A patient has pH 7.28, PaCO2 58 mmHg, HCO3- 26 mEq/L. The expected compensation for this primary respiratory acidosis and the adequacy of the measured HCO3- can be assessed by the rule that chronic respiratory acidosis raises HCO3- by:

• A 2 mEq/L per 10 mmHg rise in PaCO2 (acute) and 8 mEq/L per 10 mmHg (chronic)
• B 5 mEq/L per 10 mmHg rise in PaCO2 regardless of acute vs chronic status
• C 3 mEq/L per 10 mmHg rise in PaCO2 (acute) and 5 mEq/L per 10 mmHg (chronic)
• D 1 mEq/L per 10 mmHg rise in PaCO2 (acute) and 3.5 mEq/L per 10 mmHg (chronic) ✓

Explanation

For primary respiratory acidosis: acute compensation by blood buffers raises HCO3- by ~1 mEq/L per 10 mmHg PaCO2 rise; chronic compensation (renal HCO3- retention, over 3–5 days) raises HCO3- by ~3.5 mEq/L per 10 mmHg rise. Here PaCO2 is elevated by ~18 mmHg above normal (40 mmHg); expected chronic compensation = 18 x 3.5/10 = 6.3 mEq/L increase above 24 = ~30.3 mEq/L. Measured HCO3- of 26 is less than expected, suggesting an acute-on-chronic process or a concomitant metabolic acidosis.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

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