Central Venous Pressure and Blood Volume

The venous system contains about two-thirds of the blood volume and can be visualized as a 'venous reservoir' supplying blood flow to the heart. Central venous pressure (CVP) is therefore a balance between blood volume, venomotor tone and the demands of the cardiac pump. At a given blood volume, as cardiac output increases, the rate at which blood is removed from the venous reservoir increases and central venous pressure falls. Similarly when cardiac output decreases a rise in CVP is produced. This relationship reflects the passive pressure-volume characteristics of the venous system, and can be described by the vascular function curve (Figure CR.29) which plots CVP against cardiac output with a fixed blood volume. Alterations in blood volume, e.g. haemorrhage or transfusion will shift the vascular function curve up or down.

This relationship should be differentiated from the situation in which blood volume is actively increased to increase cardiac output. This is an application of the Frank-Starling relationship and is described by a ventricular function curve that plots cardiac output against CVP. A combination of the vascular function curve and the ventricular function curve describes ventriculovenous coupling (see page 342), which has a potential clinical application in balancing the use of IV infusion and inotropes when optimizing cardiac output.



Volume (%)



Systemic circulation

Aorta and arteries




Veins and venules


Pulmonary circulation





Veins and venules

Figure CR.28

Vascular Function Curve

Cardiac output

Figure CR.29 Vascular function curve

Cardiac output

Control of Blood Volume

The haemodynamic effects of blood volume depend on the volume in the venous reservoir. This is controlled acutely by reflex venoconstriction and redistribution from other areas of the circulatory system. Blood can be diverted from 'reservoirs' such as cutaneous vascular beds, splanchnic vessels and the liver. Longer term control of blood volume is set by the balance between intravascular fluid and interstitial fluid compartments, fluid intake and renal loss. These mechanisms are illustrated by considering the events occurring in response to haemorrhage.

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