Nose

Inhaled air enters the body through the nose or mouth. Air passing through the nose is filtered, heated to body temperature, and humidified. The external nose is only a small part of the nasal air passageway, the major portion of which lies directly behind the nose and includes three scroll-shaped turbinate bones, also called the nasal conchae.

The cartilage around the entrance to the nostrils that can flare during heavy breathing is called the alar cartilage or ala nasae (“nasal wings”). Each nostril opening (anterior naris) leads directly into the vestibule, which is the forwardly expanded portion of the nasal cavity. The vestibule is lined with cutaneous epithelium. In its lower half, it has sebaceous glands and coarse hairs, which serve to filter incoming air. The floor of the nose is at a level higher than the opening of the nostril; therefore, during nasal intubation, the apex of the nose should be elevated superiorly with gentle pressure while the tube is inserted parallel to the roof of the mouth. The tube should not be directed upward into the turbinates but rather along the floor of the nose formed by the superior aspect of the palatine bone, which forms the hard palate of the mouth directly below the nose. Prolonged nasotracheal intubation is associated with obstruction of the nasal sinuses, sinus infection, and fever. Intranasal infections can produce intracranial infection via vascular connections, as discussed later in this section.

The anterior portion of the external nose, the vestibule, expands above and behind into triangular spaces, or fossae. The fossae are separated from each other by the nasal septum, which also separates the two nostrils. The septum is formed by the ethmoid and vomer bones superiorly and the vomeronasal and nasal septal cartilages inferiorly. The nasal fossae usually communicate freely with the paranasal air sinuses (frontal, ethmoid, maxillary, and sphenoid). They open into the nasopharynx by the posterior nares (also known as choanae) and are bordered medially by the nasal septum and laterally by three turbinates arranged one above the other.

Choanal atresia is a birth defect characterized by obstruction of the posterior nasal airway. This obstruction may be life threatening in the obligate nose-breathing newborn.

The conchae are scroll-shaped prominences projecting from the lateral walls and have their free margins directed downward and inward. The conchae overlie the superior, middle, and inferior meatus, which contain the openings to the paranasal sinuses. The superior concha is by far the smallest of the three, and the middle concha extends forward much farther than the superior concha. The inferior concha, which lies along the lower part of the lateral wall of the nasal cavity, is in the pathway of airflow in the nose, and it is the one most commonly injured during nasal intubation. It extends to within approximately 2 cm of the middle of the anterior naris, and its posterior tip lies approximately 1 cm in front of the pharyngeal orifice of the eustachian tube. Eustachian drainage can become obstructed when the inferior concha or adenoid tonsils become inflamed. Such obstruction can lead to middle ear pathology.

The nasal cavities are lined with mucous membranes that are continuous with those of the pharynx. The mucosa can be divided into respiratory and olfactory areas because it not only lines the tracts followed by respired air but also covers the cells that act as the receptors for smell. The olfactory epithelium occupies the apical third of the nasal cavity. This epithelium contains afferent fibers from the olfactory nerves (cranial nerve I) that communicate through the cribriform plate of the ethmoid bone to the adjacent olfactory bulb. Signals then progress to the other parts of the rhinencephalon. The respiratory mucosa lines the lower two thirds of the nose and consists of pseudostratified ciliated columnar epithelium interspersed with goblet cells that produce mucus. Although the morphology of cells changes progressively toward the terminal bronchioles, this general arrangement of stratified ciliated epithelium with goblet cells persists throughout the majority of the air passages of the respiratory system. The direction of motion of the cilia is toward the exterior of the nasal cavity.

The principal arterial supply of the nasal fossae comes from the ophthalmic arteries through the anterior and posterior ethmoid branches and from the internal maxillary artery through the sphenopalatine arteries. Because of the location of the interior maxillary artery, it is sometimes ligated for the treatment of persistent nosebleed. The veins accompany the arteries; the ethmoid veins open into the superior sagittal sinus, and the nasal veins drain into the ophthalmic veins and then into the cavernous sinuses. Infections in the nose can result in meningitis because of this venous communication between the intracranial and intranasal circulation. The sensory nerves from the upper respiratory tract come from the ophthalmic nerve and the maxillary nerve (both are branches of cranial nerve V). Lymphatic drainage from the cavities of the nose is via the deep cervical lymph nodes adjacent to the internal jugular vein.

Through the functioning of the nasal hairs, the mucus-producing epithelium, and the rich arterial supply, the nose carries out important functions that include filtration, humidification, and heating of inspired air. As long as the incoming air is not extremely cold, the nose can warm the inspired air to nearly body temperature and moisten it to nearly 100% relative humidity. The heating and humidifying functions of the nose are affected by general anesthesia. The inspiration of cold, dry gas often dries the nasal and pharyngeal passageways, causing sore throat even if no instrumentation of the airway takes place.

