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Noninvasive Ventilatory Support in Obesity Hypoventilation SyndromeTimed Backup in Obesity Hypoventilation Syndrome: Backup Early and Often?

Lee K. Brown, MD, FCCP
Author and Funding Information

From the Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, University of New Mexico School of Medicine, and the Program in Sleep Medicine, University of New Mexico Health Sciences Center.

Correspondence to: Lee K. Brown, MD, FCCP, Department of Internal Medicine, University of New Mexico School of Medicine, 1101 Medical Arts Ave NE, Bldg No. 2, Albuquerque, NM 87102; e-mail: lkbrown@alum.mit.edu


Financial/nonfinancial disclosures: The author has reported to CHEST the following conflicts of interest: Dr Brown serves on the Polysomnography Practice Advisory Committee of the New Mexico Medical Board and on the New Mexico Respiratory Care Advisory Board. He currently receives no grant or commercial funding pertinent to the subject of this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(1):8-10. doi:10.1378/chest.12-1835
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The not common clinical scenario of acute-on-chronic ventilatory failure requiring hospital admission (the so-called “critical care syndrome” of Fletcher et al1) and the frequent occurrence of other life-threatening systemic complications of morbid obesity (recently dubbed the “malignant obesity hypoventilation syndrome” by Marik2) inevitably calls for prompt intervention in the patient with obesity hypoventilation syndrome (OHS). However, OHS is not a monolithic disorder. In a landmark study, Rapoport et al3 observed that some patients with OHS and significant obstructive sleep apnea achieved daytime eucapnia following effective treatment of their sleep-disordered breathing, whereas others remained hypercapnic despite resolution of nocturnal respiratory events. This heterogeneity in the OHS population has subsequently been confirmed by other investigators.4-6 CPAP nonresponders, christened “true Pickwickians” by Rapoport et al,3 tend to be older and exhibit lower (or even normal) apnea-hypopnea indexes (AHIs), more hypoxemia awake and asleep, and greater restrictive ventilatory impairment.6 By definition, this group requires not just a means of sustaining upper airway patency but also ventilatory support during sleep; in some cases, diurnal ventilatory support must also be provided. Moreover, there may be potentially important differences between the two groups in terms of OHS pathogenesis. In CPAP responders, mathematical modeling and empirical observation implicate renal bicarbonate retention due to the repetitive obstructive events as a fundamental mechanism.7-9 Obstructive events that are so frequent and prolonged that interevent ventilation is inadequate to excrete the CO2 load lead to sustained nocturnal hypercapnia.7,8 The ensuing metabolic alkalosis provokes hypoventilatory respiratory compensation for the acid-base disturbance and blunts the ventilatory response to CO2, resulting in daytime hypercapnia.7,8 In contrast, pathogenesis in the “true Pickwickians” may involve the usual suspects implicated in the literature since Bickelmann et al’s10 first description: impaired chest-wall mechanics, respiratory muscle weakness or fatigue, and impaired control of breathing.11 More recently, suspicion has been raised that neurohumoral factors (eg, CNS leptin resistance) may lead to a blunted ventilatory response and diurnal hypercapnia.12

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