Cardiovascular Physiology
399
reality, capillary hydrostatic pressures vary in different regions
of the body and, as will be described in a later section, are
strongly infl uenced by whether the person is lying down, sit-
ting, or standing. Moreover, capillary hydrostatic pressure in
any given region is subject to physiological regulation, medi-
ated mainly by changes in the resistance of the arterioles in
that region. As
Figure 12–43
shows, dilating the arterioles
in a particular tissue raises capillary hydrostatic pressure in
that region because less pressure is lost overcoming resis-
tance between the arteries and the capillaries. Because of the
increased capillary hydrostatic pressure, fi ltration is increased,
and more protein-free fl
uid is lost to the interstitial fl
uid. In
contrast, marked arteriolar constriction produces decreased
capillary hydrostatic pressure and favors net movement of
interstitial fl
uid into the vascular compartment. Indeed, the
arterioles supplying a group of capillaries may be so dilated or
so constricted that the capillaries manifest only fi ltration or
only absorption, respectively, along their entire length.
We have presented the story of capillary fi
ltration entirely
in terms of the Starling forces, but one other factor is involved—
the
capillary fi ltration coeffi
cient.
This is a measure of how
much fl
uid will fi lter per mmHg net fi ltration pressure. We pre-
viously ignored this factor because in most capillaries, it is not
under physiological control. A major exception, however, occurs
in the capillaries of the kidneys. As we will see in Chapter 14,
certain of the kidney capillaries fi
lter huge quantities of protein-
free fl uid because they have a very large capillary fi ltration coef-
fi cient that can be altered physiologically.
We must state again that capillary fi ltration and absorp-
tion play no signifi cant role in the exchange of nutrients and
metabolic end products between capillary and tissues. The
reason is that the total quantity of a substance, such as glu-
cose or carbon dioxide, moving into or out of a capillary as a
result of net bulk fl ow is extremely small in comparison with
the quantities moving by net diffusion.
Finally, this analysis of capillary fl uid dynamics has consid-
ered only the systemic circulation. Precisely the same Starling
forces apply to the capillaries in the pulmonary circulation,
but the relative values of the four variables differ. In particu-
lar, because the pulmonary circulation is a low-resistance, low-
pressure circuit, the normal pulmonary capillary hydrostatic
pressure—the major force favoring movement of fl uid out of
the pulmonary capillaries into the interstitium—averages only
about 7 mmHg. This is offset by a greater accumulation of
proteins in lung interstitial fl uid than is found in other tissues.
Overall, Starling’s forces in the lung slightly favor fi ltration as
in other tissues, but extensive and active lymphatic drainage
prevents the accumulation of extracellular fl uid in the inter-
stitial spaces and airways. The importance of this will be dis-
cussed further in the context of heart failure in Section E of
this chapter.
Veins
Blood fl ows from capillaries into venules and then into veins.
Some exchange of materials occurs between the interstitial
uid and the venules, just as in capillaries. Indeed, permeabil-
ity to macromolecules is often greater for venules than for cap-
illaries, particularly in damaged areas.
The veins are the last set of tubes through which blood
fl ows on its way back to the heart. In the systemic circulation,
the force driving this venous return is the pressure difference
between the peripheral veins and the right atrium. The pres-
sure in the fi rst portion of the peripheral veins is generally
quite low—only 10 to 15 mmHg—because most of the
pressure imparted to the blood by the heart is dissipated by
resistance as blood flows through the arterioles, capillaries,
and venules. The right atrial pressure is normally close to
0 mmHg. Therefore, the total driving pressure for fl ow from
the
peripheral veins
to the right atrium is only 10 to 15
mmHg. (The peripheral veins include all veins not contained
within the chest cavity.) This pressure difference is adequate
because of the low resistance to fl ow offered by the veins,
which have large diameters. Thus, a major function of the
veins is to act as low-resistance conduits for blood fl ow from
the tissues to the heart. The peripheral veins of the arms and
legs contain valves that permit fl ow only toward the heart.
In addition to their function as low-resistance conduits,
the veins perform a second important function: Their diam-
eters are refl exly altered in response to changes in blood vol-
ume, thereby maintaining peripheral venous pressure and
venous return to the heart. In a previous section, we empha-
sized that the rate of venous return to the heart is a major
determinant of end-diastolic ventricular volume and thereby
stroke volume. Thus, we now see that peripheral venous pres-
sure is an important determinant of stroke volume. We next
describe how venous pressure is determined.
Determinants of Venous Pressure
The factors determining pressure in any elastic tube are the
volume of fl uid within it and the compliance of its walls.
Consequently, total blood volume is one important determi-
nant of venous pressure because, as we will see, at any given
moment most blood is in the veins. Also, the walls of veins
are thinner and much more compliant than those of arteries.
Thus, veins can accommodate large volumes of blood with a
100
80
60
40
20
110
0
Artery
Arteriole
Capillary
Vasodilation
Vasoconstriction
Initial state
Distance along systemic blood vessels
Blood pre
ss
ure (mmH
g
)
Figure 12–43
Effects of arteriolar vasodilation or vasoconstriction on capillary
blood pressure in a single organ (under conditions of constant
arterial pressure).
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