ABSTRACT
Few simple experimental concepts have helped in improving the care of cri-
tically ill patients the way the concept of ventilator-induced lung injury
(VILI) did. The safety of mechanical ventilation for the treatment of patients
with acute respiratory failure was questioned soon after its introduction into
medical practice. Several studies showed that ventilation with high airway
pressure may result in abnormal lung function. Whereas ventilation of goats with a peak airway pressure of 13 cmH2O for two weeks proved safe pro-
vided the fraction of inspired oxygen remained low (1), atelectasis and
increased surface tension of lung extracts were seen after ventilation of dogs
with a peak airway pressure of 26 to 32 cmH2O (2). The very concept of VILI
arose from the study by Webb and Tierney (3) who showed that ventilation
of rats with high peak airway pressures [30-45 cmH2O peak inspiratory pres-
sure (PIP)] resulted in pulmonary edema, the severity of which depended on
peak airway pressure magnitude and was attenuated by the use of positive end-expiratory pressure (PEEP). Later studies showed that this edema
was due to microvascular injury and underlined the role of increased lung distension and thus high lung tissue stress in VILI development (4). If VILI
had a clinical counterpart (termed VALI, ventilation-associated lung injury),
easing the stress applied to diseased lungs would improve acute (adult)
respiratory distress syndrome (ARDS) prognosis. This has been unambigu-
ously demonstrated by the results of the ARDS network study that showed a
22% lessening of mortality in patients who received 6 mL/kg instead of the more conventional 12 mL/kg tidal volume (VT) (5).
