Marini J J
University of Minnesota, St. Paul Ramsey Medical Center, Minneapolis/St. Paul.
New Horiz. 1993 Nov;1(4):489-503.
The traditional practice of using high inflation pressures to maintain normal tidal volumes and arterial blood gases has been encouraged by the perception of uniformly distributed damage in acute lung injury. Although the frontal chest radiograph often suggests uniformity, recent work highlights the heterogeneous pathoanatomy and lung mechanics that actually characterize the adult (acute) respiratory distress syndrome. This heterogeneity is important to consider when applying mechanical ventilation, because impressive experimental evidence strongly indicates the potential for traditional selections for volume and pressure to impede lung healing or extend damage to previously unaffected areas. Because lung regions differ markedly with regard to distensibility and fragility, the acutely injured lung should be viewed as small rather than stiff. Aerated lung units appear to have nearly normal gas-to-tissue ratios and well-preserved mechanical and gas-exchanging properties. Mechanical ventilation may expose endothelial and epithelial barriers to excessive stress, allowing proteinaceous alveolar edema to form without actual membrane rupture. Such damage has been linked experimentally to an excessive transalveolar inflation pressure, to a tidal volume inappropriate to the size of the aeratable lung mass, or to damaging shear forces that develop when insufficient end-expiratory alveolar pressure is maintained to prevent tidal opening and reclosure of susceptible alveoli. Pathologic, physiologic, and theoretical arguments favor a strategy that attempts to avoid tidal alveolar collapse and to keep transalveolar pressure (not PaCO2) within normal physiologic limits. CO2 retention may be an unavoidable consequence of such a lung-protection strategy. Although the traditional paradigm for ventilation appears in need of revision, it must be recognized that few prospective, controlled trials of alternative ventilation modes have been undertaken to prove their superiority.
在急性肺损伤中,人们认为损伤是均匀分布的,这促使了传统上使用高充气压力来维持正常潮气量和动脉血气的做法。尽管胸部正位片常常显示损伤的均匀性,但最近的研究突出了成人(急性)呼吸窘迫综合征实际具有的病理解剖和肺力学的异质性。在应用机械通气时,考虑这种异质性很重要,因为大量实验证据有力地表明,传统的容量和压力选择有可能阻碍肺愈合或使损伤扩展到先前未受影响的区域。由于肺区域在可扩张性和脆弱性方面存在显著差异,急性损伤的肺应被视为小肺而非硬肺。通气良好的肺单位似乎具有近乎正常的气-组织比以及保存良好的机械和气体交换特性。机械通气可能会使内皮和上皮屏障承受过大压力,导致蛋白质性肺泡水肿形成而实际并未发生膜破裂。实验表明,这种损伤与过高的跨肺泡充气压力、与可通气肺组织大小不相适应的潮气量,或与在维持呼气末肺泡压力不足以防止易感肺泡周期性开放和关闭时产生的损伤性剪切力有关。病理、生理和理论方面的论据都支持一种试图避免肺泡周期性萎陷并将跨肺泡压力(而非动脉血二氧化碳分压)维持在正常生理范围内的策略。二氧化碳潴留可能是这种肺保护策略不可避免的后果。尽管传统的通气模式似乎需要修正,但必须认识到,很少有前瞻性、对照试验来证明替代通气模式的优越性。