Ventilator settings for patients with severe acute respiratory distress syndrome supported by venovenous extracorporeal membrane oxygenation are currently set arbitrarily. The impact on serum and pulmonary biotrauma markers of the transition to ultra-protective ventilation settings following extracorporeal membrane oxygenation implantation, and different mechanical ventilation strategies while on extracorporeal membrane oxygenation were investigated.
Randomized clinical trial.
Nine-month monocentric study.
Severe acute respiratory distress syndrome patients on venovenous extracorporeal membrane oxygenation.
After starting extracorporeal membrane oxygenation, patients were switched to the bi-level positive airway pressure mode with 1 second of 24 cm H2O high pressure and 2 seconds of 12 cm H2O low pressure for 24 hours. A computer-generated allocation sequence randomized patients to receive each of the following three experimental steps: 1) high pressure 24 cm H2O and low pressure 20 cm H2O (very high positive end-expiratory pressure–very low driving pressure); 2) high pressure 24 cm H2O and low pressure 5 cm H2O (low positive end-expiratory pressure–high driving pressure); and 3) high pressure 17 cm H2O and low pressure 5 cm H2O (low positive end-expiratory pressure–low driving pressure). Plasma and bronchoalveolar lavage soluble receptor for advanced glycation end-products, plasma interleukin-6, and monocyte chemotactic protein-1 were sampled preextracorporeal membrane oxygenation and after 12 hours at each step.
Sixteen patients on ECMO after 7 days (1–11 d) of mechanical ventilation were included. “Ultra-protective” mechanical ventilation settings following ECMO initiation were associated with significantly lower plasma sRAGE, interleukin-6, and monocyte chemotactic protein-1 concentrations. Plasma sRAGE and cytokines were comparable within each on-ECMO experimental step, but the lowest bronchoalveolar lavage sRAGE levels were obtained at minimal driving pressure.
ECMO allows ultra- protective ventilation, which combines significantly lower plateau pressure, tidalvolume, and driving pressure. This ventilation strategy significantly limited pulmonary biotrauma, which couldtherefore decrease ventilator-induced lung injury. However, the optimal ultra-protective ventilation strategy once ECMO is initiated remains undetermined and warrants further investigations.
1Sorbonne Université, UPMC Univ Paris 06, INSERM UMRS_1166-iCAN, Institute of Cardiometabolism and Nutrition, 75651 Paris Cedex 13, France.
2Assistance Publique–Hôpitaux de Paris, Pitié–Salpêtrière Hospital, Medical Intensive Care Unit, 75651 Paris Cedex 13, France.
3Département d’Immunologie, Assistance Publique–Hôpitaux de Paris, Pitié–Salpêtrière Hospital, 75651 Paris Cedex 13, France.
4Sorbonne Université, UPMC Univ Paris 06, CIMI, INSERM U_1135, Paris, France.
5Department of Cardiovascular and Thoracic Surgery, Assistance Publique–Hôpitaux de Paris, Pitié–Salpêtrière Hospital, 75651 Paris Cedex 13, France.
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Dr. Luyt received funding from MSD, Bayer Healthcare, Thermofischer Brahms, Carmot, and Faron. Dr. Combes received lecture fees from Getinge and Baxter. Dr. Schmidt received lectures fees from Getinge, Dräger, and Xenios. The remaining authors have disclosed that they do not have any potential conflicts of interest.
Address requests for reprints to: Matthieu Schmidt, MD, PhD, Service de Réanimation Médicale, iCAN, Institute of Cardiometabolism and Nutrition, Hôpital de la Pitié–Salpêtrière, 47, bd de l’Hôpital, 75651 Paris Cedex 13, France. E-mail: firstname.lastname@example.org