Respiratory failure & ventilation
Dose–Response Effects of Anterior Chest Wall Loading on Lung Mechanics, Regional Ventilation, and Hemodynamics in Acute Respiratory Distress Syndrome: A Prospective Physiologic Study
Authors' conclusion
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.
Study context
- Population
- Patients with moderate-to-severe acute respiratory distress syndrome (ARDS) (PaO2/FiO2 ≤150 mmHg)phase 1 n = 20
- Participants
- 30 patients
- Exposure
- Anterior chest wall loading (ACWL) at 5%, 10%, 15%, 20% of body weight vs baseline
- Outcome
- Transpulmonary ΔP
Methodological detailsexploratory, dose-response, random order of loads
- Exploratory
- Dose-response
- Random order of loads
Main finding
As reported in the abstract
ACWL 5%
6
median · IQR 4–7 · cm H 2 O
Baseline
7
median · IQR 5–8 · cm H 2 O
P = 0.015
Observational data: associations, not effects.
Secondary outcomes
Lung stress · ACWL at 5% body weight
P = 0.001
| Outcome | P value |
|---|---|
| End-expiratory lung volume · ACWL at 5% body weight | P < 0.001 |
End-expiratory lung volume · ACWL at 5% body weight
- Predominantly dependent decline in regional end-expiratory lung impedance, consistent with derecruitment
Nondependent lung compliance · ACWL at 5% body weight
- Increased vs baseline
Dose-response (5%–20% body weight)
- ACWL dose-dependently increased esophageal pressures, reducing transpulmonary pressures and end-expiratory lung volume, with nonlinear, baseline-dependent compliance responses
Safety
Gas exchange and hemodynamics at 5% body weight
- Gas exchange worsened; CO and oxygen delivery declined
Parts of this Brief are withheld: the automatic checks could not confirm them against the abstract.
Original publication
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