Flashcards in Seventeen Deck (12):
List some major risk factors for COPD.
Genetic Factors (α1-PI defi ciency)
Airway reactivity (methacoline reactivity)
Environmental pollution (cooking/fuel smokes)
Environmental tobacco smoke
Perinatal events and childhood illness (lung development)
Recurrent bronchopulmonary infections
When is COPD suspected in a patient? What might the physical exam be like?
COPD is suspected in a patient who presents with cough,
sputum production, and/or exertional dyspnea plus a history
of exposure to risk factors, particularly cigarette smoke.
Although COPD and asthma can coexist, careful evaluation of
specifi c clinical features can help distinguish the predominant
condition in each patient (Table 22.2).
C L I N I C A L CO R R E L AT I O N 2 2 . 1
The physical exam (Chap. 14) has low diagnostic sensitivity
and specifi city in COPD. It may be unremarkable,
particularly in patients with mild disease. In advanced
COPD or in subjects with acute exacerbations of COPD,
physical signs may include peripheral and central cyanosis,
hyperinfl ated chest with an increased anteroposterior
diameter, pursed lip breathing, use of the accessory muscles
of respiration, wheezing, diminished breath sounds, and
paradoxical inward inspiratory movement of the lower ribs
(Hoover’s sign) signifying diaphragmatic fl attening.
How is the diagnosis of COPD established and confirmed?
The diagnosis of COPD is established and confi rmed by
pulmonary function studies with bronchodilator reversibility
testing that show incompletely reversible airfl ow limitation
(Fig. 22.1). Airfl ow limitation in COPD can be defi ned
in two ways: a post-bronchodilator FEV1/FVC ratio <70%
(by the GOLD Guidelines); or a post-bronchodilator FEV1/
FVC ratio less than the lower limit of normal for age, sex, and
height (by the ATS/ERS Guidelines). The severity of obstruction
is based on the percentage of predicted FEV1 relative to
normative standards for the subject’s age, height, gender, and
race. Body plethysmography (Chap. 16) typically reveals an
increased TLC that is consistent with pulmonary hyperinfl ation
and an increased RV that is consistent with air-trapping.
Notably, the DLCO is typically decreased in emphysema,
refl ecting losses of alveolar epithelial and capillary endothelial
What might a chest x-ray show in COPD? When would a CT be advisable? When are blood gases advised? When should alpha 1 anti-trypsin levels be measured?
Chest radiographs in patients with COPD may show lung
hyperinfl ation, bullous disease, or low fl attened diaphragms due
to peripheral air-trapping (Chap. 15). Thoracic plain fi lm images
also may disclose complications of COPD such as pneumonia
or pneumothorax, or can indicate alternative diagnoses such as,
cardiomegaly with superimposed pulmonary edema. High resolution
computed tomography of the chest is performed when
the diagnosis is in question, or when bullectomy or lung volume
reduction surgery is being contemplated.
Measurement of arterial blood gases (Chap. 17) is indicated
when the FEV1 is <45 years),
or if there is a strong family history of emphysema.
Describe 3 first line smoking cessation medications and how they work? What are 2 second line medications? Why aren't they first line?
Nicotine replacements come in several delivery forms
including gum, patch, inhaler, spray, sublingual tablet, and
lozenge. By binding to nicotinic acetylcholine receptors in
the ventral tegmental area of the brain, nicotine replacement
induces the release of dopamine in the nucleus accumbens,
thereby ameliorating the withdrawal symptoms associated
with smoking cessation. Nicotine replacement appears to
increase the 6-month abstinence rates by 1.5-2 times that
of placebo. Of note, nicotine replacement therapy does not
increase the occurrence of cardiovascular events in patients
with co-existent cardiovascular disease.
Sustained-release (SR) bupropion is an antidepressant
drug that works by selectively inhibiting the reuptake of
norepinephrine and dopamine in the central nervous system.
Studies indicate that bupropion SR not only improves smoking
cessation (success odds ratio = 2.06 vs placebo), but also signifi cantly reduces the associated weight gain from quitting
smoking (1.5 kg in the bupropion SR group vs 2.9 kg in the
placebo group). Combining bupropion SR with a nicotine patch
also appears to signifi cantly increase abstinence rates versus
nicotine patch alone, although not versus bupropion alone.
Varenicline is a selective `4a2 nicotinic acetylcholine
receptor partial agonist. By binding to this class of nicotinic
receptor in the ventral tegmental area, varenicline competitively
inhibits binding by nicotine derived from tobacco smoke, and
so prevents the release of greater quantities of dopamine associated
with the reinforcing effects of smoking. Furthermore,
by inducing a regulated release of dopamine (∼60% of the
maximal response to nicotine), varenicline also ameliorates
the withdrawal symptoms from smoking cessation. Varenicline
has been shown to have superior effi cacy in promoting
continuous abstinence rates versus bupropion SR plus placebo
at 6 months, and versus placebo at 1 year. Although nortriptyline
and clonidine have been found to be superior in effi cacy
as compared to placebo in a number of trials, the often serious
side-effect profi les of both drugs preclude their widespread
use for smoking cessation.
