title: The influence of systemic hemodynamics and oxygen transport on cerebral oxygen saturation in neonates after the Norwood procedure.
abstract: OBJECTIVE
  Ischemic brain injury is an important morbidity in neonates after the Norwood procedure. Its relationship to systemic hemodynamic oxygen transport is poorly understood.
  
  
  METHODS
  Sixteen neonates undergoing the Norwood procedure were studied. Continuous cerebral oxygen saturation was measured by near-infrared spectroscopy. Continuous oxygen consumption was measured by respiratory mass spectrometry. Pulmonary and systemic blood flow, systemic vascular resistance, oxygen delivery, and oxygen extraction ratio were derived with measurements of arterial, and superior vena cava and pulmonary venous gases and pressures at 2- to 4-hour intervals during the first 72 hours in the intensive care unit.
  
  
  RESULTS
  Mean cerebral oxygen saturation was 66% +/- 12% before the operation, reduced to 51% +/- 13% on arrival in the intensive care unit, and remained low during the first 8 hours; it increased to 56% +/- 9% at 72 hours, still significantly lower than the preoperative level (P < .05). Postoperatively, cerebral oxygen saturation was closely and positively correlated with systemic arterial pressure, arterial oxygen saturation, and arterial oxygen tension and negatively with oxygen extraction ratio (P < .0001 for all). Cerebral oxygen saturation was moderately and positively correlated with systemic blood flow and oxygen delivery (P < .0001 for both). It was weakly and positively correlated with pulmonary blood flow (P = .001) and hemoglobin (P = .02) and negatively correlated with systemic vascular resistance (P = .003). It was not correlated with oxygen consumption (P > .05).
  
  
  CONCLUSIONS
  Cerebral oxygen saturation decreased significantly in neonates during the early postoperative period after the Norwood procedure and was significantly influenced by systemic hemodynamic and metabolic events. As such, hemodynamic interventions to modify systemic oxygen transport may provide further opportunities to reduce the risk of cerebral ischemia and improve neurodevelopmental outcomes.
authors.affiliation: Heart Center, the Hospital for Sick Children, Toronto, Ontario, Canada. jia.li@sickkids.ca
authors.forename: Jia
authors.initials: J
authors.lastname: Li
authors.forename: Gencheng
authors.initials: G
authors.lastname: Zhang
authors.forename: Helen
authors.initials: H
authors.lastname: Holtby
authors.forename: Anne-Marie
authors.initials: AM
authors.lastname: Guerguerian
authors.forename: Sally
authors.initials: S
authors.lastname: Cai
authors.forename: Tilman
authors.initials: T
authors.lastname: Humpl
authors.forename: Christopher A
authors.initials: CA
authors.lastname: Caldarone
authors.forename: Andrew N
authors.initials: AN
authors.lastname: Redington
authors.forename: Glen S
authors.initials: GS
authors.lastname: Van Arsdell
mesh_terms: D001692:Biological Transport; D013504:Cardiovascular Surgical Procedures; D002560:Cerebrovascular Circulation; D054022:Cerebrum / Q000098:blood supply / Q000737:chemistry*; D005260:Female; D006330:Heart Defects, Congenital / Q000503:physiopathology* / Q000601:surgery; D006439:Hemodynamics; D006801:Humans; D007231:Infant, Newborn; D008297:Male; D010092:Oximetry; D010100:Oxygen / Q000032:analysis* / Q000378:metabolism*; D011184:Postoperative Period
chemical_list: D010100:Oxygen