Obstructive Sleep Apnea: Evaluation & Management

Nearly 22 million Americans are affected by obstructive sleep apnea (OSA), making it the most common sleep disorder. Patients with undiagnosed and untreated OSA are at increased risk for cardiovascular and cerebrovascular health consequences and excessive daytime sleepiness. Here’s how you can address the symptoms and complications that make OSA a major public health concern­, and as a result, decrease economic burdens and increase quality of life.

Obstructive sleep apnea (OSA) is an increasingly common diagnosis, with nearly 22 million Americans currently affected.¹ In 2010, the diagnosis of OSA was recorded in 5.8 million office visits made by patients ages 20 or older—a 427% increase since 1999.² While nearly 50% of patients in primary care settings complain of sleep disturbances, up to 80% of OSA cases remain undiagnosed.^1,3 The high prevalence of sleep disorders in both the general population and in primary care settings, along with the underdiagnosis of OSA, illustrates the essential role of primary care providers in recognizing the signs and symptoms of OSA and evaluating patients for this condition.^1-3

BACKGROUND AND PATHOPHYSIOLOGY
OSA is the most common sleep disorder. Characterized by recurrent episodes of upper airway obstruction during sleep, it results in significantly reduced airflow (hypopnea) or complete cessation of breathing (apnea) for intervals lasting ≥ 10 seconds.^4,5 The total number of apneas or hypopneas per hour of sleep—the apnea-hypopnea index (AHI)—is one domain that can be used to classify the severity of OSA (see Table 1).⁵

Because the human upper airway lacks rigid or bony support, under normal circumstances, the pharyngeal dilator muscles act to oppose the negative pressure within the upper airway during inspiration when awake. And although the striated nature of the pharyngeal dilator muscles leads to a reduction in airway muscle tone during sleep, enough opposition is maintained to prevent airway collapse. In OSA patients, however, the reduced pharyngeal muscle tone fails to offset the negative airway pressure generated during inspiration while asleep, causing recurrent airway obstructions.⁶ In addition, anatomically narrowed upper airways can further impede airway patency during sleep.⁴ Causes include macroglossia and/or tonsillar hypertrophy, obesity with fat tissue deposits in the neck that compress the airway, and bony craniofacial abnormalities such as retrognathia.⁷

Disruptions in breathing from apneas and hypopneas result in hypercapnia and hypoxia, which trigger arousal centers in the central nervous system to increase sympathetic activity. As a result, the patient briefly awakens from sleep, which increases respiratory and pharyngeal dilator muscle tone and ultimately restores airway patency, and ventilation resumes.⁴

The sympathetic response associated with apneic and hypopneic episodes causes concomitant cardiac stimulation. This leads to transient vasoconstriction and elevations in heart rate and blood pressure. Vascular changes occur over time and result in persistent hypertension and other cardiovascular impairments.⁴

Undiagnosed and untreated OSA predisposes individuals to a multitude of health consequences and ultimately results in substantial public health and economic burdens. A recent study estimated that the economic cost of moderate-to-severe OSA in the United States is between $65 billion and $165 billion annually.⁸ Patients with OSA are at increased risk for complications such as systemic and pulmonary hypertension, congestive heart failure, cardiac arrhythmias, coronary artery disease, myocardial infarction, cerebrovascular accident, diabetes, and metabolic syndrome.⁹ Excessive daytime sleepiness from OSA has also been shown to contribute to increased rates of motor vehicle accidents, poor job performance, impaired cognitive function, and decreased quality-of-life measures.⁹

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