Closing, opening and reopening: the difficult coexistence

Volume-controlled ventilation (VCV) has always been considered as protective ventilation, in particular during spontaneous breathing, being able to avoid the administration of injurious tidal volumes (Vt) to the patient. In fact, spontaneous efforts increase transpulmonary pressure (Pl) only during pressure-regulated ventilations (1). Despite this difference in terms of Pl, the conditions of lung parenchyma determine the damage to the lung tissue and the onset of ventilator induced lung injury (VILI). In normal lung the pressures applied to a local region of the pleura are homogeneous and distributed over the whole lung (fluid-like behavior), whereas negative pleural pressures (Ppl) generated by diaphragmatic contraction are rather concentrated in dorsal parts (solid-like), once lung has been injured (2). Furthermore, when Pl is applied to the lung, a counterforce of equal intensity is developed (lung stress), whereas the associated lung deformation is called strain. These two forces are directly correlated by the specific elastance (Elsp), which reflects the intrinsic mechanical characteristics of the lung parenchyma (3). This concept is a recent introduction, but it has an important clinical relevance right away; in fact, Elsp is peculiar in each species: in pigs is about half that in human and consequently a plateau pressure (Pplat) of 30 cmH2O in pigs would approximately correspond to 60 cmH2O in humans