DISTURBANCE OF CEREBRAL OXYGENATION AND HEMODYNAMICS RELATED TO THE OPENING OF THE BYPASS BRIDGE DURING VENOARTERIAL EXTRACORPOREAL MEMBRANE-OXYGENATION

Citation
Kd. Liem et al., DISTURBANCE OF CEREBRAL OXYGENATION AND HEMODYNAMICS RELATED TO THE OPENING OF THE BYPASS BRIDGE DURING VENOARTERIAL EXTRACORPOREAL MEMBRANE-OXYGENATION, Pediatric research, 38(1), 1995, pp. 124-129
Citations number
23
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00313998
Volume
38
Issue
1
Year of publication
1995
Pages
124 - 129
Database
ISI
SICI code
0031-3998(1995)38:1<124:DOCOAH>2.0.ZU;2-S
Abstract
The objective of this study was to investigate changes of cerebral oxy genation and hemodynamics related to opening of the bypass bridge duri ng veno-arterial extracorporeal membrane oxygenation (ECMO). Ten newbo rn infants and 12 piglets were studied during opening of the bridge fo r 10 and 1 s, respectively. Changes in cerebral concentration of oxyhe moglobin (cO(2)Hb), deoxyhemoglobin (cHHb), (oxidized-reduced) cytochr ome aa(3) (cCyt.aa(3)), and blood volume (CBV) were continuously measu red by near infrared spectrophotometry. Heart rate, arterial O-2 satur ation (saO(2)), and mean arterial blood pressure (MABP) were measured simultaneously. In the piglets, central venous pressure (CVP), intracr anial pressure (ICP), and left common carotid artery blood flow (CaBF) were also measured. Opening of the bridge for 10 s in the infants res ulted in a significant decrease in MABP, saO(2), and cO(2)Hb, whereas cHHb increased. CBV did not change significantly. In piglets biphasic changes were observed for MABP CaBF, cO(2)Hb, and CBV, showing an init ial decrease followed by a smaller increase. cHHb and CVP showed rever se biphasic changes. ICP increased but saO(2) was unchanged. In all ca ses heart rate and cCyt.aa(3) did not change significantly. Opening of the bridge for 1 s resulted in minor changes in only a few variables. In conclusion, opening of the bridge resulted in a decrease of CBV an d cerebral O-2 supply due to a decrease of cerebral blood flow, follow ed by a compensatory increase of cerebral O-2 extraction and vasodilat ation. The return of oxygenated blood after reclosing resulted in an i ncrease of CBV with overcompensation of cerebral O-2 supply.