I need to refer to a range of normal PaO2 levels during CPB in a new manuscript I am preparing. Are there any guidelines or textbook chapters referring to a "target values of PaO2 during CPB", e.g. 150-250 mmHg?
This is a great question with many answers. No one really knows as it depends on what one is trying to achieve by having higher paO2s.. Hyperoxia is not adequately defined but we know that levels over 250 mmHg one gets into toxic ROS reactions resulting in cell damage after ischemic arrest, cerebral and peripheral vasoconstriction...the list goes on.
A very informative paper from the group in New Zealand (A Multicenter, Randomized, Controlled Phase IIb Trial of Avoidance of Hyperoxemia during Cardiopulmonary Bypass) showed "...avoidance of modest hyperoxemia (mean, 178 mmHg) during CPB appears safe and achievable but failed to demonstrate any difference in AKI, markers of organ damage, or length of stay." The inference being that normoxic pO2s are OK also.
We target our paO2 range from100 too 150 mmHg. We also calculate on each blood gas, our DaO2, DaO2/m2, VO2/m2 and VO2. It could be that during CPB, the paO2s are difficult to control and in order to avoid hypoxia the FiO2 s are set too high resulting in paO2s over 200 mmHg. However, I have developed a system in which the FiO2 is set according to the VO2 of the patient to achieve a paO2 of 150 mmHg. Once you use this for a few cases, it becomes automatic and one learns not only how your oxygenator responds to changes in VO2 but how the VO2 varies for each patient. I refer you to my paper and if you have any questions, please feel free to contact me at any time.
A new method to measure oxygenator oxygen transfer performance during cardiopulmonary bypass: clinical testing using the Medtronic Fusion oxygenator. DOI: 10.1177/0267659116668400
Thank you for great answers. "Optimal perfusion during cardiopulmonary bypass..." by Murphy et al. came up with no answers to my question. Many papers like this one only refer to values of SO2, because it is SO2 which determines oxygen content of blood, and not PaO2.
However, the study by McGuinness et al. was a close enough to solve my problem. It seems like, almost every author focusing on effects of hyperoxic cardiopulmonary bypass, presumes that "hyperoxia is used as a routine part of CPB in order to avoid hypoxemia", but none refers on an evidence-based manner.
Considering that more and more papers discussing side effects of hyperoxic CPB are being published every day, this presumption is going to die out.