To adapt an animal model of acute lung injury for use as a standard protocol for a screening initial evaluation of limited function, or “surge,” ventilators for use in mass casualty scenarios.
Prospective, experimental animal study.
University research laboratory.
Twelve adult pigs.
Twelve spontaneously breathing pigs (six in each group) were subjected to acute lung injury/acute respiratory distress syndrome via pulmonary artery infusion of oleic acid. After development of respiratory failure, animals were mechanically ventilated with a limited-function ventilator (simplified automatic ventilator [SAVe] I or II; Automedx, Germantown, MD) for 1 hr or until the ventilator could not support the animal. The limited-function ventilator was then exchanged for a full-function ventilator (Servo 900C; Siemens-Elema, Solna, Sweden).
Reliable and reproducible levels of acute lung injury/acute respiratory distress syndrome were induced. The SAVe I was unable to adequately oxygenate five animals with Pao2 (52.0 ± 11.1 torr) compared to the Servo (106.0 ± 25.6 torr; p = .002). The SAVe II was able to oxygenate and ventilate all six animals for 1 hr with no difference in Pao2 (141.8 ± 169.3 torr) compared to the Servo (158.3 ± 167.7 torr).
We describe a novel in vivo model of acute lung injury/acute respiratory distress syndrome that can be used to initially screen limited-function ventilators considered for mass respiratory failure stockpiles and that is intended to be combined with additional studies to definitively assess appropriateness for mass respiratory failure. Specifically, during this study we demonstrate that the SAVe I ventilator is unable to provide sufficient gas exchange, whereas the SAVe II, with several more functions, was able to support the same level of hypoxemic respiratory failure secondary to acute lung injury/acute respiratory distress syndrome for 1 hr.
From the Division of Pulmonary & Critical Care Medicine (RPD, DLH, WJEL, DJP, RWG, LR), School of Medicine, University of Washington, Seattle, WA; Division of Pulmonary, Critical Care & Sleep Medicine (DLH), The Oregon Clinic, Seattle, WA; Respiratory Care Department (CH, DJP, LR), Harborview Medical Center, Seattle, WA; Department of Physiology & Biophysics (RWG), University of Washington, Seattle, WA; and National Disaster Medical System (LR), Office of Preparedness and Emergency Operations, Office of the Assistant Secretary for Preparedness and Response, U.S. Department of Health and Human Services, Washington, DC.
Supported, in part, by the National Institute of Health grant HL07287 and Defense Department DARPA DSO Defense Sciences Research and Technology grant 07-21-Open-BAA-WP-151.
Dr. Rubinson performed this work as an employee of the University of Washington prior to joining the Office of the Assistant Secretary for Preparedness and Response, U.S. Department of Health and Human Services.
Dr. Hotchkin received funding from NIH. The remaining authors have not disclosed any potential conflicts of interest.
The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Department of Health and Human Services or its components.
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