Uykuda Solunum Bozuklukları Fizyopatolojisi Doç. Dr. Banu Eriş Gülbay AÜTF Göğüs Hastalıkları AD

Sunum Planı Normal Üst Solunum Yolu Fonksiyonları, Anatomisi Statik ve dinamik özellikleri Sağlıklı bireyler ile Uyku Apneli hastalar arasında Yumuşak doku ve kraniofasial yapılar arasındaki farklılıklar ÜSY yapılarındaki dinamik fizyolojik değişiklikler Uyku apneli Hastalarda ÜSY kalibrasyonunu arttıran Tdv yöntemleri ve mekanizmaları We review normal upper airway anatomy, static and dynamic properties of the normal upper airway, and upper airway pharyngeal muscle activation. We also examine differences in soft tissue and craniofacial structures between healthy subjects and patients with apnea and the factors leading to these differences, as well as dynamic physiologic changes in upper airway structures in patients with sleep apnea and obstruction of the pharynx during sleep. Finally, we discuss mechanisms by which the therapeutic interventions for sleep apnea increase upper airway caliber and a model for upper airway closure in patients with sleep-disordered breathing. The sleep state is associated with a decrease in motor output to pharyngeal muscles. When this occurs against the background of upper airway anatomic abnormalities, severe narrowing or closure of the pharyngeal airway can occur.

Normal ÜSY Anatomisi ÜSY;  Nazofarenks  Orofarenks Retropalatal * Retroglossal *  Hipofarenks The upper airway is separated into three regions: the nasopharynx, which is defined from the nasal turbinates to the hard palate; the oropharynx, subdivided into the retropalatal region (defined from the hard palate to the caudal margin of the soft palate) and the retroglossal region (defined from the caudal margin of the soft palate to the base of the epiglottis); and the hypopharynx, which is defined from the base of the tongue to the larynx (Fig. 82-1). The majority of patients with obstructive sleep apnea manifest upper airway closure or narrowing during sleep in the retropalatal and retroglossal regions A, Midsagittal magnetic resonance (MR) image in a normal subject showing the four upper airway regions: A is the nasopharynx, which is defined from the nasal turbinates to the hard palate; B is the retropalatal oropharynx, which extends from the hard palate to the caudal margin of the soft palate; C is the retroglossal region, which extends from the caudal margin of the soft palate to the base of the epiglottis; and D is the hypopharynx, which is defined from the base of the tongue to the larynx. B, Diagram demonstrating important midsagittal upper airway, soft tissue, and bony structures.

Normal ÜSY Anatomisi To understand airway closure in patients with obstructive sleep apnea, we need to understand how pharyngeal wall structures determine airway size, or, to put it another way, examine the doughnut as well as the hole in the doughnut. The anterior wall of the oropharynx is formed primarily by the soft palate and tongue, whereas the posterior wall of the oropharynx primarily comprises the superior, middle, and inferior constrictor muscles. The lateral oropharyngeal walls are formed by several different structures including oropharyngeal muscles (hyoglossus, styloglossus, stylohyoid, stylopharyngeus, palatoglossus, palatopharyngeus, and the pharyngeal constrictors [superior, middle, and inferior]), lymphoid tissue (palatine tonsils), and adipose tissue (parapharyngeal fat pads). The mandibular rami bound all the structures that form the lateral pharyngeal walls (Figs. 82-2 and 82-3). Figure 82-2 A, Axial magnetic resonance (MR) image in a normal subject in the retropalatal region. The tongue, soft palate, parapharyngeal fat pads (fat is white on an MR image), lateral parapharyngeal walls (muscles between the airway and lateral parapharyngeal fat pads), and mandibular rami can all be visualized on this axial MRI. B, Diagram demonstrating important soft tissue and craniofacial structures on an axial MR image in the retropalatal region. F, distance between the parapharyngeal fat pads; M, distance between the mandibular rami; P, posterior airway wall thickness; PW, lateral pharyngeal wall thickness

Normal ÜSY’nun Statik ve Dinamik Özellikleri ÜSY’nun Normal koşullar altındaki davranışı The patency of the upper airway depends on the balance of forces across it and on its compliance [6] (Fig. 10.1). The airway between the oropharynx and the larynx is a single muscular tube which conducts air in and out of the lungs, and food, drink and upper airway secretions into the oesophagus. Above the oropharynx two airways (the nasal and oral) are in parallel so that obstruction of either does not cause airflow to cease. Below the larynx the airway is supported by cartilaginous rings which prevent its collapse. Any factor which narrows the upper airway, increases the pressure around it, reduces the pressure within it, or increases its compliance, will predispose towards OSA. Airway size is determined by both dilating and collapsing forces. Dilating forces include upper airway muscle tone, mechanical force of the airway wall structure, and positive intraluminal airway pressure. Collapsing forces include tissue mass, surface adhesive forces, and negative intraluminal pressures. The resulting difference in these forces is the distending force, which acts on the wall of the upper airway. SVTH : SVTV = 1:1 (+) İntralüminal basınç Yüzeyel adeziv faktörler

Süperior faringeal constrictor Faringeal Kaslar * * * Many of the 20 or more skeletal muscles surrounding the pharyngeal airway, including the medial pterygoid, tensor palatini, genioglossus, geniohyoid, and sternohyoid, receive phasic activation during inspiration and tend to promote a patent pharyngeal lumen by dilating the airway and stiffening the airway walls.18 As shown in Figure 82-6A,B, the pharyngeal muscles have complex anatomic relationships. These muscles can be classified into muscles regulating the position of the soft palate, tongue, hyoid apparatus, and posterolateral pharyngeal walls. Schematic diagram of upper airway anatomy. The tensor palatini moves the soft palate ventrally. The genioglossus acts to displace the tongue ventrally. Coactivation of the muscles in the anterior pharyngeal wall such as the geniohyoid and sternohyoid (not shown) act on the hyoid bone to move it ventrally. Contraction of specific muscles within these groups can have antagonistic effects on the pharyngeal airway. For example, contraction of the palatal muscle levator palatini, along with the superior pharyngeal constrictor, closes the retropalatal airway; contraction of other palatal muscles, the palatopharyngeus and glossopharyngeus, opens the airway in the retropalatal region.19 Similarly, the extrinsic tongue muscles include tongue protrudors (genioglossus and geniohyoid) and retractors (hyoglossus and styloglossus). Pharyngeal muscles can have different effects when activated in concert than when activated individually. Coactivation of the hyoid muscles is a particularly good example of this phenomenon (see Fig. 82-6).20 The hyoid bone in humans, unlike that in other mammals, does not articulate with any other bony or cartilaginous structure. The position of the relatively compliant ventral pharyngeal wall is, therefore, determined by the numerous muscle attachments to this floating bony structure. Muscles inserting on the hyoid include the geniohyoid and genioglossus. Contraction of these muscles pulls the hyoid in a rostral and anterior direction. Strap muscles originating from the sternum (sternohyoid) and thyroid cartilage (thyrohyoid) also insert on the hyoid and pull it in a caudal direction. With simultaneous contraction of all four muscles, the resultant force vector acting on the hyoid is directed caudally and anteriorly. This combined effect moves the anterior pharyngeal wall outward and promotes upper airway patency. Evidence also indicates that simultaneous activation of the antagonstic protrudor and retractor tongue muscles, as occurs under hypercapnic and hypoxic conditions, has a synergistic effect in promoting upper airway patency.21,22 * ÜSY’nu Kapatan kaslar Açan kaslar Levator palatini Süperior faringeal constrictor Hyoglossus Styloglossus Palatofaringeus Glossofaringeus Genioglossus* Geniohyoid* SVTH : SVTV = 1:1

NM Tonüs Hava yolunu dilate ve kontrakte eder. Ventilasyon ile ilişkili kas tonüsü Santral respiratuar nöron drive tarafından belirlenir ve bu santral drive üzerinde;  Uyku evresi (Uyanıklık/NREM/REM)  Kimyasal kontrol (hipoksi, hiperkapni)  ÜSY mekanoreseptörleri etkilidir Diafram ve ÜSY kaslarının santral inn.; n.frenicus, n.vagus, n. glossafaringeus ve n.hypoglossus ile Kas aktivasyonu non-uniform ve aktivite  hiyerarşik Ventilatory related muscle tone is determined by central respiratory neuron drive. This drive is affected by sleep state (wake, NREM and REM sleep), chemical control (hypercarbia and hypoxia), and upper airway mechanoreceptors. Central respiratory innervation of the diaphragm and upper airway muscles is via the phrenic, vagus, glossopharyngeal, and hypoglossal nerves. Activation is nonuniform and activity is hierarchical. SVTH : SVTV = 1:1

NM Tonüs Ventilasyon ile ilişkili kas tonüsü; Ventilatuar aktivite, diaframda en fazla, ÜSY kaslarında (ventilatuar drive artmadıkça) az ya da Ø Uyku/uyanıklık durumunun ÜSY kaslarına etkisi farklı ÜSY tonik kas aktivitesi, uykunun derinleşmesi ile progresif azalır Uyanıklıkta, OUAS’lu hastalarda kas tonüsü nonapneiklere kıyasla (daha küçük ve kollabe olma eğilimli) artmıştır. Ventilatory activity is highest in the diaphragm and is reduced or absent in most upper airway muscles (inversely proportional to postural activation) unless ventilatory drive is increased. For this reason, the effects of the sleep/wake state on upper airway muscles are not uniform [16]. Postural upper airway tonic muscle activity decreases progressively with depth of sleep. A portion of this activity is maintained during NREM (but not REM) sleep (Figure 29.5). In OSA patients, muscle tone is increased during wake compared to nonapneic ‘‘normals.’’ This likely compensates for a structurally smaller and more collapsible upper airway. This augmented muscle tone is reduced during sleep (Figure 29.6). Figure 29.5 A sleep related decrease in tonic muscle tone (squares) and its associated increase in upper airway resistance (circles) with differing levels of NREM sleep are shown. Conceptually, loss of phasic upper airway reflexes (triangle) occurs acutely at sleep onset and is reduced in stage 2; increased reflex activity in stage 3/4 stabilizes ventilation despite high airway resistance. Figure 29.6 Changes in muscle tone in patients with OSA (upper) compared to normal subjects (lower). Sleep onset (arrow) is associated with decrease in tonic muscle tone in both groups. Loss of wake results in loss of phasic muscle tone in OSA (not depicted). Increased negative inspiratory pressure and arousals associated with apneas result in augmented phasic inspiratory EMG activity in OSA (seen in upper graph).

