The overnight polysomnogram is the standard diagnostic test for obstructive sleep apnea. It involves simultaneous recordings of multiple physiologic signals during sleep, including the electroencephalogram, electrooculogram, electromyogram, oronasal airflow, and oxyhemoglobin saturation. Collectively, these recordings allow identification and classification of sleep-related apneas and hypopneas. An apnea is defined as the complete cessation of airflow for at least 10 seconds. Apneas are further classified as obstructive, central, or mixed based on whether effort to breathe is present during the event. A hypopnea is defined as a reduction in airflow that is followed by an arousal from sleep or a decrease in oxyhemoglobin saturation. Commonly used definitions of a hypopnea require a 25% or 50% reduction in oronasal airflow associated either with a reduction in oxyhemoglobin saturation or an arousal from sleep (6
). Sleep apnea severity is typically assessed with the apnea–hypopnea index (AHI), which is the number of apneas and hypopneas per hour of sleep. Several additional measures of disease severity that characterize the degree of nocturnal hypoxemia (e.g., average oxyhemoglobin desaturation) and extent of sleep fragmentation (i.e., arousal frequency) are also used in the clinical and research arenas.
Although considered as a “gold-standard,” the polysomnogram is not without limitations. It requires an overnight stay in a sleep laboratory staffed with qualified personnel that can collect and interpret complex physiologic data. The process is time consuming, labor intensive, and can be costly. Moreover, despite recent attempts at standardization, inconsistencies in the collection, analysis, and interpretation of the polysomnogram across different laboratories have made it difficult to compare various studies on health-related consequences associated with obstructive sleep apnea. Issues such as abbreviated monitoring, night-to-night variability, and the “first-night” effect explain some of the variability in results across different studies. While some of aforementioned factors have modest effects, others can have a serious impact. For example, the oxyhemoglobin desaturation threshold (e.g., 3% or 4%) used for defining hypopneas can lead to varying estimates of disease severity. Awareness of such factors is vital to better understand how distinct studies with relatively comparable designs produce widely discrepant estimates of prevalence or measures of association. Methodologic issues notwithstanding, substantial advancements have been made in our knowledge of the health risks imposed by obstructive sleep apnea. In the sections that follow, this article will provide a nonexhaustive review of the prevalence, natural history, and risk factors of adult obstructive sleep apnea.