HYPERTHERMIA-INDUCED CARDIAC-ARREST IN DOGS AND MONKEYS

The pattern of dying from immersion hyperthermia was documented in 8 dogs, 9 rhesus monkeys and 12 pigtail monkeys. Under light general anesthesia and spontaneous breathing, the animals were immersed into water of 45°C, which was subsequently adjusted to control brain (parietal epidural) temperature at 42 ± 0.5°C. Transient initial hypertension, tachycardia, tachypnea and hypocarbia were followed by progressive hypotension with decreasing central venous pressure and pulmonary artery occlusion pressures (measured in three dogs only), bradycardia and bradypnea. Cardiac arrest occurred in the dogs after immersion of 288 ± 66 min and more rapidly (P < 0.02) in the rhesus monkeys (at 137 ± 75 min) and pigtail monkeys (at 178 ± 26 min). EEG silence occurred in the monkeys at MAP 40 mmHg and in the dogs at MAP 25 mmHg. Cardiac arrest occurred in form of sudden ventricular fibrillation ( 2 5 dogs, 2 9 rhesus monkeys, 3 12 pigtail monkeys), or later in electromechanical dissociation leading to electric asystole ( 3 5 dogs, 7 9 rhesus monkeys, 9 12 pigtail monkeys). The mean blood glucose levels decreased to < 30 mg/dl (P < 0.002), whereas hematocrit, serum osmolality, lactate and potassium levels increased. Necropsies revealed macroscopic petechial hemorrhages in all extracerebral organs, but not in the brain. There was no gross evidence of cerebral edema. Death seemed to be the result of primary cardiovascular failure leading to secondary (ischemic) cerebral failure (EEG silence) and apnea, which coincided with pulselessness. © 1990.