Cerebral oxygenation and hemodynamics during induction of extracorporeal membrane oxygenation as investigated by near infrared spectrophotometry.

OBJECTIVE: To investigate cerebral oxygenation and hemodynamics in relation to changes in some relevant physiologic variables during induction of extracorporeal membrane oxygenation (ECMO) in newborn infants.
METHODS: Twenty-four newborn infants requiring ECMO were studied from cannulation until 60 minutes after starting ECMO. Concentration changes of oxyhemoglobin (cO2Hb), deoxyhemoglobin (cHHb), total hemoglobin (ctHb), and (oxidized-reduced) cytochrome aa3 (cCyt.aa3) in cerebral tissue were measured continuously by near infrared spectrophotometry. Heart rate (HR), transcutaneous partial pressures of oxygen and carbon dioxide (tcPO2 and tcPCO2), arterial O2 saturation (saO2), and mean arterial blood pressure (MABP) were measured simultaneously. Intravascular hemoglobin concentration (cHb) was measured before and after starting ECMO. In 18 of the 24 infants, mean blood flow velocity (MBFV) and pulsatility index (PI) in the internal carotid and middle cerebral arteries were also measured before and after starting ECMO using pulsed Doppler ultrasound.
RESULTS: After carotid ligation, cO2Hb decreased whereas cHHb increased. After jugular ligation, no changes in cerebral oxygenation were found. At 60 minutes after starting ECMO, the values of cO2Hb, saO2, tcPO2, and MABP were significantly higher than the precannulation values, whereas the value of cHHb was lower. There were no changes in cCyt.aa3, tcPCO2, and HR, whereas cHb decreased. The MBFV was significantly increased in the major cerebral arteries except the right middle cerebral artery, whereas PI was decreased in all measured arteries. Cerebral blood volume, calculated from changes in ctHb and cHb, was increased in 20 of 24 infants after starting ECMO. Using multivariate regression models, a positive correlation of delta ctHb (representative of changes in cerebral blood volume) with delta MABP and a negative correlation with delta tcPO2 were found.
CONCLUSIONS: The alterations in cerebral oxygenation after carotid artery ligation might reflect increased O2 extraction. Despite increase of the cerebral O2 supply after starting ECMO, no changes in intracellular O2 availability were found, probably because of sufficient preservation of intracellular cerebral oxygenation in the pre-ECMO period despite prolonged hypoxemia. The increase in cerebral blood volume and cerebral MBFV may result from the following: (1) reactive hyperperfusion, (2) loss of autoregulation because of prolonged hypoxemia before ECMO and/or decreased arterial pulsatility, or (3) compensation for hemodilution related to the ECMO procedure.