The postural reduction in middle cerebral artery blood velocity is not explained by PaCO₂

Abstract

In the normocapnic range, middle cerebral artery mean velocity (MCA V _mean) changes ∼ 3.5% per mmHg carbon-dioxide tension in arterial blood (PaCO₂) and a decrease in PaCO₂ will reduce the cerebral blood flow by vasoconstriction (the CO₂ reactivity of the brain). When standing up MCA V _mean and the end-tidal carbon-dioxide tension (PETCO₂) decrease, suggesting that PaCO₂ contributes to the reduction in MCA V _mean. In a fixed body position, PETCO₂ tracks changes in the PaCO₂ but when assuming the upright position, cardiac output $(\dot {Q})$ decreases and its distribution over the lung changes, while ventilation $(\dot {V}_{{\rm E}})$ increases suggesting that PETCO₂ decreases more than PaCO₂. This study evaluated whether the postural reduction in PaCO₂ accounts for the postural decline in MCA V _mean. From the supine to the upright position, $\dot {V}_{{\rm E}},$ $\dot {Q},$ PETCO₂, PaCO₂, MCA V _mean, and the near-infrared spectrophotometry determined cerebral tissue oxygenation (CO₂Hb) were followed in seven subjects. When standing up, MCA V _mean (from 65.3±3.8 to 54.6±3.3 cm s⁻¹ ; mean ± SEM; P<0.05) and cO₂Hb (−7.2±2.2 μmol l⁻¹ ; P<0.05) decreased. At the same time, the $\dot {V}_{{\rm E}}/\dot {Q}$ ratio increased 49±14% (P<0.05) with the postural reduction in PETCO₂ overestimating the decline in PaCO₂ (−4.8±0.9 mmHg vs. −3.0±1.1 mmHg; P<0.05). When assuming the upright position, the postural decrease in MCA V _mean seems to be explained by the reduction in PETCO₂ but the small decrease in PaCO₂ makes it unlikely that the postural decrease in MCA V _mean can be accounted for by the cerebral CO₂ reactivity alone.