Control of Stroke Volume

The second variable that determines cardiac output is stroke volume, the volume of blood ejected by each ventricle during each contraction. As stated earlier, 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 (that is, the volume of blood in the

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Factors Influencing Heart Rate

FIGURE 14-28

Major factors that influence heart rate. All effects are exerted upon the SA node. The figure shows how heart rate is increased; reversal of all the arrows in the boxes would illustrate how heart rate is decreased.

FIGURE 14-28

Major factors that influence heart rate. All effects are exerted upon the SA node. The figure shows how heart rate is increased; reversal of all the arrows in the boxes would illustrate how heart rate is decreased.

PART THREE Coordinated Body Functions

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

PART THREE Coordinated Body Functions ventricles just before contraction); (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).

Relationship between Ventricular End-Diastolic Volume and Stroke Volume: The Frank-Starling Mechanism 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, as illustrated in Figure 14-29, termed 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 11, in that end-diastolic 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, a comparison of Figure 14-29 with Figure 11-25 reveals 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 hence 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.

The Sympathetic Nerves Sympathetic nerves are distributed not only to the conducting system, as described earlier, but to the entire myocardium. The effect of the sympathetic mediator norepinephrine acting on beta-adrenergic receptors is to increase ventricular contractility, defined as the strength of contraction at any given end-diastolic volume. Plasma epinephrine acting on these receptors also increases myocardial contractility. Thus, the increased force of contraction and stroke volume resulting from sympathetic-nerve stimulation or epinephrine is independent of a change in end-diastolic ventricular volume.

Note that a change in contraction force due to increased end-diastolic volume (the Frank-Starling mechanism) does not reflect increased contractility. Increased contractility is specifically defined as an increased contraction force at any given end-diastolic volume.

The relationship between the Frank-Starling mechanism and the cardiac sympathetic nerves is illustrated in Figure 14-30. The orange ventricular function curve o

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Ventricular end-diastolic volume (ml)

FIGURE 14-29

A ventricular function curve, which expresses the relationship between ventricular end-diastolic volume and stroke volume (the Frank-Starling mechanism). The horizontal axis could have been labeled "sarcomere length," and the vertical "contractile force." In other words, this is a length-tension curve, analogous to that for skeletal muscle ("see" Figure 11-25).

0 100 200 300 400

Ventricular end-diastolic volume (ml)

FIGURE 14-29

A ventricular function curve, which expresses the relationship between ventricular end-diastolic volume and stroke volume (the Frank-Starling mechanism). The horizontal axis could have been labeled "sarcomere length," and the vertical "contractile force." In other words, this is a length-tension curve, analogous to that for skeletal muscle ("see" Figure 11-25).

Sympathetic

stimulation

- /

Control

• Normal

resting

value

Ventricular end-diastolic volume (ml)

100 200 300

Ventricular end-diastolic volume (ml)

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Responses

  • Samwise
    Why is stroke volume important?
    8 years ago
  • Graziella
    What factors influence stroke volume?
    8 years ago
  • hunter
    What is the end diastolic cardiac muscle length known as?
    8 years ago
  • aryan
    How is stroke volume controlled?
    1 year ago

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