Mean Circulatory Filling Pressure
Imagine the heart arrested in diastole with no flow around the circuit. It will take a certain amount of blood just to fill the anatomical space contained by the systemic system without stretching any of its walls or developing any internal pressure. This amount is 3.56 L. Normally, however, the systemic circuit contains approximately 4.5 L of blood and is thus somewhat inflated. Because the totoal systemic circuit compliance is 140 mL/mm Hg and the "just to fill" amount of blood is 3.56 L, an extra 1000 mL (4.5 L – 3.56 L) amount of blood generate an internal pressure (deltaP) of about 7 mm Hg (deltaP = deltaV/C = 1000/140 = ~ 7 mm Hg). This theoretical pressure is called the mean circulatory filling pressure and is the actual pressure that would exist throughout the system in the absence of flow.
The two major variables that affect mean circulatory filling pressure are the circulating blood volume and the state of the peripheral venous vessel tone. In contrast, squeezing on arterioles will have a negligible effect on mean circulatory filling pressure because arterioles contain so little blood in any state. The other major components of the system (arteries and capillaries) essentially do not actively change their volume.
Flow-Induced Change in Pressure From the Base of Mean Circulatory Filling Pressure
The presence of flow around the circuit does not change the total volume of blood in the system or the mean circulatory filling pressure. The flow caused by cardiac pumping action does, however, tend to shift some of the blood volume from the venous side of the circuit to the arterial side. This causes pressure on the arterial side to rise above the mean circulatory pressure, whereas pressures on the venous side fall below it. Because veins are approximately 50 times more compliant than arteries, the flow-induced decrease in venous pressure (due to blood volume shitfed away) is only approximately 1/50th as large as the accompanying increase in arterial pressure (due to blood volume shifted into). Thus, flow or no flow, pressure in the peripheral venous compartment is normally quite close to the mean circulatory filling pressure.
Central Venous Pressure
The central venous compartment corresponds roughly to the volume enclosed by the right atrium and the great veins in the thorax. Blood leaves the central venous compartment by entering the right ventricle at a rate that is equal to the cardiac output. Venous return, in contrast, is by definition the rate at which blood returns to the thorax from the peripheral vascular beds and is thus the rate at which blood enters the central venous compartment. In any stable situation, venous return must equal cardiac output or blood would gradually accumulate in either the central venous compartment or the peripheral vasculature. However, there are often temporary differences between cardiac output and venous return. Whenever such differences exist, the volume of the central venous compartment must be changing. Because the central venous compartment is enclosed by elastic tissues, any change in central venous volume produces a corresponding change in central venous pressure.
Central venous pressure equals to the RVEDP (right venticular end diastolic pressure)/cardiac filling pressure and has an extremely important positive influence on stroke volume. On the other hand central venous pressure has an equally important negative effect on venous return. Thus, central venous pressure is always automatically driven to a value that makes cardiac output equal to venous return.
The Venous Function Curve
Anatomically the peripheral venous compartment is scatered throughout the systemic organs, but functionally it can be viewed as a single vascular space that has a particular pressure (PPV) at any instant of time. The normal operating pressure in the peripheral venous compartment is usually very close to mean circulatory filling pressure. Moreover, the same factors that influence mean circulatory filling pressure have essentially equal influences on peripheral venous pressure. Thus, "Peripheral venous pressure" can be viewed as essentially equivalent to "mean circulatory filling pressure." The blood flow rate between the peripheral venous compartment and the central venous compartment is governed by the basic flow equation (Q = deltaP/R). When the peripheral venous pressure is assumed to be 7 mm Hg, there will be no venous return when the central venous pressure (PCV) is also 7 mm Hg.
