ABSTRACT
Mechanical ventilation is a lifesaving treatment in patients with acute
respiratory failure, regardless of whether respiratory failure is associated
with acute hypoxemia, acute hypercarbia, or both. Ventilator-induced lung
injury (VILI) occurs when mechanical breaths overdistend the alveolar units (1,2). In patients with normal lungs, such as patients with neuromus-
cular disease or injuries, or patients with acute poisonings who have not
aspirated, mechanical ventilation with relatively large tidal volumes (e.g.,
10-12 mL/kg measured body weight) does not seem to harm the lungs. In
fact, some recommendations for ventilating patients with neuromuscular
disease call for the use of larger tidal volumes (> 10 mL/kg) to prevent atelectasis. However, when major areas of alveolar collapse occur, as in
acute lung injury (ALI), the effective alveolar volume is substantially reduced, and a set tidal volume of 10 mL/kg body weight may be equivalent
to a set tidal volume of 20 mL/kg body weight or greater in a reduced alveo-
lar space. Such relatively high tidal volumes have the potential to overdis-
tend and damage the alveolar walls, but as yet there is no direct way to
estimate the effective alveolar volume in order to appropriately set the tidal volume. Investigators have worked to identify biomarkers of VILI so that
protective measures can be initiated as soon as possible to reduce the
chances of further lung injury. Biological markers also could be used to
make predictions about prognosis and to stratify patients into different risk
groups in order to apply appropriate new treatments. Lastly, biological
markers are useful in studying the pathophysiology of lung injury.
