Abstract
The pressure across the lung, so-called transpulmonary pressure (PL), represents the main force acting toward to provide lung movement. During mechanical ventilation, PL is provided by respiratory system pressurization, using specific ventilator setting settled by the operator, such as: tidal volume (VT), positive end-expiratory pressure (PEEP), respiratory rate (RR), and inspiratory airway flow. Once PL is developed throughout the lungs, its distribution is heterogeneous, being explained by the elastic properties of the lungs and pleural pressure gradient. There are different methods of PL calculation, each one with importance and some limitations. Among the most known, it can be quoted: (I) direct measurement of PL; (II) elastance derived method at end-inspiration of PL; (III) transpulmonary driving pressure. Recent studies using pleural sensors in large animal models as also in human cadaver have added new and important information about PL heterogeneous distribution across the lungs. Due to this heterogeneous distribution, lung damage could happen in specific areas of the lung. In addition, it is widely accepted that high PL can cause lung damage, however the way it is delivered, whether it's compressible or tensile, may also further damage despite the values of PL achieved. According to heterogeneous distribution of PL across the lungs, the interstitium and lymphatic vessels may also interplay to disseminate lung inflammation toward peripheral organs through thoracic lymph tracts. Thus, it is conceivable that juxta-diaphragmatic area associated strong efforts leading to high values of PL may be a source of dissemination of inflammatory cells, large molecules, and plasma contents able to perpetuate inflammation in distal organs.
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