472
Chapter 13
Control by P
CO
2
Figure 13–36
i
l
lustrates
an
exper
imen
t
in
wh
ich
sub
jects
breathe air with variable quantities of carbon dioxide added.
The presence of carbon dioxide in the inspired air causes an ele-
vation of alveolar
P
CO
2
and thereby an elevation of arterial
P
CO
2
.
Note that even a very small increase in arterial
P
CO
2
causes a
marked refl
ex increase in ventilation. Experiments like this have
documented that the refl
ex mechanisms controlling ventilation
prevent small increases in arterial
P
CO
2
to a much greater degree
than they prevent equivalent decreases in arterial
P
O
2
.
Of course we don’t usually breathe bags of gas containing
carbon dioxide. What is the physiological role of this refl ex? If
a defect in the respiratory system, such as emphysema, causes
the body to retain carbon dioxide, the increase in arterial
P
CO
2
stimulates ventilation. This promotes the elimination of the
carbon dioxide. Conversely, if arterial
P
CO
2
decreases below
normal levels for whatever reason, this removes some of the
stimulus for ventilation. This reduces ventilation and allows
metabolically produced carbon dioxide to accumulate, thereby
returning the
P
CO
2
to normal. In this manner, the arterial
P
CO
2
is stabilized near the normal value of 40 mmHg.
The ability of changes in arterial
P
CO
2
to control ventila-
tion refl exly is largely due to associated changes in H
+
concen-
tration (see equation 13–11). As summarized in
Figure 13–37
,
both the peripheral and central chemoreceptors initiate the
pathways that mediate these refl exes. The peripheral chemo-
receptors are stimulated by the increased arterial H
+
concen-
tration resulting from the increased
P
CO
2
. At the same time,
because carbon dioxide diffuses rapidly across the membranes
separating capillary blood and brain tissue, the increase in
arterial
P
CO
2
causes a rapid increase in brain extracellular fl
uid
P
CO
2
. This increased
P
CO
2
increases
brain extracellular-fl
uid
H
+
concentration, which stimulates the central chemorecep-
tors. Inputs from both the peripheral and central chemorecep-
tors stimulate the medullary inspiratory neurons to increase
ventilation. The end result is a return of arterial and brain
extracellular fl
uid
P
CO
2
and H
+
concentration toward normal.
Figure 13–36
Effects on respiration of increasing arterial
P
CO
2
achieved by adding
carbon dioxide to inspired air.
04
04
44
8
5
10
15
Normal resting
level
Arterial
P
CO
2
(mmHg)
Minute ventilation (L/min)
20
Figure 13–37
Pathways by which increased arterial
P
CO
2
stimulates ventilation.
Note that the peripheral chemoreceptors are stimulated by an
increase
in H
+
concentration, whereas they are also stimulated by a
decrease
in
P
O
2
(see Figure 13–35).
Return of brain extracellular
fluid [H
+
] toward normal
Return of arterial
[H
+
] toward normal
Return of brain extracellular
fluid
P
CO
2
toward normal
Return of alveolar and
arterial
P
CO
2
toward normal
Ventilation
Respiratory muscles
Contractions
Peripheral chemoreceptors
Firing
Central chemoreceptors
Firing
Reflex via medullary
respiratory neurons
Brain extracellular fluid [H
+
]
Arterial [H
+
]
Brain extracellular fluid
P
CO
2
Arterial
P
CO
2
Breathing gas mixture
containing CO
2
Alveolar
P
CO
2
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