CPAP withdrawal as a model of the cardiovascular effects of obstructive sleep apnoea

Obstructive sleep apnoea (OSA) is associated with cardiovascular disease and hypertension. The underlying causes of cardiovascular disease and hypertension in OSA are not fully understood. Potential causes for cardiovascular disease and hypertension in OSA include; intermittent hypoxia, arousal mediated sympathetic activation, oxidative stress, endothelial dysfunction, and systemic inflammation. Continuous positive airway pressure (CPAP) is the standard treatment for OSA and CPAP withdrawal is used to model the consequences of OSA. In the CPAP withdrawal model patients with known OSA are withdrawn from their usual CPAP treatment and randomised to intervention or control for two weeks. Utilising a CPAP withdrawal model, I examined the effects of supplemental oxygen versus air (sham) during CPAP withdrawal on several outcomes, including; morning blood pressure, intermittent hypoxia, markers of arousal, and daytime sleepiness. In addition, I examined the effects of the return of OSA following CPAP withdrawal on several biomarkers. Supplemental oxygen virtually abolished the rise in morning blood pressure seen following CPAP withdrawal. Supplemental oxygen markedly attenuated intermittent hypoxia, whilst having little effect on markers of arousal, and no effect on daytime sleepiness. This suggests that intermittent hypoxia is the dominant cause of morning increases in blood pressure in OSA. Following CPAP withdrawal there was a small unexpected reduction in adrenomedullin, which is a potent vasodilator and may contribute to the blood pressure rise with CPAP withdrawal.