title: Pumpless extracorporeal CO(2) removal restores normocapnia and is associated with less regional perfusion in experimental acute lung injury.
abstract: 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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, University of Bonn, Bonn, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Kreyer
authors.forename: T
authors.initials: T
authors.lastname: Muders
authors.forename: H
authors.initials: H
authors.lastname: Luepschen
authors.forename: C
authors.initials: C
authors.lastname: Kricklies
authors.forename: K
authors.initials: K
authors.lastname: Linden
authors.forename: R
authors.initials: R
authors.lastname: Tolba
authors.forename: D
authors.initials: D
authors.lastname: Varelmann
authors.forename: J
authors.initials: J
authors.lastname: Zinserling
authors.forename: C
authors.initials: C
authors.lastname: Putensen
authors.forename: H
authors.initials: H
authors.lastname: Wrigge
mesh_terms: D000138:Acidosis / Q000097:blood; D055371:Acute Lung Injury / Q000097:blood*; D000311:Adrenal Glands / Q000098:blood supply; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood*; D002302:Cardiac Output / Q000502:physiology; D008863:Microspheres; D008969:Molecular Sequence Data; D011175:Positive-Pressure Respiration; D011652:Pulmonary Circulation / Q000502:physiology; D012039:Regional Blood Flow; D012121:Respiration, Artificial; D013152:Splanchnic Circulation / Q000502:physiology; D013552:Swine
chemical_list: D002245:Carbon Dioxide