Figure 1430

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Effects on stroke volume of stimulating the sympathetic nerves to the heart. Stroke volume is increased at any given end-diastolic volume; that is, the sympathetic stimulation has increased ventricular contractility.

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

Circulation CHAPTER FOURTEEN

Circulation CHAPTER FOURTEEN

Rate Force Development

Time

FIGURE 14-31

Effects of sympathetic stimulation on ventricular contraction and relaxation. Note that both the rate of force development and the rate of relaxation are increased, as is the maximal force developed. All these changes reflect an increased contractility.

Time

FIGURE 14-31

Effects of sympathetic stimulation on ventricular contraction and relaxation. Note that both the rate of force development and the rate of relaxation are increased, as is the maximal force developed. All these changes reflect an increased contractility.

is the same as that shown in Figure 14-29. The blue ventricular function curve was obtained for the same heart during sympathetic-nerve stimulation. The Frank-Starling mechanism still applies, but during nerve stimulation the stroke volume is greater at any given end-diastolic volume. In other words, the increased contractility leads to a more complete ejection of the end-diastolic ventricular volume.

One way of quantitating contractility is as the ejection fraction (EF), defined as the ratio of stroke volume (SV) to end-diastolic volume (EDV):

Expressed as a percentage, the ejection fraction normally averages 67 percent under resting conditions. Increased contractility causes an increased ejection fraction.

Not only does enhanced sympathetic-nerve activity to the myocardium cause the contraction to be more powerful, it also causes both the contraction and relaxation of the ventricles to occur more quickly

(Figure 14-31). These latter effects are quite important since, as described earlier, increased sympathetic activity to the heart also increases heart rate. As heart rate increases, the time available for diastolic filling decreases, but the quicker contraction and relaxation induced simultaneously by the sympathetic neurons partially compensate for this problem by permitting a larger fraction of the cardiac cycle to be available for filling.

There are multiple mechanisms by which the signal transduction pathways triggered by the binding of norepinephrine or epinephrine to their receptors causes increased contractility. These include: (1) opening more plasma-membrane calcium channels during excitation; (2) stimulating active calcium pumping into the sarcoplasmic reticulum; and (3) altering the binding of calcium by troponin. The net effect of these changes is that cytosolic calcium concentration increases to a greater value during excitation (thus facilitating contraction) and then returns to its preexci-tation value more quickly following excitation (thus facilitating relaxation).

There is little parasympathetic innervation of the ventricles (in contrast to the SA node, as described in the section on control of heart rate) and so the parasympathetic system normally has only a negligible effect on ventricular contractility.

Table 14-6 summarizes the effects of the auto-nomic nerves on cardiac function.

Afterload An increased arterial pressure tends to reduce stroke volume. This is because, in analogy to the situation in skeletal muscle (Chapter 11), the arterial pressure constitutes the "load" (technically termed the afterload) for contracting ventricular muscle; the greater this load, the less the contracting muscle fibers can shorten. This factor will not be dealt with further, however, since in the normal heart, several inherent adjustments minimize the over-all influence of arterial pressure on stroke volume. We will see, however, in the sections on high blood pressure and heart failure that long-term elevations of arterial pressure can weaken the heart and, thereby, influence stroke volume.

TABLE 14-6 Effects of Autonomic Nerves on the Heart

Area Affected

Sympathetic Nerves

Parasympathetic Nerves

SA node

Increased heart rate

Decreased heart rate

AV node

Increased conduction rate

Decreased conduction rate

Atrial muscle

Increased contractility

Decreased contractility

Ventricular muscle

Increased contractility

Decreased contractility (minor)

PART THREE Coordinated Body Functions

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

PART THREE Coordinated Body Functions

In summary (Figure 14-32), the two most important physiologic controllers of stroke volume are a mechanism (the Frank-Starling mechanism) dependent upon changes in end-diastolic volume, and a mechanism that is mediated by the cardiac sympathetic nerves and circulating epinephrine and that causes increased ventricular contractility. The contribution of each of these two mechanisms in specific physiological situations is described in later sections.

A summary of the major factors that determine cardiac output is presented in Figure 14-33, which combines the information of Figures 14-28 and 14-32.

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