Each nasal fossa is convoluted and provides approximately 60 cm² surface area per side for warming and humidifying the inspired air.² The nose is also able to prewarm inspired air to a temperature of 32° C to 34° C, over a wide range of ambient temperatures from 8° C to 40° C.³ The nasal fossa is bounded laterally by inferior, middle, and superior turbinate bones (conchae),⁴ which divide the fossa into scroll-like spaces called the inferior, middle, and superior meatuses (see Fig. 1-1).^2,^5,⁶ The inferior turbinate usually limits the size of the nasotracheal tube that can be passed through the nose, and damage to the lateral wall may occur as a result of vigorous attempts during nasotracheal intubation. The arterial supply to the nasal cavity is mainly from the ethmoid branches of the ophthalmic artery, the sphenopalatine and greater palatine branches of the maxillary artery, and the superior labial and lateral nasal branches of the facial artery. Kiesselbach’s plexus, where these vessels anastomose, is situated in Little’s area on the anterior-inferior portion of the nasal septum. This is a common source of clinically significant epistaxis. The turbinates have a rich vascular supply that affords the nasal airway the ability to expand or contract according to the degree of vascular engorgement. The vascular mucous membrane overlying the turbinates can be damaged easily, leading to profuse hemorrhage. The paired paranasal sinuses—sphenoid, ethmoid, maxillary, and frontal—drain through apertures into the lateral wall of the nose. Prolonged nasotracheal intubation may lead to infection of the maxillary sinus due to obstruction of the ostia.⁷

The olfactory area is located in the upper third of the nasal fossa and consists of the middle and upper septum and the superior turbinate bone. The respiratory portion is located in the lower third of the nasal fossa.⁶ The respiratory mucous membrane consists of ciliated columnar cells containing goblet cells and nonciliated columnar cells with microvilli and basal cells. The olfactory cells have specialized hairlike processes, called the olfactory hair, which are innervated by the olfactory nerve.⁶

The nonolfactory sensory nerve supply to the nasal mucosa is derived from the first two divisions of the trigeminal nerve, the anterior ethmoidal and maxillary nerves. Airborne chemical irritants cause firing of the trigeminal nerves, which presumably are responsible for reflexes such as sneezing and apnea.⁸ The afferent pathway for the sneezing reflex originates at the histamine-activated type C neurons of the trigeminal nerve, and the efferent pathway consists of several somatic motor nerves. The act of sneezing is associated with an increased intrathoracic air pressure of up to 100 mm Hg and may produce airflow up to 100 mph.⁸

The parasympathetic autonomic nerves reach the mucosa from the facial nerve after relay through the sphenopalatine ganglion, and sympathetic fibers are derived from the plexus surrounding the internal carotid artery through the vidian nerve.⁹ Approximately 10,000 L of ambient air passes through the nasal airway per day, and 1 L of moisture is added to this air in the process.¹⁰ The moisture is derived partly from transudation of fluid through the mucosal epithelium and partly from secretions produced by glands and goblet cells. These secretions have significant bactericidal properties. Foreign body invasion is further minimized by the stiff hairs (vibrissae), the ciliated epithelium, and the extensive lymphatic drainage of the area.

A series of complex autonomic reflexes controls the blood supply to the nasal mucosa and allows it to shrink and swell quickly. Reflex arcs also connect this area with other parts of the body. For example, the Kratschmer reflex leads to bronchiolar constriction on stimulation of the anterior nasal septum in animals. A demonstration of this reflex may be seen in the postoperative period as a patient becomes agitated when the nasal passage is packed.⁹

B Pharynx

The pharynx, 12 to 15 cm long, extends from the base of the skull to the level of the cricoid cartilage anteriorly and the inferior border of the sixth cervical vertebra posteriorly.¹¹ It is widest at the level of the hyoid bone (5 cm) and narrowest at the level of the esophagus (1.5 cm), which is the most common site for obstruction after foreign body aspiration. It is further subdivided into the nasopharynx, oropharynx, and laryngopharynx. The nasopharynx, which primarily has a respiratory function, lies posterior to the termination of the turbinates and nasal septum and extends to the soft palate. The oropharynx has primarily a digestive function, starts below the soft palate, and extends to the superior edge of the epiglottis. The laryngopharynx (hypopharynx) lies between the fourth and sixth cervical vertebrae, starts at the superior border of the epiglottis, and extends to the inferior border of the cricoid cartilage, where it narrows and becomes continuous with the esophagus (Fig. 1-3). The eustachian tubes open into the lateral walls of the nasopharynx.

