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The heart is a four-chambered biological pump that generates pressure to propel blood. The Frank-Starling law states that stroke volume (SV) increases with end-diastolic volume (EDV, preload): greater filling greater sarcomere stretch greater contraction force, up to an optimum (~2.2 m sarcomere length). This autoregulates cardiac output without the need for neurohormonal intervention.

Laplace's law applied to the left ventricle (T = P·r/2h) reveals why ventricular hypertrophy is initially adaptive: increasing h_wall reduces wall stress _wall, normalizing the load on cardiomyocytes. However, eccentric hypertrophy (increased EDV, increased r) increases _wall in the long term, leading to heart failure.

Ejection fraction (EF = SV/EDV) is the most clinically used systolic index. EF < 40% defines heart failure with reduced ejection fraction (HFrEF); EF 50% with symptoms defines HFpEF (diastolic dysfunction). Cardiac work W_ext = P dV is the area of the pressure-volume loop, which can be measured with a pressure-volume catheter (Gold Standard).

Myocardial O consumption (MVO) is proportional to the double product (HR × SBP), a clinical approximation of cardiac work. In angina, the ischemic threshold is reached when demand (MVO) exceeds supply (coronary flow). The corrected QTc is the risk marker for ventricular arrhythmia: QTc > 500 ms indicates high risk of torsades de pointes.

The hydraulic power of the heart (P = CO × MAP 12 W) is astonishingly efficient for a muscle that beats 100,000 times a day. The mechanical efficiency of the myocardium is ~2530%: the remainder of the energy consumption is dissipated as heat. In heart failure, performance decreases and MVO increases for the same useful work.

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ID:('ky', 35)

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ID:(0, 35)