Human cerebrovascular and ventilatory CO₂ reactivity to end-tidal, arterial and internal jugular vein P_CO2

This study examined cerebrovascular reactivity and ventilation during step changes in CO₂ in humans. We hypothesized that: (1) end-tidal P_CO2 (P_ET,CO2) would overestimate arterial P_CO2 (P_a,CO2) during step variations in P_ET,CO2 and thus underestimate cerebrovascular CO₂ reactivity; and (2) since P_CO2 from the internal jugular vein (P_jv,CO2) better represents brain tissue P_CO2, cerebrovascular CO₂ reactivity would be higher when expressed against P_jv,CO2 than with P_a,CO2, and would be related to the degree of ventilatory change during hypercapnia. Incremental hypercapnia was achieved through 4 min administrations of 4% and 8% CO₂. Incremental hypocapnia involved two 4 min steps of hyperventilation to change P_ET,CO2, in an equal and opposite direction, to that incurred during hypercapnia. Arterial and internal jugular venous blood was sampled simultaneously at baseline and during each CO₂ step. Cerebrovascular reactivity to CO₂ was expressed as the percentage change in blood flow velocity in the middle cerebral artery (MCAv) per mmHg change in P_a,CO2 and P_jv,CO2. During hypercapnia, but not hypocapnia, P_ET,CO2 overestimated P_a,CO2 by +2.4 ± 3.4 mmHg and underestimated MCAv-CO₂ reactivity (P < 0.05). The hypercapnic and hypocapnic MCAv-CO₂ reactivity was higher (∼97% and ∼24%, respectively) when expressed with P_jv,CO2 than P_a,CO2 (P < 0.05). The hypercapnic MCAv-P_jv,CO2 reactivity was inversely related to the increase in ventilatory change (R₂ = 0.43; P < 0.05), indicating that a reduced reactivity results in less central CO₂ washout and greater ventilatory stimulus. Differences in the P_ET,CO2, P_a,CO2 and P_jv,CO2-MCAv relationships have implications for the true representation and physiological interpretation of cerebrovascular CO₂ reactivity.