Abstract\r\nThe overlap syndrome of obstructive sleep apnoea (OSA) and chronic obstructive pulmonary disease (COPD), in\r\naddition to obesity hypoventilation syndrome, represents growing health concerns, owing to the worldwide COPD\r\nand obesity epidemics and related co-morbidities. These disorders constitute the end points of a spectrum with distinct\r\nyet interrelated mechanisms that lead to a considerable health burden. The coexistence OSA and COPD seems to occur\r\nby chance, but the combination can contribute to worsened symptoms and oxygen desaturation at night, leading to\r\ndisrupted sleep architecture and decreased sleep quality. Alveolar hypoventilation, ventilation-perfusion mismatch and\r\nintermittent hypercapnic events resulting from apneas and hypopneas contribute to the final clinical picture, which is\r\nquite different from the ââ?¬Å?usualââ?¬Â COPD. Obesity hypoventilation has emerged as a relatively common cause of chronic\r\nhypercapnic respiratory failure. Its pathophysiology results from complex interactions, among which are respiratory\r\nmechanics, ventilatory control, sleep-disordered breathing and neurohormonal disturbances, such as leptin resistance,\r\neach of which contributes to varying degrees in individual patients to the development of obesity hypoventilation.\r\nThis respiratory embarrassment takes place when compensatory mechanisms like increased drive cannot be maintained\r\nor become overwhelmed.\r\nAlthough a unifying concept for the pathogenesis of both disorders is lacking, it seems that these patients are in a\r\nvicious cycle. This review outlines the major pathophysiological mechanisms believed to contribute to the\r\ndevelopment of these specific clinical entities. Knowledge of shared mechanisms in the overlap syndrome and obesity\r\nhypoventilation may help to identify these patients and guide therapy
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