PATHOPHYSIOLOGY • TOPIC 1 / 100 • Cardiovascular
Heart Failure
Mechanistic algorithm
Myocardial injury or chronic pressure/volume overload → ↓ effective stroke volume → baroreceptor unloading → sympathetic activation + RAAS/ADH activation → vasoconstriction and Na⁺/water retention → ↑ preload/afterload → ventricular remodelling → progressive pump failure
Reduced cardiac output activates compensatory neurohormonal systems. Initially these preserve arterial pressure, but persistent catecholamine, angiotensin II and aldosterone signalling increases afterload, sodium retention, fibrosis, apoptosis and adverse remodelling.
In HFrEF, impaired systolic contraction lowers ejection fraction; in HFpEF, concentric remodelling, fibrosis and impaired relaxation raise filling pressures despite a near-normal EF.
Raised LV filling pressure is transmitted to the pulmonary veins causing interstitial/alveolar oedema and dyspnoea. Right-sided congestion produces systemic venous hypertension, oedema, ascites and hepatic congestion.
ANP/BNP rise as counter-regulatory responses, promoting natriuresis and vasodilatation, but are overwhelmed in advanced disease.
Educational learning module. The mechanism is written to emphasise clinically meaningful physiology and may be read alongside a standard textbook for deeper molecular detail.