预先受伤的肺部的低体积通风通过压力度和渐进的气囊缩降低了肺功能
Richard Zimmermann1, Franziska Roeder1, Clemens Ruppert2,3
1Institute of Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany.
概括
低体积的机械通风用microatelectases恶化肺功能通过逐步失去气泡. 由于应力度,损伤从塌的区域扩散,而不是膜洪水.
科学领域:
- 肺部医学 肺部医学
- 关键护理医学 关键护理医学
- 呼吸系统生理学 呼吸系统生理学
背景情况:
- 机械通风可以诱导肺损伤 (VILI).
- 表面活性剂功能障碍导致微乳酶可能通过对邻近气泡的应激度启动VILI.
研究的目的:
- 量化VILI.的组织病理进展.
- 测试在低阳性末尾呼气压力 (PEEP) 通风过程中,损伤是否在微电酶和通风性肺膜膜之间的接口传播.
主要方法:
- 鼠类接受了白素来诱导肺损伤和微型脱酶.
- 肺部在PEEP = 1cmH2O (低PEEP) 或PEEP = 5cmH2O (保护PEEP) 时进行机械通风,长达6小时.
- 测量了肺部机制,并固定了肺部,以对气膜结构进行立体分析.
主要成果:
- 与基线相比,低PEEP通风 (1cmH2O) 导致空气气膜额外损失26%,主要是由于崩.
- 崩的气泡的区域从半径56μm扩大到94μm,表明了微小瘤的生长.
- 气膜损失与肺弹性,服从性和吸气能力的降低相关.
结论:
- 低体积的机械通风在微小基酶的存在下加剧了肺损伤,导致逐渐的气膜损失和肺机械功能受损.
- 微电酶在缩和开放气泡之间的边界上生长,在那里压力度可能会诱导局部血管泄漏和表面活性剂功能障碍.
- 虽然存在一些膜水,但在这个模型中,它不是机械功能退化的主要驱动因素.
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