Q: I understand that patients with refractory hypertension have a high risk of obstructive sleep apnea (OSA) syndrome. Can this be screened for in an office setting?
A: You are correct: OSA is now recognized as a common, secondary cause of hypertension. When upper airway patency during sleep is compromised by tonsillar hypertrophy, pharyngeal fat deposition, macroglossia, or a redundant soft palate, the resultant loss of muscle tone may lead to functional upper airway collapse during inspiration. This in turn results in intermittent hypoxemia, hypercapnia, and acidosis, which can cause sympathetic nervous system activation and intermittent arousal from sleep.
Blood pressure tends to increase during each cycle of sleep-disordered breathing. Ambulatory blood pressure monitoring in persons with OAS demonstrates a decrease in or loss of the “nocturnal dipping effect” that is normally seen in blood pressure during sleep.
OSA is associated with daytime hypertension as well as with decreases in the nocturnal blood pressure dip. Thus, other mechanisms, in addition to sleep-disordered breathing, must be involved in the development of hypertension in patients with OSA. Obesity may help explain the connection. Obesity can cause increased pharyngeal fat deposition, and exogenous obesity is a major predisposing risk factor for hypertension as well as OSA. The other factors that contribute to daytime hypertension in patients with OSA include the increase of sympathetic nervous activity and activation of the renin-angiotensin-aldosterone system.
Presenting symptoms of OSA. Excessive daytime drowsiness is a cardinal symptom of OSA. Another is loud snoring, together with frequent pauses in normal breathing that are followed by deep inspiratory effort. Keep in mind, however, that a significant number of patients with OSA may not exhibit these classic symptoms.
Daytime fatigue, irritability, memory lapses, and difficulty with concentration have also been reported in patients with diagnosed OSA, but these alone are not sufficient to suggest the diagnosis. Nonetheless, chronic daytime sleepiness can be an important clue to the presence of OSA.
An approach to office screening. For years, the multiple sleep latency test (MSLT) has been used to provide a valid measurement of a patient’s sleepiness on the day of the test.1 It has been helpful in assessing patients with excessive daytime sleepiness for periodic limb movement disorder, narcolepsy, and idiopathic hypersomnia, as well as OSA.
Unfortunately, the MSLT is rather cumbersome, time-consuming, and expensive. It takes the better part of a full day for both the subject and the polysomnographer. Thus, it would be difficult to justify its use as a routine screening test in a large number of hypertensive patients.
An alternative test, the Epworth Sleepiness Scale (ESS), is a self-administered questionnaire that measures a patient’s general level of daytime sleepiness.2 Patients can complete the 1-page questionnaire (Box) either in the office or at home. They are asked to rate on a scale of 0 to 3 how likely they would be to doze off or fall asleep in 8 situations, assuming a typical daily schedule. The 8 responses are then totaled. It is important that patients who complete the ESS questionnaire make a distinction between dozing off and simply feeling tired.
Total ESS scores significantly distinguish normal persons and those with primary snoring (scores of less than 11) from other diagnostic groups, including persons with OSA, narcolepsy, and idiopathic hypersomnia. ESS scores of greater than 15, which indicate a high level of daytime sleepiness, are seen only in patients with these last 3 disorders.
A high ESS score, together with suggestive symptoms, would help determine whether overnight polysomnography is warranted.
How OSA is diagnosed. The diagnosis of OSA is established by overnight polysomnography.3 The rapid growth in the number of certified sleep laboratories is indicative of the increasing recognition of the importance of this problem.
In overnight polysomnography, the apneas and hypopneas the patient experiences during sleep are recorded. Both apneas and hypopneas are respiratory events that last at least 10 seconds, that are associated with an oxyhemoglobin desaturation of 4% or greater, and during which airflow or chest wall movement decreases significantly. In an apnea, airflow decreases to an amplitude that is less than 25% of the baseline amplitude; in a hypopnea, airflow decreases to less than 70% of baseline. At the end of the test, a respiratory disturbance index—the average number of apneas and hypopneas per hour of sleep—is calculated. The degree of OSA is quantified based on this index. A normal result is fewer than 5 events per hour. Mild OSA is defined as between 5 and 19 events per hour; moderate OSA, between 20 and 40 events; and severe OSA, more than 40 events per hour.
Treatment of OSA. Continuous positive airway pressure (CPAP) is the treatment of choice for OSA. It provides sustained and effective maintenance of a patent airway throughout the respiratory cycle. Effective CPAP is associated with a reduction in daytime somnolence as well as reduction in 24-hour blood pressure, including reestablishment of the nocturnal dipper effect.
In obese patients, significant weight reduction is also needed to achieve lasting results. In addition, patients with OSA should avoid nocturnal sedatives and excessive evening alcohol(Drug information on alcohol) ingestion. There is also evidence to suggest that avoiding the supine position during sleep can improve airway exchange. Effective implementation of lifestyle measures such as these is particularly important because a significant number of patients find it difficult to tolerate nocturnal CPAP on a long-term basis.
