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Anesthesiology, V 129 • No 3 394 September 2018 F UNCTIONAL impairment of respiratory muscles is considered one of the determinants of difficult weaning from the ventilator,1 which results in prolonged mechanical ventilation and is associated with worse patient outcome.2 Patients requiring invasive ventilation are exquisitely prone to the development of respiratory muscle dysfunction (including ventilator-induced diaphragmatic dysfunction), which is worsened by a number of concomitant factors like sepsis, electrolyte imbalance, malnutrition, and administration of aminoglicosides, steroids, and neuromuscular blockers. Most of the studies tackling this issue were focused on the dysfunction of inspiratory muscles, mostly the diaphragm. At variance, very few studies aimed at assessing the role of expiratory muscles. In healthy subjects at rest, expiration is a passive process: when the inspiratory muscles relax at the end of inhalation, the elastic recoil of the lung tissue (i.e., the “release” of the elastic energy stored during lung inflation) generates a positive pressure gradient between the alveoli and the atmosphere, causing the outflow of air. Although expiration is usually passive, it can become an active process involving the contraction of muscles with expiratory activity, in particular abdominal muscles (which push the diaphragm upward, reducing the volume of the chest cavity) and internal intercostal muscles (which pull the ribs downward, compressing the rib cage). This happens during forced breathing and in some pathologic conditions characterized by airways obstruction (like asthma or chronic obstructive pulmonary disease). On one hand, recruitment of expiratory muscles may facilitate the subsequent inspiration and limit hyperinflation; on the other hand, it may result in a significant increase in the oxygen consumption of respiratory muscles (i.e., in the work of breathing). Another mechanism acting to limit hyperinflation in the presence of airway obstruction is the persistence of diaphragm contraction during exhalation: this diaphragmatic “tonic activity” has been described in different experimental models and might contribute to stabilize peripheral airways and prevent expiratory lung collapse. In the current issue of ANESTHESIOLOGY, Doorduin et al.3 report the results of an interesting study exploring the role of expiratory muscle recruitment and electrical diaphragmatic postinspiratory activity in patients undergoing a weaning trial after at least 3 days of mechanical ventilation. The spontaneous breathing trial was performed with a T-tube (no positive end-expiratory pressure) for at least 60 min. Patients were instrumented with a modified nasogastric tube equipped with an esophageal and a gastric balloon and with microelectrodes for diaphragm electromyography recording, underlining the potential for electromyography as a monitoring tool,4,5 irrespective of the application of neurally adjusted ventilatory assist. Expiratory muscle recruitment was computed as the pressure–time product of gastric pressure, and tonic activity of the diaphragm was expressed as a percentage of the peak inspiratory diaphragm electromyography activity during the last quartile of neural expiration. As expected, patients who failed weaning (i.e., those who failed the spontaneous breathing trial or required reintubation within 48 h from extubation) had a higher rapid shallow breathing index, a higher inspiratory electrical activity of the diaphragm, and a significantly lower neuromechanical efficiency of diaphragm contraction (indicative Weaning from Mechanical Ventilation