The hairs at the entrance to the nostrils are of minor importance to filtration because they remove only large particles. Much more important is the removal of particles by turbulent precipitation. Air passing through the nasal passageways hits many obstructions including the septum, the turbinates, and the pharyngeal wall. When the inspired air is forced to change direction, the inhaled particles cannot change course as rapidly, and they become embedded in the mucus-covered surfaces of these processes. The particles trapped in the mucus are moved by the cilia either to the naris or posteriorly to the pharynx to be expectorated or swallowed. This occurrence is important because it denies entry of infectious, carcinogenic, or irritating substances. Nasal filtration is extremely effective for particles above 10 µm and less than 1 nm, but filtration efficiency is inverse to particle size for particles that are between 10 nm and 1 µm.¹

Pharynx

The pharynx is a wide muscular tube that is a part of both the respiratory tract and the alimentary canal. Its upper border is the base of the skull, and it extends to the level of the C6 vertebra, where it becomes continuous with the esophagus. At this level, ingested foreign bodies, such as coins, are frequently lodged. The pharynx is lined by a musculomembranous coat and divided into three parts: the nasopharynx, which extends from the posterior nares (choanae) to the end of the soft palate; the oropharynx, which is bounded superiorly by the soft palate and anteriorly by the tonsillar pillars and oral cavity and extends inferiorly to the tip of the epiglottis; and the hypopharynx (laryngopharynx), which extends from the tip of the epiglottis to the level of C6, or the beginning of the esophagus.

The pharyngeal region includes the tonsils, which are composed of three aggregations of lymphoid tissue: the palatine tonsils (major tonsils), which lie in the tonsillar fossae at the boundary of the oral cavity and oropharynx; the lingual tonsils, which extend across the tongue from the base of each palatine tonsil; and the pharyngeal tonsils (adenoids), which lie on the lateral walls of the nasopharynx. The lymphoid tissue of the tonsils forms the Waldeyer tonsillar ring, which acts as a first line of defense against bacterial invasion of the nasal and buccal passages. If inflamed, the pharyngeal tonsils may obstruct airflow through the choanae and are sometimes removed by an adenoidectomy. Likewise, chronic tonsillitis may lead to removal of the palatine tonsils by tonsillectomy.

Larynx

The adult larynx extends from vertebrae C3 to C6 and is a protective structure that prevents aspiration during swallowing; vocalization evolved secondarily. The larynx consists of one bone, nine cartilages (Table 26-1), ligaments, muscles, and membranes.

The hyoid bone is the chief support for the larynx and is the only bone that does not form a joint with another bone. Its anterior aspect can be easily palpated, and its location is sometimes used as a measure of airway assessment for laryngoscopy. The thyroid cartilage and the cricoid cartilage make up the principal part of the framework of the larynx, whereas the epiglottis guards its entrance.

Trachea

The trachea is lined by pseudostratified ciliated columnar epithelium, and it extends from the inferior larynx to the carina, where it bifurcates into the two mainstem bronchi. In adults of normal size, the distances are fairly constant: the distance from the incisors to the larynx is approximately 13 cm, as is that from the larynx to the carina. Therefore, the distance from the incisors to the carina is approximately 26 cm (note the length markings on endotracheal tubes). The blood supply to the trachea is through the inferior thyroid artery, which comes from the thyrocervical branch of the subclavian artery. Some perfusion is also received from the superior thyroid, bronchial, and internal thoracic arteries. Blood is drained by the inferior thyroid veins. Sensory innervation of the trachea is via the vagus nerve for both parasympathetic and nociceptive stimuli.

The trachea has a diameter of approximately 2.5 cm and is supported by incomplete rings of cartilage that open posteriorly and prevent tracheal collapse under the negative pressure generated during spontaneous respiration. The trachea extends down to the level of T4-T5, where the carina is located. This level corresponds anteriorly to the angle of Louis on the sternum, which is the articulation of the second rib. The trachea is not a rigid structure; it expands and contracts to accommodate head and neck movement. In an intubated patient, flexion of the neck elevates the carina. As a result, the endotracheal tube moves downward and endobronchial intubation may result. During extension of the head and neck, the trachea moves downward, the endotracheal tube moves upward, and extubation can occur. In pediatric patients, the range of this movement was demonstrated to increase with patient age and height.⁷ The apparent movement of the endotracheal tube in relation to head flexion may seem paradoxical; the mnemonic “the hose follows the nose” can be used as a memory aid. Neck rotation to the left or right tends to cause tracheal elevation and risk of endobronchial intubation.

Respiratory Zone

The respiratory bronchioles and alveolar ducts, sacs, and alveoli comprise the respiratory zone, the area where gas exchange takes place. All parts of the airway prior to this (nose to terminal bronchioles) conduct gas without exchanging gas with the blood and are referred to as the conducting zone. Some refer to the respiratory bronchioles and alveolar ducts where limited gas exchange takes place as the transitional zone because structures here function both to conduct gas and also to participate in some gas exchange. The alveoli are the air sacs that are tightly packed and closely approximated with pulmonary capillaries. The typical maximum number of approximately 300 million alveoli is reached by age 9 years. The alveoli are characterized by very thin walls composed of squamous epithelium. There are three types of cells that form the alveoli: type I pneumocytes, which are the structural cells; type II pneumocytes, which produce surfactant to reduce alveolar collapse from surface tension; and type III pneumocytes, which are macrophages. The average alveolar diameter is approximately 250 µm; therefore the total surface area available for gas exchange is 60 to 80 m².¹⁰

