To the Editor:
We read with interest the article by Doorduin et al.1 regarding weaning failure. The hypothesis was that expiratory muscle effort is higher in weaning failure patients compared to successfully weaned patients. They studied 20 patients of whom 9 had weaning failure. They found that neuromechanical efficiency of diaphragm was lower both during pressure support ventilation and during spontaneous breathing trial in the weaning failure group, despite higher neural respiratory drive. We are curious about the mechanism and possible confounders.
First, the clinical characteristics of the weaning failure group appear different. The weaning failure group had more inspiratory muscle problems at the beginning of the spontaneous breathing trial. Specifically, 56% of the weaning failure but 36% of the weaning success group received mechanical ventilation longer than 2 weeks, suggesting that the failure group had more frequent diaphragm and inspiratory muscle weakness problems.2 Studies report that diaphragm thickness progressively decreases during mechanical ventilation, and ventilator-induced diaphragm atrophy develops in patients with prolonged mechanical ventilation. In addition, 45% of the weaning success group but 67% of the weaning failure group had cardiac arrest or surgery. Cardiac surgery frequently causes diaphragm weakness.3 Additionally, patients with more cardiac problems might have developed pulmonary edema during weaning, and this may cause increased inspiratory muscle load. Can these characteristics explain higher neural respiratory drive but lower neuromechanical efficiency of the diaphragm in the failure group? Some previous studies suggest that abdominal muscles are recruited when the load on inspiratory muscles is increased.4 Second, the weaning failure group had higher Paco2 levels at the end of the trial. This may be another reason for expiratory muscle recruitment in the weaning failure group. Some studies report that expiratory muscles can be recruited when respiratory demand increases under conditions such as hypercapnia, hypoxia, or exercise.5 While expiratory activity of the diaphragm was similar during the end of the spontaneous breathing trial in both groups, expiratory gastric pressure increased in the weaning failure group compared to the success group. Contribution of the expiratory muscles to the total pressure–time product significantly increased from 13 to 24% at the end of the spontaneus breathing trial in the weaning failure group but did not change in the weaning success group. Taken together, these findings suggest that increased expiratory muscle recruitment happened in the weaning failure group as a result, not a reason. In conclusion, further information is necessary to understand the exact role of expiratory muscles in weaning failure.
Competing Interests
The authors declare no competing interests.