Rationale for Reduction of Alveolar Ventilation in ARDS

Abstract

The main evidence supporting pressure limited ventilation in the adult respiratory distress syndrome (ARDS), has come from animal studies demonstrating that mechanical ventilation (MV) can cause a form of acute parenchymal lung injury histologically similar to ARDS, resulting in progressive respiratory failure and sometimes death. In some animal models the ventilator-induced lung injury (VILI) is associated with an inflammatory response, with granulocyte sequestration in the lung and increased systemic and pulmonary vascular permeability [1], pulmonary hypertension apparently mediated at least in part by thromboxane A2 [2], the production of proinflammatory cytokines [3] and platelet activating factor [4] in the lung, and increased neutrophil accumulation in the lung and reduced chemotaxis of circulating neutrophils [5]. High pressure ventilation in rabbits [6] and in dogs [7] following tracheal inoculation of E. Coli led to reduced bacterial clearance from the lung, and more positive blood cultures than in control animals. Such consequences of MV could potentially induce or amplify a systemic inflammatory response syndrome if they occur in patients with ARDS, perhaps contributing to the development of multiple organ dysfunction syndrome. Studies of ventilator-induced lung injury are discussed in detail in other chapters.