Heat

2020 ◽  
pp. 1687-1689
Author(s):  
Michael A. Stroud
Keyword(s):  
Physical Activity ◽  
Body Temperature ◽  
Supportive Care ◽  
Physiological Responses ◽  
Heat Stroke ◽  
Heat Exposure ◽  
High Humidity ◽  
Heat Exhaustion ◽  
Clinical Presentations ◽  
Cold Core

Rising body temperature triggers behavioural and physiological responses including reduction in physical activity, alterations of clothing, skin vasodilatation, and sweating. Heat-related illness is relatively common, especially with high humidity or prolonged physical activity. Risk can be reduced by acclimatization with repeated heat exposure, but some individuals seem to be particularly susceptible. Clinical presentations of heat-related illness include (1) ‘heat exhaustion’—the commonest manifestation, with symptoms including nausea, weakness, headache, and thirst. Patients appear dehydrated, complain of being hot, and are flushed and sweaty. Treatment requires rest and fluids, given orally or (in severe cases) intravenously. (2) ‘Heat stroke’ victims often complain of headache, may be drowsy or irritable, and may claim to feel cold. Core temperature is usually 38–41°C, but the patient is shivering with dry, vasoconstricted skin. Treatment requires (a) aggressive rapid cooling; (b) close biochemical monitoring; (c) supportive care for organ failure. There is significant mortality.

Heat

2010 ◽  
pp. 1393-1395
Author(s):  
M.A. Stroud
Keyword(s):  
Physical Activity ◽  
Body Temperature ◽  
Physiological Responses ◽  
Heat Exposure ◽  
High Humidity

Rising body temperature triggers behavioural and physiological responses including reduction in physical activity, alterations of clothing, skin vasodilatation, and sweating. Heat-related illness is relatively common, especially with high humidity or prolonged physical activity. Risk can be reduced by acclimatization with repeated heat exposure, but some individuals seem to be particularly susceptible....

Hyperthermia

2018 ◽  
Author(s):  
Matt Wise ◽  
Paul Frost
Keyword(s):  
Body Temperature ◽  
Neuroleptic Malignant Syndrome ◽  
Core Body Temperature ◽  
Heat Stroke ◽  
Drug Induced ◽  
Muscle Cramps ◽  
Set Point ◽  
Heat Exhaustion ◽  
Neurological Signs ◽  
Core Body

An elevation in core body temperature due to thermoregulatory failure with a normal thermoregulatory set point is called hyperthermia. Globally, the most common heat illnesses are heat exhaustion and heat stroke, and these are major causes of morbidity and mortality. These illnesses represent a continuum of disease ranging from mild (heat exhaustion) to total (heat stroke) failure of thermoregulation. Heat exhaustion is characterized by sweating, muscle cramps, fatigue, vomiting, headaches, dizziness, and fainting. These symptoms may also occur in heat stroke but, in addition, neurological signs such as confusion, seizures, and coma predominate. While the diagnosis of these conditions may be straightforward, hyperthermia may complicate a variety of rarer illnesses, including neuroleptic malignant syndrome and drug-induced hyperthermia.

scholarly journals A Case of Exertional Heat Stroke Complicated by Hypoxic Hepatitis

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Bertram K. Woitok ◽  
Shawki Bahmad ◽  
Gregor Lindner
Keyword(s):  
Supportive Care ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Multiorgan Failure ◽  
Heat Stroke ◽  
Exertional Heat Stroke ◽  
Hypoxic Hepatitis ◽  
Threatening Condition ◽  
Life Threatening ◽  
Delayed Referral

Background.Exertional heat stroke is a life-threatening condition often complicated by multiorgan failure. We hereby present a case of a 25-year-old male presenting with syncope after a 10  km run in 28°C outside temperature who developed acute liver failure. Case Presentation. Initial temperature was found to be 41.1°C, and cooling measures were rapidly applied. He suffered from acute renal failure and rhabdomyolysis and proceeded to acute liver failure (ASAT 6100 U/l and ALAT 6561 U/l) due to hypoxic hepatitis on day 3. He did not meet criteria for emergency liver transplantation and recovered on supportive care. Conclusions. Acute liver failure due to heat stroke is a life-threatening condition with often delayed onset, which nevertheless resolves on supportive care in the majority of cases; thus, a delayed referral to transplant seems to be reasonable.

scholarly journals A novel mouse model of heatstroke accounting for ambient temperature and relative humidity

