The lungs of patients with ARDS are characterized by marked heterogeneity, resulting in the coexistence of collapsed and hyperinflated tissue.1Rezoagli E. Fumagalli R. Bellani G. Definition and epidemiology of acute respiratory distress syndrome.Ann Transl Med. 2017; 5: 282Crossref PubMed Scopus (84) Google Scholar Gravitational forces and chest wall geometry help govern the balance between these components.2Gattinoni L. Taccone P. Carlesso E. Marini J.J. Prone position in acute respiratory distress syndrome. Rationale, indications, and limits.Am J Respir Crit Care Med. 2013; 188: 1286-1293Crossref PubMed Google Scholar In this research letter, we present four cases in which chest wall compression caused an apparently “paradoxical” increase in the compliance of the respiratory system (Cpl,rs), likely explained by reduction of overdistension. Different modalities were used to detect the effect of chest wall compression on changes in: (1) partitioned respiratory mechanics using static respiratory maneuvers and an esophageal balloon; (2) distribution of the tidal ventilation and end-expiratory lung volume (EELV) by electrical impedance tomography (EIT)3Rezoagli E. Bellani G. How I set up positive end-expiratory pressure: evidence- and physiology-based!.Crit Care. 2019; 23: 412Crossref PubMed Scopus (6) Google Scholar; and (3) lung aeration by lung CT analysis. During patient positioning of a 63-year-old woman (BMI, 28 kg/m2) with severe ARDS on veno-venous extracorporeal membrane oxygenation (San Gerardo Hospital) from semi-recumbent to horizontal, we observed a “paradoxical” (at least toward common expectations) decrease of the driving pressure of the respiratory system (DP,rs) leading to a higher Cpl,rs. Three positions were formally tested: (1) supine (0°); (2) Trendelenburg (–30°); and (3) reverse Trendelenburg (30°). Increased abdominal compression on the lungs in the Trendelenburg position decreased plateau pressure and led to higher Cpl,rs, with a decreased stress index (Fig 1, panel 1). The EIT analysis suggested decreased lung overdistension in the nondependent areas in the Trendelenburg position and greater overdistension in the reverse Trendelenburg position (Fig 1, panel 2). Changes in respiratory mechanics observed during postural changes are described in the Video 1, part 1. Chest compression with a 5-kg weight is sometimes used in patients with ARDS to assess respiratory mechanics despite lack of evidence on its benefit.4Bottino N. Panigada M. Chiumello D. Pelosi P. Gattinoni L. Effects of artificial changes in chest wall compliance on respiratory mechanics and gas exchange in patients with acute lung injury (ALI).Crit Care. 2000; 4: P117Crossref Google Scholar We report the effect of a 5-kg bag applied on the chest of a 69-year-old man (BMI, 22.5 kg/m2) admitted to the Neuro-ICU (Niguarda Hospital) with legionellosis causing severe ARDS. We hypothesized that a continuous external weight on the chest might change the mechanical properties of the respiratory system, reducing overdistension of the nondependent lung areas and, in contrast, recruiting the dependent lung areas. We explored this mechanism by EIT.5Frerichs I. Amato M.B.P. Van Kaam A.H. et al.TREND study groupChest electrical impedance tomography examination, data analysis, terminology, clinical use and recommendations: consensus statement of the TRanslational EIT developmeNt stuDy group.Thorax. 2017; 72: 83-93Crossref PubMed Scopus (360) Google Scholar We tested three steps, each lasting 10 min: step A, baseline; step B, 5-kg bag continuous compression; and step C, no compression. Compared with baseline, chest weight application led to a sudden improvement of Cpl,rs by reduced DP,rs and reduced end-expiratory lung impedance (EELI), a surrogate of EELV (Fig 2, panel 1). The EELI reduction was localized mainly in the ventral regions (Fig 2, panel 2, solid lines). At the same time, we observed a change in regional tidal volume (TV) distribution from dorsal to ventral lungs, suggesting an increased regional Cpl,rs in nondependent areas (Fig 2, panel 2, dashed lines). In the nondependent lung, we observed an apparently paradoxical behavior: an increased Cpl,rs with a reduction of EELV, which we might interpret as a reduction of regional hyperinflation. In the dependent lung, we observed a decrease in both EELI and regional TV, suggesting a loss of Cpl,rs likely caused by a certain degree of de-recruitment. Time seems to be a meaningful factor, as the global EELI trend during Step B shows a progressive reduction over time (Fig 2, panel 1). In summary, this case suggests that external chest compression might improve the Cpl,rs by reducing EELV. Although this seems to lead to reduced alveolar overdistension in the nondependent areas, it might also favor dorsal de-recruitment. A 64-year-old man (21.5 kg/m2), with a medical history of Hodgkin’s lymphoma and bilateral pneumonia caused by Pneumocystis jirovecii, was admitted to the general ICU (Ospedale Maggiore Policlinico) for ARDS. To reduce tidal overdistension, 3 cm H2O of positive end-expiratory pressure (PEEP) and 6 mL/kg predicted body weight TV were used. However, ventilation was not protective (DP,rs = 25 cm H2O). A weight was therefore placed on the patient’s chest, with an immediate improvement in respiratory mechanics (Fig 2). A chest CT scan was acquired at end-inspiration and end-expiration, both with and without the weight on the chest, to optimize ventilator settings. Figure 2 (panel 3) shows a representative slice with color-mapped qualitative density analysis.6Langer T. Castagna V. Brusatori S. et al.Short-term physiologic consequences of regional pulmonary vascular occlusion in pigs.Anesthesiology. 