Santral respiratuar nöronlar NM Tonüs ÜSY fazik kas aktivitesi; Ventilatuar siklus ile bağlantılı ve inspirasyon sırasında artıyor Santral respiratuar nöron aktivitesi ve ÜSY reflekslerinden (PSS mekanoreseptörleri aracılığı ile) kaynaklanır Santral respiratuar nöronlar Upper airway phasic muscle activity is linked to the ventilatory cycle and is activated during inspiration. It results inherent from both inherent central respiratory neuron activity and reflexes mediated via peripheral nervous system mechanoreceptors. Central mechanisms preactivate upper airway muscles during inspiration. The resulting upper airway muscle activity stabilizes the upper airway prior to negative inspiratory forces generated by the diaphragm [17]. This activity is independent of upper airway mechanoreceptors Upper airway preactivation but not diaphragm activity is suppressed by various sedative medications including alcohol and benzodaizepines. With the loss of preactivation, the upper airway may be unable to compensate for negative airway pressure and other collapsing forces and upper airway obstruction may worsen. ÜSY Kasları Diaframdan daha önce aktive olur

NM Tonüs ÜSY fazik kas aktivitesi; Ventilatuar siklus ile bağlantılı ve inspirasyon sırasında artıyor Santral respiratuar nöron aktivitesi ve ÜSY reflekslerinden (PSS mekanoreseptörleri aracılığı ile) kaynaklanır Santral respiratuar nöronlar Upper airway mechanoreceptors primarily located at the level of the epiglottis react to negative airway pressure and drive phasic upper airway muscle activity [8, 18]. Both OSA and non-OSA individuals have the potential to demonstrate this reflex during wakefulness; however, in the normal airway, the reflex is not active at rest and requires augmented breathing (such as exercise). In OSA patients, this reflex primarily mediates increased upper airway muscle activity that is present during wakefulness. This reflex is also state dependent and in OSA patients is acutely lost following the transition from wake to NREM sleep [19]. Decreased phasic upper airway muscle tone worsens airway obstruction. ÜSY Kasları Diaframdan daha önce aktive olur ÜSY mekanoreseptörleri (-) hava yolu P’ına tepki verir

Normal ÜSY’nun Statik ve Dinamik Özellikleri ÜSY’nun Normal koşullar altındaki davranışı To understand why the pharyngeal airway collapses during sleep in patients with obstructive sleep apnea, one must first understand the static and dynamic properties of the upper airway under normal conditions. The mechanical behavior of the upper airway under passive conditions-that is, when neuromuscular influences have been suppressed4-7-can best be described in terms of the relationship between cross-sectional airway area (A) and transmural pressure (Ptm). As depicted in Figure 82-4A, transmural pressure is the difference between intraluminal pressure (Pl) and tissue pressure (Pti): Ptm = Pl - Pti. An increase in transmural pressure, caused either by more positive intraluminal pressure or more negative tissue pressure, distends and enlarges the airway area; conversely, a decrease in transmural pressure, caused either by more negative intraluminal pressure or more positive tissue pressure, narrows the airway. Transmural basınç: ÜSY’nu dilate eden ve kollabe eden güçler arasındaki farktır. ÜSY’nun kompliansı=ÜSY’nun kollabe olmaya eğilimini gösterir. Birim basınç karşısındaki volüm değişikliği (komplians yüksek ise transmural basınç farkı düşüktür, hava yolu kollabe olma eğilimindedir Compliance: Birim basinç degisikliginin sebep oldugu hacım degisikligidir. Formül: hacim değişimi/basınç değişimi. Airway patency is modulated by physical characteristics and neural mechanisms. The upper airway, unlike the lower respiratory tract, lacks a robust support framework of cartilaginous rings and therefore is at risk for collapse due to: (1) extraluminal tissue pressure exerted by circumferential craniofacial and soft tissue structures; and (2) negative pressure associated with inspiration. The pharyngeal dilator muscles help to maintain upper airway patency. Changes in pharyngeal transmural pressure, defined as the difference between the pressure in the airway lumen and the pressure exerted by tissues surrounding the site of collapse, modulates upper airway size. SVTH : SVTV = 1:1

Normal ÜSY’nun Statik ve Dinamik Özellikleri Faringeal hava yolu üzerinde Etkili olan Mekanik Faktörler: Statik Faktörler Yüzey adeziv güçler Boyun ve çene postürü Trakeal tug Yer çekimi Dinamik Faktörler Nazal hava yolu ve farenkste akım direnci Bernoulli etkisi Dinamik komplians A number of mechanical influences (Box 82-1) impinge on the upper airway to cause it to be fully open, narrowed, or closed. These factors can be classified as static or dynamic influences, and they interact with the tube law of the pharynx to determine, at any time, the cross-sectional area of various segments of the upper airway. SVTH : SVTV = 1:1

Normal ÜSY’nun Statik ve Dinamik Özellikleri Faringeal hava yolu üzerinde Etkili olan Mekanik Faktörler: Statik Faktörler Yüzey adeziv güçler Boyun ve çene postürü Trakeal tug Yer çekimi Dinamik Faktörler Nazal hava yolu ve farenksteki upstream direnç Bernoulli etkisi Dinamik komplians Clinical observations, as well as studies in anesthetized animals, indicate that surface adhesive forces between opposed luminal surfaces may contribute to airway patency and closure. During nasal breathing with the mouth closed, surface adhesive forces help maintain the soft palate in apposition to the base of the tongue and promote contact of the tongue with the mucosa of the fixed-space oral cavity. Mouth opening potentially destabilizes the airway by freeing the mucosal attachments of the tongue and soft palate and allowing the now freely moving structures to move posteriorly and compromise the pharyngeal airway. Nazal solunum sırasında; yumuşak damağın dil köküne yaklaşmasını ve oral kavite mukozası ile dilin kontaktını sağlar Ağız solunumu sırasında ise hava yolu destabilize olur; Dil ve yumuşak damağın mukozal yapışıklığı bozulur ve yapılar posteriora hareket ederek Faringeal hava yolunun kollabe olmasına neden olablir Surface adhesive forces may also make restoration of airway patency more difficult and may explain why the pressure needed to open an already closed airway (opening pressure) is greater than the closing pressure. Zaten kapalı olan hava yolunun açılması için, bu güçler nedeniyle daha yüksek basınca ihtiyacı (+) Increased surface tissue adhesion worsens airway collapse, and lubricants decrease airway collapse. Nazal solunum sırasında; yumuşak damağın dil köküne yaklaşmasını ve oral kavite mukozası ile dilin kontaktını sağlar. Ancak ** SVTH : SVTV = 1:1

Normal ÜSY’nun Statik ve Dinamik Özellikleri Faringeal hava yolu üzerinde Etkili olan Mekanik Faktörler: Statik Faktörler Yüzey adeziv güçler Boyun ve çene postürü Trakeal tug Yer çekimi Dinamik Faktörler Nazal hava yolu ve farenksteki upstream direnç Bernoulli etkisi Dinamik komplians Neck and Jaw Posture Body A number of studies indicate that neck flexion tends to close the airway and neck extension acts to open it.9,10 Whether the action is principally in the oropharynx or hypopharynx has not been documented, but it is likely that retropalatal and retroglossal regions of the upper airway are narrowed as the neck is flexed. Jaw posture has also been documented to influence the size of the upper airway. Opening the jaw slightly may actually increase the size of the pharynx by providing more room in the oral cavity for the tongue. This may be particularly important if the tongue is large relative to the oral cavity. However, progressive opening of the jaw leads to posterior movement of the genu of the mandible-that is, the genu moves closer to the posterior pharyngeal wall because the mandibular condyle of the temporomandibular joint is considerably rostral to the plane of the mandible (Fig. 82-5). This posterior movement of the genu of the mandible with mouth opening causes the tongue and hyoid apparatus to move posteriorly and thereby narrow the pharynx. Mouth opening causes a posterior and caudal displacement of the genu of the mandible, as well as the floating hyoid bone, through the many hyomandibular attachments. As a result, the anterior pharyngeal wall structures such as the tongue and epiglottis move in a posterior direction, decreasing pharyngeal airway size. Neck flexion would have a similar effect on the hyoid, tongue, and epiglottis even without a change in the relationship between the mandible and the maxilla. Posture — Although not a primary mechanism for upper airway obstruction, body position plays an important role in the genesis of obstructive events [16]. Some individuals with position-dependent OSA obstruct exclusively in the supine position (figure 1). When an individual is in the supine position, soft structures such as the tongue and soft palate can be drawn into the pharyngeal airway by the effects of gravity. As a result, the area behind the tongue and soft palate becomes a site of airway narrowing which can lead to upper airway obstruction (graph 3). Boyun Fleksiyonu ile ÜSY açıklığı azalır (Reropalatal ve retroglossal alan) Ekstansiyonu ile ÜSY açıklığı artar Çene açık  Farenks boyutu artar, Ancak sürekli açık kalırsa  Hyoid ve dil posteriora doğru hareket eder, farenks daralır SVTH : SVTV = 1:1

