476
Chapter 13
Alcohol inhibits the cough reflex, which may par-
tially explain the susceptibility of alcoholics to choking and
pneumonia.
Another example of a protective refl ex is the immediate ces-
sation of respiration that is often triggered when noxious agents
are inhaled. Chronic smoking may cause a loss of this refl ex.
Voluntary Control of Breathing
Although we have discussed in detail the involuntary nature of
most respiratory refl exes, the voluntary control of respiratory
movements is important. Voluntary control is accomplished
by descending pathways from the cerebral cortex to the motor
neurons of the respiratory muscles. This voluntary control of
respiration cannot be maintained when the involuntary stimuli,
such as an elevated
P
CO
2
or H
+
concentration, become intense.
An example is the inability to hold your breath for very long.
The opposite of breath-holding—deliberate hyperven-
tilation—lowers alveolar and arterial
P
CO
2
and increases
P
O
2
.
Unfortunately, swimmers sometimes voluntarily hyperventi-
late immediately before underwater swimming to be able to
hold their breath longer. We say “unfortunately” because the
low
P
CO
2
may still permit breath-holding at a time when the
exertion is lowering the arterial
P
O
2
to levels that can cause
unconsciousness and lead to drowning.
Besides the obvious forms of voluntary control, respira-
tion must also be controlled during such complex actions as
speaking, singing, and swallowing.
Refl
exes from J Receptors
In the lungs, either in the capillary walls or the interstitium, are
a group of receptors called
J receptors.
They are normally dor-
mant but are stimulated by an increase in lung interstitial pres-
sure caused by the collection of fl uid in the interstitium. Such an
increase occurs during the vascular congestion caused by either
occlusion of a pulmonary vessel
(
pulmonary embolus
)
or left
ventricular heart failure (Chapter 12), as well as by strong exer-
cise in healthy people. The main refl ex effects are rapid breathing
(tachypnea) and a dry cough. In addition, neural input from
J receptors gives rise to sensations of pressure in the chest and
dyspnea
—the feeling that breathing is labored or diffi cult.
Hypoxia
Hypoxia
is defi ned as a defi ciency of oxygen at the tissue
level. There are many potential causes of hypoxia, but they
can be classifi ed into four general categories: (1)
hypoxic
hypoxia
(also termed
hypoxemia
), in which the arterial
P
O
2
is reduced; (2)
anemic
or
carbon monoxide hypoxia,
in
which the arterial
P
O
2
is normal but the total oxygen
content
of the blood is reduced because of inadequate numbers of
erythrocytes, defi cient or abnormal hemoglobin, or compe-
tition for the hemoglobin molecule by carbon monoxide;
(3)
ischemic hypoxia
(also called hypoperfusion hypoxia), in
which blood fl ow to the tissues is too low; and (4)
histotoxic
hypoxia,
in which the quantity of oxygen reaching the tissues
is normal, but the cell is unable to utilize the oxygen because
a toxic agent—cyanide, for example—has interfered with the
cell’s metabolic machinery.
The primary causes of hypoxic hypoxia in disease are
listed in
Table 13–11
. Exposure to the reduced
P
O
2
of high
altitude also causes hypoxic hypoxia but is, of course, not a
disease. The brief summaries in Table 13–11 provide a review
of many of the key aspects of respiratory physiology and patho-
physiology described in this chapter.
This table also emphasizes that some of the diseases that
produce hypoxia also produce carbon dioxide retention and
an increased arterial
P
CO
2
(
hypercapnea
).
In such cases, treat-
ing only the oxygen defi cit by administering oxygen may be
inadequate because it does nothing about the hypercapnea.
Indeed, such therapy may be dangerous. The primary respira-
tory drive in such patients is the hypoxia, because for several
reasons the refl
ex ventilatory response to an increased
P
CO
2
may be lost in chronic situations. The administration of pure
oxygen may cause such patients to stop breathing.
Why Do Ventilation-Perfusion Abnormalities
Affect O
2
More than CO
2
?
As described in Table 13–11, ventilation-perfusion inequalities
often cause hypoxemia without associated increases in
P
CO
2
.
The explanation for this resides in the fundamental difference
between the transport of O
2
and CO
2
in the blood. Recall that
the shape of the oxygen dissociation curve is sigmoidal (see
Figure 13–26). An increase in
P
O
2
above 100 mmHg does not
Table 13–11
Causes of a Decreased Arterial
P
O
2
(Hypoxic Hypoxia) in Disease
1.
Hypoventilation
may be caused (a) by a defect anywhere
along the respiratory control pathway, from the medulla
through the respiratory muscles, (b) by severe thoracic
cage abnormalities, and (c) by major obstruction of the
upper airway. The hypoxemia of hypoventilation is always
accompanied by an increased arterial
P
CO
2
.
2.
Diffusion impairment
results from thickening of the
alveolar membranes or a decrease in their surface area.
In turn, it causes blood
P
O
2
and alveolar
P
O
2
to fail to
equilibrate. Often it is apparent only during exercise. Arterial
P
CO
2
is either normal, because carbon dioxide diffuses more
readily than oxygen, or reduced, if the hypoxemia refl exly
stimulates ventilation.
3. A
shunt
is (a) an anatomic abnormality of the cardiovascular
system that causes mixed venous blood to bypass ventilated
alveoli in passing from the right side of the heart to the left
side, or (b) an intrapulmonary defect in which mixed venous
blood perfuses unventilated alveoli (ventilation-perfusion =
0). Arterial
P
CO
2
generally does not rise because the effect
of the shunt on arterial
P
CO
2
is counterbalanced by the
increased ventilation refl exly stimulated by the hypoxemia.
4.
Ventilation-perfusion inequality
is by far the most
common cause of hypoxemia. It occurs in chronic
obstructive lung diseases and many other lung diseases.
Arterial
P
CO
2
may be normal or increased, depending upon
how much ventilation is refl exly stimulated.
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