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Regulation of Stroke Volume


Regulation of Stroke Volume
The stroke volume is regulated by three variables:
  1. the end-diastolic volume (EDV), which is the volume of blood in the ventricles at the end of diastole;
  2. the total peripheral resistance, which is the frictional resistance, or impedance to blood flow, in the arteries; and
  3. the contractility, or strength, of ventricular contraction.
    The end-diastolic volume is the amount of blood in the ven-
tricles immediately before they begin to contract. This is a work- load imposed on the ventricles prior to contraction, and thus is sometimes called a preload. The stroke volume is directly proportional to the preload; an increase in EDV results in an increase in stroke volume. (This relationship is known as the Frank-Starling law of the heart, discussed shortly.) The stroke volume is also directly proportional to contractility; when the ventricles contract more forcefully, they pump more blood.
In order to eject blood, the pressure generated in a ven- tricle when it contracts must be greater than the pressure in the arteries (because blood flows only from higher pressure to lower pressure). The pressure in the arterial system before the ventricle contracts is, in turn, a function of the total peripheral resistance—the higher the peripheral resistance, the higher the pressure. As blood begins to be ejected from the ventricle, the added volume of blood in the arteries causes a rise in mean arte- rial pressure against the “bottleneck” presented by the peripheral resistance. Ejection of blood stops shortly after the aortic pres- sure becomes equal to the intraventricular pressure. The total peripheral resistance thus presents an impedance to the ejection of blood from the ventricle, or an afterload imposed on the ven- tricle after contraction has begun. This can be medically signifi- cant; a person with a high total peripheral resistance has a high arterial blood pressure, and thus a high afterload imposed on the ventricular muscle.

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