The arterioles contain a small amount of blood, about 3% of the total blood volume. Changes in the contractile state of arterioles do not significantly affect mean circulatory pressure. Vascular function curves representing different peripheral resistances converge at a common point on the y-axis. The relationship between venous pressure (Pv) and total peripheral resistance (TPR) can be explained as follows: when cardiac output is constant, an increase in TPR causes more blood to be retained in the arterial system. This leads to an increase in arterial blood volume until the arterial pressure (Pa) rises enough to force the same amount of blood flow through the resistance vessels as the cardiac output. This increase in arterial blood volume is accompanied by a decrease in venous blood volume, resulting in a proportional decrease in Pv. This relationship between TPR and Pv, along with the inability of peripheral resistance to affect mean circulatory pressure, explains the clockwise rotation of the vascular function curves in response to increased arteriolar constriction. Arteriolar dilation, on the other hand, produces a counterclockwise rotation. When arterioles are dilated, a higher maximal level of cardiac output can be achieved compared to when they are constricted.

Cardiac output and venous return are closely linked. The heart cannot pump more blood than what is delivered to it through the venous system, and venous return must equal cardiac output over any significant time period since the circulatory system is a closed circuit. The flow around the entire closed circuit depends on the pump's capability, the circuit's characteristics, and the total fluid volume of the system. Thus, cardiac output and venous return represent the flow around this closed circuit. Cardiac output is the volume of blood pumped by the heart per unit time, while venous return is the volume of blood returning to the heart per unit time. At equilibrium, these two volumes are equal. Techniques of circuit analysis can provide insights into the control of flow around the circuit.

The cardiac function curve, according to the Frank-Starling law of the heart, shows that cardiac output closely depends on right atrial (or central venous) pressure. Right atrial pressure is approximately equal to right ventricular end-diastolic pressure due to the normal tricuspid valve acting as a low-resistance junction between the right atrium and ventricle. Cardiac function curves can be graphed as cardiac output as a function of Pv, with extrinsic regulatory influences causing shifts in these curves.

A typical cardiac function curve and a normal vascular function curve can be plotted on the same set of axes. The cardiac function curve shows that an increase in Pv leads to an increase in cardiac output, in accordance with the Frank-Starling mechanism. Conversely, the vascular function curve depicts an inverse relationship between cardiac output and Pv. Scaling Pv along the y-axis and cardiac output along the x-axis, a vascular function curve can be plotted to show how Pv varies in response to a change in cardiac output. In this chapter, the convention for the vascular function curve is arbitrarily violated to plot both curves on the same set of axes.
Fig. 19.5 . The amount of blood in the arterioles is small; these vessels contain only approximately 3% of total blood volume (see ). Changes in the contractile state of arterioles do not significantly alter mean circulatory pressure. Thus vascular function curves that represent different peripheral resistances converge at a common point on the y-axis (see
Fig. 19.5
Pv varies inversely with total peripheral resistance (TPR) when all other factors remain constant. Physiologically, the relationship between Pv and TPR can be explained as follows: if cardiac output is held constant, a sudden increase in TPR causes a progressively greater volume of blood to be retained in the arterial system. Blood volume in the arterial system continues to increase until Pa rises sufficiently to force a flow of blood equal to cardiac output through the resistance vessels. If total blood volume does not change, this increase in arterial blood volume is accompanied by an equivalent decrease in venous blood volume. Hence, an increase in TPR diminishes Pv proportionately. This relationship between TPR and Pv, together with the inability of peripheral resistance to affect mean circulatory pressure, accounts for the clockwise rotation of the vascular function curves in response to increased arteriolar constriction (see
Fig. 19.5 ). Similarly, arteriolar dilation produces a counterclockwise rotation from the same vertical axis intercept. A higher maximal level of cardiac output is attainable when the arterioles are dilated than when they are constricted (see
Fig. 19.5).
Cardiac output and venous return are tightly linked. Except for small, transient disparities, the heart cannot pump any more blood than is delivered to it through the venous system. Similarly, because the circulatory system is a closed circuit, venous return to the heart must equal cardiac output over any appreciable time interval. The flow around the entire closed circuit depends on the capability of the pump, the characteristics of the circuit, and the total fluid volume of the system.
Thus cardiac output and venous return are simply two terms for the flow around this closed circuit. Cardiac output is the volume of blood being pumped by the heart per unit time. Venous return is the volume of blood returning to the heart per unit time. At equilibrium, these two volumes are equal. In the following section, certain techniques of circuit analysis are discussed to provide some insight into the control of flow around the circuit.
Relating the Cardiac Function Curve to the Vascular Function Curve
Coupling Between the Heart and the Vasculature
In accordance with the Frank-Starling law of the heart, cardiac output depends closely on right atrial (or central venous) pressure. Furthermore, right atrial pressure is approximately equal to right ventricular end-diastolic pressure because the normal tricuspid valve acts as a low-resistance junction between the right atrium and ventricle. Graphs of cardiac output as a function of Pv are called cardiac function curves; extrinsic regulatory influences may be expressed as shifts in such curves.
A typical cardiac function curve is plotted on the same coordinates as those for a normal vascular function curve in
Fig. 19.6 . The cardiac function curve is plotted according to the usual convention; that is, the independent variable (Pv) is plotted along the x-axis, and the dependent variable (cardiac output) is plotted along the y-axis. In accordance with the Frank-Starling mechanism, the cardiac function curve reveals that a rise in Pv increases cardiac output.
Conversely, the vascular function curve characterizes an inverse relationship between cardiac output and Pv; that is, a rise in cardiac output diminishes Pv. Pv is the dependent variable (or response) and cardiac output is the independent variable (or stimulus) for the vascular function curve. Therefore, to plot a vascular function curve in the conventional manner, Pv should be scaled along the y-axis and cardiac output along the x-axis.
To plot the cardiac and vascular function curves on the same set of axes requires a modification of the plotting convention for one of these curves. The convention for the vascular function curve is violated arbitrarily in this chapter. Note that the vascular function curve in
Fig. 19.6 is intended to reflect how Pv (scaled along the x-axis) varies in response to a change in cardiac output (scaled along the y-axis).