Understanding the Basics1

The important anatomy to the airway consists of the relationship of pharynx to its surrounding structures, larynx and mobility of tissues.

Extension: Sphenoid bone to C₆

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.

Anterioriorly opens into choanae, nasal passages, and nostrils (Fig. 2).2

The nose: The nose is divided into two nasal fossae which extend uo to 10 to 14 cm from the nostrils to the nasopharynx. The two fossae are divided by a cartilaginous septum. The nasal septum is composed of the perpendicular plate of the ethmoid bone descending from the cribriform plate, septal cartilage, and the vomer.

Blood Supply (Fig. 3)

Kiesselbach's plexus, where these vessels anastomose, is situated in Little's area on the anterior-inferior portion of the nasal septum—a source of significant epistaxis.

Paranasal sinuses: Sphenoid, ethmoid, maxillary, and frontal (Fig. 4).

Nerve supply (Fig. 5): The olfactory area consists of the middle and upper septum and the superior turbinate bone, located in the upper third of the nasal fossa. The olfactory cells have specialized hairlike processes (olfactory hair) innervated by the olfactory nerve.

It starts below the soft palate, and extends to the superior edge of the epiglottis (Fig. 6).

Lies opposite C_3-6 vertebrae

Consists of 3 paired and 3 unpaired cartilages, supporting muscles and membranes (Fig. 7).

Paired: Arytenoids, corniculate, cuneiform.

Unpaired: Epiglottis, thyroid, cricoid.

Hyoid bone: U shaped, 2.5 cm wide, 1 cm thick, has greater and lesser horns (cornu).

Named so for its shield-like shape (from embryologic midline fusion of the two distinct quadrilateral laminae). In females, the sides join at approximately 120 degrees, and in males is approx 90 degrees (Adam's apple). The thyroid notch lies in the midline at the top of the fusion site of the two laminae. On the inner side of this fusion line are attached the vestibular ligaments and, below them, the vocal ligaments. The superior (greater) and inferior (lesser) cornu of the thyroid are the 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, which leads to changes in the length of the vocal folds.

The tracheal rings connect to the cricoid by ligaments and muscles and it attaches to the thyroid cartilage by the cricothyroid membrane (a site for percutaneous or sugical cricothyroidotomy).

These are shaped like three-sided pyramids, and they lie in the posterior aspect of the larynx. 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. The lateral extension of the arytenoid base is called the muscular process, where intrinsic laryngeal muscles, lateral and posterior cricoarytenoids originate. The medial extension of the arytenoid 7base 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. Broyles’ ligament connects the vocal ligament to the thyroid cartilage and contains lymphatics and blood vessels (acts as a source for extension of laryngeal cancer outside the larynx).

It is shaped like a leaf and is found between the larynx and the base of the tongue.

The epiglottis is connected to the arytenoid cartilages by the laterally placed aryepiglottic ligaments and folds. Two sets of paired fibroelastic cartilages are embedded in each aryepiglottic fold. The sesamoid cuneiform cartilage is roughly cylindrical and lies anterosuperior to the corniculate in the fold. The cuneiform may be seen laryngoscopically as a whitish elevation through the mucosa. The cuneiform and corniculate cartilages reinforce and support the aryepiglottic folds and may help the arytenoids move.

Extends from the laryngeal inlet to the lower border of the cricoid cartilage. It consists of the superiorly placed vestibular folds (false cords), and vocal folds (true vocal cords). The space between the true cords is called the rima glottidis, or the glottis. The glottis is divided into two parts—anterior intermembranous section (situated between the two vocal folds) and posterior intercartilaginous part (which passes between the two arytenoid cartilages and the mucosa, stretching between them in the midline posteriorly, forming the posterior commissure of the larynx).

The external carotid gives rise to the superior thyroid artery, which bifurcates, forming the superior laryngeal artery. This artery courses with the superior laryngeal nerve through the thyrohyoid membrane to supply the supraglottic region.

The main nerves of the larynx are the recurrent laryngeal nerves and the internal and external branches of the superior laryngeal nerves (from 11vagus nerve). The external branch of the superior laryngeal nerve supplies motor innervation to the cricothyroid muscle. All other motor supply to the laryngeal musculature is provided by the recurrent laryngeal nerve.

There is an intimate and important relationship between the nerves that supply the larynx and the vessels that supply the thyroid gland.

