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

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.