GORDON G. GIESBRECHT, PhD, *
|From the Laboratory for Exercise and Environmental Medicine; Health, Leisure and Human Performance Research Institute, University of Manitoba, Winnipeg, Manitoba, Canada|
This article considers several issues regarding cold stress, development of hypothermia, and prehospital care of the hypothermic patient. Advice is given on the use of clinical impressions and functional characteristics to determine the level of hypothermia. Response to cold water immersion is characterized as short-term (cold shock response), midterm (loss of performance), and long-term (development of hypothermia). Circum-rescue collapse is the dramatic worsening condition of the patient just before, during, or after rescue from cold stress. After rescue, the treatment priorities are to arrest the fall in core temperature, establish a steady, safe rewarming rate while maintaining the stability of the cardiorespiratory system, and provide sufficient physiological support.
Key Words: afterdrop, cardiopulmonary bypass, core temperature, heat balance, heat loss, shivering, shivering thermogenesis, rewarming
Introduction Return to Top
Wartime casualties during the first part of the 20th century stimulated a great deal of hypothermia research. This was followed by the heyday of research from the 1960s to 1980s. Despite all of this work, many controversies remain open for debate today. This article will attempt to address some of these issues.
There are several systems for describing the level of hypothermia.1–3 A common approach to classification includes core temperature (Tco) and functional characteristics (Figure 1) . Briefly, in the mild hypothermia range (Tco = 35–32°C), thermoregulatory mechanisms (ie, shivering) operate fully, with development of ataxia, dysarthria, apathy, and even amnesia.4 In moderate hypothermia (Tco = 32–28°C) the effectiveness of the thermoregulatory system diminishes until it fails, the primary effect of body cooling becomes evident, there is a progressive decrease in level of consciousness, and atrial fibrillation and other dysrhythmias occur. In severe hypothermia (Tco < 28°C), consciousness is lost, shivering is absent, acid-base disturbances develop, and the heart is susceptible to ventricular fibrillation (either spontaneous or caused by mechanical stimuli) or asystole. Death from hypothermia is generally from cardiorespiratory failure.
RESPONSES TO COOLING
The rate at which one becomes hypothermic depends mainly on the imbalance between increased heat loss and decreased heat production and inflow. First, the rate of heat loss is attenuated by insulation, either from endogenous body fat or protective garments. Heat loss can be greatly increased by the combination of cold air with wetness and wind, which can be a debilitating5 and lethal combination. Wet-wind conditions decrease effective clothing insulation6 by as much as 90%. On the other hand, increased heat production from shivering, exercise, or both can prevent or attenuate a decrease in body temperature during cold stress. At low workloads, metabolism may be 50% higher in the wet-wind conditions vs dry, calm conditions. These differences are minimized or eliminated at higher workloads. Shivering is an extremely effective source of heat production, which can reach 5 to 6 times the resting metabolic rate.7 It has recently been demonstrated that shivering endurance in otherwise healthy individuals exceeds previous expectations. A high level of shivering heat production can continue for 4 to 6 hours before it starts to decline (assuming shivering is not centrally inhibited by reaching a moderate to severe level of hypothermia).8
When long-term exposure to cold induces a reduction in shivering rate or ability to exercise, overall heat production decreases, and the rate of core cooling increases.9 The death of 4 students of the United States Army Ranger School in 1995 spawned a study by Young et al,10 which demonstrated that exertional fatigue and chronic negative energy balance greatly interfere with the ability to withstand a significant cold stress.
A great deal of misunderstanding surrounds the issue of cold water immersion. It is commonly reported that death caused by hypothermia can occur within minutes. In fact, it requires a significant length of immersion (at least 30 minutes) for hypothermia to develop. The cold shock response occurs within the first 3 to 4 minutes of cold water (head-out) immersion and will initiate peripheral vasoconstriction, the gasp reflex, hyperventilation, and tachycardia; these may lead to drowning or cause vagal arrest of the heart.
