Quantification of potential for lung recruitment may guide the ventilatory strategy in acute respiratory distress syndrome. However, there are no quantitative data on recruitability in patients with severe acute respiratory distress syndrome who require extracorporeal membrane oxygenation. We sought to quantify potential for lung recruitment and its relationship with outcomes in this cohort of patients.
A single-center, retrospective, observational cohort study.
Tertiary referral severe respiratory failure center in a university hospital in the United Kingdom.
Forty-seven adults with severe acute respiratory distress syndrome requiring extracorporeal membrane oxygenation.
In patients with severe acute respiratory distress syndrome—mainly of pulmonary origin (86%)—the potential for lung recruitment and the weight of nonaerated, poorly aerated, normally aerated, and hyperaerated lung tissue were assessed at low (5 cmH2O) and high (45 cmH2O) airway pressures. Patients were categorized as high or low potential for lung recruitment based on the median potential for lung recruitment value of the study population. The median potential for lung recruitment was 24.3% (interquartile range = 11.4–37%) ranging from –2% to 76.3% of the total lung weight. Patients with potential for lung recruitment above the median had significantly shorter extracorporeal membrane oxygenation duration (8 vs 13 d; p = 0.013) and shorter ICU stay (15 vs 22 d; p = 0.028), but mortality was not statistically different (24% vs 46%; p = 0.159).
We observed significant variability in potential for lung recruitment in patients with severe acute respiratory distress syndrome requiring extracorporeal membrane oxygenation. Patients with high potential for lung recruitment had a shorter ICU stay and shorter extracorporeal membrane oxygenation duration.
1Department of Adult Critical Care, Guy’s and St Thomas’ NHS Foundation Trust, King’s Health Partners, London, UK.
2Division of Centre of Human Applied Physiological Sciences, King’s College London, London, UK.
3Department of Emergency and Organ Transplants (DETO), Anesthesiology and Intensive Care, Università degli Studi di Bari “Aldo Moro”, Bari, Italy.
4Department of Biomedical Sciences and Human Oncology, Chair of Medical Statistics, Università degli Studi Aldo Moro, Bari, Italy.
5Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain.
6Centro de investigación biomédica en Red-Enfermedades Respiratorias, Instituto de Salud Carlos III, Madrid, Spain.
7Cardiac Critical Care Unit, University Central Hospital of Asturias, Oviedo, Spain.
8Department of Functional Biology, University of Oviedo, Oviedo, Spain.
9Peter Gorer Department of Immunobiology, School of Immunology & Microbial Sciences, King’s College, London, UK.
Drs. Camporota, Caricola, Bartolomeo, and Grasso contributed to the full access to all the data in the study and responsibility for the integrity of the data. Drs. Camporota, Caricola, Bartolomeo, Shankar-Hari, and Grasso contributed to the access to database, data analysis, and interpretation. Drs. Camporota and Grasso contributed to the study concept and design. Drs. Camporota, Caricola, and Grasso contributed to the responsibility for data acquisition. Drs. Camporota, Amado-Rodriguez, Vasques, and Grasso contributed to the article preparation and drafting. Drs. Camporota, Caricola, Di Mussi, Wyncoll, Meadows, Amado-Rodriguez, Vasques, Sanderson, Glover, Barrett, and Grasso critically revised the article for important intellectual content. Drs. Camporota and Barrett contributed to the statistical analysis
Dr. Wyncoll received funding for paid talks from Pfizer, MSD, and Fisher and Paykel. Dr. Grasso’s institution received funding from Orion Pharma, Italy, and he received funding from Maquet, Italy. The remaining authors have not disclosed any potential conflicts of interest.
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