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Ethanol ingestion prolongs orthostatic intolerance in hyperthermic humans
M D White1, C E Johnston, M P Wu
1Department of Anesthesia, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Background:
Both ethanol ingestion and hyperthermia contribute to orthostatic intolerance (OI).
Hypothesis:
Since ethanol has been cited as a major risk factor for hyperthermia-related deaths, we hypothesized that ethanol exacerbates OI induced by hyperthermia.
Methods:
There were seven subjects (four males, three females) rendered hyperthermic (esophageal temperature = 39 degrees C) in a 40 degrees C water bath on two separate days: Condition 1) Control (juice ingestion); and Condition 2) Ethanol [ethanol (1 ml x kg(-1) body mass) and juice ingestion]. To test for OI, 5-min supine periods were followed by 5-min 63 degrees head-up tilts prior to and following immersion. BPs, heart rate and esophageal temperatures were monitored throughout the experiments.
Results:
For first and second post-immersion tilts, mean arterial BP (MAP) during tilting increased by 5.9 +/- 3.6 (SE) and 9.8 +/- 2.6 mm Hg in the control condition, while it decreased by 7.9 +/- 5.8 and 0.6 +/- 4.3 mm Hg in the ethanol condition. This gave significantly lower MAP (ethanol vs. control) of 63.6 +/- 3.1 vs. 71.8 +/- 4.5 mm Hg (p < 0.05) for the first and 79.6 +/- 2.3 vs. 86.7 +/- 4.4 mm Hg (p < 0.05) for the second post-immersion tilts. These values were all significantly less (p < 0.05) than normothermic tilted values of 94.7 +/- 4.7 mm Hg in the ethanol and 93.6 +/- 2.9 mm Hg in the control condition. Prior to warm water immersion, subjects tolerated all head-up tilts. In the control condition, only one subject experienced orthostatic intolerance following the first post-heating tilt and no intolerance was experienced following 30 min post-heating. However, during the ethanol condition, 4 subjects experienced orthostatic intolerance following the first tilt with episodes of intolerance lasting as long as 80 min (8 supine/tilt cycles).
Conclusion:
Ethanol ingestion prolonged and increased the magnitude of OI in hyperthermic subjects. This may at least partly explain why ethanol is a major risk factor in hyperthermia-related deaths.