Relationship between middle cerebral artery blood velocity and end-tidal PCO2 in the hypocapnic-hypercapnic range in humans

Abstract

This study examined the relationship between cerebral blood flow (CBF) and end-tidal PCO2 (PETCO2) in humans. We used transcranial Doppler ultrasound to determine middle cerebral artery peak blood velocity responses to 14 levels of PETCO2 in a range of 22 to 50 Torr with a constant end-tidal PO2 (100 Torr) in eight subjects. PETCO2 and end-tidal PO2 were controlled by using the technique of dynamic end-tidal forcing combined with controlled hyperventilation. Two protocols were conducted in which PETCO2 was changed by 2 Torr every 2 min from hypocapnia to hypercapnia (protocol I) and vice-versa (protocol D). Over the range of PETCO2 studied, the sensitivity of peak blood velocity to changes in PETCO2 (CBF-PETCO2 sensitivity) was nonlinear with a greater sensitivity in hypercapnia (4.7 and 4.0%/Torr, protocols I and D, respectively) compared with hypocapnia (2.5 and 2.2%/Torr). Furthermore, there was evidence of hysteresis in the CBF-PETCO2 sensitivity; for a given PETCO2, there was greater sensitivity during protocol I compared with protocol D. In conclusion, CBF-PETCO2 sensitivity varies depending on the level of PETCO2 and the protocol that is used. The mechanisms underlying these responses require further investigation.

Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress

“…In the present study, linear regressions were used to assess the steady-state CBVC-PET CO 2 relationship across the reported ranges of PET CO 2 (ϳ20 Torr below and ϳ9 Torr above normocapnic values), recognizing that changes in PET CO 2 due to passive heat stress are well within this range. Consistent with the curvilinear nature of these responses (5,16), in the present study the slope of the CBVC-PET CO 2 relationship was approximately threefold greater during the hypercapnic challenge relative to the hypocapnic challenge. It is for this reason that the slopes of the CBVC-PET CO 2 relationships were separately analyzed between hypercapnic and hypocapnic trials.…”

“…These combined responses are likely to be key mechanisms responsible for reductions in orthostatic tolerance in heat-stressed individuals, although the cause(s) by which heat stress alters cerebral vascular responses is not entirely clear. Given the close relationship between cerebral perfusion and Pa CO 2 (16,36), decreases in Pa CO 2 (as reflected by decreases in PET CO 2 ) that occur during heat stress alone and combined heat and orthostatic stress (40,41) could account for passive heat stress-induced reductions in resting cerebral blood flow and augmented decreases in CBVC during combined orthostatic and heat stress. However, based on the previously reported relationship that every 1-Torr change in Pa CO 2 changes cerebral blood flow ϳ3% in the same direction under normothermic conditions (31), the decreases in PET CO 2 that are evident during heat and combined heat and orthostatic stresses are not large enough to fully account for all of the decrease in cerebral blood flow.…”

“…Recent research has shown that the relationship between cerebral blood flow and PET CO 2 is curvilinear across a wide range of hypo-and hypercapnic levels (5,16). In the present study, linear regressions were used to assess the steady-state CBVC-PET CO 2 relationship across the reported ranges of PET CO 2 (ϳ20 Torr below and ϳ9 Torr above normocapnic values), recognizing that changes in PET CO 2 due to passive heat stress are well within this range.…”

“…Although mechanisms responsible for reduced orthostatic tolerance during heat stress are unclear, they are likely associated with factors that directly or indirectly affect cerebral perfusion pressure, cerebral blood flow, and thus cerebral oxygenation (20,24,38). Cerebral perfusion is very sensitive to changes in arterial carbon dioxide tension (Pa CO 2 ), such that increases in Pa CO 2 increase cerebral perfusion, whereas decreases in Pa CO 2 decrease cerebral perfusion (16,36). Previously, our laboratory identified decreases in end-tidal carbon dioxide (PET CO 2 ; surrogate of Pa CO 2 ) of ϳ2 Torr in response to whole body passive heat stress, as well as significant reductions in cerebral perfusion and cerebral vascular conductance (40,41).…”

Cerebral Vasomotor Reactivity during Hypo- and Hypercapnia in Sedentary Elderly and Masters Athletes

“…[14][15][16] For these reasons, cerebral CO2 reactivity to hypocapnia (hyperventilation) and hypercapnia (rebreathing) was assessed separately in this study.…”