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

Abstract

End-tidal carbon dioxide tension (PetCO2) is reduced during an orthostatic challenge, during heat stress, and during a combination of these two conditions. The importance of these changes is dependent on PetCO2 being an accurate surrogate for arterial carbon dioxide tension (PaCO2), the latter being the physiologically relevant variable. This study tested the hypothesis that PetCO2 provides an accurate assessment of PaCO2 during the aforementioned conditions. Comparisons between these measures were made: 1) after two levels of heat stress ( N = 11); 2) during combined heat stress and simulated hemorrhage [via lower-body negative pressure (LBNP), N = 8]; and 3) during an end-tidal clamping protocol to attenuate heat stress-induced reductions in PetCO2 ( N = 7). PetCO2 and PaCO2 decreased during heat stress ( P < 0.001); however, there was no group difference between PaCO2 and PetCO2 ( P = 0.36) nor was there a significant interaction between thermal condition and measurement technique ( P = 0.06). To verify that this nonsignificant trend for the interaction was not due to a type II error, PetCO2 and PaCO2 at three distinct thermal conditions were also compared using paired t-tests, revealing no difference between PaCO2 and PetCO2 while normothermic ( P = 0.14) and following a 1.0 ± 0.2°C ( P = 0.21) and 1.4 ± 0.2°C ( P = 0.28) increase in internal temperature. During LBNP while heat stressed, measures of PetCO2 and PaCO2 were similar ( P = 0.61). Likewise, during the end-tidal carbon dioxide clamping protocol, the increases in PetCO2 (7.5 ± 2.8 mmHg) and PaCO2 (6.6 ± 3.4 mmHg) were similar ( P = 0.31). These data indicate that mean PetCO2 reflects mean PaCO2 during the evaluated conditions.