For those surviving the cold shock response, significant cooling of peripheral tissues, especially in the extremities, continues to occur for the first 30 minutes of immersion. This cooling has a direct deleterious effect on neuromuscular activity.5 The resultant loss of motor control makes it difficult, if not impossible, to execute survival procedures such as grasping a rescue line or hoist, signaling, etc. Thus, the ultimate cause of death is drowning, either through a failure to initiate or maintain survival performance or excessive inhalation of water under turbulent conditions.
The individual who survives the immediate and short-term phases of cold water immersion faces the possible onset of hypothermia as continuous heat loss from the body eventually decreases core temperature. Many predictive models have been developed to determine the core temperature response to cooling11–15 that are based on relationships between body composition, thermoregulatory response (ie, shivering heat production), clothing and insulation, and water temperature and sea conditions. All of these factors have been taken into account in a recent survival-time prediction model that is now used to assist in search-time decisions by various search and rescue teams.15
Behavioral variables also affect core cooling rate. Hayward et al16 demonstrated that minimizing both voluntary activity and the exposure of major heat loss areas of the skin to the cold water (ie, the HELP position) is the best way to minimize the drop in core temperature. They showed that treading water and drownproofing significantly increased the cooling rate. Despite increased metabolic heat production during exercise, the increased surface heat loss results in faster core cooling during exercise in cold water. It should be noted that this research mainly relates to lightly clothed individuals. Recent work has determined that there may be some benefit to intermittent exercise if one is wearing a well-insulatedsurvival suit.17 Under these conditions, the insulation retains the heat produced during exercise, and the rate of core cooling is significantly attenuated.
There are many clinical examples of victims being rescued from cold stress (usually from cold water immersion) in an apparently stable and conscious condition, only to experience a rewarming shock or postrescue collapse, with symptoms ranging from syncope to ventricular fibrillation and cardiac arrest. Golden et al18 have noted that deaths can occur shortly before, during, or after rescue and have used the term circum-rescue collapse. Deaths have been described just before, during, or soon after rescue, as well as up to 24 hours after rescue.18–21
Golden et al18 propose that removal from cold water results in a precipitous fall in blood pressure, inadequate coronary blood flow, and myocardial ischemia that possibly precipitates ventricular fibrillation. These authors demonstrated decreases in aortic blood pressure and central venous pressure during vertical lifting by helicopter strop from cold water. This has led to a widespread practice of using a double sling (under the arms and knees), which can raise a victim in a more horizontal position.
The importance of further cooling of the heart cannot be discounted. Fibrillation of a cold heart can be initiated by mechanical stimuli,22 hypoxia and acidosis,23 and rapid changes in pH.24 A recent review25presents data from several sources documenting afterdrop values of up to 5°C. Regardless of the etiology, it is important to note that in severely hypothermic patients, there is a significant risk of further deterioration. A summary of 21 cases of severe hypothermia indicated 4 with viable cardiac function upon rescue, with subsequent deterioration to ventricular fibrillation or asystole.25
Prehospital patient care Return to Top
TO WARM OR NOT TO WARM?
There are several views regarding methods for resuscitation of hypothermic victims. An even more fundamental question is whether or not to initiate prehospital warming at all. Some believe that such warming may be dangerous, and the advice to “prevent uncontrolled superficial rewarming”26 forms part of the Swedish Military medical doctrine. This advice has come mainly from 2 concepts. First, there is the interpretation that the “metabolic icebox” (decreased but stable cardiorespiratory activity at very low core temperatures) is a stable, safe condition and that warming the heart may bring it to a warmer range (28–32°C) where the heart is more susceptible to ventricular fibrillation. This premise seems unfounded, because the threshold for fibrillation decreases as the heart becomes cooler.27 It has been demonstrated that when shivering is pharmacologically inhibited (providing a human model for severe hypothermia) and active warming is withheld, core temperature continues to decrease by up to 2°C and remains at the lower values for several hours.28,29 Second, there is a fear of massive vasodilation and hypotension caused by surface warming. Treatment decisions are most important at moderate (28–32°C) to severe (<28°C) hypothermia. This author is unaware of any clinical or laboratory evidence that moderate surface warming could cause such vasodilation (although whole body immersion in hot water may, and is therefore contraindicated). Even immersion of the lower arms and legs in warm water has not caused hypotension.30–32
On the basis of the above work, it is seems that active warming can be conducted on severely hypothermic victims as long as care is taken not to jostle the patient in any way and core rewarming proceeds at a conservative rate to prevent rapid uncontrolled physiological changes.