The trachea extends from its attachment to the lower end of the cricoid cartilage, at the level of the 6th cervical vertebra, to its termination at the bronchial bifurcation In the preserved dissecting-room cadaver, this is at the level of the 4th thoracic vertebra and the manubriosternal junction (the angle of Louis), but in the living subject in the erect position, the lower end of the trachea can be seen in oblique radiographs of the chest to extend to the level of the 5th, or in full inspiration the 6th, thoracic vertebra. In the adult, the trachea is 15 cm long, of which 5 cm lie above the suprasternal notch; this portion is somewhat greater (nearly 8 cm) when the neck is fully extended. The diameter of the trachea is correlated with the size of the subject; a good working rule is that it has the same diameter as the patient's index finger. The patency of the trachea is due to a series of 16–20 C-shaped cartilages joined vertically by fibroelastic tissue and closed posteriorly by the nonstriated trachealis muscle. The cartilage at the tracheal bifurcation is the keel-shaped carina, which is seen as a very obvious sagittal ridge when the trachea is inspected bronchoscopically. Should the sharp edge of the carina become flattened, this usually denotes enlargement of the hilar lymph nodes or gross distortion of the pulmonary anatomy by fibrosis, tumor or other pathology

The trachea lies exactly in the midline in the cervical part of its course but within the thorax it is deviated slightly to the right by the arch of the aorta. In the neck, it is covered anteriorly by the skin and by the superficial and deep fascia, through which the rings are easily felt. The 2nd to the 4th rings are covered by the isthmus of the thyroid where, along the upper border, branches of the superior thyroid artery join from either side. In the lower part of the neck, the edges of the sternohyoid and sternothyroid muscles overlap the trachea, which is here also covered by the inferior thyroid veins 14(as they stream downwards to the brachiocephalic veins), by the cross-communication between the anterior jugular veins and, when present, by the thyroidea ima artery, which ascends from the arch of the aorta or from the brachiocephalic artery. It is because of this close relationship with the brachiocephalic artery that erosion of the tracheal wall by a tracheostomy tube may cause sudden profuse hemorrhage. It is less common for the carotid artery to be involved in this way. On either side are the lateral lobes of the thyroid gland, which intervene between the trachea and the carotid sheath and its contents (the common carotid artery, the internal jugular vein and the vagus nerve). Posteriorly, the trachea rests on the esophagus, with the recurrent laryngeal nerves lying on either side in a groove between the two. The close relationship of the unsupported posterior tracheal wall and the esophagus is revealed during esophagoscopy. The thoracic part of the trachea descends through the superior mediastinum. Anteriorly, from above downwards, lie the inferior thyroid veins, the origins of the sternothyroid muscles from the back of the manubrium, the remains of the thymus, the brachiocephalic artery and the left common carotid arterya which separate the trachea from the left brachiocephalic vein and, lastly, the arch of the aorta. Posteriorly, as in its cervical course, the trachea lies throughout on the esophagus, with the left recurrent laryngeal nerve placed in a groove between the left borders of these two structures. On the right side, the trachea is in contact with the mediastinal pleura, except where it is separated by the azygos vein and the right vagus nerve. On the left, the left common carotid and left subclavian arteries, the aortic arch and the left vagus intervene between the trachea and the pleura; the altering relationships between the major arteries and the trachea are due to the diverging, somewhat spiral, course of the arteries from their aortic origins to the root of the neck. The large tracheobronchial lymph nodes lie at the sides of the trachea and in the angle between the two bronchi. In infants, these relationships are somewhat modified; the brachiocephalic artery is higher and crosses the trachea just as it descends behind the suprasternal notch. The left brachiocephalic vein may project upwards into the neck to form an anterior relation of the cervical trachea frightening encounter, if found tensely distended with blood when performing a tracheotomy on an asphyxiating baby. In children up to the age of 2 years, the thymus is large and lies in front of the lower part of the cervical trachea.

