PMID- 24341694 OWN - NLM STAT- MEDLINE DCOM- 20140804 LR - 20131217 IS - 1399-6576 (Electronic) IS - 0001-5172 (Linking) VI - 58 IP - 1 DP - 2014 Jan TI - Pumpless extracorporeal CO(2) removal restores normocapnia and is associated with less regional perfusion in experimental acute lung injury. PG - 52-60 LID - 10.1111/aas.12217 [doi] AB - BACKGROUND: Lung protective ventilation may lead to hypoventilation with subsequent hypercapnic acidosis (HA). If HA cannot be tolerated or occurs despite increasing respiratory rate or buffering, extracorporeal CO2-removal using a percutaneous extracorporeal lung assist (pECLA) is an option. We hypothesised that compensation of HA using pECLA impairs regional perfusion. To test this hypothesis we determined organ blood flows in a lung-injury model with combined hypercapnic and metabolic acidosis. METHODS: After induction of lung injury using hydrochloric acid (HCl) aspiration and metabolic acidosis by intravenous HCl infusion in nine pigs, an arterial-venous pECLA device was inserted. In randomised order, four treatments were tested: pECLA shunt (1) with and (2) without HA, and clamped pECLA shunt (3) with and (4) without HA. Regional blood flows were measured with the coloured microsphere technique. RESULTS: HA resulted in higher perfusion in adrenal glands, spleen and parts of splanchnic area (P < 0.05) compared with normocapnia. During CO2-removal with pECLA, regional perfusion decreased to levels comparable with those without pECLA and normocapnia. Cardiac output (CO) increased during HA without a pECLA shunt and was highest during HA with a pECLA shunt compared with normocapnia. During CO2-removal with pECLA, this variable decreased but stayed higher than during normocapnia with clamped pECLA shunt (P < 0.05). CONCLUSION: In our lung-injury model, HA was associated with increased systemic and regional blood flow in several organs. pECLA provides effective CO2 removal, requiring a higher CO for perfusion of the pECLA device without improvement of regional organ perfusion. CI - (c) 2013 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd. FAU - Kreyer, S AU - Kreyer S AD - Department of Anesthesiology and Intensive Care Medicine, University of Bonn, Bonn, Germany. FAU - Muders, T AU - Muders T FAU - Luepschen, H AU - Luepschen H FAU - Kricklies, C AU - Kricklies C FAU - Linden, K AU - Linden K FAU - Tolba, R AU - Tolba R FAU - Varelmann, D AU - Varelmann D FAU - Zinserling, J AU - Zinserling J FAU - Putensen, C AU - Putensen C FAU - Wrigge, H AU - Wrigge H LA - eng SI - GENBANK/CD003844 PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20131107 PL - England TA - Acta Anaesthesiol Scand JT - Acta anaesthesiologica Scandinavica JID - 0370270 RN - 142M471B3J (Carbon Dioxide) SB - IM MH - Acidosis/blood MH - Acute Lung Injury/*blood MH - Adrenal Glands/blood supply MH - Animals MH - Carbon Dioxide/*blood MH - Cardiac Output/physiology MH - Microspheres MH - Molecular Sequence Data MH - Positive-Pressure Respiration MH - Pulmonary Circulation/physiology MH - Regional Blood Flow MH - Respiration, Artificial MH - Splanchnic Circulation/physiology MH - Swine EDAT- 2013/12/18 06:00 MHDA- 2014/08/05 06:00 CRDT- 2013/12/18 06:00 PHST- 2013/09/17 00:00 [accepted] PHST- 2013/12/18 06:00 [entrez] PHST- 2013/12/18 06:00 [pubmed] PHST- 2014/08/05 06:00 [medline] AID - 10.1111/aas.12217 [doi] PST - ppublish SO - Acta Anaesthesiol Scand. 2014 Jan;58(1):52-60. doi: 10.1111/aas.12217. Epub 2013 Nov 7.