The following rewarming classifications will be used in this article. The term spontaneous/endogenous rewarming includes shivering and exercise and emphasizes that active endogenous heat production is occurring. Exogenous external rewarming differentiates between moderate and high sources of heat that are applied to the body surface, and exogenous internal rewarming includes noninvasive and invasive methods for application of heat directly to the core.
The main priorities for treatment are to arrest the fall in core temperature and establish a steady, safe rewarming rate while maintaining the stability of the cardiovascular system and providing sufficient physiological support (ie, oxygenation, correction of metabolic and electrolyte imbalances, and intravenous volume replenishment). Although rewarming studies generally focus on the rate of warming, it is important to note that a rapid rate of rewarming does not necessarily correlate with an increased survival rate. In fact, during prehospital transport, when ability to monitor and control physiologic parameters may be limited, a safe strategy would be to promote steady but moderate warming ( 2°C·hr−1).
Hamilton and Paton33 summarized survey responses from 41 Mountain Rescue Association teams to determine common rescue and treatment practices. They reported the use (by number of teams) of the following rewarming methods: chemical pads (19); sleeping bag, spontaneous warming (16); hot water bottle (13); warm intravenous fluids (7); warm oxygen or air inhalation (3); charcoal Heatpac (Standard Telefon og Kabelfabrik, Oslo, Norway) (3); and water-perfused sarong (1). Some of these methods have been extensively researched, whereas others have not.
Figure 2 summarizes the effectiveness of various types of warming protocols (see Keatinge24 and Rogers34 for review). When shivering is present (ie, Tco above 30°C), moderate exogenous external rewarming is not any more efficient than shivering (if the patient is dry and insulated) because surface warming inhibits shivering heat production. This has been documented with body-to-body contact,35,36heating pads,35,37,38 and forced-air warming.39 Exercise causes a significant increase in postcooling afterdrop before a rapid increase in core temperature is seen.38,40 Only a high source of heat (ie, warm water immersion of the arms and legs32 or the total body,41,42 or a high-heat forced-air warming device44) will warm the core faster without an initial increase in afterdrop.
When shivering is absent in moderate to severe hypothermia, some form of exogenous external rewarming (ie, high or moderate heat) or exogenous internal rewarming (ie, invasive heat) is required; otherwise, little or no warming will occur. The charcoal-burning Heatpac (Standard) provides a thermal advantage when metabolic heat production is minimal,44 and forced-air warming also provides a warming advantage in laboratory29,39 and clinical45 studies. Further work has been done with a forced-air warming prototype designed to take advantage of preexisting commercial heating units to provide heat to a collapsible, rigid cover.46 This cover has been used in nonshivering hypothermic volunteers and has attenuated the afterdrop and resulted in effective warming, compared with a continued and extended decrease in Tco in spontaneous conditions.44
Inhalation warming with humidified air or oxygen has the core-warming effectiveness of “moderate heat” in a shivering patient42 and “no heat” in a nonshivering patient (see Figure 2 ). Inhalation rewarming reduces the metabolic heat production in mildly hypothermic shivering subjects, and the increased respiratory heat provided by inhalation rewarming did not compensate for this reduction. Studies have demonstrated a reduction of 1.4 kJ and 1.95 kJ of metabolic heat42,47 for every kilojoule of respiratory heat added. In shivering subjects, no rewarming advantages were found when rewarming trials were conducted in 2°C48 or −20°C49,50 air.
When using a human model for severe hypothermia (shivering inhibited by meperidine in hypothermic subjects28), inhalation rewarming still did not provide any core rewarming advantage over spontaneous warming during 150 minutes of recovery.29 Therefore, although inhalation warming is often presented as an effective strategy for body warming or at least prevention of further body cooling,51 the advantage regarding thermal balance is likely minimal.
