• Glauco M Plens, Maddalena T Droghi, Glasiele C Alcala, Sérgio M Pereira, Iuri C Wawrzeniak, Josué A Victorino, Chiara Crivellari, Alice Grassi, Emanuele Rezoagli, Giuseppe Foti, CostaEduardo L VELV0000-0002-6941-3626Laboratório de Pneumologia LIM-09, Disciplina de Pneumologia, Heart Institute (Incor), Hospital das Clínicas da Faculdade de Medicina da Universidade de Sao Paulo, São Paulo, Brazil.Research and Education Institute, H, AmatoMarcelo B PMBP0000-0003-3525-8282Laboratório de Pneumologia LIM-09, Disciplina de Pneumologia, Heart Institute (Incor), Hospital das Clínicas da Faculdade de Medicina da Universidade de Sao Paulo, São Paulo, Brazil., and Giacomo Bellani.
• Laboratório de Pneumologia LIM-09, Disciplina de Pneumologia, Heart Institute (Incor), Hospital das Clínicas da Faculdade de Medicina da Universidade de Sao Paulo, São Paulo, Brazil.
• Am. J. Respir. Crit. Care Med. 2024 Mar 1; 209 (5): 563572563-572.

AbstractRationale: Hypoxemia during mechanical ventilation might be worsened by expiratory muscle activity, which reduces end-expiratory lung volume through lung collapse. A proposed mechanism of benefit of neuromuscular blockade in acute respiratory distress syndrome (ARDS) is the abolition of expiratory efforts. This may contribute to the restoration of lung volumes. The prevalence of this phenomenon, however, is unknown. Objectives: To investigate the incidence and amount of end-expiratory lung impedance (EELI) increase after the administration of neuromuscular blocking agents (NMBAs), clinical factors associated with this phenomenon, its impact on regional lung ventilation, and any association with changes in pleural pressure. Methods: We included mechanically ventilated patients with ARDS monitored with electrical impedance tomography (EIT) who received NMBAs in one of two centers. We measured changes in EELI, a surrogate for end-expiratory lung volume, before and after NMBA administration. In an additional 10 patients, we investigated the characteristic signatures of expiratory muscle activity depicted by EIT and esophageal catheters simultaneously. Clinical factors associated with EELI changes were assessed. Measurements and Main Results: We included 46 patients, half of whom showed an increase in EELI of >10% of the corresponding Vt (46.2%; IQR, 23.9-60.9%). The degree of EELI increase correlated positively with fentanyl dosage and negatively with changes in end-expiratory pleural pressures. This suggests that expiratory muscle activity might exert strong counter-effects against positive end-expiratory pressure that are possibly aggravated by fentanyl. Conclusions: Administration of NMBAs during EIT monitoring revealed activity of expiratory muscles in half of patients with ARDS. The resultant increase in EELI had a dose-response relationship with fentanyl dosage. This suggests a potential side effect of fentanyl during protective ventilation.

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