The Experts below are selected from a list of 7500 Experts worldwide ranked by ideXlab platform
Jong Shiuan Yeh - One of the best experts on this subject based on the ideXlab platform.
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Stress-Induced Cardiomyopathy Caused by Heat Stroke
Annals of emergency medicine, 2011Co-Authors: Wei Ta Chen, Cheng Hsin Lin, Ming Hsiung Hsieh, Chun Yao Huang, Jong Shiuan YehAbstract:Heat Stroke is defined by central nervous system abnormalities and failure of proper maintenance of thermoregulation as a result of high core body temperature ensuing from exposure to high environmental temperatures or strenuous exercise. Common complications include acute respiratory distress syndrome, disseminated intravascular coagulation, acute renal injury, hepatic injury, and rhabdomyolysis. Myocardial injury may also occur during Heat Stroke, resulting in cardiac enzyme increase and ST-segment changes on the ECG. Such findings might behave as diagnostic pitfalls by mimicking the presentation of coronary artery occlusive myocardial infarction. A previous case report described a patient with Heat Stroke and ST-segment elevation, in which the definite cause of the ST-segment elevation was unclear; however, acute myocardial infarction caused by coronary artery disease was ruled out according to the clinical signs, serial ECG changes, and serum level of cardiac biomarkers. Stress-induced cardiomyopathy (Takotsubo cardiomyopathy) was suspected, but it could not be confirmed because of the lack of coronary angiography. We herein report a case of Heat Stroke presenting with ST-segment elevation and cardiogenic shock. Coronary angiography was performed and coronary artery occlusive myocardial infarction was ruled out because of the presence of patent coronary arteries. Left ventriculography showed midventricular and apical hypokinesis, and stress-induced cardiomyopathy was then determined to be the appropriate diagnosis. Heat Stroke causes increase of serum catecholamine levels, in which oversecretion and abnormal responses to catecholamines are a possible cause of stress-induced cardiomyopathy. Catecholamines may therefore be the key in linking Heat Stroke and stress-induced cardiomyopathy.
Lisa R. Leon - One of the best experts on this subject based on the ideXlab platform.
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Common Misconceptions in Classic and Exertional Heat Stroke
Heat Stress in Sport and Exercise, 2019Co-Authors: Orlando Laitano, Michelle A. King, Lisa R. LeonAbstract:Heat Stroke is the most severe manifestation of Heat illness. Classic Heat Stroke (CHS) is defined as central nervous system (CNS) dysfunction and severe hyperthermia as a consequence of Heat exposure at rest and affects mostly vulnerable populations (i.e., elderly during Heat waves and/or children left in vehicles). Exertional Heat Stroke (EHS) shares a similar definition as CHS, except it is triggered in young, otherwise healthy individuals during physical exertion in a hot or temperate environment. CHS and EHS have long been a topic of interest in physiology and have been extensively studied; yet, there are many misconceptions regarding the impact of Heat on organ systems as well as the etiology that predisposes certain individuals to collapse. This chapter discusses five misconceptions that have skewed our understanding of Heat Stroke pathophysiology, mainly due to misinterpretation of data, conjecture that has become dogma as well as limitations in the approaches to study the condition.
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unique cytokine and chemokine responses to exertional Heat Stroke in mice
Journal of Applied Physiology, 2017Co-Authors: Michelle A. King, Lisa R. Leon, Deborah A Morse, Thomas L ClantonAbstract:Immune modulators called cytokines are released following extreme hyperthermia leading to Heat Stroke. It is not known whether exercise in hyperthermia, leading to exertional Heat Stroke, influence...
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Pathophysiology of Heat Stroke
2015Co-Authors: Lisa R. LeonAbstract:Abstract Download Free Sample Heat illnesses exist along a continuum starting with the mild condition of Heat exhaustion and progressing to Heat injury and Heat Stroke. Heat Stroke is a life-threatening condition clinically characterized by a severe elevation in body temperature with central nervous system dysfunction that often includes combativeness, delirium, seizures, and coma. Classic Heat Stroke is experienced primarily by the very young or elderly during annual Heat waves. Exertional Heat Stroke is a condition experienced by young, fit individuals during strenuous physical activity in hot or temperate environments. Heat Stroke sequelae are a consequence of Heat injury to the tissues in combination with coagulopathies and a systemic inflammatory response syndrome (SIRS) that often culminates in multi-organ system dysfunction or death. Endotoxin leakage across ischemic-damaged gut membranes is thought to initiate the SIRS with cytokines and other inflammatory mediators involved in this multi-factoria...
