Pathophysiology of OSA

The essential culprit behind OSA is that oral and/or nasal airway flow is mechanically obstructed (Figure 2). The obstruction lies somewhere at the nexus between collapsibility of the tongue posteriorly or the soft palate and upper airway muscles losing tone during sleep resulting in an obstructed airway. A frequent site of obstruction is the oropharynx, the pharyngeal space posterior to the tongue. OSA pathophysiology includes anatomic and non-anatomic (NA) factors. NA factors include impaired pharyngeal dilator muscle function, low respiratory arousal threshold (patient will be apneic or hypopneic for longer time periods), and high loop gain (unstable control of breathing). Anatomically, narrow pharynx, longer airway lengths and lumen shape are associated with collapse while asleep. There are over 20 airway muscles. The upper airway lacks bony support. The genioglossus is the largest pharyngeal dilator. As all airway muscles do, it receives central respiratory motor output along with reflex influences via chemoreceptors and mechanoreceptors. The genioglossus exhibits a phasic pattern of activation being more active during inspiration and less active during expiration. Whereas the tensor palatini muscle exhibits tonic activity constantly throughout the breath cycle. In OSA, upper airway collapsibility (Pcrit) ranges from -5 to +5 cmH2O. Pcrit near +5 indicates a high chance of airway collapsibility.⁸

Figure 2.

Figure 2.

Depiction of the essential pathophysiology in obstructive sleep apnea. The airflow through the oral and nasal cavities (white arrows) are inhibited from reaching the lungs due to mechanical obstruction of the upper airway at the base of the tongue and posterior soft palate (gray arrows).

When airflow is prevented from reaching the lungs, there is a corresponding drop in oxygen saturation within the blood. This can be measurable by a pulse oximeter and is one component of an overnight sleep study. Repeated airway obstruction and the ensuing oxygen desaturation forces the central nervous system to take action. A patient with OSA will be displaced from deeper stages of sleep in order to breathe. These are not full awakenings but have been termed microarousals. A repetitive train of microarousals prevents the patient from enjoying the deeper, more restorative stages of sleep. As sleep architectures deteriorates, OSA patients will report poor sleep quality despite sleeping a lot (sleep quantity).