• J C Briceno and T M Runge.
• Biomedical Engineering Program, University of Texas at Austin 78712, USA.
• ASAIO J. 1994 Jul 1; 40 (3): M344-50.

AbstractEight adult goats under went 5 hr of normothermic cardiopulmonary bypass (CPB) with pulsatile (n = 3) and nonpulsatile flow (n = 5). PaCO2 was maintained at 30-40 mmHg and blood flow rate at 50 ml/min/kg. Brain tissue pH, PO2, and PCO2, arterial and venous blood gases, and other systemic variables were monitored. No significant differences in brain electrochemistry between pulsatile and nonpulsatile perfusion were observed owing to the large variability of the results and the small number of experiments. The overall data for brain tissue pH, PO2, and PCO2 were analyzed and compared to the results of arterial and venous pH, PO2, and PCO2. Brain acidosis developed at the onset of bypass, and the values for brain tissue pH dissociated from those of blood pH, suggesting that hemodilution and the initial body response to CPB are involved in its development. Brain hypercapnia also developed during CPB, the values of brain tissue PCO2 dissociated from those of blood PCO2, and brain hypercapnia appears to be secondary to brain acidosis. Brain tissue PO2 closely followed the values of PvO2, suggesting that PvO2 can be an indicator of brain tissue PO2 during normothermic CPB and must be monitored during the procedure. Brain tissue acidosis is evidently related to neurologic dysfunction after CPB, and must be addressed. Replacement of the priming solution with whole blood or artificial blood, reduction of the priming volume, and application of vigorous pulsatile flow appear feasible interventions to mitigate brain tissue acidosis during CPB.

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