Adult obstructive sleep apnea: pathophysiology and diagnosis

Abstract

Obstructive sleep apnea (OSA) is a highly prevalent disease characterized by recurrent episodes of upper airway obstruction that result in recurrent arousals and episodic oxyhemoglobin desaturations during sleep. Significant clinical consequences of the disorder cover a wide spectrum, including daytime hypersomnolence, neurocognitive dysfunction, cardiovascular disease, metabolic dysfunction, and cor pulmonale. The major risk factors for the disorder include obesity, male gender, and age. Current understanding of the pathophysiologic basis of the disorder suggests that a balance of anatomically imposed mechanical loads and compensatory neuromuscular responses are important in maintaining upper airway patency during sleep. OSA develops in the presence of both elevated mechanical loads on the upper airway and defects in compensatory neuromuscular responses. A sleep history and physical examination is important in identification of patients and appropriate referral for polysomnography. Understanding nuances in the spectrum of presenting complaints and polysomnography correlates are important for diagnostic and therapeutic approaches. Knowledge of common patterns of OSA may help to identify patients and guide therapy.

Figure 1

In the Starling resistor model, the collapsible segment of the tube is bound by an upstream and downstream segment with corresponding upstream and downstream pressures (Pus and Pds) and resistances (upstream resistance pressure and downstream resistance; data not shown). See text for further explanation (adapted in part from Gleadhill et al18). Vimax = maximal inspiratory flow; Rus = upstream resistance.

Figure 2

Illustration of the relative role of anatomically imposed mechanical loads and compensatory neuromuscular responses in maintaining upper airway patency. A Pcrit of approximately − 5 cm H₂O represents the disease threshold, the level above which obstructive hypopneas and apneas occurred. When mechanical loads on the upper airway are below the disease threshold, OSA is not present, regardless of whether neuromuscular responses are recruited. When mechanical loads on the upper airway are above the disease threshold, recruitment of compensatory neuromuscular responses are necessary to maintain upper airway patency; otherwise, OSA events will occur. Under this paradigm, the development of OSA requires a “two-hit” defect, with defects in both upper airway mechanical and neuromuscular responses (used with permission from Patil et al48).

Figure 3

A summary hypnogram and oximetry tracing in a patient with severe OSA (AHI, 84/h). Note the relatively infrequent transitions to lighter stages of sleep in the setting of severe oxyhemoglobin desaturations (Desat) [as low as 70%]. An expanded view of the sleep study is present in the lower panel. In the tracing, three obstructive apneas in association with oxyhemoglobin desaturation (pulse oximetry saturation range [SpO₂], 70 to 100%) and arousals (indicated by arrows over the EEG tracing; see text for additional details). SmEMG = submental electromyogram.

Figure 4

A summary hypnogram and oximetry tracing in a patient with moderately severe OSA (AHI, 37/h) and sleep fragmentation. Note the frequent transitions from sleep to wakefulness throughout the night. An expanded view of the sleep study is shown in the lower panel. In the tracing, five obstructive hypopneas in association with arousals (indicated by the arrows over the EEG tracing) are shown. Oxyhemoglobin desaturations of ≥ 3 to 4% were not observed in association with these events. Nocturnal oximetry alone would have missed the diagnosis of OSA (see text for further details). See Figure 3 legend for expansion of abbreviations.

Figure 5

A summary hypnogram and oximetry tracing in a patient with REM-related OSA, a pattern commonly seen in women (see text for additional details). See Figure 3 legend for expansion of abbreviations.