Unintentional hypothermia is classically defined as a decrease in core body temperature to below 35°C (95°F).¹ Victims of accidental hypothermia present year-round and in all climates. The progressive lowering of core body temperature produces a predictable pattern of organ dysfunction and associated clinical manifestations (Table 31-1). Recognition of the relationship between core temperature and physiologic manifestations is important, as it provides a blueprint and foundation for management decisions that are often unique to hypothermic victims. Cardiopulmonary resuscitation (CPR) and emergency care of hypothermic patients differ in several important respects from that of normothermic patients.

Severe hypothermia (body temperature <30°C [86°F)]) is associated with marked depression of critical body functions, which may make the victim appear clinically dead during the initial assessment.^2,3 In some cases, hypothermia may exert a protective effect on the brain and organs in cardiac arrest.^4,5 Intact neurologic recovery may be possible after prolonged periods of cardiac arrest in the hypothermic victim, although those with nonasphyxial arrest have a better prognosis than those with asphyxia-associated hypothermic arrest.^6,7,8 Therefore, lifesaving procedures should not be withheld on the basis of clinical presentation.^2,7 Victims should be transported as soon as possible to a center where monitored rewarming is possible.

Several different classification systems for hypothermia have been proposed based on core temperature.^7,9,10 For purposes of emergency management and resuscitation, hypothermia can best be characterized as either mild or severe. In mild hypothermia (core temperature 35°C–31°C [95°F–87.8°F]), the victim is conscious, still shivering, and generally not prone to developing cardiac dysrhythmias. In severe hypothermia (core temperature below 31°C [87.8°F]), the victim has an altered level of consciousness, diminished or absent shivering, and is prone to develop cardiac dysrhythmias.⁹

Since mildly hypothermic victims are still able to generate heat through shivering, they do well without invasive rewarming. Severely hypothermic victims have markedly diminished or absent thermogenesis owing to the cessation of shivering and require active internal (invasive) rewarming during resuscitation. Active internal rewarming methods include extracorporeal blood rewarming, inhalation therapy, peritoneal lavage, thoracic cavity lavage, and thoracotomy with mediastinal irrigation.

Cold stress initially stimulates tachycardia and peripheral vasoconstriction, both of which increase systemic blood pressure and cardiac afterload.^11,12 There is a resultant increase in myocardial oxygen demand. As the core temperature drops, there is a linear decrease in pulse rate. At 28°C (82.4°F) there is a 50% decrease in heart rate.^11,12,13 This bradycardia is caused by decreased spontaneous depolarization of the pacemaker cells and is, therefore, refractory to atropine administration.¹⁰

During hypothermic bradycardia, unlike normothermia, systole is prolonged longer than diastole. In addition, the conduction system is much more sensitive to cold than is the myocardium, so the cardiac cycle is lengthened.¹³

Hypothermia progressively decreases mean arterial pressure and cardiac index. Cardiac output drops to about 45% of normal at 25°C. Even after rewarming, cardiovascular function may remain temporarily depressed, with impaired myocardial contractility and peripheral vascular function.¹⁴

Characteristic electrocardiographic alterations and conduction abnormalities occur as hypothermia progresses. First the PR, then the QRS, and finally the QT intervals become prolonged.¹⁰ The J wave (Osborn wave or hypothermic hump) occurs at the junction of the QRS complex and the ST segment at temperatures below 32°C^15,16 (Fig. 31-1). Osborn waves are typically seen in leads II and V3 to V6. They are neither prognostic nor specific to hypothermia.

Below 30°C, atrial and ventricular arrhythmias are common. Hypothermia-induced VF and asystole often occur spontaneously below 25°C.¹⁷ The VF threshold and the transmembrane resting potential are decreased. VF and asystole may both result from rough handling or jostling of the victim or from sudden vertical positioning.¹⁰

The priority in the prehospital setting is to prevent further heat loss and facilitate rewarming. The rescuer should remove all wet clothing, replace it with dry clothing, and insulate the victim with sleeping bags, blankets, extra clothing, or other suitable material. Use adequate insulation underneath the victim as well as on top. If the victim is capable of purposeful swallowing (will not aspirate), encourage drinking of warm and sugary drinks.

Severely hypothermic victims require careful handling because they are prone to develop VF or asystole with handling. If in the back country, consider helicopter transport to prevent the jostling that would occur with an overland evacuation. Because of autonomic dysfunction, victims should be kept in a horizontal position whenever possible to minimize orthostatic hypotension (see also hypothermia associated with drowning in Chapter 30).⁹

Oxygen should be provided by nasal cannula or face mask or, if necessary, bag-valve-mask ventilation or endotracheal intubation. The indications for endotracheal intubation in hypothermia are identical to those in normothermia.¹⁸ Endotracheal intubation should be performed without concern for inducing VF. In a multicenter survey, endotracheal intubation was performed on 117 patients by multiple clinicians in various settings. No induced arrhythmias occurred in any of the patients.¹⁹ Fiberoptic intubation or cricothyroidotomy may be required to secure the airway when cold-induced trismus prevents direct laryngoscopy. Rapid sequence intubation with paralytic agents may not be productive, as paralytic agents will not be able to overcome the trismus produced by profound hypothermia.

Overinflation of the endotracheal tube cuff with cold air should be avoided, as the air inside the cuff will expand as the victim rewarms and potentially kink the tube or rupture the cuff.¹⁸

Administration of at least 500 mL of heated (37°C–41°C [98.6°F–105.8°F]) intravenous (IV) normal saline or 5% dextrose in normal saline may help to stabilize the conduction system of the heart and begin to reverse dehydration. Lactated Ringer’s solution should be avoided because a cold liver metabolizes lactate poorly. Intraosseous infusion provides an excellent alternative pathway for fluid replacement in a severely hypothermic patient when peripheral vessels have collapsed and are unable to be cannulated.

Meaningful rewarming of a severely hypothermic patient in the field is difficult; the goal in prehospital care should thus be to use rewarming modalities to stabilize the victim’s body temperature and prevent further cooling. Warmed IV solutions, heated humidified oxygen, and externally applied heat provide only a small amount of heat input. Hot water bottles or heat packs can be placed in the axillae and groin area and alongside the neck, where large blood vessels course near the surface. Hot water bottles should be wrapped with insulation to prevent thermal burns.