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American Journal of Respiratory and Critical Care Medicine Vol 172. pp. 1350-1351, (2005)
© 2005 American Thoracic Society


Correspondence

Effect of CPAP and Lung Volume on Obstructive Sleep Apnea

From the Authors:

We would like to thank Drs. Sivan and Pelayo for their interest in our article (1). Unfortunately, their argument is based on several incorrect assumptions. First, they state that "when we breathe, the Pa (alveolar pressure) is about negative 7–10 cm H2O", which is incorrect (2, 3). During a normal inspiration without airway obstruction, alveolar pressure falls approximately 1 cm H2O lower than the mouth pressure. At the end of inspiration and at the end of expiration alveolar pressure matches mouth pressure (= atmospheric pressure or mask pressure if CPAP is used). It is possible they were confusing alveolar with pleural pressure, which could be negative 7–10 cm H2O, but pleural pressure does not have any direct effect on airflow.

Second, they suggest that alveolar pressure changes when we manipulate end expiratory lung volume in the iron lung. This is not the case: a constant change in extrathoracic pressure influences transthoracic pressure (and results in a change in chest wall volume) but not alveolar pressure. Whatever the extrathoracic pressure is, alveolar pressure matches mouth (or mask, airway opening) pressure at the end of the breathing cycle if the airway is open (4). Moreover, the pressure gradient between mouth and alveolar pressure during unobstructed breathing is the same whether the iron lung is used or not (Figure 1). Thus, the finding that the upper airway did not collapse as easily when we increased lung volume in the iron lung, despite the fact that the upper airway was subjected to the same collapsing pressures, suggests a true mechanical change in upper airway collapsibility mediated via lung volume.



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Figure 1. The relationship between extrathoracic pressure, alveolar pressure and continuous positive airway pressure (CPAP) level.Illustrated is the CPAP level that abolishes flow limitation at rest (top) and with increased lung volume caused by negative extrathoracic pressure (bottom). All values are shown at end expiration where alveolar pressure equals mouth pressure.

 
Regarding the experiment they propose on patients with asthma and COPD, autoPEEP could occur due to active exhalation, dynamic hyperinflation, or airway closure, all of which would have very different effects on end expiratory lung volume. Thus this experiment would be very difficult to interpret.

Finally, as the head and neck are outside of the iron lung in our studies, our experimental setting is quite different from moving to a higher or lower altitude. Thus we are confident that our experimental design allowed us to separate the upper airway splinting and lung volume effects of CPAP. We can therefore draw the conclusion that changes in lung volume have important effects on the upper airway in patients with OSA.

Raphael C. Heinzer, Atul Malhotra, Amy S. Jordan, D. Andrew Wellman and David P. White

Brigham and Women's Hospital Boston, Massachusetts

FOOTNOTES

Conflict of Interest Statement: R.C.H. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. A.M. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. A.S.J. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. D.A.W. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. D.P.W. serves as a consultant to the following companies: Respironics Inc. has paid him $10,000/yr for each of the last 3 yr; Itamar Medical has paid him $10,000/yr for the last 3 yr; Alfred E. Mann has paid him $10,000/yr for the last 3 yr; WideMed has paid him $4,000/yr for the last 3 yr. He has received research grants from Respironics, Inc. ($200,000/yr for the last 3 yr); Itimar Medical ($50,000/yr for the last 3 yr); Alfred E. Mann ($10,000/yr for the last 3 yr). He has participated as a speaker in numerous scientific meetings or courses organized and financed by sleep technology companies (Cephalon, Sepracor, Orphan Medical, and Respironics).

REFERENCES

  1. Heinzer RC, Stanchina ML, Malhotra A, Fogel RB, Patel SR, Jordan AS, Schory K, White DP. Lung volume and continuous positive airway pressure requirements in obstructive sleep apnea. Am J Respir Crit Care Med 2005;172:114–117.[Abstract/Free Full Text]
  2. Dawson VD, Elliott EA. Wave-speed limitation on expiratory flow: a unifying concept. J Appl Physiol 1977;43:498–515.[Abstract/Free Full Text]
  3. West JB. Respiratory physiology, 7th ed. Baltimore: Lippincott Williams and Wilkins; 2005.
  4. Remmers JE, DeGroot WJ, Sauerland EK, Anch MA. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 1978;44:931–938.[Free Full Text]




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Copyright © 2005 American Thoracic Society