Obstructive Breathing Disorders

Obstructive sleep apnoea (OSA) is characterised by recurrent episodes of partial or complete upper airway collapse during sleep. The collapse is accompanied by a reduction in or complete cessation of airflow despite ongoing inspiratory efforts. Due to the lack of adequate lung ventilation that results from the upper airway narrowing, oxygen saturation may drop and partial pressure of carbon dioxide may occasionally rise. The events are mostly terminated by a brief awakening from sleep. Lack of sleep and low brain oxygen saturation cause excessive daytime sleepiness. There are also links between OSA and cognitive dysfunction, headaches, essential hypertension and heart failure. OSA has a reported prevalence of 2% in childhood, 2–4% in middle-aged adults (occurring more frequently in men) and more than 10% of the population over the age of 65, thus OSA is a health care issue affecting all stages of life.

The most common treatment for OSA is a Continuous Positive Airway Pressure (CPAP) device, an airpump fitted to a mask (worn at night) that maintains a positive pressure in the upper airway, thereby ensuring its patency. Another nonsurgical treatment is a mouth guard designed to advance the lower jaw in order to increase the cross-sectional area of the pharynx. There are also a variety of surgical treatments based on the principles of soft tissue stiffening/removal (soft palate, uvula, pharynx) and augmentation/displacement of bone (maxilla, mandible, hyoid) in order to dilate the airway and remove potential obstructions.

CPAP is very successful but not always well tolerated by the patient. The success of other treatments, nonsurgical and surgical alike, is mixed and appears to be related to patient-specific anatomical factors. Risk factors for OSA include smoking, obesity, excessive alcohol consumption, respiratory depressing drugs, nasal congestion, increased neck circumference and snoring.

Snoring most commonly involves the vibration of the soft palate induced by air flow through the nose and/or mouth. In pure nasal breathing the soft palate may deflect sufficiently to obstruct the nasopharynx, while if both nose and mouth are open it may also block the oral airway by contacting the tongue. Snoring may also involve the collapse of the pharyngeal walls themselves.

Snoring generally occurs during inspiration while flow rate is still increasing whereas the onset of OSA appears to be at the end of expiration, when flow rate is decreasing and in the opposite direction. However, it has been estimated that some 10% of snorers are at a much greater risk of OSA.

Open questions:

• What anatomical features of the airway make it prone to collapse?

  • Can we predict the site of collapse?

  • When in the respiratory cycle will collapse occur?

  • Is there a mechanical relation between the flow-induced oscillations typical of snoring and the airway closure in sleep apnoea?

  • Can we predict which treatment will be the most successful for a given patient?

Motivated by the need for patient-specific answers, I have been developing finite element models of the coupled fluid and solid mechanics of the human upper airway. The broad aim is to capture the salient fluid-structure interactions (FSI) and investigate the instabilities leading to flow-induced oscillations and airway collapse that are associated with snoring and sleep apnoea.