高呼气末正压使自主呼吸不产生损伤。
High Positive End-Expiratory Pressure Renders Spontaneous Effort Noninjurious.
机构信息
1 Divisao de Pneumologia, Instituto do Coracao (Incor), Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
2 Intensive Care Unit, Osaka University Hospital, Suita, Japan.
出版信息
Am J Respir Crit Care Med. 2018 May 15;197(10):1285-1296. doi: 10.1164/rccm.201706-1244OC.
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.
背景
在急性呼吸窘迫综合征（ARDS）中，不张的实变样肺组织会阻碍由膈肌收缩引起的胸膜压力（Ppl）负向波动的传递。更大的负性 Ppl 定位会通过从其他肺区域（例如非依赖区肺[pendelluft]）或呼吸机中抽取气体，相应地增加依赖区肺的拉伸。降低自主呼吸的努力程度和/或将实变样肺转化为液状样肺可能使自主呼吸不会造成损伤。
目的
确定自主呼吸是否会增加依赖区肺损伤，以及通过给予呼气末正压通气（PEEP）来募集不张的实变样肺是否会减轻这种损伤。
方法
使用已建立的严重 ARDS 模型（兔、猪）。测量区域性组织学（兔）、炎症（正电子发射断层扫描；猪）、支气管内球囊测压的区域性吸气 Ppl（intrabronchial balloon manometry）和拉伸（电阻抗断层扫描；猪）。评估了 11 例 ARDS 患者的呼吸驱动。
测量和主要结果
尽管在低 PEEP（与高 PEEP 相比）时，肌肉麻痹期间的损伤主要位于非依赖区和中肺区，但强烈的吸气努力会增加依赖区肺的损伤（通过正电子发射断层扫描和组织学来指示）。与肌肉麻痹相比，更强的努力会导致依赖区肺的局部过度拉伸和更大的潮气量募集，在依赖区肺中会产生更大的负性 Ppl 和更大的拉伸。相比之下，高 PEEP 通过更均匀地分布负性 Ppl 来最大限度地减少肺损伤，并降低自主呼吸的努力程度（即，在兔子、猪和患者中观察到的食管压力的偏差）。
结论
强烈的努力会增加依赖区肺的损伤，在那里会产生更高的局部肺应力和拉伸；在严重 ARDS 中，高 PEEP 会最大限度地减少与努力相关的肺损伤，这可能会抵消对麻痹的需求。
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