The pathophysiology and precise details of the cause of heatstroke have remained elusive. It has been suggested that methods of measuring temperature might be partially responsible (Ashland Kashmeery 1.995). Recent experimental investigations of whole-body hyperthermia (Sminia etai 1994) using esophageal temperature probes have demonstrated that there is a direct time-temperature relationship for thermal brain injury in humans and animals ( Fig 1) which is similar to the Arrhenius relation for chemical reactions and the well-established time-temperature relationship for surface burns.
Fig. 1 Time-temperature relation for cellular injury to the brain: (1) SmjnLa.ef.a/ (1994); (2) Bull (1979) (cited by Smin.La.eLal (1.9.94.).); (3) Goffnet et al. (1977) (cited by Sminia. eta[: (1994)); (4) Eshelefal (1990); (5) heart-lung prePtion fails in 10 min at 45 °C.
Most previous monitoring of human heatstroke victims and animal heatstroke experiments has relied on measurements of rectal temperature (ASh,§.D.d.,Ka.S„h.m§®ry., 1995). However, rectal temperature has shown little correlation with severity of symptoms. Fatal heatstroke has been described with a rectal temperature of 39.5 °C and survivors have registered up to 47 °C. Rapid changes in internal body temperatures may occur, and pronounced rectal temperature lag has been well documented during such rapid perturbation (Brengelmann 1987) even though many still consider it to be a reliable method of measurement.
Most emergency texts include methods of minimizing vasoconstriction and shivering, although this may indicate excessive vascular and brain cooling with lagging elevated rectal temperature. The time required to cool the brain and vascular tree below critical temperatures is probably much shorter than previously thought ( FigJ?
and Fig 3). Here, the rectal temperature lag is obvious. Esophageal, oral, and tympanic membrane temperatures follow pulmonary artery temperature closely but are subject to environmental error, particularly during treatment of heatstroke with ice water and evaporation. Tympanic membrane temperatures may vary by up to 0.5 °C in hot and cold environments. Most infrared ear thermometers are calibrated to read the midcanal temperature, and this region is more susceptible to error than the tympanic membrane. Esophageal sensor placement at the heart level is necessary for more accurate measurement. Innacurate recordings may be influenced by respiratory movement or visceral temperature. Swallowing associated with mouth breathing can also produce error. Oral temperatures require consciousness, adequate time, and close attention to proper placement without mouth breathing. Bladder temperature tends to follow visceral rather than vascular temperature (Martin elai 1994). The most accurate site is the pulmonary artery and a Swan-Ganz catheter should be used ( Brengelmann 19..8..7).
Experimental heatstroke studies in animals using routes other than rectal monitoring have shed considerable light on the problem. Experiments in dogs using tympanic rather than rectal monitoring have revealed a startlingly different chain of events and results following exposure to temperatures of 43 °C ( Ashand, Kashm.eeryJ 995). Using monkeys with epidural and esophageal monitoring during whole-body hyperthermia, Eshel et al. (1994) revealed a precise time-temperature relationship for brain injury with marked rectal lag.
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