Ventilator-induced Lung Injury

Abstract

Prevention of ventilator-induced lung injury (VILI) can attenuate multiorgan failure and improve survival in at-risk patients. Clinically significant VILI occurs from volutrauma, barotrauma, atelectrauma, biotrauma, and shear strain. Differences in regional mechanics are important in VILI pathogenesis. Several interventions are available to protect against VILI. However, most patients at risk of lung injury do not develop VILI. VILI occurs most readily in patients with concomitant physiologic insults. VILI prevention strategies must balance risk of lung injury with untoward side effects from the preventive effort, and may be most effective when targeted to subsets of patients at increased risk.

Keywords: Acute lung injury; Acute respiratory distress syndrome; Mechanical ventilation; Respiratory mechanics; Ventilator-induced lung injury.

Conflict of interest statement

Conflicts of Interest: All authors report they have no potential conflicts of interest.

Copyright © 2016 Elsevier Inc. All rights reserved.

Figures

Figure 1. Transpulmonary pressure

Transpulmonary pressure (Pairway − Ppleural) is the pertinent distending pressure of the lung. At zero flow, airway and alveolar pressure are equal, for example during an end-inspiratory plateau pressure maneuver. (a) Non-intubated patient, normal spontaneous breathing at end-inspiration. (b) Intubated patient without respiratory disease, passive on mechanical ventilator at end-inspiration. (c) Intubated patient, chest wall stiffness results in lower transpulmonary pressure and lower lung volume at end-inspiration despite higher airway pressure. (d) Intubated patient, forceful inspiratory muscle effort, such as from heightened respiratory drive, produces high transpulmonary pressure and lung volume at endinspiration even though airway pressure is reasonably low. Abbreviations: Paw, airway pressure; Ppl, pleural pressure; Ptp, transpulmonary pressure. Adapted from Slutsky AS, Ranieri VM. Ventilator-induced lung injury. N Engl J Med 2013;369(22):2126–36; with permission.

Figure 2. Atelectrauma

Local stress and strain of epithelial cells generated during alveolar recruitment. (a) Air bubble propagation down atelectatic airway generates dynamic wave of shear stress and strain at interface of air bubble and collapsed airway. As the air bubble approaches, the epithelial cell is pulled inward toward the bubble. As the air bubble passes, the cell is pushed outward. (b) Air bubble generates similar shear stress and strain of epithelial cells during propagation along flooded airway. From Ghadiali SN, Gaver DP. Biomechanics of liquid-epithelium interactions in pulmonary airways. Respir Physiol Neurobiol 2008;163(1–3):232–43; with permission.

Figure 3. Mechanical alveolar interdependence and shear strain

A–C: classic model of alveolar interdependence; each hexagon represents an alveolus in cross-section. (a) Homogeneous alveolar inflation minimizes strain. (b) Atelectasis of center alveolus induces shear strain of neighboring alveoli. (c) Asymmetric inflation of center alveolus induces shear strain of neighboring alveoli. (d) CT chest with overlying map of CT-derived regional stress concentration due to parenchymal heterogeneity in a representative patient with ARDS (light blue: low stress; orange: moderate stress; red: high stress). Figure 3A–3C from Mead J, Takishima T, Leith D. Stress distribution in lungs: a model of pulmonary elasticity. J Appl Physiol 1970;28(5):596–608. Reprinted with permission of the American Physiological Society; copyright © 2016 American Physiological Society. Figure 3D from Cressoni M, Cadringher P, Chiurazzi C, et al. Lung inhomogeneity in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2014;189(2):149–58. Reprinted with permission of the American Thoracic Society; copyright © 2016 American Thoracic Society.

Figure 4. ARDS baby lung

CT chest of representative patient with ARDS. Ventral regions are well-aerated with patchy ground-glass opacities and few areas of focal consolidation from pneumonia. Dorsal regions exhibit dense dependent atelectasis due to superimposed pressure from gravity on the edematous ARDS lung above. As a result, the volume of aerated lung available for gas exchange and mechanical insufflation is reduced—termed the “baby lung.”