Dose–Response Effects of Anterior Chest Wall Loading on Lung Mechanics, Regional Ventilation, and Hemodynamics in Acute Respiratory Distress Syndrome: A Prospective Physiological Study
Christoph Boesing, Hans Thieme, Laura Schaefer, Alice Marguerite Conrad, David Mohr, Matthias Otto, Grietje Beck, Patricia R.M. Rocco, Thomas Luecke, Joerg KrebsBackground:
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 non-dependent pleural pressure and unmask regional overdistension, but its dose-dependent effects remain uncertain. We hypothesized that low loads reduce transpulmonary driving pressure (ΔP) whereas higher loads promote derecruitment and hemodynamic compromise.
Methods:
In this prospective, exploratory study, 30 moderate-to-severe ARDS patients (PaO 2 /FIO 2 ≤150 mmHg) 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 non-linear, baseline-dependent compliance responses. At 5% body weight, ACWL reduced transpulmonary ΔP (6 [4, 7] versus 7 [5, 8] cmH
2
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Conclusions:
In moderate-to-severe ARDS, ACWL induced dose-dependent changes in pleural pressure and respiratory mechanics. By increasing non-dependent pleural pressure, it relieved non-dependent overdistension and lowered transpulmonary ΔP, but simultaneously caused dependent derecruitment and, by increasing central venous pressure, hemodynamic compromise. These findings support ACWL as a physiological probe of lung–chest wall interactions rather than a therapeutic intervention.