The heart in heatstroke

Kew, Michael C.; Tucker, R. B. K.; Bersohn, I; Seftel, H. C.

doi:10.1016/0002-8703(69)90188-4

Cited by 49 publications

(15 citation statements)

References 16 publications

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“…Kew, et al analyzed the isozyme of LDH and found that 69% of heat stroke patients showed elevated LDH levels whose isozyme patterns were indicative of a myocardial origin. 5) On the other hand, Costrini, et al did not find elevated levels of the MB fraction of CK in any of their 13 heat stroke patients. 19) The difference may be attributable to the severity of exposure of the myocardium to a high temperature and/or the severity of myocardial ischemia.…”

Section: )mentioning

confidence: 77%

“…Several cardiac complications have been documented in heat stroke cases, 5,6) and certain nonspecific ECG changes, including ST-T elevation, have been described. ST-T elevation is rare in heat stroke and is sometimes attributed to corFrom the…”

Section: )mentioning

confidence: 99%

“…Physical examination revealed a sluggish bilateral light reflex, a dry tongue, skin without any sweat, a normal heart beat without a murmur or gallop, a normal respiratory sound, and a mildly distended abdomen. The ECG revealed ST elevation in leads I, II, III, aVL, aVF, and V [3][4][5][6] , and a tall T wave in V 1-2 ( Figure 1A). The echocardiogram showed diffuse hypokinesis with a 40% ejection fraction.…”

Section: Case Reportmentioning

confidence: 99%

“…ECG was measured when the patient was transferred to the emergency room (A). ST elevation in I, II, III, aVL, aVF, and V [3][4][5][6] , and a tall T wave in V 1-2 were observed, and still remained on day 2 (B). On day 4, these changes began to be normalized (C) and were completely normalized on day 7 (D).…”

Section: Case Reportmentioning

confidence: 99%

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A Case of Severe Heat Stroke With Abnormal Cardiac Findings

et al. 2005

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SUMMARYWe document serial changes in the electrocardiogram (ECG) and myocardial markers in a case of severe heat stroke treated with cooling procedures. A 23-year-old comatose male with heat stroke was presented in the emergency room. The condition of the patient was complicated by hepatic failure, rhabdomyolysis, acute renal failure, and cardiac abnormalities. ECG revealed diffuse ST-T elevation; serum levels of myocardial markers were remarkably high and diffuse hypokinesis was observed on the echocardiogram. Cooling procedures, including applying cold vapor to the patient's skin, a gastric lavage with cold water, and an intravenous cold fluid infusion were not successful. Since multiple organ damage (heart, liver, central nervous system, and kidney) was evident, we utilized continuous hemodialysis and hemofiltration, using cold dialysate for efficient cooling. The patient recovered from the multiple organ damage and was removed from the intensive care unit 14 days after the onset. The cardiac abnormalities had normalized within several days without any damage to the myocardium. Q waves were not detected in any lead in the ECG. When interpreting ST-T elevation in the ECG of a heat stroke patient, caution should be used so as to not misdiagnose it as an acute myocardial infarction. (Int Heart J 2005; 46: 543-550) Key words: Heat stroke, Electrocardiography, Multiple organ failure, Myocardium HEAT stroke is an acute thermoregulatory failure that often results from exposure to high temperatures.1) The diagnosis of heat stroke is usually based on central nervous system dysfunction and a rectal temperature of 41°C or higher, as well as occasional multi-organ damage and dysfunction.2,3) Heat stroke can be exercise induced (exertional) or non-exercise induced (classic), and occurs when heat gain exceeds heat loss from the skin by radiation, convection, or evaporation. 4)Several cardiac complications have been documented in heat stroke cases, 5,6) and certain nonspecific ECG changes, including ST-T elevation, have been described. ST-T elevation is rare in heat stroke and is sometimes attributed to corFrom the

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confidence: 77%

Section: )mentioning

confidence: 99%

Section: Case Reportmentioning

confidence: 99%

Section: Case Reportmentioning

confidence: 99%

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A Case of Severe Heat Stroke With Abnormal Cardiac Findings

et al. 2005

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“…Tachycardia and tachypnea are common and accompanied by hypotension in approximately one third of classic heat stroke cases (42). More detailed cardiac abnormalities have been reported in heat stroke patients than animal models and include PVCs, ST segment depression, and T-wave changes consistent with myocardial ischemia and infarction, sinus tachycardia, and hypo-or hypertension that present with or without global myocardial damage (7,9,85,182,238,335,337,342,346,414). Hypocalcemia and hyperkalemia have been implicated in Q-T interval prolongation and S-T segment abnormalities, respectively, with heat stroke (7,190).…”

Section: Cardiovascular Dysfunction With Heat Strokementioning

confidence: 99%

Heat Stroke

Leon

Bouchama

2015

Comprehensive Physiology

343

356

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Heat stroke is a life-threatening condition clinically diagnosed as a severe elevation in body temperature with central nervous system dysfunction that often includes combativeness, delirium, seizures, and coma. Classic heat stroke primarily occurs in immunocompromised individuals during annual heat waves. Exertional heat stroke is observed in young fit individuals performing strenuous physical activity in hot or temperature environments. Long-term consequences of heat stroke are thought to be due to a systemic inflammatory response syndrome. This article provides a comprehensive review of recent advances in the identification of risk factors that predispose to heat stroke, the role of endotoxin and cytokines in mediation of multi-organ damage, the incidence of hypothermia and fever during heat stroke recovery, clinical biomarkers of organ damage severity, and protective cooling strategies. Risk factors include environmental factors, medications, drug use, compromised health status, and genetic conditions. The role of endotoxin and cytokines is discussed in the framework of research conducted over 30 years ago that requires reassessment to more clearly identify the role of these factors in the systemic inflammatory response syndrome. We challenge the notion that hypothalamic damage is responsible for thermoregulatory disturbances during heat stroke recovery and highlight recent advances in our understanding of the regulated nature of these responses. The need for more sensitive clinical biomarkers of organ damage is examined. Conventional and emerging cooling methods are discussed with reference to protection against peripheral organ damage and selective brain cooling.

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