BIOC63H3 Lecture Notes - Lecture 9: Blood Pressure, Cardiac Output, Stroke Volume
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The Venous System
The venules and veins return the blood from the microcirculation to the right atrium of the heart.
They do not, however, 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 that that if 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
therefore 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
compared to the arterial system. The pressure gradient require to drive the blood through the
venous system is therefore much smaller than the pressure needed in the arterial system. The
average pressure in the vena cava (the central venous pressure) is usually close to 0 mmHg (i.e.
The Veins as Capacitance Vessels
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
therefore termed capacitance vessels, and are able to serve blood volume reservoirs. During
exercise, and in hypotensive states (e.g. during hemorrhage), sympathetically mediated
constriction of the veins/venules, notably in the splanchnic (including the gastrointestinal tract
and liver) and cutaneous circulations, displaces blood to other essential vascular beds, while also
helping to maintain the blood pressure. At the same time, the resulting reduction of the venous
volume increases the volume of the blood to the heart thereby boosting cardiac output.
The volume of blood that veins can accommodate depends on the distensibility of the walls of
the vein (how much they can stretch to hold blood) and the influence of any externally applied
pressure squeezing inwardly on the veins. At a constant blood volume, as venous capacity
increases, more blood remains in the veins instead of being returned to the heart. Such venous
storage decreases the effective circulating (stressed) volume. Conversely, when venous capacity
decreases, more blood is returned to the heart and continues circulating. Thus, changes in venous
capacity directly influence the magnitude of venous return, which in turn is an important
determinant of effective circulating (stressed) blood volume.
The magnitude of total blood volume is also influenced on a short term basis by passive shifts in
bulk flow between the vascular and interstitial fluid compartments and on a long-term basis by
factors that control total ECF volume, such as salt and water balance.
Venous return refers to the volume of blood entering each atrium per minute from the veins. It is
dependent on the pressure gradient between the arterial and venous sides of the heart.
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In addition to the driving pressure imparted by cardiac contraction, five other factors enhance
venous return: 1) sympathetically induced venous vasoconstriction, 2) skeletal muscle activity,
3) the effect of venous valves, 4) respiratory activity and 5) the effect of cardiac suction (Figure
Effect of Sympathetic Activity on Venous Return
Veins are not very muscular and have little inherent tone, but venous smooth muscle is
abundantly supplied with sympathetic nerve fibers. Sympathetic stimulation produces venous
vasoconstriction, which modestly elevates venous pressure; this in turn, increases the pressure
gradient to drive more blood from the veins into the right atrium. The veins normally have such a
large diameter that the moderate vasoconstriction accompanying sympathetic stimulation has
little effect on resistance to flow. Even when constricted, the veins still have a relatively large
diameter and are still low-resistance vessels.
In addition to mobilizing the stored (unstressed) blood, venous vasoconstriction enhances venous
return by decreasing venous capacity. With the filling capacity of the veins reduced, less blood
draining from the capillaries remains in the veins but continues to flow instead toward the heart.
Effect of Skeletal Muscle Pump Activity on Venous Return
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 2). This skeletal muscle pump thus „milks‟ the
veins, driving blood towards the heart and assisting venous return. The skeletal muscle pump is
enormously potentiated during walking and running, causing a dramatic lowering of the venous
pressure in the foot.
The skeletal muscle also counters the effect of gravity on the venous system. When an individual
is lying down, the force of gravity is uniformly applied, so it does not have to be taken into
consideration. However, when an individual stands up gravitational effects are not uniform. In
addition to the usual pressure that results from cardiac contraction, vessels below the level of the
heart are subjected to pressure caused by the weight of the column of blood extending from the
heart to the level of the vessel. One important consequence of this increased pressure is that the
distensible veins yield under the increased hydrostatic pressure, further expanding so that their
capacity is increased. Even though the arteries are subjected to the same gravitation effects, they
do not expand like the veins because arteries are not nearly as distensible. Much of the blood
entering from the capillaries tends to pool in the expanded lower-leg veins instead of returning to
the heart. Because venous return is reduced, cardiac output is decreased, and the effective
circulating volume is reduced. This marked increased in capillary blood pressure resulting from
the effect of gravity causes excessive fluid to filter out of capillary beds into the lower
extremities, producing localized edema (Figure 3).
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