No abstract

Metabolic rates and rectal temperatures were continuously monitored for humans immersed in cold ocean water (4.6--18.2 degrees C) under stimulated accident conditions. The subjects wore only light clothing and a kapok lifejacket while either holding-still or swimming. While holding-still, metabolic heat production (Hm,kcal-min--1) was inversely related to water temperature (Tw, degrees C) according to the equation Hm equals 4.19 minus-0.117 Tw. This temperature response pattern is shown to be similar to that for exposure to air of the same temperature when air velocity is just over 5 m.p.h. (2.24 m/s). The thermogenic response was one-third efficient in balancing the calculated heat loss in cold water, resulting in hypothermia at a rectal temperature cooling rate (C, degrees C-min--1) dependent on water temperature (Tw, degrees C) according to the relation C equal 0.0785 - 0.0034Tw. Although swimming increased heat production to 2.5 times that of holding-still at 10.5 degrees C water temperature, cooling rate was 35% greater while swimming. A prediction equation for survival time (ts, min) of persons accidentally immersed in cold water (Tw, degrees C) has the form ts equal 15 + 7.2/(0.0785-0.0034Tw), based on the findings of this study, and it is compared to pre-existing models.

The hypothermic stress of immersion in cold water stimulates release of norepinephrine from the sympathetic nervous system. The speed and pattern of this response was studied in six healthy men by serial measurements of plasma norepinephrine concentrations before, during, and after 60 min of immersion in 10 degrees C water. After immersion for 2 min, the mean norepinephrine concentration was increased from 359+/-32 (basal) to 642+/-138 pg/ml and rose gradually to a maximum of 1.171+/-226 pg/ml after 45 min of immersion. Metabolic rate increased approximately threefold during the immersion period. After rewarming in warm water (40 degrees C), the subjects showed a transient peak in plasma norepinephrine followed by a rapid decrease to basal levels after 30 min. The fall in plasma norepinephrine after approximately 8 min of rewarming occurred despite persistent depression of the core temperature and coincided with a sudden decrease in metabolic rate and cessation of body shivering. These results suggest that the sympathetic nervous response to cold can be activated or suppressed very quickly and is dependent on the skin temperature.

During severe hypothermia, shivering is absent. To simulate severe hypothermia, shivering in eight mildly hypothermic subjects was inhibited with meperidine (1.5 mg/kg). Subjects were cooled twice (meperidine and control trials) in 8 degrees C water to a core temperature of 35.9 +/- 0.5 (SD) degrees C, dried, and then placed in sleeping bags. Meperidine caused a 3.2-fold increase in core temperature afterdrop (1.1 +/- 0.6 vs. 0.4 +/- 0.2 degree C), a 4.3-fold increase in afterdrop duration (89.4 +/- 31.4 vs. 20.9 +/- 5.7 min), and a 37% decrease in rewarming rate (1.2 +/- 0.5 vs. 1.9 +/- 0.9 degrees C/h). Meperidine inhibited overt shivering. Oxygen consumption, minute ventilation, and heart rate decreased after meperidine injection but subsequently returned toward preinjection values after 45 min postimmersion. This was likely due to the increased thermoregulatory drive with the greater afterdrop and the short half-life of meperidine. These results demonstrate the effectiveness of shivering heat production in attenuating the postcooling afterdrop of core temperature and potentiating core rewarming. The meperidine protocol may be valuable for comparing the efficacy of various hypothermia rewarming methods in the absence of shivering.