Correlation Between Cerebral and Mixed Venous Oxygen Saturation During Moderate Versus Tepid Hypothermic Hemodiluted Cardiopulmonary Bypass

Correlation Between Cerebral and Mixed Venous Oxygen Saturation During Moderate Versus Tepid Hypothermic Hemodiluted Cardiopulmonary Bypass This study was undertaken to compare cerebral oxygen saturation (RsO(2)) and mixed venous oxygen saturation (SvO(2)) in patients undergoing moderate and tepid hypothermic hemodiluted cardiopulmonary bypass (CPB).
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We undertook a multivariate logistic regression analysis of the risk factors associated with mortality in 2599 consecutive patients undergoing cardiac surgery.	Objective: This study was undertaken to compare cerebral oxygen saturation (RsO(2)) and mixed venous oxygen saturation (SvO(2)) in patients undergoing moderate and tepid hypothermic hemodiluted cardiopulmonary bypass (CPB). Methods: Fourteen patients undergoing elective coronary artery bypass graft surgery using hypothermic hemodiluted CPB. During moderate (28 degrees -30 degrees C) and tepid hypothermic (33 degrees -34 degrees C) hemodiluted CPB, RsO(2) and SvO(2) were continuously monitored with a cerebral oximeter via a surface electrode placed on the patient's forehead and with the mixed venous oximeter integrated in the CPB machine, respectively. Measurements and Main Results: Mean +/- standard deviation of RsO(2), SvO(2), PaCO(2), and hematocrit were determined prebypass and during moderate and tepid hypothermic phases of CPB while maintaining pump flow at 2.4 L/min/m(2) and mean arterial pressure in the 60- to 70-mmHg range. Compared with a prebypass value of 76.0% +/- 9.6%, RsO(2) was significantly decreased during moderate hypothermia to 58.9% +/- 6.4% and increased to 66.4% +/- 6.7% after slow rewarming to tepid hypothermia. In contrast, compared with a prebypass value of 78.6% +/- 3.3%, SvO(2) significantly increased to 84.9% +/- 3.6% during moderate hypothermia and decreased to 74.1% +/- 5.6% during tepid hypothermia. During moderate hypothermia, there was poor agreement between RsO(2) and SvO(2) with a gradient of 26%; however, during tepid hypothermia, there was a strong agreement between RsO(2) and SvO(2) with a gradient of 6%. The temperature-uncorrected PaCO(2) was maintained at the normocapnic level throughout the study, whereas the temperature-corrected PaCO(2) was significantly lower during the moderate hypothermic phase (26.8 +/- 3.1 mmHg) compared with the tepid hypothermic phase (38.9 +/- 3.7 mmHg) of CPB. There was a significant and positive correlation between RsO(2) and temperature-corrected PaCO(2) during hypothermia. Conclusions: During moderate hypothermic hemodiluted CPB, there was a significant increase of SvO(2) associated with a paradoxic decrease of RsO(2) that was attributed to the low temperature-corrected PaCO(2) values. During tepid CPB after slow rewarming, regional cerebral oxygen saturation was increased in association with an increase with the temperature-corrected PaCO(2) values. The results show that during hypothermic hemodiluted CPB using the alpha-stat strategy for carbon dioxide homeostasis, cerebral oxygen saturation is significantly higher during tepid than moderate hypothermia.
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