The Author: Dr. Isono is Associate Professor in the Department of Anesthesiology, Graduate School of Medicine of Chiba University in Chiba, Japan. His areas of research interest include respiratory physiology and sleep medicine, particularly the pathophysiology of upper airway maintenance in unconscious subjects.
Obesity and obstructive sleep apnoea: Mechanisms for increased collapsibility of the passive pharyngeal airway
Article first published online: 21 DEC 2011
© 2011 The Author. Respirology © 2011 Asian Pacific Society of Respirology
Volume 17, Issue 1, pages 32–42, January 2012
How to Cite
ISONO, S. (2012), Obesity and obstructive sleep apnoea: Mechanisms for increased collapsibility of the passive pharyngeal airway. Respirology, 17: 32–42. doi: 10.1111/j.1440-1843.2011.02093.x
SERIES EDITOR: AMANDA J PIPER
- Issue published online: 21 DEC 2011
- Article first published online: 21 DEC 2011
- Accepted manuscript online: 24 OCT 2011 10:03AM EST
- Received 5 August 2011; invited to revise 25 August 2011; revised 19 September 2011; accepted 25 September 2011.
- closing pressure;
- fat distribution;
Epidemiological evidence suggests there are significant links between obesity and obstructive sleep apnoea (OSA), with a particular emphasis on the importance of fat distribution in the development of OSA. In patients with OSA, the structure of the pharyngeal airway collapses. A collapsible tube within a rigid box collapses either due to decreased intraluminal pressure or increased external tissue pressure (i.e. reduction in transmural pressure), or due to reduction in the longitudinal tension of the tube. Accordingly, obesity should structurally increase the collapsibility of the pharyngeal airway due to excessive fat deposition at two distinct locations. In the pharyngeal airway region, excessive soft tissue for a given maxillomandibular enclosure size (upper airway anatomical imbalance) can increase tissue pressure surrounding the pharyngeal airway, thereby narrowing the airway. Even mild obesity may cause anatomical imbalance in individuals with a small maxilla and mandible. Lung volume reduction due to excessive central fat deposition may decrease longitudinal tracheal traction forces and pharyngeal wall tension, changing the ‘tube law’ in the pharyngeal airway (lung volume dependence of the upper airway). The lung volume dependence of pharyngeal airway patency appears to contribute more significantly to the development of OSA in morbidly obese, apnoeic patients. Neurostructural interactions required for stable breathing may be influenced by obesity-related hormones and cytokines. Accumulating evidence strongly supports these speculations, but further intensive research is needed.