Pulmonary Hila and Coverings

The nerve supply to the bronchi and lungs arises chiefly from the sympathetic nerves and the vagus nerve (which supplies sensory and parasympathetic innervation). All conduits to the lung pass through the hilum, which is the connection of the mediastinum to the pedicle of each lung. The structures included in each hilum include the mainstem bronchus, pulmonary artery and vein, bronchial arteries and veins (which drain into the azygos system), lymphatics, lymph nodes, pulmonary nerve plexuses, and pulmonary ligament. All of this is surrounded by connective tissue. The serous membrane covering the lung is called the pleura. The parietal pleura lines the chest wall, mediastinum, and diaphragm, and at the hilum is then reflected back to cover the lungs as the visceral pleura. Between these two layers is a potential space called the pleural cavity. The touching surfaces of the two layers of pleura are kept slippery by a small amount of serous fluid. Certain conditions can result in occupation of the pleural space by liquids or gas (Table 26-2) and may affect ventilation and lung expansion. Infected intrapleural blood can clot and organize to form a fibrothorax, which must be peeled from the surface of the lung (in a procedure called lung decortication) so the lung can reexpand.

Mediastinum

The mediastinum is the region between the two pleural sacs. It lies roughly in the center of the thoracic cavity but is slightly displaced to the left by the presence of the heart. Therefore the left lung represents 45% of the total lung capacity (TLC), whereas the right lung represents 55%. Perforation of the larynx, trachea, pharynx, or esophagus, which sometimes occurs during esophagoscopy, bronchoscopy, or traumatic intubation, can produce mediastinitis, a life-threatening infection of an area containing the trachea, esophagus, and major blood vessels and heart. The mediastinum is divided into four divisions separated by the pericardium (Table 26-3). Common procedures involving the mediastinum include coronary artery bypass, cardiac valve replacement, aortic aneurysm repair, thymectomy for myasthenia gravis, resection of tumors, and mediastinoscopy for diagnosis and staging of cancer.

Pleura

The pleura is a serous membrane that lines the thoracic wall and lungs. The parietal pleura is attached to the chest wall, diaphragm, and mediastinum but is then reflected back to cover the lungs and afterward referred to as the visceral pleura. These two layers are closely opposed, with only a capillary-thin layer of pleural fluid between them in a potential space known as the pleural space. The parietal pleura is very sensitive to pain, and conditions that cause accumulation of pleural fluid or friction between the layers can be very uncomfortable. Different areas of the pleura may produce characteristic pain patterns: the costal pleura creates localized pain, the diaphragmatic pleura creates diffuse pain, and areas supplied by the phrenic nerve may radiate pain to the neck or back. Posterior to the mediastinum, the pleura doubles up and descends downward as the “pulmonary ligament.”

If communication is created across the pleura, accumulation of air in the pleural space is referred to as pneumothorax. In a closed chest (e.g., a pulmonary bleb ruptures, creating a communication to the pleural space) a tension pneumothorax develops as inspired air accumulates in the pleural space and is not expelled. With an opening through both pleura (such as with open chest trauma) the external wound may create a simple pneumothorax, which does not tend to cause high intrathoracic pressures. In either type of pneumothorax, the elastic recoil of the lung tends to favor lung collapse once the negative pressure of the pleural space is disrupted by the breach.

Lung Compliance

Lung compliance is defined as the change in volume divided by the change in pressure (V/P). For a given change in pressure, a more compliant lung has a greater change in volume than a less compliant one. Figure 26-2 shows pressure-volume relationships for a lung. As with many concepts in respiratory physiology, the reader must make the jump from considering the application to a single alveolus (which aids in understanding) to conceptualizing the overall average state in the pulmonary system, which involves many regions existing along a continuum of conditions. In considering lung compliance, the curve in Figure 26-2 represents the collective contribution of alveoli that are almost collapsed at the beginning of inspiration, alveoli that are distended, and alveoli that exist at various intermediate volumes.

Static effective compliance describes the pressure-volume relationship for a lung when air is not moving; that is, reflecting compliance of the lung and chest wall alone. Static compliance is decreased by conditions that make the lung difficult to inflate, such as fibrosis, obesity, vascular engorgement, edema, acute respiratory distress syndrome (ARDS), and external compression (e.g., that caused by tight dressings or a surgeon leaning on the patient’s chest). Static compliance is increased by emphysema, which destroys the elastic tissue of the lung. This makes the emphysematous lung easier to inflate. The problem with emphysema is not inflation but rather deflation, because the loss of elastic tissue results in small airway collapse as the lung deflates, which causes gas trapping. It is important to note that compliance changes as lung volume changes. In other words, compliance is volume dependent. Figure 26-2 shows that the lung is less compliant both at very low and at very high lung volumes. Alveoli require greater pressure to be inflated when they are almost empty or almost full, respectively. When an alveolus is collapsed, a great increase in pressure is necessary for inflation to begin. Observe in Figure 26-2 that the slope of the inspiratory curve is less at both low volumes and very high volumes. At low volumes, it takes more energy (more negative pressure, i.e., less compliant) to begin to expand the lungs. At high volumes, the alveoli are almost at capacity, and further changes in pressure result in less change in volume (less volume per given pressure = less compliant). As you follow the curve along the expiratory side, notice that an initial increase in pressure (with slower volume change) as the chest wall relaxes is followed by a smooth reduction in volume back to the resting level. Lung compliance results from the interplay of various factors that tend to either expand the lungs or restrict lung expansion. Much of the energy required to expand the lungs, particularly at low volumes, is created by surface tension in the fluid lining of the alveoli, which tends to attract the alveoli toward a smaller volume. Perhaps counterintuitively, a lung filled with fluid (and therefore without an air/fluid interface and the resulting surface tension) has a very high compliance—it requires much less energy to expand. Although not a high-fidelity measurement, static effective compliance can be calculated easily using the following equation:

