Does normoxemic cardiopulmonary bypass prevent myocardial reoxygenation injury in cyanotic children?

Objective: To evaluate whether the deleterious effect of cardiopulmonary bypass (CPB) can be prevented by controlling PaO₂ in cyanotic children. Design: Prospective, randomized, clinical study. Setting: Single university hospital. Participants: Pediatric patients undergoing cardiac surgery for repair of congenital heart disease (n = 24). Interventions: Patients were randomly allocated into 3 groups. Patients in the acyanotic group (group I, n = 10) had CPB initiated at a fraction of inspired oxygen (F₁O₂) of 1.0 (PO₂, 300 to 350 mmHg). Cyanotic patients were subdivided as follows: Group II (n = 7) had CPB initiated at an F₁O₂ of 1.0, and group III (n = 7) had CPB initiated at an F₁O₂ of 0.21 (PO₂, 90 to 110 mmHg). A biopsy specimen of right atrial tissue was removed during venous cannulation, and another sample was removed after CPB before aortic cross-clamping. The tissue was incubated in 4 mmol/L of t-butylhydroperoxide, and the malondialdehyde (MDA) level was measured to determine the antioxidant reserve capacity. Blood samples for cytokine levels, tumor necrosis factor (TNF)-α, and interleukin (IL)-6 response to CPB were collected after induction of anesthesia and at the end of CPB before protamine administration. Measurements and Main Results: After initiation of CPB, MDA level rose markedly in the cyanotic groups compared with the acyanotic group (210 ± 118% v 52 ± 34%, p < 0.05), which indicated the depletion of antioxidants. After initiation of CPB, T.NF-α and IL-6 levels of the cyanotic groups were higher than for the acyanotic group (168 ± 77 v 85 ± 57, p < 0.001; 249 ± 131 v 52 ± 40; p < 0.001). When a comparison between the cyanotic groups was performed, group II (initiating CPB at an F₁O₂ of 1.0) had significantly increased MDA production compared with group III (initiating CPB at an F₁O₂ of 0.21) (302 ± 134% v 133 ± 74%, p < 0.05). Group II had higher TNF-α and IL-6 levels than group III (204 ± 81 v 131 ± 52, p < 0.001; 308 ± 147 v 191 ± 81, p < 0.01). Conclusion: Conventional clinical methods of initiating CPB at a hyperoxemic PO₂ may increase the possibility of myocardial reoxygenation injury in cyanotic children. This deleterious effect of reoxygenation can be modified by initiating CPB at a lower level of oxygen concentration. Subsequent long-term studies are needed to determine the best method of decreasing the oxygen concentration of the CPB circuit.