A. S. Tonnesen

C. J. Morgenweck

C. Marnock

J. M. Bull

K. D. Fallon

 Hyperthermia, to 42 degrees C, for treatment of cancer, was induced 23 times in 13 anesthetized patients utilizing an extracorporeal heat-exchange circuit. Sweating rate over the chest, abdomen, arm and forearm ranged from 0.2 to 0.9 mg sweat X min-1 X cm-2. Cardiac index (CI), stroke volume index (SVI), left ventricular stroke work index, and right ventricular stroke work index initially increased to 221 +/- 12.5, 162 +/- 9.6, 142 +/- 11, and 203 +/- 29% but later fell to 169–173, 113–120, 69, and 148–117% of control, respectively. Heart rate initially rose to 145 +/- 5.9% and then stabilized at 160–162% of control. Pulmonary arterial occlusion pressure and central venous pressure initially fell to 82 +/- 8 and 93 +/- 9% but later rose to 87–102 and 105–120% of control levels, respectively. The hemodynamic response to severe heat stress in anesthetized humans was characterized by peripheral vasodilation accompanied by compensatory increases in heart rate and CI. Ventricular function, as reflected by SVI and CI, declined with continued heat stress, despite reduced afterload and stable or increased filling pressures. Pulmonary arterial temperature rose fastest, followed by the esophageal, rectal, and bladder temperatures, respectively. Jugular bulb temperature also rose rapidly. </jats:p

Sweating, hemodynamic responses, and thermal equilibration during hyperthermia in humans

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