Fig. 19.3 ) represents the control state; that is, when cardiac output is 5 L/minute, Pv is 2 mm Hg. When the heart is arrested (cardiac output = 0), Pv becomes 7 mm Hg at equilibrium (see
Fig. 19.2C ); this pressure is the mean circulatory pressure.
The inverse relationship between Pv and cardiac output simply means that when cardiac output is suddenly decreased, the rate at which blood flows from arteries to veins through the capillaries is temporarily greater than the rate at which the heart pumps blood from the veins back •Fig. 19.3 Changes in Central Venous Pressure Produced by Changes in Cardiac Output. Themeancirculatory(orstatic)pressure(Pmc)istheequilibriumpressurethroughoutthecardiovascularsystemwhencardiacoutputis0.PointsBandArepresentthevaluesofvenouspressureatcardiacoutputsof1and5L/minute,respectively.
into the arteries. During that transient period, a net volume of blood is transferred from arteries to veins; hence, Pa falls and Pv rises.
Now suppose that cardiac output suddenly increases. This example illustrates how a third point (B in
Fig. 19.3 ) on the vascular function curve is derived. Consider that the arrested heart is suddenly restarted and immediately begins pumping blood from the veins into the arteries at a rate of 1 L/minute (see
Fig. 19.2D ). When the heart first begins to beat, the arteriovenous pressure gradient is 0, and no blood is transferred from the arteries through the capillaries and into the veins. Thus when beating resumes, blood is depleted from the veins at the rate of 1 L/minute, and arterial blood volume is replenished from venous blood volume at that same absolute rate. Hence, Pv begins to fall and Pa begins to rise. Because of the difference in arterial and venous compliance, Pa rises at a rate 19 times faster than the rate at which Pv falls. The resultant arteriovenous pressure gradient causes blood to flow through the peripheral resistance vessels. If the heart maintains a constant output of 1 L/minute, Pa continues to rise and Pv continues to fall until the pressure gradient becomes 20 mm Hg. This gradient forces a rate of flow of 1 L/minute through a peripheral resistance of 20 mm Hg/L/minute. This gradient is achieved by a 19–mm Hg rise (to 26 mm Hg) in Pa and a 1–mm Hg fall (to 6 mm Hg) in Pv. This equilibrium value of Pv (6 mm Hg) for a cardiac output of 1 L/minute also appears on the vascular function curve of
Fig. 19.3 (point B). The 1–mm Hg reduction in Pv reflects a net transfer of blood from the veins to the arteries of the circuit.
The reduction in Pv that can be evoked by a sudden increase in cardiac output is limited. At some critical maximal value of cardiac output, sufficient fluid is transferred from the veins to the arteries of the circuit for Pv to fall below ambient pressure. In a system of very distensible vessels, such as the venous system, the greater external pressure causes the vessels to collapse (see ). This •Fig. 19.4 Effectsofincreasedbloodvolume(transfusion curve) anddecreasedbloodvolume(hemorrhage curve) onthevascularfunctioncurve.Similarshiftsinthevascularfunctioncurvecanbeproducedbyincreasesanddecreases,respectively,invenomotortone.
venous collapse impedes venous return to the heart. Hence, it limits the maximal value of cardiac output to 7 L/minute in this example (see
Fig. 19.3 ), regardless of the capabilities of the pump.
Factors That Influence the Vascular Function Curve
Dependence of Venous Pressure on Cardiac Output
According to experimental and clinical observations, changes in cardiac output do indeed evoke the alterations in Pa and Pv that have been predicted by the simplified model in
Fig. 19.2