A 19-year-old girl with type 1 diabetes presents with deep, sighing respirations at a rate of 30 per minute, glucose 480 mg/dL, pH 7.08, and bicarbonate 6 mEq/L. The pattern of her breathing represents:
- A Reflex activation of pulmonary J receptors by interstitial oedema
- B Direct stimulation of peripheral chemoreceptors by acetone vapour in the blood
- C Stimulation of central chemoreceptors by ketoacid-derived hydrogen ions crossing the blood-brain barrier ✓
- D Primary brainstem dysfunction from cerebral oedema causing automatic hyperpnoea
Explanation
Kussmaul breathing in diabetic ketoacidosis is respiratory compensation for metabolic acidosis. Beta-hydroxybutyric and acetoacetic acids liberate hydrogen ions that stimulate both peripheral chemoreceptors and, after crossing the blood-brain barrier, the central chemoreceptors, driving ventilation to blow off carbon dioxide and raise pH. Acetone causes the fruity breath odour but does not stimulate chemoreceptors, eliminating option B. J receptors respond to pulmonary congestion, not acidosis.
Reference: Ganong's Review of Medical Physiology, 26th ed.
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