Hypercapnic Obstructive Sleep Apnea

Sleep-disordered breathing (SDB) syndromes reflect complex pathophysiological interactions between upper airway obstruction, chemoreflex control of breathing, sleep arousability and fragmentation, and factors altering gas exchange (hypoxia and hypercapnia). In most healthy individuals, compensation (balanced CO2 loading and unloading) for acute hypercarbia occurs with recovery supra-tidal volume breaths that follows the apnea or hypopnea. Sleep hypoventilation manifests when there is a failure of CO2 compensation and, over time, can result in chronic hypercapnia during wakefulness. Failure of CO2 compensation can be induced by sedating medications that suppress respiratory drive and may also be seen in a variety of pathologies related to the lungs (chronic obstructive pulmonary disease [COPD], interstitial lung disease [ILD]), thoracic cage (kyphosis, obesity), and respiratory muscles (neuromuscular disease [NMD]) which can coexist with OSA. Therefore, hypercapnic OSA encompasses a variety of phenotypes: OSA with sleep stage-specific hypoventilation (i.e., rapid eye movement sleep [REM] hypoventilation), obesity hypoventilation (OHS)/OSA, pulmonary overlap syndromes (most notably COPD/OSA overlap), OSA with NMD, and OSA with medication effects (sedatives and/or opioids). We describe here a new and unique pattern of SDB, hypercapnic periodic breathing, exhibiting features of obstruction, hypercapnia, and a respiratory rhythm typical of hypocapnic periodic breathing. These patients are extraordinarily difficult to treat, as several therapeutic principles are mutually antagonist. Typically, multi-modal therapy is required-positive airway pressure, CO2 stabilization, acetazolamide, and supplemental oxygen.