Anesthesiology · 2026
Dose-Response Effects of Anterior Chest Wall Loading on Lung Mechanics, Regional Ventilation, and Hemodynamics in Acute Respiratory Distress Syndrome: A Prospective Physiologic Study.
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Boesing Christoph, Thieme Hans, Schaefer Laura, Conrad Alice Marguerite, Mohr David, Otto Matthias, Beck Grietje, Rocco Patricia R M, Luecke Thomas, Krebs Joerg
Аннотация
BACKGROUND: In acute respiratory distress syndrome (ARDS), global airway pressures do not distinguish lung from chest wall mechanics, limiting bedside identification of regional overdistension. Anterior chest wall loading (ACWL) has been proposed to transiently increase nondependent pleural pressure and unmask regional overdistension, but its dose-dependent effects remain uncertain. The authors hypothesized that low loads reduce transpulmonary driving pressure (ΔP) whereas higher loads promote derecruitment and hemodynamic compromise.
METHODS: In this prospective, exploratory study, 30 patients with moderate-to-severe ARDS (Pao 2 /F i o 2 ratio of 150 mmHg or less) underwent ACWL. In a dose-response cohort (phase 1, n = 20), ACWL at 5%, 10%, 15%, and 20% of body weight was applied in random order; 5% body weight was then assessed in a separate cohort (phase 2, n = 10) using electrical impedance tomography. The primary endpoint was transpulmonary ΔP; secondary endpoints included partitioned respiratory mechanics, end-expiratory lung volume, gas exchange, and hemodynamics.
RESULTS: ACWL dose-dependently increased esophageal pressures, reducing transpulmonary pressures and end-expiratory lung volume, with nonlinear, baseline-dependent compliance responses. At 5% body weight, ACWL reduced transpulmonary ΔP (median [interquartile range], 6 [4, 7] vs. 7 [5, 8] cm H 2 O; P = 0.015) and lung stress (13.0 [10.2, 15.1] vs. 14.4 [11.8, 17.1] cm H 2 O; P = 0.001) compared with baseline, with increased nondependent lung compliance. End-expiratory lung volume was lower (1,559 [1,107, 2,051] vs. 1,784 [1,325, 2,332] ml; P < 0.001), with a predominantly dependent decline in regional end-expiratory lung impedance, consistent with derecruitment. At 5% body weight, gas exchange worsened, and cardiac output and oxygen delivery declined.
CONCLUSIONS: In moderate-to-severe ARDS, ACWL induced dose-dependent changes in pleural pressure and respiratory mechanics. By increasing nondependent pleural pressure, it relieved nondependent overdistension and lowered transpulmonary ΔP, but simultaneously caused dependent derecruitment and, by increasing central venous pressure, hemodynamic compromise. These findings support ACWL as a physiologic probe of lung-chest wall interactions rather than a therapeutic intervention.
METHODS: In this prospective, exploratory study, 30 patients with moderate-to-severe ARDS (Pao 2 /F i o 2 ratio of 150 mmHg or less) underwent ACWL. In a dose-response cohort (phase 1, n = 20), ACWL at 5%, 10%, 15%, and 20% of body weight was applied in random order; 5% body weight was then assessed in a separate cohort (phase 2, n = 10) using electrical impedance tomography. The primary endpoint was transpulmonary ΔP; secondary endpoints included partitioned respiratory mechanics, end-expiratory lung volume, gas exchange, and hemodynamics.
RESULTS: ACWL dose-dependently increased esophageal pressures, reducing transpulmonary pressures and end-expiratory lung volume, with nonlinear, baseline-dependent compliance responses. At 5% body weight, ACWL reduced transpulmonary ΔP (median [interquartile range], 6 [4, 7] vs. 7 [5, 8] cm H 2 O; P = 0.015) and lung stress (13.0 [10.2, 15.1] vs. 14.4 [11.8, 17.1] cm H 2 O; P = 0.001) compared with baseline, with increased nondependent lung compliance. End-expiratory lung volume was lower (1,559 [1,107, 2,051] vs. 1,784 [1,325, 2,332] ml; P < 0.001), with a predominantly dependent decline in regional end-expiratory lung impedance, consistent with derecruitment. At 5% body weight, gas exchange worsened, and cardiac output and oxygen delivery declined.
CONCLUSIONS: In moderate-to-severe ARDS, ACWL induced dose-dependent changes in pleural pressure and respiratory mechanics. By increasing nondependent pleural pressure, it relieved nondependent overdistension and lowered transpulmonary ΔP, but simultaneously caused dependent derecruitment and, by increasing central venous pressure, hemodynamic compromise. These findings support ACWL as a physiologic probe of lung-chest wall interactions rather than a therapeutic intervention.