Chapter 22
The Respiratory System
839
22
to increases in P
CO
2
, and a substantial decline in P
O
2
directly
stimulates them. As a result, ventilation increases as the brain
attempts to restore gas exchange to previous levels.
Within a few days, the minute ventilation stabilizes at a level
2–3 L/min higher than the sea level rate. Increased ventilation
also reduces arterial CO
2
levels, so the P
CO
2
of individuals living
at high altitudes is typically below 40 mm Hg (its value at sea
level).
High-altitude conditions always result in lower-than-normal
hemoglobin saturation levels because less O
2
is available to be
loaded. For example, at about 19,000 ± above sea level, O
2
satu-
ration of arterial blood is only 67% (compared to nearly 98%
at sea level). But Hb unloads only 20–25% of its oxygen at sea
level, which means that even at the reduced saturations at high
altitudes, the O
2
needs of the tissues are still met under resting
conditions.
Additionally, at high altitudes hemoglobin’s affinity for O
2
is reduced because BPG concentrations increase. Tis releases
more O
2
to the tissues during each circulatory round.
Although body tissues at high altitude receive adequate
oxygen under normal conditions, problems arise when all-out
efforts are demanded of the cardiovascular and respiratory sys-
tems (as athletes discovered during the 1968 Summer Olympics
on the high mesa of Mexico City, at 7370 ±). Unless a person is
fully acclimatized, such conditions almost guarantee that body
tissues will become severely hypoxic.
When blood O
2
levels decline, the kidneys produce more
erythropoietin, which stimulates bone marrow production of
RBCs (see Chapter 17, p. 636). Tis phase of acclimatization,
which occurs slowly, provides long-term compensation for liv-
ing at high altitudes.
Check Your Understanding
21.
An injured soccer player arrives by ambulance in the
emergency room. She is in obvious distress, breathing rapidly.
Her blood
P
CO
2
is 26 mm Hg and pH is 7.5. Is she suffering
from hyperventilation or hyperpnea? Explain.
22.
What long-term adjustments does the body make when
living at high altitude?
For answers, see Appendix H.
Homeostatic Imbalances
of the Respiratory System
Compare the causes and consequences of chronic
bronchitis, emphysema, asthma, tuberculosis, and lung
cancer.
Te respiratory system is particularly vulnerable to infectious
diseases because it is wide open to airborne pathogens. We con-
sidered many of these conditions, such as rhinitis and laryngitis,
earlier in the chapter.
Here we turn our attention to the most disabling respira-
tory disorders:
chronic obstructive pulmonary disease
(
COPD
),
asthma, tuberculosis,
and
lung cancer
. COPD and lung cancer
are living proof of the devastating effects of tobacco smoke
on the body. Long known to promote cardiovascular disease,
smoking is perhaps even more effective at destroying the lungs.
Chronic Obstructive Pulmonary Disease
(COPD)
Te
chronic obstructive pulmonary diseases (COPD)
, exem-
plified best by emphysema and chronic bronchitis, are a major
cause of disability and death in North America. Te key physi-
ological feature of these diseases is an irreversible decrease in
the ability to force air out of the lungs. Other features they share
in common
(Figure 22.27)
:
More than 80% of patients have a history of smoking.
Dyspnea
(disp-ne
9
ah), difficult or labored breathing o±en
referred to as “air hunger,” gets progressively worse.
Coughing and frequent pulmonary infections are common.
Most COPD victims develop respiratory failure manifested
as
hypoventilation
(insufficient ventilation in relation to
metabolic needs, causing them to retain CO
2
), respiratory
acidosis, and hypoxemia.
Emphysema
Emphysema
is distinguished by permanent enlargement of the
alveoli, accompanied by destruction of the alveolar walls. Invari-
ably the lungs lose their elasticity. Tis has three important con-
sequences: (1) Accessory muscles must be enlisted to breathe,
T
obacco smok
e
• Air pollution
Airway
obstruction
or air trapping
• Dyspnea
• Frequent infections
• Hypoventilation
• Hypoxemia
• Respiratory acidosis
α
-1 antitrypsin
deficiency
Continual bronchial
irritation and inflammation
Breakdown of elastin in
connective tissue of lungs
Emphysema
• Destruction of alveolar
wa
lls
• Loss of lung elasticity
Chronic bronchitis
• Excess mucus production
• Chronic productive cough
Figure 22.27
The pathogenesis of COPD.
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