The Venous
System
The venules and veins return the
blood from the microcirculation to the right atrium. However, they do not serve
merely as passive conduits. Instead, they have a crucial active role in
stabilizing and regulating the venous return of blood to the heart.
The venous system differs from the arterial system in two important
respects. First, the total volume (and cross-sectional area) of the venous
system is much greater than that of the arterial system. This is because there
are many more venules than arterioles; venules also tend to have larger
internal diameters than arterioles. Second, the veins are quite thin walled,
and can there-fore expand greatly to hold more blood if their internal pressure
rises.
As a result of its large cross-sectional area, the venous system offers
much less resistance to flow than the arterial system. The pressure gradient
required to drive the blood through the venous system (15 mmHg) is therefore
much smaller than the pressure needed in the arterial system (80 mmHg). The
average pressure in the venae cavae at the level of the heart (the central
venous pressure) is usually close to 0 mmHg (i.e. atmospheric pressure).
The flow of blood back to the heart is aided by the presence of one-way venous valves in the arms and especially
the legs, which prevent backflow.
The graph in Figure 22 (upper right) illustrates the relationship between
pressure and volume in a typical vein and artery. The slope of the volume – pressure
curve is referred to as the compliance. Compliance is a measure of expandability.
Veins are much more compliant than arteries at low pressures (0–10 mmHg). Small
increases in venous pressure in this range therefore cause large increases in
venous blood volume.
One reason for high venous compliance is that their thin walls allow
veins to collapse at low internal pressures. Only small increases in pressure
are needed to ‘reinflate’ a collapsed vein with blood until it has nearly
rounded up. At higher pressures, however, venous compliance decreases
dramatically (see graph) because the slack in rigid collagen fibres in the
venous wall is rapidly taken up. This limit on the expandability of the veins
is important in limiting the pooling of blood in the veins of the legs that
occurs during standing.
Because of their large volumes and
high compliance, the veins/ venules accommodate a much larger volume of the
blood (∼70%
of the total) than do the arteries/arterioles (∼12%). They are there- fore termed capacitance
vessels, and are able to serve as blood volume
reservoirs. During exercise, and in hypotensive states (e.g. during
haemorrhage), sympathetically mediated constriction of the veins/venules,
notably in the splanchnic (including the gastrointestinal tract and liver) and
cutaneous circulations, displaces blood into the rest of the cardiovascular
system. In particular, the resulting reduction of the venous volume increases
the volume of blood in the central thoracic compartment (i.e. the heart and pulmonary
circulation), thereby boosting cardiac output, assisting perfusion of other
essential vascular beds and helping to maintain
the blood pressure.
When the upright position is assumed, the pull of gravity increases the
absolute pressures within both the arteries and veins of the lower
extremities. The average arterial and venous blood pressures in a normal adult
standing quietly are about 100 and 0 mmHg, respectively, at the level of the
heart, while in the feet the pressures are about 190 and 90 mmHg, respectively.
However, gravity does not affect the pressure gradient driving the blood
circulation, because the difference
between the arterial and venous pressures is similar (100 mmHg) at both
levels. Therefore standing does not stop blood from flowing back to the heart.
The increased pressure within the veins of the lower extremities causes
them to distend, so that about 500 mL blood is shifted into this part of the
circulation. The rise in hydrostatic pressure within the capillaries of the
lower extremities increases fluid filtration, causing a progressive loss of
plasma volume into the tissues of the legs
and feet. The resulting loss of fluid from the central thoracic compartment
lowers cardiac output.
These potentially harmful effects are limited by the baroreceptor and
cardiopulmonary reflexes, which respond to a fall in the pulse pressure (see
Chapter 27). These cause an increased heart rate and widespread vasoconstriction.
This limits the loss of blood from the central thoracic compartment and
slightly raises mean arterial blood pressure (MABP) and total peripheral
resistance (TPR). The cardiac output falls by about 20%. A local sympathetic
axon reflex also reduces blood flow to the lower extremities, limiting
fluid filtration.
In the upright position, the reduction of intravascular pressures above
the heart causes the partial collapse of superficial veins, although the deeper
veins remain partly open because their walls are anchored to surrounding
tissues. Standing also causes a down- ward displacement into the spinal canal
of the cerebrospinal fluid bathing the central nervous system (CNS), creating a
negative pressure inside the rigid cranium that prevents cerebral veins from
collapsing. Because cerebral venous pressure is not able to fall as much as
arterial pressure, cerebral blood flow decreases by 10–20%.
The Skeletal Muscle Pump
Even during quiet standing, the leg muscles are stimulated by reflexes to
contract and relax rhythmically, causing swaying. During contraction, veins
within the muscles are squeezed, forcing blood towards the heart, as the venous
valves prevent retrograde flow. Upon relaxation, these veins expand, drawing in
blood from venules and from superficial veins that communicate with the muscle
veins via collaterals (Figure 22). This skeletal muscle pump thus
‘milks’ the veins, driving blood towards the heart to assist venous return. The
skeletal muscle pump is greatly potentiated during walking and running,
dramatically lowering the venous pressure in the foot to levels as low as 30
mmHg.
The Respiratory Pump
During inspiration, downward displacement of the diaphragm causes the
intrathoracic pressure to fall and the intra-abdominal pressure to rise. This
increases the pressure gradient favouring venous return, and vena caval flow
rises. An opposite effect occurs during expiration. During straining movements
in which there is forced expiration against a closed glottis (e.g. the Valsalva
manoeuvre), the rise in intrathoracic pressure severely reduces venous return.
Effect Of Cardiac Contraction
Downward displacement of the ventricles during systole pulls on the
atria, expanding them and drawing in blood from the venae cavae and pulmonary
veins. When the valves between the atria and ventricles then open during
diastole, the blood is drawn in from these veins by the expansion of the
ventricles, further aiding venous return. Venous return is therefore driven not
only by the upstream pressure, but also (to a smaller extent) by downstream
suction.