Figure 1-3 Diagrammatic representation of a sagittal section through head and neck to show divisions of the pharynx. Laryngopharynx is also known as the hypopharynx.

(Modified from Ellis H, Feldman S: Anatomy for anaesthetists, ed 6, Oxford, 1993, Blackwell Scientific.)

In the lateral walls of the oropharynx are situated the tonsillar pillars of the fauces. The anterior pillar contains the glossopharyngeus muscle, and the posterior pillar contains the palatoglossus muscle.¹² The wall of the pharynx consists of two layers of muscles, an external circular layer and an internal longitudinal layer. Each layer is composed of three paired muscles. The stylopharyngeus, salpingopharyngeus, and palatopharyngeus muscles form the internal layer. They elevate the pharynx and shorten the larynx during deglutition. The superior, middle, and inferior constrictors form the external layer; they advance the food in a coordinated fashion from the oropharynx into the esophagus.

The constrictors are innervated by filaments arising out of the pharyngeal plexus (formed by motor and sensory branches from the vagus, the glossopharyngeal, and the external branch of the superior laryngeal nerve). The inferior constrictor is additionally innervated by branches from the recurrent laryngeal and external laryngeal nerves. The internal layer is innervated by the glossopharyngeal nerve.

1 Defense Against Pathogens

Inhaled particles of size greater than 10 µm are removed by inertial impaction on the posterior nasopharynx. In addition, the inhaled airstream changes direction sharply (90 degrees) at the nasopharynx, resulting in some loss of momentum of the suspended particles. Being unable to remain suspended, the particles are trapped by the pharyngeal walls. The impacted particles are trapped by the circularly arrayed lymphoid tissue located at the entrance to the respiratory and alimentary tracts, known as the ring of Waldeyer (Fig. 1-4). The ring includes masses of lymphoid tissue or tonsils, including the two large palatine, lingual, eustachian tubal, and nasopharyngeal tonsils.

Figure 1-4 The ring of Waldeyer, a collection of lymphoid (tonsillar) tissue that guards against pathogen invasion.

(Modified from Hodder Headline PLC, London.)

The nasopharyngeal tonsils are also called adenoids.^13,¹⁴ These structures occasionally impede the passage of ETTs, especially if they are infected and enlarged. Specifically, enlarged adenoid tissue may impede passage of a nasotracheal tube or nasal airway or may simply obstruct the nasal airway passages. The lingual tonsils are located between the base of the tongue and the epiglottis. During routine anesthetic evaluation of the oropharynx, the lingual tonsils are typically not visible. Lingual tonsillar hypertrophy, which is usually asymptomatic, has been reported as a cause of unanticipated difficult intubation and fatal upper airway obstruction.¹⁵ In addition, sepsis originating from one of the numerous lymphoid aggregates may lead to a retropharyngeal or peritonsillar abscess, which poses anesthetic challenges.⁷

Ciliary activity also works to clear trapped nonsoluble particles that are held in an outer mucus layer within the nares. This function is influenced by temperature, viscosity of the mucus, and the osmotic properties of the discharge. The ciliary movement can be negatively affected by many factors, such as viral infections or environmental agents, including air pollution and cigarette smoke. The loss of ciliary function leads to chronic and recurrent infections and can gradually severely injure the respiratory tract, leading to conditions such as chronic bronchitis, sinusitis, and otitis.³

2 Upper Airway Obstruction

a Sedation and Anesthesia

The pharynx is the common pathway for food and the respiratory gases. Patency of the pharynx is vital to the patency of the airway and proper gas exchange in unintubated patients. Proper placement of an ETT requires an understanding of the distance relationships from the oropharynx to the vocal cords and carina. Complications such as a cuff leak at the level of the vocal cords and endobronchial intubation may thus be avoided (Fig. 1-5). Traditionally, it has been taught that upper airway obstruction in patients who are sedated or anesthetized (without an ETT), or who have altered levels of consciousness for other reasons, occurs as a result of the tongue’s falling back onto the posterior pharyngeal wall. Specifically, it is thought that a reduction in genioglossus muscle activity leads to posterior displacement of the tongue with subsequent obstruction.¹⁶ However, a number of publications offer a different explanation. The velopharyngeal segment of the upper airway adjacent to the soft palate has recently become the primary focus. This area is particularly prone to collapse and has been found to be the predominant flow-limiting site during sedation and anesthesia,¹⁷ speech disorders, and obstructive sleep apnea (OSA) (Fig. 1-6).

