Body temperature is tightly regulated by a combination of behavioral, neuroendocrinologic, and cardiovascular responses to cold stress. Core temperature will fall when the amount of heat lost to the environment exceeds the amount of heat produced.
Heat is lost from a warm body by conduction, convection, evaporation, and radiation. Conduction occurs when a warm body makes direct contact with a cold object. Conductive heat loss can be minimized by avoiding contact with cold or poorly insulated objects (e.g., metal backboards or stretchers). Convective cooling occurs when a fluid (usually air or water) comes in contact with a warm body. The amount of heat lost via convection can be considerable and is proportional to the amount of fluid that flows around the body, the specific heat capacity of the fluid, and the temperature difference between the fluid and the body. Practically, the emergency physician needs to understand that exposure to cool air or water will result in heat loss, that water can absorb a large amount of heat in a short period of time, and that windy conditions or flowing water can significantly increase the rate of cooling. Evaporative heat loss occurs due to the energy required for water to phase change from a liquid to a gas. The amount of heat lost to evaporation is proportional to the temperature difference between the body and the air and the wind speed over the body and is inversely proportional to the humidity. Therefore, a warm moist body exposed to cold, dry, windy air will lose a significant amount of heat. A vapor barrier (e.g., a plastic bag or sheet), placed around the patient, effectively prevents evaporative cooling but is often not practical when repeated access to the patient's skin is required. Radiant cooling occurs because all warm bodies "radiate" heat, in the form of electromagnetic waves. Increasing the temperature of the room can minimize radiant heat loss, and some losses can be recovered using special reflective fabrics (likely low yield in most clinical situations). In summary, it is important to minimize heat loss in the hypothermic patient, and a basic understanding of the physics of heat transfer can be helpful. Practically, heat loss can be minimized by heating the room, removing wet clothes, drying the patient (or wrapping the patient in a vapor barrier), providing insulation, and protecting the patient from wind.
HEAT CONSERVATION AND PRODUCTION
The most important responses to cold include behavior (e.g., putting on warm clothing, seeking a warm environment), peripheral vasoconstriction, increased metabolic rate, and muscular thermogenesis (voluntary or shivering). Shivering is a remarkably efficient method of heat production, and care is required to preserve this important source of heat. Unfortunately, shivering can be suppressed by medications (e.g., analgesics, sedatives), by the application of warming devices (e.g., hot packs, forced air blankets, warm humidified air), if energy stores are exhausted, or if the core temperature drops below a critical level (~31°C).5 The suppression of shivering by various warming methods is one of the reasons why the rewarming literature is so controversial.
Core temperature may continue to drop after a patient is removed from the cold environment,9,10 a process often referred to as afterdrop. The amount of continued core cooling will depend on the stage of hypothermia, the degree of thermoregulatory dysfunction, the ongoing cold stress (often significant in the prehospital care environment), and the physics of heat transfer (heat from the relatively warmer core will be transferred to the cooler periphery by direct conduction or by convection from blood flow). The relative importance of the various mechanisms and the impact of various rewarming techniques are the source of much debate, due in part to the desire to avoid iatrogenic core cooling. Historically, there was concern that rewarming or active movement could cause convection of cold blood from the periphery to the core with a potential increase in morbidity. Careful experimental studies have demonstrated an ~1°C drop in core temperature during minimally invasive rewarming when shivering is inhibited with narcotics11 or during exercise,12 but case series have not demonstrated any clinically significant afterdrop or morbidity when minimally invasive rewarming is used.6,13 In general, healthy uninjured patients who are able to shiver and have adequate fuel reserves (or can drink warm sweet drinks) will be able to self-rewarm once removed from further cold stress. In contrast, patients who have lost the ability to shiver are at significant risk of further temperature decline unless active rewarming is used.6,14,15 The use of aggressive immersion rewarming techniques such as hot baths or showers should likely be avoided due to the potential risks of vasodilatory hypotension or convective cooling.16
Cases of secondary hypothermia can be conveniently organized into those caused predominantly by increased heat loss, those caused predominantly by impaired thermoregulation, and those caused by multiple factors (Table 209-1). This classification is somewhat arbitrary, but in general, the multifactorial cases have a higher risk of missed diagnosis and are less likely to fully resolve with rewarming and supportive care. Iatrogenic causes of hypothermia deserve special attention, particularly in trauma patients, where the loss of just a few degrees of core temperature can create a profound coagulopathy and more than double patient mortality.17 Massive transfusion and large-volume crystalloid resuscitation are common iatrogenic causes of hypothermia unless proper fluid warmers are used. Inadequate insulation, repeated or prolonged exposure to the cool air of the resuscitation or operating room, and inadequate core temperature monitoring all contribute to iatrogenic heat loss, which may increase morbidity and mortality.
