title: Mechanical ventilation with lower tidal volumes and positive end-expiratory pressure prevents alveolar coagulation in patients without lung injury.
abstract: BACKGROUND
  Alveolar fibrin deposition is a hallmark of acute lung injury, resulting from activation of coagulation and inhibition of fibrinolysis. Previous studies have shown that mechanical ventilation with high tidal volumes may aggravate lung injury in patients with sepsis and acute lung injury. The authors sought to determine the effects of mechanical ventilation on the alveolar hemostatic balance in patients without preexistent lung injury.
  
  
  METHODS
  Patients scheduled for an elective surgical procedure (lasting > or = 5 h) were randomly assigned to mechanical ventilation with either higher tidal volumes of 12 ml/kg ideal body weight and no positive end-expiratory pressure (PEEP) or lower tidal volumes of 6 ml/kg and 10 cm H2O PEEP. After induction of anesthesia and 5 h later bronchoalveolar lavage fluid and blood samples were obtained, and markers of coagulation and fibrinolysis were measured.
  
  
  RESULTS
  In contrast to mechanical ventilation with lower tidal volumes and PEEP (n = 21), the use of higher tidal volumes without PEEP (n = 19) caused activation of bronchoalveolar coagulation, as reflected by a marked increase in thrombin-antithrombin complexes, soluble tissue factor, and factor VIIa after 5 h of mechanical ventilation. Mechanical ventilation with higher tidal volumes without PEEP caused an increase in soluble thrombomodulin in lavage fluids and lower levels of bronchoalveolar activated protein C in comparison with lower tidal volumes and PEEP. Bronchoalveolar fibrinolytic activity did not change by either ventilation strategy.
  
  
  CONCLUSIONS
  Mechanical ventilation with higher tidal volumes and no PEEP promotes procoagulant changes, which are largely prevented by the use of lower tidal volumes and PEEP.
authors.affiliation: Dept. of Intensive Care Medicine, Center for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. godachoi@mail.com
authors.forename: Goda
authors.initials: G
authors.lastname: Choi
authors.forename: Esther K
authors.initials: EK
authors.lastname: Wolthuis
authors.forename: Paul
authors.initials: P
authors.lastname: Bresser
authors.forename: Marcel
authors.initials: M
authors.lastname: Levi
authors.forename: Tom
authors.initials: T
authors.lastname: van der Poll
authors.forename: Misa
authors.initials: M
authors.lastname: Dzoljic
authors.forename: Margreeth B
authors.initials: MB
authors.lastname: Vroom
authors.forename: Marcus J
authors.initials: MJ
authors.lastname: Schultz
mesh_terms: D000368:Aged; D000768:Anesthesia, General; D000991:Antithrombins / Q000378:metabolism; D001778:Blood Coagulation Disorders / Q000150:complications*; D001992:Bronchoalveolar Lavage Fluid; D002985:Clinical Protocols; D005260:Female; D005342:Fibrinolysis / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010960:Plasminogen Activators / Q000378:metabolism; D011175:Positive-Pressure Respiration; D011650:Pulmonary Alveoli / Q000098:blood supply / Q000502:physiology*; D011652:Pulmonary Circulation / Q000502:physiology; D012121:Respiration, Artificial; D013514:Surgical Procedures, Operative; D013917:Thrombin / Q000378:metabolism; D013990:Tidal Volume / Q000502:physiology*
chemical_list: D000991:Antithrombins; D010960:Plasminogen Activators; D013917:Thrombin