title: Cerebral oxygen supply and utilization during infant cardiac surgery.
abstract: The survival of infants with congenital heart disease has improved dramatically. However, the incidence of neurological injury in infants surviving cardiac surgery remains considerable. These neurological sequelae are attributable at least in part to hypoxia-ischemia/reperfusion, which inevitably accompanies infant heart surgery with deep hypothermia, cardiopulmonary bypass, and circulatory arrest. To begin to identify mechanisms of brain injury during infant cardiac surgery, we used near-infrared spectroscopy to study the relationship between cerebral intravascular (hemoglobin) and mitochondrial (cytochrome aa3) oxygenation in 63 infants (aged 1 day to 9 months) undergoing deep hypothermic repair of congenital heart defects, throughout the intraoperative period. Moreover, we assessed the effect of postnatal age on these changes. The cerebral concentration of oxidized cytochrome aa3 decreased from the onset of deep hypothermic cardiopulmonary bypass, despite apparent abundant intravascular oxygenation manifested by a simultaneous increase in the cerebral concentration of oxyhemoglobin. During this interval infants older than 2 weeks had a greater decrease in oxidized cytochrome aa3 than did infants 2 weeks old or younger. During deep hypothermic circulatory arrest, cerebral levels of oxidized cytochrome aa3 remained depressed while those of oxyhemoglobin declined. With reperfusion following circulatory arrest, the recovery of oxidized cytochrome aa3 was delayed, despite a rapid recovery of intravascular oxygenation (HbO2). After rewarming and 60 minutes of reperfusion, only 46% of infants recovered to the baseline level of cerebral oxidized cytochrome aa3. These findings demonstrate a paradoxical dissociation of changes in intravascular and mitochondrial oxygenation during hypothermic cardiopulmonary bypass; a pronounced decrease of mitochondrial oxygenation is established during induction of hypothermia and a delay in recovery of mitochondrial oxygenation occurs following circulatory arrest. These effects were more pronounced in infants older than 2 weeks than in younger infants. The data suggest potentially deleterious impairments of intrinsic mitochondrial function or of delivery of intravascular oxygen to the mitochondrion or both, effects previously undetected and apparently influenced by cerebral maturation.
authors.affiliation: Department of Neurology, Children's Hospital, Harvard Medical School, Boston, MA, USA.
authors.forename: A J
authors.initials: AJ
authors.lastname: du Plessis
authors.forename: J
authors.initials: J
authors.lastname: Newburger
authors.forename: R A
authors.initials: RA
authors.lastname: Jonas
authors.forename: P
authors.initials: P
authors.lastname: Hickey
authors.forename: H
authors.initials: H
authors.lastname: Naruse
authors.forename: M
authors.initials: M
authors.lastname: Tsuji
authors.forename: A
authors.initials: A
authors.lastname: Walsh
authors.forename: G
authors.initials: G
authors.lastname: Walter
authors.forename: D
authors.initials: D
authors.lastname: Wypij
authors.forename: J J
authors.initials: JJ
authors.lastname: Volpe
mesh_terms: D001921:Brain / Q000098:blood supply / Q000378:metabolism*; D002315:Cardiopulmonary Bypass; D002560:Cerebrovascular Circulation; D006330:Heart Defects, Congenital / Q000601:surgery*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D009422:Nervous System Diseases / Q000209:etiology; D010101:Oxygen Consumption; D011183:Postoperative Complications / Q000209:etiology; D013055:Spectrophotometry, Infrared