title: Hemodynamic and respiratory changes during lung recruitment and descending optimal positive end-expiratory pressure titration in patients with acute respiratory distress syndrome.
abstract: OBJECTIVE
  To investigate respiratory and hemodynamic changes during lung recruitment and descending optimal positive end-expiratory pressure (PEEP) titration.
  
  
  METHODS
  Prospective auto-control clinical trial.
  
  
  METHODS
  Adult general intensive care unit in a university hospital.
  
  
  METHODS
  Eighteen patients with acute respiratory distress syndrome.
  
  
  METHODS
  Following baseline measurements (T0), PEEP was set at 26 cm H2O and lung recruitment was performed (40/40-maneuver). Then tidal volume was set at 4 mL/kg (T26R) and PEEP was lowered by 2 cm H2O in every 4 mins. Optimal PEEP was defined at 2 cm H2O above the PEEP where Pao2 dropped by > 10%. After setting the optimal PEEP, the 40/40-maneuver was repeated and tidal volume set at 6 mL/kg (T(end)).
  
  
  RESULTS
  Arterial blood gas analysis was done every 4 mins and hemodynamic measurements every 8 mins until T(end), then in 30 (T30) and 60 (T60) mins. The Pao2 increased from T0 to T(end) (203 +/- 108 vs. 322 +/- 101 mm Hg, p < .001), but the extravascular lung water (EVLW) did not change significantly. Cardiac index (CI) and the intrathoracic blood volume (ITBV) decreased from T0 to T26R (CI, 3.90 +/- 1.04 vs. 3.62 +/- 0.91 L/min/m2, p < .05; ITBVI, 832 +/- 205 vs. 795 +/- 188 m/m2, p < .05). There was a positive correlation between CI and ITBVI (r = .699, p < .01), a negative correlation between CI and central venous pressure (r = -.294, p < .01), and no correlation between CI and mean arterial pressure (MAP).
  
  
  CONCLUSIONS
  Following lung recruitment and descending optimal PEEP titration, the Pao2 improves significantly, without any change in the EVLW up to 1 hr. This suggests a decrease in atelectasis as a result of recruitment rather than a reduction of EVLW. There is a significant change in CI during the maneuver, but neither central venous pressure, heart rate, nor MAP can reflect these changes.
authors.affiliation: Department of Anaesthesia and Intensive Therapy, University of Pécs, Hungary.
authors.forename: Ildiko
authors.initials: I
authors.lastname: Toth
authors.forename: Tamas
authors.initials: T
authors.lastname: Leiner
authors.forename: Andras
authors.initials: A
authors.lastname: Mikor
authors.forename: Tamas
authors.initials: T
authors.lastname: Szakmany
authors.forename: Lajos
authors.initials: L
authors.lastname: Bogar
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Molnar
mesh_terms: D000328:Adult; D000368:Aged; D000399:Air Pressure; D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology*; D002496:Central Venous Pressure / Q000502:physiology; D015633:Extravascular Lung Water / Q000502:physiology; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006785:Hospitals, University; D006801:Humans; D008168:Lung / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood*; D011175:Positive-Pressure Respiration / Q000379:methods*; D011650:Pulmonary Alveoli / Q000503:physiopathology; D001261:Pulmonary Atelectasis / Q000503:physiopathology / Q000628:therapy; D012123:Pulmonary Ventilation / Q000502:physiology*; D012128:Respiratory Distress Syndrome / Q000503:physiopathology* / Q000628:therapy; D013318:Stroke Volume / Q000502:physiology*; D013990:Tidal Volume / Q000502:physiology*
chemical_list: D010100:Oxygen