You see a 59-year-old man previously diagnosed as having COPD
in the clinic 3 months following discharge from the Intensive Care
Unit (ICU) for a severe exacerbation of COPD. The patient was advised
to stop smoking, but failed on several attempts. He had received
influenza virus vaccine in the past fall. Following an outing for
Christmas shopping, the patient developed a cold, which “settled
in his chest.” Increased sputum with purulence and fever
was followed by worsening dyspnea. He suddenly became extremely
dyspneic and was admitted to the ICU via the emergency room. Following
treatment with oxygen, antibiotics, and systemic corticosteroids,the
patient improved slowly and was discharged on home oxygen delivered
by a concentrator. Corticosteroids were not continued after discharge.
When seen in your clinic 1 month later, the patient was accompanied
by his daughter, who is wheeling the oxygen E-cylinder that was
prescribed for portability. Your patient reported that he remained
severely short of breath and could not regain the 10 pounds of weight
that he had lost during the acute exacerbation. He commented on
being “depressed” over the fact that he needed to “wear
oxygen.” His appetite was poor and he had difficulty sleeping.
He had rarely gone outside of his home since discharge. The patient
was receiving albuterol by MDI three times daily, ipratropium by
MDI three times daily, and sustained release theophylline, 600 mg
at bedtime. Your patient is moderately short of breath. He is alert
and cooperative. Physical examination reveals decreased breath sounds.
Cardiac and extremity examination are normal. Edema is absent. The
patient’s FEV1 is 1.10 L/s (29% of
predicted), FVC is 3.42 (75% of predicted), and FEV1/FVC
ratio is 46%. (No previous spirometric tests had ever been
done before!) The patient’s oxygen saturation, measured
by a pulse oximeter, is 97%, while receiving oxygen by
a nasal cannula at 2 L/min. You consider the following
treatment options (choose the one most appropriate for this patient):
- 1. Add a selective serotonin
reuptake inhibitor (SSRI) antidepressant
- 2. Add oral corticosteroids
- 3. Measure theophylline blood
- 4. Add a salmeterol MDI
- 5. Stop oxygen and do oximetry
after 20 min
- 6. Continue the present treatment
and see the patient again in 3 months
Comment: Of course, any patient’s
problem may suggest more than one therapeutic option. This patient, with
severe COPD, who has just recovered from his first bout of acute
respiratory failure and is now depressed and receiving oxygen, is
in need of aggressive systematic therapy to prevent relapse and
readmission. But of greater importance is the challenge of improving
the patient to a state of general health and quality of life.
Probably the choice least likely to help would be to add an antidepressant.
Depression, anxiety, and somatic preoccupation are common in patients
with advanced COPD. In most cases, the depression is reversible
through methods of pulmonary rehabilitation and adjustments in therapy. More
recent studies of patients who receive home oxygen have shown a
high prevalence of depression, often a result of reduced mobility
and opportunities for social interaction.
You might be tempted to add corticosteroids once again, as they
have been shown to be helpful in acute exacerbations of disease.
In fact, there is some suggestion from uncontrolled clinical trials that
long-term administration of corticosteroids may slow the rate of
decline in ventilatory function, but no randomized controlled clinical
trials have shown an improvement in survival.
Theophylline often has a beneficial effect on respiratory muscle
function, and usually does not lead to insomnia in patients with
COPD. The effect on respiratory muscle function is not directly related
to blood theophylline levels. These measurements are also expensive.
Thus, in the absence of gastrointestinal upset or cardiac arrhythmias,
measurement of theophylline blood levels is not commonly done to
guide theophylline therapy.
Salmeterol, a long-acting β-agonist, may be
useful in the maintenance management of COPD. Salmeterol provides
equal clinical benefit when compared with ipratropium.However,
salmeterol cannot be used for breakthrough attacks because of its
prolonged duration of action. Either albuterol or ipratropium is
required for this purpose. Using the combination of albuterol with
ipratropium in a single MDI would be a reasonable and useful strategy
in either exacerbations or in maintenance management.
