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  • Title: Impaired oxygen utilization during rapid cooling on cardiopulmonary bypass.
    Author: Irita K, Kai Y, Takahashi S.
    Journal: Fukuoka Igaku Zasshi; 1999 Jan; 90(1):14-22. PubMed ID: 10087669.
    Abstract:
    UNLABELLED: Little attention has been paid to oxygen demand/supply balance during the cooling phase of cardiopulmonary bypass (CPB). We examined the changes in systemic oxygen utilization caused by the initiation of deep hypothermic CPB. METHODS: We calculated the changes in systemic oxygen consumption (VO2) and its related parameters in 5 patients who underwent reconstruction of the aortic arch using deep hypothermic CPB. Rectal temperature was decreased to 18 centigrade on average. RESULTS: VO2 decreased immediately after the initiation of hypothermic CPB. VO2 decreased by an average of 50% and 64%, while rectal temperatures decreased from 35 to 34 and 32 centigrade, respectively. Hemoglobin-bound oxygen accounted for 68% of VO2 just before CPB and 28% after the rectal temperature decreased to 32 centigrade. This decrease in VO2 correlated with the maximum temperature gradient between the venous and the arterial blood during the cooling phase. The abrupt decrease in VO2 by initiating CPB was associated with an increase in mixed venous oxygen saturation and a decrease in oxygen extraction ratio. VO2 values during the cooling phase were much lower than those during the rewarming phase at any given rectal temperatures. VO2 values at rectal temperatures of 34 and 32 centigrade during the cooling phase of CPB were 40% and 29% of those during the rewarming phase of CPB, respectively. This difference was caused by the changes in VO2 derived from hemoglobin-bound oxygen, and VO2 derived from dissolved oxygen did not show any significant changes during the cooling and the rewarming phase. Hysteresis of VO2 was also observed as a function of the nasopharyngeal temperature. The arterial lactate concentration showed an insignificant but gradual increase during the cooling phase. CONCLUSION: These observations suggested that an immediate decrease in VO2 and the following low values of VO2 caused by the initiation of deep hypothermic CPB could not be simply due to a decrease in the metabolic rate for oxygen but rather due to disturbances in oxygen utilization, one of which seemed to be caused by the impaired oxygen release from hemoglobin. It was also suggested that an increase in mixed venous oxygen saturation by initiating hypothermic CPB did not necessarily indicate an adequate oxygen/demand supply balance.
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