The body attempts to preserve normothermia through mechanisms such as increased metabolic rate, peripheral vasoconstriction, increased preshivering muscle tone, or shivering. As the core temperature drops below ~35°C, progressive impairment occurs affecting all of the body's organ systems. CNS impairment can progress from poor judgment, amnesia, and dysarthria, to ataxia and apathy, unconsciousness, areflexia, and eventually electroencephalographic arrest.5 Paradoxical undressing is a potentially deadly behavior that occurs in up to 30% of fatal hypothermia cases.18 Below ~29°C, the pupils may become dilated and fixed, and below ~23°C, corneal reflexes may be absent; neither are reliable for neurologic prognosis in hypothermia.5
Cardiovascular responses to cold include profound peripheral vasoconstriction and an initial increase in heart rate and blood pressure, usually followed by progressive bradycardia, hypotension, and myocardial irritability. Below ~32°C, the risk of cardiac arrest increases as malignant cardiac arrhythmias become more common, particularly below 28°C.19 The term rescue collapse is used to describe cardiac arrest that can commonly occur during extrication, transport, or treatment of a deeply hypothermic patient. The cause of rescue collapse is multifactorial but ultimately related to the profound irritability of the cold myocardium. Atrial fibrillation and flutter are expected arrhythmias and not necessarily markers of cardiac instability.6 ECG changes in hypothermia are variable but classically include bradycardia with prolonged PR, then QRS widening, and then prolonged QTc. ECGs are often complicated by muscle tremors or shivering, and hypothermia can cause almost any heart block or atrial or ventricular arrhythmias. The classic Osborn J waves (Figure 209-1) usually occur below 32°C, can be misdiagnosed as ST elevation myocardial infarction, and can also be caused by intracranial pathology or sepsis.5 Occasionally patients may be in a low-flow state, with a very difficult to detect pulse that may provide some oxygen delivery. Asystole is the common final arrhythmia, but in accidental hypothermia, it does not exclude the possibility of a successful resuscitation.6
ECG strip from a patient with a temperature of 25°C (77°F) showing atrial fibrillation with a slow ventricular response, muscle tremor artifact, and Osborn (J) wave (arrow).
Respiratory changes include initial tachypnea, followed by a progressive decrease in minute ventilation and eventual respiratory arrest. Pulmonary edema is an inconsistent complication of hypothermia but is common after resuscitation from stage IV hypothermia.
The renal response to hypothermia is termed cold diuresis and is a response to vasoconstriction-induced hypervolemia. It results in significant fluid losses, which may be further increased in patients with a history of cold water immersion or alcohol intoxication.5 Rhabdomyolysis is a potential complication of hypothermia20; however, the clinician should always exclude a missed compartment syndrome or extensive frostbite when an elevated creatine kinase is detected. Hypothermia can also cause muscle rigidity, termed pseudo-rigor mortis; hence, rigor mortis cannot be used as a reliable marker of death in the cold patient. Hypothermia has a somewhat dramatic impact on coagulation and blood viscosity, and these effects are often underrecognized by clinicians because blood samples are heated to 37°C prior to analysis. Coagulopathy is a concern below 34°C, particularly in trauma patients in whom hypothermia can compromise the chance for a surgical cure and exponentially increase mortality,17 partly due to poor activity of clotting factors and platelet dysfunction.21 Hypothermic patients can also be hypercoagulable from a combination of increased viscosity, hemoconcentration, and an inflammatory cascade similar to disseminated intravascular coagulation; these factors can put hypothermic patients at an increased risk for venous thromboembolic disease as well as coronary and cerebral artery occlusion.5
Cellular oxygen consumption decreases as core temperature drops and, in an otherwise healthy patient who has adequate oxygen delivery prior to cooling, may provide protection against ischemia. It is estimated that cerebral oxygen requirements are approximately 50% at 28°C, 19% at 18°C, and 11% at 8°C.5,22 This neuroprotective effect of hypothermia is exploited in certain cardiac surgeries. The most dramatic technique is deep hypothermic circulatory arrest, where patients are cooled to ~18°C and cardiac arrest is induced and maintained for up to ~30 minutes.23 The combination of the potential to survive prolonged periods of ischemia, with the uncertainty of knowing if a patient has been in a low-flow state (difficult to detect cardiac activity that provides some oxygen delivery) versus cardiac arrest, increases the complexity of termination of resuscitation decisions for hypothermic patients unless the history clearly indicates death prior to cooling.