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may aggravate lung injury/collapse and decrease oxygenation.
Intratracheal aspiration and sepsis are leading causes of acute lung injury that frequently necessitate mechanical ventilation (MV), which may aggravate lung injury thereby potentially increasing the risk of acute kidney injury (AKI).
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Mechanical ventilation (MV) with high tidal volumes may induce or aggravate lung injury in critical ill patients.
See related letter by Ng et al., Mechanical ventilation (MV) may aggravate pre-existing lung injury or even cause lung injury in healthy lungs, a phenomenon frequently referred to as ventilator-induced lung injury (VILI).
While the risk of ARDS development may be reduced by lowering tidal volumes, MV with low tidal volumes still seems to aggravate lung injury and further tidal volume reduction is limited by hypercapnia, which aggravates acidosis.
Obviously, the highest risk is to aggravate lung oedema.
However, MV can cause or aggravate lung injury, an entity referred to as ventilator-induced lung injury (VILI) [ 4].
However, high pressure and volume associated with tidal ventilation are known to aggravate lung injury in this setting [ 1].
Therefore, if solely guided by PaO2, ventilator adjustments may aggravate alveolar instability, particularly when lung injury is evolving secondary to volume resuscitation and a progressing systemic inflammatory response syndrome (SIRS) [20].
Laboratory studies have suggested that partial recruitment may aggravate cytokine production in the lung.
Animal studies demonstrate that mechanical ventilation with conventional tidal volume not only may aggravate, but also may initiate lung injury [ 1, 2].
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