Figure 1-5 Important distances for proper endotracheal tube placement.

(From Stone DJ, Bogdonoff DL: Airway considerations in the management of patients requiring long-term endotracheal intubation. Anesth Analg 74:276, 1992.)

Figure 1-6 A, Medial sagittal view of upper airway showing site of airway obstruction in sedated patients. In the obstructed state, the soft palate is in contact with the posterior pharyngeal wall. CD, Minimum anteroposterior diameter at level of tongue; EF, minimum anteroposterior diameter at level of epiglottis. B, The velopharynx (VP) and its relation to the soft palate (SP), nasopharynx (NP), oropharynx (OP), tonsil (TON), hypopharynx (HP), and larynx (L).

(From Shorten GD, Opie NJ, Graziotti P, et al: Assessment of upper airway anatomy in awake, sedated and anaesthetized patients using magnetic resonance imaging. Anaesth Intensive Care 22:165, 1994.)

Nandi and colleagues, using lateral radiographs in patients under general inhalational anesthesia, showed that obstructive changes in the airway occurred at the level of the soft palate and epiglottis.¹⁸ Shorten and coworkers, using magnetic resonance imaging (MRI), found that patients receiving intravenous sedation for anxiolysis with midazolam had anterior-posterior dimensional changes in the upper airway also at the level of the soft palate and epiglottis while sparing the tongue (see Fig. 1-6).¹⁹ In addition, Mathru and coauthors, using MRI to evaluate volunteers receiving propofol anesthesia, found that obstruction occurs at the level of the soft palate and not the tongue.²⁰ Therefore, it appears that the soft palate and epiglottis may play a more significant role than the tongue in pharyngeal upper airway obstruction.

b Obstructive Sleep Apnea

Reduction in the size of the pharynx is also a factor in the development of respiratory obstruction in patients with OSA.²¹ This problem has been studied with the use of imaging techniques including computed tomography (CT) and MRI, nasopharyngoscopy, fluoroscopy, and acoustic reflection.²² Structural changes that include tonsillar hypertrophy, retrognathia, and variations in craniofacial structures have been linked to sleep apnea risk, presumably by increasing upper airway collapsibility. CT and MRI studies in awake subjects have shown increased fatty tissue deposition and submucosal edema in the lateral walls of the pharynx, both of which can narrow the pharyngeal lumen and predispose to obstruction during sleep, when protective neuromuscular mechanisms wane.²³ Obesity, the major risk factor for OSA, has been shown to increase pharyngeal collapsibility through reductions in lung volumes, especially decreases in functional residual capacity (FRC), which are accentuated with the onset of sleep. This decrease in FRC may increase pharyngeal collapsibility through reductions in tracheal traction on the pharyngeal segment.^23,²⁴ In awake male patients with OSA, CT has revealed a reduced airway caliber at all levels of the pharynx when compared with normal patients, with the narrowest portion posterior to the soft palate.²⁵

The subatmospheric intra-airway pressure created by contraction of the diaphragm against the resistance of the nose can lead to a reduction in size of the pharyngeal airway. The collapsible segments of the pharynx are divided into three areas: retropalatal, retroglossal, and retroepiglottic. Patency depends on the contractile function of pharyngeal dilator muscles in these segments. The muscles involved are the tensor palatini, which retracts the soft palate away from the posterior pharyngeal wall; the genioglossus, which moves the tongue anteriorly; and the muscles that move the hyoid bone forward, including the geniohyoid, sternohyoid, and thyrohyoid muscles.^23,²⁶ In patients with OSA, elevated genioglossal and tensor palatini muscle activity has been observed in the awake state. In contrast, normal subjects have lower activity in these muscles. Observations like these suggest that increased upper airway dilator muscle activity compensates for a more anatomically narrow upper airway in OSA. The reduction in upper airway muscle activity during sleep has been implicated in leading to increased likelihood of upper airway obstruction in patients with OSA compared with healthy subjects.^23,²⁴ Studies also show that the configuration of the airway may differ in patients with OSA. Normally, the longer axis of the pharyngeal airway is transverse; however, in OSA patients the anterior-posterior axis is predominant. It is believed that this orientation is less efficient and may affect upper airway muscle function. Continuous positive airway pressure (CPAP) has been found to be effective in treating airway obstruction in these patients. The application of CPAP appears to increase the volume and cross-sectional area of the oropharynx, especially in the lateral axis.²⁷