Stopping oxygen for 20 min and repeating pulse oximetry would
be the most important option. Because this patient has a 97% saturation
on 2 L, it could be that room air hypoxemia is not present. Too
many patients are encumbered by oxygen, often inappropriately delivered
via a stationary system, which may, in fact, result in reduced activities
of daily living and depression. Today, ambulatory oxygen is the
standard of care for patients who can and will increase their activities
and exercise both inside and outside of the home.
Continuing with the same treatment and seeing the patient again
3 months later might be the treatment option selected by some physicians.
However, this would probably promote a further period of unnecessary
self-exile, because of the patient’s preoccupation with
the need for oxygen therapy. The continued use of an inappropriate
home oxygen system would not be desirable. A more active treatment
strategy would be more appropriate.
What happened? Oxygen was stopped at the time of the physical
examination and counseling. After 20 min patients with hyperinflation
and air trapping, as a result of increased RV and temporary “storage” of
oxygen, reach a steady state. Following the discontinuation of oxygen,
pulse oximetry was repeated on room air and oxygen saturation was
92%. On walking around the clinic while breathing air,
the patient’s oxygen saturation was 90% with an
accompanying pulse of 88.
Stopping the oxygen 3 months after discharge is important because
it helps both the physician and the patient understand that oxygen
is no longer necessary, at least at the present time. By learning this
fact, the patient can be encouraged to gradually increase walking
to 20–30 min or more each day. This can be accomplished
by walking outside on good weather days or walking in shopping malls
or within other covered structures to improve exercise tolerance
during periods of poor weather. Regular daily exercise is the key
ingredient of pulmonary rehabilitation.
Pulmonary rehabilitation, the details of which go beyond the
scope of this chapter, can briefly be described as focusing on patient
education, breathing retraining, physical reconditioning, and the adjustment
of pharmacological agents. Oxygen is useful only in those patients
with chronic stable hypoxemia. The Nocturnal Oxygen Therapy Trial
(NOTT) demonstrated a survival benefit from long-term ambulatory
oxygen, compared with shorter periods of oxygen administration via
a stationary system. Whether the improved survival with ambulatory
oxygen in the NOTT study (Figure 7–1) was due
to the duration of oxygen or the method of delivery has never been
adequately studied. A reevaluation of the NOTT study strongly suggests
that patients who had better walk tolerance during exercise training
prior to receiving oxygen, compared with those with poorer walk
tolerance, had a much better survival with ambulatory oxygen than
with stationary oxygen alone. Even patients with poor exercise tolerance
did better with ambulatory oxygen than with stationary oxygen.
Comparison of survival in nocturnal oxygen (NOT) patients
compared with continuous oxygen therapy (COT) patients. Survival
is significantly better at each year of observation (Nocturnal Oxygen
The prognosis for patients with advanced COPD has been improving
in recent years. This is probably due to the fact that today more
aggressive therapy is given to prevent exacerbations of COPD, which
helps to prevent acute respiratory failure. More effective strategies
to achieve smoking cessation, advances in the treatment of acute
respiratory failure, and the use of oxygen and pulmonary rehabilitation
have together improved the length and quality of life for many patients
with advanced COPD.
You see a 41-year-old woman in the clinic because of her concerns
about emphysema and lung cancer. Her worry is over the fact that
her mother, who has severe emphysema, has recently been found to
have lung cancer, which is inoperable because of its location near
the carina. The patient had started smoking at age 13, and had consumed,
on average, 1.5 packs of cigarettes per day (42 pack-years). She
reports a “cigarette cough” and poor pep and energy.
She is still able to work as a secretary in a large law firm. Because
smoking in the office is prohibited, she takes numerous “coffee
breaks” and smokes outside of the building to deal with
her nicotine craving. Her mother is receiving radiation therapy
for lung cancer in an attempt to improve the staging, with the possibility
of a lung resection later.
Physical examination is normal. Which one of the following diagnostic
procedures would be appropriate at this time?
