582
U N I T 6
Respiratory Function
affords the potential for impaired gas exchange because
of mismatching of ventilation and perfusion. The FVC
is the amount of air that can be forcibly exhaled after
maximal inspiration. In patients with chronic lung
disease, the FVC is decreased, the FEV
1.0
is decreased,
and the ratio of FEV
1.0
to FVC is decreased. Lung vol-
ume measurements reveal a marked increase in RV, an
increase in TLC, and elevation of the RV-to-TLC ratio.
These and other measurements of expiratory flow are
determined by spirometry and are used in the diagno-
sis and severity of COPD (see Chapter 21, Fig. 21-15).
Other diagnostic measures become important as the
disease advances. Measures of exercise tolerance, nutri-
tional status, hemoglobin saturation, and arterial blood
gases can be used to assess the overall impact of COPD
on health status and to direct treatment.
The treatment of COPD depends on the stage of
the disease and often requires an interdisciplinary
approach.
10,44
Smoking cessation is the only measure
that slows the progression of the disease. Maintaining
and improving physical and psychosocial functioning is
an important part of the treatment program. A long-
term pulmonary rehabilitation program can significantly
reduce hospitalizations and increase a person’s ability to
manage and cope with his or her impairment in a posi-
tive way. This program includes breathing exercises that
focus on restoring the function of the diaphragm, reduc-
ing the work of breathing, and improving gas exchange.
Physical conditioning with appropriate exercise training
increases maximal oxygen consumption and reduces
ventilatory effort and heart rate for a given workload.
Work simplification and energy conservation strategies
may be needed when impairment is severe.
Respiratory tract infections can prove life-threaten-
ing to persons with severe COPD. A person with COPD
should avoid exposure to others with known respira-
tory tract infections and should avoid attending large
gatherings during periods of the year when influenza or
respiratory tract infections are prevalent. Immunization
for influenza and pneumococcal infections decreases the
likelihood of their occurrence. Although antibiotics are
used to treat acute exacerbations of COPD due to bacte-
rial infection, there is no evidence that the prophylactic
use of antibiotics prevents acute exacerbations.
The pharmacologic treatment of COPD includes
the use of bronchodilators, including inhaled adrener-
gic and anticholinergic agents.
10,44
Inhaled
β
2
-agonists
have been the mainstay of treatment of COPD for many
years. It has been suggested that long-acting inhaled
β
2
-
agonists may be even more effective than the short-act-
ing forms of the drug. The anticholinergic drugs, which
are administered by inhalation, produce bronchodila-
tion by blocking parasympathetic cholinergic receptors
that produce contraction of bronchial smooth muscle.
They also reduce the volume of sputum without alter-
ing its viscosity. Because these drugs have a slower onset
and longer duration of action, they typically are used
on a regular basis rather than as needed. Inhalers that
combine an anticholinergic drug with a
β
2
-adrenergic
agonist are available. Oral theophylline may be used
in treatment of persons who fail to respond to inhaled
bronchodilators. The long-acting theophylline prepara-
tions may be used to reduce overnight declines in respi-
ratory function. When theophylline is prescribed, blood
levels are used as a guide in arriving at an effective dose
schedule.
Although inhaled corticosteroids often are used in
treatment of COPD, there is controversy regarding their
usefulness. There is evidence that inflammation in COPD
is not suppressed by inhaled or oral corticosteroids.
44
Because corticosteroids are useful in relieving asthma
symptoms, they may benefit persons with asthma con-
comitant with COPD. Inhaled corticosteroids also may
be beneficial in treating acute exacerbations of COPD,
minimizing the undesirable effects that often accompany
systemic use.
Oxygen therapy is prescribed for selected persons
with significant hypoxemia (arterial PO
2
< 55 mm Hg).
Administration of continuous low-flow (1 to 2 L/min)
oxygen to maintain arterial PO
2
levels between 55 and
65 mm Hg decreases dyspnea and pulmonary hyper-
tension and improves neuropsychological function and
activity tolerance.
10,44
The overall goal of oxygen ther-
apy is to maintain a hemoglobin oxygen saturation of at
least 90%. Portable oxygen administration units, which
allow mobility and the performance of activities of daily
living, are often used in severe COPD. Because the ven-
tilatory drive associated with hypoxic stimulation of the
peripheral chemoreceptors does not occur until the arte-
rial PO
2
has been reduced to about 60 mm Hg or less,
increasing the arterial PO
2
above 60 mm Hg tends to
depress the hypoxic stimulus for ventilation and often
leads to hypoventilation and carbon dioxide retention.
Bronchiectasis
Bronchiectasis is characterized by a permanent dilation
of bronchi caused by destruction of the bronchial muscle
wall and elastic supporting tissue
16,46,47
(Fig. 23-11). It is
not a primary disease but occurs secondary to a number of
abnormalities that profoundly obstruct the airways
or produce persistent infection, including atelectasis,
obstruction of the smaller airways, diffuse bronchitis,
and cystic fibrosis.
15
In the past, bronchiectasis often fol-
lowed a necrotizing bacterial pneumonia that frequently
complicated measles, pertussis (whooping cough), or
influenza. Tuberculosis was also commonly associated
with bronchiectasis. Thus, with the advent of antibiotics
that more effectively treat respiratory infections such as
tuberculosis, and with immunization against pertussis
and measles, there has been a marked decrease in the
prevalence of bronchiectasis.
Etiology and Pathogenesis
Two processes are critical to the pathogenesis of bron-
chiectasis: obstruction and chronic persistent infec-
tion.
15,16
Regardless of which may come first, both cause
damage to the bronchial walls, leading to weakening
and dilation. On gross examination, bronchial dila-
tion is classified as saccular, cylindrical, or varicose.
16,47
Saccular bronchiectasis involves the proximal third to
