Infrared Spectrophotometry

Abstract

Objective. To investigate cerebral oxy­ genation and hemodynamics in relation to changes in some relevant physiologic variables during induction of extracorporeal membrane oxygenation (ECMO) in new­ born infants. Methods. Twenty-four newborn infants requiring ECMO were studied from cannulation until 60 minutes after starting ECMO. Concentration changes of oxyhemo­ globin (c02Hb), deoxyhemoglobin (cHHb), total hemo­ globin (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 0 2 saturation (sa02), 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, c 0 2Hb decreased whereas cHHb increased. After jugular ligation, no changes in cerebral oxygenation were found. At 60 min­ utes after starting ECMO, the values of cOaHb, saO^ tcPo^ and MABP were significantly higher than the pre- cannulation values, whereas the value of cHHb was lower. There were no changes in cCyt.aa3, toPco^, 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 regres­ sion models, a positive correlation of ActHb (representa­ tive of changes in cerebral blood volume) with AMABP and a negative correlation with AtcPo2 were found. Conclusions. The alterations in cerebral oxygenation after carotid artery ligation might reflect increased Oz extraction. Despite increase of the cerebral 0 2 supply after starting ECMO, no changes in intracellular 0 2 avail­ ability were found, probably because of sufficient pres­ ervation 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 hyperperfu­ sion, (2) loss of autoregulation because of prolonged