEF ≤40%), ACC/AHA Stage C, NYHA Class III–IV at admission. His neurohormonal compensation — RAAS hyperactivation, sympathetic overdrive, atrial remodelling — is working against him. His medications will target exactly those cascades: an ACE inhibitor or ARNI to interrupt Ang II, a beta-blocker (once euvolaemic) to reverse adrenergic toxicity, an MRA to block aldosterone-mediated fibrosis, an SGLT2 inhibitor for additional cardioprotective benefit, and furosemide to relieve the immediate congestion. Think now about what it means to explain to this man why he needs four different heart medications that each work in a completely different way. Which of these would you explain first? How would you frame the concept of neurohormonal compensation — the body helping in the short term and hurting in the long term — in language a patient with limited health literacy would understand? The clinician who can explain the mechanism simply enough for the patient to understand is the clinician whose patient will take all four medications long enough to live longer.