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Kazuyuki Miyamoto ◽  
Keisuke Suzuki ◽  
Hirokazu Ohtaki ◽  
Motoyasu Nakamura ◽  
Hiroki Yamaga ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Temperature ◽  
Relative Humidity ◽  
Ambient Temperature ◽  
Core Body Temperature ◽  
Heat Exposure ◽  
Organ Damage ◽  
Core Body ◽  
The Impact ◽  
Treatment Water

Abstract Background Heatstroke is associated with exposure to high ambient temperature (AT) and relative humidity (RH), and an increased risk of organ damage or death. Previously proposed animal models of heatstroke disregard the impact of RH. Therefore, we aimed to establish and validate an animal model of heatstroke considering RH. To validate our model, we also examined the effect of hydration and investigated gene expression of cotransporter proteins in the intestinal membranes after heat exposure. Methods Mildly dehydrated adult male C57/BL6J mice were subjected to three AT conditions (37 °C, 41 °C, or 43 °C) at RH > 99% and monitored with WetBulb globe temperature (WBGT) for 1 h. The survival rate, body weight, core body temperature, blood parameters, and histologically confirmed tissue damage were evaluated to establish a mouse heatstroke model. Then, the mice received no treatment, water, or oral rehydration solution (ORS) before and after heat exposure; subsequent organ damage was compared using our model. Thereafter, we investigated cotransporter protein gene expressions in the intestinal membranes of mice that received no treatment, water, or ORS. Results The survival rates of mice exposed to ATs of 37 °C, 41 °C, and 43 °C were 100%, 83.3%, and 0%, respectively. From this result, we excluded AT43. Mice in the AT 41 °C group appeared to be more dehydrated than those in the AT 37 °C group. WBGT in the AT 41 °C group was > 44 °C; core body temperature in this group reached 41.3 ± 0.08 °C during heat exposure and decreased to 34.0 ± 0.18 °C, returning to baseline after 8 h which showed a biphasic thermal dysregulation response. The AT 41 °C group presented with greater hepatic, renal, and musculoskeletal damage than did the other groups. The impact of ORS on recovery was greater than that of water or no treatment. The administration of ORS with heat exposure increased cotransporter gene expression in the intestines and reduced heatstroke-related damage. Conclusions We developed a novel mouse heatstroke model that considered AT and RH. We found that ORS administration improved inadequate circulation and reduced tissue injury by increasing cotransporter gene expression in the intestines.

TEMPERATURE REGULATION IN EXERCISE

PEDIATRICS ◽  
1963 ◽  
Vol 32 (4) ◽  
pp. 691-702
Author(s):  
Sid Robinson
Keyword(s):  
Blood Flow ◽  
Body Temperature ◽  
Heat Stroke ◽  
The Body ◽  
Physiological Regulation ◽  
Temperature Changes ◽  
Metabolic Heat ◽  
Warm Blood ◽  
Hot Environments ◽  
Large Increments

The central body temperature of a man rises gradually during the first half hour of a period of work to a higher level and this level is precisely maintained until the work is stopped; body temperature then slowly declines to the usual resting level. During prolonged work the temperature regulatory center in the hypothalamus appears to be reset at a level which is proportional to the intensity of the work and this setting is independent of environmental temperature changes ranging from cold to moderately warm. In hot environments the resistance to heat loss may be so great that all of the increased metabolic heat of work cannot be dissipated and the man's central temperature will rise above the thermostatic setting. If this condition of imbalance is continued long enough heat stroke will ensue. We have found that in a 3 mile race lasting only 14 minutes on a hot summer day a runner's rectal temperature may rise to 41.1°C., with heat stroke imminent. The physiological regulation of body temperature of men in warm environments and during the increased metabolic heat production of work is dependent on sweating to provide evaporative cooling of the skin, and on adjustments of cutaneous blood flow which determine the conductance of heat from the deeper tissues to the skin. The mechanisms of regulating these responses during work are complex and not entirely understood. Recent experiments carried out in this laboratory indicate that during work, sweating may be regulated by reflexes originating from thermal receptors in the veins draining warm blood from the muscles, summated with reflexes from the cutaneous thermal receptors, both acting through the hypothalamic center, the activity of which is increased in proportion to its own temperature. At the beginning of work the demand for blood flow to the muscles results in reflex vasoconstriction in the skin. As the body temperature rises the thermal demand predominates and the cutaneous vessels dilate, increasing heat conductance to the skin. Large increments in cardiac output and compensatory vasoconstriction in the abdominal viscera make these vascular adjustments in work possible without circulatory embarrassment.

