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(aCO2)) as reflected by 3 to 5 Torr reductions in end-tidal carbon dioxide tension (P(ETCO2)). Heat stress also reduces cerebrovascular conductance (CBVC) by up to 30%. While is a strong regulator of CBVC, it is unlikely that the relatively small change in during heating is solely responsible for the reductions in CBVC. This study tested the hypothesis that P(aCO2), referenced by P(ETCO2), is not the sole mechanism for reductions in CBVC during heat stress. Mean arterial blood pressure (MAP), P(ETCO2), 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(ETCO2) 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 approximately 1.3 degrees C, which resulted in decreases in P(ETCO2), 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 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(ETCO2), 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 , as referenced by P(ETCO2), 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.

Figure 1. End-tidal carbon dioxide tension and middle cerebral artery blood velocity (MCA V_mean) during the three conditions

The reduction in end-tidal carbon dioxide () concentration observed with heat stress was completely abolished by the clamping procedure (A). Heat stress reduced MCA V_mean relative to normothermia. Restoration of to the normothermic level while subjects were heat stressed (heat stress + clamp) attenuated the decrease in MCA V_mean relative to control heat stress without the clamp; however, MCA V_mean remained reduced when compared to normothermia (B). These data indicate that mechanisms other than reduced contribute to the reduced cerebral perfusion that occurs in heat-stressed individuals. *Significantly different relative to normothermia. §Significantly different relative to control heat stress.

Figure 2. Representative illustration of middle cerebral artery blood velocity (MCA V_mean) and end-tidal carbon dioxide waveforms during the three conditions

The MCA V_mean and end-tidal carbon dioxide () waveforms during normothermia are depicted in A and B, respectively, whereas the MCA V_mean and waveforms during heat stress (left of the vertical dashed line) and heat stress + clamp (right of the vertical line) are depicted in C and D, respectively. The transition in the signals between normothermia and control heat stress is not continuous whereas the transition between heat stress and heat stress + clamp is continuous. The numerical values indicate mean responses for each condition and variable. During the heat stress + clamp protocol, when was successfully restored to the normothermic level, MCA V_mean was elevated relative to heat stress; however, it remained reduced when compared to normothermia.