Clinical problems can arise from both the exaggeration and the depression of upper airway reflexes. A heightened reflex response can lead to laryngospasm and prolonged paroxysm of cough, whereas depressed reflexes can increase the risk of aspiration and compromised airway.²⁸

The velopharynx, an area of the pharynx adjacent to the soft palate, is assuming increased importance in the understanding of OSA, speech disorders, and airway obstruction under anesthesia (see Fig. 1-6 B).²⁹ Fiberoptic nasendoscopy and MRI are recommended for studying velopharyngeal dysfunction.²⁹^–³¹ Six skeletal muscles—the tensor veli palatini, levator veli palatini, musculus uvulae, palatoglossus, palatopharyngeus, and superior constrictor—help form the so-called velopharyngeal sphincter. The proper function of the sphincter is vital to opening and closing of the nasal passages to airflow during deglutition and normal breathing.

C Larynx

The larynx, which lies in the adult neck opposite the third through sixth cervical vertebrae,¹² is situated at the crossroads between the food and air passages (or conduits). It is made up of cartilages forming the skeletal framework, ligaments, membranes, and muscles. Its primary function is to serve as the “watchdog” of the respiratory tract, allowing passage only to air and preventing secretions, food, and foreign bodies from entering the trachea. In addition, it functions as the organ of phonation. The larynx may be located somewhat higher in females and children. Until puberty, no differences in laryngeal size exist between males and females. At puberty, the larynx develops more rapidly in males than in females, almost doubling in the anteroposterior diameter. The female larynx is smaller and more cephalad.¹² The measurements of the length, transverse diameter, and sagittal diameter of the adult larynx are 44, 36, and 43 mm, respectively, in the male and 41, 36, and 26 mm, respectively, in the female.³² Most larynxes develop somewhat asymmetrically.³³ The inlet to the larynx is bounded anteriorly by the upper edge of the epiglottis, posteriorly by a fold of mucous membrane stretched between the two arytenoid cartilages, and laterally by the aryepiglottic folds.⁹

1 Bones of the Larynx

The hyoid bone (Fig. 1-7) suspends and anchors the larynx during respiratory and phonatory movement. It is U shaped, and its name is derived from the Greek word hyoeides, meaning shaped like the letter upsilon. It has a body, which is 2.5 cm wide by 1 cm thick, and greater and lesser horns (cornu). The hyoid does not articulate with any other bone. It is attached to the styloid processes of the temporal bones by the stylohyoid ligament and to the thyroid cartilage by the thyrohyoid membrane and muscle. Intrinsic tongue muscles originate on the hyoid, and the pharyngeal constrictors are also attached there.^4,^12,³⁴

Figure 1-7 External frontal (left) and anterolateral (right) views of the larynx. Notice the location of cricothyroid membrane and thyroid gland in relation to thyroid and cricoid cartilage in the frontal view. The horn of the thyroid cartilage is also known as the cornu. In the anterolateral view, the shape of the cricoid cartilage and its relation to thyroid cartilage are shown.

(Modified from Ellis H, Feldman S: Anatomy for anaesthetists, ed 6, Oxford, 1993, Blackwell Scientific.)

2 Cartilages of the Larynx

Nine cartilages provide the framework of the larynx (Fig. 1-8; see also Fig. 1-7). These are the unpaired thyroid, cricoid, and epiglottis and the paired arytenoids, corniculates, and cuneiforms. They are connected and supported by membranes, synovial joints, and ligaments. The ligaments, when covered by mucous membranes, are called folds. The thyroid, cricoid, and arytenoid cartilages consist of hyaline cartilage, whereas the other cartilages are elastic cartilage. Hyaline cartilage tends to ossify in the adult, and this occurs earlier in men than in women.³

Figure 1-8 Cartilages and ligaments of the larynx seen posteriorly. Notice the location of the corniculate cartilage within the aryepiglottic fold.