Plateau pressure is the pressure observed if you retard exhalation momentarily when the lungs are at end-inspiration. An inspiratory pause on the ventilator is an easy way to observe the plateau pressure. After subtracting the added pressure of PEEP, the plateau pressure is then divided into the measured tidal volume of that breath, producing a measure of lung compliance. A static compliance of 60 to 100 mL/cm H₂O is considered normal. However, the most useful clinical application of compliance measurement is in monitoring trends to evaluate changing physical status or the effectiveness of positive end-expiratory pressure (PEEP) or other treatment modalities.

Dynamic compliance is the compliance of the lung while the air is moving. Dynamic compliance is influenced by the forces involved in static compliance as well as the effects of airway resistance. Airway obstruction (e.g., that caused by bronchospasm or the presence of foreign bodies in the airway) can greatly decrease dynamic compliance.¹¹ Dynamic compliance is calculated as the tidal volume divided by peak inspiratory pressure − PEEP. Many modern anesthesia ventilators can calculate and trend compliance through tracing of pressure-volume curves.

Lung Elastic Recoil

The forces that cause elastic recoil of the lung are responsible for emptying the lung during exhalation and have a significant influence on lung compliance. In addition to actual elastic fibers, the surface tension of the liquid film that lines the alveoli contributes to elastic recoil of the lung. Surface tension occurs at a gas/liquid interface and is generated by the cohesive forces among the molecules of the liquid. Surface tension is what causes water to bead and form droplets.

Surface tension at the gas-fluid interface between the alveolar walls and the gas inside them contributes to reducing the size of alveoli, particularly when the alveoli are at low volumes. At end-expiration, surface tension increases the pressure required to inflate the alveoli, contributing to the flat portion of the lung compliance curve. This concept is often attributed to the law of Laplace (P = T/r), which states that if surface tension (T) is constant, pressure (P) would increase as radius (r) decreases. Pulmonary surfactant secreted by alveolar type II cells counteracts the influence of surface tension on the lungs. With surfactant present, as alveolar radius decreases, surface tension also decreases, so that pressure remains more constant. Surfactant consists of proteins and phospholipids, primarily, dipalmitoylphosphatidylcholine. The surface active agent serves to lower the surface tension of the fluid lining the alveoli and decrease the work of breathing.

Although the law of Laplace has traditionally been applied to understanding alveolar pressure-tension relationships, there is controversy over whether alveoli should be treated as spherical (and thus subject to the law) or not. Geometricians postulate that closely packed alveoli would not maintain the shape of spheres, but rather of polyhedrons because their sides would be flattened against each other. The classical application of LaPlace described the concept of alveoli as distinct balloon-like structures wherein pressure differentials can cause small alveoli to collapse and expel their gas into larger ones. The fact that alveoli are not individually suspended, but rather part of a connective tissue mesh, argues against this concept. The presence of pores of Kohn also argues against this theory, because the pores allow pressure equalization between adjacent alveoli. Connective tissue and elastic forces probably play the most important role in preventing alveolar closure.¹²

In any case, it is clear that surfactant is crucial for reducing surface tension and preventing collapse of alveoli and, perhaps more importantly, small airways. The cylindrical shape of airways lends to the application of the law of LaPlace to the role of surfactant in these structures. Surfactant probably also helps prevent fluid bridging (connection of fluid lining from opposite sides of an airway at low volumes), which could impair gas flow.¹³ In the fetus, surfactant is not produced until approximately 28 to 32 weeks of gestation and does not reach mature levels until approximately 35 weeks’ gestation. The lack of surfactant is the prevalent cause of respiratory distress syndrome (RDS) in premature infants. Formation of surfactant can be hastened by the administration of glucocorticoids (particularly a steroid that crosses the placenta, such as betamethasone) to the parturient mother when premature delivery is threatened or imminent. The direct administration of synthetic surfactant to the airways of premature newborns has also greatly reduced the incidence of RDS. Amniocentesis is sometimes performed to determine whether mature surfactant levels are present in the premature fetus. The ratio of lecithin to sphingomyelin (the L/S ratio) indicates the amount of mature surfactant (dipalmitoyl lecithin) in proportion to the amount of surfactant precursor (sphingomyelin).

