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 ventricles immediately before they begin to contract. This is a workload 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 ventricle when it contracts must be greater than the pressure in the arteries (since 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 arterial pressure against the "bottleneck" presented by the peripheral resistance; ejection of blood stops shortly after the aortic pressure 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 ventricle after contraction has begun.

In summary, the stroke volume is inversely proportional to the total peripheral resistance; the greater the peripheral resistance, the lower the stroke volume. It should be noted that this lowering of stroke volume in response to a raised peripheral resistance occurs for only a few beats. Thereafter, a healthy heart is able to compensate for the increased peripheral resistance by beating more strongly. This compensation occurs by means of a mechanism described in the next section (Frank-Starling Law of the Heart).

The proportion of the end-diastolic volume that is ejected against a given afterload depends on the strength of ventricular contraction. Normally, contraction strength is sufficient to eject 70 to 80 ml of blood out of a total end-diastolic volume of 110 to 130 ml. The ejection fraction is thus about 60%. More blood is pumped per beat as the EDV increases, and thus the ejection fraction remains relatively constant over a range of end-diastolic volumes. In order for this to be true, the strength of ventricular contraction must increase as the end-diastolic volume increases.

Frank-Starling Law of the Heart

Two physiologists, Otto Frank and Ernest Starling, demonstrated that the strength of ventricular contraction varies directly with the end-diastolic volume (fig. 14.2). Even in experiments where the heart is removed from the body (and is thus not subject to neural or hormonal regulation) and where the still-beating heart is filled with blood flowing from a reservoir, an increase in EDV within the physiological range results in increased contraction strength and, therefore, in increased stroke volume. This relationship between EDV, contraction strength, and stroke volume is thus a built-in, or intrinsic, property of heart muscle, and is known as the Frank-Starling Law of the Heart.

Intrinsic Control of Contraction Strength

The intrinsic control of contraction strength and stroke volume is due to variations in the degree to which the myocardium is stretched by the end-diastolic volume. As the EDV rises within the physiological range, the myocardium is increasingly stretched and, as a result, contracts more forcefully.

As discussed in chapter 12, stretch can also increase the contraction strength of skeletal muscles (see fig. 12.20). The resting length of skeletal muscles, however, is close to ideal, so that significant stretching decreases contraction strength. This is

Clinical Investigation Clue

Remember that when they found Charlie crawling along the road, he had a fast, weak pulse.

What physiological mechanism was responsible for Charlie's rapid pulse?

not true of the heart. Prior to filling with blood during diastole, the sarcomere lengths of myocardial cells are only about 1.5 |im. At this length, the actin filaments from each side overlap in the middle of the sarcomeres, and the cells can contract only weakly (fig. 14.3).

Frank-Starling law

Frank-Starling law

Ventricular end-diastolic volume (ml)

Figure 14.2 The Frank-Starling law and sympathetic nerve effects. The graphs demonstrate the Frank-Starling law: As the end-diastolic volume is increased, the stroke volume is increased. The graphs also demonstrate, by comparing the three curves, that the stroke volume is higher at any given end-diastolic volume when the ventricle is stimulated by sympathetic nerves. This is shown by the steeper curves to the left (see the red arrow).

Ventricular end-diastolic volume (ml)

Figure 14.2 The Frank-Starling law and sympathetic nerve effects. The graphs demonstrate the Frank-Starling law: As the end-diastolic volume is increased, the stroke volume is increased. The graphs also demonstrate, by comparing the three curves, that the stroke volume is higher at any given end-diastolic volume when the ventricle is stimulated by sympathetic nerves. This is shown by the steeper curves to the left (see the red arrow).

As the ventricles fill with blood, the myocardium stretches so that the actin filaments overlap with myosin only at the edges of the A bands (fig. 14.3). This increases the number of interactions between actin and myosin, allowing more force to be developed during contraction. Since this more advantageous overlapping of actin and myosin is produced by stretching of the ventricles, and since the degree of stretching is controlled by the degree of filling (the end-diastolic volume), the strength of contraction is intrinsically adjusted by the end-diastolic volume.

As shown in figure 14.4, muscle length has a more pronounced effect on contraction strength in cardiac muscle than in skeletal muscle. That is, a particular increase in sarcomere length will stimulate contraction strength more in cardiac muscle than in skeletal muscle. This is believed to be due to an increased sensitivity of stretched cardiac muscle to the stimulatory effects of Ca2+.

The Frank-Starling law explains how the heart can adjust to a rise in total peripheral resistance: (1) a rise in peripheral resistance causes a decrease in the stroke volume of the ventricle, so that (2) more blood remains in the ventricle and the end-diastolic volume is greater for the next cycle; as a result, (3) the ventricle is stretched to a greater degree in the next cycle and contracts more strongly to eject more blood. This allows a healthy ventricle to sustain a normal cardiac output.

A very important consequence of these events is that the cardiac output of the left ventricle, which pumps blood into the systemic circulation with its ever-changing resistances, can be adjusted to match the output of the right ventricle (which pumps blood into the pulmonary circulation). Clearly, the rate of blood msec - Time -

Resting sarcomere lengths

2 35

Actin

- Myosin

Figure 14.3 The Frank-Starling Law of the Heart. When the heart muscle is subjected to an increasing degree of stretch (a through d), it contracts more forcefully. The contraction strength is indicated on the y-axis as the tension. Notice that the time required to reach maximum contraction remains constant, regardless of the degree of stretch.

Cardiac Output, Blood Flow, and Blood Pressure flow through the pulmonary and systemic circulations must be equal in order to prevent fluid accumulation in the lungs and to deliver fully oxygenated blood to the body.

Extrinsic Control of Contractility

The contractility is the strength of contraction at any given fiber length. At any given degree of stretch, the strength of ventricular contraction depends on the activity of the sympathoadrenal system. Norepinephrine from sympathetic nerve endings and epi-nephrine from the adrenal medulla produce an increase in contraction strength (see figs. 14.2 and 14.4). This positive inotropic effect results from an increase in the amount of Ca2+ available to the sarcomeres.

The cardiac output is thus affected in two ways by the activity of the sympathoadrenal system: (1) through a positive in-otropic effect on contractility and (2) through a positive chronotropic effect on cardiac rate (fig. 14.5). Stimulation through parasympathetic nerve endings to the SA node and conducting tissue has a negative chronotropic effect but does not directly affect the contraction strength of the ventricles. However, the increased EDV that results from a slower cardiac rate can increase contraction strength through the mechanism described by the Frank-Starling Law of the Heart.

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