Lab: Heart Failure

This laboratory session applies physiological principles of heart failure to clinical examination and case-based reasoning, reinforcing the haemodynamic and structural consequences of a failing heart.

Heart failure can result from: pump damage (MI → scar tissue, cardiomyopathy, myocarditis); pump dysfunction with normal anatomy (arrhythmia, valvular disorders, pericarditis); or pump overload (hypertension — chronic pressure overload; high-output failure from anaemia or hyperthyroidism driving resting tachycardia → eventual failure).

Chronic hypertension drives concentric LV hypertrophy (thicker wall, smaller cavity) as an initial compensation (Laplace: T = Pr/w; thicker wall reduces tension). Over time, fibrosis and impaired relaxation lead to diastolic dysfunction. If the hypertensive load is not controlled, systolic dysfunction follows and the heart dilates (eccentric hypertrophy) → Laplace now works against it (↑r, ↓w → ↑tension demand) → failure.

Approximately 4-5 litres of excess interstitial fluid must accumulate before peripheral oedema becomes clinically visible. In heart failure, fluid comes from RAAS-driven Na+/H2O retention. Baroreceptors are tonically active; hypotension → ↓baroreceptor firing → brainstem → ↑SNS → ↑adrenergic tone. Hypertension → ↑baroreceptor firing → ↓SNS.

Breathlessness in left heart failure: impaired LV output → ↑LVEDP → ↑LA pressure → ↑pulmonary venous pressure → fluid into pulmonary interstitium → ↓lung compliance → ↑work of breathing → dyspnoea. At night (supine), venous return increases → ↑cardiac filling → worsens LV failure → ↑pulmonary oedema → ↑dyspnoea (PND). Examination: chest X-ray shows white lungs (increased density); auscultation reveals bibasal crepitations. Apex beat displaced laterally (e.g. to 5th ics anterior axillary line) → indicates cardiac dilation/enlargement.