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Rouen, France
Dr. Cuvelier is Assistant Professor, and Dr. Muir is Professor and Chairman of the Pulmonary and Intensive Care Department, Rouen University Hospital.
Correspondence to: Antoine Cuvelier, Service de Pneumologie et Soins Intensifs Respiratoires, Hôpital de Bois-Guillaume, CHU de Rouen 76031 Rouen Cedex, France; e-mail: antoine.cuvelier{at}chu-rouen.fr
Obesity is of growing concern all over the world since > 312 millions of individuals have a body mass index > 30 kg/m2. Respiratory consequences of obesity are now of major concern in the pulmonary specialty, including asthma, obstructive sleep apnea syndrome (OSAS), obesity-hypoventilation syndrome (OHS), and some acute situations like hypercapnic respiratory failure and respiratory postsurgical complications. OHS is commonly defined as the association of obesity with daytime hypercapnia (PaCO2 > 45 mm Hg) in the absence of any other respiratory disease. OHS is one of the many etiologies of chronic respiratory failure and has become a frequent indication to initiate long-term noninvasive mechanical ventilation (NIV) in most European countries.1 Nocturnal NIV has been shown to be clinically effective in OHS because of a rapid and sustained improvement of daytime arterial blood gas levels2 and a net reduction of daytime sleepiness. However, mechanisms of improvement under NIV remain unclear, as well as the physiopathology and the natural history of the disease.
In this issue of CHEST (see page 148), Chouri-Pontarollo et al3 give new insights about OHS physiopathology and associated symptoms. Fifteen patients were thoroughly evaluated by nocturnal polysomnography and therefore stratified according to their diurnal CO2 ventilatory responses. The authors3 showed that a subjective sleepiness index such as the Epworth sleepiness scale could not predict the presence of impaired CO2 ventilatory response at baseline but that a more objective technique for sleepiness measurement like the OSLER test could. Indeed, sleep latencies were significantly shorter in patients having low CO2 sensitivity. Under NIV, the Epworth sleepiness scale and OSLER test scores significantly improved only in patients having low CO2 sensitivity. These results suggest that daytime sleepiness intensity may be an objective way to assess the efficacy of domiciliary NIV in OHS patients.24 It should be now demonstrated to which extent an OSLER test may have the appropriate sensitivity and specificity to discriminate the heterogeneous population of OHS patients, and to which extent it may be incorporated in clinical practice when following up domiciliary NIV patients.
Another interesting point arising from the results of Chouri-Pontarollo et al3 concerns the impact of bilevel NIV in OHS. Indeed, 7 of 15 of their patients had low CO2 response at baseline, displaying a typical situation of chronic alveolar hypoventilation. No clinical characteristics could differentiate the patients having normal or impaired CO2 sensitivity at baseline since they had similar body mass index, similar daytime hypoxemia and daytime hypercapnia levels, similar indexes of nocturnal respiratory disturbances, and similar severity of desaturation during sleep. According to our current understanding of how NIV works, we would have anticipated that domiciliary NIV would have reset the respiratory centers and therefore improved CO2 sensitivity, but this was not the case for five of seven patients (71%). Clearly, NIV improved PaCO2, restored sleep architecture (increased stage 3–4 and rapid eye movement sleep), corrected nocturnal desaturations, and decreased respiratory disturbance index and microarousals. The mechanisms of such sleep and daytime PaCO2 improvements, without any significant change in CO2 sensitivity and without concomitant weight loss, have to be clarified. Because assessments were performed after only 5 nights under NIV, further studies should appraise the time course evolution of ventilatory responses in OHS patients receiving domiciliary NIV.
It may be suggested that the coexistence of OSAS in all the OHS patients included by Chouri-Pontarollo et al3 is an explanation for the observed improvement of PaCO2 values. OSAS occurs in approximately 70 to 90% of all OHS cases,45 but previously published studies in these patients did not analyze the response to NIV according to the nocturnal pattern (ie, hypoventilation with or without OSAS). Perhaps the patients in the present study took advantage of bilevel NIV because the ventilatory assistance suppressed underlying obstructive apneas and hypopneas and partly prevented CO2 load by the same way. Because NIV regularly improves OHS patients but not always normalizes CO2 response, the specific impact of the ventilatory assistance has now to be evaluated on each component of the OHS puzzle: correction of OSAS, correction of hypoventilation, respiratory muscles unload,6 improvement of FVC,7 or factors that have been recently identified like leptin resistance, inflammation, or genetic factors.8 As stated by the authors,3 a study comparing NIV vs continuous positive airway pressure is needed and may clarify the impact of OSAS during OHS. The natural history of OHS is still unknown, and we have to assess to which extent CO2 sensitivity has a role in the development of the disease, or if it is a consequence of it, and what is the evolution of the impaired ventilatory drive during the course of the disease.
Footnotes
The authors have no conflicts of interest to disclose.
References
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