Obstructive sleep apnea and hypertension: Mechanisms, evaluation, and management

Abstract

Obstructive sleep apnea (OSA) is a recognized cause of secondary hypertension. OSA episodes produce surges in systolic and diastolic pressure that keep mean blood pressure levels elevated at night. In many patients, blood pressure remains elevated during the daytime, when breathing is normal. Contributors to this diurnal pattern of hypertension include sympathetic nervous system overactivity and alterations in vascular function and structure caused by oxidant stress and inflammation. Treatment of OSA with nasal continuous positive airway pressure (CPAP) abolishes apneas, thereby preventing intermittent arterial pressure surges and restoring the nocturnal "dipping" pattern. CPAP treatment also has modest beneficial effects on daytime blood pressure. Because even small decreases in arterial pressure can contribute to reducing cardiovascular risk, screening for OSA is an essential element of evaluating patients with hypertension.

Obstructive Sleep Apnea in Patients on Conventional and Short Daily Hemodialysis

“…Despite all the evidence, there is a lack of studies on the impact of OSA in patients on hemodialysis. OSA is now a recognized cause of secondary hypertension in the general population [6]. The observation that patients with OSA needed more pills for the same optimal BP control than patients without OSA is consistent with the hypothesis that OSA is associated with a tendency to high levels of BP in patients on hemodialysis.…”

“…In the general population, OSA is recognized as a secondary cause of hypertension [6] and has also been associated with cardiac septal hypertrophy [7], heart failure [8] and ultimately death of cardiovascular origin [9]. However, the association of OSA with cardiovascular outcomes in the population of patients on hemodialysis is not well established.…”

Epworth Sleepiness Scale may be an indicator for blood pressure profile and prevalence of coronary artery disease and cerebrovascular disease in patients with obstructive sleep apnea

“…In some subjects, the normal nocturnal fall in BP is <10%, which is referred to as a nondipping pattern (the ratio of nighttime/daytime BP> 0.9), in contrast to the normal dipping pattern [32]. In OSA patients, because of sympathetic nervous system overactivity and alterations in hemodynamic mechanism and vascular function, OSA episodes produce surges in systolic and diastolic pressure that keep mean BP levels elevated at night [33], which result in the lack of dipping and the elevated nocturnal BP is carried over into the early waking hours in patients with OSA and causes elevated morning BP [34]. In this article, significant statistical difference can be found in the ratio of nighttime/daytime average BP between EDS and non-EDS.…”

Cardiovascular Performance Following Continuous Positive Airway Pressure in Patients with Severe Obstructive Sleep Apnea

“…It is probable that this discrepancy is related to severity of OSA, with severe OSA resulting in higher MAP but mild to moderate OSA causing no measurable effect on MAP. OSA is a recognized cause of hypertension (Dopp, Reichmuth, & Morgan, 2007). OSA episodes produce increases in SBP and DBP and hence MAP.…”