Advances in ventilator-associated lung injury: prevention is the target

Abstract

Mechanical ventilation (MV) is the main supportive treatment in respiratory failure due to different etiologies. However, MV might aggravate ventilator-associated lung injury (VALI). Four main mechanisms leading to VALI are: 1) increased stress and strain, induced by high tidal volume (V_T); 2) increased shear stress, i.e. opening and closing, of previously atelectatic alveolar units; 3) distribution of perfusion and 4) biotrauma. In severe acute respiratory distress syndrome patients, low V_T, higher levels of positive end expiratory pressure, long duration prone position and neuromuscular blockade within the first 48 hours are associated to a better outcome. VALI can also occur by using high V_T in previously non injured lungs. We believe that prevention is the target to minimize injurious effects of MV. This review aims to describe pathophysiology of VALI, the possible prevention and treatment as well as monitoring MV to minimize VALI.

Keywords::

• acute respiratory distress syndrome
• mechanotransduction
• positive end-expiratory pressure
• tidal volume
• transpulmonary pressure
• ventilator-associated lung injury

Financial & competing interests disclosure

The authors have no 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. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.

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

Key issues

• The main mechanisms of ventilator-associated lung injury (VALI) are high inspiratory transpulmonary pressure (barotrauma), alveolar overdistention (volutrauma), repetitive opening and closing of collapsed alveoli (atelectrauma) and biotrauma.

• Mechanotransduction is the activation of lung (epithelium, endothelium, extracellular matrix and peripheral airways) response process induced by mechanical forces transduced into biochemical signal and leading to release of inflammatory mediators.

• VALI can be described by a ‘multiple-hit’ model: predisposing conditions (old age, excessive pulmonary perfusion, transfusion of blood products, sepsis) acting synergistically with injurious mechanical ventilation, and leading to pulmonary inflammation.

• Protective ventilation (low V_T/predicted body weight and moderate-to-high positive end-expiratory pressure) is the recommended treatment in acute respiratory distress syndrome (ARDS).

• In non-injured lungs, protective ventilation with low V_T and low-to-moderate positive end-expiratory pressure during surgery can decrease postoperative pulmonary complications.

• Assisted ventilation may be the alternative options for preventing further VALI in mild-to-moderate ARDS.

• Stem cell therapy is an alternative approach for treatment and prevention of ARDS.

• Respiratory monitoring at the bedside is mandatory to prevent VALI or to optimize ventilation strategies in patients with and without ARDS.

Notes