How Epinephrine Works

Increased Preload. Figure 14.7B shows a pressure-volume loop from the same heart in the presence of increased preload. After opening of the mitral valve at point 1 in Figure 14.7B, diastolic pressure and volume increase to a higher value than in Figure14.7A. When isovolumetric contraction begins at point 2, end-diastolic volume is higher. Because afterload is unchanged, the aortic valve opens at the same pressure (point 3). In the idealized graph in Figure 14.7B, the greater force of contraction associated with higher preload causes the ventricle to eject all of the extra volume that entered during diastole. This means that, when the aortic valve closes at point 4, the volume and pressure of the ventricle are identical to the values in Figure 14.7A. The difference in volume between points 3 and 4 is larger, representing the larger stroke volume associated with increased preload.

Increased Afterload. Figure 14.7C shows the effect of increased afterload on the pressure-volume loop. In this situation, the aortic valve opens (point 3) at a higher pressure because aortic pressure is increased, as compared with Figure 14.7A. The higher aortic pressure decreases stroke volume, and the aortic valve closes (point 4) at a higher pressure and volume. Mitral valve opening and ventricular filling (point 1) begin at a higher pressure and volume because more blood is left in the ventricle at the end of systole. Filling of the ventricle proceeds along the same diastolic pressure-volume curve from point 1 to point 2.

Because the ventricle did not empty as much during systole and the atrium delivers as much blood during diastole, end-diastolic volume and pressure (preload) are increased.

Increased Contractility. Figure 14.7D shows the effect of increased contractility on the pressure-volume loop. In this idealized situation, there is no change in end-diastolic volume, and mitral valve closure occurs at the same pressure and volume (point 2). Afterload is also the same,- therefore, the aortic valve opens at the same arterial pressure (point 3). The increased force of contraction causes the ventricle to eject more blood and the aortic valve closes at a lower end-systolic volume (point 4). This means that the mitral valve opens at a lower end-diastolic volume (point 1). Because diastolic compliance is unchanged, filling proceeds along the same pressure-volume curve from point 1 to point 2.

When there are changes in diastolic compliance, the pressure-volume curve between (1) and (2) is changed. This and other changes, such as heart failure, are beyond the scope of this text.

Heart Rate Interacts With Stroke Volume to Influence Cardiac Output

Heart rate can vary from less than 50 beats/min in a resting, physically fit individual to greater than 200 beats/min during maximal exercise. If stroke volume is held constant, in creases in heart rate cause proportional increases in cardiac output. However, heart rate affects stroke volume,- changes in heart rate do not necessarily cause proportional changes in cardiac output. In considering the influence of heart rate on cardiac output, it is important to recognize that as the heart rate increases and the duration of the cardiac cycle decreases, the duration of diastole decreases. As the duration of diastole decreases, the time for filling of the ventricles is diminished. Less filling of the ventricles leads to a reduced end-diastolic volume and decreased stroke volume.

Effect of Decreased Heart Rate on Cardiac Output. A

consequence of the reciprocal relationship between heart rate and the duration of diastole is that, within limits, decreasing the rate of a normal resting heart does not decrease cardiac output. The lack of a decrease in cardiac output is because stroke volume increases as heart rate decreases. Stroke volume increases because as the heart rate falls, the duration of ventricular diastole increases, and the longer duration of diastole results in greater ventricular filling. The resulting elevated end-diastolic fiber length increases stroke volume, which compensates for the decreased heart rate. This balance works until the heart rate is below 20 beats/min. At this point, additional increases in end-dias-tolic fiber length cannot augment stroke volume further because the maximum of the ventricular function curve has been reached. At heart rates below 20 beats/min, cardiac output falls in proportion to decreases in heart rate.

