4.5 Environmental Emergencies: Core Temperature Control (Hypo/Hyperthermia)

4.5 Environmental Emergencies: Core Temperature Control (Hypo/Hyperthermia)

Critical care transport teams frequently encounter patients with disrupted thermoregulation. Hypothermia and hyperthermia require precise physiological management because rapid or incorrect temperature corrections can trigger fatal cardiovascular collapse.

Pathophysiology of Accidental Hypothermia

Defined as a core body temperature <35°C (95°F). Transport medicine providers must classify hypothermia accurately to guide resuscitation:

• Mild Hypothermia (32–35°C / 89.6–95°F): Shivering is active. The patient exhibits tachypnea, tachycardia, and cold diuresis. Cold diuresis occurs when peripheral vasoconstriction shifts blood to the central circulation, tricking the body into sensing hypervolemia, which reduces ADH (vasopressin) and increases ANP.
• Moderate Hypothermia (28–32°C / 82.4–89.6°F): Shivering ceases as thermoregulatory mechanisms fail. Bradycardia, hypoventilation, altered mental status, and dilated pupils occur. The ECG demonstrates prolongation of all intervals (PR, QRS, QT) and the appearance of Osborn waves (J waves) at the junction of the QRS and ST segments.
• Severe Hypothermia (<28°C / 82.4°F): High risk of spontaneous ventricular fibrillation and asystole. Cold-induced coagulopathy is a major complication; clotting cascade enzymes are temperature-dependent and fail to function. Note that standard laboratory coagulation tests (PT/PTT) are run at 37°C in the laboratory, so they will artificially appear normal despite severe in-vivo coagulopathy.

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Rewarming Modalities and Transport Hazards

Passive External Rewarming

Removing wet clothing and insulating the patient with dry blankets. Only effective in mild hypothermia where the patient's thermogenesis is intact.

Active External Rewarming

Forced warm air blankets (e.g., Bair Hugger), radiant heat, and hot water bottles applied to the axillae and groin. Useful for mild to moderate hypothermia.

[!WARNING] Active external rewarming of the limbs can trigger peripheral vasodilation, resulting in afterdrop. Afterdrop is the return of cold, acidotic, hyperkalemic blood from the extremities to the core, causing a secondary drop in core temperature and precipitating "rewarming shock" or ventricular fibrillation.

Active Core (Internal) Rewarming

Crucial for severe hypothermia. This includes:

• Warmed IV fluids (38–42°C)
• Warmed humidified oxygen (40–42°C)
• Warmed irrigation of body cavities (bladder, stomach, thoracic/peritoneal cavity via chest tubes)
• Extracorporeal Membrane Oxygenation (ECMO) or Cardiopulmonary Bypass (CPB): The definitive active core rewarming strategy for cardiac arrest, providing rewarming rates of 5–10°C/hour.
• Rewarming Rate: For non-arrested patients, the target rate is 1 to 2°C/hour to avoid hemodynamically significant vasodilation (rewarming shock) and fluid shifts.

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Cardiac Arrest Resuscitation in Hypothermia

The hypothermic myocardium is highly irritable; rough handling can precipitate ventricular fibrillation. Transport patients very gently.

ACLS modifications are required based on core temperature:

• "Not dead until warm and dead": Core temperature should exceed 32–35°C before resuscitation is terminated.
• Core Temp <30°C: The myocardium is highly resistant to defibrillation and vasoactive medications. Attempt defibrillation once. If unsuccessful, defer further attempts until core temperature is >30°C. Withhold IV medications (epinephrine, antiarrhythmics) entirely, as they accumulate in the inactive peripheral circulation and can cause toxicity when the patient is rewarmed. Focus on active core rewarming.
• Core Temp 30–35°C: Double the interval between vasoactive medication doses (e.g., epinephrine every 6–10 minutes instead of every 3–5 minutes). Resume standard defibrillation.
• Core Temp >35°C: Resume standard ACLS protocols.

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Hyperthermia and Heat Stroke

Heat exhaustion presents with diaphoresis, headache, and weakness, but mental status remains intact and core temperature is <40°C. Heat stroke is a medical emergency defined by a core temperature >40°C (104°F) associated with altered mental status (confusion, delirium, seizures, coma) and often anhydrosis.

Pathophysiology

Extreme heat denatures proteins, damages cell membranes, and triggers a systemic inflammatory response syndrome (SIRS)-like cascade, leading to disseminated intravascular coagulation (DIC), rhabdomyolysis (releasing myoglobin which causes acute kidney injury), and multi-organ dysfunction.

Cooling Techniques in Transport

1. Evaporative Cooling: Spraying the patient with tepid water and directing high-velocity fans across the skin. This is highly effective and easily performed in the helicopter or fixed-wing aircraft.
2. Conductive Cooling: Applying ice packs to the neck, axilla, and groin. Cold water immersion is the gold standard for exertional heat stroke but is impractical during transport. Cold IV fluids (4°C saline) can be infused, but with caution to avoid shivering.
3. Target Temperature Endpoint: Discontinue active cooling measures when the core temperature reaches 38 to 39°C (100.4–102.2°F). Stopping at this range prevents overshoot hypothermia, shivering (which increases heat production), and cardiovascular instability.
4. Avoid Antipyretics: Acetaminophen and aspirin are contraindicated. The hypothalamic temperature set point is not elevated in heat stroke (unlike in infectious fever); therefore, antipyretics are ineffective and will only exacerbate hepatic and renal damage.