Central Venous Pressure

Venous pressure is a term that represents the average blood pressure within the venous
compartment. The term "central venous pressure" (CVP) describes the pressure in the thoracic
vena cava near the right atrium (therefore CVP and right atrial pressure are essentially the same).
CVP is an important concept in clinical cardiology because it is a major determinant of the filling
pressure and therefore the preload of the right ventricle, which regulates stroke volume through
the Frank-Starling mechanism.

A change in CVP (ΔCVP) is determined by the change in volume (ΔV) of blood within the thoracic
veins divided by thecompliance (Cv) of the these veins according to the following equation:

ΔCVP = ΔV / Cv

Therefore, CVP is increased by either an increase in venous blood volume or by a decrease in

venous compliance.  The latter change can be caused by contraction of the smooth muscle within
the veins, which increases the venous vascular tone and decreases compliance.  The effects of
increased venous blood volume and decreased venous compliance on CVP are illustrated in the
figure to the right. In this figure, point A represents a control operating point for the venous
vasculature. The curve that point A is on is the compliance curve for the thoracic veins. If the volume
of blood within these veins is increased, then the operating point will shift up and to the right (from A
to B) along the same compliance curve. This will lead to an increase in pressure that is determined
by the change in volume and the venous compliance (slope of the curve). CVP will also be increased
if venous smooth muscle contraction is enhanced (e.g., by sympathetic nerve stimulation). When this
occurs, the venous compliance decreases (dashed red line), and the new operating point C will
reflect a smaller venous volume but at a greater venous pressure.

It is important to note for a proper conceptual understanding that the compliance of the large thoracic
veins (especially the vena cava) does not undergo large changes.  Instead, the major site for venous
compliance changes is smaller veins located outside of the thorax. These smaller veins are can
undergo significant compliance changes. When the compliance of these veins decreases (e.g., by
sympathetic nerve stimulation), constriction of these veins and the resulting increased pressure is
transmitted up to the thoracic veins, which increases their volume and therefore pressure.

In the body, venous compliance and venous volume are not static, but dynamic, with many factors
influences these two variables, such as cardiac output, respiratory activity,contraction of skeletal
muscles (particularly legs and abdomen),sympathetic vasoconstrictor tone, and hydrostatic
forces (i.e., gravity). Venodilator drugs, which are often used in the treatment of acute heart
failure and angina, relax venous vessels (increase their compliance) and thereby lower central
venous pressure. All of the above factors influence central venous pressure by either changing
thoracic venous blood volume or venous compliance. These factors or mechanisms are summarized
in the following table:

Primarily a change in
Factors Increasing Central Venous compliance (C) or
Pressure volume (V)
Decreased cardiac output V
Increased blood volume V
Venous constriction C
Changing from standing to supine body posture V
Arterial dilation V
Forced expiration (e.g., Valsalva) C
Muscle contraction (abdominal and limb) V, C
 A decrease in cardiac output either due to decreased heart rate or stroke volume (e.g.,
in ventricular failure) results in blood backing up into the venous circulation (increased
venous volume) as less blood is pumped into the arterial circulation.  The resultant
increase in thoracic blood volume increases CVP.
 An increase in total blood volume as occurs in renal failure or fluid retention through
activation of the renin-angiotensin-aldosterone system increases venous pressure.
 Venous constriction caused by sympathetic activation of veins, or by circulating
vasoconstrictor substances (e.g.,catecholamines, angiotensin II) decreases venous
compliance, which increases CVP.
 A shift in blood volume into the thoracic venous compartment that occurs when a
person changes from standing to supine position increases CVP.
 Arterial dilation as occurs during withdrawal of sympathetic tone or with arterial
vasodilator drugs causes increased blood flow from the arterial into the venous
compartments. This increases venous blood volume and CVP.  This is what occurs
when the heart is functioning normally.  It is important to note, however, that arterial
dilation in ventricular failure leads to a decrease in CVP instead of an increase.  This
occurs because the arterial dilation decreases afterload on the ventricle leading to an
 increase in stroke volume.  Ventricular stroke volume is more strongly influenced by
afterload when the ventricular is in failure than when it has normal function.
 CVP is also increased during a force expiration, particularly against a high resistance
(as occurs with a Valsalva maneuver) due to external compression of the thoracic
vena cava as intrapleural pressure rises. This mechanical compression of the vena
cava functionally reduces the compliance of the vena cava.
 Muscle contraction, particularly of the limbs and abdomen, compresses the veins (i.e.,
decreases compliance) and forces blood into the thoracic compartment, thereby
increasing thoracic blood volume and CVP.