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Heat Stroke role of the systemic inflammatory response
Journal of Applied Physiology, 2010Co-Authors: Lisa R. Leon, Bryan G HelwigAbstract:Heat Stroke is a life-threatening illness that is characterized clinically by central nervous system dysfunction, including delirium, seizures, or coma and severe hyperthermia. Rapid cooling and support of multi-organ function are the most effective clinical treatments, but many patients experience permanent neurological impairments or death despite these efforts. The highest incidence of Heat Stroke deaths occurs in very young or elderly individuals during summer Heat waves, with ∼200 deaths per year in the United States. Young, fit individuals may experience exertional Heat Stroke while performing strenuous physical activity in temperate or hot climates. Factors that predispose to Heat Stroke collapse include pre-existing illness, cardiovascular disease, drug use, and poor fitness level. For decades the magnitude of the hyperthermic response in Heat Stroke patients was considered the primary determinant of morbidity and mortality. However, recent clinical and experimental evidence suggests a complex interplay between Heat cytotoxicity, coagulation, and the systemic inflammatory response syndrome (SIRS) that ensues following damage to the gut and other organs. Cytokines are immune modulators that have been implicated as adverse mediators of the SIRS, but recent data suggest a protective role for these proteins in the resolution of inflammation. Multi-organ system failure is the ultimate cause of mortality, and recent experimental data indicate that current clinical markers of Heat Stroke recovery may not adequately reflect Heat Stroke recovery in all cases. Currently Heat Stroke is a more preventable than treatable condition, and novel therapeutics are required to improve patient outcome.
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Heat Stroke and cytokines.
Progress in brain research, 2007Co-Authors: Lisa R. LeonAbstract:Heat Stroke is a life-threatening illness that affects all segments of society, including the young, aged, sick, and healthy. The recent high death toll in France (Dorozynski, 2003) and the death of high-profile athletes has increased public awareness of the adverse effects of Heat injury. However, the etiology of the long-term consequences of this syndrome remains poorly understood such that preventive/treatment strategies are needed to mitigate its debilitating effects. Cytokines are important modulators of the acute phase response (APR) to stress, infection, and inflammation. Current data implicating cytokines in Heat Stroke responses are mainly from correlation studies showing elevated plasma levels in Heat Stroke patients and experimental animal models. Correlation data fall far short of revealing the mechanisms of cytokine actions such that additional research to determine the role of these endogenous substances in the Heat Stroke syndrome is required. Furthermore, cytokine determinations have occurred mainly at end-stage Heat Stroke, such that the role of these substances in progression and long-term recovery is poorly understood. Despite several studies implicating cytokines in Heat Stroke pathophysiology, few studies have examined the protective effect(s) of cytokine antagonism on the morbidity and mortality of Heat Stroke. This is particularly surprising since Heat Stroke responses resemble those observed in the endotoxemic syndrome, for which a role for endogenous cytokines has been strongly implicated. The implication of cytokines as mediators of endotoxemia and the presence of circulating endotoxin in Heat Stroke patients suggests that much knowledge can be gained from applying our current understanding of endotoxemic pathophysiology to the study of Heat Stroke. Heat shock proteins (HSPs) are highly conserved proteins that function as molecular chaperones for denatured proteins and reciprocally modulate cytokine production in response to stressful stimuli. HSPs have been shown repeatedly to confer protection in Heat Stroke and injury models. Interactions between HSPs and cytokines have received considerable attention in the literature within the last decade such that a complex pathway of interactions between cytokines, HSPs, and endotoxin is thought to be occurring in vivo in the orchestration of the APR to Heat injury. These data suggest that much of the pathophysiologic changes observed with Heat Stroke are not a consequence of Heat exposure, per se, but are representative of interactions among these three (and presumably additional) components of the innate immune response. This chapter will provide an overview of current knowledge regarding cytokine, HSP, and endotoxin interactions in Heat Stroke pathophysiology. Insight is provided into the potential therapeutic benefit of cytokine neutralization for mitigation of Heat Stroke morbidity and mortality based on our current understanding of their role in this syndrome.
Yoram Epstein - One of the best experts on this subject based on the ideXlab platform.
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Heat Stroke
Sports Medicine, 2004Co-Authors: Eran Hadad, Moshe Rav-acha, Yuval Heled, Yoram Epstein, Daniel S. MoranAbstract:The prognosis of Heat Stroke in patients is directly related to the degree of hyperthermia and its duration. Therefore, the most important feature in the treatment of Heat Stroke is rapid cooling. Several cooling methods have been presented in the literature including immersion in water at different temperatures, evaporative cooling, ice pack application, pharmacological treatment and invasive techniques. This article describes the various cooling techniques in terms of efficacy, availability, adverse effects and mortality rate. Data suggest that cooling should be initiated immediately at time of collapse and should be based on feasible field measures including ice or tepid water (1–16°C), which are readily available. In the emergency department, management should be matched to the patient’s age and medical background and include immersion in ice water (1–5°C) or evaporative cooling.
