Chronic Obstructive Pulmonary Disease

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

To view the entire topic, please or .

The Washington Manual is an award-winning, complete mobile solution for nurses and students. Look up information on diseases, tests, and procedures; then consult the database with 5,000+ drugs or refer to 65,000+ dictionary terms. Explore these free sample topics:

-- The first section of this topic is shown below --

General Principles

Definition

  • Chronic obstructive pulmonary disease (COPD) is defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) as a mostly preventable and treatable disorder characterized by an expiratory airflow limitation that is not fully reversible. Exposure to noxious particles and gases, as well as abnormalities in lung development, predisposes individuals to the development of COPD. The trajectory of the disease is variable and not necessarily progressive.
  • Recently, there has been a suggestion to expand the diagnostic criteria of COPD from a single measure of lung function (expiratory airflow limitation) to include environmental exposure, symptoms, and abnormal findings on CT scans. There is now recognition that a COPD definition that solely relies on lung function misses patients in the early stages of the disease.
  • 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 the absence of associated fibrosis. However, fibrosis can coexist with emphysema in a syndrome called combined pulmonary fibrosis and emphysema (CPFE).
    • The airway disease in COPD occurs primarily 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 a productive cough, on most days, for at least 3 consecutive months per year and for at least 2 consecutive years, and in the absence of other lung diseases that could account for this symptom.
    • Emphysema and chronic bronchitis can be insidious and present in the absence of airflow obstruction. Even in the absence of airflow obstruction, COPD is still associated with adverse health outcomes.

Epidemiology

  • Although the true prevalence of COPD is difficult to determine, COPD is estimated to affect approximately 15 million people in the US.
  • Prior to the COVID-19 pandemic, COPD and other chronic lower respiratory diseases represented the third leading cause of death in the US.1 In 2020, COVID-19 was the third leading underlying cause of death after heart disease and cancer, with COPD and chronic lower respiratory disease ranking sixth. The mortality rate for COPD has steadily increased since 2012, and globally the burden remains high. The World Health Organization estimated that approximately 3.2 million deaths were caused by COPD in 2015, accounting for 5% of all worldwide deaths that year.
  • COPD is protracted in time and is responsible for more years lived with disability (3.6%) than all other respiratory diseases combined.1

Etiology

  • Most cases of COPD are attributable to cigarette smoking in the US.
  • Environmental and occupational dusts (e.g., wood-burning stoves, fumes, gases, and chemicals) are other common causes of COPD worldwide. Household indoor air pollution is a major cause of fatal COPD, particularly in developing countries and rural areas.2
  • α1-Antitrypsin (A1AT) deficiency is found in 1%–2% of COPD patients. Clinical characteristics of affected patients may include a minimal or nonexistent smoking history, early-onset COPD (e.g., younger than 45 years), a family history of lung disease, or lower lobe–predominant panacinar emphysema.

Pathophysiology

  • The pathogenesis of COPD involves inflammation, immune reactions, imbalance of proteinases and antiproteinases, turnover of the 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.3

Prevention

  • In Western countries, abstinence from smoking is the most effective measure for preventing COPD.
  • Domestic biomass fuel smoke inhalation is responsible for COPD in nonsmoking patients in rural settings and developing countries, who sometimes have comparatively low cigarette smoking rates. Strategies aimed at improving access to cookstoves and cleaner fuel sources along with increased ventilation are essential in these populations (e.g., the Global Alliance for Clean Cookstoves has been established for this purpose).
  • In patients with COPD, smoking cessation may result in a reduction in the rate of lung function decline and improved survival.4,5
  • Tobacco cessation attempts warrant repeating until the patient stops smoking. Most smokers fail initial attempts at smoking cessation, and relapse reflects the nature of the nicotine dependence and not the failure of the patient or the physician.
  • A multimodality approach is recommended to optimize smoking cessation.
    • 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.
    • The US Department of Health and Human Services has developed a telephone-based support system (1-800-QUIT-NOW) with an Internet analog (smokefree.gov).
Table 9-1: Pharmacotherapy for Smoking Cessation
ProductDosingSide Effects/Precautions
Nicotine Replacement Therapya
Transdermal 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
Nonnicotine Pharmacotherapy
Bupropion ER (Zyban)150 mg/d × 3 d, 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 d, 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

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 or gum) used for breakthrough cravings.

