Obstructive sleep apnea/hypopnea syndrome (OSAHS) is one of the most important medical conditions identified in the last 50 years. It is a major cause of morbidity, a significant cause of mortality, and the most common medical cause of daytime sleepiness. Central sleep apnea is a rare clinical problem. Other sleep disorders are discussed in Chap. 27.
OSAHS is defined as the coexistence of unexplained excessive daytime sleepiness with at least five obstructed breathing events (apnea or hypopnea) per hour of sleep (Table 265-1). This event threshold may have to be increased in the elderly. Apneas are defined in adults as breathing pauses lasting ≥10 s and hypopneas as events ≥10 s in which there is continued breathing but ventilation is reduced by at least 50% from the previous baseline during sleep. As a syndrome, OSAHS is the association of a clinical picture with specific abnormalities on testing; asymptomatic individuals with abnormal breathing during sleep should not be labeled as having OSAHS.
Table 265-1 Clinical Indicators in the Sleepy Patient
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Table 265-1 Clinical Indicators in the Sleepy Patient
|Age of onset (years)||35–60||10–30||10–30|
|Time of day||Afternoon/evening||Afternoon/evening||Morning|
|Duration||<1 h||<1 h||>1 h|
Apneas and hypopneas are caused by the airway being sucked closed on inspiration during sleep. This occurs as the upper-airway dilating muscles—like all striated muscles—relax during sleep. In patients with OSAHS, the dilating muscles fail to oppose negative pressure within the airway during inspiration. The primary defect is not in the upper-airway muscles, which function normally in OSAHS patients when awake. These patients have narrow upper airways already during wakefulness, but when they are awake, their airway dilating muscles have increased activity, which ensures airway patency. However, during sleep, muscle tone falls and the airway narrows; snoring may commence before the airway occludes, and apnea results. Apneas and hypopneas terminate when the subject arouses, i.e., wakens briefly, from sleep. This arousal is sometimes too subtle to be seen on the electroencephalogram but may be detected by cardiac acceleration, blood pressure elevation, or increase in sympathetic tone. The arousal results in return of upper-airway dilating muscle tone, and thus airway patency is resumed.
Factors predisposing to OSAHS by narrowing the pharynx include obesity—in Western populations around 50% of OSAHS patients have a body mass index (BMI) >30 kg/m2—and shortening of the mandible and/or maxilla. This change in jaw shape may be subtle and can be familial. Hypothyroidism and acromegaly predispose to OSAHS by narrowing the upper airway with tissue infiltration. Other predisposing factors for OSAHS include male sex and middle age (40–65 years), myotonic dystrophy, Ehlers-Danlos syndrome, and, perhaps, smoking.
OSAHS occurs in around 1–4% of middle-aged males and is about half as common in women. The syndrome also occurs in childhood—usually associated with tonsil or adenoid enlargement—and in the elderly, although the frequency is slightly lower in old age. Irregular breathing during sleep without daytime sleepiness is much more common, occurring in perhaps a quarter of the middle-aged male population. As these individuals are asymptomatic, they do not have OSAHS, but there is increasing epidemiologic evidence of an association of irregular breathing during sleep with increased vascular risk even in the nonsleepy.
Randomized controlled treatment trials have shown that OSAHS causes daytime sleepiness; impaired vigilance, cognitive performance and driving; depression; disturbed sleep; and hypertension. Daytime sleepiness may range from mild to irresistible and can be indistinguishable from that in narcolepsy (Chap. 27). The sleepiness may cause inability to work effectively, damage interpersonal relationships, and prevent socializing. The somnolence is dangerous, with a three- to sixfold risk of road accidents. Experiments with normal subjects repeatedly aroused from sleep indicate that the sleepiness results, at least in part, from the repetitive sleep disruption associated with the breathing abnormality. Other symptoms include difficulty concentrating, unrefreshing nocturnal sleep, nocturnal choking, nocturia, and decreased libido. Partners report nightly loud snoring in all postures, which may be punctuated by the silence of apneas.
Cardiovascular and Cerebrovascular Events
OSAHS raises 24-h mean blood pressure. The increase is greater in those with recurrent nocturnal hypoxemia, is at least 4–5 mmHg, and may be as great as 10 mmHg in those with >20% arterial oxygen desaturations per hour of sleep. This rise probably results from a combination of surges in blood pressure accompanying each arousal at apnea/hypopnea termination and from the associated 24-h increases in sympathetic tone.
Epidemiologic data in normal populations indicate that this rise in blood pressure would increase the risk of myocardial infarction by around 20% and that of stroke by about 40%. Although there are no long-term randomized controlled trials to indicate whether this is true in OSAHS patients—such studies would be unethical—observational studies suggest an increase in cardiovascular and stroke risk in patients with untreated OSAHS. Furthermore, epidemiologic studies suggest increased vascular risk in normal subjects with raised apneas and hypopneas during sleep. Patients with recent stroke have a high frequency of apneas and hypopneas during sleep. These seem largely to be a consequence, not a cause, of the stroke and to decline over the weeks after the vascular event. There is no evidence that treating the apneas and hypopneas improves stroke outcome.
The association of OSAHS with diabetes mellitus is not due only to the fact that obesity is common in both ...