The pathophysiology of OSAS

The pharynx is the site of upper airway obstruction during sleep in OSAS. In general, any pathological change or normal variant that narrows the upper airway when awake will predispose the individual to obstructive apnoea or hypopnoea when asleep. Obesity is the single most common predisposing factor, but patients with OSAS may have other contributory factors that narrow the upper airway, such as a large tongue, enlarged tonsils, increased total soft tissue in the pharynx or a retropositioned mandible (receding jaw) (figure 1).

During inspiration, the air pressure in the pharynx is below atmospheric pressure, and the size of the pharyngeal lumen depends on the balance between the narrowing force that results from this suction pressure and the dilating force generated by the small muscles attached to the upper airway, which contract with each inspiration and normally stabilise the floppy walls of the pharynx. At sleep onset, there is a reduction in pharyngeal luminal area and a reduction in upper airway muscle activity, both of which are exaggerated in OSAS. Surface mucosal factors may also influence airway patency, especially in subjects with mucosal inflammation from repetitive trauma and resultant loss of sensation.

Each apnoea or hypopnoea is terminated by an arousal, which is accompanied by a surge in heart rate and blood pressure. In many individuals, the increased blood pressure persists by day, with its attendant risk of developing cardiovascular disease and stroke.

Risk factors for OSAS

The prevalence of OSAS increases with age and reaches a plateau after 60 years of age. However, recent cross-sectional data on more than 5000 subjects have shown significant proportions of people ≥70 years of age continuing to present with symptomatic disease.

An association between obesity and OSAS has been noted in many studies, with moderate or severe obesity (body mass index (BMI) > 30 kg·m-2) in 60–90% of patients with OSAS. Central obesity, characterised by a high waist-to-hip ratio or large neck circumference, correlates better with OSAS than BMI, even in people with a normal BMI.

OSAS is more common in men than women. This has been attributed to differences in anatomical and functional properties of the upper airway, differences in craniofacial morphology and fat deposition, and different ventilatory responses to arousal from sleep. However, health professionals need to be particularly alert to the possibility of OSAS  in women, as male bed partners may be less aware of the symptoms of obstructive breathing during sleep. The disease prevalence is higher in post-menopausal women and hormone replacement therapy is associated with a lower prevalence; the prevalence of OSAS increases during pregnancy, particularly in the third trimester.

First-degree relatives of patients with OSAS have an increased risk of developing the disorder. The genetic determinants of craniofacial features, obesity and regional fat distribution are also relevant. Congenital conditions affecting craniofacial development, such as Marfan syndrome, Down syndrome and the Pierre Robin sequence, predispose to OSAS, as do acromegaly and hypothyroidism.

Smoking is associated with a higher prevalence of snoring and OSAS, and alcohol can increase upper airway collapsibility leading to apnoeas.

Muscle-relaxant medication (sedative hypnotic drugs, opiates), sleep deprivation and supine posture can all exacerbate OSAS, although the degree to which sleep disordered breathing is worsened in the individual may depend on the predominant pathological mechanism in the individual patient and his or her intrinsic physiological responses.

Reduced nasal patency, due to congestion or anatomical defects, as well as respiratory allergy are also potential contributors.

See the entire Sleep breathing disorders Chapter