title: Pumpless extracorporeal lung assist for protective mechanical ventilation in experimental lung injury.
abstract: OBJECTIVE
  To test the hypothesis that ventilation with 3 mL/kg tidal volume combined with extracorporeal CO2 removal by arteriovenous interventional lung assist reduces ventilator-associated organ injury in experimental acute lung injury when compared with ventilation with 6 mL/kg tidal volume without interventional lung assist.
  
  
  METHODS
  Prospective, randomized, controlled trial.
  
  
  METHODS
  A university research laboratory.
  
  
  METHODS
  A total of 14 pigs weighing 46 +/- 4 kg (mean +/- sd).
  
  
  METHODS
  Acute lung injury was induced by repeated lung lavages until Pao2 was <100 mm Hg, with Fio2 of 1.0 and positive end-expiratory pressure of 5 cm H2O, for 1 hr without additional lavages. Animals were randomized to an interventional group with a tidal volume of 3 mL/kg with interventional lung assist (n = 7) or to a control group with a tidal volume of 6 mL/kg without interventional lung assist (n = 7) for 24 hrs. Organ function in vivo was determined by laboratory analyses, including calculations of pulmonary ventilation/perfusion distribution. Histologic assessment of organ injury was performed post mortem after 24 hrs.
  
  
  RESULTS
  In both groups, gas exchange improved in the course of the study (p < .05). However, in contrast to control animals, animals with lower tidal volumes and interventional lung assist had severe ventilation/perfusion mismatch, as indicated by increased perfusion to lung areas with a low ventilation/perfusion ratio (p < .05). Other variables of organ function in vivo and results of histologic examination post mortem did not reveal any statistical difference between groups.
  
  
  CONCLUSIONS
  Combined ventilation with lower tidal volumes and extracorporeal CO2 removal as compared with traditional low tidal volumes without extracorporeal CO2 removal is not associated with differences in organ injury. Obviously, ventilation with tidal volumes of <6 mL/kg may cause pulmonary de-recruitment when positive end-expiratory pressure is not adequately increased.
authors.affiliation: Department of Surgical Intensive Care Medicine, and Institute of Pharmacology and Toxicology, University Aachen, Aachen, Germany. rolf.dembinski@post.rwth-aachen.de
authors.forename: Rolf
authors.initials: R
authors.lastname: Dembinski
authors.forename: Nadine
authors.initials: N
authors.lastname: Hochhausen
authors.forename: Sandra
authors.initials: S
authors.lastname: Terbeck
authors.forename: Stefan
authors.initials: S
authors.lastname: Uhlig
authors.forename: Constanze
authors.initials: C
authors.lastname: Dassow
authors.forename: Monika
authors.initials: M
authors.lastname: Schneider
authors.forename: Akexander
authors.initials: A
authors.lastname: Schachtrupp
authors.forename: Dietrich
authors.initials: D
authors.lastname: Henzler
authors.forename: Rolf
authors.initials: R
authors.lastname: Rossaint
authors.forename: Ralf
authors.initials: R
authors.lastname: Kuhlen
mesh_terms: D000818:Animals; D012121:Respiration, Artificial; D012128:Respiratory Distress Syndrome / Q000628:therapy*; D013552:Swine