Electrocardiographic Abnormalities in Patients With Heat Stroke

Akhtar, Mohammed Jawaid; Al-Nozha, Mansour M.; Al-Harthi, Saad S.; Nouh, Mohamed S.

doi:10.1378/chest.104.2.411

Cited by 74 publications

(41 citation statements)

References 14 publications

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“…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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Section: )mentioning

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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“…However, further testing will likely be necessary to determine how any TnI released from damaged myocytes during exertional HS could affect the specificity of the test. Although cardiovascular damage was previously observed in our passive rat HS model (57) as well as clinical conditions (3,9,18,35,47,48), it is important to point out that our primary purpose in evaluating cTnI levels in the present study was not as an indicator of cardiovascular insult, and we did not measure cardiomyocyte or tissue damage directly in the present study. Instead, we are suggesting that measuring cTnI in circulation can serve as a very sensitive and specific marker of total systemic HS pathology, not just cardiac damage.…”

Section: Discussionmentioning

confidence: 92%

Point-of-care cardiac troponin test accurately predicts heat stroke severity in rats

Audet

Quinn

Leon

2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Audet GN, Quinn CM, Leon LR. Point-of-care cardiac troponin test accurately predicts heat stroke severity in rats. Am J Physiol Regul Integr Comp Physiol 309: R1264 -R1272, 2015. First published August 19, 2015; doi:10.1152/ajpregu.00286.2015.-Heat stroke (HS) remains a significant public health concern. Despite the substantial threat posed by HS, there is still no field or clinical test of HS severity. We suggested previously that circulating cardiac troponin (cTnI) could serve as a robust biomarker of HS severity after heating. In the present study, we hypothesized that (cTnI) point-of-care test (ctPOC) could be used to predict severity and organ damage at the onset of HS. Conscious male Fischer 344 rats (n ϭ 16) continuously monitored for heart rate (HR), blood pressure (BP), and core temperature (Tc) (radiotelemetry) were heated to maximum Tc (Tc,Max) of 41.9 Ϯ 0.1°C and recovered undisturbed for 24 h at an ambient temperature of 20°C. Blood samples were taken at Tc,Max and 24 h after heat via submandibular bleed and analyzed on ctPOC test. POC cTnI band intensity was ranked using a simple four-point scale via two blinded observers and compared with cTnI levels measured by a clinical blood analyzer. Blood was also analyzed for biomarkers of systemic organ damage. HS severity, as previously defined using HR, BP, and recovery Tc profile during heat exposure, correlated strongly with cTnI (R 2 ϭ 0.69) at Tc,Max. POC cTnI band intensity ranking accurately predicted cTnI levels (R 2 ϭ 0.64) and HS severity (R 2 ϭ 0.83). Five markers of systemic organ damage also correlated with ctPOC score (albumin, alanine aminotransferase, blood urea nitrogen, cholesterol, and total bilirubin; R 2 Ͼ 0.4). This suggests that cTnI POC tests can accurately determine HS severity and could serve as simple, portable, cost-effective HS field tests. field test; heat stroke; cardiac troponin; point of care; rat HEAT-RELATED ILLNESSES remain a substantial public health threat. Heat stroke (HS) is the most severe form of heat illness, typically presenting as a core temperature (T c ) of Ͼ40°C (104°F) accompanied by central nervous system (CNS) dysfunction, visceral organ failure, and cardiovascular damage (2,6,12,13,16,22,49,51,59). Heat-related illness is associated with considerable pathological variability, and both during heat stress and recovery there is a wide spectrum of physiological responses between individuals. This, in combination with the extremely complex systemic etiology of HS, has meant that testing for HS severity at any time point, but specifically early in recovery, has proven extremely challenging. Presently, there are no validated clinical or field-expedient tests capable of delineating severity during heat or acute recovery.We have shown in mice that the T c response during recovery, specifically the depth of post-HS hypothermia, is a marker of HS severity (39 -41). Hypothermia during recovery has been observed in clinical cases and documented in the most severe HS cases, including deaths (43). More recently, we es...

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“…This is followed by hyperkalemia attributed to heatstroke-associated rhabdomyolysis and cellular leakage. 81 Furthermore, increased glucose utilization results in hypophosphataemia, which might be masked by hyperphosphataemia due to cellular leakage and ensuing renal impairment. 89 …”

Section: Biochemical Findings Associated With Heatstrokementioning

confidence: 99%

Clinical biochemistry of hyperthermia

Hashim

2010

Ann Clin Biochem

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Heatstroke is the most severe form of heat-related disorders that include mild heat intolerance, heat exhaustion and heat stress. The incidence of heat-related disorders is increasing due to several factors that include climate change, co-morbidities and drug usage. Patients with heatstroke present with a core body temperature above 408C, multiorgan dysfunction and central nervous system disorder. The pathogenesis of heatstroke is not fully understood; however, heat-shock proteins, inflammatory cytokines and their modulators have been implicated. The clinical biochemistry laboratory plays an important role in the management of patients with heatstroke. Biochemical findings in patients with heatstroke include elevated urea, creatinine, cardiac and skeletal muscle enzymes, myoglobin and troponin. There is also biochemical evidence of metabolic acidosis, respiratory alkalosis, hepatic injury with elevated enzyme levels as well as abnormal hematological and coagulation indices. This review article aims at increasing awareness of the biochemical changes seen in patients with heatstroke and their possible role in prognosis and in elucidating the pathogenesis of heatstroke.

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Electrocardiographic Abnormalities in Patients With Heat Stroke

Cited by 74 publications

References 14 publications

A Case of Severe Heat Stroke With Abnormal Cardiac Findings

A Case of Severe Heat Stroke With Abnormal Cardiac Findings

Point-of-care cardiac troponin test accurately predicts heat stroke severity in rats

Clinical biochemistry of hyperthermia

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