Ventilator-Induced Lung Injury

Michele Umbrello and Paolo Formenti

Introduction

The vast majority of critically ill patients undergo invasive mechanical ventilation (MV) during their stay in the intensive care unit, and patients with ARDS are almost invariably managed by invasive mechanical ventilation. Despite extensive research over nearly half a century, no effective pharmacological therapies exist for ARDS, and supportive care with mechanical ventilation remains the cornerstone of treatment [1]. Indeed, mechanical ventilation, per se, does not substitute the function of the lungs: indeed, it is a substitute for the activity of respiratory muscles. Moreover, mechanical ventilation is a procedure that aims to improve the gas exchange, and, since it does not act either on the etiology or on the pathophysiology of ARDS, it is a measure to buy time for healing to take place [2]. On the other side, mechanical ventilation is not devoid of side effects and, namely, the hemodynamic instability secondary to the increased intrathoracic pressures and the mechanical trauma to the lung structure. Indeed, mechanical ventilation can further damage the lung, activating a biological inflammatory response and promoting the development of the so- called ventilator-induced lung injury (VILI). The present chapter will focus on the latter aspect, i.e., VILI. The classic distinction among factors related to the lung parenchyma, factors related to the mechanical ventilator, and extrapulmonary factors will be employed to classify the causes of VILI. The recently introduced theory of mechanical power, as a unifying hypothesis for all the mechanical ventilator- associated causes, will also be presented and discussed.

M. Umbrello (*) • P. Formenti

Unita Operativa di Anestesia e Rianimazione, Ospedale San Paolo-Polo Universitario, ASST Santi Paolo e Carlo, Via A. Di Rudini, 8, 20142 Milan, Italy

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© Springer International Publishing Switzerland 2017 D. Chiumello (ed.), Acute Respiratory Distress Syndrome (ARDS), DOI 10.1007/978-3-319-41852-0_13

 
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