Respiratory Rate as a Factor in Lung Injury - Not Just What You Set, but How You Set
Respiratory Rate as a Factor in Lung Injury - Not Just What You Set, but How You Set
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呼吸频率是肺损伤的一个因素 - 不仅仅是您设置的呼吸频率，还有您如何设置
DOI：
10.1097/aln.0000000000004502
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发表时间：
2023
期刊：
影响因子：
8.8
通讯作者：
Uchida Kanji
中科院分区：
文献类型：
--
作者：
Saita;K.;Moriuchi;Y.;Iwagawa;T.;Aihara;M.;Takai;Y.;Uchida;K.;Watanabe;S.;Uchida Kanji
机械通气的呼吸支持对于患有急性呼吸窘迫综合征（ARDS）等疾病的危重患者至关重要，这些疾病的肺部气体交换能力受损。然而，通气本身将肺部暴露在非生理性环境中，这本身就会伤害肺部。有关呼吸机设置影响患者预后的报告主要集中在低潮气量（VT） 1和适当的驱动压力上。2此外，压力（气压损伤）、VT（容积损伤）和肺单元循环开闭（肺不电损伤）的概念已被提出作为通气性肺损伤的机制。随后研究和讨论了将这些因素最小化的呼吸机设置。呼吸频率虽然是呼吸机调定中必不可少的一项，但由于是在VT调定后被动调整，因此很少受到重视。动物研究表明，呼吸频率增加会加剧通气引起的肺损伤3，支持这一现象的证据正在逐渐积累。基于认识到肺损伤的严重程度受一定时间内施加于肺组织的静态肺损伤因子数量的影响，提出了机械功率（由体积、压力、流量和呼吸频率组成）的概念来量化这些因子。与其他静态因素相比，这些动态因素是所谓的“ergotrauma”的原因。因此，呼吸频率作为一个动态因素正在引起人们的注意；然而，关于特定呼吸频率设置如何影响肺损伤的报道仍然很少。在本期《麻醉学》杂志上，Xavier等人发表了一项有趣的研究，可能会为这一领域增添一些见解。作者提出了这样一个假设，即如果呼吸速率是逐渐而不是突然增加而达到理想的呼吸速率，则高呼吸速率机械通气引起的肺损伤将会减弱。在气管内脂多糖诱导的轻度ARDS实验模型中，作者随机给予不同呼吸速率模式的大鼠进行机械通气（压力控制模式，维持VT为6 ml/kg，呼气末正压为3 cm H2O），共2 h。骤增组呼吸速率从70次/min突然增加到130次/min，逐渐适应组呼吸速率从70次/min突然增加到130次/min。呼吸频率在30或60 min内由70次/min逐渐增加到130次/min。在每组中，作者评估了以130次呼吸/分钟通气1小时后肺损伤的病理表现、肺通气、炎症介质和细胞损伤标志物的异质性评分。在另一个系列中，另一个组在呼吸频率突然从70次/分钟增加到130次/分钟之前进行肺补充操作（持续气道正压30 cm H2O 30秒）。作者发现，呼吸频率的突然增加导致更高的组织学肺损伤评分，更差的肺通气异质性，以及更高水平的炎症和细胞损伤标志物。在逐渐适应组中，所有这些变化都减弱了。此外，在呼吸频率突然增加之前进行肺再募集操作，可以防止高呼吸频率机械通气后炎症和细胞损伤标志物的增加。
Respiratory support with mechanical ventilation is crucial for critically ill patients with diseases such as acute respiratory distress syndrome (ARDS), in which the pulmonary gas exchange capacity is impaired. However, ventilation itself exposes the lungs to a nonphysiologic environment, which in itself injures the lungs. Reports on ventilator settings that have been shown to affect patient outcomes have focused on low tidal volume (VT) 1 and adequate driving pressure. 2 Additionally, the concepts of pressure (barotrauma), VT (volutrauma), and cyclic opening–closing of the lung units (atelectrauma) have been proposed as mechanisms of ventilationinduced lung injury. Ventilator settings that minimize each of these factors were subsequently studied and discussed. Although the respiratory rate is an essential item in the ventilator setting, it has received little attention because it is passively adjusted after the VT setting. Animal studies have shown that increasing the respiratory rate exacerbates ventilation-induced lung injury, 3 and evidence in support of this phenomenon is gradually accumulating. Based on the recognition that the severity of lung injury is affected by the number of static lung injury factors applied to the lung tissue over a certain period of time, the concept of mechanical power (consisting of volume, pressure, flow, and respiratory rate) was proposed to quantify these factors. These dynamic factors are the cause of so-called “ergotrauma,” in contrast to other static factors. 4 Thus, the respiratory rate is gaining attention as a dynamic factor; however, there are still few reports describing how specific respiratory rate settings affect lung injury. In this issue of Anesthesiology, Xavier et al. 5 published an interesting study that may add some insights to this field. The authors addressed the hypothesis that lung injury induced by mechanical ventilation with a high respiratory rate would be attenuated if the desired respiratory rate was reached by gradual rather than abrupt increases. In an experimental model of mild ARDS induced by intratracheal administration of lipopolysaccharide, the authors randomly assigned rats to receive mechanical ventilation (pressure control mode to maintain a VT of 6 ml/kg with 3 cm H2O positive end-expiratory pressure) with various respiratory rate patterns for a total of 2 h. In the abrupt increase group, the respiratory rate was abruptly increased from 70 to 130 breaths/min, while in the gradual adaptation group, the respiratory rate was gradually increased from 70 to 130 breaths/min in 30 or 60 min. In each group, the authors evaluated pathologic findings of lung injury after 1 h of ventilation at 130 breaths/min, heterogeneity scores of lung aeration, inflammatory mediators, and markers of cellular damage. In another series, an additional group underwent a pulmonary recruitment maneuver (continuous positive airway pressure of 30 cm H2O for 30 s) before the respiratory rate was abruptly increased from 70 to 130 breaths/min. The authors found that the abrupt increase in the respiratory rate resulted in a greater histologic lung injury score, worse lung aeration heterogeneity, and higher levels of markers of inflammation and cellular damage. In the gradual adaptation group, all of these changes were attenuated. Additionally, the lung recruitment maneuver before the abrupt increase in the respiratory rate prevented the increase in the markers of inflammation and cell damage after mechanical ventilation with a high respiratory rate.