Normal ÜSY’nun Statik ve Dinamik Özellikleri Faringeal hava yolu üzerinde Etkili olan Mekanik Faktörler: Statik Faktörler Yüzey adeziv güçler Boyun ve çene postürü Trakeal tug Yer çekimi Dinamik Faktörler Nazal hava yolu ve farenkste akım direnci Bernoulli etkisi Dinamik komplians Increases in lung volume are thought to increase pharyngeal cross-sectional area, reduce closing pressure, and stiffen the upper airway.11-14 This action is probably exerted through axial forces in the trachea-a so-called tracheal tug. Increasing lung volume causes a caudal displacement of the intrathoracic trachea that, in turn, exerts caudally directed forces on the pharynx. The resulting passive axial tension in the pharyngeal wall tends to open the pharynx. Figure 29.9 The effects of tracheal tug and longitudinal tension on the airway are demonstrated. Inferior displacement of the trachea and/or hyoid bone increases longitudinal tension of the pharyngeal airway and decreases collapsibility. The upper airway diameter falls through a reflex mechanism as the lung volume, and in particular the functional residual capacity, decreases. Changes in lung volume significantly alter pharyngeal upper airway size. This ‘‘lung volume dependence’’ of pharyngeal airway size occurs during wakefulness and sleep [45]. Increased lung volumes increase pharyngeal size and decreased lung volumes contribute to pharyngeal collapse. Although when initially observed, reflex activation of upper airway dilator muscles was speculated, subsequent studies have demonstrated that changes are a mechanical effect of tracheal and thoracic traction. Thoracic traction, commonly referred to as ‘‘tracheal tug,’’ markedly influences pharyngeal size and patency and is mediated through the mediastinum, intrathoracic pressures, and the trachea. Changes are independent of neuromuscular activity or upper airway muscle support, with a likely mechanism being passive tracheal traction altering pharyngeal collapsibility by increasing longitudinal tension and stability on the pharyngeal wall (Figure 29.9) Another effect of the horizontal sleep posture is a decrease in lung volume. Reductions in lung volume have been shown to cause upper airway narrowing, possibly by reducing caudal traction on the airway [1,17]. However, upper airway narrowing has not been reported in patients with reduced lung volumes due to intrinsic lung restriction. This may be due to the differential effects of intrinsic lung restriction on diaphragm position and pleural pressure AC volümü artarsa  İntratorasik trakeanın caudal hareketi ile ÜSY kesit alanı artar (Faringeal duvarda pasif aksiyel gerilim) (Mekanik etki) SVTH : SVTV = 1:1

Normal ÜSY’nun Statik ve Dinamik Özellikleri Faringeal hava yolu üzerinde Mekanik Etkiler: Statik Faktörler Yüzey adeziv güçler Boyun ve çene postürü Trakeal tug Yer çekimi Dinamik Faktörler Nazal hava yolu ve farenksteki upstream direnç Bernoulli etkisi Dinamik komplians Gravity is thought to have an important influence on pharyngeal airway patency, and it is common for patients with obstructive sleep apnea to have a higher apnea-hypopnea index in the supine than in the nonsupine position. When the patient is supine, gravity can narrow the pharyngeal airway by pulling the tongue and soft palate in a posterior direction. Body position alters airway size and collapsibility. Airway size decreases following movements from sitting to supine as well as lateral decubitus to supine [43]. Changes are greater in OSA. Tissue mass, change in lung volume, tracheal tug, and vascular volume may contribute. Gravity affects the lower pharynx and retroepiglottic airway more than other segments during parabolic flight [43]. Gravity has minimal effect on the position and airway of the upper pharynx and upper tongue base in nonapneic individuals. Dil ve yumuşak damağı posterior yönünde çekerek, faringeal havayolunun daralmasına neden olur SVTH : SVTV = 1:1

Normal ÜSY’nun Statik ve Dinamik Özellikleri Hava akımı  nazal giriş ile nazofarenks arasındaki basınç düşmesinden kaynaklanır Diafram ve inspiratuar kasların kontrakte olmasına sekonder olarak nazofaringeal basınç düşer (Hava akımı için drive basınç) Burunda yüksek ve türbülan basınç (+) Nazal rezistansta artış  daha negatif faringeal intraluminal basınç oluşturarak faringeal kesit alanı daraltır (segmentin kompliansı önemli) Faringeal hava yolu üzerinde Etkili olan Mekanik Faktörler: Statik Faktörler Yüzey adeziv güçler Boyun ve çene postürü Trakeal tug Yer çekimi Dinamik Faktörler Nazal hava yolu ve farenkste akım direnci Bernoulli etkisi Dinamik komplians A model of the upper airway under dynamic conditions that has been advanced and effectively employed is derived from an analogy of the upper airway to a Starling resistor.15,16 In essence, Starling resistor is a term used to describe a highly collapsible tube having infinite compliance at one transmural pressure and low compliance at a higher or lower transmural pressure. The tube is completely closed at one luminal pressure and completely open at a higher luminal pressure. The luminal pressure at which the airway shifts from fully open to fully closed (i.e., the point of infinite compliance) is determined by the extramural pressure and is referred to as the critical pressure (Pcrit). Airflow is generated through the nose owing to a pressure drop between the nasal inlet and the nasopharynx. This driving pressure for airflow is generated by a reduction in nasopharyngeal pressure secondary to active contraction of the diaphragm and other inspiratory pump muscles.Body_ID: P082024The nose has a relatively high resistance and turbulent flow. The resistance is enhanced in situations where the nasal airway is narrowed by mucosal congestion. Accordingly, the increase in nasal resistance that occurs during inspiration is alinear relative to inspiratory airflow such that greater inspiratory airflow leads to disproportionately more negative nasopharyngeal intraluminal pressure.Body_ID: Nasopharyngeal pressure is, effectively, the equivalent of intraluminal pressure for the pharynx if the resistance within the pharynx is relatively low. All other factors being equal, increases in nasal resistance will produce a greater negative pharyngeal intraluminal pressure and reduced pharyngeal cross-sectional area. The extent to which the lumen narrows depends on regional airway compliance, that is, the relative compliance of each segment. As is the case with nasal resistance, a high resistance within the pharynx is associated with a decrease in intraluminal pressure at more caudal (more downstream) segments during inspiration. In other words, a narrowing at the retropalatal region is associated with a further decline in intraluminal pressure during inspiration at sites caudal to the retropalatal region, thereby increasing the tendency for closure in the retroglossal region and hypopharynx. Diğer bir deyişle retropalatal bölgede bir daralma intraluminal basınçta inspiriyum sırasında retropalatal bölgenin kaudalinde daha fazla basınç düşmesine yol açarak retroglossal bölge ve hipofarinksin kapanmaya eyiliminin artışına neden olur. SVTH : SVTV = 1:1

Normal ÜSY’nun Statik ve Dinamik Özellikleri Faringeal hava yolu üzerinde Etkili olan Mekanik Faktörler: Statik Faktörler Yüzey adeziv güçler Boyun ve çene postürü Trakeal tug Yer çekimi Dinamik Faktörler Nazal hava yolu ve farenkste akım direnci Bernoulli etkisi Dinamik komplians Nazal obstrüksiyon; NM Tonüsün devam ettirilmesi için gerekli afferent reflekslerin azalmasına Ağzın açık kalması ile alt faringeal hava yolu destabilizasyonuna Yüzey gerilim güçlerinin artmasında Yukarı hava yolu rezistans artışı ile alt hava yolunda kollapsa yol açar Nasal obstruction contributes to the presence and severity of OSA [37]. Nasal blockage may (1) reduce nasal afferent reflexes, which help to maintain muscular tone, (2) augment the tendency for mouth opening, which destabilizes the lower pharyngeal airway (by posterior rotation, vertical opening, and inferior displacement of the hyoid), (3) reduce humidification, increase mucus viscosity, and increase surface tension forces, and (4) increase upstream airway resistance, thus increasing downstream airway collapse [14, 38]. A multitude of pathologies cause nasal obstruction and warrant appropriate evaluation. SVTH : SVTV = 1:1