The trachea bifurcates in the supine cadaver at the level of the 4th thoracic vertebra into the right and left bronchi. In the erect position in full inspiration in life, the level of bifurcation is at T₆. The right main bronchus is shorter, wider and more vertically placed than the left: shorter because it gives off its upper lobe bronchus sooner (after a course of only 2.5 cm); 15wider because it supplies the larger lung; and more vertically placed (at 25° to the vertical compared with 45° on the left) because the left bronchus has to extend laterally behind the aortic arch to reach its lung hilum. Thus, inhaled foreign bodies are more inclined to enter the wider and more vertical right bronchus than the narrower and more obliquely placed left. The right pulmonary artery is first below and then in front of the right main bronchus, and the azygos vein arches over it. The left main bronchus is 5 cm long. It passes under the aortic arch, in front of the esophagus, thoracic duct and descending aorta, and has the left pulmonary artery lying first above and then in front of it. Because the right upper lobe bronchus arises only a short distance below the carina, it is not possible to place a tube in that bronchus without the risk of obstruction of the lower lobe. To overcome this difficulty, right-sided endobronchial tubes have an orifice in the lateral surface of the tube that coincides with the opening of the right upper lobe. No special arrangement has to be made for tubes placed in the left bronchus, as the 5 cm distance between the carina and the left upper lobe bronchus leaves ample room for the cuffed end of an endobronchial tube.

Each lung is roughly conical, with an apex, a base, a lateral (or costal) and a medial surface and with three borders—anterior, posterior and inferior. Each lung lies freely within its pleural cavity apart from its attachments at the hilum. The right lung is the larger, weighing on average 620 g compared with 570 g on the left. The lung of the male is larger and heavier than that of the female. Each lung is divided by a deep oblique fissure, and the right lung is further divided by a transverse fissure. Thus, the right lung is trilobed and the left bilobed.

The nose, mouth and pharynx conduct air to the larynx, humidify and filter the air gases. The larynx aids phonation and conducts the gas into the trachea (18 mm diameter and 11 cm length).

Type 1 alveolar cells: Derived from type II alveolar cells, provide a thin layer of cytoplasm which covers about 80% of the gas exchange zone. 0.1 mm thick, have 1 nm gap junctions, impermeable to albumin, allow extravasation of mf's—unable to divide—highly sensitive to hyperoxia.

Type II alveolar cells: These cells allow the formation of surfactant and other enzymes. They are rounded cells at septal junctions, resistant to hyperoxia.

Type III alveolar cells: These cells are the main lung defence system—alveolar macrophages.

A thin film of liquid lines the alveoli and the surface tension of this film is an important factor in the pressure-volume relationship of the lung. The surface tension arises because the attractive forces between adjacent molecules of the liquid are much stronger than those between the liquid and the gas. As a result of that the liquid surface area becomes as small as possible. At the interface between the liquid and the alveolar gas, intermolecular forces in the liquid tend to cause the area of the lining to shrink (the alveoli tend to get smaller). The surface tension contributes to the pressure-volume behavior of the lungs because when the lungs are inflated with saline they have much larger compliance that when they are filled with air (because saline abolishes the surface tension).

This generates a pressure predicted from Laplace's law:

Surfactant is stored in the lamellar bodies of type II alveolar cells and made up of phospholipids, plasma proteins and carbohydrate. It is an amphipathic molecule with a charged hydrophilic head and hydrophobic tail.

Functions of surfactant are:

Primary lung volumes:

Secondary derived capacities:

The volume of gas left in the lungs at the end of normal tidal expiration

FRC acts as a buffer:

Factors decreasing FRC:

Age, posture—supine position, anesthesia—muscle relaxants, surger—laparoscopic, pulmonary fibrosis/pulmonary edema, obesity, abdominal swelling, pregnancy—increased abdominal pressure.

Factors increasing FRC:

Increasing height of patient, erect position—diaphragm and abdominal organs less able to encroach upon bases of the lungs, emphysema—decreased elastic recoil of lung therefore less tendency of lung to collapse, asthma—air trapping.

This is the volume at which the small airways close during expiration. Under normal circumstances the FRC is always greater than the CC however, if the FRC was to decrease then this would no longer be the case and the small airways may close at the end of normal tidal expiration. This leads to hypoxemia, atelectasis and worsening gas exchange due to increasing V/Q mismatch.

Inhaled air passes through the conducting airways and eventually reaches the respiratory epithelium of the lungs. The trachea divides into right and left main bronchi, which in turn divide into lobar, then segmental 12 bronchi. 24This process continues down to the terminal bronchioles (the smallest airways without alveoli).

Dead space: volume of gas which does not take part in gas exchange (Figs. 20 and 21).

