The Respiratory System
to increases in P
, and a substantial decline in P
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
levels, so the P
of individuals living
at high altitudes is typically below 40 mm Hg (its value at sea
High-altitude conditions always result in lower-than-normal
hemoglobin saturation levels because less O
is available to be
loaded. For example, at about 19,000 ± above sea level, O
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
needs of the tissues are still met under resting
Additionally, at high altitudes hemoglobin’s aﬃnity for O
is reduced because BPG concentrations increase. Tis releases
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
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
An injured soccer player arrives by ambulance in the
emergency room. She is in obvious distress, breathing rapidly.
is 26 mm Hg and pH is 7.5. Is she suffering
from hyperventilation or hyperpnea? Explain.
What long-term adjustments does the body make when
living at high altitude?
For answers, see Appendix H.
of the Respiratory System
Compare the causes and consequences of chronic
bronchitis, emphysema, asthma, tuberculosis, and lung
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-
chronic obstructive pulmonary disease
. 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
chronic obstructive pulmonary diseases (COPD)
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
More than 80% of patients have a history of smoking.
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
(insuﬃcient ventilation in relation to
metabolic needs, causing them to retain CO
acidosis, and hypoxemia.
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,
• Air pollution
or air trapping
• Frequent infections
• Respiratory acidosis
irritation and inflammation
Breakdown of elastin in
connective tissue of lungs
• Destruction of alveolar
• Loss of lung elasticity
• Excess mucus production
• Chronic productive cough
The pathogenesis of COPD.