Dental sleep medicine series 4: Upper airway physiology

Sleep disordered breathing is a medical condition that requires a different approach in thinking than the dentistry that we are used to. A solid knowledge of airway anatomy and physiology is essential in understanding and treating OSA.

From Sleep medicine 6th edition

Numerous factors contribute to ventilation and mechanical properties of the thoracopulmonary system. Because sleep interacts with several of these factors, it has an impact on ventilation and gas exchanges through its effect on airway resistance, thoracopulmonary compliance, and lung volumes. As a consequence of its effect on upper airway muscle control and chest mechanics, sleep has a strong influence on upper airway stability. Accordingly, persons with compromised upper airway anatomy are at increased risk for development of obstructive sleep-induced disordered breathing, especially during the transition between wakefulness and sleep.

Anatomy and physiology
The upper airway includes the nasal cavity, pharynx and larynx. It is hypothesised that the development of speech which requires mobility of the pharynx led to a loss of rigid support of the upper airway which makes it more collapsible in humans. Breathing is possible through either the nose or the mouth but nasal breathing is the physiologic breathing route. The lower airway includes the trachea and lungs.

Capillaries lining the alveoli allow gas exchange between lung air and blood. The dual aim of breathing is to provide oxygen to the body and to remove carbon dioxide from cell metabolism. deoxygenated, carbon dioxide loaded blood enters the right side of the heart and is pumped to the lungs where gas is exchanged. The blood returns to the left side of the heart and is pumped around the body. The ribs articulate with the transverse process of the thoracic vertebrae and have anterior flexible cartilagenous connections with the sternum. The lungs are lined with visceral pleura which is separated by a few millimeters of lubricating fluid to the parietal fluid lining the hemothorax. The expansion of the rib cage provides negative pressure in the lungs (like a syringe drawing air in) and allows an expansion in volume.

The diaphragm is the main muscle of respiration. The phrenic nerve provides innervation to the diaphragm. During inspiration, the diaphragm contracts increasing intrathoracic volume. Intercostal muscles can also increase the intrathoracic volume by elevating the ribs and increasing the anterior posterior dimension of the thorax The scalene or SCM muscles are not active during normal breathing but can be activated during effort or in thoracopulmonary disorders.

The lung has an inherent contractive force due to its elastic tissue which is balanced by the outward resting force of the ribcage. During expiration the inspiratory muscles relax and the elasticity of the lung takes over allowing expiration to be a passive process. However, during active expiration, abdominal and external intercostal muscles enhance the change in pressure. The average rate of respiration is 10-18/minute.

Effects of obesity and body position
The supine position causes a reduction in total lung capacity compared to the upright position thought to be use to an increase in intrathoracic blood volume or due to the gravitational effect of abdominal contents pushing the relaxed diaphragm into a more rostral position reducing its ability to contract therefore also increasing breathing effort. Decreased lung volume can also increase upper airway resistance  by reducing the caudal traction of the mediastenum and trachea on the pharyngeal walls making them more collapsible on inspiration.

In obese subjects, a similar restriction in the lung volume is observed in the sitting position. due to Contrary to expectations, a lesser decline in total lung capacity from sitting to supine is noted in obese subjects possibly because the diaphragm is already shifted to a more rostral position (due to abdominal contents) and the supine shift has less of an effect of the diaphram (i.e the normal effects of the supine position are already present in obese patients regardless of their position).

Effects of sleep on the airway
Lung functional residual capacity decreases during sleep. in NREM2, SWS and REM sleep. Possible mechanisms include rostral displacement of the diaphragm due to muscle hypotonia, alteration of respiratory timing from the CNS, decrease in lung and thoracic compliance and central pooling of blood. Reduction of tidal volume is due to a faster and shallower breathing pattern especially in REM sleep.

Upper airway
The upper airway plays a unique role in ventilation as sleep dramatically affects its mechanical properties. Intrathoracic airway structures are kept patent by cartilagenous structures and the nasopharynx is non collapsible. However, the pharynx that lies between these is prone to closure during an imbalance between forces that tend to dilate or close them (acting as a starling resistor).
Collapsing forces
The collapsible forces are the negative pressure applied by the lung and the pressure applied by upper airway tissue. Change from a laminar to a turbulent flow tends to increase air velocity near the walls further reducing intraluminal pressure. Increased weight of the upper airway tissue on the hyoid arch (muscular and adipose tissue) reduces its stability.
Dilator forces
The contraction of upper airway dilators are the main factors affecting airway dilation. Tracheal traction due to the movement of the diaphragm, intercostals and accessory muscles unloads the upper airway. Upper airway stabilising muscles e.g genioglossus, levator palatini, tensor palatini, geniohyoid, musculus uvulae and palatopharyngeus contribute to upper airway patency. Activation of the masseter and pterygoid muscles may also contribute to stabilising upper airway by their position on the mouth and mandible. Negative pressure developed in the upper airway has a positive feedback on muscle activity through activation of tensoreceptor and mechanoreceptor pathways.

Sleep may compromise upper airway stability by altering the pattern of preactivation of upper airway muscles leading to a rise in upper airway resistance and airway closure. The loss of wakefulness stimulus contributes to the decrease in upper airway muscle activity. The tensor palitini has tonic activity but the genioglossus, palatoglossus and levator palatini have phasic activities. Obstructive breathing disorders are mainly observed during N1, N2 and REM sleep when ventilation is physiologically unstable and rarely during SWS when breathing is regular.