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 pressure.





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