what is OSA

Sleep apnoea is defined as a cessation of airflow at the nose and mouth lasting at least 10 seconds, due to abnormal respiratory events. These abnormal respiratory events may take two forms: apnoeas and hypopnoeas. There are three distinct forms of sleep apnoea (Brown, 1994): central, defined by the absence of respiratory effort; obstructive, defined as continued respiratory effort against an occluded upper airway and mixed, which begins with a period of central apnoea and concludes with one or more obstructed breaths.

Hypopnoea has been defined as a reduction in tidal volume of greater than 50 per cent measured by a validated means, or a reduction in flow of 30-50 per cent associated with either an arousal or a desaturation of 3 per cent or greater, lasting more than 10 seconds.

The AHI, represents the number of apnoeas and hypopnoeas occurring per hour of sleep and thus gives an indication of the severity of OSA. The American Academy of Sleep Medicine Task Force (1999) defined mild OSA as an AHI of 5-15 events per hour, moderate OSA as an AHI of 16-30 events per hour and severe OSA as an AHI greater than 30 events per hour. It should be noted that any cut off in AHI score attempting to stratify the severity of OSA is arbitrary, as the severity can vary from night-to-night and symptoms from day-to-day in any individual. However, such stratification can be used when considering treatment strategies. The original definition of OSA by Guilleminault (1982), was the occurrence of five or more abnormal respiratory events per hour of sleep. However, there appears to be no universally accepted defining point for starting treatment for OSA subjects, with reported ranges from 5 to 20 (Guilleminault, 1982; Riley et al., 1983). Stradling (2001), proposed that rather than define a threshold for normality it would be better to accept that there is a spectrum of upper airway narrowing during sleep and the presence of snoring, hypopnoeas and apnoeas are arbitrary points along this spectrum. The adoption of this symptom-based approach to care avoids much of the ambiguity and encompasses less defined conditions, such as upper airways resistance syndrome.

Sleep related breathing disorders demonstrate, to varying degrees, the collapsibility of the pharyngeal airway, which characteristically occurs at the onset of sleep (Remmers et al., 1978). In OSA, despite the continued respiratory effort, the more severe degree of collapse and obstructed pharyngeal airway prevents effective ventilation, resulting in either apnoea or hypopnoea. In turn, hypoxia and hypercapnia quickly develop, necessitating arousal to re-establish airway patency and normal ventilation (White, 1995). The site of the obstruction is at the level of the velopharynx (behind the uvula and soft palate), oropharynx (behind the tongue), hypopharynx (behind the epiglottis and base of tongue) or some combination of the above (Pringle and Croft, 1993; Ryan