Marini John J, Gattinoni Luciano
Department of Medicine, University of Minnesota, Minneapolis, Saint Paul, MN, USA.
Crit Care Med. 2008 Dec;36(12):3252-8. doi: 10.1097/CCM.0b013e31818f0e68.
To describe the clinical implications of an often neglected mechanism through which localized acute lung injury may be propagated and intensified.
Experimental and clinical evidence from the medical literature relevant to the airway propagation hypothesis and its consequences.
The diffuse injury that characterizes acute respiratory distress syndrome is often considered a process that begins synchronously throughout the lung, mediated by inhaled or blood-borne noxious agents. Relatively little attention has been paid to possibility that inflammatory lung injury may also begin focally and propagate sequentially via the airway network, proceeding mouth-ward from distal to proximal. Were this true, modifications of ventilatory pattern and position aimed at geographic containment of the injury process could help prevent its generalization and limit disease severity. The purposes of this communication are to call attention to this seldom considered mechanism for extending lung injury that might further justify implementation of low tidal volume/high positive end-expiratory pressure ventilatory strategies for lung protection and to suggest additional therapeutic measures implied by this broadened conceptual paradigm.
描述一种常被忽视的机制的临床意义，通过该机制局部急性肺损伤可能会扩散并加重。
来自医学文献的与气道传播假说及其后果相关的实验和临床证据。
急性呼吸窘迫综合征的特征性弥漫性损伤通常被认为是一个在整个肺部同步开始的过程，由吸入性或血源性有害物质介导。相对而言，人们很少关注炎性肺损伤也可能从局部开始并通过气道网络依次传播，从远端向近端向口腔方向发展的可能性。如果这是真的，旨在对损伤过程进行区域控制的通气模式和体位的调整可能有助于防止其扩散并限制疾病的严重程度。本通讯的目的是提醒人们注意这种很少被考虑的扩大肺损伤的机制，这可能进一步证明实施低潮气量/高呼气末正压通气策略以保护肺部是合理的，并提出这种扩展的概念范式所暗示的其他治疗措施。