Hayward and Steinman52 have suggested other benefits of inhalation warming, including rehydration, stimulation of mucociliary activity in the respiratory tract, and direct heat transfer from the upper airways to the hypothalamus, brain stem, and other brain structures. Any resultant warming of the respiratory and cardiovascular centers could help stabilize cardiorespiratory parameters even if total body heat content were not increased significantly. There are a few anecdotal reports in which application of inhalation warming to hypothermic victims in the field significantly improved the patient’s pulse rate and mental state within 20 to 40 minutes. Although this is consistent with inhalation therapy warming the brain stem or other brain structures without significantly increasing core body heat content, the improvement could also have been caused by improved oxygenation. In summary, there is no reason to preclude the use of inhalation warming, either by itself or in combination with other invasive or noninvasive measures.
The past decade has seen research on 2 new warming methods that use the principle of warming via the patient’s appendages. Vanggaard and Gjerloff53 proposed a simple rewarming technique that supplies exogenous heat by immersing hands, forearms, feet, and lower legs in 44 to 45°C water. The proposed advantages of this method are 3-fold. First, warming of the distal extremities opens the arteriovenous anastomoses in the fingers and toes. Second, this greatly increases the venous return to the heart via the superficial venous rete in the forearms and lower legs. Third, the warmed venous blood returns to the heart with minimal countercurrent heat exchange (loss), because the superficial veins are not in close proximity to the arteries.
Two previous studies warming either the hands and forearms only31 or hands and feet only30 concluded that this method is ineffective. However, when arms, forearms, lower legs, and feet were immersed in 42 or 45°C water, very impressive warming rates were seen (6.1 and 9.9°C·hr−1, respectively).32Because of technical limitations, this method may not be practical for field use or in small transport vehicles; however, it was adopted by the Royal Danish Navy in 1970 for use on ships.54 As a precaution against burns, the safest application of this method may be to start with 42°C water and gradually increase it to only 44°C.
In a related procedure, Grahn et al55 applied negative pressure to enhance arteriovenous anastomoses warming in hypothermic (Tco = 34.8°C) postoperative patients recovering from general anesthetics. They applied a water-perfused blanket (45–46°C) to a single forearm and hand that had been placed in a subatmospheric pressure environment (−30 to −40 mm Hg). This method resulted in a 10-fold increase in rewarming rate (13.6 °C·hr−1 over 5–15 minutes) compared with external warming only (1.4 °C·hr−1). This promising methodology has been applied to 4 hypothermic Norwegian soldiers (tympanic temperature [Tty] = 35–36.2°C measured by infrared thermometer) reporting to a field hospital after prolonged exposure to a cold environment.56 Negative pressure heating caused rapid cessation of shivering, increased thermal comfort, and abruptly increased Tco to normal values within 15 minutes. There were no comparisons with control treatments conducted in other patients, but the results seem promising for victims rendered mildly hypothermic because of environmental exposure. Not all results from the use of this technique have been positive. Smith et al57 showed no difference in warming efficacy between negative pressure warming and standard surface warming in postanesthesia care unit patients. We have applied this methodology to hypothermic subjects (Tco = 35°C) after cold-water immersion and found no rewarming benefits compared with spontaneous warming, both in shivering subjects and those in whom shivering was inhibited with meperidine. The discrepancy in results may be caused by the much greater overall cooling of the water-immersed subjects compared with the postoperative patients and cold-air–exposed soldiers. The greater cooling, and thus greater integrated cold thermal signal to the thermoregulatory center, might make it more difficult to overcome the cold-induced closing of the arteriovenous anastomoses.
General care Return to Top
In conclusion, Figure 3 provides an algorithm for first aid prehospital care of the hypothermic patient. In all cases, patients should be treated gently, removed from the cold stress, and have wet clothing removed; if the patient is moderately to severely hypothermic, clothes should be cut off to minimize movement. Care should then be taken to insulate and provide a vapor barrier, if possible, to minimize conductive/convective and evaporative heat loss, respectively. If responsive and shivering vigorously, the patient should rewarm spontaneously; however, exogenous external heating could be instituted in any condition.
