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Transient electroencephalographic suppression with initiation of cardiopulmonary bypass in pigs: blood versus nonblood priming

Division of Cardiothoracic Anesthesiology and the Charles R Allen Research Laboratories, Department of Anesthesiology, University of Texas Medical Branch, Galveston, Texas

Cheng Y Lin

Division of Cardiothoracic Anesthesiology and the Charles R Allen Research Laboratories, Department of Anesthesiology, University of Texas Medical Branch, Galveston, Texas

Larry W Jenkins

Division of Cardiothoracic Anesthesiology and the Charles R Allen Research Laboratories, Department of Anesthesiology, University of Texas Medical Branch, Galveston, Texas

Douglas S DeWitt

Division of Cardiothoracic Anesthesiology and the Charles R Allen Research Laboratories, Department of Anesthesiology, University of Texas Medical Branch, Galveston, Texas

William E Johnston

Division of Cardiothoracic Anesthesiology and the Charles R Allen Research Laboratories, Department of Anesthesiology, University of Texas Medical Branch, Galveston, Texas, william.johnston{at}utmb.edu

Electroencephalographic (EEG) changes have been reported with cardiopulmonary bypass (CPB). We tested whether the type of priming solution (blood versus nonblood) affected the EEG. Twenty-six anesthetized pigs (29.5 ± 1.6 kg) were cannulated for CPB primed with 1 liter plasmalyte and 500 ml 6% hetastarch (nonblood prime). EEG signals were recorded during the initiation of normothermic CPB. Three minutes later, animals were weaned from CPB and allowed to stabilize. CPB was reinstituted using the animals’ hemodiluted blood as prime. We found that with nonblood prime, abrupt and marked EEG suppression lasting 12.6 ± 0.7 s was found in all animals, followed by gradual resumption of baseline EEG activity. In contrast, CPB with blood prime caused no detectable EEG changes. We conclude that severe reductions in EEG activity occur after initiating CPB with nonblood prime; these reductions are not seen when using blood prime. The cause of EEG suppression is unknown, but may represent transient impairment of oxygen delivery to the brain caused by nonblood perfusion.

Perfusion, Vol. 14, No. 5, 337-340 (1999)
DOI: 10.1177/026765919901400504


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