• The hallmark pathophysiologic mechanism in COPD is irreversible progressive obstruction of expiratory airflow due to chronic bronchitis and/or emphysema.
  • In emphysema, chronic exposure to cigarette smoke destroys the alveolar walls, enlarging the airspace. These airways eventually collapse and cause obstruction, leading to air trapping and hyperinflation.
  • In chronic bronchitis, cigarette smoke causes the proliferation of mucinous-secreting cells (goblet cells) and impairs ciliary function. These effects lead to excess mucous secretion, mucus plug formation, and airflow obstruction.
• Smoking is responsible for over 90% of cases of COPD.

• The primary cell lines that are increased in the airways of patients with COPD are neutrophils, macrophages, and CD8+ T lymphocytes.  These cells release cytotoxic enzymes and proteases that cause alveolar damage, reduced ciliary motion, and increased mucus secretion by goblet cells.  Although more abundant, the infiltrating inflammatory cells show impaired ability to phagocytize bacterial pathogens, contributing to increased risk of respiratory infections such as community-acquired pneumonia.
• Chronic obstructive pulmonary disease (COPD) manifests with progressively worsening dyspnea, end-expiratory wheezing, a prolonged expiratory phase, and spirometry findings of a decreased FEV1/FVC ratio, a decreased FEV1, and increased TLC (due to increased lung compliance).

<aside> 🚬 A patient has a significant smoking history and has symptoms that meet the criteria for chronic bronchitis, (productive cough for ≥ 3 months each year for ≥ 2 consecutive years), a form of chronic obstructive pulmonary disease (COPD).

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• However, an important feature that distinguishes chronic bronchitis from emphysema is a normal DLCO (since chronic bronchitis, unlike emphysema, is not associated with alveolar destruction).
• Emphysema-predominant COPD can manifest with cachexia (due to increased work of breathing) and an occasional dry cough.
  • Decreased DLCO levels indicate a decreased surface area for air exchange from the destruction of the alveoli present in emphysema.

• It is important to note that clearly distinguishing between emphysema and chronic bronchitis via clinical features may not always be possible because most patients with COPD have a combination of emphysema and chronic bronchitis.

• ABGs in COPD

  • ↓ PaO2 (n:90) → hypoxemic @ rest
  • ↑ PaCO2 (n :40) → chronic respiratory acidosis
  • ↑ HCO3 (n:24) → renal compensation
  • ↓/↔︎ pH (n:7.4) → may be decreased or normal if there is adequate compensation
  • A decrease in urinary HCO3- excretion is a compensatory measure in response to hypercapnia and chronic respiratory acidosis, which often occur in patients with COPD as a result of expiratory airway collapse and respiratory muscle fatigue.
    • The proximal convoluted tubules reabsorb HCO3-, improving the buffer capacity of the serum against lower pH.
    • The distal convoluted tubules and collecting ducts in the kidneys also increase excretion of H+ (in the form of H2PO4‑ and NH4+), raising the blood pH to compensate for respiratory acidosis.

  note: in CHF, ABGs will show hypoxemia with ↓↓ PaCO2 ≠ ↑ (like in COPD) → due to hyperventilation

• COPD causes air trapping and hyperinflation of the lungs, so these patients breathe at higher baseline lung volumes (higher functional residual capacity).

  • The volume of air in the lungs that is not respired, the residual volume (RV), is substantially increased.
  • The total lung capacity (TLC) increases as well, but to a lesser extent than RV.
  • Therefore, the fraction of air in the lungs that is not involved in respiration, the RV/TLC ratio, is also increased.
  • A high RV/TLC ratio correlates with poor outcomes in patients with COPD.

CXR showing hyperinflation in a COPD patient

• PFTs & Flow-volume loops in COPD

Acute COPD Exacerbation (AECOPD)

• A patient with a history of chronic obstructive pulmonary disease (COPD) has increasing dyspnea and purulent sputum production consistent with an acute exacerbation (AECOPD). Precipitants of AECOPD can be divided into infectious and noninfectious causes.  Infectious etiologies account for roughly two-thirds of all cases of AECOPD:
  • The 3 bacteria most commonly isolated during AECOPD are nontypeable Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae.
  • The 3 most common viral triggers of AECOPD are human rhinovirus, influenza, and respiratory syncytial virus.
  • MCC of COPD exacerbation:
    • respiratory viruses are the MCC → Rhinovirus
    • bacteria are the second MCC → “respiratory triad” → S.pneumoniae, H.influenzae, M.catarrhalis
• Infection results in direct damage to respiratory ciliated epithelium, cytokine-mediated airway inflammation, and mucus hypersecretion, all of which worsen the baseline symptoms of COPD.  The presence of purulent (eg, greenish, malodorous) sputum merely denotes the influx of activated neutrophils (myeloperoxidase produces the green hue) and does not reliably distinguish between viral or bacterial infection.