The relationship between systemic oxygen uptake and del ivery during moderate hypothermic cardiopulmonary bypass: critical values and effects of vasodilation by hydralazine

Abstract

The relationship between oxygen delivery (DO2) and uptake (VO2) has been studied during moderately hypothermic cardiopulmonary bypass (CPB) in 15 patients undergoing myocardial revascularization. As soon as nasopharyngeal temperature was lowered to 32°C, blood flow was decreased from 2.4 to 2.0 l/min/m 2. Arterial and mixed venous blood gas analyses were performed five and eight minutes later and DO2 and VO2 were calculated; VO2 stabilized in five minutes after changing blood flow and neither DO2 nor VO2 values changed three minutes later (DO 2: 217 ± 19 versus 215 ± 17 ml/min/m2; VO2: 63 ± 12 versus 66 ± 14 ml/min/m2). Blood flow then was increased to 2.3 l/min/m2 and DO2 and VO2 were determined again, five minutes later; they both increased significantly, to 243 ± 20 and 74 ± 13 ml/min/m 2, respectively. However, a further blood flow increase to 2.6 l/min/m 2 which caused DO2 to increase to 277 ± 24 ml/min/m 2, did not affect VO2 which was unchanged five minutes later (76 ± 13 ml/min/m2); VO2 dependence on DO2 values higher than 243 ± 20 ml/min/m2 was consequently ruled out. Ten patients, having a mean arterial pressure higher than 80 mmHg, were eventually vasodilated with hydralazine, 0.1 mg/kg intravenously, and DO2 and VO2 were determined after five and ten minutes. As blood flow did not change, DO2 was unaffected while a slight increase in VO2 mean values was observed which was not statistically significant (prior to hydralazine: 78 ± 15 ml/min/m2; five minutes later: 82 ± 17 ml/min/m2; 10 minutes later: 76 ± 18 ml/min/m2). In conclusion, during hypothermic CPB at 32°C, VO2 plateau ranges between 48 and 102 mi/min/m 2 (mean ± 2 SD) in 95% of patients, corresponding to 66 and 141 ml/min/m 2 at 37°C; this finding closely matches other literature reports. Consequently, lower VO2 values suggest inadequate oxygen supply to tissues. Critical DO2 at 32°C is lower than 283 ml/min/m2 in 97.5% of patients. Finally, arterial vasoconstriction does not seem to play a significant role in tissue hypoperfusion.