The equilibrium point of the cardiovascular system is determined by the intersection of the cardiac and vascular function curves. This point represents the stable values of cardiac output and central venous pressure at which the system tends to operate. Any deviation from these values is only temporary as long as the cardiac and vascular function curves accurately depict the system.

To illustrate the tendency to operate around the equilibrium point, let's consider a sudden change. If there is a sudden increase in central venous pressure (Pv) from the equilibrium point to point A, it would cause changes in cardiac output. This increase in Pv could be caused by injecting a given volume of blood into the venous vessels while simultaneously withdrawing an equal volume from the arterial vessels. Despite the rise in Pv, the total blood volume remains constant.

According to the cardiac function curve, the elevated Pv would lead to an increase in cardiac output from point A to point B during the next ventricular systole. This increased cardiac output would cause a net transfer of blood from the veins to the arteries, resulting in a reduction in Pv. However, the reduction in Pv during one heartbeat would be small because only a fraction of the total venous blood volume is transferred to the arteries. As a consequence of this reduction in Pv, cardiac output during the next beat decreases from point C to point D, as dictated by the cardiac function curve. Since point C is still above the intersection point, the heart pumps blood from the veins to the arteries at a rate higher than the flow across the peripheral resistance from arteries to veins. Consequently, Pv continues to decrease. This process continues in diminishing steps until the intersection point is reached. 

The equilibrium point, where the curves intersect, represents the specific combination of cardiac output and Pv that satisfies the requirements of the cardiac and vascular function curves simultaneously. At this point, cardiac output equals venous return, and the system remains stable.

By examining different combinations of cardiac and vascular function curves, we can also understand the effects of changes in ventricular contractility on cardiac output and Pv. In Fig. 19.7, the lower cardiac function curve depicts the control state, while the upper curve represents increased myocardial contractility. These curves are similar to the ventricular function curves shown in Fig. 18.12.

Enhanced ventricular contractility, as represented by the upper curve, causes a shift in the equilibrium values of cardiac output and Pv from the intersection point of the control vascular and cardiac function curves (continuous curve) to the intersection point of the same vascular function curve with the cardiac function curve (dashed curve) that reflects the response to sympathetic stimulation.
When the cardiovascular system is represented by a given pair of cardiac and vascular function curves, the intersection of these two curves defines the equilibrium point of that system. The coordinates of this equilibrium point represent •Fig. 19.6 Typical Vascular and Cardiac Function Curves Plotted on the Same Coordinate Axes. Toplotbothcurvesonthesamegraph,thex-axisandy-axisforthevascularfunctioncurveshadtobeswitched;comparetheassignmentofaxeswiththosein
Figs.
19.3,19.4,and19.5.
Thecoordinatesoftheequilibriumpoint,attheintersectionofthecardiacandvascularfunctioncurves,representthestablevaluesofcardiacoutputandcentralvenouspressureatwhichthesystemtendstooperate.Anyperturbation(e.g.,asuddenincreaseinvenouspressuretopointA)institutesasequenceofchangesincardiacoutputandvenouspressurethatrestorethesevariablestotheirequilibriumvalues.
the values of cardiac output and Pv at which the system tends to operate. Only transient deviations from such values of cardiac output and Pv are possible, as long as the given cardiac and vascular function curves characterize the system accurately.
The tendency to operate about this equilibrium point may best be illustrated by the response to a sudden change. Consider the changes caused by a sudden rise in Pv from the equilibrium point to point A in
Fig. 19.6 . This change in Pv might be caused by the rapid injection, during ventricular diastole, of a given volume of blood on the venous vessels of the circuit and simultaneous withdrawal of an equal volume from the arterial vessels of the circuit. Thus although Pv rises, total blood volume remains constant.
As defined by the cardiac function curve, this elevated Pv would increase cardiac output (from point A to point B in
Fig. 19.6 ) during the next ventricular systole. The increased cardiac output would then cause the transfer of a net quantity of blood from the veins to the arteries of the circuit, with a consequent reduction in Pv. In one heartbeat, the reduction in Pv would be small (from point B to point C) because the heart would transfer only a fraction of the total venous blood volume to the arteries. As a result of this reduction in Pv, cardiac output during the very next beat diminishes (from point C to point D) by an amount dictated by the cardiac function curve. Because point C is still above the intersection point, the heart pumps blood from the veins to the arteries at a rate greater than that at which blood flows across the peripheral resistance from arteries to veins. Hence, Pv continues to fall. This process continues in diminishing steps until the point of •Fig. 19.7 Enhancementofmyocardialcontractility,asbystimulationofcardiacsympatheticnerves,causestheequilibriumvaluesofcardiacoutputandcentralvenouspressure(Pv)toshiftfromtheintersection(pointA)ofthecontrolvascularandcardiacfunctioncurves(continuous curve) totheintersection(pointD)ofthesamevascularfunctioncurvewiththecardiacfunctioncurve(dashed curve) thatrepresentstheresponsetosympatheticstimulation.
intersection is reached. Only one specific combination of cardiac output and venous pressure—the equilibrium point, denoted by the coordinates of the point at which the curves intersect—satisfies the requirements of the cardiac and vascular function curves simultaneously. At the equilibrium point, cardiac output equals venous return, and the system is stable.
Combinations of cardiac and vascular function curves also help explain the effects of alterations in ventricular contractility on cardiac output and Pv. In
Fig. 19.7, the lower cardiac function curve represents the control state, whereas the upper curve reflects the influence of increased myocardial contractility. This pair of curves is analogous to the ventricular function curves shown in
Fig. 18.12.
The enhanced ventricular contractility represented by the upper curve in