Question 1 · Hard
A 55-year-old woman with a BMI of 49 kg/m2 has daytime sleepiness and morning headaches. She has no lung disease, vomiting or diuretic use. Her chemistry panel shows total CO2 32 mmol/L (reference 22-29) and chloride 96 mmol/L, and the ward asks whether she has a metabolic alkalosis. Arterial results: pH 7.36 (reference 7.35-7.45), pCO2 7.6 kPa (57 mm Hg), HCO3- 31 mmol/L. For every 10 mm Hg rise in pCO2, HCO3- rises by about 1 mmol/L in acute and about 3.5 mmol/L in chronic respiratory acidosis (±2 mmol/L). Which interpretation fits best?
- AAcute respiratory acidosis without compensation
- BChronic respiratory acidosis with expected compensation
- CMetabolic alkalosis with respiratory compensation
- DRespiratory acidosis plus metabolic alkalosis
Show answerHide answer
Answer: B · Chronic respiratory acidosis with expected compensation
The pCO2 is high and the pH sits at the acid end of the range, so the primary disorder is a respiratory acidosis; a primary metabolic alkalosis would leave the pH alkaline. The pCO2 is 17 mm Hg above 40, so a chronic disorder should raise HCO3- by about 3.5 × 1.7 = 6 mmol/L, to about 30 (28-32), and an acute one by only about 2, to about 26. The measured 31 mmol/L fits chronic renal compensation, and the low chloride reflects bicarbonate retained in its place. No extra metabolic alkalosis is needed to explain the results. The pattern fits obesity hypoventilation, and the raised total CO2 on the panel is compensation, not a separate disorder.
- A: Acute retention would raise HCO3- only to about 26 mmol/L.
- C: Compensation does not overshoot; a primary alkalosis would make the pH alkaline.
- D: HCO3- 31 mmol/L lies within the expected 28-32, so no extra alkalosis is present.