Obesity hypoventilation syndrome: From sleep-disordered breathing to systemic comorbidities and the need to offer combined treatment strategies

Research and Development Department AGIR à dom, Meylan, France.
Respirology (Impact Factor: 3.35). 11/2011; 17(4):601-10. DOI: 10.1111/j.1440-1843.2011.02106.x
Source: PubMed


Obesity hypoventilation syndrome (OHS) is defined as a combination of obesity (body mass index ≥ 30 kg/m(2)), daytime hypercapnia (partial arterial carbon dioxide concentration ≥45 mm Hg) and sleep-disordered breathing after ruling out other disorders that may cause alveolar hypoventilation. Through the prism of the International Classification of Functioning, OHS is a chronic condition associated with respiratory, metabolic, hormonal and cardiovascular impairments, leading to a decrease in daily life activities, a lack of social participation and high risk of hospitalization and death. Despite its severity, OHS is largely underdiagnosed and the health-related costs are higher than those of apnoeic or obese eucapnic patients. The present review discusses the definition, epidemiology, physiopathology and treatment modalities of OHS. Although nocturnal positive airway pressure therapies represent first-line treatment and are effective in improving patient outcomes, there is a need to offer combined treatment strategies and to assess the effect of multimodal therapeutic strategies on morbidity and mortality.

Download full-text


Available from: Anne-Laure Borel, Nov 12, 2014
1 Follower
46 Reads
  • Source
    • "Syndrome obésité-hypoventilation [5] "
    Revue des Maladies Respiratoires Actualites 03/2014; 6(1):55–62. DOI:10.1016/S1877-1203(14)70510-5
  • Source
    • "In obese subjects, respiratory system mechanics can become disturbed, in isolation or in association with upper airway pathology, and obesity hypoventilation syndrome (OHS) may develop as a result [4-6]. According to the International Classification of Functioning, OHS is a chronic condition associated with respiratory, metabolic, hormonal and cardiovascular impairments, leading to a decrease in daily life activities, a lack of social participation and a high risk of hospitalisation and death (Figure 1) [7]. OSA and COPD are both prevalent disorders [8-10], which are gaining more importance, due to the obesity epidemic in Western countries [11,12] in addition to smoking behaviour over previous decades [13]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The overlap syndrome of obstructive sleep apnoea (OSA) and chronic obstructive pulmonary disease (COPD), in addition to obesity hypoventilation syndrome, represents growing health concerns, owing to the worldwide COPD and obesity epidemics and related co-morbidities. These disorders constitute the end points of a spectrum with distinct yet interrelated mechanisms that lead to a considerable health burden. The coexistence OSA and COPD seems to occur by chance, but the combination can contribute to worsened symptoms and oxygen desaturation at night, leading to disrupted sleep architecture and decreased sleep quality. Alveolar hypoventilation, ventilation-perfusion mismatch and intermittent hypercapnic events resulting from apneas and hypopneas contribute to the final clinical picture, which is quite different from the “usual” COPD. Obesity hypoventilation has emerged as a relatively common cause of chronic hypercapnic respiratory failure. Its pathophysiology results from complex interactions, among which are respiratory mechanics, ventilatory control, sleep-disordered breathing and neurohormonal disturbances, such as leptin resistance, each of which contributes to varying degrees in individual patients to the development of obesity hypoventilation. This respiratory embarrassment takes place when compensatory mechanisms like increased drive cannot be maintained or become overwhelmed. Although a unifying concept for the pathogenesis of both disorders is lacking, it seems that these patients are in a vicious cycle. This review outlines the major pathophysiological mechanisms believed to contribute to the development of these specific clinical entities. Knowledge of shared mechanisms in the overlap syndrome and obesity hypoventilation may help to identify these patients and guide therapy.
    Respiratory research 11/2013; 14(1):132. DOI:10.1186/1465-9921-14-132 · 3.09 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: While the impact of obesity on respiratory function has been extensively studied, and several definitive conclusions have emerged, its impact on exercise performance is complex, with the available data sometimes providing contradictory or inconclusive information. Based on the literature discussed, it appears that resting alterations in lung volumes and gas exchange become attenuated during exercise in the obese, while oxygen cost of breathing and dyspnoea are increased. Respiratory muscle function also seems to be impaired, such that inspiratory muscle strength is reduced and respiratory drive is increased. Furthermore, while there is no reduction in the absolute values of maximal oxygen uptake compared with normal-weight subjects, oxygen uptake at a given workload is increased and maximal workload is reduced in the obese, caused by increases in body mass and/or basal metabolic rate. To date, obesity has not been listed as an indication for pulmonary rehabilitation (PR), hence the reason why conclusive data on the impact of obesity per se on PR are lacking. The majority of evidence discussed is based on comparative data from obese versus normal-weight patients, with respiratory disorders currently established as indications for PR. The best evidence currently available regarding the impact of obesity on PR is for patients with chronic obstructive pulmonary disease (COPD); here, it appears that obesity per se has no negative impact on PR. Otherwise, there are no conclusive data on the impact of obesity on PR in respiratory disorders other than COPD, and this remains to be investigated in the future.
    Respirology 02/2012; 17(6):899-907. DOI:10.1111/j.1440-1843.2012.02151.x · 3.35 Impact Factor
Show more