Grieco Domenico Luca, Chen Lu, Brochard Laurent
Interdepartmental Division of Critical Care Medicine, University of Toronto, Toronto, Canada.
Keenan Research Centre and Li Ka Shing Institute, Department of Critical Care, St Michael's Hospital, Toronto, Canada.
Ann Transl Med. 2017 Jul;5(14):285. doi: 10.21037/atm.2017.07.22.
Transpulmonary pressure (P) is computed as the difference between airway pressure and pleural pressure and separates the pressure delivered to the lung from the one acting on chest wall and abdomen. Pleural pressure is measured as esophageal pressure (P) through dedicated catheters provided with esophageal balloons. We discuss the role of P in assessing the effects of mechanical ventilation in patients with acute respiratory distress syndrome (ARDS). In the supine position, directly measured P represents the pressure acting on the alveoli and airways. Because there is a pressure gradient in the pleural space from the non-dependent to the dependent zones, the pressure in the esophagus probably represents the pressure at a mid-level between sternal and vertebral regions. For this reason, it has been proposed to set the end-expiratory pressure in order to get a positive value of P. This improves oxygenation and compliance. P can also be estimated from airway pressure plateau and the ratio of lung to respiratory elastance (elastance-derived method). Some data suggest that this latter calculation may better estimate P in the nondependent lung zones, at risk for hyperinflation. Elastance-derived P at end-inspiration (P) may be a good surrogate of end-inspiratory lung stress for the "baby lung", at least in non-obese patients. Limiting end-inspiratory P to 20-25 cmHO appears physiologically sound to mitigate ventilator-induced lung injury (VILI). Last, lung driving pressure (∆P) reflects the tidal distending pressure. Changes in P may also be assessed during assisted breathing to take into account the additive effects of spontaneous breathing and mechanical breaths on lung distension. In summary, despite limitations, assessment of P allows a deeper understanding of the risk of VILI and may potentially help tailor ventilator settings.
跨肺压(P)通过气道压力与胸膜压力之差计算得出,它将作用于肺部的压力与作用于胸壁和腹部的压力区分开来。胸膜压力通过配备食管气囊的专用导管测量为食管压力(P)。我们讨论了P在评估急性呼吸窘迫综合征(ARDS)患者机械通气效果中的作用。在仰卧位时,直接测量的P代表作用于肺泡和气道的压力。由于胸膜腔内从非依赖区到依赖区存在压力梯度,食管内的压力可能代表胸骨和脊柱区域之间中间水平的压力。因此,有人提议设置呼气末压力以使P值为正。这可改善氧合和顺应性。P也可从气道压力平台和肺与呼吸弹性之比(弹性推导法)估算得出。一些数据表明,后一种计算方法在非依赖肺区可能能更好地估算P,这些区域有发生过度充气的风险。吸气末弹性推导的P(P)对于“婴儿肺”可能是吸气末肺应力的良好替代指标,至少在非肥胖患者中如此。将吸气末P限制在20 - 25 cmH₂O在生理上似乎合理,可减轻呼吸机诱导的肺损伤(VILI)。最后,肺驱动压(∆P)反映潮气量扩张压力。在辅助呼吸期间也可评估P的变化,以考虑自主呼吸和机械通气对肺扩张的叠加效应。总之,尽管存在局限性,但对P的评估有助于更深入地了解VILI风险,并可能有助于调整呼吸机设置。