• Christian J Hunter, Arlin B Blood, John M Bishai, Adam D Hickerson, Debbie D Wall, Ricardo L Peverini, Gordon G Power, and Andrew O Hopper.
• Center for Perinatal Biology, Loma Linda University School of Medicine, Loma Linda, CA, USA.
• Pediatr Crit Care Me. 2004 Sep 1; 5 (5): 475-81.

BackgroundConcern exists that extracorporeal membrane oxygenation (ECMO) may decrease cerebral blood flow (CBF), impair cerebral autoregulation, and thereby increase the risk of neurologic injury.ObjectiveThis study was undertaken in newborn lambs to compare the effects of initiation of venoarterial and venovenous ECMO on CBF and cerebral oxygen delivery as measured by laser-Doppler flowmetry. This study also evaluates the effects of carotid artery and jugular vein ligation on CBF.DesignCBF, arterial blood pressure, sagittal sinus pressure, heart rate, cardiac output, arterial blood gases, and hemoglobin saturation were measured. After anesthesia, instrumentation, and a 1-2 hr stabilization period, values were recorded during a 30-min control period, and the carotid artery or jugular vein was cannulated. The animals were then studied during venoarterial or venovenous ECMO for 1 hr.Main ResultsCarotid ligation resulted in a transient decrease in right cortex CBF that resolved within 60 secs. Next, during a 60-min period of venoarterial ECMO (flow rate of 100 mL.min(-1).kg(-1), n = 11), cerebral resistance to flow increased, CBF decreased 25%, and cerebral oxygen delivery decreased by 30%. Native cardiac output and Paco(2) remained constant. Pulsatility in the lingual artery, representing the pulsatility of arterial flow to the brain, decreased throughout venoarterial ECMO. In contrast, in those lambs receiving ECMO in the venovenous mode (n = 7), resistance to flow, CBF, cerebral oxygen delivery, and pulsatility did not change.ConclusionsThere was no sustained decrease in CBF after ligation of either the carotid artery or jugular vein. Venoarterial but not venovenous ECMO induced decreases of CBF that could not be attributed to changes in blood gases or blood pressure but that may relate to diminished pulsatility in cerebral resistance vessels or to differences in levels of circulating vasoactive compounds.

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