CardiologyTier 2Topic

Regulation of cardiac output

Definition

Cardiac output (CO) = heart rate x stroke volume - regulated by the determinants of stroke volume (preload, afterload, contractility) plus heart rate itself
Understanding these determinants is the physiological basis for classifying and treating heart failure and shock

Preload (Frank-Starling mechanism) - increased venous return/ventricular filling stretches myocardial fibres, increasing the force of the subsequent contraction, up to a physiological limit beyond which further stretch reduces output (the descending limb, seen in decompensated heart failure)
Afterload - the resistance the ventricle must overcome to eject blood (systemic vascular resistance for the LV, pulmonary vascular resistance for the RV) - inversely related to stroke volume, all else equal
Contractility - intrinsic force of contraction independent of preload/afterload, modulated by sympathetic tone (inotropes increase it) and impaired in systolic heart failure
Heart rate - CO rises with heart rate up to a point, beyond which shortened diastolic filling time reduces stroke volume enough to offset the rate increase

This framework underlies haemodynamic classification of shock (cardiogenic - reduced contractility; hypovolaemic - reduced preload; distributive - reduced afterload/SVR) and guides targeted therapy for each
Heart failure classification, cardiogenic shock, Frank-Starling mechanism, shock differentiation

Heart failure therapy targets these determinants: diuretics (reduce preload), vasodilators (reduce afterload), inotropes (increase contractility, used cautiously given long-term harm in chronic HF)

Chronic neurohormonal activation that initially supports cardiac output (via preload/afterload/rate increases) becomes maladaptive over time - the physiological basis for why heart failure treatment blocks these compensatory pathways rather than augmenting them

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