• Domenico Luca Grieco, Gian Marco Anzellotti, Andrea Russo, Filippo Bongiovanni, Barbara Costantini, Marco D'Indinosante, Francesco Varone, Fabio Cavallaro, Lucia Tortorella, Lorenzo Polidori, Bruno Romanò, Valerio Gallotta, Antonio Maria Dell'Anna, Liliana Sollazzi, Giovanni Scambia, Giorgio Conti, and Massimo Antonelli.
• From the Department of Anesthesiology and Intensive Care Medicine, Catholic University of The Sacred Heart (D.L.G., G.M.A., A.R., F.B., F.C., L.P., B.R., A.M.D., L.S., G.C., M.A.) Anesthesia, Emergency and Intensive Care Medicine, Fondazione Policlinico Universitario A. Gemelli IRCCS (D.L.G., G.M.A., A.R., F.B., F.C., L.P., B.R., A.M.D., L.S., G.C., M.A.) Department of Obstetrics and Gynecology, Catholic University of The Sacred Heart (B.C., M.D., L.T., V.G., G.S.) Gynecologic Oncology, Fondazione Policlinico Universitario A. Gemelli IRCCS (B.C., M.D., L.T., V.G., G.S.) Department of Internal Medicine, Catholic University of The Sacred Heart (F.V.) Respiratory Medicine, Fondazione Policlinico Universitario A. Gemelli IRCCS (F.V.), Rome, Italy.
• Anesthesiology. 2019 Jul 1; 131 (1): 58-73.

BackgroundAirway closure causes lack of communication between proximal airways and alveoli, making tidal inflation start only after a critical airway opening pressure is overcome. The authors conducted a matched cohort study to report the existence of this phenomenon among obese patients undergoing general anesthesia.MethodsWithin the procedures of a clinical trial during gynecological surgery, obese patients underwent respiratory/lung mechanics and lung volume assessment both before and after pneumoperitoneum, in the supine and Trendelenburg positions, respectively. Among patients included in this study, those exhibiting airway closure were compared to a control group of subjects enrolled in the same trial and matched in 1:1 ratio according to body mass index.ResultsEleven of 50 patients (22%) showed airway closure after intubation, with a median (interquartile range) airway opening pressure of 9 cm H2O (6 to 12). With pneumoperitoneum, airway opening pressure increased up to 21 cm H2O (19 to 28) and end-expiratory lung volume remained unchanged (1,294 ml [1,154 to 1,363] vs. 1,160 ml [1,118 to 1,256], P = 0.155), because end-expiratory alveolar pressure increased consistently with airway opening pressure and counterbalanced pneumoperitoneum-induced increases in end-expiratory esophageal pressure (16 cm H2O [15 to 19] vs. 27 cm H2O [23 to 30], P = 0.005). Conversely, matched control subjects experienced a statistically significant greater reduction in end-expiratory lung volume due to pneumoperitoneum (1,113 ml [1,040 to 1,577] vs. 1,000 ml [821 to 1,061], P = 0.006). With airway closure, static/dynamic mechanics failed to measure actual lung/respiratory mechanics. When patients with airway closure underwent pressure-controlled ventilation, no tidal volume was inflated until inspiratory pressure overcame airway opening pressure.ConclusionsIn obese patients, complete airway closure is frequent during anesthesia and is worsened by Trendelenburg pneumoperitoneum, which increases airway opening pressure and alveolar pressure: besides preventing alveolar derecruitment, this yields misinterpretation of respiratory mechanics and generates a pressure threshold to inflate the lung that can reach high values, spreading concerns on the safety of pressure-controlled modes in this setting.

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