A 30-year-old woman is hyperventilating acutely due to anxiety. pH 7.52, PaCO2 24 mmHg, HCO3− 19 mEq/L. Which buffering response accounts for the fall in HCO3−?
- A Acute intracellular buffering: H+ from cells exchange with Na+ and K+, titrating HCO3 extracellularly; HCO3 falls ~2 mEq/L per 10 mmHg fall in PaCO2 ✓
- B Renal excretion of HCO3 via bicarbonate wasting in the proximal tubule, occurring within minutes
- C Respiratory alkalosis stimulates chloride-bicarbonate exchange in erythrocytes, raising plasma chloride and consuming HCO3
- D Liver switches from consuming to producing lactate, which titrates HCO3 to lactic acid
Explanation
In acute respiratory alkalosis, the fall in PaCO2 shifts the bicarbonate buffer equilibrium (H+ + HCO3 ⇌ H2CO3 ⇌ H2O + CO2). The immediate compensation is intracellular buffering: H+ ions leave cells (moving down their concentration gradient as extracellular pH rises) in exchange for Na+ and K+; these H+ ions then consume extracellular HCO3. The expected acute fall is approximately 2 mEq/L per 10 mmHg fall in PaCO2. Here, PaCO2 fell by 16 mmHg, so expected HCO3 = 24 − (2 × 1.6) ≈ 20.8, consistent with the measured 19. Renal HCO3 wasting (option B) is the chronic compensation and takes 24–48 hours. Option C is a minor erythrocyte chloride shift that contributes minimally. Option D is incorrect.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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