oxygen content. In intensive care settings, if
arterial oxygen saturation is normal, reduced
Sv02 is usually caused by underperfusion of
organs resulting from reduced cardiac output,
which causes greater extraction of oxygen from
the blood, thereby lowering venous oxygen
saturation and content.
An experiment is done on a human
subject that measures the P02 of venous
blood leaving the forearm during
reactive hyperemia following a period
of ischemia. During the initial phase
of reactive hyperemia, venous P02
is transiently lower than normal and
then becomes elevated. As blood flow
returns toward normal near the end of
the hyperemic response, the venous P02
also returns to its normal value. How
would you explain these findings?
Carbon Dioxide Diffusion
Carbon dioxide is a by-product of oxidative
metabolism and must be removed from the
tissue and transported to the lungs by the
blood. Like oxygen, carbon dioxide is very
lipid-soluble and readily diffuses from cells
into the blood. In fact, its diffusion constant is
about 20 times greater than oxygen in aque-
ous solutions. The removal of carbon diox-
ide from tissues is not diffusion-limited; its
removal depends primarily on the blood flow.
Therefore, reduced tissue perfusion leads to an
increase in tissue and venous PC02. Increased
oxidative metabolism of a tissue (e.g., contract-
ing muscle) increases C02 production by cells,
thereby increasing the concentration gradient
for C02 diffusion from the tissue to the blood
and increasing venous PC02. The magnitude
of the increase in venous P02 depends on the
relative increase in metabolism and blood flow.
The body is comprised of two basic fluid com-
partments: intravascular and extravascular.
The intravascular compartment contains fluid
(i.e., blood) within the cardiac chambers and
blood vessels of the body. The extravascular
system is everything outside of the intravascu-
lar compartment. The extravascular compart-
ment is made up of many subcompartments
such as the cellular, interstitial, and lymphatic
subcompartments and a specialized system
containing cerebrospinal fluid within the cen-
tral nervous system.
Fluid readily exchanges between the intra-
vascular and extravascular
Fluid leaves blood vessels (primarily capil-
laries) and enters the tissue interstitium of
the extravascular compartment. This is called
fluid filtration (Fig. 8.5). It is estimated that
about 1% of the plasma is filtered into the
interstitium in a typical organ. The intersti-
tial fluid is exchanged with the fluid found
within the subcompartments of the extracel-
lular compartment. It is crucial that a steady
state is achieved in which the same volume
of fluid that leaves the vasculature is returned
to the vasculature; otherwise, the extravascu-
lar compartment would swell with fluid (i.e.,
become edematous).
There are two routes by which fluid is
returned to the blood. First, fluid reabsorp-
tion returns most of the filtered fluid to the
blood at the venular end of capillaries or at
postcapillary venules (see Fig. 8.5). The rate
of reabsorption is less than filtration; there-
fore, a second mechanism is required to main-
tain fluid balance. This second mechanism
involves lymphatic vessels. These specialized
vessels, similar in size to venules, comprise
an endothelium with intercellular gaps sur-
rounded by a highly permeable basement
membrane. Terminal lymphatics end as blind
sacs within the tissue. The terminal lymphatics
take up the excess filtered fluid (including elec-
trolytes and macromolecules) and transport it
into larger lymphatics that leave the tissue. It is
estimated that 5% to 10% of capillary filtration
is transported out of tissues by the lymphat-
ics. The larger lymphatics have smooth muscle
cells that undergo spontaneous vasomotion
that serves to “pump” the lymph. Vasomo-
tion is spontaneous rhythmic contraction and
relaxation of the lymphatic vessels. Evidence
exists that as a lymphatic vessel fills with fluid,
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