Source: Williams DM, Bourdet SV. Chronic Obstructive Pulmonary Disease. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. http://accesspharmacy.com/content.aspx?aid=7975888. Accessed June 23, 2012.
- Chronic obstructive lung disease (COLD)
- Lung disease characterized by chronic obstruction of airflow
that interferes with normal breathing and is not fully reversible.
- Cigarette smoking accounts for 85–90% of
- Other causes include environmental exposures and host factors.
- Inhalation of noxious particles and gases activates neutrophils,
macrophages, and lymphocytes that release tumor necrosis factor-α and
other inflammatory mediators, causing destructive lung changes.
- Oxidants from cigarette smoke cause tissue damage, promote
inflammation, and inhibit antiprotease activity.
- Hereditary deficiency of α1-antitrypsin
increases risk for premature emphysema.
- Inflammatory exudate leads to increased number and size of
goblet cells, increased mucus secretion, and impaired ciliary motility.
- Airway smooth muscle and connective tissue thickens; chronic
inflammation causes fibrosis and narrowing of small airways.
- Late structural changes increase pulmonary pressures; in severe
COPD, secondary pulmonary hypertension leads to right-sided heart
- 12.1 million Americans over age 25 years have COPD.
- COPD accounts for about 126,00 deaths in the United States
annually, representing one in every 20 deaths.
- Mortality rate is higher in men, but death rate in women has
doubled over last 25 years.
- Mortality rate is higher in whites than blacks.
- Abstention from cigarette smoking best means of preventing
- Environmental exposures: tobacco smoke, occupational dusts
and chemicals, air pollution
- Host factors: genetic predisposition (e.g., α1-antitrypsin
deficiency), airway hyperresponsiveness, impaired lung growth
- Initially, chronic cough and sputum production; symptoms
may be present for several years before dyspnea develops.
- Physical examination often normal in mild disease. With more
severe disease, patients may have cyanosis, “barrel chest,” resting
tachypnea, shallow breathing, pursing of lips during expiration, and
use of accessory respiratory muscles.
- During COPD exacerbations, patients may have worsening dyspnea,
increased sputum volume and purulence, chest tightness, increased
need for bronchodilators, malaise, fatigue, and decreased exercise
Means of Confirmation and Diagnosis
- Diagnosis based in part on symptoms and history of exposure
to risk factors.
- Arterial blood gases (ABG) with low Pao2 (45–60
mm Hg) and elevated Paco2 (50–60
mm Hg) in more severe disease
- Spirometry shows reduced forced expiratory volume in 1
second (FEV1), forced vital capacity (FVC), and FEV1:FVC
ratio to <70%.
- Postbronchodilator FEV1 <80% of predicted
confirms airflow limitation not fully reversible.
- Prevent or minimize disease progression.
- Relieve symptoms.
- Improve exercise tolerance.
- Improve health status.
- Prevent and treat exacerbations.
- Reduce morbidity and mortality.