Thermal and cardiovascular changes during three methods of resuscitation from mild hypothermia

Hayward, J. S.; Eckerson, J. D.; Kemna, D.

doi:10.1016/0300-9572(84)90031-5

Cited by 133 publications

(99 citation statements)

References 13 publications

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“…Core temperature was measured by a thermocouple in the esophagus (T es) at the level of the cardiac atria. This site has previously been shown to provide the closest correlation to intracardiac temperature (15). Single-channel electrocardiogram and heart rate were also monitored for the duration of each trial and recorded at 30-s intervals with the metabolic information.…”

Section: Instrumentationmentioning

confidence: 99%

Thermal effects of whole head submersion in cold water on nonshivering humans

Pretorius

Bristow²,

Steinman³

et al. 2006

Journal of Applied Physiology

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. Thermal effects of whole head submersion in cold water on nonshivering humans. J Appl Physiol 101: 669 -675, 2006. First published April 13, 2006; doi:10.1152/japplphysiol.01241.2005This study isolated the effect of whole head submersion in cold water, on surface heat loss and body core cooling, when the confounding effect of shivering heat production was pharmacologically eliminated. Eight healthy male subjects were studied in 17°C water under four conditions: the body was either insulated or uninsulated, with the head either above the water or completely submersed in each body-insulation subcondition. Shivering was abolished with buspirone (30 mg) and meperidine (2.5 mg/kg), and subjects breathed compressed air throughout all trials. Over the first 30 min of immersion, exposure of the head increased core cooling both in the body-insulated conditions (head out: 0.47 Ϯ 0.2°C, head in: 0.77 Ϯ 0.2°C; P Ͻ 0.05) and the body-exposed conditions (head out: 0.84 Ϯ 0.2°C and head in: 1.17 Ϯ 0.5°C; P Ͻ 0.02). Submersion of the head (7% of the body surface area) in the body-exposed conditions increased total heat loss by only 10%. In both body-exposed and body-insulated conditions, head submersion increased core cooling rate much more (average of 42%) than it increased total heat loss. This may be explained by a redistribution of blood flow in response to stimulation of thermosensitive and/or trigeminal receptors in the scalp, neck and face, where a given amount of heat loss would have a greater cooling effect on a smaller perfused body mass. In 17°C water, the head does not contribute relatively more than the rest of the body to surface heat loss; however, a cold-induced reduction of perfused body mass may allow this small increase in heat loss to cause a relatively larger cooling of the body core.hypothermia; heat loss; submersion; perfused body mass; thermal model; symptomless hypothermia; thermal core; cold-water near drowning MANY RECREATIONAL, COMMERCIAL, and military activities involve cold water and the possible development of accidental hypothermia. Several studies (6,11,14,21) have addressed the effect of cold-water immersion on the rate of body core cooling. The initiation and degree of hypothermia are related to many variables, including water temperature, insulation, duration of exposure, and the amount of body surface area (BSA) exposed to the water. The effect of whole head cold-water submersion on core cooling is unknown.One hypothesis predicts a substantial heat loss through the head due to the great amount of surface blood flow in the scalp and because scalp blood vessels do not vasoconstrict in response to cold as do surface vessels in other body areas (8). An alternative hypothesis predicts minimal heat loss from the head because submersion of the head and neck would only involve 7-9% more of the body surface area (20). As well, mathematical modeling predicts minimal conductive heat loss directly through the scalp and skull (27). This topic has important practical implications for conditions where th...

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Section: Instrumentationmentioning

confidence: 99%

Thermal effects of whole head submersion in cold water on nonshivering humans

Pretorius

Bristow²,

Steinman³

et al. 2006

Journal of Applied Physiology

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“…To this end, we have implemented an underwater exercise method, similar to that by Park and colleagues (24) to prevent increases in core temperature during exercise. As such, this allowed an assessment for an interaction between esophageal temperature (T es ), used as an index of central blood temperature (10), and isocapnic hypoxia on exercise ventilation. We hypothesized a greater exercise ventilation would be evident because of an increased sensitivity of the peripheral chemoreceptors to hypoxia during a low-intensity "hyperthermic" exercise relative to a low-intensity "normothermic" exercise when esophageal temperature was maintained at resting levels.…”

mentioning

confidence: 99%

The effects of hyperthermia and hypoxia on ventilation during low-intensity steady-state exercise

