Advances in perfusion strategies have played an important role in improving outcomes following repair of complex congenital heart defects. The influence of cooling strategy, temperature, duration of circulatory arrest, and specific method of cerebral perfusion on neurologic morbidity have been extensively characterized. Similarly, the ability of pharmacologic agents to modulate the post-cardiopulmonary bypass (CPB) inflammatory response has been previously elucidated in both the laboratory and clinical arena. However, modification of the circuit and priming components have received comparably less attention. We recently showed that employment of a miniaturized circuit and a bloodless prime reduce inflammation and have salutary effects on cardiopulmonary function following hypothermic low-flow perfusion (HLF), and that this circuit may also improve cerebral protection following both deep hypothermic circulatory arrest and HLF. The current report, therefore, reviews current strategies utilized to minimize post-CPB inflammation and highlights the empirical evidence from our laboratory demonstrating the beneficial role of a miniaturized extracorporeal circuit in this context.
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