We thank the authors for their comments and appreciate the opportunity to clarify several aspects of our study.

The 12 to 15 ml/kg was not the volume of the first breath after sugammadex, but rather was the tidal volume required during paralysis to alleviate the subjects’ dyspnea. This was the expiratory volume, so the measured values would not have been elevated by any mask leak. Consistent with this, the end-tidal partial pressure of carbon dioxide was between 30 and 35 mmHg during neuromuscular blockade compared to 37 to 42 mmHg before paralysis.

We agree that arterial carbon dioxide measurements would have been ideal; however, in healthy adults the end-tidal closely tracks arterial values. Provided the end-tidal partial pressure of carbon dioxide is measured appropriately from the alveolar plateau, in healthy adults the difference from arterial values is less than 3 to 5 mmHg.  The studies cited—one involving patients spontaneously breathing on halothane, the other in children—may not be the most relevant comparisons for our awake and paralyzed adult volunteers.

The description from one subject of the airway feeling like a “small crack” suggests an altered proprioception of tongue and pharynx during neuromuscular blockade. We doubt it was an accurate indication of airway size, especially as we could easily deliver large tidal volumes.

We suggest that the dyspnea was due to factors other than inadequate gas exchange. Breathing movements are known to alter the sensation of dyspnea, even when the arterial carbon dioxide measurements is held constant.  A classic example of this is the effect of rebreathing expired air on the breakpoint. Chronically ventilated patients often require much greater tidal volumes than are required for gas exchange alone. Consequently, they often have very low arterial carbon dioxide measurements.  In our study, the dyspnea may have been due to the reduced functional residual capacity from the neuromuscular blockade, which generated a sensation of abnormally deflated lungs. If this were the mechanism, then addition of positive end-expiratory pressure may also have been effective in alleviating it.

For further insight into the complex interplay of factors involved in the control of ventilation and the sensation of dyspnea, we recommend “Air Hunger: A Primal Sensation and a Primary Element of Dyspnea” by Banzett et al., which provides an excellent overview of the topic.