title: Influence of tidal volume on pulse pressure variations in hypovolemic ventilated pigs with acute respiratory distress-like syndrome.
abstract: BACKGROUND
  Sensitivity and specificity of respiratory change in pulse pressure (DeltaPP) to predict preload dependency has been questioned at small tidal volumes (VT) in critically ill patients suffering from acute respiratory distress syndrome (ARDS). We studied DeltaPP in pigs with ARDS-like syndrome during reversible hemorrhagic shock.
  
  
  METHODS
  Prospective, observational animal study in a Laboratory Investigation Unit. Sixteen deeply sedated mechanically ventilated pigs were successively ventilated with VT of 10 ml/kg at a respiratory rate of 15 breaths/min (RR15) and VT of 6 ml/kg at RR15 and RR25. ARDS-like syndrome was produced by lung lavage in eight pigs (ARDS group). Severe hemorrhagic shock was induced by removal of 40% of total blood volume followed by restoration.
  
  
  RESULTS
  After bleeding, in the control group ventilated with a VT of 10 ml/kg, DeltaPP increased from 8.5 (95% confidence interval [CI], 7.1 to 9.9%) to 18.5% (CI, 15.3 to 21.7%; P<0.05). In the ARDS group, this index increased similarly, from 7.1% (95% CI, 5.3 to 9.0%) to 20.1% (CI, 15.3 to 24.9%; P<0.05). In control lungs, reduction in VT from 10 to 6 ml/kg reduced the DeltaPP reaction by 40%, although it remained a statistically valid indicator of hypovolemia regardless of the RR value. In contrast, in the ARDS group, DeltaPP was an unreliable hypovolemia marker at low VT ventilation, regardless of the RR value (p=not statistically significant).
  
  
  CONCLUSIONS
  The present study suggests that DeltaPP is a reliable indicator of severe hypovolemia in pigs with healthy lungs regardless of VT or RR. In contrast, in pigs with ARDS-like syndrome ventilated with small VT, DeltaPP is not a good indicator of severe hemorrhage. However, in this setting, indexing DeltaPP to respiratory changes in transpulmonary pressure allows this marker to significantly indicate the occurrence of hypovolemia.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
authors.forename: Claes U
authors.initials: CU
authors.lastname: Wiklund
authors.forename: Denis R
authors.initials: DR
authors.lastname: Morel
authors.forename: Hélène
authors.initials: H
authors.lastname: Orbring-Wiklund
authors.forename: Jacques-Andre
authors.initials: JA
authors.lastname: Romand
authors.forename: Vincent
authors.initials: V
authors.lastname: Piriou
authors.forename: Jean-Louis
authors.initials: JL
authors.lastname: Teboul
authors.forename: Karim
authors.initials: K
authors.lastname: Bendjelid
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D020896:Hypovolemia / Q000503:physiopathology*; D012121:Respiration, Artificial / Q000379:methods; D012128:Respiratory Distress Syndrome / Q000503:physiopathology* / Q000628:therapy*; D012680:Sensitivity and Specificity; D034421:Sus scrofa; D013990:Tidal Volume / Q000502:physiology*