The effects of reduced end‐tidal carbon dioxide tension on cerebral blood flow during heat stress

Abstract

Passive heat stress reduces arterial carbon dioxide partial pressure (P aCO 2 ) as reflected by 3 to 5 Torr reductions in end-tidal carbon dioxide tension (P ETCO 2 ). Heat stress also reduces cerebrovascular conductance (CBVC) by up to 30%. While P aCO 2 is a strong regulator of CBVC, it is unlikely that the relatively small change in P ETCO 2 during heating is solely responsible for the reductions in CBVC. This study tested the hypothesis that P aCO 2 , referenced by P ETCO 2 , is not the sole mechanism for reductions in CBVC during heat stress. Mean arterial blood pressure (MAP), P ETCO 2 , middle cerebral artery blood velocity (MCA V mean ), and calculated CBVC (MCA V mean /MAP) were assessed in seven healthy individuals, during three separate conditions performed sequentially: (1) normothemia, (2) control passive heat stress and (3) passive heat stress with P ETCO 2 clamped at the normothermic level (using a computer-controlled sequential gas delivery breathing circuit). MAP was similar in the three thermal conditions (P = 0.55). Control heat stress increased internal temperature ∼1.3• C, which resulted in decreases in P ETCO 2 , MCA V mean and calculated CBVC (P < 0.001 for all variables). During heat stress + clamp conditions internal temperature remained similar to that during the control heat stress condition (P = 0.31). Heat stress + clamp successfully restored P ETCO 2 to the normothermic level (P = 0.99) and increased MCA V mean (P = 0.002) and CBVC (P = 0.008) relative to control heat stress. Despite restoration of P ETCO 2 , MCA V mean (P = 0.005) and CBVC (P = 0.03) remained reduced relative to normothermia. These results indicate that heat stress-induced reductions in P aCO 2 , as referenced by P ETCO 2 , contribute to the decrease in MCA V mean and CBVC; however, other factors (e.g. perhaps elevated sympathetic nerve activity) are also involved in mediating this response.

Blood Flow Distribution during Heat Stress: Cerebral and Systemic Blood Flow

“…3 In addition, it is well known that heat stress modifies distribution of blood flow toward cutaneous circulation while decreasing renal and splanchnic blood flows by enhanced vasoconstriction. 15,19 Maintained or decreased cerebral blood velocity during heat stress has been reported [10][11][12][20][21][22][23] but the mechanism remains unclear. The present study demonstrated that CBF conductance in MCAV mean , ICA, and VA gradually decreased during whole body heating, whereas CVC forehead and ECA conductance increased by 3 times and 2.5 times from the baseline, respectively.…”

“…However, their follow-up study showed that MCAV mean did not return to the baseline level during heat stress (internal temperature increased by 1.41C) even when P ET CO 2 was clamped to the preheating. 11,12 In the present study, we also calculated the relationship between changes in P ET CO 2 and changes in ICA and VA blood flows throughout heat stress, but there was no significant relationship. We did not perform any perturbation to change P ET CO 2 in this study.…”

“…In contrast, heat stress reduced rather than augmented CBF despite an increase in Q, 10 indicating that the role of systemic circulation is unlikely to have an important role in CBF regulation during heat stress. The mechanism of the decrease in CBF during heat stress has been explained partly by heat stress-induced hypocapnia via hyperventilation, 11 but it has not been understood completely. 11,12 It is well established that heat stress modified the blood distribution of Q to the systemic circulation by an increase in cutaneous blood flow for thermoregulation.…”

“…The mechanism of the decrease in CBF during heat stress has been explained partly by heat stress-induced hypocapnia via hyperventilation, 11 but it has not been understood completely. 11,12 It is well established that heat stress modified the blood distribution of Q to the systemic circulation by an increase in cutaneous blood flow for thermoregulation. 4,[13][14][15] Similar to systemic circulation, the contribution of Q to CBF may be altered by heat stress.…”

End-tidal carbon dioxide tension reflects arterial carbon dioxide tension in the heat-stressed human with and without simulated hemorrhage

“…Studies using end-tidal carbon dioxide tension (PET CO 2 ) to estimate Pa CO 2 during passive heat stress (i.e., increase in internal temperature ϳ1.2-1.5°C) suggest that heat stress reduces Pa CO 2 ϳ4 -8 mmHg (3,5,15,26). A potential limitation to these studies is the assumption that PET CO 2 is an accurate surrogate for Pa CO 2 , the latter being the physiologically relevant variable.…”