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3 Pathophysiology of Sleep‐Related Breathing Disorders
Conceptual Overview
The origin and cause of sleep‐related breathing disorders (SRBDs) are ongoing areas of study and interest, as well as the many contributing factors. The pathophysiology of SRBD is multifactorial, involving the anatomy, the function of the airway physiologically and other contributing factors such as the control of respiration neurologically, age, sex, weight and other sleep disorders. In addition, SRBDs are often times progressive. This may begin simply as chronic mouth breathing, especially during sleep, and progress to snoring and then to obstructive sleep apnea (OSA) [1]. In addition, there may be neurogenic changes that can impact the sensory and motor activity of the upper airway related to vibration, inflammation, and even hypoxia [2]. There may also be a developmental aspect to the evolution of SRBD in the human. This involves the loss of the eppiglottic‐soft palatal lock‐up that in other primates prevents the tongue from collapsing into the airway during sleep. This has been attributed to the acquisition of speech, associated with the descent of the larynx, termed the great leap forward [3] (Figure 3.1).
Insomnia also needs to be considered and may be associated with painful conditions, psychological issues such as anxiety or depression, and may be residual to adequately managed SRBD. This association was first reported in 1973 [4]. It has been reported that about 50% of patients presented with both the SRBD and insomnia, and it was termed sleep breathing disorder plus [5] also referred to as complex insomnia [6].
Normal Respiration
A brief discussion and review of respiration needs to be addressed. Under normal circumstances respiration is mostly considered to be involuntary. It is primarily under the control of the diaphragm that is innervated by the phrenic nerve, composed primarily of muscle fibers that cause contraction. The phrenic nerve is derived from the cervical nerves at the C‐3 to C‐5 level. During passive breathing the diaphragm contracts and moves downward causing an increase in the negative pressure within the lungs and the alveoli. This negative pressure causes air to enter the lungs to fill them. In addition, this action may be impacted by the action of the intercostal muscles as well as the scalenes. Expiration during quiet breathing is passive and there is no active muscle activity. The process is related to the elastic recoil of the lungs and the rib cage.
Forced inspiration and expiration is different. With forced or exertional inspiration the scalenes and the sternocleidomastoid (SCM) muscles are active. They impact the first and second ribs as well as the sternum, and this results in the elevation of the bony cage in an effort to increase lung volume. Forced expiration is primarily an action of the intercostal muscles that pull the thoracic cage inward and force air out of the lungs.
Figure 3.1 Evolution of SRBD based on the acquisition of speech and the loss of the epiglottic‐soft palatal lockup. This allows the tongue base to occupy more of the oropharynx.
Anatomy and Function of the Airway
The understanding and focus is related to the pathophysiology of SRBD that begins with an understanding of the anatomy of the airway most often implicated in the onset and perpetuation of these conditions. The anatomy of the airway here focuses mainly on the upper airway, primarily the musculature that directly controls airway function, which has been broken down by anatomic location [7]. These same muscles are also involved in the function of speech and eating, hence breathing while awake is likely impacted by these functions but not during sleep and this then increases the likelihood for the SRBD.
The airway may be divided into three regions: the retropalatal area (nasopharynx), the retroglossal area (oropharynx), and the hypopharynx, also known as the laryngopharynx [8]. The oropharynx is at the level of the second and third cervical vertebrae (C‐2 to C‐3). The hypopharynx is at the level of C‐4 to C‐6, is a continuation of the oropharynx demarcated by the epiglottis, and starts at the level of the hyoid bone. In these three regions there are structures that need to be considered that have an impact on the airway as well as breathing (Figure 3.2).
Soft Palate
The muscles involved here are mainly designed to elevate and tense the soft palate. In addition, during the act of swallowing these muscles close off the nasopharynx (Table 3.1).
The palatopharyngeus and palatoglossus muscles are included with the soft palate because their origin is from the palatine aponeurosis, and the control of these muscles is the same as the musculus uvulae and levator veli palatini. The palatoglossus muscle is one of the four extrinsic muscles of the tongue, the only one that is not innervated by hypoglossal nerve (cranial nerve XII), and is innervated by the pharyngeal branch of the vagus nerve (cranial nerve X) [9]. The palatopharyngeus muscle goes from the area of the palate to the pharynx. Its primary function is associated with swallowing and is also innervated by the same nerve as the palatoglossis.
Figure 3.2 Illustration of the three regions of the upper airway: N, nasopharynx;