Silva Pedro Leme, Gama de Abreu Marcelo
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Ann Transl Med. 2018 Oct;6(19):385. doi: 10.21037/atm.2018.10.03.
The pressure across the lung, so-called transpulmonary pressure (P), represents the main force acting toward to provide lung movement. During mechanical ventilation, P is provided by respiratory system pressurization, using specific ventilator setting settled by the operator, such as: tidal volume (V), positive end-expiratory pressure (PEEP), respiratory rate (RR), and inspiratory airway flow. Once P 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 P calculation, each one with importance and some limitations. Among the most known, it can be quoted: (I) direct measurement of P; (II) elastance derived method at end-inspiration of P; (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 P 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 P can cause lung damage, however the way it is delivered, whether it's compressible or tensile, may also further damage despite the values of P achieved. According to heterogeneous distribution of P 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 P may be a source of dissemination of inflammatory cells, large molecules, and plasma contents able to perpetuate inflammation in distal organs.
跨肺压力,即所谓的跨肺压(P),是促使肺运动的主要作用力。在机械通气过程中,P由呼吸系统增压提供,通过操作者设置的特定通气参数来实现,如:潮气量(V)、呼气末正压(PEEP)、呼吸频率(RR)和吸气气道流量。一旦P在整个肺内形成,其分布是不均匀的,这可以用肺的弹性特性和胸膜压力梯度来解释。P的计算方法有多种,每种方法都有其重要性和局限性。其中最知名的方法有:(I)P的直接测量;(II)吸气末P的弹性推导法;(III)跨肺驱动压。最近在大型动物模型以及人体尸体中使用胸膜传感器的研究,为肺内P的不均匀分布增添了新的重要信息。由于这种不均匀分布,肺的特定区域可能会发生损伤。此外,人们普遍认为高P会导致肺损伤,然而,无论P是以可压缩还是拉伸的方式施加,尽管达到的P值相同,施加方式也可能会进一步造成损伤。根据P在肺内的不均匀分布,间质和淋巴管也可能相互作用,通过胸段淋巴途径将肺部炎症扩散到外周器官。因此,可以想象,与高P值相关的膈肌附近区域可能是炎症细胞、大分子和血浆成分扩散的来源,这些成分能够使远端器官的炎症持续存在。