Abbreviations used in equation:

FeCO₂- CO₂ from mixed expired gases

Expiration is usually passive and relies on the elastic recoil of the lungs and the chest wall.

Elastic recoil is usually measured in terms of compliance.

A variety of factors affect this like lung volume, pulmonary blood volume, extravascular lung water and pathological processes (inflammation, fibrosis)

Factors affecting compliance are:

Disease: In atelectasis, when the lung is relatively stiff, the point of balance (resting expiratory volume) will be reached at a lower lung volume, as there will be greater pull inwards; this will predispose to further atelectasis. The excessively compliant emphysematous lung has less elastic recoil; resting expiratory volume will then be greater, since the natural tendency for the chest wall to expand is maintained.

Age: The immature lung in the infant is less elastic than in adulthood. Elasticity is highest in young adults and it decreases slowly with advancing age—lung compliance is therefore lowest in young adults. Chest wall compliance is highest at birth and slowly declines with age.

Posture: Thoracic compliance is lower in the supine position, as the gravitational pull of the abdomen, which existed in the upright position, is reversed and the diaphragm is pushed into the chest by the abdominal contents.

Anesthesia: Several factors (supine position, airway closure, changes in intrathoracic blood volume, accumulation of fluid, direct effect of drugs, altered muscle tone, external pressure) influence compliance under anesthesia; generally compliance is decreased.

Obesity: The effect is compounded by supine or lithotomy position.

It is the work required by the respiratory muscles to overcome the mechanical impedance to respiration. It is the sum of work requires to overcome both elastic and airflow resistance.

Breathing is mainly controled at the level of brainstem. The normal automatic and periodic nature of breathing is triggered and controled by the respiratory centers located in the pons and medulla.

It is located in the lower pons.

It is located in the upper pons.

These receptors are placed in the walls of bronchi and bronchioles of the lung. The main function of these receptors is to prevent the overinflation of the lungs. Inflation of the lungs activates these receptors and activation of the stretch receptors in turn inhibits the neurones in inspiratory center via vagus nerve. When the expiration starts activation of the stretch receptors gradually ceases allowing neurones in the inspiratory neurones become active again (Hering-Breuer Reflex). It is particularly important for infants. In adults it is functional only during exercise when the tidal volume is larger than normal.

The respiratory system maintains concentrations of O₂, CO₂ and the pH of the body fluids within a normal range. Any deviation from these values has a marked influence on the respiration. Chemoreceptors are specialized neurones activated by changes in O₂ or CO₂ levels in the blood and the brain tissue, respectively. They are involved in the regulation of respiration according to the changes in PO₂ and pH. O₂-sensitive chemoreceptors (Peripheral chemoreceptors) are located at the bifurcation of the carotid artery in the neck and the aortic arch. They are small vascular sensory organs encapsulated with the connective tissue. They are connected to the respiratory center in the medulla by glossopharyngeal nerve (carotid body chemoreceptors) and the vagus nerve (aortic body). Central chemoreceptors are located bilaterally in the chemosensitive area of the medulla oblongata and exposed to the cerebrospinal fluid (CSF), local blood flow and local metabolism. They actually respond to changes in H⁺ concentration in these compartments. When the blood partial PCO₂ is increased CO₂ diffuses into the CSF from cerebral vessels and liberates H⁺. (When CO₂ combines with water forms carbonic acid and liberates H⁺ and HCO₃⁻).

At high altitude because the ability of the lung to eliminate CO₂ is not affected, in response to increased respiration, blood PCO₂ is decreased. If PO₂ drops under certain level respiratory system does not respond and death will occur.

Alveolar pressure is the same throughout the lung; therefore, the more negative intrapleural pressure at the apex (or the least gravity-dependent area) results in larger, more distended apical alveoli than in other areas of the lung (Fig. 28). The transpulmonary pressure (Paw – Ppl), or distending pressure of the lung, is greater at the top and lower at the bottom, where intrapleural pressure is less negative. Despite the smaller alveolar size, more ventilation is delivered to dependent pulmonary areas. The decrease in intrapleural pressure at the base of the lungs during inspiration is greater than at the apex because of diaphragmatic proximity. Thus, because the dependent area of the lung generates the greatest change in transpulmonary pressure, more gas is sucked into dependent areas of the lung.

