Role of Strain Rate in the Pathogenesis of Ventilator-Induced Lung Edema.

Objective: Lungs behave as viscoelastic polymers. Harms of mechanical ventilation could then depend on not only amplitude (strain) but also velocity (strain rate) of lung deformation. Herein, we tested this hypothesis.

Lung anatomy, energy load, and ventilator-induced lung injury.

Background: High tidal volume can cause ventilator-induced lung injury (VILI), but positive end-expiratory pressure (PEEP) is thought to be protective. We aimed to find the volumetric VILI threshold and see whether PEEP is protective per se or indirectly.

Methods: In 76 pigs (22 ± 2 kg), we examined the lower and upper limits (30.

Validation of computed tomography for measuring lung weight.

Background: Lung weight characterises severity of pulmonary oedema and predicts response to mechanical ventilation. The aim of this study was to evaluate the accuracy of quantitative analysis of thorax computed tomography (CT) for measuring lung weight in pigs with or without pulmonary oedema.

Methods: Thirty-six pigs were mechanically ventilated with different tidal volumes and positive end-expiratory pressures that did or did not induce pulmonary oedema.

High positive end-expiratory pressure: only a dam against oedema formation?

Introduction: Healthy piglets ventilated with no positive end-expiratory pressure (PEEP) and with tidal volume (VT) close to inspiratory capacity (IC) develop fatal pulmonary oedema within 36 h. In contrast, those ventilated with high PEEP and low VT, resulting in the same volume of gas inflated (close to IC), do not. If the real threat to the blood-gas barrier is lung overinflation, then a similar damage will occur with the two settings.