Should vascular pressures be lowered to avert ventilator-induced lung injury?
Given that elevation in pulmonary vascular inflow pressure accentuated VILI, it seems logical that reduction in postalveolar vascular pressure would also be protective. The merit of reducing left atrial pressure might be expected for at least two reasons. The edematous lungs tend to collapse under their own weight and to develop dependent atelectasis, which could lead to cyclic opening and collapse, intensified shear stresses, and a tendency toward VILI in dependent areas. Moreover, exudation of protein-rich fluid has the potential to inactivate surfactant, further altering membrane permeability by increasing both surface tension and radial traction on pulmonary microvessels. On the other hand, increased left atrial pressure might help to limit VILI by flooding the alveoli of dependent regions, thereby reducing regional mechanical stresses. Reducing capillary pressure could promote cyclic vascular recruitment and derecruitment as the lungs transition from West’s zone III to zone II con