(Modified from Ellis H, Feldman S: Anatomy for anaesthetists, ed 6, Oxford, 1993, Blackwell Scientific.)

a Thyroid Cartilage

The thyroid cartilage, the longest laryngeal cartilage and the largest structure in the larynx, acquires its shieldlike shape from the embryologic midline fusion of the two distinct quadrilateral laminae.³⁵ In females, the sides join at an angle of approximately 120 degrees; in males, the angle is closer to 90 degrees. This smaller thyroid angle explains the greater laryngeal prominence (“Adam’s apple”), longer vocal cords, and lower-pitched voice in males.³⁶ The thyroid notch lies in the midline at the top of the fusion site of the two laminae.³⁷ On the inner side of this fusion line are attached the vestibular ligaments and, below them, the vocal ligaments (Fig. 1-9). The superior (greater) and inferior (lesser) cornua of the thyroid are slender, posteriorly directed extensions of the edges of the lamina. The lateral thyrohyoid ligament attaches the superior cornu to the hyoid bone, and the cricoid cartilage articulates with the inferior cornu at the cricothyroid joint. The movements of this joint are rotatory and gliding and result in changes in the length of the vocal folds.

Figure 1-9 Sagittal (lateral) view of the larynx. The vocal and vestibular folds and the thyroepiglottic ligament attach to the midline of the inner surface of the thyroid cartilage. Also notice the relationship between the cricovocal membrane and the vocal folds.

(Modified from Ellis H, Feldman S: Anatomy for anaesthetists, ed 6, Oxford, 1993, Blackwell Scientific.)

b Cricoid Cartilage

The cricoid cartilage (see Fig. 1-9) represents the anatomic lower limit of the larynx and helps support it.³⁵ The name cricoid is derived from the Greek words krikos and eidos, meaning shaped like a ring, and it is frequently said to have a signet-ring shape. It is thicker and stronger than the thyroid cartilage and represents the only complete cartilaginous ring in the airway. For this reason, cautious downward pressure on the cricoid cartilage to prevent passive regurgitation is possible without subsequent airway obstruction. Traditionally, it was thought that the pediatric airway was narrowest at the level of the cricoid, and recommendations for ETT size were made based on the size of the cricoid ring. However, studies done with video bronchoscopes on anesthetized and paralyzed children have shown that the glottic opening may be narrower than the cricoid region.³⁸ Therefore, an ETT tube may cause more damage to the vocal cords than to the subglottic area.

The bulky portion or lamina is located posteriorly. The tracheal rings are connected to the cricoid by ligaments and muscles. The cricoid lamina forms ball-and-socket synovial articulations with the arytenoids posterosuperiorly and with the thyroid cartilage inferolaterally and anteriorly.³⁵ It also attaches to the thyroid cartilage by means of the cricothyroid membrane (CTM), a relatively avascular and easily palpated landmark in most adults (see Figs. 1-8 and 1-9).

The inner diameters of the cricoid cartilage have been measured in cadavers, with great variability noted. Randestad and colleagues reported that the smallest diameter is in the frontal plane, which in females ranged from 8.9 to 17.0 mm (mean, 11.6 mm) and in males from 11.0 to 21.5 mm (mean, 15.0 mm).³⁹ They pointed out that placement of a standard size ETT (7 mm inner diameter for females, 8 mm for males) through the cricoid cartilage while preventing mucosal necrosis may be difficult in certain individuals.³⁹ The CTM represents an important identifiable landmark, providing access to the airway by percutaneous or surgical cricothyroidotomy.

