OBJECTIVE: To evaluate whether the deleterious effect of cardiopulmonary bypass (CPB) can be prevented by controlling PaO(2) 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 (groupI, n = 10) had CPB initiated at a fraction of inspired oxygen (F(I)O(2)) of 1.0 (PO(2), 300 to 350 mmHg). Cyanotic patients were subdivided as follows: Group II (n = 7) had CPB initiated at an F(I)O(2) of 1.0, and group III (n = 7) had CPB initiated at an F(I)O(2) of 0.21 (PO(2), 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)-alpha, 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, TNF-alpha 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 F(I)O(2) of 1.0) had significantly increased MDA production compared with group III (initiating CPB at an F(I)O(2) of 0.21) (302 +/- 134% v 133 +/- 74%, p < 0.05). Group II had higher TNF-alpha 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 PO(2) 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. Copyright 2002, Elsevier Science (USA). All rights reserved.
RCT Entities:
OBJECTIVE: To evaluate whether the deleterious effect of cardiopulmonary bypass (CPB) can be prevented by controlling PaO(2) 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 (F(I)O(2)) of 1.0 (PO(2), 300 to 350 mmHg). Cyanotic patients were subdivided as follows: Group II (n = 7) had CPB initiated at an F(I)O(2) of 1.0, and group III (n = 7) had CPB initiated at an F(I)O(2) of 0.21 (PO(2), 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)-alpha, 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, TNF-alpha 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 F(I)O(2) of 1.0) had significantly increased MDA production compared with group III (initiating CPB at an F(I)O(2) of 0.21) (302 +/- 134% v 133 +/- 74%, p < 0.05). Group II had higher TNF-alpha 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 PO(2) 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. Copyright 2002, Elsevier Science (USA). All rights reserved.