The physical basis of ventilator-induced lung injury

Abstract

Although mechanical ventilation (MV) is a life-saving intervention for patients with acute respiratory distress syndrome (ARDS), it can aggravate or cause lung injury, known as ventilator-induced lung injury (VILI). The biophysical characteristics of heterogeneously injured ARDS lungs increase the parenchymal stress associated with breathing, which is further aggravated by MV. Cells, in particular those lining the capillaries, airways and alveoli, transform this strain into chemical signals (mechanotransduction). The interaction of reparative and injurious mechanotransductive pathways leads to VILI. Several attempts have been made to identify clinical surrogate measures of lung stress/strain (e.g., density changes in chest computed tomography, lower and upper inflection points of the pressure–volume curve, plateau pressure and inflammatory cytokine levels) that could be used to titrate MV. However, uncertainty about the topographical distribution of stress relative to that of the susceptibility of the cells and tissues to injury makes the existence of a single ‘global’ stress/strain injury threshold doubtful.

Keywords::

• acute lung injury
• acute respiratory distress syndrome
• esophageal pressure
• lung strain
• lung stress
• mechanical ventilation
• mechanotransduction
• plateau pressure
• ventilator-induced lung injury

Financial & competing interests disclosure

This study was supported by NIH grant HL63178. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Notes

LIP: Lower inflection point; P_es: Esophageal pressure; P_plat: Plateau pressure; P_tp: Transpulmonary pressure; P–V: Pressure–volume; UIP: Upper inflection point.