Imaging atelectrauma in Ventilator-Induced Lung Injury using 4D X-ray microscopy

Luca Fardin,Sam Bayat,Alberto Bravin,Alberto Mittone,Goran Lovric,Ludovic Broche,Anders Larsson,Olivier Stephanov

doi:10.1038/s41598-020-77300-x

Abstract

Mechanical ventilation can damage the lungs, a condition called Ventilator-Induced Lung Injury (VILI). However, the mechanisms leading to VILI at the microscopic scale remain poorly understood. Here we investigated the within-tidal dynamics of cyclic recruitment/derecruitment (R/D) using synchrotron radiation phase-contrast imaging (PCI), and the relation between R/D and cell infiltration, in a model of Acute Respiratory Distress Syndrome in 6 anaesthetized and mechanically ventilated New-Zealand White rabbits. Dynamic PCI was performed at 22.6 µm voxel size, under protective mechanical ventilation [tidal volume: 6 ml/kg; positive end-expiratory pressure (PEEP): 5 cmH2O]. Videos and quantitative maps of within-tidal R/D showed that injury propagated outwards from non-aerated regions towards adjacent regions where cyclic R/D was present. R/D of peripheral airspaces was both pressure and time-dependent, occurring throughout the respiratory cycle with significant scatter of opening/closing pressures. There was a significant association between R/D and regional lung cellular infiltration (p = 0.04) suggesting that tidal R/D of the lung parenchyma may contribute to regional lung inflammation or capillary-alveolar barrier dysfunction and to the progression of lung injury. PEEP may not fully mitigate this phenomenon even at high levels. Ventilation strategies utilizing the time-dependence of R/D may be helpful in reducing R/D and associated injury.

Highlights

Mechanical ventilation can damage the lungs, a condition called Ventilator-Induced Lung Injury (VILI)
It is necessary in the treatment of patients with acute respiratory distress syndrome (ARDS)[1], a pathologic condition characterized by severe lung inflammation, diffuse alveolar damage and infiltration, increased microvascular permeability edema, surfactant dysfunction and widespread patchy a telectasis[2]
Static CT images acquired upon expiration (5 cmH2O) and inspiration (25 cmH2O) are shown in a representative animal. These images were acquired at baseline and the end of the two phases of our lung injury model: lavage-induced surfactant depletion followed by injurious ventilation

Summary

Introduction

Mechanical ventilation can damage the lungs, a condition called Ventilator-Induced Lung Injury (VILI). The overall mortality of ARDS remains high: between 35 and 45%3, in part because despite its vital role in improving oxygenation, mechanical ventilation can damage the lungs, a condition referred to as Ventilator-Induced Lung Injury (VILI). Overdistension due to high regional tidal volumes can induce mechanical injury to the lung, through exaggerated stress and strain Evidence to support this hypothesis is mainly based on clinical studies showing the improvement in the mortality of ARDS patients by reducing tidal v olume[5]. Positive end-expiratory pressure (PEEP) is usually applied in ARDS to improve oxygenation by preventing end-expiratory lung collapse It should theoretically prevent atelectrauma and reduce the inhomogeneities responsible for stress concentration. The importance of atelectrauma in the development of VILI is still unclear

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