Respiratory Physiology
461
on the two sides of the alveolar-capillary membrane result in
the net diffusion of oxygen from alveoli to blood and of car-
bon dioxide from blood to alveoli. As this diffusion occurs,
the
P
O
2
in the pulmonary capillary blood rises and the
P
CO
2
falls. The net diffusion of these gases ceases when the capillary
partial pressures become equal to those in the alveoli.
In a normal person, the rates at which oxygen and carbon
dioxide diffuse are so rapid and the blood fl
ow through the cap-
illaries so slow that complete equilibrium is reached well before
the blood reaches the end of the capillaries (
Figure 13–23
).
Thus, the blood that leaves the pulmonary capillaries to
return to the heart and be pumped into the systemic arteries
has essentially the same
P
O
2
and
P
CO
2
as alveolar air. (They are
not exactly the same, for reasons given later.) Accordingly, the
factors described in the previous section—atmospheric
P
O
2
,
cellular oxygen consumption and carbon dioxide production,
and alveolar ventilation—determine the alveolar gas pressures,
which then determine the systemic arterial gas pressures.
Given that diffusion between alveoli and pulmonary capil-
laries normally achieves complete equilibration, the more capil-
laries that participate in this process, the more total oxygen
and carbon dioxide is exchanged. Many of the pulmonary
capillaries at the apex (top) of each lung are normally closed at
rest. During exercise, these capillaries open and receive blood,
thereby enhancing gas exchange. The mechanism by which
this occurs is a simple physical one; the pulmonary circula-
tion at rest is at such a low blood pressure that the pressure in
these apical capillaries is inadequate to keep them open, but
the increased cardiac output of exercise raises pulmonary vas-
cular pressures, which opens these capillaries.
The diffusion of gases between alveoli and capillar-
ies may be impaired in a number of ways (see Figure 13–23),
resulting in inadequate oxygen diffusion into the blood. For
one thing, the total surface area of all of the alveoli in contact
with pulmonary capillaries may be decreased. In lung infec-
tions or
pulmonary edema,
for example, some of the alveoli
may become fi lled with fl uid. Diffusion may also be impaired
if the alveolar walls become severely thickened with connective
tissue, as, for example, in the disease called
diffuse interstitial
brosis
.
Pure diffusion problems of these types are restricted
to oxygen and usually do not affect the elimination of carbon
dioxide, which is much more diffusible than oxygen.
Matching of Ventilation and Blood Flow
in Alveoli
The major disease-induced cause of inadequate oxygen
movement between alveoli and pulmonary capillary blood
is not a problem with diffusion, but instead is due to the
mismatching of the air supply and blood supply in individual
alveoli.
The lungs are composed of approximately 300 million
alveoli, each capable of receiving carbon dioxide from, and sup-
plying oxygen to, the pulmonary capillary blood. To be most
effi cient, the correct proportion of alveolar air fl
ow (ventilation)
and capillary blood fl ow (perfusion) should be available to
each
alveolus. Any mismatching is termed
ventilation-perfusion
inequality
.
The major effect of ventilation-perfusion inequality is to
lower the
P
O
2
of systemic arterial blood. Indeed, largely because
of gravitational effects on ventilation and perfusion, there is
enough ventilation-perfusion inequality in normal people to
lower the arterial
P
O
2
about 5 mmHg. One effect of upright pos-
ture is to increase the fi lling of blood vessels at the bottom of the
lung due to gravity, which contributes to a difference in blood
fl ow distribution in the lung. This is the major explanation of
Table 13–7
Normal Gas Pressure
Venous Blood
Arterial Blood
Alveoli
Atmosphere
P
O
2
40 mmHg
100 mmHg*
105 mmHg*
160 mmHg
P
CO
2
46 mmHg
40 mmHg
40 mmHg
0.3 mmHg
*The reason that the arterial
P
O
2
and alveolar
P
O
2
are not exactly the same is described later in this chapter.
0
20
40
60
80
100
20
0
40
60
80
100
120
% of capillary length
Pulmonary capillary
P
O
2
(mmHg)
Systemic venous
P
O
2
Alveolar
P
O
2
Normal lung
Diseased lung
Figure 13–23
Equilibration of blood
P
O
2
with an alveolus with a
P
O
2
of 105
mmHg along the length of a pulmonary capillary. Note that an
abnormal alveolar diffusion barrier (diseased alveolus) does not fully
oxygenate the blood.
Figure 13–23
physiological
inquiry
What is the effect of exercise on
P
O
2
at the end of a capillary in a
normal region of the lung? In a region of the lung with diffusion
limitation due to disease?
Answer can be found at end of chapter.
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