- 1. Chest x-ray
- 2. Arterial blood gases
- 3. Spirometry
- 5. Sputum cytology
- 6. CT scan of chest
Because her mother has lung cancer, and lung cancer has a familial
component, you might be tempted to do a chest x-ray, even at the
patient’s young age. In fact, most physicians are now beginning
to realize that women are more susceptible to developing lung cancer
than men at a given age and level of smoking.In fact,
women tend to have lung cancer at a younger age than men. A chest
x-ray, however, is not nearly as sensitive as CT scanning in diagnosing
early-stage lung cancer. Low-radiation dose spiral CT scanning would
be appropriate if airflow obstruction were present. The risk of
lung cancer is four- to sixfold greater in patients with airflow
obstruction, compared with normal airflow, with all other background
factors being equal (ie, smoking, occupational risk, and family
Accordingly, spirometry is the most practical and necessary option
in this patient. It is the most important method of diagnosing COPD
and assessing responses to therapy.
α1-Antitrypsin could be considered
in view of the family history of emphysema, but only about 3% of
COPD is due to α1-antitrypsin deficiency.
It is much more important to identify airflow obstruction by spirometry
in assessing patients with a family history of emphysema. Sputum
cytology could also be considered and, because of heavy smoking
and airflow obstruction, could reveal dysplastic premalignant lesions
or even roentgenographically occult lung cancer.
Her spirometry results are as follows: FEV1 is 2.05
(67% of predicted), FVC is 4.10 (110% of predicted),
and FEV1/FVC ratio is 51%. Thus, this
patient clearly has airflow obstruction with an FEV1 of
less than 70% of predicted and the interesting fact that
the FVC is 110% of predicted. By the GOLD criteria, the
stage of this woman’s COPD would be classified as moderate.
Other ATS and BTS criteria would classify her as mild. Of greater
importance, in view of her young age and significant loss of airflow,
most experienced clinicians would consider her severity as moderate
and in need of treatment immediately.
Of course, the most important therapy for this patient is smoking
cessation. The Lung Health Study has clearly shown that patients
between the ages of 35 and 60 have a significant improvement in
FEV1 following smoking cessation, compared with accelerated
losses during continued smoking, over a 5-year period (see Figure
7–2). Today, there are improved strategies in
smoking cessation, with a growing number of pharmacological agents
available to use before or on the quit date. These products are
listed in Table 7–3. Assuming this patient had normal ventilatory
function at age 20, which may not be true since she started smoking
as a teenager, she has lost a total of 1500 mL in 21 years, or a
loss of over 71 mL per year. Normal losses for a person this age
and height (5 foot 5 inches) are approximately 25 mL per year. Thus,
with a similar decline over the next 20 years with continued smoking,
at 61 years (her mother’s age) she will have lost another
1420 mL. By age 61 her FEV1 will have declined to 0.73
L, which is in the range of far advanced and disabling emphysema
(see Figure 7–3). By contrast, if she stops smoking
and only loses FEV1 at the rate of 25 mL per year, she
will lose 500 mL and her FEV1 will be 1.55 at age 61, which
is compatible with a state of reasonably good health (see Figure
7–3). Thus, a key to success in this patient is smoking
cessation to prevent a disastrous outcome.
Mean postbronchodilator forced expiratory volume at
1 s (FEV1) for participating in the smoking intervention
and placebo groups who were sustained quitters and continuing smokers.
The two curves diverge sharply after baseline. (Adopted
from Anthonisen NR et al: Effects of smoking intervention and the
use of an inhaled anticholinergic bronchodilator on the rate of
decline of FEV1. The Lung Health Study. JAMA 1994;272:1502.)
Patient 2 case example: FEV1 projections. This
illustrates the accelerated losses of FEV1 that have occurred
at age 41, assuming that the patient’s lung function was
normal at age 20. The two projections portray a slower decline in
FEV1 due to stopping smoking, compared with a more rapid
decline if she continues to smoke.