Effect of Increased Heart Rate as a Result of Electronic

Pacing. If an electronic pacemaker is attached to the right atrium and the heart rate is increased by electrical stimulation, surprisingly little increase in cardiac output results. This is because as the heart rate increases, the interval between beats shortens and the duration of diastole decreases. The decrease in diastole leaves less time for ventricular filling, producing a shortened end-diastolic fiber length, which subsequently reduces both the force of contraction and the stroke volume. The increased heart rate is, therefore, offset by the decrease in stroke volume. When the rate increases above 180 beats/min secondary to an abnormal pacemaker, stroke volume begins to fall as a result of poor diastolic filling. A person with abnormal tachycardia (e.g., caused by an ectopic ventricular pacemaker) may have a reduction in cardiac output despite an increased heart rate.

Events in the myocardium compensate to some degree for the decreased time available for filling. First, increases in heart rate reduce the duration of the action potential and, thus, the duration of systole, so the time available for dias-tolic filling decreases less than it would otherwise. Second, faster heart rates are accompanied by an increase in the force of contraction, which tends to maintain stroke volume. The increased contractility is sometimes called treppe or the staircase phenomenon. These internal adjustments are not very effective and, by themselves, would be insufficient to permit increases in heart rate to raise cardiac output.

Effects of Increased Heart Rate as a Result of Changes in Autonomic Nerve Activity. Increased heart rate usually occurs because of decreased parasympathetic and increased sympathetic neural activity. The release of norep-

inephrine by sympathetic nerves not only increases the heart rate (see Chapter 13) but also dramatically increases the force of contraction (see Fig. 14.3). Furthermore, nor-epinephrine increases conduction velocity in the heart, resulting in a more efficient and rapid ejection of blood from the ventricles. These effects, summarized in Figure 14.8, maintain the stroke volume as the heart rate increases. When the heart rate increases physiologically as a result of an increase in sympathetic nervous system activity (as during exercise), cardiac output increases proportionately over a broad range.

Influences on Stroke Volume and Heart Rate Regulate Cardiac Output

In summary, cardiac output is regulated by changing stroke volume and heart rate. Stroke volume is influenced by the contractile force of the ventricular myocardium and by the force opposing ejection (the aortic pressure or afterload). Myocardial contractile force depends on ventricular end-diastolic fiber length (Starling's law) and my-ocardial contractility. Contractility is influenced by four major factors:

1) Norepinephrine released from cardiac sympathetic nerves and, to a much lesser extent, circulating norepinephrine and epinephrine released from the adrenal medulla

2) Certain hormones and drugs, including glucagon, isoproterenol, and digitalis (which increase contractility) and anesthetics (which decrease contractility)

How Epinephrine Effect Heart Rate

^jpflHBIBII^ Effects of increased sympathetic neural activity on heart rate, stroke volume, and cardiac output. Various effects of norepinephrine on the heart compensate for the decreased duration of diastole and hold stroke volume relatively constant, so that cardiac output increases with increasing heart rate. The words "Increase" and "Decrease" in small type denote quantitatively less important effects than the same words in large type.

^jpflHBIBII^ Effects of increased sympathetic neural activity on heart rate, stroke volume, and cardiac output. Various effects of norepinephrine on the heart compensate for the decreased duration of diastole and hold stroke volume relatively constant, so that cardiac output increases with increasing heart rate. The words "Increase" and "Decrease" in small type denote quantitatively less important effects than the same words in large type.

3) Disease states, such as coronary artery disease, myocarditis (see Chapter 10), bacterial toxemia, and alterations in plasma electrolytes and acid-base balance

4) Intrinsic changes in contractility with changes in heart rate and/or afterload

Heart rate is influenced primarily by sympathetic and parasympathetic nerves to the heart and, by a lesser extent, by circulating norepinephrine and epinephrine. The effect of heart rate on cardiac output depends on the extent of concomitant changes ventricular filling and contractility.

Heart failure is a major problem in clinical medicine (see Clinical Focus Box 14.1).

Essentials of Human Physiology

Essentials of Human Physiology

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Responses

  • Marja Pasanen
    How epinephrine effect Heart Rate?
    5 years ago
  • reilly
    How epinephrine works?
    4 years ago

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