It has been well documented that mechanical ventilation can injure the lungs, causing ventilator-induced lung injury (VILI). Known as “respirator lung,” VILI can include air leaks and surfactant dysfunction. Mechanical ventilation can trigger a complex array of pro- and anti-inflammatory mediators, according to Martin C. J. Kneyber, et al.
In a seminal study led by HH Webb and DF Tierney, it was discovered that:
- The ventilation of normal lungs with low pressures (PIP 14 cmH2O) does not cause significant injury
- Ventilation with high pressures (30 or 45 cmH2O) produces perivascular edema, and that ventilation at high airway pressures (45 cmH2O) without PEEP leads to severe lung injury (gross pulmonary edema, severe hypoxia) and
- PEEP confers protection from alveolar edema due to high inspiratory pressure ventilation.
Webb and Tierney put forth a number of thoughts based on the above results:
- That lungs from patients with ARDS have some “normal alveoli scattered among collapsed or fluid-filled alveoli, and that although the flooded alveoli “may be protected from overinflation... we are concerned that the normal alveoli may be overinflated and damaged.”
- That “tissue disruption secondary to a high inspiratory pressure is probably not the mechanism of the changes we observed.”
- That surfactant dysfunction with certain ventilatory strategies likely contributed to the development of lung injury.
What Causes Lung Injury?
Dreyfuss et al, found that high pressure (PIP 45 cmH2O) ventilation of rat lungs increases extravascular water and lung albumin uptake rapidly, and longer ventilation of up to 20 minutes causes a progressive increase in lung injury.
There are also a number of factors that predispose someone to VILI, including:
- underlying lung disease
- systemic inflammation
- surfactant dysfunction
- pulmonary edema
- extremes of age
Zhongheng Zhang, et al, write: “Extracorporeal membrane oxygenation (ECMO) provides an alternative to rescue patients with severe respiratory failure that MV fails to maintain adequate gas exchange. The timing of ECMO initiation based on the risks and benefits of ECMO has been widely investigated. In the running of ECMO, the protective ventilation strategy can be employed without worrying about catastrophic hypoxemia and carbon dioxide retention.”