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  • Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation that is not fully reversible. Two principal conditions (referred to as phenotypes) include:

    • Chronic bronchitis: Chronic or recurrent excess mucus secretion with cough that occurs on most days for at least 3 months of the year for at least 2 consecutive years.

    • Emphysema: Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls, without fibrosis.


  • The most common cause of COPD is exposure to tobacco smoke. Inhalation of noxious particles and gases activates neutrophils, macrophages, and CD8+ lymphocytes, which release chemical mediators, including tumor necrosis factor-α, interleukin-8, and leukotriene B4. Inflammatory cells and mediators lead to widespread destructive changes in airways, pulmonary vasculature, and lung parenchyma, resulting in chronic airflow limitation.

  • Oxidative stress and imbalance between aggressive and protective defense systems in the lungs (proteases and antiproteases) may also occur. Oxidants generated by cigarette smoke react with and damage proteins and lipids, contributing to cell and tissue damage. Oxidants also promote inflammation and exacerbate protease–antiprotease imbalance by inhibiting antiprotease activity.

  • The protective antiprotease α1-antitrypsin (AAT) inhibits protease enzymes, including neutrophil elastase. AAT deficiency increases risk for premature emphysema.

  • Inflammatory exudate in airways leads to increased number and size of goblet cells and mucus glands. Mucus secretion increases and ciliary motility is impaired. There is thickening of the smooth muscle and connective tissue in airways. Chronic inflammation leads to scarring, fibrosis, and airflow obstruction.

  • Arterial blood gas (ABG) abnormalities result from impaired gas transfer due to parenchymal damage and loss of alveolar-capillary networks. Significant ABG changes are usually not present until airflow limitation is very severe. In such patients, hypoxemia (low arterial oxygen tension—PaO2 45–60 mm Hg [6.0–8.0 kPa]) and hypercapnia (elevated arterial carbon dioxide tension—Paco2 50–60 mm Hg [6.7–8.0 kPa]) can become chronic problems. Hypoxemia is initially associated with exertion but develops at rest as the disease progresses. Hypoxemia results from hypoventilation (V) of lung tissue relative to perfusion (Q) of the area. This low V/Q ratio progresses over several years, resulting in a consistent decline in PaO2. As gas exchange worsens with disease progression, patients may exhibit chronic hypercapnia and are referred to as CO2 retainers. In such patients, central respiratory response to chronically increased Paco2 is blunted. Serum pH is usually near normal because the kidneys compensate by retaining bicarbonate. If acute respiratory distress develops (eg, as with pneumonia or COPD exacerbation with respiratory failure) Paco2 may rise sharply, resulting in worsening respiratory acidosis.

  • Chronic hypoxemia and changes in pulmonary vasculature lead to increases in pulmonary pressures, especially during exercise. Sustained elevated pulmonary pressures can lead to right-sided heart failure (cor pulmonale) characterized by right ventricle hypertrophy in response to increased pulmonary vascular resistance.

  • Chronic airflow obstruction leads to air trapping, ...

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