Cardiac output at pre‐syncope in the heat‐stressed human

Maintenance of arterial blood pressure is governed by a combination of vascular resistance and cardiac output. Although heat stress compromises the control of arterial blood pressure during simulated hemorrhage, it remains unknown whether this response is due to inadequate vascular resistance and/or cardiac output responses. This study evaluated cardiac output responses at the onset of syncopal symptoms in heat‐stressed individuals. Simulated hemorrhage was imposed via lower body negative pressure (LBNP) to pre‐syncope in 11 subjects during passive heating (increase core temperature 1.2 ± 0.2 °C). Cardiac output was measured via thermodilution while subjects were normothermic, heat stressed, and throughout subsequent LBNP. Heat stress increased cardiac output from 7.1 ± 1.1 L/min to 11.9 ± 2.0 L/min (P < 0.001). Although cardiac output at the onset of syncopal symptoms was 37 ± 13% lower relative to pre‐LBNP, absolute cardiac output was not different than normothermic values (7.5 ± 1.8 L/min; P = 0.46). These data indicate that, in the setting of profound cutaneous vasodilation associated with heat stress combined with a simulated hemorrhagic challenge sufficient to cause syncopal symptoms, a cardiac output that is adequate to maintain blood pressure while normothermic is no longer adequate while heat stressed. Supported by NIH Grants HL61388 & HL84072