Epidemiology

The prevalence of OSA is estimated at 3% to 7% of adult men and 2% to 5% of adult women. Some groups of people have a higher disease prevalence, including older adults and those who are overweight (Figure 108-1). Most OSA remains undiagnosed and, as the population ages and the obesity epidemic explodes, a surge in disease prevalence is expected.

Pathophysiology

The upper airway from the hard palate to the larynx has evolved as a multipurpose complex structure. Its ability to collapse and change shape is essential for the functions of breathing, swallowing, and speaking. The airways of patients with OSA are narrow and more prone to collapse (Figure 108-2). These individuals are more dependent on increased tone of the airway dilator muscles during wakefulness to maintain airway patency. Decreased tone at the onset of sleep in healthy patients and those with OSA causes breathing instability. Patients who are highly dependent on increased muscle tone during wakefulness are much more vulnerable to airway obstruction during the transition from wakefulness to sleep. Arousal from sleep helps the patient restore normal respiratory patterns, but the end result is poor-quality fragmented sleep.

Obstructive sleep apnea, obesity, cardiovascular risk, and metabolic syndrome

The patient with OSA who presents to the operating room has more than a single condition. These patients have multiple intertwined comorbid conditions that make their care complicated to manage. Obesity, often an accompaniment to OSA, presents the anesthesia provider’s first set of challenges. Deposition of fat in the pharyngeal tissues exacerbates the underlying narrowness and collapsibility of the pharyngeal airway. Obese patients also accumulate more visceral fat, which appears to affect the severity of the OSA. Symptom severity correlates with weight loss and gain. In the Wisconsin Sleep Cohort Study, the authors demonstrated that a 10% gain in weight in patients with OSA led to a 32% increase in the number of apneas and hypopneas experienced per hour of sleep (i.e., the apnea-hypopnea index, or AHI; Table 108-1). A modest 10% decrease in weight led to a 26% improvement in the AHI. Weight loss results in a dose-dependent decrease in the severity of the syndrome.

OSA and obesity also play a significant role in cardiovascular morbidity. Obesity increases the risk of hypertension, heart failure, stroke, and coronary heart disease (Figure 108-3). OSA independently increases the risk of cardiovascular disease regardless of age, sex, or comorbid conditions such as tobacco use, alcohol use, diabetes, and obesity. The Sleep Heart Health Study data indicate that the odds ratios of atrial fibrillation, coronary heart disease, and tachycardia are all elevated in patients with OSA. The mechanism of increased cardiovascular risk in patients with OSA has not been entirely delineated but appears to involve the sustained sympathetic activation, oxidative stress, and resulting vascular inflammation that occur with the repetitive episodes of hypercarbia and hypoxia. These patients have higher levels of inflammatory mediators such as C-reactive protein and interleukin 6 in conjunction with elevated levels of endothelin and decreased levels of nitric oxide. Treatment of OSA with continuous positive airway pressure (CPAP) improves hypertension, decreases levels of inflammatory mediators, and in some patients with dyslipidemia, promotes regression of atherogenic plaque.