Cardiac stroke volume is the volume of blood ejected by each ventricle during each contraction, equal to the difference between the end-diastolic volume and the end-systolic volume. So, stroke volume determines cardiac output. Let us remember that the ventricles do not completely empty themselves of blood during contraction. Therefore, a more forceful contraction can produce an increase in stroke volume by causing greater emptying. Changes in the force of contraction can be produced by a variety of factors, but three are dominant under most physiological and pathophysiological conditions: 1) changes in the end-diastolic volume (the volume of blood in the ventricles just before contraction, sometimes referred to as the pre-load); 2) changes in the magnitude of sympathetic nervous system input to the ventricles; and 3) afterload, that is, the arterial pressures against which the ventricles pump.
The mechanical properties of cardiac muscle are the basis for an inherent mechanism for altering stroke volume: The ventricle contracts more forcefully during systole when it has been filled to a greater degree during diastole. In other words, all other factors being equal, the stroke volume increases as the end-diastolic volume increases. This is illustrated graphically as a ventricular function curve. This relationship between stroke volume and end-diastolic volume is known as the Frank-Starling mechanism (also called Starling’s law of the heart) in recognition of the two physiologists who identified it. What accounts for the Frank-Starling mechanism? Basically it is simply a length-tension relationship, as described for skeletal muscle in Chapter 9, in that enddiastolic volume is a major determinant of how stretched the ventricular sarcomeres are just before contraction. Thus, the greater the end-diastolic volume, the greater the stretch, and the more forceful the contraction.
However, there is an important difference between the length-tension relationship in skeletal and cardiac muscle. The normal point for cardiac muscle in a resting individual is not at its optimal length for contraction, as it is for most resting skeletal muscles, but is on the rising phase of the curve. For this reason, additional stretching of the cardiac muscle fibers by greater filling causes increased force of contraction. The significance of the Frank-Starling mechanism is as follows: At any given heart rate, an increase in the venous return—the flow of blood from the veins into the heart—automatically forces an increase in cardiac output by increasing end-diastolic volume and thus stroke volume. One important function of this relationship is maintaining the equality of right and left cardiac outputs. Should the right heart, for example, suddenly begin to pump more blood than the left, the increased blood flow to the left ventricle would automatically produce an increase in left ventricular output. This ensures that blood will not accumulate in the lungs.