462
Chapter 13
the fact, given earlier, that the
P
O
2
of blood in the pulmonary
veins and systemic arteries is normally about 5 mmHg less
than that of average alveolar air (see Table 13–7).
In disease states, regional changes in lung compliance,
airway resistance, and vascular resistance can cause marked
ventilation-perfusion inequalities. The extremes of this phe-
nomenon are easy to visualize: (1) There may be ventilated
alveoli with no blood supply at all (dead space or wasted ven-
tilation) due to a blood clot, for example, or (2) there may be
blood fl
owing through areas of lung that have no ventilation
(this is termed a
shunt
) due to collapsed alveoli, for example.
But the inequality need not be all-or-none to be signifi cant.
Carbon dioxide elimination is also impaired by
ventilation-perfusion inequality, but not nearly to the same
degree as oxygen uptake. Although the reasons for this are
complex, small increases in arterial CO
2
lead to increases in
alveolar ventilation, which usually prevent increases in arterial
P
CO
2
. Nevertheless, severe ventilation-perfusion inequalities in
disease states can lead to some elevation of arterial
P
CO
2
.
There are several local homeostatic responses within the
lungs that minimize the mismatching of ventilation and blood
fl ow and thereby maximize the effi ciency of gas exchange
(
Figure 13–24
). Probably the most important of these is a
direct effect of low oxygen on pulmonary blood vessels. A
decrease in ventilation within a group of alveoli—which might
occur, for example, from a mucous plug blocking the small air-
ways—leads to a decrease in alveolar
P
O
2
and the area around
it, including the blood vessels. A decrease in
P
O
2
in these alve-
oli and nearby blood vessels leads to vasoconstriction, divert-
ing blood fl ow away from the poorly ventilated area. This local
adaptive effect, unique to the pulmonary arterial blood vessels,
ensures that blood fl ow is directed away from diseased areas of
the lung toward areas that are well-ventilated. Another factor
to improve the match between ventilation and perfusion can
occur if there is a local decrease in blood fl ow within a lung
region due to, for example, a small blood clot in a pulmonary
arteriole. A local decrease in blood fl ow brings less systemic
CO
2
to that area, resulting in a local decrease in
P
CO
2
. This
causes local bronchoconstriction, which diverts air fl ow away
to areas of the lung with better perfusion.
The net adaptive effects of vasoconstriction and bron-
choconstriction are to (1) supply less blood fl ow to poorly ven-
tilated areas, thus diverting blood fl ow to well-ventilated areas,
and (2) redirect air away from diseased or damaged alveoli
and toward healthy alveoli. These factors greatly improve the
effi ciency of pulmonary gas exchange, but they are not per-
fect even in the healthy lung. There is always a small mismatch
of ventilation and perfusion, which, as just described, leads to
the normal alveolar-arterial O
2
gradient of about 5 mmHg.
Gas Exchange Between Tissues and Blood
As the systemic arterial blood enters capillaries throughout the
body, it is separated from the interstitial fl uid by only the thin
capillary wall, which is highly permeable to both oxygen and
carbon dioxide. The interstitial fl uid, in turn, is separated from
the intracellular fl uid by the plasma membranes of the cells,
which are also quite permeable to oxygen and carbon dioxide.
Metabolic reactions occurring within cells are constantly con-
suming oxygen and producing carbon dioxide. Therefore, as
shown in Figure 13–21, intracellular
P
O
2
is lower and
P
CO
2
higher
than in blood. The lowest
P
O
2
of all—less than 5 mmHg—is in
the mitochondria, the site of oxygen utilization. As a result,
a net diffusion of oxygen occurs from blood into cells and,
within the cells, into the mitochondria, and a net diffusion of
carbon dioxide occurs from cells into blood. In this manner, as
blood fl ows through systemic capillaries, its
P
O
2
decreases and
its
P
CO
2
increases. This accounts for the systemic venous blood
values shown in Figure 13–21 and Table 13–7.
In summary
, the supply of new oxygen to the alveoli
and the consumption of oxygen in the cells create
P
O
2
gradi-
ents that produce net diffusion of oxygen from alveoli to blood
in the lungs and from blood to cells in the rest of the body.
Conversely, the production of carbon dioxide by cells and its
elimination from the alveoli via expiration create
P
CO
2
gradients
that produce net diffusion of carbon dioxide from cells to blood
in the rest of the body and from blood to alveoli in the lungs.
Figure 13–24
Local control of ventilation-perfusion matching.
Decreased blood flow
Local perfusion decreased
to match a local decrease
in ventilation
Local ventilation decreased
to match a local decrease
in perfusion
Diversion of blood
flow and air flow
away from local
area of disease
to healthy areas
of the lung
Pulmonary blood
P
O
2
Alveoli
P
CO
2
Decreased air flow to
region of lung
Vasoconstriction of
pulmonary vessels
Decreased air flow
Decreased blood flow
to region of lung
Bronchoconstriction
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