We thank Drs. Zhou and Wang for their thoughtful comments on our study.1 Certainly, many factors may influence the tidal volume during anesthesia induction. We previously reported that progressive muscle paralysis induced by rocuronium injection did not change the tidal volume during facemask ventilation without airway maneuvers in adult subjects with normal upper airway anatomy.2 In contrast to Ikeda et al.’s study,2 the tidal volume progressively improved in both non–sleep disordered breathing and sleep disordered breathing groups in Sato et al.’s study.1 We believe there are three major differences between Ikeda et al.’s and Sato et al.’s study designs: anesthesia depth, initial airway patency, and airway maneuvers by the anesthetists. It is our opinion that anesthesia depth contributes little to time dependence of the tidal volume, given that pharyngeal collapsibility increases only slightly by increasing anesthesia depth with propofol, however, the pharyngeal collapsibility profoundly increases immediately after loss of consciousness.3 The pharyngeal airway was initially open in Ikeda et al.’s study but was not controlled in Sato et al.’s study. We suspect that the pharyngeal airway initially closed, particularly in Sato et al.’s patients with sleep disordered breathing; subsequently, surface adhesive forces of the pharyngeal airway mucosa may have played a role in making reopening of the airway difficult.4 We believe that minor adjustments made for each individual patient throughout the airway maneuver process by the anesthetists, as well as the gradual progression of muscle paralysis and anesthesia depth, will lead to achievement of a more successful and constant airway maneuver. Regrettably, we did not measure the change in rigidity of the neck and mandible, nor the process of proper head extension and mandible advancement during mask ventilation.
In addition to the upper airway mechanisms discussed above, Drs. Zhou and Wang also pointed out the possible contribution of mechanical changes in the lower airways to the results of this study. During progressive increase of muscle paralysis, chest wall compliance increase and laryngeal resistance decrease are expected. Without any doubt, the tidal volume measured in this study is an outcome of interaction between these lower airway and upper airway mechanisms. Drs. Zhou and Wang suggest use of peak inspiratory pressure during volume-controlled ventilation instead of tidal volume during pressure-controlled ventilation. We disagree with their suggestion because higher peak pressure induced during the volume-controlled ventilation causes gastric gas insufflation, particularly in obese subjects, which would consequently increase study risk for the participants.5 It is our hope that future studies will clarify the mechanisms while controlling the concerns raised by Drs. Zhou and Wang and lead to better techniques of improving the mask ventilation process.
Drs. Wang and Wei raised the possibility of circulatory influence on the onset of muscle paralysis between sleep disordered breathing and non-sleep disordered breathing groups. The techniques used in rocuronium injection ideally should be identical between the groups; however, to our regret, perfect control was not obtained, while rocuronium was rapidly injected through a forearm intravenous line in all participants. Delayed onset time may have influenced the tidal volume due to difficulty in performing airway maneuvers under less paralyzed condition. It should be noted, however, that the train-of-four ratio did not differ between the subgroups in which significant tidal volume difference was confirmed. The idea of reduced cardiac output in patients with sleep disordered breathing as an explanation for the results of this study is interesting, but would not explain the reason for a smaller tidal volume in sleep disordered breathing patients even with two-hand mask ventilation under complete paralysis. The techniques of shortening rocuronium onset time may be worth using in clinical practice, however, for maximizing the positive impact of muscle relaxant on mask ventilation during anesthesia induction, particularly in patients with sleep disordered breathing, as recent airway guidelines strongly recommend.6,7
As commented by Drs. Buffington, Wells, and Soose, the results of this study strongly support expiratory flow limitation as an important mechanism for difficult or impossible mask ventilation during anesthesia induction. Although we agree with the possibility of “valve-like behavior of the soft palate” as a cause of expiratory flow limitation, we did not directly confirm it in this study. We have certainly experienced that triple airway maneuvers, including mouth opening with two hands and/or use of an oral airway, eliminate the expiratory flow limitation on the airflow tracing and improve mask ventilation. Furthermore, as they pointed out, the valve-like behavior of the soft palate may or may not be all-or-none and the “partial expiratory flow limitation” waveform pattern in figure 2 could be caused by expiratory airflow through the mouth. It is of paramount importance to explore the mechanisms of expiratory flow limitation. We completed a clinical study to address these issues and are preparing for publication (University Hospital Medical Information Network; UMIN000011821: Dynamic behavior of the soft palate during mask ventilation).
The authors declare no competing interests.