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CIRCULATORY PHYSIOLOGY
The interaction between myosin and actin, coupled with ATP produced by oxidative phosphorylation, is thought to be the basis for the contraction of each myofibril and therefore the contraction of the whole muscle. Each myofibril exhibits a property called contractility (or inotropic state) that represents the ability of the fiber to develop contractile force. The force exhibited by the fiber is influenced not only by its contractile state but also by its initial length, or preload, according to the Starling curve (Fig. 1-7). This concept can be expanded from the single fiber to describe the function of the entire ventricle. Thus, the abscissa, formerly preload or fiber length, becomes left ventricular filling pressure or volume (i.e., the amount of stretch on the myocardial fibers in diastole); and the ordinate, formerly tension, becomes stroke volume or stroke work (i.e., the ability of the heart to generate tension). Note that as diastolic pressure increases, the normal heart is able to increase its stroke volume, up to a point. This relationship is referred to as a ventricular function curve and, given identical states of contractility and afterload (see below), defines the amount of work that a heart is able to perform. Several factors determine left ventricular filling The term afterload describes the “impedance” or resistance against which the heart must contract. Like preload, afterload also can refer either to a single myofibril or to the heart as a whole. The afterload is approximated by the arterial pressure, the major determinant of the impedance to left ventricular contraction. In the intact heart, the afterload determines the amount of blood the heart can pump given a fixed preload and fixed state of contractility; that is, the higher the workload against which the heart must function, the less blood it can eject, and vice versa. Therefore, the ventricular function curve will be shifted up and to the left with decreasing afterload and shifted down and to the right with increasing afterload. Shifts in ventricular function with changes in afterload are minimal in normal ventricles but prominent in failing ventricles.