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COPD and Respiratory Acidosis: Why Blood pH Becomes Acidic

In COPD, chronic airflow obstruction impairs CO2 excretion → chronic respiratory acidosis (elevated PaCO2, low pH).

Pathophysiology

  • Airway narrowing + loss of elastic recoil → air trapping, hyperinflation.
  • V/Q mismatch → dead space ventilation ↑.
  • Respiratory muscle fatigue (flattened diaphragm, increased work of breathing).
  • Chronic hypercapnia (PaCO2 >45 mmHg) → renal compensation: HCO3- retention → pH partially corrected (compensated respiratory acidosis).
  • Acute exacerbation → acute-on-chronic respiratory acidosis: pH drops sharply (uncompensated).

ABG Interpretation

ParameterNormalChronic CompensatedAcute Exacerbation
pH7.35-7.457.35-7.40 (near normal)<7.35 (acidemia)
PaCO235-45>45 (e.g., 55-65)↑↑ from baseline
HCO3-22-26>26 (e.g., 30-36)Baseline elevated

Clinical Management

  • Controlled O2 (target SpO2 88-92%) — avoid hypoxic drive suppression.
  • Bronchodilators (SABA + SAMA), systemic steroids.
  • NIV (BiPAP) for acute hypercapnic respiratory failure: ↓ intubation, mortality.
  • Treat triggers (infection, PE, cardiac).
  • Chronic: long-acting bronchodilators, pulmonary rehab, vaccinations, smoking cessation.

CO2 retention is a hallmark of advanced COPD; understanding compensation guides safe oxygen therapy.

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