Respiratory Pressure

Although the elastic forces of the lung tend to favor lung collapse, the chest wall is constantly under tension to expand. This is why normal inspiration requires very little energy. At the end of eupneic exhalation, the outward recoil of the chest wall is balanced by the inward elastic recoil of the lung. At this resting end-expiratory point, the opposing forces of the lungs and chest wall produce negative pressure in the pleural space.

The difference between intraalveolar pressure and intrapleural pressure is called the transpulmonary pressure. Under normal circumstances, the pleural pressure is always slightly negative, owing to the opposing forces of lung tissue contraction and chest wall expansion. The intrapleural pressure becomes slightly more negative during inspiration and slightly less negative during expiration. The transpulmonary pressure fluctuates as the alveolar pressure oscillates between slightly negative during inspiration to slightly positive during expiration, returning to zero whenever airflow is stopped at end-inspiration or end-expiration (Figure 26-3). During normal inspiration, intraalveolar pressure fluctuates only by 1 to 2 mmHg. Therefore very little pressure is applied during eupneic ventilation. During maximal expiration with a closed glottis (such as during coughing), intraalveolar pressure may exceed 100 mmHg, whereas during obstructed inspiration, it may be reduced to as low as −90 mmHg. During the first few breaths of life, a newborn can attain an intraalveolar pressure from −40 to −60 mmHg as the fluid-filled lungs are first aerated. In conditions of low lung compliance, more work is required to expand the lung, and the transpulmonary pressure rises (greater difference between intrapleural and intraalveolar pressure required to increase the lung volume).

Resistance to Breathing

In addition to the static elastic recoil of the lung, frictional resistance of lung tissues and resistance to airflow opposes inflation of the lung. Rheologic characteristics of airflow affect its ability to pass through conducting airways. Laminar flow is an orderly movement, where molecules are moving along a generally straight path. In laminar flow, the gas in the center of the stream moves faster than that closer to the wall because frictional resistance slows molecules near the vessel wall. Laminar flow is characterized by lower pressure than turbulent flow. During turbulent flow, resistance greatly increases because molecules move in various directions. The rheologic calculation of Reynolds number predicts when flow of a fluid (or gas) will be laminar or turbulent. Reynolds number (Re) is calculated as follows:

Throughout the airways, both laminar and turbulent flows occur. True laminar flow occurs in smaller airways, where the diameter is small and linear velocity is very low. Linear velocity is inversely proportional to cross-sectional area for any flow rate. Turbulence is greatest in large airways, and turbulence caused by branching of the airways produces the breath sounds heard on auscultation. Resistance to laminar flow follows Poiseuille’s law (R = 8ηl/r⁴, where η equals viscosity). Resistance (R) to laminar airflow is directly proportional to the length (l) of the tube and inversely proportional to the fourth power of the radius (r). Therefore doubling the radius of the tube decreases resistance 16 (2⁴) times. Normally, about 40% of the total airway resistance resides in the upper airways (nasal cavity, pharynx, and larynx).

Although resistance to airflow is greatest in individual small airways, the net total resistance to airflow of the small airways is very low because they represent a massive number of parallel pathways. Under normal circumstances, the greatest resistance to airflow resides in medium-sized bronchi, whose smooth muscle tone greatly affects airway resistance. During lung inflation, increasing lung volumes exert retractive forces on the airways, resulting in a reduction in airway resistance. During forced expiration, dynamic compression of the airways increases airway resistance and may promote airway collapse (most likely in small airways with no cartilaginous support).

The clinical application of these concepts resides in strategies to reduce airflow resistance. Bronchodilators will reduce resistance to airflow by increasing the radius of the pathway, as predicted by Poiseuille. Selection of an endotracheal tube size may confer greater or lesser resistance, based on the length and (much more significantly) the internal diameter of the tube. Clinical application of Reynolds number suggests that lower velocity (lower inspiratory flow or lower inspiratory:expiratory ratio) and lower density would promote laminar flow and create lower ventilating pressures. The reduction in density is the conceptual basis for combining helium with oxygen (“heliox”) to improve pulmonary gas distribution in obstructive lung disease.¹⁴

Other influences on airflow include the autonomic nervous system and pathologic conditions. The autonomic nervous system affects the tone of the bronchial smooth muscle. The sympathetic nervous system, as well as sympathomimetic drugs (e.g., norepinephrine, epinephrine, and isoproterenol), produce bronchodilation. The parasympathetic nerves and parasympathomimetic drugs (e.g., acetylcholine) cause bronchoconstriction. Parasympatholytic drugs (e.g., atropine and ipratropium) therefore cause bronchodilation (though mildly). Irritation of the airway by foreign bodies or inhaled irritants causes reflex bronchoconstriction.