scholarly journals Alpha-Lipoic Acid Protects Cardiomyocytes against Heat Stroke-Induced Apoptosis and Inflammatory Responses Associated with the Induction of Hsp70 and Activation of Autophagy

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Hsin-Hsueh Shen ◽  
Yu-Shiuan Tseng ◽  
Ni-Chun Kuo ◽  
Ching-Wen Kung ◽  
Sherif Amin ◽  
...  
Keyword(s):  
Lipoic Acid ◽  
Myocardial Injury ◽  
Inflammatory Responses ◽  
Heat Stroke ◽  
Heat Exposure ◽  
Antioxidant Properties ◽  
Mitochondrial Enzymes ◽  
Protective Effects ◽  
Anion Formation ◽  
Anti Inflammatory

Heat stroke (HS) is a life-threatening illness and defined as when body temperature elevates above 40°C accompanied by the systemic inflammatory response syndrome that results in multiple organ dysfunctions. α-Lipoic acid (ALA) acts as a cofactor of mitochondrial enzymes and exerts anti-inflammatory and antioxidant properties in a variety of diseases. This study investigates the beneficial effects of ALA on myocardial injury and organ damage caused by experimental HS and further explores its underlying mechanism. Male Wistar rats were exposed to 42°C until their rectal core temperature reached 42.9°C and ALA was pretreared 40 or 80 mg/kg (i.v.) 1.5 h prior to heat exposure. Results showed that HS-induced lethality and hypothermia were significantly alleviated by ALA treatment that also improved plasma levels of CRE, LDH, and CPK and myocardial injury biomarkers myoglobin and troponin. In addition, ALA reduced cardiac superoxide anion formation and protein expression of cleaved caspase 3 caused by HS. Proinflammatory cytokine TNF-α and NF-κB pathways were significantly reduced by ALA treatment which may be associated with the upregulation of Hsp70. ALA significantly increased the Atg5-12 complex and LC3B II/LC3B I ratio, whereas the p62 and p-mTOR expression was attenuated in HS rats, indicating the activation of autophagy by ALA. In conclusion, ALA ameliorated the deleterious effects of HS by exerting antioxidative and anti-inflammatory capacities. Induction of Hsp70 and activation of autophagy contribute to the protective effects of ALA in HS-induced myocardial injury.

scholarly journals Exertional dyspnoea in COPD: the clinical utility of cardiopulmonary exercise testing

2016 ◽  
Vol 25 (141) ◽  
pp. 333-347 ◽  
Author(s):  
Denis E. O'Donnell ◽  
Amany F. Elbehairy ◽  
Azmy Faisal ◽  
Katherine A. Webb ◽  
J. Alberto Neder ◽  
...  
Keyword(s):  
Physical Activity ◽  
Exercise Testing ◽  
Physiological Responses ◽  
Cardiopulmonary Exercise Testing ◽  
Chronic Obstructive ◽  
Exertional Dyspnoea ◽  
Obstructive Pulmonary Disease ◽  
Respiratory Impairment ◽  
Laboratory Exercise ◽  
Cardiopulmonary Exercise

Activity-related dyspnoea is often the most distressing symptom experienced by patients with chronic obstructive pulmonary disease (COPD) and can persist despite comprehensive medical management. It is now clear that dyspnoea during physical activity occurs across the spectrum of disease severity, even in those with mild airway obstruction. Our understanding of the nature and source of dyspnoea is incomplete, but current aetiological concepts emphasise the importance of increased central neural drive to breathe in the setting of a reduced ability of the respiratory system to appropriately respond. Since dyspnoea is provoked or aggravated by physical activity, its concurrent measurement during standardised laboratory exercise testing is clearly important. Combining measurement of perceptual and physiological responses during exercise can provide valuable insights into symptom severity and its pathophysiological underpinnings. This review summarises the abnormal physiological responses to exercise in COPD, as these form the basis for modern constructs of the neurobiology of exertional dyspnoea. The main objectives are: 1) to examine the role of cardiopulmonary exercise testing (CPET) in uncovering the physiological mechanisms of exertional dyspnoea in patients with mild-to-moderate COPD; 2) to examine the escalating negative sensory consequences of progressive respiratory impairment with disease advancement; and 3) to build a physiological rationale for individualised treatment optimisation based on CPET.

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