Cardiac output and blood pressure are regulated by four factors: heart rate, myocardial contractility, preload, and afterload. These factors are controlled by various neural and humoral mechanisms. Preload and afterload, which are mutually dependent on the function of the heart and the vasculature, play a crucial role in determining cardiac output. They are considered coupling factors as they establish a functional connection between the heart and blood vessels.

The four major factors that determine cardiac output are heart rate, myocardial contractility, preload, and afterload. Preload and afterload are known as coupling factors because they create a functional connection between the heart and blood vessels. Understanding the nature of this coupling is essential for comprehending the regulation of cardiac output.

Peripheral chemoreceptors (carotid and aortic bodies) and central chemoreceptors in the medulla oblongata respond to a decrease in blood PaO2 and an increase in blood PCO2. Activation of these chemoreceptors leads to an increase in the rate and depth of respiration but also results in peripheral vasoconstriction. Cardiopulmonary baroreceptors found in the cardiac chambers and large pulmonary vessels have a lesser impact on blood pressure but participate in regulating blood volume.

Stimuli originating from the skin, viscera, lungs, and brain affect peripheral resistance and consequently blood pressure. Neural and local metabolic factors work together to distribute blood to active tissues and divert it from inactive ones. Metabolic factors have a greater influence on blood flow in vital structures such as the heart, brain, and contracting skeletal muscles.

The operating point of the cardiovascular system occurs at the intersection of the vascular and cardiac function curves. The evaluation of these curves enables clinicians to determine the effects of changes in blood volume, vascular tone, and contractility on cardiac output.

The central nervous system, heart, and systemic vasculature possess mechanisms that allow cardiac output to increase during vigorous exercise. These mechanisms ensure that the necessary levels of cardiac output are achieved.

Hemorrhage leads to cardiovascular consequences, and compensatory mechanisms come into play to restore arterial pressure and cardiac output.

Please answer the following questions based on the information provided:

1. What are the four major factors that determine cardiac output? Which two of these factors are said to be “coupling factors,” and what is the reason for that description?
2. What is a cardiac function curve, and how is it related to the Frank-Starling mechanism?
3. What is a vascular function curve, and how is it affected by changes in total peripheral resistance, blood volume, and venous tone?
4. Why does the operating point of the cardiovascular system occur at the intersection of the vascular and cardiac function curves?
5. How does evaluation of the cardiac function curve and the vascular function curve enable clinicians to determine the effect of changes in blood volume, vascular tone, and contractility on cardiac output?
6. What mechanisms in the central nervous system, heart, and systemic vasculature allow cardiac output to increase to the necessary levels during vigorous exercise?
7. What are the cardiovascular consequences of hemorrhage, and what are the compensatory mechanisms that tend to restore arterial pressure and cardiac output?
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predominate over those in the aorta, and they respond more vigorously to changes in pressure (stretch) than to elevated or reduced nonpulsatile pressure.
9.
Peripheral chemoreceptors (carotid and aortic bodies) and central chemoreceptors in the medulla oblongata are stimulated by a decrease in blood PaO2 and by an increase in blood PCO2. Stimulation of these chemoreceptors increases the rate and depth of respiration, but it also produces peripheral vasoconstriction. Cardiopulmonary baroreceptors are also present in the cardiac chambers and large pulmonary vessels. They have less influence on blood pressure but do participate in regulation of blood volume.
10.
Peripheral resistance and hence blood pressure are affected by stimuli that arise in the skin, viscera, lungs, and brain. The combined effect of neural and local metabolic factors distributes blood to active tissues and diverts it from inactive tissues. In vital structures, such as in the heart and brain and in contracting skeletal muscle, the metabolic factors predominate.
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Timmers HJ, Wieling W, Karemaker JM, et al. Cardiovascular responses to stress after carotid baroreceptor denervation in humans. Ann N Y Acad Sci. 2004;1018:515.
Zhang P, Mende U. Regulators of G-protein signaling in the heart and their potential as therapeutic targets. Circ Res. 2011;109: 320.
Upon completion of this chapter, the student should be able to answer the following questions: 1.
What are the four major factors that determine cardiac output? Which two of these factors are said to be “coupling factors,” and what is the reason for that description?
2.
What is a cardiac function curve, and how is it related to the Frank-Starling mechanism?
3.
What is a vascular function curve, and how is it affected by changes in total peripheral resistance, blood volume, and venous tone?
4.
Why does the operating point of the cardiovascular system occur at the intersection of the vascular and cardiac function curves?
5.
How does evaluation of the cardiac function curve and the vascular function curve enable clinicians to determine the effect of changes in blood volume, vascular tone, and contractility on cardiac output?
6.
What mechanisms in the central nervous system, heart, and systemic vasculature allow cardiac output to increase to the necessary levels during vigorous exercise?
7.
What are the cardiovascular consequences of hemorrhage, and what are the compensatory mechanisms that tend to restore arterial pressure and cardiac output?
Regulation of Cardiac Output and Blood Pressure
Four factors control cardiac output: heart rate, myocardial contractility, preload, and afterload (
Fig. 19.1). Heart rate and myocardial contractility are strictly cardiac factors, although they are controlled by various neural and humoral mechanisms. Preload and afterload are factors that are mutually dependent on function of the heart and the vasculature and are important determinants of cardiac output. Preload and afterload are themselves determined by cardiac output and by certain vascular characteristics. Preload and afterload are called coupling factors because they constitute a functional coupling between the heart and blood vessels.
To understand regulation of cardiac output, the nature of the coupling between the heart and the vascular system must be appreciated.