Pathophysiology

Body temperature reflects the balance between heat production and heat loss. The four physiologic mechanisms of heat loss are evaporation, convection, radiation, and conduction. Conduction is enhanced by exposure to water, which increases thermal conductivity 20- to 30-fold. In response to cold stress, the hypothalamus attempts to stimulate heat production through shivering and increasing thyroid, catecholamine, and adrenal activity. Vasoconstriction simultaneously minimizes heat loss in hypothermic patients.

Clinical Manifestations

As the hypothermic patient’s compensatory mechanisms are overwhelmed, temperature-dependent physiologic changes occur. Patients with mild hypothermia demonstrate tachypnea, tachycardia, ataxia, dysarthria, impaired judgment, shivering, and diuresis. Moderate hypothermia is characterized by decreased pulse and cardiac output, hypoventilation, central nervous system depression, hyporeflexia, decreased renal blood flow, and loss of shivering. Atrial fibrillation and other arrhythmias may be seen. The electrocardiogram may manifest an Osborn or J wave (Figure 55.1); this secondary wave follows the S wave, most prominently in leads aVL, aVF, and V_1–6. In severe hypothermia, coma, hypotension, pulmonary edema, oliguria, areflexia, bradycardia, ventricular arrhythmias, and asystole occur. Ventricular fibrillation is the most common fatal arrhythmia, as hypothermia lowers the heart’s fibrillation threshold. The differential diagnosis for hypothermia and predisposing factors are shown in Box 55.1.

The diagnosis of hypothermia depends on the use of a low-reading electronic thermometer to determine core temperature. It is important to know the low limit of the thermometer being used, as it is possible for the patient’s temperature to be lower than the device’s lowest reading. After making the diagnosis, laboratory evaluation should be undertaken to identify potential complications. Characteristic findings are presented in Table 55.1.

Management

The management of hypothermia starts by stabilizing the airway, breathing, and circulation. It also includes preventing further heat loss, initiating rewarming, and treating complications (Figure 55.2). Early endotracheal intubation facilitates clearing of secretions produced by cold-induced bronchorrhea in patients with altered mental status or a decreased gag reflex. Blood pressure may be supported by crystalloid infusions. Dopamine administration should be considered in cases refractory to volume resuscitation. Core temperature should be monitored closely during therapy to prevent iatrogenic worsening of hypothermia or overshoot hyperthermia.

Rewarming techniques are divided into passive external rewarming, active external rewarming, and active internal rewarming. Passive external rewarming is the method of choice for mild hypothermia. After wet clothing is removed, blankets or other types of insulation are applied, allowing the patient’s intrinsic heat production to generate passive warming. This process requires sufficient physiologic reserve to generate heat by shivering or increasing metabolic rate.

Active external rewarming techniques provide heat to the patient directly. These include warm blankets, heating pads, radiant heat, or warm baths directly to the patient’s skin. These methods are indicated for moderate to severe hypothermia or for patients with mild hypothermia who lack physiologic reserve, are unstable, or fail to respond to passive external rewarming. A risk of active external rewarming is core-temperature afterdrop. This complication occurs when the extremities and trunk are warmed simultaneously. As extremities are rewarmed, cold, acidotic blood that has pooled in the vasoconstricted extremities of the hypothermic patient flows into the core circulation, causing a drop in core temperature. This can be avoided by rewarming the trunk before the extremities by active internal warming.

Active internal rewarming is the most aggressive therapeutic strategy and may be used alone or combined with active external rewarming in moderate or severe hypothermia. Effective techniques include pleural and peritoneal irrigation with warm saline, continuous arteriovenous or conventional hemodialysis, the use of endovascular warming devices, and cardiopulmonary bypass. Giving humidified, inspired gas; warm intravenous fluids; and bladder or gastrointestinal irrigation with warm saline is adjunctive.

The hypothermic heart is sensitive to movement; rough handling, especially of the severely hypothermic patient, may precipitate arrhythmias. This becomes more likely at core temperatures less than 30° C (86° F). Although atrial fibrillation or flutter often resolves spontaneously with rewarming, management of ventricular arrhythmias may be problematic. The administration of Advanced Cardiac Life Support (ACLS) medications in this setting is controversial, as ventricular arrhythmias and asystole may prove refractory until the patient has been rewarmed to a core temperature greater than 30° C (86° F). Hypothermic patients in cardiac arrest should receive defibrillation and a first bolus of the appropriate medications as indicated. However, if unsuccessful, cardiopulmonary resuscitation and aggressive rewarming must be initiated promptly. Further efforts at resuscitation should be attempted once the core temperature is 30° C and continued until the temperature is 32° to 35° C.