Human cerebrovascular and ventilatory CO2 reactivity to end‐tidal, arterial and internal jugular vein PCO2

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Abstract
This study examined cerebrovascular reactivity and ventilation during step changes in CO2 in humans. We hypothesized that: (1) end‐tidal P (P) would overestimate arterial P (P) during step variations in P and thus underestimate cerebrovascular CO2 reactivity; and (2) since P from the internal jugular vein (P) better represents brain tissue P , cerebrovascular CO2 reactivity would be higher when expressed against P than with P , 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 , 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 and P . During hypercapnia, but not hypocapnia, P overestimated P 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 than P (P < 0.05). The hypercapnic MCAv–P 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 , P and P–MCAv relationships have implications for the true representation and physiological interpretation of cerebrovascular CO2 reactivity.