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Sweating, hemodynamic responses, and thermal equilibration during hyperthermia in humans
Journal of Applied Physiology (Bethesda, Md. : 1985)
|April 1, 1987
Summary
Induced hyperthermia for cancer treatment caused significant cardiovascular changes in anesthetized patients. Heart rate and cardiac index initially increased but later declined, indicating impaired ventricular function under severe heat stress.
Area of Science:
- Cardiovascular Physiology
- Thermoregulation
- Oncology
Background:
- Cancer treatment often involves hyperthermia, raising body temperature to therapeutic levels.
- Understanding the physiological responses to induced hyperthermia is crucial for patient safety.
Purpose of the Study:
- To investigate the hemodynamic and thermoregulatory responses to induced hyperthermia in anesthetized cancer patients.
Main Methods:
- Induced hyperthermia up to 42°C using an extracorporeal heat-exchange circuit in 13 anesthetized patients.
- Monitored sweating rate, cardiac index (CI), stroke volume index (SVI), ventricular stroke work indices, heart rate, pulmonary arterial occlusion pressure, central venous pressure, and body temperatures.
Main Results:
- Peripheral vasodilation occurred, leading to initial increases in heart rate and CI.
- Ventricular function (SVI, CI) declined with sustained heat stress, despite reduced afterload.
- Body temperatures increased rapidly, with pulmonary artery temperature rising fastest, followed by esophageal, rectal, and bladder.
Conclusions:
- Severe heat stress during hyperthermia treatment induces significant cardiovascular strain in anesthetized patients.
- Compensatory mechanisms initially maintain cardiac output, but prolonged heat exposure impairs ventricular function.
- Close hemodynamic monitoring is essential during hyperthermia cancer therapy.