Up to a Point, Increases in End-Diastolic VentricuIarVoIume Cause Increases in Stroke Volume
Stroke volume equals end-diastolic volume minus end- systolic volume. Therefore, as shown in Figure 21-2, stroke volume can be increased only by increasing end-diastolic volume (i.e., filling the ventricles more during diastole) or by decreasing end-systolic volume (i.e., emptying the ventricles more completely during systole), or both.
The effect of increasing end-diastolic ventricular volume (EDV) on stroke volume is plotted in Figure 21-3, A. The detailed physiological mechanisms underlying this relationship are complex. Basically, however, greater ventricular filling during diastole places the ventricular muscle fibers in a more favorable geometry for the ejection of blood during the next systole. Also, stretching the ventricular muscle fibers during diastole causes a greater amount of calcium (Ca2+) to be released from the sarcoplasmic reticulum during the subsequent systolic contraction, and this enhances the force of contraction. Resting conditions in a normal animal are somewhere around the middle of this ventricular function curve. Therefore, increases or decreases from normal ventricular end-diastolic volume result in approximately proportional increases or decreases in stroke volume.