Basics of Airway Dynamics
There are two basic principles of airway dynamics that come into play, the Venturi effect and the Bernoulli principle. The Venturi effect says that if the diameter of a tube is decreased, in this case the airway, then for a given volume of fluid to pass through the tube the velocity has to increase. A classic example or comparison is the garden hose. This basic concept relates to snoring, as the airway caliber is narrowed, soft tissues within the airway may vibrate. The Bernoulli principle states that as fluid flows through a tube and with an increase in the flow of that substance, there is an increase in negative pressure at the periphery. This then contributes to an increased potential for airway collapse. An example is a paper straw; as more force is applied the straw is more likely to collapse.
Another concept is that of the variable resistor. In this situation, as the rate of flow increases so does the resistance to that flow. However, the classic explanation that involves airway collapse related to flow is the starling resistor concept. In this situation, a collapsible tube is positioned between two rigid structures. In this case, the collapsible tube is the airway and is between the craniofacial structures, nasal airway, and the trachea. When the airflow increases and the pressure outside the tube is greater than the pressure inside the tube, this leads to collapse. In the awake state, the airway is not subject to these fluctuations in pressure and the airway remains open. However, during sleep when the airway relaxes and negative pressure increases the transmural forces that support the airway are not capable of resisting the negative pressure and this leads to airway restriction or obstruction. During respiration, the flow through the tube (airway) may be unimpeded, causes flutter, or becomes blocked depending on the variation in pressure. This correlates with normal breathing, snoring, and obstruction associated with apnea [17].
Another consideration is the critical closing pressure, known as Pcrit. The Pcrit is related to the ability of the upper airway muscles to resist collapse. Being associated with the collapsibility of the airway this may be related to upper airway anatomy [18]. One study found that certain cephalometric measurements were predictive of the Pcrit. In particular, the airway length and the relationship of the hyoid to the mandibular plane are relevant.
The concept of loop gain (LG) has become a known factor related to the airway and to successful management of SRBD, especially with oral appliance therapy (OAT). LG is related to an unstable ventilatory response to a disturbance in respiration [19]. When the LG is low, a more desirable situation, then the response to a respiratory disturbance more easily returns to a stable pattern [20]. If the LG is higher, then the response is greater and hence unstable. This results in more difficulty managing the respiratory disturbance. A lower LG is favorable to successful OAT.
Conclusion
The upper airway is a complex area with many muscles designed to support the airway for normal breathing and also to facilitate swallowing and to some degree speech. Over time and with age the airway becomes less compliant and hence may be more likely to experience collapse as well as obstruction.
References
1 1 Lindberg, E., Elmasry, A., Gislason, T. et al. (1999). Evolution of sleep apnea syndrome in sleep snorers a population‐based prospective study. Am. J. Respir. Crit. Care Med. 159: 2024–2027.
2 2 Sabolsky, J.P., Stashuk, D.W., Hamilton‐Wright, A. et al. (2012). Neurogenic changes in the upper airway of patients with obstructive sleep apnea. Am. J. Respir. Crit. Care Med. 185 (3): 322–329.
3 3 Davidson, T.M. (2003). The Great Leap Forward: the anatomic basis for the acquisition of speech and obstructive sleep apnea. Sleep Med. 4 (3): 185–194.
4 4 Guilleminault, C., Eldridge, F.S., and Dement, W.C. (1973). Insomnia with sleep apnea: a new syndrome. Science 181: 856–858.
5 5 Krakow, B., Melendres, D., Ferreira, E. et al. (2001). Prevalence of insomnia symptoms in patients with sleep‐disordered breathing. Chest 120: 1923–1929.
6 6 Neubauer, D.N. (2015). What is complex insomnia? Neurol. Rev. 23 (11): 18.
7 7 Norton, N.S. (2007). Netter's Head and Neck Anatomy for Dentistry. Saunders Elsevier.
8 8 Dempsey JA, Veasey SC, Morgan BJ, O'Donnell CP. Pathophysiology of sleep apnea. Physiol. Rev. 2010; 90(1):47–112. doi: https://doi.org/10.1152/physrev.00043.2008.
9 9 Standring, S. (ed.) (2008). Gray's Anatomy: The Anatomical Basis of Clinical Practice, 40e. London: Churchill Livingstone.
10 10 Sanders, I. and Mu, L. (2013). A 3‐dimensional atlas of human tongue muscles. Anat. Rec. (Hoboken) 296 (7): 1102–1114. https://doi.org/10.1002/ar.22711.
11 11 Gardner, E., Gray, D.J., and O'Rahilly, R. (1969). Anatomy A Regional Study of Human Structure, 694. WB Saunders Co.
12 12 Broderick, M. and Guilleminault, C. (2008). Neurological aspects of obstructive sleep apnea. Ann. N.Y. Acad. Sci. 1142: 44–57.
13 13 Saboisky, J.P., Stashuk, D.W., Hamilton‐Wright, A. et al. (2012). Neurogenic changes in the upper airway of patients with obstructive sleep apnea. Am. J. Resp. Crit. Care Med. 185 (3): 322–329.
14 14 Friberg, D., Ansved, T., Borg, K. et al. (1998). Histological indications of a progressive snorers disease in an upper airway muscle. Am. J. Resp. Crit. Care Med. 157: 586–593.
15 15 Almendros, I., Acerbi, I., Puig, F. et al. (2007). Upper‐airway inflammation triggered by vibration in a rat model of snoring. Sleep 30 (2): 225–227.
16 16 Lee, S.A., Amis, T.C., Byth, K. et al. (2008). Heavy snoring as a cause of carotid artery atherosclerosis. Sleep 31 (9): 1207–1213.
17 17 Lee‐Chiong, T. (2006). Sleep: A Comprehensive Handbook, 213–214. Wiley‐Liss/Wiley.
18 18 Genta, P.R., Eckert, D.J., Danzi, N.J. et al. (2011). Critical closing pressure and upper airway anatomy. Am. J. Respir. Crit. Care Med. 183: A3693.
19 19 Strohl, K.P., Yamauchi, M., and Dick, T.E. (2007). Loop gain and sleep disordered breathing. Curr. Respir. Med. 3: 85–92.
20 20 Kryger, M.H., Roth, T., and Dement, W.C. (2017). Principles and Practice of Sleep Medicine. Elsevier Saunders.
4 The Classification of Sleep Disorders
Conceptual Overview
The classification of sleep disorders has evolved over time as research has contributed to a better understanding of these disorders. As with other areas or disciplines related to clinical dentistry, a classification system for sleep disorders will facilitate a comprehension of the various disorders, especially with regard to supporting evidence, signs and symptoms, pathophysiology, etiology, and clinical management. However, for a greater appreciation of the full spectrum of sleep disorders, the practitioner is encouraged to at least be familiar with the more common sleep disorders. This chapter is intended as a review of the third edition of the International Classification of Sleep Disorders (ICSD‐3) [1] with the emphasis placed on the sleep disorders that are more likely to be encountered by the practicing dentist.
Classification Systems
A classification system assists with the development of a differential diagnosis of various health and medically related disorders. There are currently four classification systems for sleep disorders that should be