In a study of heat stroke, more than 250 observations were made on healthy adult human subjects. Data were obtained on body heat storage, sweat rate, sweat replacement, blood pressure, venous pressure, oxygen consumption, blood gas analyses, hemoconcentration, and osmolarity; and on cardiac output, cardiac shadows, and auscultatory and electrocardiographic findings. During extreme heat exposure there was an increased venous pressure and operational arteriovenous shunt (or its functional equivalent) in the presence of cardiac failure. It is postulated that (1) the primary event in the circulatory collapse of heat pyrexia is highoutput cardiac failure, (2) the cessation of sweating is a result of rising venous pressure, (3) older persons are more susceptible because of irreversible circulatory changes, and (4) an effective treatment may be the intravenous administration of saline solution together with rapid digitalization.
Gold J. DEVELOPMENT OF HEAT PYREXIA. JAMA. 1960;173(11):1175–1182. doi:10.1001/jama.1960.03020290001001