supplementation Symptoms include profound weakness and fatigue, frontal headache, anorexia, nausea, vomiting, diarrhea, and severe muscle cramps Tachycardia and orthostatic hypotension may be noted Hyponatremia, hemoconcentration, and significantly diminished urine sodium are consistent findings Children with cystic fibrosis, particularly those who are young and unable to meet increased salt requirements, are at risk for electrolyte depletion because salt losses in their sweat apparently not respond to acclimatization and aldosterone stimulation of the sweat gland Heat stroke is a life-threatening emergency Classic signs are hyperpyrexia (41°C [105.8°F] or higher); hot, dry skin that is pink or ashen (anhidrosis) depending on the circulatory state; and severe CNS dysfunction Often sweating ceases before the onset of heat stroke The onset of the CNS disturbance may be abrupt, with sudden loss of consciousness Often, however, premonitory signs and symptoms exist These include a sense of impending doom, headache, dizziness, weakness, confusion, euphoria, gait disturbance, and combativeness Posturing, incontinence, seizures, hemiparesis, and pupillary changes may occur Any level of coma may be noted Cerebrospinal fluid findings are usually normal The extent of damage to the CNS is related to the time and extent of hyperpyrexia and to the adequacy of circulation In severe cases, coma may persist even after the body temperature is lowered Patients able to maintain cardiac output adequate to meet the enormously elevated circulatory demand are most likely to survive Initially, the pulse is rapid and full, with an increased pulse pressure Total peripheral vascular resistance falls as a result of vasodilation in the skin and muscle beds, and splanchnic flow diminishes If hyperpyrexia is not corrected, ashen cyanosis and a thin, rapid pulse herald a falling cardiac output The cause may be either direct thermal damage to the myocardium or significant pulmonary hypertension with secondary right ventricular failure Even after body temperature is returned to normal, cardiac output remains elevated and peripheral vascular resistance remains low for several hours, resembling the compensatory hyperemia after ischemia noted in post-trauma, post-shock, and post-septic states Persistently circulating vasoactive substances probably account for this phenomenon