During sleep the muscles of the airway become relaxed. The relaxation of these muscles in turn reduces the diameter of the airway. Typically, the airway of a UARS patient is already restricted or reduced in size, and this natural relaxation reduces the airway further. Therefore, breathing becomes labored. It can be likened to breathing through a coffee straw.

Pathophysiology of UARS is similar to obstructive sleep apnea / hypopnea syndrome in that abnormal airway resistance in the upper airway during sleep leads to unwanted physiologic consequences. Increased upper airway resistance in this disorder does not lead to cessation of airflow (apnea) or decrease in airflow (hypopnea), but instead leads to an arousal secondary to increased work of breathing to overcome the resistance. Repeated and multiple arousals (which the patient is usually unaware of) result in an abnormal sleep architecture and daytime somnolence (sleepiness). Arousals result in sympathetic activation, and UARS is therefore likely to cause hypertension similar to obstructive sleep apnea syndrome (This has not been verified in large clinical populations because of the relatively small number of patients with UARS in the larger epidemiologic studies so far. However, repeated arousals in individuals have clearly been shown to be related to sympathetic activation and elevation in blood pressure.)^[1]

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