2019; 131: 336-343Crossref PubMed Scopus (7) Google Scholar Application of the weight reduced EELV, with an end-expiratory reduction and increase of hyperinflated and poorly aerated lung tissue, respectively. A 62-year-old man (BMI, 28 kg/m2) with severe COVID-19 ARDS was in the ICU (Milan Fair)7Rezoagli E. Magliocca A. Bellani G. Pesenti A. Grasselli G. Development of a critical care response—experiences from Italy during the Covid19 pandemic.Anesthesiol Clin. 2021; 39: 265-284Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar on volume-controlled ventilation with the following settings: TV, 400 mL; respiratory rate, 35 beats/min; PEEP, 8 cm H2O; Fio2, 0.9; and peak inspiratory pressure (PIP), 42 cm H2O. The patient experienced decreased PIP when the head of the bed was lowered to 0° for nursing. To test whether this observation was related to an increased transmission of the abdominal pressure to the chest wall, we performed a transient abdominal compression in semi-recumbent position (~15 s). A sudden decrease of PIP to 26 cm H2O was observed. After releasing the abdominal compression, PIP immediately increased to 38 cm H2O. Blood oxygen saturation and hemodynamics were unaffected by the transient change in PIP (Video 1, part 2). To further investigate this mechanism, we performed a formal test applying a 5-kg saline bag to the abdomen for 10 min while recording airway and esophageal pressures during end-inspiratory and end-expiratory holds. The following was noted after application of the abdominal weight: DP,rs decreased (28 to 17 cm H2O); driving pressure of the chest wall increased (1 to 3 cm H2O); and driving pressure of the lung decreased by 13 cm H2O. Consequently, compliance of the lung doubled (15 to 29 mL/cm H2O), whereas compliance of the chest wall worsened (400 to 133 mL/cm H2O). During this test, Pao2/Fio2 and Paco2 remained unchanged. This finding suggests that the improvement of the lung mechanical properties is unlikely determined by lung recruitment, and more likely the consequence of a decreased lung resting volume preventing end-inspiratory overdistention. The presented cases show that, in some patients with ARDS, compression on the chest wall decreases the amount of hyperinflation, improving respiratory mechanics without causing alveolar recruitment. Our explanation resides in a right shift of the chest wall pressure-volume loop, which decreases lung volume, causing ventilation to occur in a more compliant region of the lung pressure-volume loop (Fig 1, panel 3). The measurement of partitioned respiratory mechanics suggests that an extrinsic weight does not worsen the compliance of the chest wall in a clinically relevant way. However, it reduces chest wall and lung volume, similarly to what is observed in obese patients.8Behazin N. Jones S.B. Cohen R.I. Loring S.H. Respiratory restriction and elevated pleural and esophageal pressures in morbid obesity.J Appl Physiol. 2010; 108: 212-218Crossref PubMed Scopus (158) Google Scholar This might be an additional explanation for the protective effects determined by prone position9Katira B.H. Osada K. Engelberts D. et al.Positive end-expiratory pressure, pleural pressure, and regional compliance during pronation: an experimental study.Am J Respir Crit Care Med. 2021; 203: 1266-1274Crossref PubMed Scopus (13) Google Scholar and for the obesity paradox.10Ni Y.-N. Luo J. Yu H. et al.Can body mass index predict clinical outcomes for patients with acute lung injury/acute respiratory distress syndrome? A meta-analysis.Crit Care. 2017; 21: 36Crossref PubMed Scopus (100) Google Scholar Chest wall compression does not seem to favor alveolar recruitment, which is also unlikely given the decreased airway pressure during weight placement. Our work suggests that an increase of respiratory system compliance during chest or abdominal compression should be regarded as a sign of tidal overinflation and should be taken into account to optimize mechanical ventilation. It remains unknown if improvement of lung mechanics due to patient positioning or chest wall compression has an impact on gas exchange and, ultimately, on patient outcome. Other contributions: The authors are highly grateful to Laurent Brochard, MD, for helpful discussions and his constructive feedback in regard to this work. The authors are indebted to Dario Manzolini, MD, and Manuela Marotta, MD, Department of Medicine and Surgery of the University of Milano-Bicocca, Monza, Italy, for their valuable support with the making of the Video about case 1; to Serena Brusatori, MD, Department of Pathophysiology and Transplantation of the University of Milan , for her valuable support with qualitative color-mapped analysis of Figure 2, panel 3; and to Manuela Chiodi, MD, Department of Pathophysiology and Transplantation of the University of Milan, for her valuable support with quantitative CT analysis of Figure 2, panel 3. Additional information: The Video can be found in the Supplemental Materials section of the online article. https://journal.chestnet.org/cms/asset/cabced99-9b78-4a23-8b0e-fdcaa1c5c3e4/mmc1.mp4Loading ... Download .mp4 (231.45 MB) Help with .mp4 files Video 1