Pereira Sérgio M, Sinedino Bruno E, Costa Eduardo L V, Morais Caio C A, Sklar Michael C, Adkson Sales Lima Cristhiano, Nakamura Maria A M, Ranzani Otavio T, Goligher Ewan C, Tucci Mauro R, Ho Yeh-Li, Taniguchi Leandro U, Vieira Joaquim E, Brochard Laurent, Amato Marcelo B P
Division of Pneumology (Laboratory of Medical Investigation 09), Faculty of Medicine, University of São Paulo, São Paulo, Brazil; Department of Anesthesia and Pain Medicine, Unity Health Toronto; Interdepartmental Division of Critical Care; and Keenan Center for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada.
Anesthesiology Discipline, Department of Surgery, Faculty of Medicine, University of São Paulo, São Paulo, Brazil.
Anesthesiology. 2022 May 1;136(5):763-778. doi: 10.1097/ALN.0000000000004161.
Strong spontaneous inspiratory efforts can be difficult to control and prohibit protective mechanical ventilation. Instead of using deep sedation and neuromuscular blockade, the authors hypothesized that perineural administration of lidocaine around the phrenic nerve would reduce tidal volume (VT) and peak transpulmonary pressure in spontaneously breathing patients with acute respiratory distress syndrome.
An established animal model of acute respiratory distress syndrome with six female pigs was used in a proof-of-concept study. The authors then evaluated this technique in nine mechanically ventilated patients under pressure support exhibiting driving pressure greater than 15 cm H2O or VT greater than 10 ml/kg of predicted body weight. Esophageal and transpulmonary pressures, electrical activity of the diaphragm, and electrical impedance tomography were measured in pigs and patients. Ultrasound imaging and a nerve stimulator were used to identify the phrenic nerve, and perineural lidocaine was administered sequentially around the left and right phrenic nerves.
Results are presented as median [interquartile range, 25th to 75th percentiles]. In pigs, VT decreased from 7.4 ml/kg [7.2 to 8.4] to 5.9 ml/kg [5.5 to 6.6] (P < 0.001), as did peak transpulmonary pressure (25.8 cm H2O [20.2 to 27.2] to 17.7 cm H2O [13.8 to 18.8]; P < 0.001) and driving pressure (28.7 cm H2O [20.4 to 30.8] to 19.4 cm H2O [15.2 to 22.9]; P < 0.001). Ventilation in the most dependent part decreased from 29.3% [26.4 to 29.5] to 20.1% [15.3 to 20.8] (P < 0.001). In patients, VT decreased (8.2 ml/ kg [7.9 to 11.1] to 6.0 ml/ kg [5.7 to 6.7]; P < 0.001), as did driving pressure (24.7 cm H2O [20.4 to 34.5] to 18.4 cm H2O [16.8 to 20.7]; P < 0.001). Esophageal pressure, peak transpulmonary pressure, and electrical activity of the diaphragm also decreased. Dependent ventilation only slightly decreased from 11.5% [8.5 to 12.6] to 7.9% [5.3 to 8.6] (P = 0.005). Respiratory rate did not vary. Variables recovered 1 to 12.7 h [6.7 to 13.7] after phrenic nerve block.
Phrenic nerve block is feasible, lasts around 12 h, and reduces VT and driving pressure without changing respiratory rate in patients under assisted ventilation.
强烈的自主吸气努力可能难以控制，并妨碍保护性机械通气。作者推测，与使用深度镇静和神经肌肉阻滞剂不同，在膈神经周围进行利多卡因神经周围给药可降低急性呼吸窘迫综合征自主呼吸患者的潮气量（VT）和经肺峰值压力，而不是使用深度镇静和神经肌肉阻滞剂。
在一项概念验证研究中，使用了一种已建立的六只雌性猪的急性呼吸窘迫综合征动物模型。然后，作者在九名接受压力支持且驱动压力大于15 cm H2O或VT大于预测体重的10 ml/kg的机械通气患者中评估了该技术。在猪和患者中测量了食管和经肺压力、膈肌电活动和电阻抗断层扫描。使用超声成像和神经刺激器识别膈神经，并在左右膈神经周围依次给予神经周围利多卡因。
结果以中位数[四分位间距，第25至75百分位数]表示。在猪中，VT从7.4 ml/kg[7.2至8.4]降至5.9 ml/kg[5.5至6.6]（P<0.001），经肺峰值压力（25.8 cm H2O[20.2至27.2]降至17.7 cm H2O[13.8至18.8]；P<0.001）和驱动压力（28.7 cm H2O[20.4至30.8]降至19.4 cm H2O[15.2至22.9]；P<0.001）也下降。最依赖部位的通气从29.3%[26.4至29.5]降至20.1%[15.3至20.8]（P<0.001）。在患者中，VT下降（8.2 ml/kg[7.9至11.1]降至6.0 ml/kg[5.7至6.7]；P<0.001），驱动压力也下降（24.7 cm H2O[20.4至34.5]降至18.4 cm H2O[16.8至20.7]；P<0.001）。食管压力、经肺峰值压力和膈肌电活动也下降。依赖部位通气仅从11.5%[8.5至12.6]略有下降至7.9%[5.3至8.6]（P = 0.005）。呼吸频率没有变化。膈神经阻滞后1至12.7小时[6.7至13.7]变量恢复。
膈神经阻滞是可行的，持续约12小时，可降低辅助通气患者的VT和驱动压力，而不改变呼吸频率。
