Cerebral cortical perfusion during and following resuscitation from cardiac arrest in dogs.

Perfusion of the cerebral cortex during closed chest CPR in dogs, generating systolic pressures of 60 to 70 mmHg, is only 10% of pre-arrest blood flow. In contrast, internal cardiac massage produces normal cortical perfusion rates. Following a 20-min perfusion arrest, during pressure controlled reperfusion, cortical flow rates decay to less than 20% normal after 90 min of reperfusion. This appears to be due to increasing cerebral vascular resistance, and is not due to rising intracranial pressure. The post-arrest cortical hypoperfusion syndrome is prolonged with cortical flow remaining below 20% normal up to 18 hr post arrest. The use of a variety of calcium antagonists, including flunarizine, lidoflazine, verapamil, and Mg2+, immediately post-resuscitation maintains cerebral vascular resistance and cortical perfusion at normal levels. A prospective blind trial of the calcium antagonist lidoflazine following a 15-min cardiac arrest in dogs and resuscitation by internal massage, demonstrates amelioration of neurologic deficit in the early postresuscitation period.

Early amelioration of neurologic deficit by lidoflazine after fifteen minutes of cardiopulmonary arrest in dogs.

A prospective, controlled, blind study was done to test the effect of a calcium entry blocker on the neurologic integrity of dogs after cardiopulmonary arrest. Ten male mongrel dogs were anesthetized, prepared with sterile technique, and instrumented for pulmonary arterial (PA) and systematic arterial pressure monitoring. A left thoracotomy and pericardotomy were performed. Cardiac arrest was produced by injecting KCl (1 mEq/kg) through the PA line, and the respirator was stopped. Full arrest was maintained for 15 minutes. Thereafter, the dogs were resuscitated with ventilation, internal massage, fluids, bicarbonate, epinephrine, and internal defibrillation. All dogs were resuscitated within 6 to 10 minutes. Five control dogs received saline placebo, and five dogs were treated with lidoflazine (1 mg/kg) IV drip immediately post resuscitation. All dogs were scored neurologically every two hours by a deficit grading scale. All treated dogs had spontaneous ventilation, reactive pupils and corneals, voluntary movements, and responses to tactile stimulation at 12 hours post resuscitation. Four of five control dogs had maximum deficit scores without improvement. The difference in neurologic scores between the treated and control groups became increasingly divergent with time, and was statistically significant (P less than .05) by four hours post resuscitation. Thus the calcium antagonist lidoflazine produces improvement in neurologic recovery in the first 12 hours after cardiopulmonary arrest in dogs.

Prolonged hypoperfusion in the cerebral cortex following cardiac arrest and resuscitation in dogs.

Increasing cerebral vascular resistance and brain perfusion failure occur within 90 minutes following cardiac arrest and resuscitation. This study followed cortical perfusion for 18 hours after a 15-minute cardiac arrest. Six dogs were anesthetized with ketamine and gallamine and then mechanically ventilated. They were instrumented for arterial pressure, central venous pressure, and regional cerebral cortical blood flow (rCCBF) determined by thermodilution. A left thoracotomy and pericardiotomy were done. Two dogs served as non-arrest controls. Cardiac arrest was produced in four dogs with an intravenous bolus of KCl at 1 mEq/kg. After 15 minutes of cardiac arrest, the animals were resuscitated with internal massage, NaHCO3, epinephrine, and internal defibrillation. Cortical blood flow was followed for 18 hours. Arterial core temperature was never less than 35 C. Pre-arrest cortical blood flows were 0.86 cc/min/g (+/- 0.11). The two control animals had stable rCCBF (0.74 +/- 0.17) for all determinations during the 18-hour follow-up period. Determinations of rCCBF from 6 to 18 hours in post-arrest animals were 7% to 14% of pre-arrest values. We conclude that the post-resuscitation perfusion failure in the cortex is prolonged. Any potential for neuronal recovery, unless perfusion is protected, would not be realized given this phenomenon.