Lung Volumes

The following discussion of lung volumes uses the parameters of a normal 70-kg male. Table 26-4 gives an overview of related terms and normal values. The amount of gas that enters and leaves the body with each eupneic breath is approximately 350 to 500 mL and represents the tidal volume (V_T). The minute volume (MV) equals V_T multiplied by the respiratory rate. However, because some ventilation occupies the conducting zone, only a portion of the minute ventilation (e) participates in gas exchange. The amount of alveolar ventilation in a minute equals V_T minus anatomic dead space (the volume of the conducting airways, which is approximately 2 mL per kg of body weight) multiplied by the ventilatory rate. The rate of alveolar ventilation will be indirectly proportional to the arterial CO₂ tension. The residual volume (RV) is the volume of gas left in the lung after a maximal exhalation (approximately 1.5 L). The RV cannot be removed from the lungs voluntarily and is important because it is a component of the functional residual capacity, which represents alveolar gas used for oxygenation of the blood between breaths or in periods of apnea. The expiratory reserve volume is the volume of gas expelled from the lungs during a maximal forced exhalation, starting at the end of a normal tidal exhalation. The inspiratory reserve volume is the volume of gas inhaled into the lungs during a maximal forced inhalation, starting at the end of a normal tidal inspiration (2.5 L).

The sum of the four basic lung volumes is the total lung capacity (TLC). Several types of lung capacity measures exist, each of which is the sum of two or more lung volumes. TLC is the volume of air in the lungs after a maximal inspiratory effort (approximately 6 L in a 70-kg adult). The vital capacity is the amount of air that can be forcibly exhaled from the lungs after a maximal inspiratory effort (approximately 4.5 L). The functional residual capacity (FRC) is the volume of gas contained in the lungs after normal quiet expiration. It is the sum of the RV and expiratory reserve volume (approximately 3 L). The inspiratory capacity is the volume of air inhaled into the lungs during a maximal inspiratory effort that begins at FRC (approximately 3 L). Figure 26-4 gives a graphic representation of lung volumes and normal flow measurements.

Closing volume describes the phenomenon during exhalation when small airways collapse, hindering further emptying of lung units distal to them. Closing volume is defined as the volume above residual volume where small airways close, whereas closing capacity describes the absolute volume of gas in the lung when small airways close (the closing capacity is the sum of the closing volume plus the residual volume). The closing volume increases from approximately 30% of the TLC at age 20 years to approximately 55% at age 70 years. Certain conditions increase the closing volume, such as supine positioning, pregnancy, obesity, COPD, congestive heart failure, and aging.¹⁵ In abnormal conditions, if the closing volume exceeds the FRC, airway closure occurs during tidal breathing, resulting in poorly ventilated or unventilated alveoli and intrapulmonary shunting. The shearing forces of repetitive airway opening and closing also leads to airway injury.¹⁶ Measurement of closing volume analyzing washout characteristics of inert gas is a more sensitive indicator of small airway disease (such as from smoking) than is measurement of spirometry.¹⁵

Dead Space

Dead space refers to ventilation that does not participate in gas exchange. The volume of the conducting airways represents the anatomic dead space and normally equals approximately 2 mL/kg of body weight. Alveoli that are ventilated but not perfused comprise the alveolar dead space because they do not deliver oxygen nor do they remove CO₂ from the blood. The sum of the anatomic dead space plus the alveolar dead space is the physiologic dead space (V_D). Because perfused ventilation equilibrates with arteriolar CO₂ and nonperfused (dead space) ventilation does not, the proportion of dead space ventilation can be calculated by comparing the ratio of CO₂ in the arterial blood and in the exhaled gas. This is calculated with the Bohr equation:

Regional Distribution of Alveolar Ventilation

Gravity and other factors influence ventilation and perfusion such that both are unevenly distributed throughout the lungs. In the normal upright lung, the alveoli at the base are more compliant than those at the apex, meaning that those at the base exhibit a greater change in volume with each breath. This is considered to be a result of the effect of gravity on the interconnected parenchyma of the lung, whereby the greatest “pull” is exerted on the more superior portions of lung. Therefore, the alveoli in those areas are held in a more open state even at rest, whereas alveoli at the base are more compressed. During inspiration then, the alveoli at the bases are able to accept more new gas (Figure 26-5). Alterations to the resting volume or impingements on lung compliance may change this relationship. Pregnancy or obesity may hinder expansion of lower units or may cause compression that results in collapsed dependent areas. In that case, other lung areas become the most compliant. The sigmoidal shape of the compliance curve (see Figure 26-2) reveals that alveoli become less compliant at higher volumes (e.g., in nondependent alveoli at high lung volume) and also at very low volumes (e.g., in dependent alveoli at very low resting lung volumes).

Alveolar Oxygen and Carbon Dioxide Levels

The levels of O₂ and CO₂ in alveolar gas are determined by several factors. These include the amount of alveolar ventilation, the inspired concentrations of O₂ and CO₂, the flow of mixed venous blood to the lungs, and the body’s consumption of O₂ and production of CO₂. In a person spontaneously breathing room air, each breath brings approximately 350 mL of fresh air (21% of which is O₂) into the alveoli, which already contain over 2 L of gas (the FRC). Each exhalation removes approximately 350 mL of gas consisting of 5% to 6% CO₂. Every minute, approximately 250 mL of O₂ diffuse from the alveoli into the pulmonary capillary blood, whereas approximately 200 mL of CO₂ diffuse from the pulmonary capillary blood into the alveoli. The ratio of the amount of CO₂ produced to the quantity of O₂ consumed is called the respiratory quotient (RQ = 200 mL CO₂ produced divided by 250 mL O₂ consumed = 0.8). The proportion of CO₂ production and O₂ consumption varies with energy source (greater with more carbohydrates and lower with more fat), but 0.8 is the typical result from a mixed diet.

