Changes of supply and demand in cerebral oxygen after resuscitation from cardiac arrest and the effect of hypertensive reperfusion in dogs

Objective To observe the changes of cerebral oxygen metabolism during the process of reperfusion after resuscitation from cardiac arrest (CA) in dogs and the effects of hypertensive reperfusion. Methods Twelve dogs were subjected to 8 min of ventricular fibrillation resulted from electric shock followed by open chest cardiopulmonary resuscitation (CPR). Dogs were randomly assigned to group NT (normotensive reperfusion, i.e. MAP was at the baseline level before cardiac arrest, n =6) and group HT (hypertensive reperfusion, i.e. MAP was elevated by 10%-15% higher than the baseline, n =6). Cerebral arteriovenous (saggital) oxygen content difference (Ca ssDO 2) and venous (saggital sinus) PO 2 (PssO 2) were determined before cardiac arrest (CA) and at 30, 60, 120, and 240 min after CA. Results In group NT, the Ca ssDO 2 before CA was higher ( P 0.05) than that at 30 min after arrest and lower ( P 0.01) than that at 240 min after arrest. In group HT, the Ca ssDO 2 was not significantly different from that in group NT before arrest, but it was significantly higher ( P 0 01) than that in group NT at 30 min after CA. These values were not significantly different between group NT and HT thereafter( P 0.05). In two groups, PssO 2 was higher ( P 0.01) at 30 min after reperfusion and lower ( P 0.05) at 240 min after reperfusion than that before arrest. At 30 min after reperfusion, PssO 2 was higher ( P 0.01) in group HT than that in group NT. There was no significant difference ( P 0.01) between the two groups thereafter ( P 05). Conclusion There is an imbalance between cerebral oxygen supply and oxygen demand after cardiac arrest and resuscitation. Hypertensive reperfusion can improve early cerebral oxygen supply after cardiac arrest.