Control of Cardiac Output: Coupling of Heart and Blood Vessels

Preload or Filling Pressure of the Heart

The greater the preload of the heart, the greater the cardiac output. In the intact circulation, it will be the pressure in the great veins (i.e., the central venous pressure [CVP]) that constitutes the preload of the heart. In the whole heart, the stretch of the ventricles before systole will determine the strength of the subsequent contraction, by the cellular mechanisms discussed earlier (see Chapter 4 ). The cardiac output is the output of the left ventricle, but it is the preload of the right ventricle that ultimately actually determines the cardiac output. The reason is that, during periods when cardiac output is constant, and within limits, the left ventricle will pump whatever volume of blood comes to it, from the right side of the heart. Thus it is the filling pressure on the right side of the heart that ultimately determines the output on the left. The filling pressure on the right side of the heart is functionally equal to the central venous pressure. In the intact circulation, the preload is considered to be the CVP, which is approximately equal to the mean right atrial pressure ( ${\overline{\text{P}}}_{\text{ra}}$ ), which, when the tricuspid valve is open, is approximately equal to the right ventricular pressure. The relationship between preload or filling pressure and stroke volume (or cardiac output) is shown in the cardiac function curve. Cardiac function curves are also known as “Starling curves” or ventricular function curves. Partial curves can be obtained in human subjects, through the use of intracardiac pressure and volume transducers. The cardiac function curve is a manifestation of the Frank-Starling relationship or length-dependence of cardiac contraction.

Cardiac Function Curve

The CFC will be derived by using left ventricular pressure-volume (P-V) loops to illustrate the effect that varying preload has on the stroke volume (SV). In the CFC, stroke volume (or the proportional quantity, CO) is plotted as a function of filling pressure, or preload. For the left ventricle, a measure of preload is the left ventricular end-diastolic pressure (LVEDP). In an experimental situation in which an isolated animal heart is used, the preload of the left ventricle may be varied by changing the height of a reservoir of blood that is connected to the left ventricle. Raising or lowering the reservoir increases or decreases the pressure in the left ventricle and is one way in which preload can be changed in an experimental setting. In humans in an experimental setting, brief transient vena caval occlusion may be used to reduce, on one beat, the filling pressure of the left ventricle (by reducing the return of blood first to right ventricle and then subsequently to the left ventricle). This constitutes a reduction of the preload of the left ventricle. The effect of changing preload in this way on the left ventricular P-V loop in humans is shown in Fig. 10.2A . It can be seen that decreased preload is associated with markedly decreased end-diastolic volume, decreased end-systolic volume, and decreased arterial blood pressure during the ejection period. The net effect is decreased stroke volume. Increased preload is associated with the opposite changes, and the net effect is increased stroke volume. Note that in this case, the end-systolic pressure volume points (see Fig. 4.18 , point F in the schematic P-V loop) all lie on a single line for the different P-V loops. When this occurs, it is an indication that the contractility of the left ventricle was the same for all the different preloads. (This line is known as the end-systolic pressure-volume relationship, or ESPVR, as explained previously in Chapter 4 .) When the different stroke volumes are then plotted against the preload pressures at which they occurred (see Fig. 10.2B ), the entire relationship yields the cardiac function curve, or CFC. An individual CFC describes the way that stroke volume changes with preload, at a constant contractility. The CFC shows that the effect of increased preload is to increase stroke volume or, when heart rate is factored in, to increase cardiac output. Of course, changes in contractility are central to the physiological control of stroke volume and cardiac output, and the way in which changed contractility alters the cardiac function curve is explained later in this chapter (see Fig. 10.4A and B ). A CFC obtained from measurements in 75 patients in whom left ventricular end-diastolic pressure was varied (by various means other than transient vena caval occlusion) ( Fig. 10.3 ) also verifies that the CFC is a feature of cardiac function in humans.

Factors That Change the Cardiac Function Curve

Cardiac Function Curves and Physiological Function

Heart rate (HR) is a major physiological determinant of cardiac output, because CO = HR × SV. Thus it is useful to plot cardiac output, rather than stroke volume, as a function of preload ( Fig. 10.7 ). Increased heart rate, increased contractility, and decreased afterload are all factors that increase cardiac output at a given preload. Conversely, decreased heart rate, decreased contractility, increased afterload, and decreased compliance all decrease cardiac output at a given preload. Physiologically, the changes in cardiac function are rarely (if ever) as simple as can be achieved in isolated heart preparations, as illustrated in the simple schemes shown in Figs. 10.2, and 10.4 through 10.6 ). For example, an increase in contractility produced by increased sympathetic drive to the heart (increased release of norepinephrine) tends to raise stroke volume as shown (see Fig. 10.4 ), but heart rate also increases, with a resultant greater cardiac output. Because mean arterial pressure is the arithmetic product of cardiac output and total peripheral resistance, there is an increase in mean arterial pressure, which constitutes an increase in afterload, an effect that tends to decrease stroke volume. Thus it is important to remember that physiologically, multiple changes usually occur simultaneously. Most importantly, the filling pressure of the heart is greatly influenced by conditions in the systemic blood vessels. The effect that factors in the systemic vasculature have on the filling pressure of the heart, and hence on cardiac output, are quantified with the vascular function curve, or VFC , as discussed next.