Changes in arterial blood pressure elicited by severe passive heating at rest is associated with hyperthermia-induced hyperventilation in humans

The arterial blood pressure and ventilatory responses to severe passive heating at rest varies greatly among individuals. We tested the hypothesis that the increase in ventilation seen during severe passive heating of resting humans is associated with a decrease in arterial blood pressure. Passive heating was performed on 18 healthy males using hot water immersion to the level of the iliac crest and a water-perfused suit. We then divided the subjects into two groups: MAP_NOTINC (n = 8), whose mean arterial blood pressure (MAP) at the end of heating had increased by ≤3 mmHg, and MAP_INC (n = 10), whose MAP increased by >3 mmHg. Increases in esophageal temperature (T _es) elicited by the heating were similar in the two groups (+2.3 ± 0.3 vs. +2.4 ± 0.4 °C). Early during heating (increase in T _es was <1.5 °C), MAP, minute ventilation (\( \dot{V}_{\text{E}} \)), and end-tidal CO₂ pressure (\( P_{{{\text{ET}}_{\text{CO2}} }} \)) were similar between the groups. However, during the latter part of heating (increase in T _es was ≥1.5 °C), the increase in \( \dot{V}_{\text{E}} \) and decrease in \( P_{{{\text{ET}}_{\text{CO2}} }} \) were significantly greater or tended to be greater, while the increase in MAP was significantly smaller in MAP_NOTINC than MAP_INC. Among all subjects, heating-induced changes in \( \dot{V}_{\text{E}} \) significantly and negatively correlated with heating-induced changes in MAP during the latter part of heating (r = −0.52 to −0.74, P < 0.05). These results suggest that, in resting humans, 25−50 % of the variation in the magnitude of the arterial blood pressure response to severe passive heating can be explained by the magnitude of hyperthermia-induced hyperventilation.