This patient succeeds in stopping smoking and you see her again
on follow-up 1 year later. On this occasion, her FEV1 is
2.20 L/s. She is now concerned about a 12-pound weight
gain and has further concerns about the future, because her mother
has died of a massive hemorrhage. She again asks about her risk
of lung cancer. The following should be considered now:
- 1. Sputum cytology
- 2. CT scan
- 3. Reassurance that her smoking
cessation at a young age will be sufficient
- 4. Chest x-ray
- 5. Appetite suppressants
This patient is certainly at high risk for lung cancer, even
though she has stopped smoking. Today more lung cancer is found
in former smokers than in current smokers.Although still
controversial, it would be appropriate, based upon recent studies,
to order a low-radiation dose spiral CT scan looking for an occult
peripheral nodule, and sputum cytology to find indications of dysplastic
preneoplastic or neoplastic lesions. Today, the combination of sputum cytology
and CT scanning offers the greatest promise in early identification
of lung cancer. Both sputum cytology and CT scans identify patients
in early stages, where the likelihood of cure is 60% to
80%. When lung cancer is diagnosed by accident by chest
x-rays that are done for other reasons, or on the basis of symptoms,
the 5-year survival is a dismal 14%. Chest x-rays are not
as sensitive as CT scans in the diagnosis of early lung cancer.
Many smokers gain some weight on stopping, but this occurs mostly
in the initial stage of quitting and often does not progress. Dietary
counseling would be appropriate because of the weight gain, but
the use of anorectic agents should be avoided.
A 45-year-old man sees you for a “routine physical.” He
prides himself on a state of good physical fitness. He plays golf
each weekend, and jogs at least 30 min per day. This program was
begun after an earlier diagnosis of hypertension, hypercholesterolemia,
and insulin resistance. Following the exercise and weight loss program,
the patient’s blood pressure returned to normal. Serum
lipids became high-density lipoprotein (HDL) 60, low-density lipoprotein
(LDL) 105, triglycerides 200, and fasting blood sugar 90. He had
smoked a pack per day for 21 years, but stopped 2 years ago when
he began his physical reconditioning program.
You review the patient’s records and find that a chest
x-ray, EKG, and SMA-22 done in the past year as a part of an insurance
evaluation were normal. Spirometric tests have never been done on this
patient. His height is 5 foot 11 inches. Spirometry reveals FEV1 is
3.43 L/s (80%), FVC is 5.28 (100%), and
FEV1/FVC ratio is 65%. You recognize
that this patient has early stage COPD because the FEV1/FVC
ratio is less than 70%, even though his FEV1 is
only borderline low. The patient’s FEV1 elevates
by 350 mL to 3.84 L/s, an increase of 12%, in
response to albuterol. This patient asks you if there is any therapy
that will prevent the decline of his FEV1 over his lifetime.
You consider one of the following options:
- 1. Reassurance that stopping
smoking is sufficient to ensure good health
- 2. Ipratropium, two puffs, three
- 3. Salmeterol, two puffs, twice
- 4. Inhaled corticosteroids
- 5. Oral theophylline
Although this patient meets the criterion of a significant bronchodilator
response, ie, a 12% improvement of FEV1 in response
to an inhaled agent, there is no evidence that the long-term use
of either a β-agonist or an anticholinergic will
alter the rate of decline in ventilatory function. During the Lung Health
Study, ipratropium remained effective during the 5 years that it
was used, but it did not change the rate of decline of baseline
FEV1. Another study, however, showed that ipratropium had
the effect of elevating baseline lung function. Thus, if a bronchodilator
were to be used, ipratropium would probably be superior to a β-agonist.
It would also have fewer side effects of tremor, tachycardia, or
Recently there has been great interest in determining whether
corticosteroids can slow the rate of decline in FEV1 in
COPD. Five studies have failed to show a sustained benefit in baseline
FEV1. One study showed a slight improvement in a subset
of patients, but an overall rate of decline equal to that of placebo.
At least two studies have shown an improvement in symptoms and quality
of life,whereas one study has shown a statistically significant
reduction in bone density.
In this patient, who has previously demonstrated insulin resistance,
steroid systemic effects might worsen insulin resistance and ultimately
result in diabetes. Thus, inhaled corticosteroids should not be
used. Judged by his FEV1 and state of physical fitness,
this patient does not face premature morbidity and mortality from COPD.
He does not require any medications for his lungs as long as he
remains asymptomatic and maintains a near normal FEV1.
New drugs are under study that may slow the rate of decline in FEV1 by
opposing the inflammatory and other damaging mechanisms that result
in airway inflammation and loss of alveolar walls.