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

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]

-- To view the remaining sections of this topic, please or --

General Principles

Definition

  • Chronic obstructive pulmonary disease (COPD) is defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) as a mostly preventable and treatable disorder characterized by an expiratory airflow limitation that is not fully reversible. Exposure to noxious particles and gases, as well as abnormalities in lung development, predisposes individuals to the development of COPD. The trajectory of the disease is variable and not necessarily progressive.
  • Recently, there has been a suggestion to expand the diagnostic criteria of COPD from a single measure of lung function (expiratory airflow limitation) to include environmental exposure, symptoms, and abnormal findings on CT scans. There is now recognition that a COPD definition that solely relies on lung function misses patients in the early stages of the disease.
  • 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 the absence of associated fibrosis. However, fibrosis can coexist with emphysema in a syndrome called combined pulmonary fibrosis and emphysema (CPFE).
    • The airway disease in COPD occurs primarily 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 a productive cough, on most days, for at least 3 consecutive months per year and for at least 2 consecutive years, and in the absence of other lung diseases that could account for this symptom.
    • Emphysema and chronic bronchitis can be insidious and present in the absence of airflow obstruction. Even in the absence of airflow obstruction, COPD is still associated with adverse health outcomes.

Epidemiology

  • Although the true prevalence of COPD is difficult to determine, COPD is estimated to affect approximately 15 million people in the US.
  • Prior to the COVID-19 pandemic, COPD and other chronic lower respiratory diseases represented the third leading cause of death in the US.1 In 2020, COVID-19 was the third leading underlying cause of death after heart disease and cancer, with COPD and chronic lower respiratory disease ranking sixth. The mortality rate for COPD has steadily increased since 2012, and globally the burden remains high. The World Health Organization estimated that approximately 3.2 million deaths were caused by COPD in 2015, accounting for 5% of all worldwide deaths that year.
  • COPD is protracted in time and is responsible for more years lived with disability (3.6%) than all other respiratory diseases combined.1

Etiology

  • Most cases of COPD are attributable to cigarette smoking in the US.
  • Environmental and occupational dusts (e.g., wood-burning stoves, fumes, gases, and chemicals) are other common causes of COPD worldwide. Household indoor air pollution is a major cause of fatal COPD, particularly in developing countries and rural areas.2
  • α1-Antitrypsin (A1AT) deficiency is found in 1%–2% of COPD patients. Clinical characteristics of affected patients may include a minimal or nonexistent smoking history, early-onset COPD (e.g., younger than 45 years), a family history of lung disease, or lower lobe–predominant panacinar emphysema.

Pathophysiology

  • The pathogenesis of COPD involves inflammation, immune reactions, imbalance of proteinases and antiproteinases, turnover of the 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.3

Prevention

  • In Western countries, abstinence from smoking is the most effective measure for preventing COPD.
  • Domestic biomass fuel smoke inhalation is responsible for COPD in nonsmoking patients in rural settings and developing countries, who sometimes have comparatively low cigarette smoking rates. Strategies aimed at improving access to cookstoves and cleaner fuel sources along with increased ventilation are essential in these populations (e.g., the Global Alliance for Clean Cookstoves has been established for this purpose).
  • In patients with COPD, smoking cessation may result in a reduction in the rate of lung function decline and improved survival.4,5
  • Tobacco cessation attempts warrant repeating until the patient stops smoking. Most smokers fail initial attempts at smoking cessation, and relapse reflects the nature of the nicotine dependence and not the failure of the patient or the physician.
  • A multimodality approach is recommended to optimize smoking cessation.
    • 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.
    • The US Department of Health and Human Services has developed a telephone-based support system (1-800-QUIT-NOW) with an Internet analog (smokefree.gov).
Table 9-1: Pharmacotherapy for Smoking Cessation
ProductDosingSide Effects/Precautions
Nicotine Replacement Therapya
Transdermal 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
Nonnicotine Pharmacotherapy
Bupropion ER (Zyban)150 mg/d × 3 d, 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 d, 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

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 or gum) used for breakthrough cravings.

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

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]

There's more to see -- the rest of this topic is available only to subscribers.