Ventilator-associated lung injury (VALI) refers to an acute lung injury that develops during mechanical ventilation.
It is termed ventilator-induced lung injury (VILI) if it can be proven that the mechanical ventilation caused the acute lung injury.
Most patients receive pressure or volume, controlled, invasive, mechanical ventilation, receive a constant, or nearly constant, title, volume with each breath.
Constant ventilation with either small or large tidal volumes, delivered for even short periods, alter surfactant, increases surface tension, cause atelectasis, generates inflammatory cytokines, and produces ventilator induced lung injury.
Atelectasis is a major factor that becomes because cyclic opening and closing of atelectatic spaces and over extension of patent alveoli adjacent to the atelactic regions occur, both of which cause Ventilator induced lung injury, and result in systemic inflammation (biotrauma).
Barotrauma is the most harmful aspect of mechanical ventilation: over-stretching of the airways and alveoli.
During mechanical ventilation, gas flows into the lung will take the path of least resistance.
As a result areas of the lung that are collapsed or filled with secretions are underinflated with mechanical ventilation.
Areas of the lung that are relatively normal will be overinflated with mechanical ventilation, and will become overdistended and injured.
Reducing tidal volumes reduces over inflation risks.
With positive pressure ventilation, atelectatic regions inflate, but alveoli will collapse during the expiratory phase of the breath.
The repeated alveolar collapse and expansion is suggested to be caused by VALI.
Ventilator-associated lung injury is known as biotrauma.
Biotrauma involves the lung injury from any mediators of the inflammatory response or from bacteremia.
Finally oxygen toxicity contributes to ventilator-associated lung injury through several mechanisms including oxidative stress.
Possible reasons for predisposition to VALI include:
Overdistension of alveoli and cyclic atelectasis are the primary causes for alveolar injury during positive pressure mechanical ventilation.
Alveolar injury causes swelling of the tissues, bleeding of the alveoli, loss of surfactant, and complete alveoli collapse due to biotrauma.
Surfactant is normally in activated and/or depleted continuously and must be continuously secreted to maintain low surface tension and prevent atelectasis.
Surfactant’s stimulus to secrete is the mechanical stress resulting from stretching type II pneumocytes.
The sigh recruits more surfactant.
Short term, administration of size improves lung compliance and gas exchange, decreases ventilation heterogeneity, and regional lung strain, reverses and prevents atelectasis and reduces inflammatory, cytokine production.
High flow rates are associated with rheotrauma of the lung, high volumes with volutrauma and pressures with barotrauma.
Alveolar overdistension is limited by using small tidal volumes, maintaining a low plateau pressure, and most effectively by using volume-limited ventilation.
Low tidal volume ventilation reduced post operative pneumonia and reduced the requirement for both invasive and non invasive ventilation after surgery.
To prevent cyclic atelectasis positive end-expiratory pressure (PEEP) is the principal method used to keep the alveoli open.
Open lung ventilationn combines small tidal volumes and an applied PEEP above the low inflection point on the pressure-volume curve, to lessen cyclic atelectasis.
High frequency ventilation also reduces ventilator-associated lung injury.
Permissive hypercapnia and hypoxemia and allowing ventilation at less aggressive settings can mitigate all forms of ventilator-associated lung injury
VALI occurs most commonly when receiving mechanical ventilation for acute lung injury or acute respiratory distress syndrome.