Since its introduction in the treatment of the Acute Respiratory Distress Syndrome, mechanicalventilation has been so strongly interwoven with its side effects that someone started to consider itas invariably dangerous. Over the decades, attention has shifted from gross barotrauma tovolutrauma and, more recently, atelectrauma and biotrauma. In this manuscript, we will describe theanatomical and physiological framework in which Ventilator-Induced Lung Injury (VILI) mayoccur. We will address the concept of lung stress/strain as applied to the whole lung or specificpulmonary regions. We will challenge some of the common beliefs, such as the claim of studyingseparately the dangerous effects of different tidal volumes (end-inspiration) and end-expiratorypositive pressures (PEEP). Based on available data, we will suggest that stress at rupture is onlyrarely reached and that high tidal volume induces VILI by augmenting the pressure heterogeneity atthe interface between open and constantly closed units. We believe that VILI occurs only when agiven threshold is exceeded; below this limit, mechanical ventilation is likely to be safe.

Ventilator-induced lung injury: the anatomical and physiological framework

Protti A;
2010

Abstract

Since its introduction in the treatment of the Acute Respiratory Distress Syndrome, mechanicalventilation has been so strongly interwoven with its side effects that someone started to consider itas invariably dangerous. Over the decades, attention has shifted from gross barotrauma tovolutrauma and, more recently, atelectrauma and biotrauma. In this manuscript, we will describe theanatomical and physiological framework in which Ventilator-Induced Lung Injury (VILI) mayoccur. We will address the concept of lung stress/strain as applied to the whole lung or specificpulmonary regions. We will challenge some of the common beliefs, such as the claim of studyingseparately the dangerous effects of different tidal volumes (end-inspiration) and end-expiratorypositive pressures (PEEP). Based on available data, we will suggest that stress at rupture is onlyrarely reached and that high tidal volume induces VILI by augmenting the pressure heterogeneity atthe interface between open and constantly closed units. We believe that VILI occurs only when agiven threshold is exceeded; below this limit, mechanical ventilation is likely to be safe.
Acute lung injury; Acute respiratory distress syndrome; Chest wall elastance; Lung elastance; Lung mechanics; Lung strain; Lung stress; Lung volumes; Transpulmonary pressure; Ventilator-induced lung injury
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11699/3283
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