Approximately 21% of dry atmospheric air is O₂; therefore, at the standard barometric pressure of 760 mmHg, Po₂atm equals 0.21 × 760 mmHg, or 160 mmHg. Only 0.04% of atmospheric air is CO₂, so Pco₂atm = 0.3 mm Hg. As the inspired air passes through the upper airways, it is heated to body temperature and humidified to a relative humidity of nearly 100%. The partial pressure of water vapor at body temperature is a fairly constant 47 mmHg. The Po₂ of inspired air (Pio₂) saturated with water vapor at standard atmospheric pressure = 0.21 × (760 mmHg − 47 mmHg), or 149 mmHg.

The inspired gas mixes with the gas already in the alveoli (FRC) and rapidly equilibrates with the pulmonary capillary blood. The alveolar Po₂ (Pao₂) can be calculated with the alveolar air equation:

Effects of Alveolar Ventilation on Carbon Dioxide and Oxygen

Within certain limits Paco₂ is inversely proportional to alveolar ventilation. If alveolar ventilation is doubled, then Paco₂ and Paco₂ are reduced by half (if CO₂ production remains unchanged).

As alveolar ventilation increases, Pao₂ also increases slightly. However, doubling alveolar ventilation does not double Pao₂; according to the alveolar air equation, reduction of the Paco₂ raises the Pao₂, bringing Pao₂ closer to the Pio₂.

Influences on Pulmonary Blood Flow

Although pulmonary vessels have less muscular content than systemic arteries, the low pressure of the system makes pulmonary blood flow very sensitive to small changes in arterial tone. Unlike the systemic circulation, where hemodynamic influences are more global, pulmonary blood flow is more prevalently regulated locally by changes in oxygen and carbon dioxide tension. In contrast to the systemic circulation, high oxygen tension and hypocapnea vasodilates pulmonary vessels (which helps those vessels pick up more oxygen), whereas hypercarbia and acidosis cause vasoconstriction. Having the strongest influence on pulmonary local regulation, blood flow to hypoxic or atelectatic alveoli is actively diverted at a precapillary site by a process known as hypoxic pulmonary vasoconstriction. This decreases blood flow away from focal diseased areas of the lung and improves matching of ventilation and perfusion. See Chapter 27 for a discussion of the significance of hypoxic pulmonary vasoconstriction during pulmonary surgery.

Relationship of Pulmonary Blood Flow and Ventilation

In the normal upright lung, a greater portion of the blood flow is distributed to the dependent regions because of the effects of hydrostatic pressure and greater distention of dependent pulmonary vessels. Likewise, differences in compliance of the ventilating tissue also result in a general increase in the proportion of ventilation from nondependent (least ventilation) to dependent (most ventilation) of the lungs. There are two caveats to these rules. Although they fit the spontaneously breathing patient fairly well, the spatial distribution of these relationships are altered during positive-pressure ventilation. Also, the lung zones are commonly portrayed in textbooks in nicely demarcated lines of latitude, a model appreciated for its simple elegance.

Although there may be a general increase in perfusion from top to bottom of the lung, it should be noted that gravity alone does not determine physiologic perfusion. If it did, then it would be observed that the greatest blood flow in the body would be in the lower extremities, with the least in the head, a cogent point of explanation offered by Levitzki.²¹ Gravity interacts with elastic forces to influence ventilation and with vessel recruitment to alter distribution of perfusion. There is evidence that regional perfusion zones may be situated with the greatest blood flow in the lower, core areas of the lungs, with zones 2 and 1 more resembling concentric spheres radiating toward the periphery.²² Nonetheless, the classic explanation of ventilation-perfusion zones described by West in 1964 serves as a useful model for considering the relationships between ventilation and perfusion,²³ and more specifically, the conditions under which intraalveolar pressure may impede vascular flow.²⁴ In this model, regions of the lung are considered in zones, according to the relative intravascular and intraalveolar pressure (Figure 26-6).

In the parts of the lung where alveoli exist at a greater resting volume, alveolar pressure can exceed pulmonary artery pressure (PAP), so that perfusion is impeded. This is called zone 1 and represents alveolar dead space because the region is ventilated but not perfused. Normally, zone 1 exists only in a very small margin of lung area around the apical border during spontaneous ventilation, but the use of PEEP or high airway pressures during mechanical ventilation can create or expand this zone.

The intermediate zone, where there is a variable relationship between vascular and alveolar pressure, is zone 2. A point is described in zone 2 along the continuum of decreasing intraalveolar pressure where arterial pressure exceeds alveolar. Below that point, flow is solely dependent upon arterial flow, and unrelated to alveolar or venous pressure. This concept is described as a waterfall zone, as when rising water finally overflows a dam. At that point, the height of the dam does not influence the flow, only the upstream inflow does. The zone 2 relationship is not static, but fluctuation in alveolar pressure related to respiration can variably occlude capillary flow.

