We thank Dr. Duvaldestin for his comments regarding our article.1
Dr. Duvaldestin points out that our assessor-blinded study is at odds with his own findings.2
We believe that findings from both studies can be easily reconciled by taking into account some overlapping findings as well as a few obvious methodologic differences between these studies.1,2
In accordance with our data, Duvaldestin et al. did not observe flow limitation during normal breathing. However, our data show that integrity was impaired during airway challenges.
Duvaldestin and coworkers2
correctly point out that, in their study, volunteers were breathing via
a mouthpiece whereas we used a nasal mask during our experiments.1
Indeed, this is an important methodologic difference. In fact, our approach allows for analysis of the pressure–flow relationship of the whole supraglottic airway, whereas the method of Dr. Duvaldestin is restricted to the oropharyngeal airway only. However, it is clinically important to evaluate both, the retropharyngeal and retroglossal upper airway.
We have shown that the effects of partial neuromuscular blockade on the upper airway muscles are significantly greater in the retropalatal compared with the retroglossal airway.3
In accordance, Schwab and coworkers4
showed that the soft palate plays the predominant role in mediating airway narrowing during sleep, and this is thought to be related to a decrease in upper airway dilator muscle activity. Thus, the retropalatal area seems to be particularly susceptible to a decrease in upper airway dilator tone. Accordingly, the technique used by Dr. Duvaldestin and coworkers is not sensitive to detect upper airway collapse in its most collapsible segment.
Although in Dr. Duvaldestin's opinion this circumstance is the main difference between the two studies, we believe that further differences in methodology exist with far greater impact on the results.
First, Dr. Duvaldestin and coworkers studied six volunteers, and there is no information provided how the number of volunteers was determined. Our study was performed following a power analysis based on pilot experiments and we examined 15 volunteers. Thus, one might speculate that Dr. Duvaldestin's study lacked the power to demonstrate significant results—absence of significance does not reflect significance of absence.
Second, Dr. Duvaldestin and coworkers conducted a negative pressure challenge using a stepwise decrease in airway pressure from ambient pressure to −40 cm H2
O with a decrease in airway pressure by 5 cm H2
O implemented every three respiratory cycles. This technique is assumed to assess active dynamic responses to airway obstruction, and the critical airway pressure obtained is thus the so-called active Pcrit.5
Depending on the volunteers' respiratory rates, the time between the onset and the nadir of the negative pressure challenge with this technique varies and occurs over time. Most likely, this results in differences in compensatory mechanisms such as airway muscle activation or changes in respiratory drive. In our study, in contrast, volunteers were exposed to short random pressure drops alternating with longer periods of breathing at a (slightly positive) holding pressure. This latter technique is suitable to assess the passive mechanical properties of the upper airway and has thus been coined the passive Pcrit.5
This variable reflects the mechanical integrity of the upper airway and, potentially, the patient's ability to compensate for challenges such as a forced inspiration.
Although not addressed in any of the publications, upper airway muscles are likely more susceptible to neuromuscular blocking agents than the diaphragm. Whether this is due to particular resistance of the diaphragm to such drugs or to particular susceptibility of the upper airway muscles has not been elaborated.
Accordingly, although we agree with Dr. Duvaldestin that further work on the susceptibility of the airway muscles is warranted, this issue does not alter our findings or dilute their significance.
Frank Herbstreit, Dr. Med.,*
Jürgen Peters, Prof. Dr. Med.
Matthias Eikermann, PD Dr. Med.
*Klinik fuer Anaesthesiologie und Intensivmedizin, Universitaetsklinikum Essen, Essen, Germany. email@example.com
1. Herbstreit F, Peters J, Eikermann M: Impaired upper airway integrity by residual neuromuscular blockade. Anesthesiology 2009; 110:1253–60
2. D'Honneur G, Lofaso F, Drummond GB, Rimaniol JM, Aubineau JV, Harf A, Duvaldestin P: Susceptibility to upper airway obstruction during partial neuromuscular block. Anesthesiology 1998; 88:371–8
3. Eikermann M, Vogt FM, Herbstreit F, Vahid-Dastgerdi M, Zenge MO, Ochterbeck C, de Greiff A, Peters J: The predisposition to inspiratory upper airway collapse during partial neuromuscular blockade. Am J Respir Crit Care Med 2007; 175:9–15
4. Trudo FJ, Gefter WB, Welch KC, Gupta KB, Maislin G, Schwab RJ: State-related changes in upper airway caliber and surrounding soft-tissue structures in normal subjects. Am J Respir Crit Care Med 1998; 158:1259–70
5. Patil SP, Schneider H, Marx JJ, Gladmon E, Schwartz AR, Smith PL: Neuromechanical control of upper airway patency during sleep. J Appl Physiol 2007; 102:547–56
© 2010 American Society of Anesthesiologists, Inc.