Chu¹,

Jay²,

White³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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This study assessed whether the elevated sensitivity of ventilation to hypoxia during exercise is accounted for by an elevation of esophageal temperature (Tes). Eleven males volunteered for two exercise sessions on an underwater, headout cycle ergometer at a steady-state rate of oxygen consumption (V O 2) of ϳ0.87 l/min (SD 0.07). In one exercise session, 31.5°C (SD 1.4) water held Tes at a normothermic level of ϳ37.1°C, and in the other exercise session, water at 38.2°C (SD 0.1) maintained a hyperthermic Tes of ϳ38.5°C. After a 30-min rest and 20-min warm-up, exercising participants inhaled air for 10 min [Euoxia 1 (E1)], an isocapnic hypoxic gas mixture with 12% O2 in N2 (H1) for the next 10 min and air again [Euoxia 2 (E2)] for the last 10 min. A significant increase in V E during all hyperthermia conditions (0.01Ͻ P Ͻ 0.048) was evident; however, during hyperthermic hypoxia, there was a disproportionate and significant (P ϭ 0.017) increase in V E relative to normothermic hypoxia. This was the main explanation for a significant esophageal temperature and gas type interaction (P ϭ 0.012) for V E. Significant effects of hyperthermia, isocapnic hypoxia, and their positive interaction remained evident after removing the influence of V O2 on V E. Serum lactate and potassium concentrations, as well as hemoglobin oxygen saturation, were each not significantly different between normothermic and hyperthermic-hypoxic conditions. In conclusion, the elevated sensitivity of exercise ventilation to hypoxia during exertion appears to be modulated by elevations in esophageal temperature, potentially because of a temperature-mediated stimulation of the peripheral chemoreceptors. oxygen consumption; isocapnia; hyperpnea; chemosensitivity; immersion THERE HAVE BEEN SEVERAL PROPOSED mechanisms for the hyperpnea that occurs during exercise (16,25,37). A neurogenic hypothesis (16) implicates core temperature as a central mediating stimulus in the control of pulmonary ventilation during both actively and passively induced hyperthermia (2, 37). It suggests that increases in core temperature could increase pulmonary ventilation by several mechanisms. One proposed mechanism suggests an increase in core temperature is associated with an increase in carbon dioxide sensitivity (30), while another suggests a direct physical effect of increased temperature in the respiratory control center and the peripheral chemoreceptors (5). The increased sensitivity to carbon dioxide (CO 2 ) appears to be evident during exercise (35), and during postexercise hyperthermia (28). Another hypothesis suggests a direct effect of an increase in core temperature causing a change in the equilibrium constants of the CO 2 buffer system, resulting in a diminished capacity to buffer CO 2 by body fluids (32). Pulmonary ventilation is then elevated after hydrogen ion (H ϩ ) concentration is increased in the regions of the central respiratory centers in the medulla oblongata.Hypoxia is another well-established modulator of pulmonary ventilation. Low inspired O 2 parti...

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“…It has long been recognised, although not always appreciated, that an insulated auditory canal temperature reliably tracks variations in deep-body temperature (Cooper et al, 1964;Greenleaf and Castle, 1972;Edwards et al, 1978;Hayward et al, 1984;Cotter et al, 1995;Taylor et al, 2014), particularly within higher air temperatures, and certainly when the ears are further insulated by the wearing of a motorcycle helmet. This was perhaps most clearly illustrated by Todd et al (2014) who sinusoidally varied heat production and deep-body temperature, finding the auditory canal index tracked oesophageal temperature, and therefore central blood temperature (Cooper et al, 1964;Hayward et al, 1984). Earlier work by the same group established the phase delay between these two indirect indices to be about 90 s (Russell, 1999).…”

Section: Discussionmentioning

confidence: 99%

Thermal and cardiovascular strain imposed by motorcycle protective clothing under Australian summer conditions

et al. 2015

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Motorcycle protective clothing can be uncomfortably hot during summer, and this experiment was designed to evaluate the physiological significance of that burden. Twelve males participated in four, 90-min trials (cycling 30 W) across three environments (25, 30, 35 °C [all 40% relative humidity]). Clothing was modified between full and minimal injury protection. Both ensembles were tested at 25 °C, with only the more protective ensemble investigated at 30 and 35 °C. At 35 °C, auditory canal temperature rose at 0.02 °C min(-1) (SD 0.005), deviating from all other trials (p < 0.05). The thresholds for moderate (>38.5 °C) and profound hyperthermia (>40.0 °C) were predicted to occur within 105 min (SD 20.6) and 180 min (SD 33.0), respectively. Profound hyperthermia might eventuate in ~10 h at 30 °C, but should not occur at 25 °C. These outcomes demonstrate a need to enhance the heat dissipation capabilities of motorcycle clothing designed for summer use in hot climates, but without compromising impact protection. Practitioner's Summary: Motorcycle protective clothing can be uncomfortably hot during summer. This experiment was designed to evaluate the physiological significance of this burden across climatic states. In the heat, moderate (>38.5 °C) and profound hyperthermia (>40.0 °C) were predicted to occur within 105 and 180 min, respectively. Disciplines Medicine and Health Sciences | Social and Behavioral Sciences

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Thermal and cardiovascular changes during three methods of resuscitation from mild hypothermia

Cited by 133 publications

References 13 publications

Thermal effects of whole head submersion in cold water on nonshivering humans

Thermal effects of whole head submersion in cold water on nonshivering humans

The effects of hyperthermia and hypoxia on ventilation during low-intensity steady-state exercise

Thermal and cardiovascular strain imposed by motorcycle protective clothing under Australian summer conditions

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