Normal ÜSY’nun Statik ve Dinamik Özellikleri Faringeal hava yolu üzerinde Mekanik Etkiler: Statik Faktörler Yüzey adeziv güçler Boyun ve çene postürü Trakeal tug Yer çekimi Dinamik Faktörler Nazal hava yolu ve farenksteki upstream direnç Bernoulli etkisi Dinamik komplians İntraluminal basınç azalması, Enerji kaybı ve Bernoulli etkisi ile Enerji  hava akımı direncini yenmek için harcanır Bernoulli etkisi  Lümen daraldığında hava akım hızındaki artıştan kaynaklanan enerjinin statikten kinetiğe döner ve hava yollarını kollabe eder Sonuçta, faringeal intraluminal basıncın inspirasyon sırasında azalmasına neden olur. Two physical phenomena cause a reduction in intraluminal pressure as gas flows through a tube: loss of energy and the Bernoulli effect. Energy is lost by work done in overcoming flow-resistance aspects of the airway; the Bernoulli effect is the conversion of energy from static to kinetic caused by an increase in the velocity of airflow when the lumen size decreases. The first phenomenon relates to upstream resistance to airflow. Whenever gas flows through a resistance, potential energy is dissipated in overcoming friction; consequently, intraluminal pressure decreases. The second phenomenon relates to acceleration of gas as it flows through a narrowed segment of a tube. Both phenomena contribute to decreasing pharyngeal intraluminal pressure during inspiration; therefore, both tend to narrow the pharynx during inspiration. To generate an inspiratory flow through the high-resistance air passage presented by the nose, pharyngeal pressure must fall below pressure at the nares. Nasal resistance contributes to the development of negative intraluminal pressure in the absence of inspiratory flow limitation. However, once inspiratory flow limitation is present, the relatively rigid nasal passage does not contribute to further pressure drop across the collapsible airway segment. By contrast, progressive narrowing of the pharyngeal upstream segment would produce progressively more negative intraluminal pressures caudal to the site of narrowing, regardless of inspiratory flow limitation, because of increased viscous energy losses in the narrowed region.Body_ID: P082029If the cross-sectional area of the pharyngeal lumen decreases in some regions, the velocity of airflow will be elevated in these regions. This increase in airflow velocity implies an increase in kinetic energy of the airstream and, hence, a decrease in lateral wall pressure. This reduction in lateral wall pressure allows further narrowing of the tube according to the tube law of the pharynx. Tüp boyunca gaz akımına bağlı olarak intraluminal basınç azalması iki mekanizmayla oluşur: Enerji kaybı ve Bernoulli etkisi. Enerji hava akımı sırasında hava yolu direncinin üstesinden gelinirken kaybolur. Bernoulli etkisi, lümen daraldığında artan hava akım hızının yarattığı enerjinin hava yollarını kollabe etmesidir. Bernoulli etkisi daralan tüpte artan hava akımı hızı ile ilişkilidir. Her iki mekanizma da inspirasyon sırasında faringeal intraluminal basıncı azaltır. Bu durum inspirasyonda farinksi daralmaya yöneltir. SVTH : SVTV = 1:1

Normal ÜSY’nun Statik ve Dinamik Özellikleri Faringeal hava yolu üzerinde Mekanik Etkiler: Statik Faktörler Yüzey adeziv güçler Boyun ve çene postürü Trakeal tug Yer çekimi Dinamik Faktörler Nazal hava yolu ve farenksteki upstream direnç Bernoulli etkisi Dinamik komplians İnspirasyon sırasında ÜSY’nun herhangi bir noktasında intraluminal basınçtaki azalma  ÜSY segmentinin dinamik kompliansı ile etkileşime girer During inspiration, the decrease in intraluminal pressure at any point in the upper airway interacts with the dynamic compliance of that segment of the upper airway.17 If intraluminal pressure at the beginning of inspiration is a value that lies on the steep portion of the pressure-area relationship, the upper airway narrows as intraluminal pressure decreases during inspiration. The degree to which pharyngeal cross-sectional area decreases depends on the dynamic compliance of the upper airway. This mechanical property also influences the likelihood of yet further airway collapse. Specifically, narrowing during inspiration due to a decrease in intraluminal pressure might decrease the area significantly, which in turn increases the velocity of gas flowing through that segment. The velocity increase causes further reductions in intraluminal pressure because of the conversion of static to kinetic energy with decreased lateral wall (or distending) pressure. Such a decline in luminal pressure tends to further decrease airway area. This sequence of events describes dynamic narrowing of the upper airway, which is typically observed under normal conditions if the pharyngeal muscles are relatively hypotonic. SVTH : SVTV = 1:1

Normal ÜSY’nun Statik ve Dinamik Özellikleri Faringeal hava yolu üzerinde Mekanik Etkiler: Statik Faktörler Yüzey adeziv güçler Boyun ve çene postürü Trakeal tug Yer çekimi Dinamik Faktörler Nazal hava yolu ve farenksteki upstream direnç Bernoulli etkisi Dinamik komplians İnspirasyon sırasında ÜSY’nun herhangi bir noktasında intraluminal basınçtaki azalma  ÜSY segmentinin dinamik kompliansı ile etkileşime girer During inspiration, the decrease in intraluminal pressure at any point in the upper airway interacts with the dynamic compliance of that segment of the upper airway.17 If intraluminal pressure at the beginning of inspiration is a value that lies on the steep portion of the pressure-area relationship, the upper airway narrows as intraluminal pressure decreases during inspiration. The degree to which pharyngeal cross-sectional area decreases depends on the dynamic compliance of the upper airway.Body_ID: P082031This mechanical property also influences the likelihood of yet further airway collapse. Specifically, narrowing during inspiration due to a decrease in intraluminal pressure might decrease the area significantly, which in turn increases the velocity of gas flowing through that segment. The velocity increase causes further reductions in intraluminal pressure because of the conversion of static to kinetic energy with decreased lateral wall (or distending) pressure. Such a decline in luminal pressure tends to further decrease airway area. This sequence of events describes dynamic narrowing of the upper airway, which is typically observed under normal conditions if the pharyngeal muscles are relatively hypotonic. Akım hızı arttıkça  İntralüminal basınçta daha fazla azalma olur (statik enerjinin, kinetik enerjiye konversiyonu nedeniyle) İntralüminal P (-)’leşir  ÜSY daralır  Akım hızı artar SVTH : SVTV = 1:1

Faringeal Kas Aktivasyonunu Modüle eden Faktörler: Activation of pharyngeal muscles can alter the mechanical characteristics of the upper airway. The effect of pharyngeal dilator muscle activation on the tube law of the pharynx is shown in Figure 82-7. Under active conditions, the pressure-area relationship is shifted upward and to the left. At any given transmural pressure, muscle activation increases area and stiffens the airway; that is, it decreases effective compliance. Figure 82-7 Airway area under passive conditions (i.e., no muscle activation) can be increased by a rise in transmural pressure (Ptm). Such a change occurs with the application of a positive intraluminal pressure, such as with nasal continuous positive airway pressure (CPAP). Contraction of pharyngeal dilators shifts the passive curve up and to the left. The muscle contraction increases Ptm, and (P2-P1) now represents Pmus (muscle pressure). Figure 82-8 Balance of forces that sustain upper airway patency. The two major forces are airway suction pressure and upper airway muscle tone that dilates and stiffens the airway. These in turn are influenced by other factors.The effect of muscle activation on the tube law is quantified by the term Pmus, the effective pressure exerted by muscle activation, which is equivalent to the change in transmural pressure required to yield the equivalent change in area on the passive curve (see Fig. 82-7). Under certain conditions, pharyngeal dilating muscles generally display inspiratory bursting activity together with tonic expiratory activity. Alcohol, sleep deprivation, anesthesia, and sedative-hypnotics suppress respiratory-related pharyngeal muscle activation.26 Additional factors that modulate respiratory-related activity of pharyngeal airway motor neurons include changes in state, proprioceptive feedback, and chemical drive (Fig. 82-8). SVTH : SVTV = 1:1

Faringeal Kas Aktivasyonunu Modüle eden Faktörler Uykuya Geçiş ile birlikte Supraglottik direnç artar (Normal) OUAS’lularda uyanıklıkta bile yüksek Bu gözlemler, Nöral durumdaki değişiklik ile birlikte ÜSY kalibrasyonunda reversible bir değişiklik olduğunu göstermektedir. Sonuç olarak, Uyanıklıktan  uykuya ve/veya REM’e geçiş ile birlikte Faringeal havayolundaki kaslara giden Nörol outputta değişiklik Perhaps the most convincing evidence demonstrating the overall importance of changes in state on the neuromuscular maintenance of airway patency is that obstructive sleep apnea is a sleep disorder. Modification of neuromuscular factors by sleep is a normal phenomenon; this fact can be inferred from measurements of supraglottic resistance in healthy persons-that is, resistance from the nares to the region above the glottis. With sleep onset, this resistance rises from the low values (e.g., 1 to 2 cm H2O/L/sec) to high values (e.g., 5 to 10 cm H2O/L/sec).27,28 Supraglottic airway resistance is abnormally high in patients with obstructive sleep apnea while they are awake, and the resistance rises significantly with sleep onset, reaching infinity with complete airway closure These observations in healthy persons, snorers, and patients with obstructive sleep apnea indicate that a reversible change in upper airway caliber occurs with a shift in neural state. Such behavior is explained by a change in neural output to upper airway muscles, which causes a decrease in Pmus at one or more sites within the pharyngeal airway. Electromyographic (EMG) recordings of pharyngeal muscles, such as the genioglossus and tensor palatini, confirm this decrease in pharyngeal muscle activity during the transition from wakefulness to sleep.28,30 An even more pronounced reduction in motor output to pharyngeal muscles occurs in rapid eye movement (REM) sleep, particularly in phasic REM.31,32 Although there is compelling evidence that sleep compromises the neural output to pharyngeal dilator muscles, the corresponding effects on inspiratory pump muscles are much less convincing. SVTH : SVTV = 1:1

