Function of the Left Heart

Systolic contraction of the left ventricle is due to sliding of myosin filaments past actin filaments within sarcomeres, which are very simple contractile units. How can these simple sarcomere building blocks yield the complex functional characteristics of the left ventricle? That is, the ventricle must respond to changes in an individual’s level of activity and organ function to deliver all of the oxygen and metabolites required by all organ systems. Function of the ventricle can be understood by first considering that muscle tension-length properties assembled into a three-dimension ventricular chamber yield ventricular pressure-volume properties. Diastolic and systolic properties of the ventricle can be explained by considering cardiac muscle to have a time-varying elastance (ΔP/ΔV). Elastance is maximum (Emax) near end systole which indicates that end-systolic properties can be characterized by an end-systolic pressure-volume relationship (ESPVR) with a slope of Emax, which is synonymous with contractility. The sloped ESPVR means that stroke volume (and hence cardiac function) is decreased by an increase in afterload, a decrease in contractility, and a decrease in diastolic compliance, and vice versa. Area on a pressure-volume diagram has units of energy, or work. It follows that myocardial oxygen consumption is directly related to pressure-volume area on a ventricular pressure–volume diagram. Thus, consideration of the cardiac cycle illustrated on a ventricular pressure-volume diagram yields an understanding of underlying features which determine cardiac function and the myocardial oxygen consumption that is required to generate these functional characteristics.