Cerebral and systemic arteriovenous oxygen monitoring after cardiac arrest. Inadequate cerebral oxygen delivery

Abstract

Background: After prolonged cardiac arrest, under controlled normotension, cardiac output and cerebral blood flow are reduced for several hours. This dog study documents for the first time the postarrest reduction in oxygen (O 2) delivery in relation to O 2 uptake for brain and entire organism. Methods: In eight dogs we used our model of ventricular fibrillation (VF) cardiac arrest of 12.5 min, reperfusion with brief cardiopulmonary bypass, and controlled normotension, normoxemia, and mild hypocapnia to 24 h. Results: Between 4 and 24 h after cardiac arrest, cardiac output decreased by about 25% and the systemic arteriovenous Oz content difference doubled, while the calculated systemic O 2 utilization coefficient (O 2 UC) increased and the systemic venous PO 2 decreased, both not to critical levels. The cerebral arteriovenous O 2 content difference however, which was 5.6 ± 1.7 ml/dl before arrest, increased between 1 and 18 h, to 10.8 ± 3.2 ml/dl at 4 h. The cerebral O 2 UC increased and the cerebral venous Poz decreased, both to critical levels. Conclusions: After prolonged cardiac arrest in dogs with previously fit hearts, the reduction of O 2 transport to the brain is worse than its reduction to the whole organism. Monitoring these values might help in titrating life-support therapies.