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found that low mean nocturnal arterial oxygen saturation was the factor most strongly associated with hypoventilation, suggesting that recurrent nocturnal hypoxaemia may blunt central respiratory drive.57 Chouri-Pontarollo et?al. identified two groups of OHS individuals: those with CO2 responses within the normal range and those who were low responders. Those with blunted responses were objectively sleepier http://www.selleckchem.com/products/blz945.html and had more severe rapid eye movement hypoventilation than those with more normal responses.58 Banerjee et?al. showed that extremely obese subjects (BMI ��50?kg/m2) without OHS are still able to maintain eucapnia even in the presence of OSAS. Despite similar BMI, severities of apnoea/hypopnoea index, arousal indices and sleep architecture, patients with OHS exhibited more severe oxygen desaturation compared with the eucapnic obese group. One-night CPAP treatment significantly improved the apnoea/hypopnoea https://en.wikipedia.org/wiki/Oxymatrine index and sleep architecture abnormalities. In the OSAS without OHS group, only 9% continued to spend >20% of total sleep time with SpO2 http://www.selleckchem.com/products/nutlin-3a.html is a CO2 retainer because of decreased central drive or increased dead space, alveolar PO2 will be lower, leading to lower alveolar oxygen stores and more rapid desaturation.43,56,60 It is possible that persistent hypoxaemia is accompanied by defective ventilatory load compensation or that the ventilatory response to hypoxia and/or hypercapnea is so depressed in OHS subjects that inadequate alveolar ventilation is accompanied by blood gas derangements.59,60 In obese individuals with OSAS, there may be a difference in ventilatory pattern following apnoeic events between individuals who are able to maintain eucapnia and those who are hypercapnic, suggesting that under certain conditions, repetitive abnormal breathing during sleep may induce a depression of ventilatory drive.43,61�C63 When apnoeas or hypopnoeas occur during sleep, ventilation is intermittently reduced, permitting acute episodes of hypercapnea to arise. However, most obese individuals can sufficiently hyperventilate following apnoea to eliminate the accumulated CO2, and therefore maintain overall eucapnia.63 In contrast, when there is inadequate compensatory hyperventilation (failure to sufficiently increase inter-event ventilation or reduce inter-event duration) immediately after each episode or if the response to the accumulated CO2 is blunted, increased PaCO2 during sleep can occur.43 Thus, in order for hypercapnic OSAS to develop, other factors (e.g.