michigan hypertension core curriculum - State of Michigan

Obstructive Sleep Apnea
Susan Steigerwalt, MD
Obstructive sleep apnea (OSA) is a common cause of secondary HTN and is also an identified
cause of non-dipping of the nocturnal BP as well as masked HTN (normal office BP with elevated
ambulatory BP). At-risk hypertensives should be screened for obstructive sleep apnea, at least with a
symptom questionnaire, as diagnosis and subsequent treatment of OSA with CPAP (continous positive
pressure to avoid airway occlusion) may lower BP. In established uncontrolled hypertensives, treatment
of OSA decreases blood pressure by on average 5/3 mmHg (23). In population studies, OSA has been
associated with an increased risk for congestive heart failure, stroke, coronary artery disease, and sudden
cardiac death. Stroke survivors have a 43-91% prevalence of OSA. 1
Clinical clues to OSA include neck size greater than or equal to 17 inches, partner witnessed loud
snoring, choking and/or gasping at night, and excessive daytime sleepiness. Two useful tools are the
Epworth Sleepiness scale (downloadable from the internet) and the Berlin Sleep Questionnaire. If patient
has a positive screening test for OSA, further evaluation with an overnight polysomnogram is indicated.
Treatment is suboptimal, but CPAP is indicated for symptomatic relief of daytime sleepiness and has also
been shown to improve hypertension control as well as to lower CVD risk.
The severity of sleep apnea can be characterized by apnea (complete cessation of airflow for
10 seconds)-hypopnea (reduction of airflow followed by arousal from sleep or a drop in oxyhemoglobin
saturation) index (AHI). OSA is a collapse of the upper airway that results in activation of the sympathetic
nervous system which arouses the patient from sleep. Multiple mechanisms appear to cause/contribute
to OSA-related elevations in BP (fig1).
Secondary Hypertension
NKFM & MDCH 87