ABSTRACT
Initial description of ventilator-induced lung injury (VILI) was made by
ventilating normal lungs with high peak inspiratory pressures (PIP) (1). However, mechanical ventilation is most often used in patients with dis-
eased lungs. These lungs are inhomogenous, normal zones coexisting with
edematous or atelectatic ones (2). Thus it is conceivable that inflation of
lungs with heterogeneously distributed lesions may lead to greater regional
stress and local overinflation than that of uniform uninjured ones. Mead
et al. were the first to conceptualize the increased risk of tissue injury during
inflation when lungs had zones of atelectasis (3). They calculated that the
pressure tending to expand an atelectatic region surrounded by a fully expanded lung would be approximately 140 cmH2O at a transpulmonary
pressure of 30 cmH2O (3). They further speculated that ‘‘mechanical venti-
lators, by applying high transpulmonary pressure to the nonuniformly
expanded lungs of some patients who would otherwise die of respiratory
insufficiency, may cause the hemorrhage and the formation of hyaline mem-
branes found in such patients’ lungs at death’’ (3). Other abnormalities that
may increase lung tissue stress are the presence of significant areas excluded from the ventilation. In that case, the bulk of ventilation is delivered to
smaller (and likely less damaged) lung volume that thus would be at a
greater risk of overinflation.
