G-35 Free Communication/Poster - Heat Stress II: JUNE 5, 2010 7:30 AM - 11:00 AM: ROOM: Hall C
During moderate to pronounced passive heat stress end-tidal carbon dioxide tension (PETCO2) is reduced by approximately 3 - 8 mmHg, which in part contributes to the decreases in cerebral blood flow and cerebrovascular conductance that occur in this thermal condition. Clamping devices have been used to manipulate PETCO2 in normothermic humans, however, their effectiveness in clamping arterial carbon dioxide tension (PaCO2) while heat stressed is unknown.
PURPOSE: The aim of this study was to test the hypothesis that in the heat stressed human PETCO2 accurately tracks PaCO2 when PETCO2 is clamped at normothermic levels.
METHODS: Internal temperature (telemetry pill), PaCO2 (radial artery catheter), and PETCO2 (capnograph) were assessed in 7 healthy individuals during three conditions performed sequentially; 1) normothermia (NT), 2) passive heat stress (HS), and 3) passive heat stress when PETCO2 was clamped at normothermic levels (HS+Clamp). Clamping was achieved using a computer controlled sequential gas delivery breathing circuit (RespiractTM).
RESULTS: Heat stress increased internal temperature from 37.0 ± 0.3 to 38.4 ± 0.4 °C (P < 0.001). While normothermic values of PaCO2 (40.4 ± 3.4 mmHg) and PETCO2 (38.8 ± 3.5 mmHg; P = 0.12) were similar, HS resulted in significantly greater reductions in PaCO2 (D 10.1 ± 3.0 mmHg) relative to PETCO2 (D 7.8 ± 3.5 mmHg; P = 0.04). HS+Clamp caused comparable increases in PaCO2 (D 6.6 ± 3.4 mmHg) and PETCO2 (D 7.5 ± 2.8 mmHg: P = 0.30), however, because the decrease in PaCO2 due to HS was greater than PETCO2, absolute PaCO2 during HS+Clamp remained significantly lower (PaCO2: 36.8 ± 4.9 mmHg; PETCO2: 38.5 ± 5.2 mmHg; P < 0.01).
CONCLUSION: These results indicate that despite a difference in absolute PETCO2 and PaCO2 during heat stress+clamp conditions, clamping caused similar increases between PETCO2 and PaCO2.
Supported by NIH Grants HL61388 & HL84072