Faringeal Kas Aktivasyonunu Modüle eden Faktörler Proprioceptif Stimulus Torasik ve ÜSY reseptörlerinden kalkan proprioceptif feedback’ler faringeal kaslara giden motor outputu modüle eder ÜSY obstrüksiyonu Süper,or laringeal Glossofarengeal trigeminal sinir Süperior laringeal sinir Proprioceptive StimuliBody 'proprioception' was awareness of movement derived from muscular, tendon, and articular sources. Such a system of classification has kept physiologists and anatomists searching for specialised nerve endings which transmit data on joint capsule and muscle tension (such as muscle spindles and Pacini corpuscles). Poprioceptive feedback from thoracic and upper airway receptors can modulate the motor output to pharyngeal muscles. During non-rapid eye movement (NREM) sleep and general anesthesia in animals, withdrawal of vagally mediated phasic volume feedback by tracheal occlusion during inspiration results in an immediate large augmentation in motor output to many upper airway and chest wall inspiratory pump muscles.33-35 Neurally mediated upper airway muscle activation also occurs with introduction of subatmospheric pressure into an isolated, sealed upper airway in spontaneously breathing tracheotomized animals.36,37 Because topical anesthesia of the upper airway inactivates the response, the upper airway receptors mediating this reflex activation are believed to be located superficially in the airway wall.37,38 The majority of upper airway respiratory-related afferents appear to be located in the upper trachea and larynx and are carried in the internal branch of the superior laryngeal nerve. Proprioceptive information from the upper airway is also transmitted in the glossopharyngeal and trigeminal nerves.37,39Body_ID: P082047page 989page 990Body_ID: P0990Both intrathoracic and upper airway proprioceptive information may also reduce motor output to the thoracic inspiratory muscles, thereby increasing intraluminal pressure below the site of airway obstruction.40 The reflex effects elicited in animals on upper airway and respiratory pump muscles could represent a powerful defense mechanism for the maintenance of upper airway patency during sleep. Presumably, neural reflex activation of pharyngeal muscles by upper airway and thoracic receptors are initiated by upper airway obstruction and tend to compensate for airway obstruction by dilating and stiffening the pharynx ÜSY ve torasik reseptörler (glossofaringeal ve trigeminal sinir ile taşınır) tarafından faringeal kasların nöral refleks aktivasyonu  ÜSY obstrüksiyonu tarafından başlatılır ve amaç farenksi dilate (motor output süperior laringeal sinir ile getirilir) etmektir. Farengeal kasların nöral aktivasyonu ÜSY + torasik reseptörlerce alınır Amaç: Faringeal kaslara dilatasyon sağlamak SVTH : SVTV = 1:1

Faringeal Kas Aktivasyonunu Modüle eden Faktörler Kimyasal Stimulus ÜSY ve frenik motor nöronların hipokapniye yanıtları arasındaki farklılıklar ile ilişkilidir. ÜSY motor nöronları Solunum kasları motor nöronları Kas aktivasyonu için gerekli C02 eşik değeri Daha yüksek Daha düşük Hiperventilasyonu takiben, fazik motor aktivite ÖNCE ÜSY motor aktivitesi kaybolur Daha sonra kaybolur C02’in yükselmesine tekrar izin verilirse Fazik motor aktivite daha sonra başlar Fazik motor aktivite ÖNCE başlar Solunum ile ilişkili Faringeal kas aktivitesi genellikle hiperkapnik ve hipoksik durumlarda görülür (Sakin solunumda Ø)Chemical StimuliBody_ID: HC082019Respiratory-related pharyngeal muscle activity, which can be absent during quiet breathing, usually appears under hypercapnic or hypoxic conditions.41,42 These EMG differences are only significant as they relate to their mechanical effects. These electromechanical relationships are largely unexplored, but it appears unlikely that changes in electrical output to upper airway or thoracic pump muscles have a direct, linear relationship to the resulting mechanical changes in the pharyngeal airway.Body_ID: P082049Upper airway and phrenic motor neurons also differ in their response to hypocapnia. Upper airway motor neurons appear to have a higher CO2 threshold for activation than respiratory pump muscles. With passive hyperventilation in a tracheotomized, vagotomized, anesthetized animal, phasic upper airway motor neuron activity disappears prior to phrenic activity. When the CO2 level is then allowed to rise, phasic activity first reappears in the phrenic nerve. Thus, cyclic changes in arterial CO2 around the CO2 threshold for activation of upper airway motor neuron activity could lead to an imbalance of forces acting on the pharyngeal airway and favor closure SVTH : SVTV = 1:1

Faringeal Kas Aktivasyonunu Modüle eden Faktörler Sonuçta, Arteriyel CO2 seviyesindeki siklik değişiklikler faringeal hava yolu üzerine olan güçler üzerinde dengesizliğe yol açarak hava yolu kapanmasına eğilimi arttırabilir. Kimyasal Stimulus ÜSY ve frenik motor nöronların hipokapniye yanıtları arasındaki farklılılar ile ilişkilidir. ÜSY motor nöronları Solunum kasları motor nöronları Kas aktivasyonu için gerekli C02 eşik değeri Daha yüksek Daha düşük Hiperventilasyonu takiben, fazik motor aktivite ÖNCE ÜSY motor aktivitesi kaybolur Daha sonra kaybolur C02’in yükselmesine tekrar izin verilirse Fazik motor aktivite daha sonra başlar Fazik motor aktivite ÖNCE başlar Solunum ile ilişkili Faringeal kas aktivitesi genellikle hiperkapnik ve hipoksik durumlarda görülür (Sakin solunumda Ø)Chemical StimuliBody_ID: HC082019Respiratory-related pharyngeal muscle activity, which can be absent during quiet breathing, usually appears under hypercapnic or hypoxic conditions.41,42 These EMG differences are only significant as they relate to their mechanical effects. These electromechanical relationships are largely unexplored, but it appears unlikely that changes in electrical output to upper airway or thoracic pump muscles have a direct, linear relationship to the resulting mechanical changes in the pharyngeal airway.Body_ID: P082049Upper airway and phrenic motor neurons also differ in their response to hypocapnia. Upper airway motor neurons appear to have a higher CO2 threshold for activation than respiratory pump muscles. With passive hyperventilation in a tracheotomized, vagotomized, anesthetized animal, phasic upper airway motor neuron activity disappears prior to phrenic activity. When the CO2 level is then allowed to rise, phasic activity first reappears in the phrenic nerve. Thus, cyclic changes in arterial CO2 around the CO2 threshold for activation of upper airway motor neuron activity could lead to an imbalance of forces acting on the pharyngeal airway and favor closure SVTH : SVTV = 1:1

[Dilatasyon aktivitesinin kaybı + (-) inspiratuar intralüminal basınç] OUAS’da Temel olarak; Uyku sırasında faringeal hava yolu kollapsı (+) Bu kollapsın nedeni ve mekanizması multifaktöriyel (ÜSY’nun yapısal sorunları + uykuda müsküler tonüs kaybı) *Aktif mekanizma Pasif mekanizma [Dilatasyon aktivitesinin kaybı + (-) inspiratuar intralüminal basınç] Historically, two basic schools of thought existed to describe the genesis of airway collapse—‘‘active’’ versus ‘‘passive’’ mechanisms. The active theory proposed by Weitzman and coworkers [1] in 1978 resulted from observations of spasmodic closure of the lateral pharyngeal walls and closure of the velopharynx timed at the end of expiration. This sphincteric closure ‘‘apparently by active muscle contraction’’ was maintained for the duration of inspiration and was followed by airway openings occurring following arousals. Since, in humans, electromyographic studies of pharyngeal constrictors fail to demonstrate collapse combined with expiratory muscle activity, the concept of active muscular contraction causing airway closure in OSA has been replaced in favor of other mechanisms [2]. As an alternative to the active theory, a theory based on passive mechanisms does not require active neuromuscular contraction of pharyngeal muscle to close the airway. Obstruction instead results from the interaction of loss of dilating activity of pharyngeal muscles, the mass of the tongue and other tissues, and negative inspiratory intraluminal pressures [3] SVTH : SVTV = 1:1 *Weitzman ED, 1978.

Sağlıklı bireyler ile Uyku Apneli hastalar arasında “Anatomik farklılıklar” Faringeal Obstrüksiyonun Yeri ve Paterni Obstrüksiyon;  Retropalatal alanda daha fazla  Sıklıkla birden fazla noktada Site and Patterns of Pharyngeal Obstruction The retropalatal region is the most common primary site of airway narrowing or closure during sleep in patients with obstructive sleep apnea, although upper airway narrowing can also occur in the retroglossal region.1,3,19,48,100-102 However, most patients with obstructive sleep apnea have more than one site of narrowing.101 The retropalatal region usually collapses in a sphincter-like fashion, which is characterized by movement of both the anterior and lateral walls rather than the more rigid posterior wall.103 Studies examining state-dependent changes in the upper airway also demonstrate that airway narrowing during sleep occurs in both the lateral and anterior-posterior dimensions (Fig. 82-14) Figure 82-14 Magnetic resonance image in the retropalatal region of a normal subject during wakefulness and sleep. Airway area is smaller during sleep in this normal subject. The state-dependent change in airway caliber is a result of decreases in the lateral and anterior-posterior airway dimensions. Thickening of the lateral pharyngeal walls is demonstrated during sleep. Uykuda lateral ve ön-arka çap azalıyor, lateral faringeal duvarlar kalınlaşıyor. SVTH : SVTV = 1:1

Sağlıklı bireyler ile Uyku Apneli hastalar arasında “Anatomik farklılıklar” Uyku Apneli hastalarda; ÜSY, sağlıklı bireylerdekinden daha küçük Hava yolu darlığı en sık retropalatal bölgede Apneik ÜSY boyutundaki azalma; Çevreleyen yd’da genişleme Kranio fasial yapıların Boyutlarında küçülme ya da Yapılarda değişikliğe sekonder Most studies have shown that the upper airway is smaller in patients with sleep apnea compared with normal subjects.1,43-48 The airway narrowing found in these studies is primarily in the retropalatal region.43,49,50 Figure 29.1 Differences in upper airway length between infants (left), nonapneic adults (middle), and OSA adults (right) are shown. In infants, the tongue compromises a shorter segment of the pharyngeal airway and the larynx may reside at the level of the second cervical vertebra. In nonapneic adults, the larynx may reside at the fourth cervical vertebra and both airway length and tongue area are greater in obstructive sleep apnea. SVTH : SVTV = 1:1