How are inhaled bronchodilators and glucocorticoids used in COPD? What do they accomplish?
Inhaled bronchodilators include β2-adrenergic agonists
and anticholinergics that provide symptomatic relief. However,
as a class of therapeutics these have not been shown to
alter the long-term declines in pulmonary function described
above (Table 22.5). Use of theophylline as a bronchodilator
has waned due to its serious side effects including nausea,
vomiting, arrhythmia, seizures, and generally a narrow therapeutic
window. Although inhaled glucocorticoids (ICs) (eg,
beclomethasone, budesonide, fl uticasone, and triamcinolone)
also do not ameliorate declines in lung function, they improve
airway reactivity and respiratory symptoms that decrease the
need for health care utilization. Combining an inhaled glucocorticoid
with a long-acting β2-adrenergic agonist (LABA),
such as the budesonide/formoterol or salmeterol/fl uticasone
formulations available, provides greater improvements in dyspnea
and lung function than does each component alone. Systemic
steroids are not recommended for maintenance therapy
of COPD because of their long-term side effects of osteoporosis,
steroid myopathy, adrenal insuffi ciency, and immunosuppression.
Rather, systemic steroids are reserved for signifi cant
acute exacerbations of COPD.
When is long term O2 therapy used in COPD? What does it accomplish?
Aside from smoking cessation, long-term O2 therapy
(>15 h/day) is the only treatment that has been demonstrated
to increase survival in COPD patients with chronic respiratory
failure or cor pulmonale. Chronic respiratory failure is
defi ned as a Pao2 ≤55 mm Hg or a Sao2 ≤88%. Cor pulmonale
is defi ned as a Pao2 of 55-60 mm Hg or Sao2 ≤89% with
pulmonary hypertension, peripheral edema, or polycythemia.
Oxygen therapy has other health benefi ts, including improved
pulmonary hemodynamics, reduced polycythemia, increased
exercise capacity, enhanced lung mechanics, and improved
What is recommended concerning vaccinations in COPD?
Immunization against respiratory infections is recommended
in patients with COPD (Table 22.4). Infl uenza vaccines
should be given to all COPD patients, since these can
signifi cantly reduce serious illness and death by about 50%.
The multivalent pneumococcal polysaccharide vaccine that
is generally recommended for all persons ≥65 years old is
indicated for COPD patients <40% predicted, since the vaccine can reduce the incidence of
community-acquired pneumonia (CAP) in this cohort.
What is pulmonary rehab? When is it recommended? What does it accomplish?
Pulmonary rehabilitation is recommended for patients
with moderate COPD and breathlessness (Table 22.4). In this
context, such rehabilitation is defi ned as a combination of
patient education plus participation in physical therapy that
involves muscle strengthening exercises, including the primary
and accessory muscles associated with breathing. Benefi
ts of pulmonary rehabilitation include improvements in a
patient’s exercise capacity and quality of life, as well as reductions
in their dyspnea, anxiety, depression, and health care utilization.
The American Lung Association (ALA) is one of
several nonprofi t groups that organizes and/or supervises local
pulmonary rehabilitation clinics for COPD patients.
What are some surgical treatments for COPD? When are they used and what do they accomplish?
Bullectomy, lung volume reduction surgery, and lung
transplantation are surgical treatment options for selected
patients with advanced COPD. Bullectomy may reduce dyspnea
and improve lung function in patients with bullous disease
(Chap. 37). When lung volume reduction surgery was performed
in a subset of patients with very severe COPD (FEV1
50 mm Hg, and secondary pulmonary hypertension.
What is considered an acute exacerbation? What normally causes it? How is it managed?
The GOLD Guidelines defi ne a COPD exacerbation as
“an event in the natural course of disease characterized by
a change in the patient’s baseline dyspnea, cough, and/or
sputum that is beyond normal day-to-day variations, is acute
in onset, and may warrant a change in regular medications.”
Although most COPD exacerbations are triggered by respiratory
infectious agents and air pollution, the exact cause is not
known in about one-third of these episodes.
Common infectious agents associated with COPD exacerbations
include respiratory viruses and bacterial pathogens
such as Haemophilus infl uenzae, Streptococcus pneumoniae,
and Moraxella catarrhalis. Managing acute exacerbations of
COPD requires increasing the dosage and frequency of inhaled
short-acting β-agonist bronchodilators (eg, albuterol). Adding
a short-acting anticholinergic bronchodilator (eg, ipratropium)
then is considered if a response to the short-acting β-agonist
medication does not occur. Systemic steroid therapy (eg,
prednisone, 30-40 mg orally for 7-10 days) has been shown
to improve lung function, oxygenation, and time to recovery
in COPD patients experiencing acute exacerbations. Systemic
steroids should be started in hospitalized patients with COPD,
and should be considered in ambulatory patients whose FEV1
<50% of predicted at the time of presentation.