634 SECTION VIIRespiratory Physiology
EFFECTS OF SLEEP
Respiration is less rigorously controlled during sleep than in
the waking state, and brief periods of apnea occur in normal
sleeping adults. Changes in the ventilatory response to hy-
poxia vary. If the PCO 2 falls during the waking state, various
stimuli from proprioceptors and the environment maintain
respiration, but during sleep, these stimuli are decreased and a
decrease in PCO 2 can cause apnea. During rapid eye move-
ment (REM) sleep, breathing is irregular and the CO 2 re-
sponse is highly variable.
RESPIRATORY ABNORMALITIES
ASPHYXIA
In asphyxia produced by occlusion of the airway, acute hyper-
capnia and hypoxia develop together. Stimulation of respira-
tion is pronounced, with violent respiratory efforts. Blood
pressure and heart rate rise sharply, catecholamine secretion is
increased, and blood pH drops. Eventually the respiratory ef-
forts cease, the blood pressure falls, and the heart slows. As-
phyxiated animals can still be revived at this point by artificial
respiration, although they are prone to ventricular fibrillation,
probably because of the combination of hypoxic myocardial
damage and high circulating catecholamine levels. If artificial
respiration is not started, cardiac arrest occurs in 4 to 5 min.
DROWNING
Drowning is asphyxia caused by immersion, usually in water.
In about 10% of drownings, the first gasp of water after the los-
ing struggle not to breathe triggers laryngospasm, and death
results from asphyxia without any water in the lungs. In the re-
maining cases, the glottic muscles eventually relax and fluid
enters the lungs. Fresh water is rapidly absorbed, diluting the
plasma and causing intravascular hemolysis. Ocean water is
markedly hypertonic and draws fluid from the vascular system
into the lungs, decreasing plasma volume. The immediate goal
in the treatment of drowning is, of course, resuscitation, but
long-term treatment must also take into account the circula-
tory effects of the water in the lungs.
PERIODIC BREATHING
The acute effects of voluntary hyperventilation demonstrate
the interaction of the chemical mechanisms regulating respi-
ration. When a normal individual hyperventilates for 2 to 3
min, then stops and permits respiration to continue without
exerting any voluntary control over it, a period of apnea oc-
curs. This is followed by a few shallow breaths and then by an-
other period of apnea, followed again by a few breaths
(periodic breathing). The cycles may last for some time be-
fore normal breathing is resumed (Figure 37–12). The apnea
apparently is due to a lack of CO 2 because it does not occur
following hyperventilation with gas mixtures containing 5%
CO 2. During the apnea, the alveolar PO 2 falls and the PCO 2 ris-
es. Breathing resumes because of hypoxic stimulation of the
carotid and aortic chemoreceptors before the CO 2 level has re-
turned to normal. A few breaths eliminate the hypoxic stimu-
lus, and breathing stops until the alveolar PO 2 falls again.
Gradually, however, the PCO 2 returns to normal, and normal
breathing resumes. Changes in breathing patterns can be
symptomatic of disease (Clinical Box 37–3).
EFFECTS OF EXERCISE
Exercise provides a physiological example to explore many of
the control systems discussed above. Of course, many cardio-
vascular and respiratory mechanisms must operate in an inte-
grated fashion if the O 2 needs of the active tissue are to be met
and the extra CO 2 and heat removed from the body during ex-
ercise. Circulatory changes increase muscle blood flow while
maintaining adequate circulation in the rest of the body. In
addition, there is an increase in the extraction of O 2 from the
blood in exercising muscles and an increase in ventilation.
This provides extra O 2 , eliminates some of the heat, and ex-
cretes extra CO 2. A focus on regulation of ventilation and tis-
sue O 2 is presented below, as many other aspects of regulation
have been presented in previous chapters.
CHANGES IN VENTILATION
During exercise, the amount of O 2 entering the blood in the
lungs is increased because the amount of O 2 added to each
FIGURE 37–12 Changes in breathing and composition of
alveolar air after forced hyperventilation for 2 min. Bars in bottom
indicate breathing, whereas blank spaces are indicative of apnea.
0
40
80
120
160
Partial pressure (mm Hg)
Breathing 01 23456
pattern
Alveolar PO 2
Alveolar PCO 2
Time after stopping hyperventilation
(min)