Blood flow to and around the lung is similar to any other organ but at much lower pressures than the systemic system (Fig. 29).37

Blood flow within the lung is mainly gravity-dependent. Since the alveolar-capillary beds are not composed of rigid vessels, the pressure of the surrounding tissues can influence the resistance to flow through the individual capillaries. Thus, blood flow depends on the relationship between pulmonary artery pressure (Ppa), alveolar pressure (PA), and pulmonary venous pressure. West et al. and West and Dollery created a lung model which divides the lung into three zones (Fig. 30).

The efficiency with which oxygen and carbon dioxide exchange at the alveolar-capillary level highly depends on the matching of capillary perfusion and alveolar ventilation. At this level, the combination of lung and the circulatory system must be well-matched.

The majority of blood flow is distributed to the gravity-dependent part of the lung. During a spontaneous breath, the largest portion of the tidal volume also reaches the gravity-dependent part of the lung.40

Thus, the nondependent area of the lung receives a lower proportion of both ventilation and perfusion, and dependent lung receives greater proportions of ventilation and perfusion. But, ventilation and perfusion are not matched perfectly, and various V/Q ratios result throughout the lung (Fig. 32).

The partial pressure of oxygen that is inhaled from our natural environment through normal inhalation is not maintained at the same partial pressure by the time it reaches the alveoli and indeed the mitochondria. The process by which this decrease in partial pressure occurs is called the oxygen cascade.42

Oxygen is carried in 2 forms in the blood:

Oxygen dissociation curve (Fig. 35):

Carbon dioxide is carried in the blood in 3 ways:

The Haldane effect:

This phenomenon refers to the increased ability of blood to carry CO₂ when hemoglobin is deoxygenated. Deoxyhemoglobin is 3.5 times more effective than oxyhemoglobin in forming carbamino compounds.

The value for the A-a gradient gives the clinician some idea about the amount of VQ mismatch and shunt that is present in the lungs. A typical normal value would be around 0.5-1 kPa (5 mm Hg) though values up to around 15 mm Hg may be accepted.

True shunt refers to a VQ = 0.

The shunt equation: Qs = Shunted blood flow Qt = Cardiac output Qt-Qs = Blood flow through the lungs minus the shunted blood CcO₂ = Oxygen content of end pulmonary capillary blood CaO₂ = Oxygen content of arterial blood CvO₂ = Oxygen content of mixed venous blood shunt equation (Fig. 38).

Because PO₂ in the pulmonary capillary blood varies with time as it moves through the pulmonary capillary bed, oxygen cannot be used to assess diffusing capacity. A gas mixture containing carbon monoxide is the traditional diagnostic gas used to measure diffusing capacity. Its partial pressure in the blood is nearly zero, and its affinity for hemoglobin is 200 times that of oxygen. Carbon monoxide diffusing capacity (D_LCO) collectively measures all the factors that affect the diffusion of gas across the alveolar-capillary membrane. The D_LCO is recorded in mL CO/min/mm Hg at standard temperature and pressure, dry.

Used in patients with significant pulmonary dysfunction.

The flow-volume loop graphically demonstrates the flow generated during a forced expiratory maneuver followed by a forced inspiratory maneuver, plotted against the volume of gas expired.49

The subject forcefully exhales completely, then immediately and forcefully inhales to vital capacity. The expired and inspired volumes are plotted on the abscissa and flow is plotted on the ordinate. Although various numbers can be generated from the flow-volume loop, the configuration of the loop itself is probably the most informative part of the test. It helps in distinguishing an extrathoracic from intra thoracic obstruction and guide in its management.50

Direct laryngoscopy and introduction of tracheal tube are noxious stimuli that can provoke a response of cardiovascular, respiratory and other physiological systems.

Hypertension, tachycardia—exaggerated with increased duration an force of laryngoscopy. Increase in arterial pressures starts within 5 seconds of laryngoscopy, peaks in 1–2 minutes and returns to control levels in 5 minutes. Also noted with use of ILMA.

Laryngospasm—if laryngoscopy attempted during light plane of anesthesia; bronchospasm, coughing, bucking.

Elevation of ICT/IOP.

Vomiting, aspiration, latex allergy (Patients with spina bifida, rubber industry workers, atopic patients, and patients with a multiple surgery history are most at risk. Patients with type I hypersensitivity are at risk for developing anaphylaxis with hypotension, rash, and bronchospasm).