title: Ventilation-perfusion distributions in different porcine lung injury models.
abstract: BACKGROUND
  Acute lung injury is characterized by hypoxemia which may be caused by hypoventilation, ventilation-perfusion (V(A)/Q) mismatch, intrapulmonary shunting and oxygen diffusion impairment. The multiple inert gas elimination technique (MIGET) allows analysis of these four causes of hypoxemia and is therefore the most comprehensive approach to investigate blood gas abnormalities. Using MIGET, we studied whether specific patterns of gas exchange abnormalities occur in different lung injury models and whether gas exchange abnormalities can be related to pathogenic aspects of lung injury.
  
  
  METHODS
  Lung injury was induced with oleic acid injection, endotoxin infusion or repeated lung lavage in groups of 6 mechanically ventilated pigs.
  
  
  RESULTS
  PaO2 decreased and PaCO2 increased significantly in all three lung injury models, but gas exchange was more impaired in the oleic acid and lavage, as compared to the endotoxin group. Shunt was the major cause of hypoxemia in our lung injury models, whereas V(A)/Q mismatch contributed to venous admixture only after oleic acid injection and lung lavage. Oxygen diffusion limitation was not observed. Although alveolar ventilation was maintained after induction of lung injury, hypercapnia developed due to an increase of the ventilatory mean towards higher V(A)/Q ratios, increased shunt and increased carbon dioxide production.
  
  
  CONCLUSIONS
  Shunt and ventilation-perfusion mismatch fully explain the gas exchange disturbances observed in our lung injury models. Although V(A)/Q distributions can be related to pathogenic aspects of the three study groups, we did not observe specific V(A)/Q patterns which allow diagnosis of the type of lung injury from a recovered V(A)/Q distribution.
authors.affiliation: Department of Clinical Physiology, University of Uppsala, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Neumann
authors.forename: G
authors.initials: G
authors.lastname: Hedenstierna
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004731:Endotoxins / Q000633:toxicity; D015633:Extravascular Lung Water / Q000187:drug effects / Q000378:metabolism; D006439:Hemodynamics / Q000187:drug effects; D008171:Lung Diseases / Q000139:chemically induced / Q000503:physiopathology*; D019301:Oleic Acid / Q000633:toxicity; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology; D011659:Pulmonary Gas Exchange / Q000187:drug effects; D012121:Respiration, Artificial; D015656:Respiratory Mechanics / Q000187:drug effects / Q000502:physiology; D013552:Swine; D007507:Therapeutic Irrigation; D014692:Ventilation-Perfusion Ratio / Q000502:physiology*
chemical_list: D004731:Endotoxins; D019301:Oleic Acid; C044101:endotoxin, Escherichia coli