Chronic Obstructive Pulmonary Disease

Chronic Obstructive Pulmonary Disease is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles


Chronic obstructive pulmonary disease (COPD) is a mostly preventable and treatable disorder characterized by expiratory airflow limitation that is not fully reversible. The airflow limitation is often progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases, principally cigarette smoke.1

The airflow obstruction in COPD is caused by emphysema and airway disease.

  • Emphysema is defined pathologically as permanent enlargement of air spaces distal to the terminal bronchiole accompanied by destruction of the alveolar walls and absence of associated fibrosis.
  • The airway disease in COPD occurs principally in small airways (i.e., those with an internal diameter of <2 mm). Chronic bronchitis is a common feature of COPD and is defined clinically as productive cough on most days for at least three consecutive months per year for at least two consecutive years, in the absence of other lung diseases that could account for this symptom. Individuals with chronic bronchitis but without airflow obstruction do not have COPD.


  • Although the prevalence of COPD is difficult to determine, it is estimated to affect approximately 15 million Americans.
  • COPD and other chronic lower respiratory diseases represent the third leading cause of death in the United States.2
  • In the United States, the age-adjusted mortality rate remains higher among Caucasians compared with African Americans, Hispanics, or Pacific Islanders, but rate differences between men and women have closed.


  • Most cases of COPD are attributable to cigarette smoking. Although only a minority of cigarette smokers develop clinically significant COPD, a much higher proportion develop abnormal lung function.3
  • Environmental (e.g., wood-burning stoves) and occupational dusts, fumes, gases, and chemicals are other etiologic agents of COPD. Household indoor air pollution is a major cause of fatal COPD in underdeveloped countries.4
  • α1-Antitrypsin deficiency is found in 1%–2% of COPD patients. Clinical characteristics of affected patients may include a minimal smoking history, early-onset COPD (e.g., younger than 45 years of age), a family history of lung disease, or lower lobe–predominant 
panacinar emphysema. Despite its relative rarity, some authorities recommend diagnostic testing for this condition in all patients with COPD.


  • The pathogenesis of COPD involves inflammation, immune reactions, imbalance of proteinases and antiproteinases, turnover of extracellular matrix, oxidative stress, and apoptosis.
  • Pathologic features include destruction of alveolar tissue and small airways, airway wall inflammation, edema and fibrosis, and intraluminal mucus.
  • Pulmonary function changes include decreased maximal expiratory airflow, hyperinflation, air trapping, and alveolar gas exchange abnormalities.
  • An increased incidence of osteoporosis, skeletal muscle dysfunction, and coronary artery disease occur in COPD, perhaps indicating a systemic component of inflammation.5


  • Abstinence from smoking is the most effective measure for preventing COPD.
  • In patients with COPD, smoking cessation may result in a reduction in the rate of lung function decline and improve survival.6,7
  • Tobacco dependence warrants repeated treatment until patients stop smoking.8 Most smokers fail initial attempts at smoking cessation, and relapse reflects the nature of the dependence and not the failure of the patient or the physician.
  • A multimodality approach is recommended to optimize smoking quit rates.
    • Counseling on the preventable health risks of smoking, providing advice to stop smoking, and encouraging further attempts to stop smoking even after previous failures
    • Providing smoking cessation materials to patients
    • Prescribing pharmacotherapy (Table 9-1); providers should take every advantage to counsel and provide pharmacotherapy (including in the inpatient setting)
      Table 9-1: Pharmacotherapy for Smoking Cessation
      ProductDosingSide Effects/Precautions
      Nicotine Replacement Therapya
      Trandermal patchb7, 14, or 21 mg/24 h
      Usual regimen = 21 mg/d = 6 wk, 14 mg/d × 2 wk, 7 mg/d × 2 wk
      Headache, insomnia, nightmares, nausea, dizziness, blurred vision (applies to all nicotine products)
      Chewing gum, lozenges2–4 mg q1–8h
      Gradually taper use

      Inhaler10 mg/cartridge (4 mg delivered dose)
      6–16 cartridges/d

      Nasal spray0.5 mg/spray
      1–2 sprays in each nostril q1h

      Non-nicotine Pharmacotherapy
      Bupropion ER (Zyban)150 mg/d × 3 days, then bid × 7–12 wk
      Start 1 wk before quit date
      Dizziness, headache, insomnia, nausea, xerostomia, hypertension, seizure
      Avoid monoamine oxidase inhibitors
      Varenicline (Chantix)0.5 mg/d × 3 days, bid × 4 days, then 1 mg bid × 12–24 wk
      Start 1 wk before quit date
      Nausea, vomiting, headache, insomnia, abnormal dreams
      Worsening of underlying psychiatric illness

      See also Fiore MC, Baker TB. Clinical practice. Treating smokers in the health care setting. N Engl J Med. 2011;365:1222-1231 for strategies and approach.  [PMID:21991895]

      aCombination therapy is often used. A long-acting product (e.g., patch) is used for basal nicotine replacement, with a short-acting product (e.g., inhaler) used for breakthrough cravings.

      bIf patient smokes less than a half pack per day, start at 14-mg dose.

  • Formal smoking cessation programs, often administered in a group setting, can be more effective than non–face-to-face methods.
  • The US Department of Health and Human Services has developed a telephone-based support system (1-800-QUIT NOW) with an Internet analog (

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