Chapter 22
The Respiratory System
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22
blood takes O
2
away more quickly than ventilation can replen-
ish it
(Figure 22.19a)
. As a result, the terminal arterioles con-
strict, redirecting blood to respiratory areas where P
O
2
is high
and oxygen pickup is more efficient.
In alveoli where ventilation is maximal, high P
O
2
dilates pul-
monary arterioles and blood flow into the associated pulmonary
capillaries increases (Figure 22.19b). Notice that the autoregula-
tory mechanism controlling pulmonary vascular muscle is the
opposite of the mechanism controlling arterioles in the systemic
circulation.
Influence of Local P
CO
2
on Ventilation
Bronchioles servicing
areas where alveolar CO
2
levels are high dilate, allowing CO
2
to
be eliminated from the body more rapidly. Bronchioles serving
areas where P
CO
2
is low constrict.
Balancing Ventilation and Perfusion
Te changing diam-
eter of local bronchioles and arterioles synchronizes alveolar
ventilation and pulmonary perfusion. Poor alveolar ventilation
results in low oxygen and high carbon dioxide levels in the al-
veoli. Consequently, pulmonary arterioles constrict and airways
dilate, bringing blood flow and air flow into closer physiological
match. High P
O
2
and low P
CO
2
in the alveoli cause bronchioles
serving the alveoli to constrict, and promote flushing of blood
into the pulmonary capillaries.
Although these homeostatic mechanisms provide appropri-
ate conditions for efficient gas exchange, they never completely
balance ventilation and perfusion in every alveolus due to other
factors. In particular, (1) gravity causes regional variations in
both blood and air flow in the lungs, and (2) the occasional
alveolar duct plugged with mucus creates unventilated areas.
Tese factors, together with blood shunted from the bron-
chial veins, account for the slight drop in P
O
2
from alveolar air
(104 mm Hg) to pulmonary venous blood (100 mm Hg), as
shown in Figure 22.17.
Internal Respiration
Internal respiration involves capillary gas exchange in body tis-
sues. In internal respiration, the partial pressure and diffusion
gradients are reversed from the situation we have just described
for external respiration and pulmonary gas exchange. However,
the factors promoting gas exchanges between systemic capillar-
ies and tissue cells are essentially identical to those acting in the
lungs (see Figure 22.17).
±issue cells continuously use O
2
for their metabolic activities
and produce CO
2
. Because P
O
2
is always lower in tissues than
it is in systemic arterial blood (40 mm Hg versus 100 mm Hg),
O
2
moves rapidly from blood into tissues until equilibrium is
reached. At the same time, CO
2
moves quickly along its pressure
gradient into blood. As a result, venous blood draining the tissue
capillary beds and returning to the heart has a P
O
2
of 40 mm Hg
and a P
CO
2
of 45 mm Hg.
In summary, the gas exchanges that occur between blood
and alveoli and between blood and tissue cells take place by
Mismatch of ventilation and perfusion
ventilation and/or
perfusion of alveoli
causes local
P
CO
2
and
P
O
2
Pulmonary arterioles
serving these alveoli
constrict
O
2
autoregulates
arteriolar diameter
O
2
autoregulates
arteriolar diameter
Match of ventilation
and perfusion
ventilation,
perfusion
Mismatch of ventilation and perfusion
ventilation and/or
perfusion of alveoli
causes local
P
CO
2
and
P
O
2
Pulmonary arterioles
serving these alveoli
dilate
Match of ventilation
and perfusion
ventilation,
perfusion
(a) Ventilation less than perfusion
(b) Ventilation greater than perfusion
Figure 22.19
Ventilation-perfusion coupling.
Autoregulatory events result in local matching
of blood flow (perfusion) through the pulmonary capillaries with the amount of alveolar ventilation.
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