Brain tissue oxygen pressure and cerebral metabolism in an animal model of cardiac arrest and cardiopulmonary resuscitation

Objective: Direct measurement of brain tissue oxygenation (PbtO(2)) is established during spontaneous circulation, but values of PbtO(2) during and after cardiopulmonary resuscitation (CPR) are unknown. The purpose of this study was to investigate: (1) the time-course of PbtO(2) in an established model of CPR, and (2) the changes of cerebral venous lactate and S-100B. Methods: In 12 pigs (12-16 weeks, 35-45kg), ventricular fibrillation (VF) was induced electrically during general anaesthesia. After 4min of untreated VF, all animals were subjected to CPR (chest compression rate 100/min, FiO(2) 1.0) with vasopressor therapy after 7, 12, and 17min (vasopressin 0.4, 0.4, and 0.8U/kg, respectively). Defibrillation was performed after 22min of cardiac arrest. After return of spontaneous circulation (ROSC), the pigs were observed for 1 h. Results: After initiation of VF, PbtO(2) decreased compared to baseline (mean +/- SEM; 22 +/- 6 versus 2 +/- 1 mmHg after 4 min of VF; P < 0.05). During CPR, PbtO(2) increased, and reached maximum values 8 min after start of CPR (25 7 mmHg; P < 0.05 versus no-flow). No further changes were seen until ROSC. Lactate, and S-100B increased during CPR compared to baseline (16 +/- 2 versus 85 +/- 8 mg/dt, and 0.46 +/- 0.05 versus 2.12 +/- 0.40 mu g/l after 13min of CPR, respectively; P < 0.001); lactate remained elevated, while S-100B returned to baseline after ROSC. Conclusions: Though PbtO(2) returned to pre-arrest values during CPR, PbtO(2) and cerebral lactate were lower than during post-arrest reperfusion with 100% oxygen, which reflected the cerebral. tow-flow state during CPR. The transient increase of S-100B may indicate a disturbance of the blood-brain-barrier. (c) 2006 Elsevier Ireland Ltd. All rights reserved.