Hypercapnia causes cerebral vasodilation and increases CBF. The primary mechanism mediating this response is:

• A CO2 diffuses across vessel walls, lowering perivascular pH; this local acidosis directly relaxes cerebrovascular smooth muscle ✓
• B CO2 stimulates central chemoreceptors in the medulla, which send descending signals to dilate cerebral vessels
• C CO2 binds carbamino groups on cerebrovascular haemoglobin, triggering eNOS activation and NO release
• D Hypercapnia-induced systemic hypertension passively increases CBF through pressure-dependent vasodilation

Explanation

Carbon dioxide is a potent cerebral vasodilator. CO2 freely diffuses across the blood-brain barrier and vascular walls. In the perivascular space, CO2 combines with water (catalysed by carbonic anhydrase) to form carbonic acid, which dissociates to H+ and HCO3−. This localised extravascular acidosis (fall in pH) directly causes cerebrovascular smooth muscle relaxation through opening of ATP-sensitive K+ channels (KATP) and reduced intracellular calcium sensitivity. CBF increases linearly with PaCO2 between ~20 and 80 mmHg (approximately 2–3% change per mmHg). This is a local phenomenon, not mediated by central neural reflexes (option B). Options C and D are not the operative mechanism.

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

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Written and medically reviewed by the StethoPrep medical team.