• Brian D Kubiak, Scott P Albert, Louis A Gatto, Girish Trikha, Ola El-Zammar, and Gary F Nieman.
• Department of Surgery, Upstate Medical University, Syracuse, New York 13210, USA. kubiakb@upstate.edu
• J. Surg. Res. 2010 Aug 1; 162 (2): 250-7.

BackgroundPatients with acute respiratory distress syndrome (ARDS) are often ventilated with high airway pressure. Brief loss of airway pressure may lead to an extended loss of oxygenation. While using high frequency oscillatory ventilation (HFOV) in a porcine acute lung injury model, two animals became disconnected from the ventilator with subsequent loss of airway pressure. We compared the two disconnected animals to the two animals that remained connected to determine causes for the extended reduction in oxygenation.MethodsARDS was induced using 5% Tween. Thirty min of nonprotective ventilation (NPV) followed before placing the pigs on HFOV. Measurements were made at baseline, after lung injury, and every 30min during the 6-h study. Disconnections were treated by hand-ventilation and a recruitment maneuver before being placed back on HFOV. The lungs were histologically analyzed and wet/dry weights were measured to determine lung edema.ResultsHemodynamics and lung function were similar in all pigs at baseline, after injury, and following NPV. The animals that remained connected to the oscillator showed a continued improvement in PaO(2)/FiO(2) (P/F) ratio throughout the study. The animals that experienced the disconnection had a significant loss of lung function that never recovered. The disconnect animals had more diffuse alveolar disease on histologic analysis.ConclusionsA significant fall in lung function results following disconnection from HFOV, which remains depressed for a substantial period of time despite efforts to reopen the lung. Dispersion of edema fluid is a possible mechanism for the protracted loss of lung function.Copyright 2010 Elsevier Inc. All rights reserved.

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