Heart Failure Physiology

Heart failure is the chronic inability of the heart to pump blood at a rate that maintains adequate tissue perfusion or matches systemic metabolic requirements. The principal pathophysiological feature is reduced myocardial contractility — the Starling curve is shifted downward, meaning a lower SV is produced for any given EDV.

In mild heart failure, CO at rest may be nearly normal (compensated failure) because increased EDV — from impaired emptying — recruits the Starling mechanism to partially restore SV. In severe failure, CO is subnormal at rest (decompensated failure). Stroke volume is not a reliable indicator of cardiac function in heart failure; ejection fraction (EF = SV/EDV, normal 50-70%) is more useful. EF is reduced in heart failure and fails to rise normally on exercise because: (1) the Starling curve is flat and increased EDV produces little additional SV; (2) β1-adrenoceptors are downregulated, impairing the sympathetic contractility response.

Compensatory mechanisms in chronic heart failure include: increased adrenergic activity (peripheral vasoconstriction → ↑TPR to maintain MABP; venoconstriction → ↑venous return → ↑EDV); RAAS activation (↓renal perfusion → renin → angiotensin II → aldosterone → Na+/H2O retention → ↑ECF volume by up to 30% → ↑EDV); elevated endothelin-1 (vasoconstrictor). Blood flow is preferentially maintained to brain, coronary, and skeletal muscle; reduced to kidney (RAAS), skin (cold peripheries), and gut (malabsorption).

Oedema in heart failure results from elevated venous hydrostatic pressure. Right heart failure → ↑systemic venous pressure → peripheral oedema (ankles in ambulant patients, sacrum in bed-ridden). Left heart failure → ↑pulmonary venous pressure → ↑pulmonary capillary pressure → fluid into lung interstitium → pulmonary oedema → reduced lung compliance → dyspnoea. In the supine position (at night), fluid distributes more evenly through the lungs → paroxysmal nocturnal dyspnoea (PND).

Ventricular dilation worsens prognosis: Laplace''s Law (T = Pr/w) shows that increased radius requires greater wall tension to maintain the same intraventricular pressure → ↑O2 demand. Additionally, dilated AV valve annuli cause regurgitation, reducing effective SV. Treatments aim to reduce cardiac work (afterload reduction), reduce plasma volume (diuretics), and improve contractility (inotropes) — without undermining the compensatory EDV increase.