Resuscitation from hypothermia-induced cardiac arrest Mark R. Kristjanson, MD; Gerald K. Bristow, MD, FRCPC

M ore than 10 people die each year in Manitoba of accidental hypothermia; across Canada 186 died in 1986.' Resuscitation of a hypothermic victim is different from that of a normothermic victim, especially with respect to appreciation of the length of time between clinical death (the absence of vital signs) and biologic or brain death. The following case report graphically demonstrates this feature.

Case report In March 1989 at about midnight a farmer had seen a car parked at the side of a highway about 32 km from Stonewall, Man. At approximately 7 am the farmer noticed that the car was still there; he found a young woman lying inside. The police, who arrived at 8 am, found her to be unresponsive and without a pulse or respiration. An ambulance from Stonewall General Hospital arrived at 8:25 am. One crew member thought he saw a muscular twitch in the patient's neck, so cardiopulmonary resuscitation (CPR) was started. The patient was received in the emergency department at 8:45 am. She was unconscious, had no pulse or respiration and was cold to the touch. Cardiac monitoring revealed asystole. CPR and mechanical ventilation with a bag-valve-mask device were continued. Rapid examination revealed fixed and dilated pupils, cold, slightly stiff and areflexic extremities, a clear chest with good air entry during mechanical ventilation, a strong femoral pulse with chest compressions and no evidence of trauma. Orders were given to warm intravenous solutions and blankets, the use of which began at, 8:55 am and was continued throughout the resuscitation. Initially the warmed solutions (500-ml bags of nor-

mal saline and Ringer's lactate) were run through a wide-open intravenous tube. The blankets were placed on the trunk and wrapped around the extremities. In addition, the patient was given epinephrine, 1.3 mg intravenously, sodium bicarbonate, 50 mmol intravenously, and calcium chloride, 500 mg intravenously. Cardioversion was unsuccessful. The patient's rectal temperature, measured with a clinical thermometer whose lower limit was 30°C, was 30.2°C at 9:20 am. Ten minutes later a widecomplex rhythm at a rate of 36 beats/min was visible on the heart monitor, and the blood pressure was 30/0 mm Hg. At 9:45 am another thermometer, whose lower limit was -20°C, revealed the rectal temperature to be 26°C; the blood pressure was 40/0 mm Hg, and the wide-complex rhythm persisted at the same rate. Chest compressions were stopped. Mechanical ventilation, with a 7-mm endotracheal tube and a bag-valve device, was continued. At 10:05 am the rectal temperature was 27.5°C, the blood pressure 50/0 mm Hg and the pulse rate 36. Fifteen minutes later the blood pressure rose to 70/40 mm Hg, and the pulse rate increased to 38. The patient was transferred to the intensive care unit, Health Sciences Centre, Winnipeg, at 10:45 am. The pulse rate and the blood pressure continued to return to normal with rewarming, which now included peritoneal lavage. Electrocardiography revealed that the wide complexes were progressively narrowing and that the rhythm was junctional or nodal. Later that evening the patient became conscious and oriented, and she recognized family and friends. However, she could not remember any events that had occurred in the 24 hours or so before she regained consciousness. She was transferred to a medical ward 24 hours later and discharged home 2 days after that. Neuropsychologic findings at discharge were normal.

From Stonewall General Hospital, Stonewall, Man., and the Department ofAnesthesia, Health Sciences Centre, Winnipeg

Reprint requests to: Dr. Gerald K Bristow, Department of Medical Education, Rm. S204, 750 Bannatyne Ave., Winnipeg, Man. R3E OW3

Faculty ofMedicine, University ofManitoba, CAN MED ASSOC J 1990; 142 (7)



on the biologic survival time the woman was successfully resuscitated. This event clearly underscores the As the body temperature falls the length of time truth in the dictum when dealing with hypothermic between clinical death and biologic or brain death victims in cardiac arrest: "No one is dead until without CPR increases, from 5 minutes at normo- warm and dead".4 thermia to perhaps as long as 30 minutes at temperatures approaching 251C.23 The mechanism of this References extension of survival time has been studied but is not completely understood.3 Although the exact 1. Causes of Death. Vital Statistics, vol 4, Statistics Canada, Ottawa, 1986: 166 length of time of cardiorespiratory arrest in the case Bering EA Jr: Effects of profound hypothermia and circulatory we have reported will never be known it was at least 2. arrest on cerebral oxygen metabolism and cerebrospinal fluid 25 minutes (the elapsed time from the police's electrolyte composition in dogs. J Neurosurg 1974; 39: 199205 discovery of no vital signs to the onset of CPR by the 3. Hickey PR: Deep hypothermic circulatory arrest: current status ambulance crew). future directions. Mount Sinai J Med 1985; 52: 541-547 Because of the keen observation of the ambu- 4. and Southwick FS, Dalglish PH Jr: Recovery after prolonged lance crew and the awareness of both the crew and asystolic cardiac arrest in profound hypothermia. JAMA 1980; 243: 1250-1253 the attending physicians of the effect of hypothermia

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Resuscitation from hypothermia-induced cardiac arrest.

CASE REPORT * ETUDE DE CAS Resuscitation from hypothermia-induced cardiac arrest Mark R. Kristjanson, MD; Gerald K. Bristow, MD, FRCPC M ore than 10...
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