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Liver transplantation in exertional Heat Stroke: a medical dilemma.
Intensive care medicine, 2004Co-Authors: Eran Hadad, Yuval Heled, Daniel S. Moran, Ziv Ben-ari, Y Shani, Yoram EpsteinAbstract:Background Exertional Heat Stroke (EHS) is a life-threatening condition caused by an extreme elevation in core body temperature. Hepatic involvement is one of the hallmarks of Heat Stroke, affecting nearly all Heat Stroke patients. It is usually manifested by increased serum levels of liver enzymes, but acute liver failure has also been reported. Liver transplantation has been proposed as a potential treatment in cases of severe liver failure, but there are no unanimous criteria pointing to the right stage in which to conduct the transplantation.
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Dantrolene and recovery from Heat Stroke.
Aviation Space and Environmental Medicine, 1999Co-Authors: Daniel S. Moran, Yoram Epstein, M. Wiener, Michal HorowitzAbstract:: Several authors have shown that dantrolene may be effective in the treatment of Heat Stroke patients. However, the scant data available are still controversial. The aim of this investigation was to establish an animal experimental model for studying the efficacy of this drug both as a prophylactic agent and as a means of hastening the cooling process after Heat Stroke. Male albino rats were divided into five groups: Sedentary controls (SC), Sedentary+dantrolene (S+D), Exercise controls (EC), and Exercise+dantrolene (E+D, E+D1). The drug (140 mg x kg(-1) body weight) was administered i.v. either prior to subjection to Heat stress (40 degrees C) (S+D, E+D) or upon development of Heat Stroke syndrome (E+D1). In the S+D group, dantrolene administered prior to Heat stress (HS) delayed the development of Heat Stroke by 70%, although colonic temperature (Tc) at the onset of Heat Stroke was similar to that in group SC (43.0 +/- 0.1 degrees C and 43.2 +/- 0.4 degrees C for S+D and SC, respectively). In E+D animals, dantrolene shortened exercise endurance in the Heat by 17.5%, but concomitantly hindered severe Tc rise (40.9 +/- 0.2 degrees C and 40.0 +/- 0.2 degrees C for EC and E+D, respectively). Administration of dantrolene on the development of Heat Stroke appeared to improve cooling in the exercise group (0.25 degrees C x min(-1) and 0.18 degrees C x min(-1), for the first 1 5 min of cooling, for E+D1 and EC, respectively). The results suggest that dantrolene is effective as a prophylactic agent in sedentary animals only. It also might have application on development of Heat Stroke. It is hypothesized that the observed rapid cooling is associated with dantrolene's effect on muscle contraction, thus leading to attenuated Heat production and peripheral vascular relaxation.
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Exertional Heat Stroke: a case series.
Medicine and science in sports and exercise, 1999Co-Authors: Yoram Epstein, Daniel S. Moran, Yair Shapiro, Ezra Sohar, Joshua ShemerAbstract:ABSTRACTExertional Heat Stroke: a case series. Med. Sci. Sports Exerc., Vol. 31, No. 2, pp. 224-228, 1999. Exertional Heat Stroke (EHS) is a state of extreme hyperthermia that occurs when excess Heat that is generated by muscular exercise exceeds the body's ability to dissipate it at the same rate.
Wei Ta Chen - One of the best experts on this subject based on the ideXlab platform.
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Stress-Induced Cardiomyopathy Caused by Heat Stroke
Annals of emergency medicine, 2011Co-Authors: Wei Ta Chen, Cheng Hsin Lin, Ming Hsiung Hsieh, Chun Yao Huang, Jong Shiuan YehAbstract:Heat Stroke is defined by central nervous system abnormalities and failure of proper maintenance of thermoregulation as a result of high core body temperature ensuing from exposure to high environmental temperatures or strenuous exercise. Common complications include acute respiratory distress syndrome, disseminated intravascular coagulation, acute renal injury, hepatic injury, and rhabdomyolysis. Myocardial injury may also occur during Heat Stroke, resulting in cardiac enzyme increase and ST-segment changes on the ECG. Such findings might behave as diagnostic pitfalls by mimicking the presentation of coronary artery occlusive myocardial infarction. A previous case report described a patient with Heat Stroke and ST-segment elevation, in which the definite cause of the ST-segment elevation was unclear; however, acute myocardial infarction caused by coronary artery disease was ruled out according to the clinical signs, serial ECG changes, and serum level of cardiac biomarkers. Stress-induced cardiomyopathy (Takotsubo cardiomyopathy) was suspected, but it could not be confirmed because of the lack of coronary angiography. We herein report a case of Heat Stroke presenting with ST-segment elevation and cardiogenic shock. Coronary angiography was performed and coronary artery occlusive myocardial infarction was ruled out because of the presence of patent coronary arteries. Left ventriculography showed midventricular and apical hypokinesis, and stress-induced cardiomyopathy was then determined to be the appropriate diagnosis. Heat Stroke causes increase of serum catecholamine levels, in which oversecretion and abnormal responses to catecholamines are a possible cause of stress-induced cardiomyopathy. Catecholamines may therefore be the key in linking Heat Stroke and stress-induced cardiomyopathy.
