Maintenance of the Body
and victims are perpetually exhausted because breathing re-
quires 15–20% of their total body energy supply (as opposed to
5% in healthy individuals). (2) For complex reasons, the bron-
chioles open during inspiration but collapse during expiration,
trapping huge volumes of air in the alveoli. Tis hyperinﬂation
leads to development of a permanently expanded “barrel chest”
and ﬂattens the diaphragm, thus reducing ventilation eﬃciency.
(3) Damage to the pulmonary capillaries as the alveolar walls
disintegrate increases resistance in the pulmonary circuit, forc-
ing the right ventricle to overwork and consequently become en-
larged. In addition to smoking, hereditary factors (e.g., alpha-1
antitrypsin deﬁciency) cause emphysema in some patients.
, inhaled irritants lead to chronic produc-
tion of excessive mucus. Te mucosae of the lower respiratory
passageways become inﬂamed and ﬁbrosed. Tese responses
obstruct the airways, severely impairing lung ventilation and
gas exchange. Pulmonary infections are frequent because bacte-
ria thrive in the stagnant pools of mucus. However, the degree
of dyspnea is usually moderate compared to emphysema.
As with emphysema, smoking is a major risk factor. Environ-
mental pollution also promotes chronic bronchitis.
COPD: Symptoms and Treatments
In the clinical setting you might see two very diﬀerent patterns
that represent the extremes of patients with COPD. One pat-
tern has traditionally been called the “pink puﬀer”: Tese pa-
tients work so hard to maintain adequate ventilation that they
lose weight, becoming thin but still having nearly normal blood
gases. In contrast, “blue bloaters,” commonly of stocky build, be-
come suﬃciently hypoxic that they are obviously cyanotic. Te
hypoxia causes constriction of pulmonary blood vessels, lead-
ing to pulmonary hypertension and right-sided heart failure.
±raditionally, “pink puﬀers” were associated with emphysema
while “blue bloaters” were associated with chronic bronchitis. As
usual, things are not that clear-cut. It turns out that patients with
the same underlying disease can display either of these clinical
patterns, and this may depend on a third factor—the strength of
their innate respiratory drive. Most COPD patients fall between
these two clinical extremes.
COPD is routinely treated with bronchodilators and cortico-
steroids in aerosol form (inhalers). Severe dyspnea and hypoxia
mandate oxygen use. For a few patients, surgical treatment for
lung volume reduction surgery
, may be beneﬁcial.
In this procedure, part of the grossly enlarged lungs is removed
to give the remaining lung tissue room to expand. While this
surgery does not prolong life, it can oﬀer certain COPD patients
better quality of life, although at a high cost.
COPD patients in acute respiratory distress are commonly
given oxygen. Oxygen must be administered with care, how-
ever. In some of these patients, giving pure oxygen can increase
the blood P
(and lower blood pH) to life-threatening levels.
Why does this happen? First, oxygen dilates pulmonary arteri-
oles, increasing perfusion and worsening an already poor ven-
tilation-perfusion mismatch. Second, oxygen drives more CO
oﬀ of hemoglobin (the Haldane eﬀect), dumping it into alveoli
from which it cannot be removed because of the underlying
disease. Te solution is to use the minimum concentration of
oxygen that relieves the patient’s hypoxia.
is characterized by episodes of coughing, dyspnea,
wheezing, and chest tightness—alone or in combination. A
sense of panic accompanies most acute attacks. Although some-
times classed with COPD because it is an obstructive disorder,
asthma is marked by acute episodes followed by symptom-free
periods—that is, the obstruction is
Te cause of asthma has been hard to pin down. Initially
it was viewed as a consequence of bronchospasms triggered
by various factors such as cold air, exercise, or allergens. How-
ever, bronchoconstriction has relatively little eﬀect on air ﬂow
through normal lungs. Researchers have found that in allergic
asthma (the most common kind), active inﬂammation of the
airways comes ﬁrst. Te inﬂammation is an immune response
controlled by ±
2 cells, a subset of ± lymphocytes. By secreting
certain interleukins, ±
2 cells stimulate the production of IgE
and recruit inﬂammatory cells (notably eosinophils) to the site.
Once someone has allergic asthma, the inﬂammation per-
sists even during symptom-free periods and makes the airways
hypersensitive. (Te most common triggers are in the home—
the allergens from dust mites, cockroaches, cats, dogs, and
fungi.) Once the airway walls are thickened with inﬂammatory
exudate, the eﬀect of bronchospasm is vastly magniﬁed and can
dramatically reduce air ﬂow.
About one in ten people in North America suﬀer from
asthma—children more than adults. Over the past 20 years, the
number of cases has risen dramatically, an increase which may
now be plateauing.
While asthma remains a major health problem, better treat-
ment options have reduced the number of asthma-related
deaths. Instead of merely treating the symptoms with fast-acting
bronchodilators, we now treat the underlying inﬂammation us-
ing inhaled corticosteroids. Newer approaches limit airway in-
ﬂammation by using antileukotrienes and antibodies against the
patient’s own IgE class of antibodies.
, the infectious disease caused by the bac-
, is spread by coughing and
primarily enters the body in inhaled air. ±B mostly aﬀects the
lungs but can spread through the lymphatics to other organs.
One-third of the world’s population is infected, but most
people never develop active ±B because a massive inﬂammatory
and immune response usually contains the primary infection
in ﬁbrous, or calciﬁed, nodules (tubercles) in the lungs. How-
ever, the bacteria survive in the nodules and when the person’s
immunity is weakened, they may break out and cause sympto-
matic ±B. Symptoms include fever, night sweats, weight loss,
racking cough, and coughing up blood.