Heat Related Mortality Miklós Székely,Luís Carletto,and András Garami Department of Pathophysiology and Gerontology; Medical School; University of Pécs; Pécs, Hungary Climate Change and Health: A Position Paper of American College of PhysiciansRyan A. Crowley, BSJ As the climate warms, more people could be susceptible to heat-related illness. Extreme heat exposure caused more than 7400 deaths in the United States. Excessive heat exposure caused more than 7400 deaths in the United States from 19190-2010. In France, 6 heat waves occuring from 1971 to 2003 were associated with significant excess mortality, contributing to 13,700 deaths in 2003 alone, Across Europe, about 70,000 premature deaths were attributed to the 2003 heat wave. Heat exposure of the body can result in different physiological/pathological outcomes. Physiologically, successful activation of the effectors results in warmth tolerance. In case of repeated, chronic heat exposure the tolerance intensifies leading to heat acclimation . Heat-related illnesses develop when the pathological effects of heat load are not prevented. Syndromes vary from less severe, such as heat syncope to severe forms as lethal heat stroke. Activation of autonomic heat-defense effectors affects the regulation of homeostatic systems other than thermoregulation. Increased cutaneous vasodilation and decreased venous tone reduce ventricular filling, which, in an orthostatic position, may lead to low brain perfusion and heat syncope (with unconsciousness). Electrolyte imbalance can develop due to sweating, and promote the occurrence of heat cramps, i.e. short-lived, painful contractions of skeletal muscles during or after prolonged work in the heat. In severe hypovolemia, heat exhaustion develops with domination of water- or salt-depletion. The former is mainly due to insufficient fluid replacement and consists of thirst, progressive hypovolemia, hyperosmolarity and hyperthermia. Salt-depletion dominates when sweating-induced water loss is replaced, but salt is not (e.g., by soft drinks), leading to hypoosmolarity and its consequences (e.g., cell swelling). In patients with compensated heart failure, the need for a higher cardiac output during heat exposure may manifest heart failure: high end-diastolic volume/pressure with backward (venous congestion, edema) and forward (insufficient muscle/renal/intestinal perfusion) failure symptoms. Consequently, the patient collapses because of muscle weakness. Although consciousness is maintained, the developing heat decompensation is more severe than heat syncope.