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ICVTS on-line discussion A Further testing is warranted to detect more subtle degrees...

University Hospital Sestre Milosrdnice, Zagreb 10000, Croatia

Does poor oxygenation during one-lung ventilation impair aerobic myocardial metabolism in patients with symptomatic coronary artery disease?

eComment: The authors stated that they are not able to provide a safety margin of tolerable minimal PaO₂-values above the anaerobic threshold of the myocardial metabolism [1]. Not such a long time ago, we conducted a study of controlled cardiac reoxygenation, in a lethal ischemic swine model, utilizing normoxic bypass and normoxic cardioplegia solution which called into question the beneficial effects of controlled cardiac reoxygenation when employing normoxic conditions. In this study, we specifically combined a normoxic protocol for CPB without titration to hyperoxic levels and tested whether there was any value for controlled cardiac reoxygenation and limiting cardiac dysfunction. We were unable to show any significant advantage to controlled cardiac reoxygenation over normoxic cardioplegia resuscitation utilizing substrate-enhanced cardioplegia. Utilizing a resuscitative protocol, the value of controlling for reoxygenation during the cardioplegic resuscitation was compared in two groups of animals. Its effect on cardiac function following a lethal injury and whether it enabled recovery in acutely injured ventricles were measured utilizing the degree of myocite damage and peroxidative injury based on CK, CK-MB, nitric oxide and specifically conjugated diene levels in the coronary sinus blood. It was shown that even normoxic bypass, although attenuating the liberation of oxygen free radicals, does not prevent reperfusion injury in a hypoxic or ischemic setting when the FiO₂ tension is further raised, either gradually or abruptly, to hyperoxic levels [2]. It remains to be proven whether or not there can be further benefit to cardiac resuscitation by gradual reoxygenation to hyperoxic levels while utilizing a normoxic CPB circuit. A major value to titrating the oxygen tension both in the CPB circuit and cardioplegia (to limit reoxygenation injury both on CPB and in myocardial resuscitation) is its clinical simplicity and applicability to both congenital surgery as well as adult cardiac surgery.

The subtle but real difference in conjugated dienes in the controlled reoxygenation brings to question whether further testing is warranted to detect more subtle degrees of improved cardiac preservation with a controlled reoxygenation protocol in the face of normoxic bypass under nonlethal surgical patterns. Further investigation could include comparing the effect of normoxic versus hypoxic CPB in a lethal ischemia model with and without controlled cardiac reoxygenation as it relates to reperfusion injury with determination of nitric oxide, conjugated diene analysis, creatinine kinase serum assays with measuring of subsequent formation of adenosine triphosphate in coronary sinus blood samples.

I am hoping that the above mentioned statements could improve the determination of myocardial metabolism, and that we will be able to provide a safety margin of tolerable minimal PaO₂-values above the anaerobic threshold.

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1. Mierdl S, Meininger D, Dogan S, Wimmer-Greinecker G, Westphal K, Bremerich DH, Byhahn C. Does poor oxygenation during one-lung ventilation impair aerobic myocardial metabolism in patients with symptomatic coronary artery disease? Interact CardioVasc Thorac Surg 2007; 6:209–213.[Abstract/Free Full Text]
2. Buckberg GD. Studies of hypoxemic/reoxygenation injury. J Thorac Cardiovasc Surg 1995; 110:1163–1286.[CrossRef]

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