A MODEL OF OBSTRUCTIVE SLEEP APNEA IN NORMAL HUMANS

D. Stanescu and C. Veriter

Université Catholique de Louvain, Pulmonary Laboratory and Division Cliniques, Universitaires St Luc, Brussels, Belgium

	To the Editor :

In the June 2000 issue of the journal, King and colleagues (1) have reported on their findings on upper airway obstruction induced during sleep in normal subjects by lowering nasal pressure to 10 cm H₂O.

Because upper airways are compliant structures, it is not surprising that a change in their transmural pressure will modify their permeability. A negative transmural pressure would necessarily narrow (2) or close these airways, as described in this paper (1). A positive transmural pressure would open a closed airway, as during application of CPAP in the sleep apnea syndrome.

What is surprising, however, is the explanation offered by the authors for the restoration of the upper airway patency during arousal. The allegation of King and colleagues (1) is that during arousal the transmural pressure of the upper airways became positive. Furthermore, to explain how, in the presence of a continuous negative intraluminal pressure, transmural pressure became positive, the authors assert that "the pressure surrounding the site of pharyngeal collapse fell below the level of subatmospheric intraluminal pressure," attributed to "the activation of upper airway muscles." If, in their example, the luminal pharyngeal pressure is 10 cm H₂O, the outside pressure must become less than 10 cm H₂O (i.e., 15 or 20 cm H₂O)! But how can the activation of upper airway muscles decrease the surrounding pressure? In contrast to the intrathoracic airways, where the outside pressure is the pleural pressure, the surrounding pressure of the extrathoracic airways is the atmospheric pressure and of course, cannot change. In fact, despite the negative intraluminal pressure, the activation of upper airway muscles restores the patency of upper airways by dilating and stabilizing them.

Curiously enough, in the only recording illustrating the respiratory and the polysomnographic response in one subject breathing with 10 cm H₂O during non-REM sleep (Figure 2), contrary to the comments of the authors (1), oxyhemoglobin saturation increased during obstructive sleep apnea, instead of decreasing, as one would expect. Neither was there, except in two breaths, a "progressive increase in esophageal pressure swings."

	References

1. King ED, O'Donnell CP, Smith PL, Schwartz AR. A model of obstructive sleep apnea in normal humans: role of the upper airway. Am J Respir Crit Care Med 2000; 161: 1979-1984 [Abstract/Free Full Text].

2. Sanna A, Veriter C, Kurtansky A, Stanescu D. Contraction and relaxation of upper airway muscles during expiratory application of negative pressure at the mouth. Sleep 1994; 17: 220-225 [Medline].

	From the Authors:

We appreciate that some confusion exists concerning the surrounding pressure used to determine the upper airway transmural pressure. In our model (1) we define transmural pressure as the difference between the intraluminal pressure and the pressure within the tissues surrounding the airway lumen. With the activation of upper airway dilator muscles, the surrounding tissue pressure would fall, thereby increasing the transmural pressure. We refer the reader to a more complete discussion of the theoretical basis for our model, and the influence of muscle activation on transmural pressure (2).

Johns Hopkins University, Baltimore, Maryland

	References

1. King ED, O'Donnell CP, Smith PL, Schwartz AR. A model of obstructive sleep apnea in normal humans: role of the upper airway. Am J Respir Crit Care Med 2000; 161: 1979-1984 .

2. Gold AR, Schwartz AR. The pharyngeal critical pressure: the whys and hows of using nasal continuous positive airway pressure diagnostically. Chest 1996; 110: 1077-1088 [Free Full Text].

3. Rowley JA, Permutt S, Willey S, Smith PL, Schwartz AR. Effect of tracheal and tongue displacement on upper airway airflow dynamics. J Appl Physiol 1996; 80: 2171-2178 [Abstract/Free Full Text].

4. Rowley JA, Williams BC, Smith PL, Schwartz AR. Neuromuscular activity and upper airway collapsibility: mechanisms of action in the decerebrate cat. Am J Respir Crit Care Med 1997; 156: 515-521 [Abstract/Free Full Text].