Department of Anesthesiology, Emergency and Intensive Care Medicine, University of Göttingen, Robert-Koch-Straße 40, 37075, Göttingen, Germany.
University of Minnesota, Minneapolis/Saint Paul, MN, USA.
Crit Care. 2017 Jul 12;21(1):183. doi: 10.1186/s13054-017-1750-x.
The adverse effects of mechanical ventilation in acute respiratory distress syndrome (ARDS) arise from two main causes: unphysiological increases of transpulmonary pressure and unphysiological increases/decreases of pleural pressure during positive or negative pressure ventilation. The transpulmonary pressure-related side effects primarily account for ventilator-induced lung injury (VILI) while the pleural pressure-related side effects primarily account for hemodynamic alterations. The changes of transpulmonary pressure and pleural pressure resulting from a given applied driving pressure depend on the relative elastances of the lung and chest wall. The term 'volutrauma' should refer to excessive strain, while 'barotrauma' should refer to excessive stress. Strains exceeding 1.5, corresponding to a stress above ~20 cmHO in humans, are severely damaging in experimental animals. Apart from high tidal volumes and high transpulmonary pressures, the respiratory rate and inspiratory flow may also play roles in the genesis of VILI. We do not know which fraction of mortality is attributable to VILI with ventilation comparable to that reported in recent clinical practice surveys (tidal volume ~7.5 ml/kg, positive end-expiratory pressure (PEEP) ~8 cmHO, rate ~20 bpm, associated mortality ~35%). Therefore, a more complete and individually personalized understanding of ARDS lung mechanics and its interaction with the ventilator is needed to improve future care. Knowledge of functional lung size would allow the quantitative estimation of strain. The determination of lung inhomogeneity/stress raisers would help assess local stresses; the measurement of lung recruitability would guide PEEP selection to optimize lung size and homogeneity. Finding a safety threshold for mechanical power, normalized to functional lung volume and tissue heterogeneity, may help precisely define the safety limits of ventilating the individual in question. When a mechanical ventilation set cannot be found to avoid an excessive risk of VILI, alternative methods (such as the artificial lung) should be considered.
急性呼吸窘迫综合征(ARDS)机械通气的不良影响主要有两个原因:正压或负压通气时跨肺压的不生理性增加和胸膜压的不生理性增加/降低。与跨肺压相关的副作用主要导致呼吸机相关性肺损伤(VILI),而与胸膜压相关的副作用主要导致血流动力学改变。给定应用驱动压力引起的跨肺压和胸膜压的变化取决于肺和胸壁的相对弹性。“容积伤”一词应指过度应变,而“气压伤”应指过度应力。在实验动物中,应变超过 1.5,对应于约 20cmH2O 以上的应力,会造成严重损伤。除了高潮气量和高跨肺压外,呼吸频率和吸气流量也可能在 VILI 的发生中起作用。我们不知道有多少与通气相关的死亡率可归因于 VILI,这些通气与最近临床实践调查中报告的通气相似(潮气量约 7.5ml/kg,呼气末正压(PEEP)约 8cmH2O,频率约 20bpm,相关死亡率约 35%)。因此,需要更完整和个性化地了解 ARDS 肺力学及其与呼吸机的相互作用,以改善未来的护理。对功能性肺大小的了解可以允许对应变进行定量估计。肺不均匀性/应变量增加的确定有助于评估局部应力;肺可复张性的测量可以指导 PEEP 选择,以优化肺大小和均匀性。找到机械功率的安全阈值,归一化为功能性肺体积和组织异质性,可能有助于精确定义有关个体通气的安全限制。当找不到机械通气设置来避免过度的 VILI 风险时,应考虑替代方法(如人工肺)。