• J Golej, H Kahlbacher, G Schöffmann, P Winter, G Burda, H Boigner, and G Trittenwein.
• Department of Neonatology and Pediatric Intensive Care, University Children's Hospital of Vienna, Vienna, Austria. johann.golej@akh-wien.ac.at
• Perfusion. 2002 Nov 1; 17 (6): 421-6.

AbstractThere is evidence that haemodynamic fluctuations on extracorporeal membrane oxygenation (ECMO) increase the risk of cerebral damage. We hypothesized that initiation of venovenous (VV) or venoarterial (VA) ECMO itself causes haemodynamic fluctuations and, thus, established an infant animal ECMO model in order to discuss this hypothesis. Five piglets were cannulated using the jugular and femoral veins (VV group) and five using the jugular vein and carotid artery (VA group). All animals were subjected to hypoxic ventilation (FiO2 8%) for 10 min, leading to a PaO2 of < 40 mmHg, and subsequently rescued by ECMO. The heart rate (HR) and mean arterial blood pressure (MAP) were recorded at 5-min intervals; the arterial blood lactate was measured prior to and after 5 and 10 min of hypoxia, as well as 30, 60 and 120 min after initiation of ECMO. The response to initiation of ECMO was similar in the VV and VA groups with regard to HR and lactate, but differed significantly in MAP. HR decreased significantly from 135 +/- 7 to 103 +/- 6 beats/min (p < 0.05) and from 132 +/- 8 to 84 +/- 9 beats/min (p < 0.01) at 5 min (p = NS) after installation; lactate increased from 1.4 +/- 0.1 to 1.8 +/- 0.2 mmol/l (p = NS) and from 1.4 +/- 0.2 to 1.6 +/- 0.5 mmol/l (p = NS) after 30 min (p = NS); MAP decreased from 80 +/- 5 to 63 +/- 3 mmHg (p = NS) and increased from 75 +/- 4 to 84 +/- 3 mmHg (p = NS) at 5 min (p = 0.001), respectively. The initiation of ECMO is associated with haemodynamic fluctuations in both modalities, which differ with regard to blood pressure reaction.

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