Sağlıklı bireyler ile Uyku Apneli hastalar arasında “Anatomik farklılıklar” Uyku Apneli hastalarda; ÜSY, sağlıklı bireylerdekinden daha küçük Hava yolu darlığı en sık retropalatal bölgede Apneik ÜSY boyutundaki azalma; Çevreleyen yd’da genişleme Kranio fasial yapıların Boyutlarında küçülme ya da Yapılarda değişikliğe sekonder gelişebilir Why is the upper airway smaller in patients with sleep apnea? The reduction in the size of the apneic upper airway compared with the normal airway must be secondary to enlargement of the surrounding soft tissues and to reductions in or changes to the craniofacial structures.46,47 Studies using cephalometrics have demonstrated reductions in mandibular body length (retrognathia), inferiorly positioned hyoid bone, and retroposition of the maxilla in patients with sleep apnea compared with normal subjects.51-54 Reduction in mandibular body length, in particular, has been shown to be an important risk factor for obstructive sleep apnea.55 In addition to craniofacial differences, enlargement of the upper airway soft tissue structures (tongue, lateral pharyngeal walls, soft palate, parapharyngeal fat pads) has also been demonstrated in patients with sleep apnea compared with normal subjects.46,47 SVTH : SVTV = 1:1

Sağlıklı bireyler ile Uyku Apneli hastalar arasında “Anatomik farklılıklar”  Retrognati*  Hyoidin aşağı yerleşimi Maksillanın retropozisyonu ÜSY’da genişlemiş yumuşak dokular Dil/ Lateral faringeal duvar/YD/ Parafaringeal yağ Uyku Apneli hastalarda; ÜSY, sağlıklı bireylerdekinden daha küçük Hava yolu darlığı en sık retropalatal bölgede Apneik ÜSY boyutundaki azalma; Çevreleyen yd’da genişleme Kranio fasial yapıların Boyutlarında küçülme ya da Yapılarda değişikliğe sekonder gelişebilir Why is the upper airway smaller in patients with sleep apnea? The reduction in the size of the apneic upper airway compared with the normal airway must be secondary to enlargement of the surrounding soft tissues and to reductions in or changes to the craniofacial structures.46,47 Studies using cephalometrics have demonstrated reductions in mandibular body length (retrognathia), inferiorly positioned hyoid bone, and retroposition of the maxilla in patients with sleep apnea compared with normal subjects.51-54 Reduction in mandibular body length, in particular, has been shown to be an important risk factor for obstructive sleep apnea.55 In addition to craniofacial differences, enlargement of the upper airway soft tissue structures (tongue, lateral pharyngeal walls, soft palate, parapharyngeal fat pads) has also been demonstrated in patients with sleep apnea compared with normal subjects.46,47 SVTH : SVTV = 1:1

Sağlıklı bireyler ile Uyku Apneli hastalar arasında “Anatomik farklılıklar” Studies using cephalometrics have demonstrated reductions in mandibular body length (retrognathia), inferiorly positioned hyoid bone, and retroposition of the maxilla in patients with sleep apnea compared with normal subjects.51-54 Reduction in mandibular body length, in particular, has been shown to be an important risk factor for obstructive sleep apnea.55 In addition to craniofacial differences, enlargement of the upper airway soft tissue structures (tongue, lateral pharyngeal walls, soft palate, parapharyngeal fat pads) has also been demonstrated in patients with sleep apnea compared with normal subjects.46,47 Midsagittal magnetic resonance (MR) image of a normal subject (left) and a patient with sleep apnea (right). The upper airway is smaller and the soft palate is longer in the patient with sleep apnea. The amount of subcutaneous fat (white area at the back of the neck) is greater in the apneic than in the normal subject. Midsagittal magnetic resonance (MR) image of a normal subject (left) and a patient with sleep apnea (right). The upper airway is smaller and the soft palate is longer in the patient with sleep apnea. The amount of subcutaneous fat (white area at the back of the neck) is greater in the apneic than in the normal subject. B, Axial MR image in the retropalatal region of a normal subject (left) and a patient with sleep apnea (right). The upper airway is smaller (primarily narrowed in the lateral dimension) in the patient with sleep apnea. SVTH : SVTV = 1:1

Schwab RJ, et al. Am J Respir Crit Care Med 2003 Sağlıklı bireyler ile Uyku Apneli hastalar arasında “Anatomik farklılıklar” Figure 82-10 Volumetric reconstruction of axial magnetic resonance (MR) images in a normal subject and a patient with sleep apnea. The mandible is depicted in white, the tongue in light blue, the soft palate in dark blue, the lateral parapharyngeal fat pads in medium blue, and the lateral/posterior pharyngeal walls in gray. Both subjects had an elevated body mass index (32.5 kg/m2). The normal subject has a larger airway than the patient with sleep apnea. The tongue, soft palate, and lateral pharyngeal walls of the patient with sleep apnea are all larger than in the normal subject. Recently, a case-control study demonstrated that the volume of the upper airway soft tissue structures (tongue, lateral pharyngeal walls, soft palate, parapharyngeal fat pads; Fig. 82-10) was significantly greater in apneic patients than normal ones.46 The volume of the lateral pharyngeal walls, tongue, and total soft tissue surrounding the upper airway remained significantly larger in apneic patients than in normal persons after covariate adjustments for sex, age, ethnicity, craniofacial size, and fat surrounding the upper airway. Moreover, this study demonstrated that increased volume of the lateral pharyngeal walls, tongue, and total upper airway soft tissue significantly increased the risk for sleep apnea even after the covariate adjustments.46 SVTH : SVTV = 1:1 Schwab RJ, et al. Am J Respir Crit Care Med 2003

ÜSY Y.Dokularının Genişleme Nedenleri Ödem Obezite ve Kilo artışı Kas hasarı Cinsiyet Genetik Faktörler Why are the upper airway soft tissue structures enlarged in patients with sleep apnea? Although there is not a specific answer to this question, there are several possible mechanisms explaining the etiology of the enlargement of the upper airway soft tissue structures in apneic persons, including edema secondary to negative pressure from airway closure or trauma, weight gain, muscle injury, gender, and genetic factors. SVTH : SVTV = 1:1

ÜSY Y.Dokularının Genişleme Nedenleri Ödem Obezite ve Kilo artışı Kas hasarı Cinsiyet Genetik Faktörler Negative pressure during airway closure or trauma from repeated apneic events may cause edema in the soft tissue structures surrounding the upper airway. This edema could increase the size of these soft tissue structures. The soft palate is especially at risk for the development of edema because it can be tugged caudally and traumatized during apneas. CPAP is thought to reduce upper airway edema.56 Quantitative MR mapping has indicated that there is more edema or fat, or both, in the genioglossus muscles of apneic persons than in normal ones.59,60 Histologic studies have also shown that patients with sleep apnea have increased edema in the uvula compared with normal persons.61Body_ID: P082058  Hava yolu kapanması sırasında (-) basınç ya da  Tekrarlayan apnelere sek. travma Özellikle YD, uvula risk altında SVTH : SVTV = 1:1

ÜSY Y.Dokularının Genişleme Nedenleri Ödem Obezite ve Kilo artışı Kas hasarı Cinsiyet Genetik Faktörler  Faringeal hava yolu boyutu daha küçük  Hava yolu kollapsibilitesi daha fazla BÇ, yağ dağılımı açısından BMİ’den daha iyi bir gösterge Obez + uyku apneli hastalarda, Lateral parafaringeal yağ yastıklarında Dil ve YD’da Kilo artışı yağ+kas doku artışı Obesity is known to be an important risk factor for obstructive sleep apnea.62,63 Although the relationship between obesity and sleep apnea is not well understood, it appears that obesity decreases pharyngeal airway size and increases airway collapsibility. Increased neck size, a better surrogate of upper airway fat distribution than body mass index (BMI), has been demonstrated to be an excellent predictor of sleep apnea.63,64 It is thought that the increased neck size in obese patients with obstructive sleep apnea is related to fat deposition in the neck Upper airway imaging studies have demonstrated increased adipose tissue surrounding the airway (primarily enlargement of the lateral parapharyngeal fat pads-see Figs. 82-2, 82-9B, and 82-10) in obese patients with sleep apnea.1,43,65-68 These studies suggest that obesity increases fat deposition in the lateral pharyngeal fat pads, which, in turn, has been hypothesized to compress the lateral walls and reduce upper airway size.1,43,65-68 Fat deposition within the tongue or soft palate may also be important in increasing the size of the soft tissue structures and reducing the caliber of the upper airway. Fat has been shown to be deposited in the uvula of patients with sleep apnea, which supports the hypothesis that fat deposited outside of the parapharyngeal fat pads may be important in the pathogenesis of sleep apnea.69,70Body_ID: P082060It has also been argued that the total amount of fat surrounding the upper airway may be a more important contributor to sleep apnea than fat localized in a particular anatomic site. Shelton and coworkers67 have hypothesized that fat deposition in the space bounded by the mandibular rami increases tissue pressure, which in turn would lead to airway narrowing.Body_ID: P082061In addition to direct deposition of fat, weight gain may also alter the muscle tissue surrounding the upper airway. Weight gain not only increases adipose tissue but also has been shown to increase muscle mass.71,72 Approximately 25% of the increased weight in obese patients is secondary to fat-free tissue72,73; it has been shown that patients with sleep apnea have a larger percentage of muscle in the uvula than normal subjects do.69,74 These data suggest that weight gain may predispose to obstructive sleep apnea by increasing the size of the muscular soft tissue structures (tongue, soft palate, lateral pharyngeal walls) surrounding the upper airway in addition to the direct deposition of fat in the parapharyngeal fat pads. This hypothesis is supported by data in obese nonapneic women that show that weight loss decreases the volume of the lateral pharyngeal walls and parapharyngeal fat pads (Fig. 82-11A,B).75Body_ID: P082062Other explanations for the relationship between obesity and sleep apnea include changes in upper airway compliance and alterations in the biomechanical relationships of the upper airway muscles.76 Thus, although obesity has been shown to be an important risk factor for sleep apnea, the specific effect of weight gain on the upper airway soft tissue structures is not entirely understood. SVTH : SVTV = 1:1