One of the most difficult decisions in the field is whether or not to start cardiopulmonary resuscitation (CPR).58 At very low core temperatures, it may be difficult to confirm ventilation or cardiac activity, and initiation of CPR on someone with diminished but viable cardiac function will likely trigger ventricular fibrillation. If respiration cannot be detected, a short period of ventilation should be initiated with care not to cause hyperventilation. This increased oxygenation may improve cardiac function to the point where it can be detected. At this point, a concerted effort should be made to feel a carotid pulse (ie, 60 seconds). If pulse or breathing still cannot be detected, it may be assumed that there is no cardiac function, and CPR should be initiated with standard procedures.
Finally, the balance of factors (time of transport vs more advanced medical facilities) is something that should be considered when transport decisions are made. It may be advantageous to transport the more severely hypothermic cases to more advanced care facilities, even though transport time may be greater.
References Return to Top
- Antretter H, Dapunt OE, Bonatti J. Management of profound hypothermia.Br J Hosp Med.1995;54:215–220.2. Danzl DF, Pozos RS, Hamlet MP., Accidental hypothermia. In: Auerbach PS, ed. Wilderness Medicine: Management of Wilderness and Environmental Emergencies. St Loius, MO: Mosby 1995:51–103.3. Forgey WW, ed. Wilderness Medical Society Practice Guidelines for Wilderness Emergency Care.Merrillville, In: ICS Books Inc; 1995.
4. Castellani JW, Young AJ, Sawka MN, Backus VL, Canete JJ. Amnesia during cold water immersion: a case report. Wilderness Environ Med. 1998;9:153–155.
5. Vanggaard L. Physiological reactions to wet-cold. Aviat Space Environ Med. 1975;46:33–36.
6. Pugh LGCE. Cold stress and muscular exercise, with special reference to accidental hypothermia. Br Med J. 1967;2:333–337.
7. Eyolfson D, Tikuisis P, Giesbrecht GG., Measurement and prediction of maximal shivering capacity in humans. In: Hodgdon JA, Heaney JH, Buono MJ, ed. Environmental Ergonomics VIII. International Series of Environmental Ergonomics. Vol.1: San Diego, CA: Naval Health Research Center and San Diego State University. 2000;315–317.
8. Tikuisis P, Eyolfson DA, Xu X, Giesbrecht GG., Evidence of shivering fatigue: verification of a prediction model. Proceedings of the International Conference on Physiological and Cognitive Performance in Extreme Environments. 2000; Canberra, Australia. Australian Institute of Sport.2000:115–117.
9. Thompson RL, Hayward JS. Wet-cold exposure and hypothermia: thermal and metabolic responses to prolonged exercise in rain. J Appl Physiol. 1996;81:1128–1137.
10. Young AJ, Castellani JW, O’Brien C. Exertional fatigue, sleep loss, and negative energy balance increase susceptibility to hypothermia. J Appl Physiol. 1998;85:1210–1217.
11. Wissler EH, Mathematical simulation of human thermal behavior using whole body models. In: Shitzer A, Eberhart RC, ed. Heat Transfer in Medicine and Biology. New York, NY: Plenum Press. 1985:325–373.
12. Xu X, Werner J. A dynamic model of the human/clothing/environment—system. Appl Human Sci.1997;16:61–75.
13. Werner J, Webb P. A six-cylinder model of human thermoregulation for general use on personal computers. Ann Physiol Anthropol. 1993;12:123–134.
14. Holmer I. Prediction of responses to cold. Arct Med Res. 1995;54:48–54.
15. Tikuisis P. Prediction of survival time at sea based on observed body cooling rates. Aviat Space Environ Med. 1997;68:441–448.
16. Hayward JS, Eckerson JD, Collis ML. Effect of behavioral variables on cooling rate of man in cold water. J Appl Physiol. 1975;38:1073–1077.
17. Reinertsen RE, Volla TT, Sandsund M, Eid T, Bakkevig MK, Comparison of thermal responses between rest and exercise during cold water immersion. In: Carey C, Florant GL, Wunder BA, Horwitz B, eds. Life in the Cold. Boulder, CO: Westiew Press; 1993.
18. Golden FSC, Hervey GR, Tipton MJ. Circum-rescue collapse: collapse, sometimes fatal, associated with rescue of immersion victims. J Roy Nav Med Serv. 1991;77:139–149.
