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Hyperthermic hyperventilation is not mitigated by cardiopulmonary baroreceptor loading

This study tested the hypothesis that cardiopulmonary baroreceptor loading would reverse increases in ventilation and decreases in end‐tidal carbon dioxide (CO2) that accompany hyperthermia. Ten individuals (29±5 y; 76±12 kg) underwent passive heat stress via a water perfused suit while intestinal temperature (HQ Inc.), mean skin temperature, central venous pressure (central venous catheter, CVP, n=8), minute ventilation, tidal volume (Parvo‐Medics) and end‐tidal CO2 (capnograph, PETCO2) were monitored. After intestinal temperature was elevated 1.9 ±0.5°C, causing a sustained rise in ventilation (by 2.9 ±2.8 L/min), and reductions in PETCO2 (by 4 ±3 mm Hg) and CVP (by 4 ±1 mm Hg), 19 ±2 ml/kg of warmed saline was rapidly (over 5–10 min) infused intravenously to increase CVP and return cardiopulmonary baroreceptor loading towards normothermic levels. Saline infusion increased CVP by 5 ±1 mm Hg (P <0.01) but did not change (P >;0.05) ventilation, tidal volume or PETCO2. Intestinal and skin temperatures did not change (P >;0.05) with saline infusion. The absence of a reduction in ventilation upon returning cardiopulmonary baroreceptor loading to pre‐heat stress levels indicates that hyperthermic hyperventilation is not caused by cardiopulmonary baroreceptor unloading coincident with the heat stress. Supported by NIH Grant HL061388