Expansion
Sympathetic activation, renin-angiotensin activation, and ventricular remodelling
Expansion
Compensatory mechanisms
- Sympathetic activation - raises rate and contractility, and constricts vessels
- Renin-angiotensin-aldosterone activation - retains salt and water, raising preload
- Frank-Starling - increased filling raises stroke volume
- Ventricular remodelling - hypertrophy reduces wall stress, dilatation preserves stroke volume
Why they fail
- Tachycardia and increased contractility raise myocardial oxygen demand and shorten diastole
- Salt and water retention raise filling pressures, causing pulmonary and peripheral oedema
- Vasoconstriction raises afterload, further reducing output
- Chronic catecholamine exposure is directly cardiotoxic and downregulates beta receptors
- Dilatation raises wall stress by Laplace, worsening efficiency
This is precisely why the drugs that improve survival, namely ACE inhibitors, beta blockers, mineralocorticoid antagonists and neprilysin inhibition, all block compensation, whereas positive inotropes relieve symptoms but worsen mortality.