Thomas Luecke

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.

Purpose: Right ventricular impairment (RVI) can be alleviated by the initiation of veno-venous extracorporeal membrane oxygenation (V-V ECMO), which enhances gas exchange and allows for less invasive mechanical ventilation. However, the progression of RVI during V-V ECMO remains unclear. This study assesses echocardiographic changes in RVI over a five-day period in twenty acute respiratory distress syndrome (ARDS) patients with V-V ECMO support. Material and Methods: Over a five-day period of V-V ECMO support, we examined echocardiographic markers of RVI, including right and left ventricular end-diastolic area ratio (RVEDA/LVEDA), tricuspid annular plane systolic excursion (TAPSE), tricuspid valve lateral anulus peak systolic velocity ( S ′), right ventricular fractional area change (FAC), and right ventricular myocardial performance index. Secondary objectives included changes in mechanical power transmitted to the respiratory system, hemodynamics and gas-exchange. Results: RVEDA/LVEDA ratio remained elevated (0.8 [0.7-0.8] vs 0.7 [0.7-0.9]; p = .986), TAPSE decreased (2.0[1.6-2.5] cm vs 1.7 [1.4-2.2] cm; p = .024) while no changes were observed in S ′ (16 [13-21] cm/s vs 15 [12-18] cm/s; p = .136) and FAC (38 [27-47] % vs 36 [29-43] %; p = .627). The right ventricular myocardial performance index improved (0.74 [0.45-1.00] vs 0.51 [0.42-0.80]; p = .004). Lung mechanical power was significantly reduced due to a decrease in lung elastic and resistive components. Conclusions: Despite preserved longitudinal function and improved global performance, RVI persisted in severe ARDS patients on V-V ECMO, as indicated by the RVEDA/LVEDA ratio. These findings suggest that mechanisms beyond hypoxemia, hypercapnia and the invasiveness of mechanical ventilation contribute to RVI in these patients. Trial registration: This trial was registered with the German Clinical Trials Register (DRKS00028584) on March 28, 2022. https://drks.de/search/en/trial/DRKS00028584