How does CVP influecne venous return
If the peripheral venous pressure remains at 7 mm Hg, decreasing central venous pressure will increase the pressure drop across the venous reistance and consequently cause an elevation in venous return. This relationship is summarized by the venous function curve, which shows how venous return increases as central venous pressure drops. If central venous pressure reaches very low values and falls below the intrathoracic pressure, the veins in the thorax are compressed, which therefore tends to limit venous return. In the example in Figure 8-4, intrathoracic pressure is taken to be 0 mm Hg and the flat portion of the venous function curve indicates that lowering central venous pressure below 0 mm Hg produces no additional increase in venous return.
How does peripheral venous pressure influence venous return
If the central venous remains constant and the peripheral increases, the pressure difference between the two will be enhanced, which increases venous return as a drop in central venous pressure. The two ways in which peripheral venous pressure can change were: first, because veins are elastic vessels changes in the volume of blood contained within the peripheral veins would alter the peripheral venous pressure. Moreover, because the veins are much more compliant than any other vascular segment, changes in circulating blood volume produce larger changes in the volume of blood in the veins than in any other vascular segment. Second, peripheral venous pressure can be altered through changes in venous tone produced by increasing or decreasing the activity of sympathetic vasoconstrictor nerves supplying the venous smooth muscle. In addition, an increase in any force compressing veins from the outside has the same effect on the pressure inside veins as an increase in venous tone. Thus, such things as muscle exercise and wearing elastic stockings tend to elevate peripheral venous pressure.
Shift of the venous function curve
Whenever peripheral venous pressure is altered, the relationship between central venous pressure and venous return is also altered. For example, whenever peripheral venous pressure is elevated by increase in blood volume or by sympathetic stimulation, the venous function curve shifts upward and to the right. By similar logic, decreased peripheral venous pressure caused by blood loss or decreased sympathetic vasoconstriction of peripheral veins shifts the venous function curve downward and to the left.
Determination of Cardiac Output and Venous Return by Central Venous Pressure
The significance of the fact that central venous pressure simultaneously affects both cardiac output and venous return can be best seen by plotting the cardiac function curve and the venous function curve on the same graph (Figure 8-5).
Central venous pressure, as defined earlier, is the filling pressure of the right heart. Strictly speaking, this pressure directly affects only the stroke volume and output of the right heart pump. In most contexts, however, "cardiac output" implies the output of the left heart pump. How is it then, as we have previously implied, that central venous pressure profoundly affects the output of the left side of the heart? The proper answer is that changes in central venous pressure automatically cause essentially parallel changes in the filling pressure of the left side of the heart (i.e., in left atrial pressure). Consider, for example, the following sequence of consequences that a small step increase in central venous pressure has on a heart that previously was in a steady state:
- Increased central venous pressure.
- Increased right ventricular stroke volume via Starling's law of the heart.
- Increased output of the right side of the heart.
- The right side of the heart output temporarily exceeds that of the left side of the heart.
- As long as this imbalance exists, blood accumulates in the pulmonary vasculature and raises pulmonary venous and left atrial pressures.
- Increased left atrial pressure increases left ventricular stroke volume via Starling's law.
- Very quickly, a new steady state will be reached when left atrial pressure has risen sufficiently to make left ventricular stroke volume exactly equal to the increased right ventricular stroke volume.
The major conclusion here is that left atrial pressure will automatically change in the correct direction to match left ventricular stroke volume to the current right ventricular stroke volume. Consequently, it is usually an acceptable simplification to say that central venous pressure affects cardiac output as if the heart consisted only of a single pump.
Note that in Figure 8-5, cardiac output and venous return are equal (at 5 L/min) only when the central venous pressure is 2 mm Hg. If central venous pressure were to decrease to 0 mm Hg for any reason, cardiac output would fall (to 2 L/min) and venous return would increase (to 7 L/min). With a venous return of 7 L/min and a cardiac output of 2 L/min, the volume of the central venous compartment would necessarily increase and this would produce a prgoressive increasing central venous pressure. In this manner, central venous pressure would return to the original level (2 mm Hg) in a very short time. Conversely, in the same logic the similar thing would happen when cenral venous pressure were to increase. The conclusion is that the cardiovascular system automatically adjusts to operate at the point where the cardiac and venous function curve intersect.