ÜSY Y.Dokularının Genişleme Nedenleri Ödem Obezite ve Kilo artışı Kas hasarı Cinsiyet Genetik Faktörler  Faringeal hava yolu boyutu daha küçük  Hava yolu kollapsibilitesi daha fazla BÇ, yağ dağılımı açısından BMİ’den daha iyi bir gösterge Obez + uyku apneli hastalarda, Lateral parafaringeal yağ yastıklarında Dil ve YD’da Kilo artışı yağ+kas doku artışı Obesity is known to be an important risk factor for obstructive sleep apnea.62,63 Although the relationship between obesity and sleep apnea is not well understood, it appears that obesity decreases pharyngeal airway size and increases airway collapsibility. Increased neck size, a better surrogate of upper airway fat distribution than body mass index (BMI), has been demonstrated to be an excellent predictor of sleep apnea.63,64 It is thought that the increased neck size in obese patients with obstructive sleep apnea is related to fat deposition in the neck Upper airway imaging studies have demonstrated increased adipose tissue surrounding the airway (primarily enlargement of the lateral parapharyngeal fat pads-see Figs. 82-2, 82-9B, and 82-10) in obese patients with sleep apnea.1,43,65-68 These studies suggest that obesity increases fat deposition in the lateral pharyngeal fat pads, which, in turn, has been hypothesized to compress the lateral walls and reduce upper airway size.1,43,65-68 Fat deposition within the tongue or soft palate may also be important in increasing the size of the soft tissue structures and reducing the caliber of the upper airway. Fat has been shown to be deposited in the uvula of patients with sleep apnea, which supports the hypothesis that fat deposited outside of the parapharyngeal fat pads may be important in the pathogenesis of sleep apnea.69,70Body_ID: P082060It has also been argued that the total amount of fat surrounding the upper airway may be a more important contributor to sleep apnea than fat localized in a particular anatomic site. Shelton and coworkers67 have hypothesized that fat deposition in the space bounded by the mandibular rami increases tissue pressure, which in turn would lead to airway narrowing.Body_ID: P082061In addition to direct deposition of fat, weight gain may also alter the muscle tissue surrounding the upper airway. Weight gain not only increases adipose tissue but also has been shown to increase muscle mass.71,72 Approximately 25% of the increased weight in obese patients is secondary to fat-free tissue72,73; it has been shown that patients with sleep apnea have a larger percentage of muscle in the uvula than normal subjects do.69,74 These data suggest that weight gain may predispose to obstructive sleep apnea by increasing the size of the muscular soft tissue structures (tongue, soft palate, lateral pharyngeal walls) surrounding the upper airway in addition to the direct deposition of fat in the parapharyngeal fat pads. This hypothesis is supported by data in obese nonapneic women that show that weight loss decreases the volume of the lateral pharyngeal walls and parapharyngeal fat pads (Fig. 82-11A,B).75Body_ID: P082062Other explanations for the relationship between obesity and sleep apnea include changes in upper airway compliance and alterations in the biomechanical relationships of the upper airway muscles.76 Thus, although obesity has been shown to be an important risk factor for sleep apnea, the specific effect of weight gain on the upper airway soft tissue structures is not entirely understood. SVTH : SVTV = 1:1

ÜSY Y.Dokularının Genişleme Nedenleri Ödem Obezite ve Kilo artışı Kas hasarı Cinsiyet Genetik Faktörler The remodeling of the upper airway muscles in patients with sleep apnea may be a primary or secondary phenomenon; in other words, it might be a consequence rather than the cause of apneas. Carrera and coworkers78 studied the structure and function of the genioglossus in apneic subjects and nonapneic subjects and demonstrated that the myopathy is a secondary phenomenon (Tekrarlayan Denervasyon/ İnnervasyon hasarı ile) . These investigators found increased type II fibers in the genioglossus muscle of apneic subjects; however, the changes in the genioglossus muscle were reversed with CPAP. ÜSY kaslarındaki “Remodelling” nedenden çok bir sonuç gibi Apneik hastalarda genioglossus kasında,  Tip II liflerde progresif artış (hipertrofi)  CPAP ile düzelme SVTH : SVTV = 1:1

ÜSY Y.Dokularının Genişleme Nedenleri Ödem Obezite ve Kilo artışı Kas hasarı Cinsiyet Genetik Faktörler Erkek Kadın ÜSY boyutu Daha büyük Daha küçük Boyun çevresi Daha geniş Daha dar Yağ dağılımı Gövdenin üst kısmı + Karın Gövdenin alt kısmı + ekstremiteler Dil/YD/ Lateral faringeal duvar Parafaringeal yağ yastıkçıkları* Fark yok Gender may also have an important effect on the size of the upper airway soft tissue structures. Several studies have demonstrated that upper airway size is smaller in women than in men.80,81 In addition, studies have shown that neck size is smaller in women than in men82 so the size of the upper airway soft tissue structures (tongue, soft palate, lateral pharyngeal walls, lateral parapharyngeal fat pads) are hypothetically also smaller in women than men. Moreover, fat distribution is different in women than in men.83,84 In men, fat is deposited primarily in the upper body and trunk, whereas in women it is deposited primarily in the lower body and extremities.83,84 These gender-related differences in overall fat distribution suggest that the size of the lateral parapharyngeal fat pads may be greater in men than in women.Body_ID: P082066Two studies have used MR imaging to examine gender-related differences in upper airway soft tissue structures in normal subjects.85,86 Both studies showed that the tongue size, soft palate size, and total soft tissue were greater in normal men than in women.85,86 Whittle and colleagues85 demonstrated that the total volume of soft tissues and the size of both the tongue and soft palate were larger in men than in women. Malhotra and coworkers86 demonstrated that airway length, soft palate size, and tongue size were greater in men than women. Surprisingly, neither study found significant differences in the size of the lateral pharyngeal fat pads in the normal men and women.85,86 These data suggest that gender may not have a significant effect on the amount of visceral (parapharygneal fat pads) neck fat but may have an important effect on the size of the other upper airway soft tissue structures. SVTH : SVTV = 1:1

ÜSY Y.Dokularının Genişleme Nedenleri Ödem Obezite ve Kilo artışı Kas hasarı Cinsiyet Genetik Faktörler Genetic FactorsBody_ID: HC082026Although some researchers hypothesize that genetic factors play an important role in determining the size of the upper airway soft tissue structures, few data support this hypothesis. Family aggregation of craniofacial anatomy (reduction in posterior airway space, increase in mandible-to-hyoid distance, inferior hyoid placement) has been shown in patients with sleep apnea.82,87 The data from these studies suggest that elements of craniofacial structure are likely inherited in apneic patients, but studies examining the heritability of the upper airway soft tissue structures (tongue, soft palate, lateral pharyngeal walls, lateral parapharyngeal fat pads) have not yet been performed. Macroglossia has been shown to be a risk factor for sleep apnea in patients with trisomy 21,88 but otherwise the effect of genetic factors on the size of upper airway soft tissue structures has not been well studied. Nonetheless it seems plausible that the size of the tongue, soft palate, and lateral pharyngeal walls is at least partially genetically mediated.  Kraniofasial anatominin ailesel agregasyonu  Makroglossi (Trizomi 21)  Dil/ YD/ Lateral faringeal duvar boyutunun kısmen genetik yatkınlık olasılığı (+) SVTH : SVTV = 1:1

ÜSY Yapılarında Dinamik Fizyolojik Değişiklikler ÜSY ile ilgili statik çalışmalar ile uyku apne için “anatomik risk faktörleri” tanımlanmış ÜSY’nun Dinamik davranışı da önemli Although we have gained important insights into the anatomic risk factors for sleep apnea with static studies of the upper airway, examination of the dynamic behavior of the upper airway is also necessary to completely understand the pathogenesis of sleep-disordered breathing. CT, MR imaging, and nasopharyngoscopy have been used to examine dynamic changes in upper airway caliber and the surrounding soft tissue structures during the respiratory cycle.48,89-93 Dinamik çalışmalar ile Normal ve uyku apnelilerde solunumun 4 farklı evresinde üst solunum yolu gösterilmiştir. Electron beam CT has been used to demonstrate that upper airway size changes during four distinct phases of the respiratory cycle in normal subjects and patients with sleep apnea (Fig. 82-12).45,49 In early inspiration (phase 1, see Fig. 82-12) there is a small increase in upper airway size, but during most of inspiration (phase 2, see Fig. 82-12) upper airway caliber remains relatively constant. The finding that upper airway caliber is relatively constant in inspiration during wakefulness suggests a balance between the action of the upper airway dilator muscles to increase airway size and negative intraluminal pressure to decrease airway size. In early expiration, upper airway caliber increases (phase 3, see Fig. 82-12) secondary to positive intraluminal pressure (the upper airway dilator muscles are not active during expiration). Upper airway caliber was largest in early expiration.45,49 At the end of expiration (phase 4, see Fig. 82-12) there is a large reduction in upper airway caliber. Diagram of the changes in upper airway area as a function of tidal volume during the respiratory cycle. Airway caliber is relatively constant in inspiration (phases 1 and 2), whereas airway size increases in early expiration (phase 3) and decreases in late expiration (phase 4). Researchers have hypothesized that the end of expiration is a vulnerable time for upper airway narrowing or collapse because the upper airway is no longer kept open by the phasic action of the upper airway dilator muscles (phases 1 and 2, during inspiration) or positive intraluminal pressure (phase 3, early expiration).45,49 In these investigations, upper airway caliber was smallest at the end of expiration.45,49 This finding may have important implications with regard to the timing of sleep-induced upper airway closure. Apneic events during sleep are thought to occur during inspiration secondary to negative intraluminal pressure generated by contraction of the chest wall.94 However, studies examining airway resistance have demonstrated that airway closure in patients with sleep apnea can occur during both expiration and inspiration.95,96 Studies using nasopharygoscopy have also shown that airway closure during sleep occurs during expiration and that subatmospheric intraluminal pressure was not required for pharyngeal closure.43,97 These data indicate that the upper airway is vulnerable to collapse at the end of expiration in addition to collapse during inspiration. Collapse and increased resistance occur during both inspiration and expiration in OSA. Expiratory collapse is a more static process. Dividing various forces into static forces include structure (craniofacial and soft tissue), tonic muscle tone, and passive changes in airway luminal pressures. Apneler;  End-ekspiratuar (dilatör kas aktivitesi ve (+) intraluminal basınç Ø  İnspirasyon sırasında (-) intraluminal basınç var SVTH : SVTV = 1:1

