Hypercapnia does not improve hyperthermic simulated hemorrhagic tolerance

This study tested the hypothesis that hypercapnia induced increases in cerebral perfusion improves tolerance to a simulated hemorrhagic challenge in heat stressed individuals. Seven individuals (32±9 y; 73±15 kg) underwent passive heat stress followed by a hemorrhagic challenge on two separate days (randomized). Hemorrhage was simulated via progressive lower body negative pressure (LBNP) to pre‐syncope after body core (intestinal) temperature was raised ~1.5 °C using a water perfused suit. From 30 Torr LBNP to pre‐syncope, subjects inhaled either (blinded) a hypercapnic gas mixture (5% carbon dioxide [CO 2 ], 21% oxygen, balance nitrogen) or normal room air (SHAM). Middle cerebral artery blood velocity (MCAv, transcranial Doppler) and end tidal CO 2 (P ET CO 2 , capnograph) were measured. 5% CO 2 increased P ET CO 2 at 30 Torr LBNP (15±3 mmHg) and pre‐syncope (19±3 mmHg), compared to SHAM (P<0.01). Subsequently, MCAv was higher in the 5% CO 2 trial at 30 Torr (24±10 cm.s −1 , ~33%) and presyncope (21±14 cm.s −1 , ~30%) relative to the SHAM (P<0.01). However, hypercapnia did not alter LBNP tolerance time (5% CO2: 7.5±3.5 min; SHAM: 9.1±3.6 min; P=0.33). These data indicate that inhaling a hypercapnic gas mix and circumventing hyperventilatory‐induced hypocapnia does not improve an individualˈs tolerance to a hyperthermic hemorrhagic challenge, despite improving cerebral perfusion. Supported by NIH Grant HL061388