HEAT RELATED SYNCOPE
Part of the initial adaptation to high ambient temperatures involves dilatation of peripheral blood vessels, which allows for dissipation of excess heat through the skin. Thus, at any one point in time, more of an individual’s intravascular volume will be located in the periphery. This leads to a relative decrease in effective circulating volume (Wilson, 2011).
Concomitant dehydration, volume loss through sweating, and heat edema may further reduce the effective circulating volume. Eventually, this will result in inadequate venous return leading to a transient loss of consciousness as cerebral perfusion temporarily becomes inadequate to maintain consciousness. This loss of consciousness in response to heat exposure is referred to as heat related syncope (Wilson, 2011).
Common risk factors for the development of heat related syncope include:
CLINICAL PRESENTATION & DIAGNOSIS
Heat related syncope is typically seen in elderly patients who stand for prolonged periods of time or make abrupt postural changes in hot environments. The actual syncopal event will be preceded by a prodrome of non-specific symptoms such as nausea, lightheadedness, vertigo, etc. While the actual symptoms are less important, the presence of a prodrome is highly supportive of a benign etiology for the syncopal event. Conversely, the assessing clinician should be concerned for cardiogenic (and to a lesser extent, neurogenic) etiologies if a prodrome is lacking.
The actual loss of consciousness should be brief and self-limited. Initially, after regaining consciousness, patients may experience similar symptoms to those which occurred during their prodrome. Again, this is reassuring of a benign cause for the patient’s syncope (Bouchama A, 2002). Cardiac syncope will often result in an immediate return to baseline which should prompt a higher degree of concern and further investigations. Eventually, the patient should return to baseline. Any focal neurologic deficit or failure to return to baseline should prompt transport to hospital for evaluation.
Heat related syncope is self-limited and will resolve upon placing the patient in a horizontal position to increase effective circulating volume available to the brain. Additionally, the patient should be moved to a cooler, preferably shaded environment for assessment. Avoidance of prolonged standing and abrupt postural changes may reduce occurrence (Toru Hifumi, 2018).
Authors: Dr. Erik Leci and Dr. Graham Briscoe (May 10, 2020 PR ND)
Wilson, C. (2011). Effects of Thermal Stress on Cardiac Function . Exercise Sport Science Review, 39: 12-17 .
Bouchama A, K. J. (2002). Heat stroke. New England Jounral of Medicine , 346:1978–88.
Toru Hifumi, Y. K. (2018). Heat stroke. Journal of Intensive Care , 320-328.