The dimensions of the CTM have been identified in cadaveric specimens.⁴⁰^–⁴² However, the actual methods of obtaining the anatomic measurements varied, making comparisons difficult to interpret. Caparosa and Zavatsky described the CTM as a trapezoid with a width ranging from 27 to 32 mm, representing the actual anatomic limit of the membrane, and a height of 5 to 12 mm.⁴¹ Bennett and coauthors⁴⁰ reported the width as 9 to 19 mm and the height as 8 to 19 mm, whereas Dover and coworkers⁴² reported a width of 6.0 to 11.0 mm and a height of 7.5 to 13.0 mm, using the distance between the cricothyroid muscles as their horizontal limit. The width and height of the membrane are reported to be smaller in females than in males.^10,⁴²

Anteriorly, vascular structures overlie the membrane and pose a risk of hemorrhage.^40,⁴²^–⁴⁴ Cadaveric studies have reported the presence of a transverse cricothyroid artery, a branch of the superior thyroid artery, traversing the upper half of the membrane. Therefore, a transverse incision in the lower third of the membrane is recommended. The superior thyroid artery courses along the lateral edge of the membrane, and various branches of the superior and inferior thyroid veins and the jugular veins are also reported to traverse the membrane.

c Arytenoids

The two light arytenoid cartilages (see Fig. 1-8) are shaped like three-sided pyramids, and they lie in the posterior aspect of the larynx.⁴⁵ The arytenoid’s medial surface is flat and is covered with only a firm, tight layer of mucoperichondrium.^45,⁴⁶ The base of the arytenoid is concave and articulates by a true diarthrodial joint with the superior lateral aspect of the posterior lamina of the cricoid cartilage. It is described as a ball and socket with three movements—rocking or rotating, gliding, and pivoting—that control adduction and abduction of the vocal cords. All such synovial joints can be affected by rheumatoid arthritis. Cricoarytenoid arthritis is present in a majority of patients with rheumatoid arthritis and has been identified as a cause of life-threatening upper airway obstruction.⁴⁷ Cricoarytenoid arthropathy has also been reported as a rare but potentially fatal cause of acute upper airway obstruction in patients with systemic lupus erythematosus.⁴⁸

The lateral extension of the arytenoid base is called the muscular process. Important intrinsic laryngeal muscles, the lateral and posterior cricoarytenoids, originate here. The medial extension of the arytenoid base is called the vocal process. Vocal ligaments, the bases of the true vocal folds, extend from the vocal process to the midline of the inner surface of the thyroid lamina (see Fig. 1-9). The fibrous membrane that connects the vocal ligament to the thyroid cartilage actually penetrates the body of the thyroid. This membrane is called Broyles’ ligament. This ligament contains lymphatics and blood vessels and therefore can act as an avenue for extension of laryngeal cancer outside the larynx.^35,⁴⁹ The relationship between the anterior commissure of the larynx and the inner aspect of the thyroid cartilage is important to otolaryngologists, who perform thyroplasties and supraglottic laryngectomies on the basis of its location. A study of cadavers reported that the anterior commissure of the larynx can usually be found above the midpoint of the vertical midline fusion of the thyroid cartilage ala.^46,⁵⁰

d Epiglottis

The epiglottis is considered to be vestigial by many authorities.⁵¹ Composed primarily of fibroelastic cartilage, the epiglottis does not ossify and maintains some flexibility throughout life.^35,^45,⁵² It is shaped like a leaf and is found between the larynx and the base of the tongue (see Figs. 1-8 and 1-9).^34,⁴⁶ The anterior surface of the epiglottis is concave, and this, in combination with laryngeal elevation, aids in airway protection during deglutition.¹ In approximately 1% of the population, the tip and posterior aspect of the epiglottis are visible during a pharyngoscopic view with the mouth opened and tongue protruded. Contrary to reports, this does not always predict ease of intubation.⁵³ The upper border of the epiglottis is attached by its narrow tip or petiole to the midline of the thyroid cartilage by the thyroepiglottic ligament (see Fig. 1-9). The hyoepiglottic ligament connects the epiglottis to the back of the body of the hyoid bone.^34,⁵⁴ The mucous membrane that covers the anterior aspect of the epiglottis sweeps forward to the tongue as the median glossoepiglottic fold and to the pharynx as the paired lateral pharyngoepiglottic folds.³⁵ The pouchlike areas found between the median and lateral folds are the valleculae (Fig. 1-10). The tip of a properly placed Macintosh laryngoscope blade rests in this area. The vallecula is a common site of impaction of foreign bodies, such as fish bones, in the upper airway.