Hypothermia after cardiac arrest: Beneficial, but slow to be adopted
ABSTRACTSurvivors of cardiac arrest due to ventricular tachycardia or ventricular fibrillation have improved neurologic outcomes if they are cooled to a core body temperature of 32°C to 34°C for 24 hours as soon as possible after reaching the hospital.
KEY POINTS
- This treatment is indicated for comatose adult patients who have had a witnessed cardiac arrest, whose initial cardiac rhythm is ventricular fibrillation or pulseless ventricular tachycardia, and who have return of spontaneous circulation with basic and advanced cardiac life support.
- Contraindications include hemorrhagic stroke, a Glasgow Coma Scale score of 8 or higher, cardiac arrest due to drug overdose, and preexisting hypothermia. Relative contraindications include baseline coagulopathy and severe hypotension (mean arterial pressure < 60 mm Hg) that is not correctable by fluid infusion, vasopressors, or invasive hemodynamic support.
- Adverse effects have included hypokalemia, bradyarrhythmia, ventricular tachycardia, hypotension, seizures, hyperglycemia, a transient decrease in the glomerular filtration rate, abnormal coagulation studies, and an increased incidence of pneumonia and sepsis.
ADVERSE EFFECTS OF MILD THERAPEUTIC HYPOTHERMIA
Some of these effects are predictable. Decreasing the body temperature causes potassium to shift into the cells, and this same potassium will leave the intracellular space during the rewarming phase. For this reason, aggressive potassium repletion for mild hypokalemia (potassium levels of 3.0–3.5 mmol/L) during mild therapeutic hypothermia can result in dangerous hyperkalemia during rewarming and should generally be avoided.
As another example, the enzymes involved in coagulation are less effective at lower temperatures. Thus, if it occurs, active bleeding requiring transfusion warrants consideration of stopping the hypothermia.
Adverse effects should be watched for (eg, by checking electrolyte levels frequently, monitoring blood glucose, continuous electroencephalographic monitoring during the cooling phase, and avoiding placement of intracardiac catheters once the goal temperature is reached) and addressed as they happen. However, in a recent review of this subject42 the balance of evidence continued to indicate that the benefit of this treatment exceeds its risks.
OUR PATIENT RECOVERS
After 24 hours of therapeutic hypothermia, our patient was gradually rewarmed to a normal temperature, and sedation and paralysis were discontinued.
Analysis of his prearrest and postarrest 12-lead electrocardiograms revealed a type I Brugada pattern (coved ST elevation and negative T waves in V1, V2, and V3, caused by abnormal repolarization due to inherited mutations in SCN5A). Cardiac catheterization revealed normal coronary arteries, and MRI revealed no evidence of arrhythmogenic right ventricular cardiomyopathy or other structural abnormalities.
In the next 72 hours the patient was successfully extubated, and he gradually returned to full neurologic function. Before he went home a few days later, a single-lead cardioverter-defibrillator was implanted to prevent sudden cardiac death. All of his first-degree relatives were encouraged to undergo genetic screening for SCN5A mutations. The patient is currently back to his previous high level of functioning as a marketing manager, husband, and father of two young children.
