High Positive End-Expiratory Pressure Renders Spontaneous Effort Noninjurious
High Positive End-Expiratory Pressure Renders Spontaneous Effort Noninjurious
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DOI：
10.1164/rccm.201706-1244oc
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发表时间：
2018-05-15
影响因子：
24.7
通讯作者：
Fujino, Yuji
中科院分区：
文献类型：
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作者：
Morais, Caio C. A.;Koyama, Yukiko;Fujino, Yuji
基本原理：在急性呼吸窘迫综合征（ARDS）中，肺不张的实性肺组织损害了由胸壁收缩引起的胸膜压（Ppl）负波动的传递。更负的Ppl的定位通过从其他肺区域（例如，非依赖性肺[pendelluft]）或呼吸机。降低自发性努力水平和/或将固体样肺转换为液体样肺可能使自发性努力无损伤。目的：确定自发性努力是否增加依赖性肺损伤，以及是否通过呼气末正压（PEEP）恢复肺不张的固体样肺来减少这种损伤。测量局部组织学（兔）、炎症（正电子发射断层扫描;猪）、局部吸气Ppl（支气管内球囊测压）和拉伸（电阻抗断层扫描;猪）。呼吸驱动进行了评估，在11例ARDS. Measures和主要结果：虽然在肌肉麻痹损伤主要是在非依赖性和中间的肺区域在低（与高）PEEP，强吸气努力增加损伤（正电子发射断层扫描和组织学）依赖性肺。较强的努力（相对于肌肉麻痹）导致局部过度拉伸和依赖性肺中更大的潮汐募集，其中更负的Ppl被定位并且产生更大的拉伸。相反，高PEEP通过更均匀地分布负Ppl和降低自发努力的幅度（即，结论：用力过猛增加了依赖性肺损伤，其中产生了较高的局部肺应力和拉伸;在严重ARDS中，通过高PEEP使用力依赖性肺损伤最小化，这可能抵消了麻痹的需要。
Rationale: In acute respiratory distress syndrome (ARDS), atelectatic solid-like lung tissue impairs transmission of negative swings in pleural pressure (Ppl) that result from diaphragmatic contraction. The localization of more negative Ppl proportionally increases dependent lung stretch by drawing gas either from other lung regions (e.g., nondependent lung [pendelluft]) or from the ventilator. Lowering the level of spontaneous effort and/or converting solid-like to fluid-like lung might render spontaneous effort noninjurious.Objectives: To determine whether spontaneous effort increases dependent lung injury, and whether such injury would be reduced by recruiting atelectatic solid-like lung with positive end-expiratory pressure (PEEP).Methods: Established models of severe ARDS (rabbit, pig) were used. Regional histology (rabbit), inflammation (positron emission tomography; pig), regional inspiratory Ppl (intrabronchial balloon manometry), and stretch (electrical impedance tomography; pig) were measured. Respiratory drive was evaluated in 11 patients with ARDS.Measurements and Main Results: Although injury during muscle paralysis was predominantly in nondependent and middle lung regions at low (vs. high) PEEP, strong inspiratory effort increased injury (indicated by positron emission tomography and histology) in dependent lung. Stronger effort (vs. muscle paralysis) caused local overstretch and greater tidal recruitment in dependent lung, where more negative Ppl was localized and greater stretch was generated. In contrast, high PEEP minimized lung injury by more uniformly distributing negative Ppl, and lowering the magnitude of spontaneous effort (i.e., deflection in esophageal pressure observed in rabbits, pigs, and patients).Conclusions: Strong effort increased dependent lung injury, where higher local lung stress and stretch was generated; effort-dependent lung injury was minimized by high PEEP in severe ARDS, which may offset need for paralysis.