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.
Original language | English (US) |
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Pages (from-to) | 373-385 |
Number of pages | 13 |
Journal | Expert Review of Respiratory Medicine |
Volume | 4 |
Issue number | 3 |
DOIs | |
State | Published - Jun 2010 |
Keywords
- Acute lung injury
- Acute respiratory distress syndrome
- Esophageal pressure
- Lung strain
- Lung stress
- Mechanical ventilation
- Mechanotransduction
- Plateau pressure
- Ventilator-induced lung injury
ASJC Scopus subject areas
- Immunology and Allergy
- Pulmonary and Respiratory Medicine
- Public Health, Environmental and Occupational Health