Abstract
Mechanical ventilation associated lung injury (VALI) negatively impacts the outcomes of critically ill patients. Research during the past two decades has led to a better understanding of key physiologic mechanisms of injury, yet uncertainty over the topographical distribution of these mechanisms continues to fuel controversies over "best ventilation practice" in injured lungs. In this issue Pavone and colleagues have explored the temporal and spatial evolution of VALI in an elegant use of intravital microscopy. Their findings reinforce the notion that regions which receive most of the inspired gas, in Pavone's case the non-dependent lung of a rat supported in the lateral decubitus posture, are particularly susceptible to injury. However, the inability to measure tissue strain remote from the pleura keeps important questions about small scale intra-acinar stress and strain distributions unanswered.
Highlights
Mechanical Ventilation Associated Lung Injury (VALI) is a prevalent complication of supportive care and greatly impacts outcomes of critically ill patients [1,2]
Research during the past two decades has identified deforming stress as a major determinant of “biotrauma”[3], and has drawn attention to four interrelated lung injury mechanisms: regional overexpansion caused by the application of a local stress or pressure that forces cells and tissues to assume shapes and dimensions they normally would not during unassisted breathing; so-called “low volume injury” associated with the repeated recruitment and de-recruitment of unstable lung units, causing the abrasion of the epithelial airspace lining by interfacial tension; the inactivation of surfactant triggered by large alveolar surface area oscillations, that stress surfactant adsorption and desorption kinetics and are associated with surfactant aggregate conversion; and interdependence mechanisms that raise cell and tissue shear stress between neighboring structures with differing mechanical properties.[4]
Using the lateral decubitus posture to compare the evolution of VALI between dependent and nondependent lung regions, Pavone and colleagues conclude that instability is first manifest in non-dependent lung, that positive end expiratory pressure (PEEP) prevents alveolar instability, but does not reduce lung water and that alveolar instability, as defined, does not correlate with measures of pulmonary gas exchange
Summary
Mechanical Ventilation Associated Lung Injury (VALI) is a prevalent complication of supportive care and greatly impacts outcomes of critically ill patients [1,2]. Research during the past two decades has identified deforming stress as a major determinant of “biotrauma”[3], and has drawn attention to four interrelated lung injury mechanisms: regional overexpansion caused by the application of a local stress or pressure that forces cells and tissues to assume shapes and dimensions they normally would not during unassisted breathing; so-called “low volume injury” associated with the repeated recruitment and de-recruitment of unstable lung units, causing the abrasion of the epithelial airspace lining by interfacial tension; the inactivation of surfactant triggered by large alveolar surface area oscillations, that stress surfactant adsorption and desorption kinetics and are associated with surfactant aggregate conversion; and interdependence mechanisms that raise cell and tissue shear stress between neighboring structures with differing mechanical properties.[4] the many degrees of freedom in ventilator settings and uncertainty about the topographical distribution of mechanical properties in injured lungs continue to fuel controversies about best positive end expiratory pressure (PEEP)” and safe tidal volumes[5].
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