OUAS’lu hastalarda Sonuç olarak, hava yolu obstrüksiyonunun patogenezinde; ÜSY’nun anormal anatomisi ÜSY’nun dilatör kaslarının yetersiz refleks aktivasyonu ÜSY’nun artmış kollapsibilitesi rol oynar ve Hastalarda Daha küçük ve kollabe olma eğiliminde bir hava yolu (+) Kollaps riski temel olarak, doku basıncının intralüminal basınçtan daha fazla olduğu ekspirasyon sonunda When all data are taken into account, it is quite clear that OSAHS patients have a smaller and more collapsible airway. The airway is most at risk for complete collapse at the end of an expiration, where the tissue pressure may be larger than the intraluminal pressure. SVTH : SVTV = 1:1

SVTH : SVTV = 1:1

Anatomik ve nörolojik faktörlerin ilişkisi: Normal kişide uykuda faringeal lumende daralma olmaktadır; Uykuda, ÜSY kas aktivitesinde azalma ve İnspirasyondaki intraluminal subatmosferik negatif basınç en temel nedenidir. Sonuçta, uyanıklığa göre  uykuda ÜSY’da daralma olmaktadır, ancak bu şiddetli değildir. OUAS’lu hastada ise uykuda ciddi ve tıkayıcı bir daralma oluşmaktadır. Ve, Uykuda meydana gelen ÜSY aktivite kaybı, altta yatan anatomik bozulma nedeni ile oluşan ÜSY daralmasını daha ciddi hale getirmektedir.

Anatomik ve Nöral Hipotez Uyku, faringeal kas aktivitesini (normal insanlarda ve uyku apnelilerde) azaltır. OUAS’nun patogenezinde dilatör kas motor fonksiyon azalması mı yoksa farinksi daraltan anatomik yapı mı olduğu önemli sorudur. Uyku ilişkili faringeal nöral aktivitedeki azalma OUAS’lu hastalarda normalden fazla mıdır?

Anatomik Hipotez Anatomik hipotezi destekleyen veriler: Obez ve kraniofasiyal anormallikleri olanlarda dilde, lateral faringeal duvarlarda, tonsillerde ve total yumuşak dokuda genişleme ile OUAS’nun ilişkisi gözlemlenmiştir. Uyku apneleri; Kilo verme, Tonsillektomi ve kraniofasiyal anormalliklerin onarılması ile düzeltilebiliyor olması, bu anormalliklerin hastalığın başlaması ile ilişkili olduğunu desteklemektedir.

Nöral Hipotez  Uyku ilişkili nöromusküler anormallik OUAS’na yol açıyor mu?  Günümüzde OUAS’lu hastalarda patogenezde primer bir nöral anormalliğin olduğuna dair kanıt Ø  Ancak, Anatomik faktörler uykuya geçişte aniden değişemezken, faringeal havayolunu dilate eden nöromusküler etkiler uykunun başlamasıyla baskılanmaktadır.  Bulgular sinir sisteminin obstruktif uyku apnenin patogenezine sekonder olarak katıldığını göstermektedir.  OUAS ile birlikte görülen uyku fragmantasyonu faringeal kaslardaki motor out-put da azalmaya yol açarak hastalığı arttırmaktadır.

Uyku apneli Hastalarda ÜSY kalibrasyonunu arttıran Tedavi yöntemleri ve mekanizmaları  Zayıflama  CPAP  Ağız içi araçlar  Cerrahi uygulamalar  ÜSY boyutuna  Çevredeki yumuşak dokuya  Kraniofasial yapıya yönelik on the effect of weight loss, CPAP, oral appliances, and surgery on upper airway size and the surrounding soft tissue and craniofacial structure. SVTH : SVTV = 1:1

Uyku apneli Hastalarda ÜSY kalibrasyonunu arttıran Tedavi yöntemleri ve mekanizmaları  Zayıflama  CPAP  Ağız içi araçlar  Cerrahi uygulamalar  ÜSY boyutuna  Çevredeki yumuşak dokuya  Kraniofasial yapıya yönelik on the effect of weight loss, CPAP, oral appliances, and surgery on upper airway size and the surrounding soft tissue and craniofacial structure. %5-10’luk bir kayıp OUAS tedavisinde başarılı Havayolu kollapsibilesini azaltıyor Tam olarak OUAS ciddiyetini ve Üsy kalibrasyonunu ve konfigürasyonunu nasıl değiştiriyor (?) Zayılama parafaringeal yağ yastıkçıklarında azalma SVTH : SVTV = 1:1

Uyku apneli Hastalarda ÜSY kalibrasyonunu arttıran Tedavi yöntemleri ve mekanizmaları  Zayıflama  CPAP  Ağız içi araçlar  Cerrahi uygulamalar  ÜSY boyutuna  Çevredeki yumuşak dokuya  Kraniofasial yapıya yönelik CPAP üst hava yolu kas aktivitesini suprese etmesine rağmen farinks girişinden itibaren pozitif transmural basınç uygulayarak hava yolunu genişletir.  CT ve MR çalışmaları CPAP ile hava yolu dilatasyonunun anterior-posterior mesafeden ziyade lateral mesafede olduğunu göstermiştir.  CPAP basıncının progressif olarak arttırılması(>15 cm H2O) hava yolu çapını yalnızca lateral yönde arttırmakla kalmaz hava yolu volümünü (üç kat) ve retropalatal ve retroglossal bölgeleri de önemli ölçüde arttırır. Figure 82-15 A, Volumetric reconstruction of the upper airway with progressively greater continuous positive airway pressure (CPAP) (0 to 15 cm H2O) settings in a normal subject. There are significant increases in upper airway volume in the retropalatal and retroglossal regions with higher levels of CPAP. B, Axial magnetic resonance image in a normal subject at two levels of CPAP (0 and 15 cm H2O) in the retropalatal region. Airway area is significantly greater at 15 cm H2O. The airway enlargement is predominantly in the lateral dimension. Airway enlargement with CPAP results in thinning of the lateral pharyngeal walls, although the parapharyngeal fat pads are not displaced SVTH : SVTV = 1:1

Uyku apneli Hastalarda ÜSY kalibrasyonunu arttıran Tedavi yöntemleri ve mekanizmaları  Zayıflama  CPAP  Ağız içi araçlar  Cerrahi uygulamalar  ÜSY boyutuna  Çevredeki yumuşak dokuya  Kraniofasial yapıya yönelik  Oral mandibular ilerletme aygıtlarının, posterior hava yolu boşluğunu özellikle de retroglossal bölgeyi dili öne çekerek genişlettiği gösterilmiştir.  Ancak son çalışmalar mandibular ilerletme apereylerin retropalatal bölgeyi de retroglossal bölge gibi genişlettiğini göstermiştir. (öncelikle lateral yönde)  Bu da oral apereylerin etki mekanizmalarının basitçe dil ve yumuşak damağı öne çekmekten daha komplike olduğunu düşündürmektedir. on the effect of weight loss, CPAP, oral appliances, and surgery on upper airway size and the surrounding soft tissue and craniofacial structure. SVTH : SVTV = 1:1

Uyku apneli Hastalarda ÜSY kalibrasyonunu arttıran Tedavi yöntemleri ve mekanizmaları  Zayıflama  CPAP  Ağız içi araçlar  Cerrahi uygulamalar  ÜSY boyutuna  Çevredeki yumuşak dokuya  Kraniofasial yapıya yönelik  UPPP en çok uygulanan prosedürdür.  UPPP de tonsiller, uvula, yumuşak damağın distal kenarı, faringeal aşırı dokular kaldırılmaktadır. UPPP’nin başarı oranları tıkanan hava yolu bölümünün yerine bağlıdır. Retropalatal bölgede daha başarılı  MR çalışmalarında UPPP de alınan yumuşak dokuların olduğu yerlerde genişleme olmakta ancak cerrahi uygulanmayan bölümlerde hava lümeni küçük kalmaktadır. Uvulopalatopharyngoplasty (UPPP) uyku apneli hastalarda en çok uygulanan prosedürdür. UPPP de tonsiller, uvula, yumuşak damağın distal kenarı, faringeal aşırı dokular kaldırılmaktadır. UPPP nin başarı oranları tıkanan hava yolu bölümünün yerine bağlıdır. Retropalatal bölgede tıkanıklığı olan hastalar retroglossal bölgede tıkanma yaşayanlara oranla UPPP den daha fazla fayda sağlarlar. Maalesef bu hastalarda başarı oranı %50 dir ve kabul edilemeyecek düşüklüktedir. MR çalışmalarında UPPP de alınan yumuşak dokuların olduğu yerlerde genişleme olmakta ancak cerrahi uygulanmayan bölümlerde hava lümeni küçük kalmaktadır. Bu da UPPP nin uyku apneli hastalarda neden çok başarılı olamadığını açıklamaktadır. SVTH : SVTV = 1:1

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