Since the early clinical descriptions of OSA in the 1970s, our understanding of the pathogenesis and adverse consequences of this chronic disease has advanced substantially. Initially, it was recognized that apneic events fragmented sleep, induced cardiovascular instability, and led to excessive daytime sleepiness., Given the hemodynamic and sleep-related effects of obstructive apneas, it comes as no surprise that the apnea index, which tallies the number of apneas per hour of sleep, became the primary disease-defining metric for OSA. Over time, as the full spectrum of upper-airway collapse during sleep became more apparent, the simple concept of only quantifying apneas quickly evolved into something more complex. It is now obvious that obstructive apneas, the original sine qua non for the disease, are not the only events of interest because obstructive hypopneas can also have similar effects (eg, arousals, BP swings)., As the clinical impact of hypopneas became widely recognized, these events were incorporated into quantifying disease activity, and the original apnea index gave way to the now commonly used apnea-hypopnea index (AHI). Although defining hypopneas continues to be plagued with many challenges,,, the AHI has become a ubiquitous measure in sleep medicine. In fact, the AHI not only is used to diagnose OSA but also is central to assessing disease severity.