The current understanding of adverse central nervous system (CNS) events following cardiac surgery involves several identifiable, evidence-based mechanisms: athero-sclerotic emboli, microgaseous and microparticulate emboli, and hypoperfusion.1 Secondary factors, including patient co-morbidities and inherent genetic susceptibilities, as well as systemic inflammatory processes and a suboptimal metabolic milieu may interact to potentiate the extent of injury.2 In this review a number of these factors and their potential interactions will be explored with a view towards developing a comprehensive management strategy to minimize CNS injury.
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