As the overall mortality declines following repair of complex congenital cardiac malformations, attention has focused on reducing the lasting morbidity of these interventions, particularly the observed neurodevelopmental deficiencies. Both cardiopulmonary bypass and deep hypothermic circulatory arrest produce transient alterations in cerebral hemodynamics and metabolism. In studies performed in animals, deep hypothermic circulatory arrest, as compared to cardiopulmonary bypass alone, has been shown to produce excess injury to, and death of, neuronal and glial cells.1 In neonates, deep hypothermic circulatory arrest of greater duration than one hour is a risk factor for early post-operative seizures, and for subsequent neurodevelopmental deficits.2 The Boston Circulatory Arrest Study suggests that, at follow-up of eight years, infants subjected to greater than 41 minutes of deep hypothermic circulatory arrest had excess deficits in full-scale, verbal and performance intelligence quotient, the Mayo apraxia test, and grooved pegboard testing.3 The independent adverse effects of deep hypothermic circulatory arrest have encouraged clinicians to develop the alternative technique of intermittent global perfusion, or continuous regional perfusion at low flow perfusion, in an attempt to reduce the degree of injury to the central nervous system.4–7
Evaluation of cerebral metabolism and quantitative electroencephalography after hypothermic circulatory, arrest and low-flow cardiopulmonary bypass at different temperatures
