Global lung stress varies considerably with low tidal volume ventilation for acute respiratory distress syndrome. High stress despite low tidal volumes may worsen lung injury and increase risk of death. No widely available parameter exists to assess global lung stress. We aimed to determine whether the volume delivered during a recruitment maneuver (VRM) is inversely associated with lung stress and mortality in acute respiratory distress syndrome.
Substudy of an acute respiratory distress syndrome clinical trial on esophageal pressure-guided positive end-expiratory pressure titration.
U.S. academic medical center.
Forty-two patients with acute respiratory distress syndrome in whom airflow, airway pressure, and esophageal pressure were recorded during the recruitment maneuver.
A single recruitment maneuver was performed before initiating protocol-directed ventilator management. Recruitment maneuvers consisted of a 30-second breath hold at 40 cm H2O airway pressure under heavy sedation or paralysis. VRM was calculated by integrating the flow-time waveform during the maneuver. End-inspiratory stress was defined as the transpulmonary (airway minus esophageal) pressure during end-inspiratory pause of a tidal breath and tidal stress as the transpulmonary pressure difference between end-inspiratory and end-expiratory pauses.
VRM ranged between 7.4 and 34.7 mL/kg predicted body weight. Lower VRM predicted high end-inspiratory and tidal lung stress (end-inspiratory: β = –0.449; 95% CI, –0.664 to –0.234; p < 0.001; tidal: β = –0.267; 95% CI, –0.423 to –0.111; p = 0.001). After adjusting for PaO2/FIO2 and either driving pressure, tidal volume, or plateau pressure and positive end-expiratory pressure, VRM remained independently associated with both end-inspiratory and tidal stress. In unadjusted analysis, low VRM predicted increased risk of death (odds ratio, 0.85; 95% CI, 0.72–1.00; p = 0.026). VRM remained significantly associated with mortality after adjusting for study arm (odds ratio, 0.84; 95% CI, 0.71–1.00; p = 0.022).
Low VRM independently predicts high lung stress and may predict risk of death in patients with acute respiratory distress syndrome.
1Division of Pulmonary and Critical Care Medicine, University of California, San Diego, San Diego, CA.
2School of Medicine, University of California, San Diego, San Diego, CA.
3Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN.
4Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Boston, MA.
5Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, MA.
*See also p. 244.
Drs. Beitler and Hubmayr conceived the study. Drs. Beitler, Hubmayr, Malhotra, Loring, and Talmor designed the study. Drs. Beitler, Malhotra, Loring, and Talmor contributed the primary data. Dr. Beitler, Mr. Majumdar, and Dr. Loring performed the primary data analysis. All authors contributed to the interpretation of results. Dr. Beitler prepared the first draft of the article, and all authors revised the draft critically for important intellectual content. All authors gave approval of the final article submitted for publication.
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Supported, in part, by a grant R01-HL052586 from the National Heart, Lung, and Blood Institute.
Dr. Hubmayr served as a board member for the American Thoracic Society, consulted for Philips Research NA, and received grant support from the National Heart, Lung, and Blood Institute (NHLBI) (RO1 116826). Dr. Malhotra received support for article research from the National Institutes of Health (NIH) (k24). Dr. Thompson served as a board member on Data Monitoring Boards for Roche Genentec, Ferring Labs, Bristol Myers Squibb, and the NHLBI, and he received support for article research from the NIH. He and his institution consulted (one time consulting) for GlaxoSmithKline and Ra Pharmaceuticals on acute respiratory distress syndrome (ARDS) trial design. His institution received grant support from the NHLBI (funding for the conduct of ARDS prevention trials and for the use of carbon monoxide and mesenchymal stem cells for the treatment of ARDS). Dr. Owens consulted for Philips Respironics (prior, < $5,000). He and his institution received grant support from the NIH/NHLBI (K23 Award). Dr. Loring received support for article research from the NIH. He and his institution received grant support from the NIH. Dr. Talmor received grant support from the NHLBI (RO1 HL52586, UM1 HL108724) and received support for article research from the NIH. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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