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(Chest. 2005;127:698-699.)
© 2005 American College of Chest Physicians

The Saga of Obstructive Sleep Apnea Syndrome and Daytime Hypercapnia

Work in Progress

Gökhan M. Mutlu, MD, FCCP and Israel Rubinstein, MD, FCCP

Chicago, IL
Dr. Mutlu is an Assistant Professor of Medicine, Northwestern University, Feinberg School of Medicine and Dr. Rubenstein is a Professor of Medicine, University of Illinois at Chicago.

Correspondence to: Gökhan M. Mutlu, MD, FCCP, Northwestern University, 240 E. Huron, McGaw 2300, Chicago, IL 60611; e-mail: g-mutlu{at}northwestern.edu

The current body of clinical evidence suggests that the majority of patients with obstructive sleep apnea syndrome (OSAS) are eucapnic during wakefulness, and that detection of daytime hypercapnia attests to mechanical impairment of the respiratory system due to obesity (ie, obesity hypoventilation syndrome) and/or COPD.123 While OSAS may contribute to CO2 retention in these patients, no correlation exists between the severity of OSAS and presence of daytime hypercapnia. Conceivably, OSAS could predispose to daytime hypercapnia by causing nocturnal hypoxemia and sleep fragmentation that, in turn, impair mass load compensation, thereby predisposing obese patients to hypercapnia.4

In this issue of CHEST (see page 710), Dr. Laaban and colleagues report that daytime hypercapnia is present in patients with OSAS even in the absence of COPD.5 The most striking finding is the presence of hypercapnia in nonobese patients, suggesting that OSAS itself could lead to daytime hypercapnia. While the possibility of OSAS alone evokes daytime hypercapnia in the absence of significant obesity or COPD has been reported before,6 this is first large-scale study that evaluated the incidence of daytime hypercapnia in patients with OSAS in the absence of COPD.

There are several limitations to this study. Firstly, pH data were not reported, which forestalls proper data analysis and interpretation because the observed rise in CO2 could also be attributed to a compensatory response to underlying metabolic alkalosis rather than to alveolar hypoventilation. This notion is supported by the relatively mild degree of hypercapnia observed in these patients. Secondly, no information is provided on alveolo-arterial oxygen gradient so the mechanism(s) underlying hypoxemia (ie, hypoventilation vs ventilation-perfusion mismatching) in nonobese individuals cannot be delineated. Lastly, a selection bias may exist because only 2,217 of approximately 30,000 patients with OSAS who were prescribed nasal continuous positive airway pressure underwent pulmonary function testing and arterial blood gas analysis. The presence of hypoxemia at rest may have triggered these procedures. Irrespective, these data suggest that patients with OSAS who present with daytime hypoxemia are more likely to have daytime hypercapnia as well, so the latter should be sought by arterial blood gas analysis.2

The mechanism(s) underlying alveolar hypoventilation in patients with OSAS in the absence of mechanical impairment of the respiratory system due to obesity and/or COPD is uncertain. Leptin-related abnormalities in ventilatory control and respiratory muscle "fatigue" are intriguing possibilities but fail to explain the presence of hypercapnia in nonobese patients with OSAS.7 Loss of the so-called normal CO2 response to apnea that protects against the development of hypercapnia by stimulating respiratory compensation for each apnea during the interapnea period is thought to predispose to daytime hypercapnia in patients with OSAS.8 Whether genetic aberration(s) underlies alveolar hypoventilation in these patients or whether it is an acquired, maladaptive response to longstanding OSAS resetting of ventilatory regulation is uncertain because this phenomenon is observed only in a minority of patients. Given this ongoing controversy and its implications for patient care, further large-scale, community-based controlled studies are warranted to elucidate the incidence of daytime hypercapnia in patients with OSAS in the absence of mechanical impairment due to obesity and/or COPD.

References

  1. Guilleminault, C, Tilkian, A, Dement, WC (1976) The sleep apnea syndromes. Annu Rev Med 27,465-484[CrossRef][ISI][Medline]
  2. Leech, JA, Onal, E, Baer, P, et al Determinants of hypercapnia in occlusive sleep apnea syndrome. Chest 1987;92,807-813[Medline]
  3. Bradley, TD, Rutherford, R, Lue, F, et al Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnea. Am Rev Respir Dis 1986;134,920-924[ISI][Medline]
  4. Lopata, M, Önal, E Mass loading, sleep apnea, and the pathogenesis of obesity hypoventilation. Am Rev Respir Dis 1982;126,640-645[ISI][Medline]
  5. Laaban-JP Chailleux, E, Antadir, OG Daytime hypercapnia in adult patients with obstructive sleep apnea syndrome in France, before initiating nocturnal nasal CPAP therapy. Chest 2005;127,710-715[Medline]
  6. Kessler, R, Chaouat, A, Schinkewitch, P, et al The obesity-hypoventilation syndrome revisited: a prospective study of 34 consecutive cases. Chest 2001;120,369-376[CrossRef][ISI][Medline]
  7. Tankersley, C, Kleeberger, S, Russ, B, et al Modified control of breathing in genetically obese (ob/ob) mice. J Appl Physiol 1996;81,716-723[Abstract/Free Full Text]
  8. Rapoport, DM, Garay, SM, Epstein, H, et al Hypercapnia in the obstructive sleep apnea syndrome: a reevaluation of the "Pickwickian syndrome." Chest 1986;89,627-635[Medline]




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