Student Level: Honours

Obstructive sleep apnoea (OSA) is characterised by recurrent nocturnal upper airway (UA) obstruction, airflow limitation and oxygen desaturation events. A low end-expiratory lung volume 
(EELV: the volume of gas remaining in the lung at the end of a tidal expiration), potentially arising as a consequence of obesity, supine posture and sleep, has been widely proposed as a key pathophysiological mechanism promoting increased UA collapsibility and nocturnal UA obstruction in OSA patients. The volume of the gas in the lung is also important in determining the severity of apnea related  oxygen desaturation, and may additionally influence the ability of the upper airway muscles to reopen the upper airway. Our recent published animal study suggests that the onset of upper airway closure occurs once there has been a threshold reduction in lung volume. We now propose to extend this work, and using both a well established animal model and human subjects with OSA we propose to test the following hypotheses:-
1.There is a critical EELV below which obstructive apnoeic events are likely to develop.
2. Low EELV levels promote more severe oxygen desaturation levels during apnoea.
3. Low EELV reduces UA dilator muscle fractional shortening for a given level of stimulus (input drive), reducing the ability of UA muscles to both dilate the UA lumen and lower its resistance to airflow.
4. In OSA patients, low EELV values during sleep are associated with more frequent and longer apnoeic events accompanied by more severe levels of oxygen desaturation.

Supervisor: Associate Professor Kristina Kairaitis - kristina.kairaitis@sydney.edu.au