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OSA Pathogenesis

OSA is increasingly recognized as a multifactorial disorder i.e., different people have OSA for different reasons. Although an anatomical predisposition (collapsibility of the upper airway) is required, other factors are important as well, including a low respiratory arousal threshold (wake up too easily), dysfunction in upper airway dilator muscles and instability in ventilatory control (which we quantify using the engineering term loop gain [LG]), which leads to periods of decreased pharyngeal tone as well periods of increased respiratory effort.  I have been actively involved in efforts to characterize the different endotypes – defined as a subtype of a condition that has a distinct functional or pathobiological mechanism – important for OSA. The ultimate goal of this work is to personalize therapy for OSA one day by addressing the underlying endotype to treat OSA effectively in an individual with targeted therapy.


Currently, we can measure these endotypes through careful manipulation of the airway during the night during sleep, and see how the person's muscles, respiratory drive and arousal mechanisms compensate.


In an individual, we can model how the traits go together.


This is important because two people might have the same severity of OSA for DIFFERENT reasons.  Ultimately we hope to treat the underlying cause and personalize therapy.

We do have alternate therapies, such as oral appliances and upper airway surgery, but we are pretty bad at predicting who can use these.  With a knowledge of the underlying physiology we can model outcomes from surgery more accurately.