In metabolic acidosis, the immediate respiratory compensation (hyperventilation) is triggered by chemoreceptors. The sequence of events in this compensatory ventilatory response is:

• A Peripheral carotid body chemoreceptors detect decreased pH first (within minutes); central chemoreceptors (responding to CSF pH change) supplement this after 12-24 hours as CSF bicarbonate adjusts ✓
• B Central chemoreceptors detect decreased HCO3- directly and stimulate the respiratory center within minutes
• C Central chemoreceptors are primary because blood-brain barrier prevents H+ entry; peripheral chemoreceptors play no role
• D Decreased PaO2 secondary to hyperventilation triggers peripheral chemoreceptors to sustain compensation

Explanation

In metabolic acidosis, the initial ventilatory response is rapid (within minutes) because peripheral carotid body chemoreceptors directly sense the decrease in arterial pH. Central chemoreceptors (on the ventral medullary surface) detect changes in CSF H+ concentration, which is initially buffered by CSF HCO3-; as CSF bicarbonate is depleted (over 12-24 hours), central chemoreceptor drive is enhanced. Thus the full compensatory hyperventilation (Kussmaul breathing) reflects both peripheral and central chemoreceptor activation. The maximal compensatory response is not achieved until 12-24 hours, during which central chemoreceptor contribution increases.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.