Relatonship Of Arterial Oxygen Partial Pressure With Brain Injury During Cardioulonmary Bypass In Finfant With Caynotic Cogential Heart Dises

ObjectiveThe study was to probe into the relationship of arterial oxygen partial pressure(PaO₂) with brain injury and to investgate the optimal PaO₂ during cardiopulmonarybypass (CPB) in infants with cyanotic congenital heart disease, by controllinng PaO₂at different levels during CPB, and measuring markers of brain injury and regionalcerebral oxygen saturation (rSO₂) at different time points.MethodsEnrolled in the study were forty-five cyannotic infants, who were less than threeyears old and underwent corrective cardiac surgery from August 1st, 2010 to January31st, 2011 at Guangdong general Hospital. All the infants were lower than 85% bypulse oxygen saturation (SpO₂) and were confirmed with cyanotic congenital heartdisease by cardiac echo or CT scan. The study was approved by the Research Ethics Committee of Guangdong General Hospital and parental informed consent wasgained the day before the operation for all infants'parents.The infants were randomly allocated into three groups by a specific computerprogramme: Controlled group 1 (G1 group), in which PaO₂ levels of all the 15 infantswere controlled at 80-120mmHg during CPB; Controlled group 2 (G2 group), inwhich PaO₂ levels of all the 15 infants were controlled at 120-200 mmHg during CPB;Uncontrolled group (G3 group), in which PaO₂ levels of all the 15 infants werecontrolled over 200mmHg during CPB. Percutaneous blood-gas was continuouslymonitored and PaO₂ was controlled at three stratified levels with an oxygen-airmixture by adjusting fraction of inspired oxygen. Except for the perfusionists, thesurgical team and the laboratory team were blind to the treatment allocation.Blood samples were collected and rSO₂ was measured respectively just beforestarting CPB, at the end of CPB, and at 3hr, 5hr, and 24hr after CPB (T1, T2, T3, T4,T5). Samples were centrifuged to separate the serum and then frozen to -80℃untilthe determination. Serum concentrations of protein S100β, neuron specific enolase(NSE), adrenomedullin (ADM), superoxide dismutase (SOD), and malondialdehyde(MDA) were determined by one technician at the same time.ResultsTotally forty-five infants were enrolled in this study, with 32 infnats being maleand 13 female. Infants ranged in age from 1 month to 3 years, with an average agebeing 9.97±8.24 months, and 15 infants being 1-6 months old, 15 being 6-12 months,and 5 being 1-3 years; ranged in weight from 3.2 to 14.2 kg, with an average weightbeing 7.79±2.53 kg, and 9 infants being less than 5 kg, 31 being 5-10 kg, and 5 morethan 10 kg. The infants were randomly allocated into three groups by a specificcomputer programme, and there were similar age, weight, and SpO₂ before operationamong the groups. Except for SpO₂ during CPB, all the managements were identical among the groups.S100β: Serum concentrations of protein S100βin three groups were similar beforeCPB was initiated, but all rose significantly after starting CPB. Protein S100βlevelsof group G3 reached a peak of 699±139 pg/ml by the end of CPB, significantly higherthan those in group G1 and group G2, and were positively correlated with SpO₂ levels(r=0.526, p=0.008). After CPB, protein S100βdropped gradually to a close pre-CPBlevel 24 hr later, while that in group G1 was still rising little by little and that in groupG2 maintianed a relatively high level.NSE: There was a similar NSE level in the groups before CPB was initiated. NSElevel of group G1 was continuously rising after starting CPB and reached asignificantly high level at 3 hr or 5 hr after CPB, while that of group G2 rosesignificantly during CPB and even higher at 3 hr or 5 hr after CPB. NSE levels ofgroup G1 and group G2 showed a dropping trend at 24 hr after CPB. NSE levels ofgroup G3 rose significantly during CPB and maintianed at a high level afterwards.There was no significant difference of serum NSE concentrations among these threegroups.ADM: There was no significant difference of serum ADM concentrations amongdiffenrent time points in each group and among these three groups.SOD: There was no significant difference of serum SOD concentrations amongdiffenrent time points in each group and among these three groups.MDA: Serum concentrations of MDA in three groups were similar before CPB wasinitiated, but all rose significantly by the end of CPB. At 24 hr after CPB, MDA levelof group G1 still maintained at a high level, while that of group G3 showed a trend ofdropping and that of group G2 dropped gradually to a close pre-CPB level. There wasno significant difference of serum MDA concentrations among these three groups.rSO₂: There was a similar rSO₂ level in the groups before CPB was initiated. rSO₂ of group G3 dropped by the end of CPB, but rose significantly at 3 hr after CPB andmaintained at a high level afterwards. rSO₂ of group G2 rose with starting CPB butmaintained at a stable level afterwards. rSO₂ of group G1 increased gradually afterstarting CPB. There was no significant difference of rSO₂ among these three groupsexcept that of group G3 and group G2 in T2 time point.ConclusionsHigh PaO₂ during CPB in infants with cyanotic congenital heart disease mightcause an increase of serum protein S100β, NSE and MDA, and a decrease of brainrSO₂, indicating that brain injury might become worse with a higher PaO₂ and mightbe positively correlated with PaO₂ during CPB. Biochemical markers of brain injurychanged mainly at the time of CPB, showing that the therapeutic window time islocated in the period of CPB and in the early stage after CPB. PaO₂ should still belimited to an optimal level even after the end of CPB to prevent a secondary braininjury.