19. McCance RA, Ungley CC, Crosfill JWL, Widdowson EM, The Hazards to Men in Ships Lost at Sea, 1940–44. Medical Research Council Special Report Series. Report 291. London, UK: Her Majesty’s Stationery Office.1956:1–44.
20. Keatinge WR. Death after shipwreck. Br Med J. 1965;25:1537–1541.
21. Golden FSC. Death after rescue from immersion in cold water. J R Nav Med Serv. 1973;59:5–7.
22. Osborne L, Kamal El, Din AS, Smith JE. Survival after prolonged cardiac arrest and accidental hypothermia. Br Med J Clin Res Educ. 1984;289:881–882.
23. Niazi SA, Lewis EJ. Profound hypothermia in the dog. Surg Gynecol Obstet. 1956;102:98–106.
24. Keatinge WR, Survival in Cold Water. Oxford, UK: Blackwell Scientific Publishing; 1969.
25. Giesbrecht GG. Cold stress, near drowning and accidental hypothermia: a review. Aviat Space Environ Med. 2000;71:733–752.
26. Socialstyrelsen, Hypothermia—Cold-Induced Injuries. Stockholm, Sweden: National Board of Health and Welfare; 1997.
27. Covino BG, Beavers WR. Effect of hypothermia on ventricular fibrillary threshold. Proc Soc Exp Biol Med. 1957;95:631–634.
28. Giesbrecht GG, Goheen MSL, Johnston CE, Kenny GP, Bristow GK, Hayward JS. Inhibition of shivering increases core temperature afterdrop and attenuates rewarming in hypothermic humans. J Appl Physiol. 1997;83:1630–1634.
29. Goheen MSL, Ducharme MB, Kenny GP. Efficacy of forced-air and inhalation rewarming by using a human model for severe hypothermia. J Appl Physiol. 1997;83:1635–1640.
30. Daanen HAM, Van De Linde FJG. Comparison of four noninvasive rewarming methods for mild hypothermia. Aviat Space Environ Med. 1992;63:1070–1076.
31. Cahill CJ, Balmi PJ, Tipton MJ. An evaluation of hand immersion for rewarming individuals cooled by immersion in cold water. Aviat Space Environ Med. 1995;66:418–423.
32. Vanggaard L, Eyolfson D, Xu X, Weseen G, Giesbrecht GG. Immersion of distal arms and legs in warm water (AVA rewarming) effectively rewarms hypothermic humans. Aviat Space Environ Med.1999;70:1081–1088.
33. Hamilton RS, Paton BC. The diagnosis and treatment of hypothermia by mountain rescue teams: a survey. Wilderness Environ Med. 1996;7:28–37.
34. Rogers I. Which rewarming therapy in hypothermia? A review of the randomised trials. Emerg Med.1997;9:213–220.
35. Harnett RM, O’Brien EM, Sias FR, Pruitt JR. Initial treatment of profound accidental hypothermia.Aviat Space Environ Med. 1980;51:680–687.
36. Giesbrecht GG, Sessler DI, Mekjavic IB, Schroeder M, Bristow GK. Treatment of mild immersion hypothermia by direct body-to-body contact. J Appl Physiol. 1994;76:2373–2379.
37. Collis ML, Steinman AM, Chaney RD. Accidental hypothermia: an experimental study of practical rewarming methods. Aviat Space Environ Med. 1977;48:625–632.
38. Giesbrecht GG, Bristow GK, Uin A, Ready AE, Jones RA. Effectiveness of three field treatments for induced mild (33.0°C) hypothermia. J Appl Physiol. 1987;63:2375–2379.
39. Giesbrecht GG, Schroeder M, Bristow GK. Treatment of mild immersion hypothermia by forced-air warming. Aviat Space Environ Med. 1994;65:803–808.
40. Giesbrecht GG, Johnston CE, Bristow GK. The convective afterdrop component during hypothermic exercise decreases with delayed exercise onset. Aviat Space Environ Med. 1998;69:17–22.
41. Hoskin RW, Melinyshyn MJ, Romet TT, Goode RC. Bath rewarming from immersion hypothermia.J Appl Physiol. 1986;61:1518–1522.
