Effects of Physical Hyperthermia Upon Blood Gas Equilibria in Man

Abstract
Eight human subjects were studied at both normal (6 expts.) and elevated body temp. (40.1 to 41.2[degree]C, 15 expts.) induced physically in a hot humid air cabinet. Sedative drugs were given in some and withheld in other fever expts. By means of the classical tonometer technique detns. were made of alkali reserve, arterial pH, arterial pCO2, and the arterial pO2-Independently arterial pCO2 and pO2 were also found by the aeror tonometer technique. In vitro a rise in temp. of 3.5 C was found to cause a reduction in T40 of the blood of 3 vol.%. When a correction was applied for diminished solubility of CO2, this reduction amounted to 1.3 vol.%. The change in pH due to the same rise in temp. was +0.02 while the oxygen dissociation curve shifted to the right by an increment in pO2 of 13% over that at 37[degree]C. During physical fever in unsedated patients, pH rose (avg. 7.48) and pCO2 fell (avg. 33 mg.Hg) with minor changes in alkali reserve (un-compensated alkalosis). In sedated patients, pH was normal or slightly reduced (avg. 7.38) with corresponding deviations in arterial pCO2. As measured by both the tonometer and aerotono-meter techniques the arterial PO2 at elevated body temp. showed no alteration from control levels. This finding applied equally to sedated and unsedated patients and fails to confirm the generally held opinion that hyperthermia produces an anoxic anoxia.

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