The Journal of thoracic and cardiovascular surgery · 2011
Perioperative cerebral and somatic oxygenation in neonates with hypoplastic left heart syndrome or transposition of the great arteries.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Uebing Anselm, Furck Anke K, Hansen Jan H, Nufer Elisabeth, Scheewe Jens, Dütschke Peter, Jung Olaf, Kramer Hans-Heiner
Аннотация
OBJECTIVE: Significant depression in cerebral oxygen saturation has been observed in patients with hypoplastic left heart syndrome (HLHS) undergoing Norwood operations. We monitored cerebral oxygen saturation with near-infrared spectroscopy before and after this procedure. Patients with transposition of great arteries (TGA) before and after arterial switch operation were also studied to elucidate whether post-cardiopulmonary bypass (CPB) changes in cerebral oxygen saturation are related to CPB or hemodynamic alterations inherent in single-ventricle physiology.
METHODS: We monitored 33 patients with HLHS and 20 with TGA 24 hours before and 48 hours after CPB. In addition to cerebral oxygen saturation, routine measurements of oxygen transport and delivery were performed.
RESULTS: Preoperatively, cerebral oxygen saturation was higher in patients with HLHS than with TGA (61% ± 7% vs 56% ± 8%, P = .04). After CPB, cerebral oxygen saturation was markedly depressed in both groups but increased toward end of monitoring (HLHS vs TGA minimal value 42% ± 12% vs 54% ± 11%, P < .001, value 48 hours after CPB 62% ± 7% vs 80% ± 8%, P < .0001). Routine measures of oxygen delivery, such as arterial and central venous oxygen saturations, were similar at minimal cerebral oxygen saturation and 48 hours after CPB.
CONCLUSIONS: Depression of cerebral oxygen saturation is prevalent among neonates with congenital heart disease regardless of whether univentricular or biventricular circulation is present, suggesting that cerebral desaturation is mainly induced by CPB's effect on cerebral blood flow. Routine measures of oxygen delivery fail to indicate cerebral desaturation.
METHODS: We monitored 33 patients with HLHS and 20 with TGA 24 hours before and 48 hours after CPB. In addition to cerebral oxygen saturation, routine measurements of oxygen transport and delivery were performed.
RESULTS: Preoperatively, cerebral oxygen saturation was higher in patients with HLHS than with TGA (61% ± 7% vs 56% ± 8%, P = .04). After CPB, cerebral oxygen saturation was markedly depressed in both groups but increased toward end of monitoring (HLHS vs TGA minimal value 42% ± 12% vs 54% ± 11%, P < .001, value 48 hours after CPB 62% ± 7% vs 80% ± 8%, P < .0001). Routine measures of oxygen delivery, such as arterial and central venous oxygen saturations, were similar at minimal cerebral oxygen saturation and 48 hours after CPB.
CONCLUSIONS: Depression of cerebral oxygen saturation is prevalent among neonates with congenital heart disease regardless of whether univentricular or biventricular circulation is present, suggesting that cerebral desaturation is mainly induced by CPB's effect on cerebral blood flow. Routine measures of oxygen delivery fail to indicate cerebral desaturation.