42. Romet TT, Hoskin RW. Temperature and metabolic responses to inhalation and bath rewarming protocols. Aviat Space Environ Med. 1988;59:630–634.
43. Ducharme MB, Giesbrecht GG, Frim J, Forced-air rewarming in −20°C simulated field conditions. In: Blatteis CM, ed. Thermoregulation: Tenth International Symposium on the Pharmacology of Thermoregulation. Vol.813: New York, NY: New York Academy of Sciences. 1997;676–681.
44. Hultzer M, Xu X, Marrao M, Chochinov A, Giesbrecht GG, Efficacy of torso rewarming using a human model for severe hypothermia [abstract]. Proceedings of the World Congress on Wilderness Medicine. 1999; Whistler, Canada: Wilderness Medical Society.1999:80
45. Steele MT, Nelson MJ, Sessler DI. Forced air speeds rewarming in accidental hypothermia. Ann Emerg Med. 1996;27:479–484.
46. Giesbrecht GG, Pachu P, Xu X. Design and evaluation of a portable rigid forced-air warming cover for prehospital transport of cold patients. Aviat Space Environ Med. 1998;69:1200–1203.
47. Morrison JB, Conn ML, Hayes PA. Influence of respiratory heat transfer on thermogenesis and heat storage after cold immersion. Clin Sci (Lond). 1982;63:127–135.
48. Sterba JA. Efficacy and safety of prehospital rewarming techniques to treat accidental hypothermia.Ann Emerg Med. 1991;20:896–901.
49. Mekjavic IB, Eiken O. Inhalation rewarming from hypothermia: an evaluation in −20°C simulated field conditions. Aviat Space Environ Med. 1995;66:424–429.
50. Ducharme MB, Kenny GP, Johnston CE, Nicolaou G, Bristow GK, Giesbrecht GG, Efficacy of forced-air and inhalation rewarming in humans during mild (Tco = 33.9°C) hypothermia. In: Shapiro Y, Moran DS, Epstein Y, eds. Environmental Ergonomics: Recent Progress and New Frontiers. London, UK: Freund Publishing Co; 1996:147–150.
51. Weinberg AD. The role of inhalation rewarming in the early management of hypothermia.Resuscitation. 1998;36:101–104.
52. Hayward JS, Steinman AM. Accidental hypothermia: an experimental study of inhalation rewarming. Aviat Space Environ Med. 1975;46:1236–1240.
53. Vanggaard L, Gjerloff CC. A new simple technique of rewarming in hypothermia. Int Rev Army Navy Air Force Med Serv. 1979;52:427–430.
54. Vanggaard L, Ny Laegebog for Sofarende (Authorized Ship Captain’s Guide). Copenhagen, Denmark: Tellus; 1987:1–380.
55. Grahn D, Brock-Utne JG, Watenpaugh DE, Heller HC. Recovery from hypothermia can be accelerated by mechanically distending blood vessels in the hand. J Appl Physiol. 1998;85:1643–1648.
56. Soreide E, Grahn DA, Brock-Utne JG, Rosen L. A non-invasive means to effectively restore normothermia in cold stressed individuals: a preliminary report. J Emerg Med. 1999;17:725–730.
57. Smith CE, Parand A, Pinchak AC, Hagen JF, Hancock DE. Failure of negative pressure rewarming (Thermostat™) to accelerate recovery from mild hypothermia in postsurgical patients. Anesth Analg.1999;89:1541–1545.
58. Steinman AM, Cardiopulmonary resuscitation and hypothermia. Circulation. 1986;74: IV.29–32.
*Corresponding author: Gordon G. Giesbrecht, PhD, Laboratory for Exercise and Environmental Medicine; Health, Leisure and Human Performance Research Institute, University of Manitoba, 211 Max Bell Centre, Winnipeg, Manitoba, Canada, R3T 2N2 (E-mail: email@example.com).
Figures Return to Top
Click on thumbnail for full-sized image.
Figure 1. Criteria for classification of hypothermia.
Click on thumbnail for full-sized image.
Figure 2. Schematic representation of relative effectiveness of various types of rewarming protocols for shivering and nonshivering patients.
Click on thumbnail for full-sized image.
Figure 3. First aid prehospital care of the hypothermic victim.