Insufficient cutaneous vasoconstriction leading up to and during syncopal symptoms in the heat stressed human.
As much as 50% of cardiac output can be distributed to the skin in the hyperthermic human, and therefore the control of cutaneous vascular conductance (CVC) becomes critical for the maintenance of blood pressure. Little is known regarding the magnitude of cutaneous vasoconstriction in profoundly hypotensive individuals while heat stressed. This project investigated the hypothesis that leading up to and during syncopal symptoms associated with combined heat and orthostatic stress, reductions in CVC are inadequate to prevent syncope. Using a retrospective study design, we evaluated data from subjects who experienced syncopal symptoms during lower body negative pressure (N = 41) and head-up tilt (N = 5). Subjects were instrumented for measures of internal temperature, forearm skin blood flow, arterial pressure, and heart rate. CVC was calculated as skin blood flow/mean arterial pressure × 100. Data were obtained while subjects were normothermic, immediately before an orthostatic challenge while heat stressed, and at 5-s averages for the 2 min preceding the cessation of the orthostatic challenge due to syncopal symptoms. Whole body heat stress increased internal temperature (1.25 ± 0.3°C; P < 0.001) and CVC (29 ± 20 to 160 ± 58 CVC units; P < 0.001) without altering mean arterial pressure (83 ± 7 to 82 ± 6 mmHg). Mean arterial pressure was reduced to 57 ± 9 mmHg (P < 0.001) immediately before the termination of the orthostatic challenge. At test termination, CVC decreased to 138 ± 61 CVC units (P < 0.001) relative to before the orthostatic challenge but remained approximately fourfold greater than when subjects were normothermic. This negligible reduction in CVC during pronounced hypotension likely contributes to reduced orthostatic tolerance in heat-stressed humans. Given that lower body negative pressure and head-up tilt are models of acute hemorrhage, these findings have important implications with respect to mechanisms of compromised blood pressure control in the hemorrhagic individual who is also hyperthermic (e.g., military personnel, firefighters, etc.).
Crandall
C G
CG
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Dallas, TX 75231, USA. craigcrandall@texashealth.org
Shibasaki
M
M
Wilson
T E
TE
D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D001831:Body Temperature / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D005260:Female; D005334:Fever / Q000503:physiopathology; D018475:Head-Down Tilt / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D018882:Heat Stress Disorders / Q000503:physiopathology*; D006801:Humans; D008150:Lower Body Negative Pressure; D008297:Male; D012039:Regional Blood Flow / Q000502:physiology*; D012189:Retrospective Studies; D012867:Skin / Q000098:blood supply*; D013575:Syncope / Q000503:physiopathology*; D014661:Vasoconstriction / Q000502:physiology*