OBJECTIVE: To investigate the cerebrovascular response to changes in arterial CO2 tension during extracorporeal membrane oxygenation (ECMO) in normoxaemic and hypoxaemic piglets. METHODS: Four groups of six anaesthetized, paralysed and mechanically ventilated piglets: group 1-normoxaemia without ECMO, group 2-ECMO after normoxaemia, group 3-hypoxaemia without ECMO, and group 4-ECMO after hypoxaemia, were exposed successively to hypercapnia and hypocapnia. Changes in cerebral concentrations of oxyhaemoglobin (cO2Hb), deoxyhaemoglobin (cHHb), (oxidized-reduced) cytochrome aa3 (cCyt.aa3) and blood volume (CBV) were continuously measured using near infrared spectrophotometry. Heart rate, arterial O2 saturation, arterial blood pressure, central venous pressure, intracranial pressure (ICP) and left common carotid artery blood flow (LCaBF) were measured simultaneously. RESULTS: Hypercapnia resulted in increased CBV, cO2Hb and ICP in all groups, while cHHb was decreased. No changes in LCaBF were found. Hypocapnia resulted in decreased cO2Hb and increased cHHb except in group 3. LCaBF decreased in all groups except group 2. CBV decreased only in groups 2 and 4. No effect on ICP was observed in any of the groups. The other variables showed no important changes either during hypercapnia or hypocapnia. ECMO after hypoxaemia resulted in a greater response of cO2Hb and cO2Hb and cHHb during hypocapnia. The effect of hypercapnia on CBV while on ECMO was greater than without ECMO. CONCLUSION: Since cerebrovascular reactivity to CO2 remains intact during ECMO in piglets, it is important to keep arterial CO2 tension stable and in normal range during clinical ECMO.
OBJECTIVE: To investigate the cerebrovascular response to changes in arterial CO2 tension during extracorporeal membrane oxygenation (ECMO) in normoxaemic and hypoxaemic piglets. METHODS: Four groups of six anaesthetized, paralysed and mechanically ventilated piglets: group 1-normoxaemia without ECMO, group 2-ECMO after normoxaemia, group 3-hypoxaemia without ECMO, and group 4-ECMO after hypoxaemia, were exposed successively to hypercapnia and hypocapnia. Changes in cerebral concentrations of oxyhaemoglobin (cO2Hb), deoxyhaemoglobin (cHHb), (oxidized-reduced) cytochrome aa3 (cCyt.aa3) and blood volume (CBV) were continuously measured using near infrared spectrophotometry. Heart rate, arterial O2 saturation, arterial blood pressure, central venous pressure, intracranial pressure (ICP) and left common carotid artery blood flow (LCaBF) were measured simultaneously. RESULTS:Hypercapnia resulted in increased CBV, cO2Hb and ICP in all groups, while cHHb was decreased. No changes in LCaBF were found. Hypocapnia resulted in decreased cO2Hb and increased cHHb except in group 3. LCaBF decreased in all groups except group 2. CBV decreased only in groups 2 and 4. No effect on ICP was observed in any of the groups. The other variables showed no important changes either during hypercapnia or hypocapnia. ECMO after hypoxaemia resulted in a greater response of cO2Hb and cO2Hb and cHHb during hypocapnia. The effect of hypercapnia on CBV while on ECMO was greater than without ECMO. CONCLUSION: Since cerebrovascular reactivity to CO2 remains intact during ECMO in piglets, it is important to keep arterial CO2 tension stable and in normal range during clinical ECMO.