PMID- 23603884 OWN - NLM STAT- MEDLINE DCOM- 20140203 LR - 20130610 IS - 1537-1921 (Electronic) IS - 0898-4921 (Linking) VI - 25 IP - 3 DP - 2013 Jul TI - The effect of pumpless extracorporeal CO2 removal on regional perfusion of the brain in experimental acute lung injury. PG - 324-9 LID - 10.1097/ANA.0b013e3182905e6a [doi] AB - BACKGROUND: Lung-protective mechanical ventilation with low tidal volumes (V(T)) is often associated with hypercapnia (HC), which may be unacceptable in patients with brain injury. CO2 removal using a percutaneous extracorporeal lung assist (pECLA) enables normocapnia despite low V(T), but its effects on regional cerebral blood flow (rCBF) remain ambiguous. We hypothesized that reversal of HC by pECLA impairs rCBF in a porcine lung injury model. METHODS: Lung injury was induced in 9 anesthetized pigs by hydrochloric acid aspiration. rCBF and systemic hemodynamics were measured by colored microsphere technique and transpulmonary-thermodilution during a randomized sequence of 4 experimental situations: pECLA shunt-on (1) with HC and (2) without HC, pECLA shunt-off (3) with HC and (4) without HC. RESULTS: HC increased rCBF (P<0.05). CO2 removal with pECLA resulting in normocapnia, decreased rCBF to levels comparable to those without pECLA and normocapnia. HC resulted in increased cardiac output (+25.5%). Cardiac output was highest during HC with pECLA shunt (+44.9%). During pECLA with CO2 removal, cardiac output (+38.1%) decreased compared with pECLA without CO2 removal, but stayed higher than during normocapnia/no pECLA shunt (P<0.05). CONCLUSIONS: In this animal model, mechanical ventilation with low V(T) was associated with HC and increased rCBF. CO2 removal by pECLA restored normocapnia, reduced rCBF to levels of normocapnia, but required a higher systemic blood flow for the perfusion of the pECLA device. If these results could be transferred to patients, extracorporeal CO2 removal might be an option for treatment of combined lung and brain injury in condition of a sufficient cardiac flow reserve. FAU - Kreyer, Stefan AU - Kreyer S AD - Department of Anesthesiology and Intensive Care Medicine, University Hospital Bonn, Bonn, Germany. stefan.kreyer@uni-bonn.de FAU - Muders, Thomas AU - Muders T FAU - Luepschen, Henning AU - Luepschen H FAU - Kricklies, Corinna AU - Kricklies C FAU - Linden, Katharina AU - Linden K FAU - Soehle, Martin AU - Soehle M FAU - Zinserling, Joerg AU - Zinserling J FAU - Putensen, Christian AU - Putensen C FAU - Wrigge, Hermann AU - Wrigge H LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - J Neurosurg Anesthesiol JT - Journal of neurosurgical anesthesiology JID - 8910749 RN - 142M471B3J (Carbon Dioxide) RN - QTT17582CB (Hydrochloric Acid) SB - IM MH - Acidosis/physiopathology MH - Acute Lung Injury/chemically induced/*physiopathology MH - Animals MH - Blood Gas Analysis MH - Carbon Dioxide/*analysis MH - Cardiac Output/physiology MH - Cerebrovascular Circulation/*physiology MH - Extracorporeal Membrane Oxygenation/*adverse effects MH - Hemodynamics/physiology MH - Hydrochloric Acid MH - Hydrogen-Ion Concentration MH - Hypercapnia/etiology/*physiopathology MH - Microspheres MH - Respiratory Mechanics/physiology MH - Swine EDAT- 2013/04/23 06:00 MHDA- 2014/02/04 06:00 CRDT- 2013/04/23 06:00 PHST- 2013/04/23 06:00 [entrez] PHST- 2013/04/23 06:00 [pubmed] PHST- 2014/02/04 06:00 [medline] AID - 10.1097/ANA.0b013e3182905e6a [doi] PST - ppublish SO - J Neurosurg Anesthesiol. 2013 Jul;25(3):324-9. doi: 10.1097/ANA.0b013e3182905e6a.