The dependent portion of the lung, where both pulmonary arterial and venous pressures exceed alveolar pressure, is known as zone 3. This zone represents continuous blood flow, and it is in this zone that the tip of a pulmonary artery catheter should lie, for example, to ensure continuous communication with the left heart. Alveoli in this zone rest at a lower volume than in zone 1, and so they have greater compliance and represent the greatest proportion of ventilation in the lung; however, the perfusion is also greatest here, and so there is no obstruction to blood flow. West later described a fourth zone in the most dependent portions of lung, wherein extravascular pressure from mechanical compression or interstitial fluid compresses the vessels and occludes their flow.²⁵

Pulmonary Edema

The normal distance for diffusion from the alveolar air space into the pulmonary capillary blood cells is less than 1 micrometer. The gas must traverse the surfactant layer, the flat alveolar type I cells, the interstitial space, the endothelial cells that make up the wall of the pulmonary capillary, a minute amount of plasma, and then finally the membrane of the red blood cell. The pulmonary system is designed to allow free passage of gases across this series of structures, collectively called the respiratory membrane. However, that inherent “leakiness” does predispose this area to unintended movement of fluid.

There is a fine balance between the plasma colloid oncotic pressure, which tends to hold fluid in the pulmonary capillaries, and the capillary hydrostatic pressure, interstitial fluid colloid oncotic pressure, and negative interstitial fluid pressure, which all tend to favor fluid movement into the interstitial space. In normal circumstances, the net of these forces favors movement into the interstitium, helping to divert fluid from the adjacent “leaky” capillaries away from the alveoli and thereby prevent accumulation there.²⁶ Although the interstitium has a large compliance for removing accumulating transudated fluid, derangements in the factors above can lead to fluid accumulation in the interstitium or alveoli and disrupt gas exchange.

Pulmonary vascular congestion causes increased capillary leakage into the interstitium, which can increase the distance for gas diffusion. If the capillary leak overcomes the compliance of the interstitial space, the fluid may then begin to pass into the alveoli. Pulmonary edema affects oxygenation more than CO₂ excretion because CO₂ is 20 times more diffusible than O₂. Many conditions can result in pulmonary edema. The high capillary pressures associated with heart failure or the excessive administration of intravenous fluids can increase lung water content. The size of the pulmonary capillary pores can be increased by sepsis, smoke inhalation, and other toxic conditions. Brain trauma can produce an intense sympathetic discharge, resulting in neurogenic pulmonary edema.

A condition that occasionally occurs during emergence from anesthesia is postobstructive pulmonary edema, also referred to as negative-pressure pulmonary edema (NPPE). After extubation, if the patient experiences laryngospasm and then attempts forceful inhalation against the closed glottis, the drastic decrease in intrathoracic pressure pulls fluid from the pulmonary capillaries. The onset of pulmonary edema is rapid and relatively easy to treat. The symptoms resolve rapidly; in most cases, patients are discharged within 24 hours. Treatment includes removing the precipitating condition (relieving airway obstruction) and general supportive measures: oxygen, maintenance of a patent airway, noninvasive continuous positive airway pressure (CPAP), and intubation with PEEP if required to maintain oxygenation. Unlike pulmonary edema related to fluid overload, NPPE does not call for diuretic therapy. However, many reported cases do include the use of controversial treatments of diuretics and corticosteroids.²⁷ The three mainstays of treatment remain treatment of the precipitating condition, normalization of ventilation and oxygenation, and reduction of lung congestion and fluid. Treatment summary is in Box 26-4.

Ventilation-Perfusion Relationships in the Lung

Normally, ventilation () is approximately 4 L/min, whereas pulmonary blood flow () is approximately 5 L/min. Therefore, the ventilation-perfusion ratio () for the whole lung is 0.8. However, and must be matched at the alveolar-capillary level for gas exchange to occur in the lung.

Dependent portions of the lung receive relatively more blood flow than nondependent portions because of the effects of gravity and vessel recruitment and distensibility. Additionally, ventilation goes to the more compliant portions of the lung. Normally at FRC, the dependent regions of the lung are more compliant, and the alveoli of the nondependent portions are more inflated (“tented open”) and less compliant. Therefore, relatively more ventilation and perfusion go to the dependent portions, and this results in optimal gas exchange.

Although distribution of ventilation normally decreases moving from dependent to nondependent regions of the lung, the accompanying decrease in perfusion is even greater; therefore the ratio, , increases as measured progressively from dependent to nondependent lung areas (Figure 26-7). Also, varies: in alveoli that are ventilated but not perfused, equals 0, so equals infinity (i.e., dead space); in alveoli that are perfused but not ventilated, equals 0, so equals 0 (i.e., a shunt). Similarly, alveoli that are ventilated but poorly perfused are described as “deadspace-like,” whereas alveoli that are perfused but poorly ventilated are termed shuntlike

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