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© Cambridge University Press 2013. Continuous positive airway pressure Obstructive sleep apnea (OSA) is characterized by a repetitive collapse of the pharynx during sleep resulting in apnea and hypopnea, which are associated with intrathoracic pressure changes, oxygen desaturations, and arousals from sleep. It was not until 1982, when Colin Sullivan in Australia invented continuous nasal positive airway pressure ventilation (CPAP), that a fully effective, noninvasive treatment for OSA became available [1]. Nocturnal application of CPAP via a nasal or face mask is the standard therapy for patients with obstructive sleep apnea syndrome (OSAS). The positive airflow pressure that is generated by an airflow turbine pump forces open the pharynx, thereby preventing apneas, hypopneas, snoring, and any acute physiological consequences of OSA. Continuous positive airway pressure has been shown to improve daytime symptoms such as excessive sleepiness, quality of life, blood pressure, and other measures of cardiovascular risk in patients with moderate to severe OSAS [2,3]. There is also some evidence that CPAP has the same beneficial effects on sleepiness and quality of life in patients with minimally symptomatic OSA without excessive daytime sleepiness [2]. As OSAS is often a lifelong condition, CPAP usually needs to be used indefinitely. Approximately 30%–50% of all patients diagnosed with OSAS will not tolerate CPAP in the long term, and nightly adherence to this therapy shows a considerable interindividual variability, which is particularly true for patients with milder forms of OSA who may not perceive improvement in daytime symptoms such as sleepiness with this treatment [4,5]. However, currently there is no data on the minimum time of CPAP use per night that is required for patients to fully benefit from this therapy in terms of improvement in symptoms, quality of life, blood pressure, or any other measure of cardiovascular risk. This needs to be taken into account when considering the effects of CPAP on postulated stroke risk factors and cerebrovascular events, which are discussed in the following sections of this chapter.

Original publication

DOI

10.1017/CBO9781139061056.012

Type

Chapter

Book title

Sleep, Stroke, and Cardiovascular Disease

Publication Date

01/01/2010

Pages

115 - 126