Looking beyond macroventilatory parameters and rethinking ventilator-induced lung injury

• Published in: Journal of applied physiology (1985) 2018-05, Vol.124 (5), p.1214-1218
• Main Authors: Kollisch-Singule, Michaela C., Jain, Sumeet V., Andrews, Penny L., Satalin, Joshua, Gatto, Louis A., Villar, Jesús, De Backer, Daniel, Gattinoni, Luciano, Nieman, Gary F., Habashi, Nader M.
• Format: Article
• Language: English
• Subjects: Alveoli; Critical care; Edema; Human behavior; Injuries; Lungs; Mechanical ventilation; Respiratory distress syndrome; Strain; Ventilation; Viewpoint
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00412.2017

Clinicians recognize that although mechanical ventilation is a necessary tool in managing critically ill patients that develop acute respiratory distress syndrome (ARDS), it can simultaneously induce and propagate injury in the lung it is meant to support. The mechanism of this ventilator induced lung injury (VILI) is thought to be related to dynamic strain and cyclic alveolar collapse and reopening; however, an all-encompassing single mechanism for VILI remains elusive. Conceptually, the lung is often illustrated by a single compartment balloon model in which reducing stress reduces volumetric distortion and strain in the balloon wall. This approach, however, is an oversimplification of the complex geometry of the finely partitioned, interdependent, and four-dimensional behavior of the human lung at the level of the microenvironment. The balloon model also docs not account for lung heterogeneity, a hallmark of ARDS, as collapsed or edema-filled alveoli generate regional stress, inducing strain on the neighboring open alveoli.