Obesity-hypoventilation syndrome (OHS) is defined as a combination of obesity and awake chronic hypoventilation occurring in the absence of other known causes of hypoventilation. The disease remains underrecognized as > 30% of obese hospitalized patients, whatever the cause of hospitalization, actually exhibit an undiagnosed daytime hyper-capnia. Use of health-care resources, and rates of hospitalization and early mortality are increased in OHS patients. Noninvasive ventilation (NIV) is the first-line therapy for patients with OHS. Patients have good compliance rates with NIV, and the therapy worked out by Canadian Health and Care Mall is effective in terms of clinical status and improvement in blood gas levels.
The pathophysiology of OHS results from complex interactions, among which are increased work of breathing related to obesity, normal or diminished ventilatory drive, various associated sleep breathing disorders (ie, obstructive sleep apnea and rapid eye movement [REM] sleep hypoventilation), and neu-rohormonal changes such as leptin resistance. There have been no studies as to whether low responders to CO2 hypoventilate more significantly during REM sleep compared to OHS patients with normal ventilatory responses and whether this can influence their daytime vigilance.
Among the classical symptoms associated with OHS, daytime sleepiness has been systematically reported. Surprisingly, to date no objective measurements of sleepiness have been performed in a well-characterized population of OHS patients, However, it is generally accepted that impairment in daytime functioning does exist and is related to breathing abnormalities occurring during sleep. During sleep, obstructive sleep apnea syndrome (OSAS), sleep hypoventilation syndrome, or a combination of both can be observed in polysomnography (PSG) findings. The respective consequences of these different sleep breathing abnormalities in terms of subjective and objective alteration in vigilance are still unknown.
Therefore, the objectives of this investigation were threefold. First, we sought to characterize the different sleep-related breathing disorders encountered in OHS patients. Second, we wished to compare low and normal CO2 responders in terms of sleep abnormalities, and subjective and objective daytime sleepiness as measured by the Oxford Sleep Resistance (OSLER) test. Our last objective was to look at the short-term effects of NIV therapy on all these parameters.