A 55-year-old woman with COPD and chronic CO2 retention has ABG: pH 7.37, PaCO2 58 mmHg, HCO3⁻ 33 mEq/L. Her serum Cl⁻ is 92 mEq/L and Na⁺ is 140 mEq/L. Which statement best characterises her acid-base status and the renal mechanism responsible?

• A Compensated chronic respiratory acidosis; renal compensation involves increased proximal tubular H⁺ secretion, enhanced HCO3⁻ reabsorption, and increased ammoniagenesis—raising plasma HCO3⁻ by ~3.5 mEq/L per 10 mmHg rise in PaCO2 ✓
• B Mixed respiratory acidosis and metabolic alkalosis; the HCO3⁻ is too high for expected renal compensation, indicating a primary metabolic alkalosis superimposed on COPD
• C Compensated chronic respiratory acidosis; the expected HCO3⁻ should be 22 + (58−40)×0.5 = 31 mEq/L, so the actual 33 mEq/L indicates a concomitant metabolic alkalosis
• D Uncompensated respiratory acidosis; the kidney cannot increase HCO3⁻ above 30 mEq/L due to aldosterone-independent reabsorption limits

Explanation

In chronic respiratory acidosis, renal compensation raises HCO3⁻ by approximately 3.5 mEq/L per 10 mmHg increase in PaCO2 (chronic rule). Expected HCO3⁻ = 24 + [(58−40)/10] × 3.5 = 24 + 1.8 × 3.5 = 24 + 6.3 = ~30.3 mEq/L; the observed 33 mEq/L is slightly above this, which could suggest a small additional metabolic component, but option A best describes the primary physiology. The renal mechanism involves increased apical NHE3-mediated H⁺ secretion, enhanced carbonic anhydrase activity, HCO3⁻ reabsorption, and particularly increased NH4⁺ excretion. Option C's formula (0.5 per 10 mmHg) applies to acute respiratory acidosis (HCO3⁻ rises ~1 mEq/L per 10 mmHg acutely), not chronic compensation.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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