Daniel S. Moran - One of the best experts on this subject based on the ideXlab platform.
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Heat Stroke
Sports Medicine, 2004Co-Authors: Eran Hadad, Moshe Rav-acha, Yuval Heled, Yoram Epstein, Daniel S. MoranAbstract:The prognosis of Heat Stroke in patients is directly related to the degree of hyperthermia and its duration. Therefore, the most important feature in the treatment of Heat Stroke is rapid cooling. Several cooling methods have been presented in the literature including immersion in water at different temperatures, evaporative cooling, ice pack application, pharmacological treatment and invasive techniques. This article describes the various cooling techniques in terms of efficacy, availability, adverse effects and mortality rate. Data suggest that cooling should be initiated immediately at time of collapse and should be based on feasible field measures including ice or tepid water (1–16°C), which are readily available. In the emergency department, management should be matched to the patient’s age and medical background and include immersion in ice water (1–5°C) or evaporative cooling.
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Liver transplantation in exertional Heat Stroke: a medical dilemma.
Intensive care medicine, 2004Co-Authors: Eran Hadad, Yuval Heled, Daniel S. Moran, Ziv Ben-ari, Y Shani, Yoram EpsteinAbstract:Background Exertional Heat Stroke (EHS) is a life-threatening condition caused by an extreme elevation in core body temperature. Hepatic involvement is one of the hallmarks of Heat Stroke, affecting nearly all Heat Stroke patients. It is usually manifested by increased serum levels of liver enzymes, but acute liver failure has also been reported. Liver transplantation has been proposed as a potential treatment in cases of severe liver failure, but there are no unanimous criteria pointing to the right stage in which to conduct the transplantation.
-
Dantrolene and recovery from Heat Stroke.
Aviation Space and Environmental Medicine, 1999Co-Authors: Daniel S. Moran, Yoram Epstein, M. Wiener, Michal HorowitzAbstract:: Several authors have shown that dantrolene may be effective in the treatment of Heat Stroke patients. However, the scant data available are still controversial. The aim of this investigation was to establish an animal experimental model for studying the efficacy of this drug both as a prophylactic agent and as a means of hastening the cooling process after Heat Stroke. Male albino rats were divided into five groups: Sedentary controls (SC), Sedentary+dantrolene (S+D), Exercise controls (EC), and Exercise+dantrolene (E+D, E+D1). The drug (140 mg x kg(-1) body weight) was administered i.v. either prior to subjection to Heat stress (40 degrees C) (S+D, E+D) or upon development of Heat Stroke syndrome (E+D1). In the S+D group, dantrolene administered prior to Heat stress (HS) delayed the development of Heat Stroke by 70%, although colonic temperature (Tc) at the onset of Heat Stroke was similar to that in group SC (43.0 +/- 0.1 degrees C and 43.2 +/- 0.4 degrees C for S+D and SC, respectively). In E+D animals, dantrolene shortened exercise endurance in the Heat by 17.5%, but concomitantly hindered severe Tc rise (40.9 +/- 0.2 degrees C and 40.0 +/- 0.2 degrees C for EC and E+D, respectively). Administration of dantrolene on the development of Heat Stroke appeared to improve cooling in the exercise group (0.25 degrees C x min(-1) and 0.18 degrees C x min(-1), for the first 1 5 min of cooling, for E+D1 and EC, respectively). The results suggest that dantrolene is effective as a prophylactic agent in sedentary animals only. It also might have application on development of Heat Stroke. It is hypothesized that the observed rapid cooling is associated with dantrolene's effect on muscle contraction, thus leading to attenuated Heat production and peripheral vascular relaxation.
-
Exertional Heat Stroke: a case series.
Medicine and science in sports and exercise, 1999Co-Authors: Yoram Epstein, Daniel S. Moran, Yair Shapiro, Ezra Sohar, Joshua ShemerAbstract:ABSTRACTExertional Heat Stroke: a case series. Med. Sci. Sports Exerc., Vol. 31, No. 2, pp. 224-228, 1999. Exertional Heat Stroke (EHS) is a state of extreme hyperthermia that occurs when excess Heat that is generated by muscular exercise exceeds the body's ability to dissipate it at the same rate.