Initially, the laryngotracheal diverticulum includes the esophagus and the trachea as a single tube. Then longitudinal ridges begin to develop along the tube and form a septum (wall), which separates the esophagus from the trachea. Failure of this septum to develop leads to a tracheoesophageal fistula (abnormal opening), leaving a communication between the esophagus and the trachea. This abnormality occurs about once in every 2500 births. Approximately 90% of the cases of esophageal atresia (blind pouch) are of the type seen in Figure 21-1, A. Parts B through D show variations of tracheoesophageal fistulas.¹

Fetal lung development can be divided into the following four periods:

The respiratory system can be divided into two major anatomic areas: the upper airway and the lower airway. The upper airway consists of the nasopharyngeal cavity (nasopharynx, oropharynx, laryngopharynx) (Figure 21-2). The lower airway contains the larynx, trachea, bronchi, bronchopulmonary segments, terminal bronchioles, and the acinus (the alveolar region supplied by one terminal bronchiole, which includes numerous alveoli) (see Figure 21-2).

Air is filtered by the large hairs (vibrissae) of the nasal cavity and cilia that line the nasal cavity. The cilia sweep foreign particles trapped by mucus into the nasopharynx, where they are swallowed or expectorated. An electron micrograph of the tracheobronchial lining is shown in Figure 21-3. Pseudostratified ciliated columnar epithelium lines the trachea and bronchi. Goblet cells and mucus-producing glands are contained in this area and are responsible for synthesizing approximately 100 ml/day in the adult, more with disease. The composition of mucus is 95% water with the remaining 5% consisting of mucopolysaccharides, mucoproteins, and lipids. Maintenance of water content and fluid balance is important to the mobilization of secretions. A child has more mucus-producing glands and therefore produces more mucus than an adult. Consequently, in an ill child the overproduction of mucus in combination with small airway size may precipitate tracheobronchial obstruction.^2,3

Cilia (Figure 21-4) beat in a sweeping motion like oars rowing a boat at approximately 1000 to 1500 strokes per minute.^2,3 Mucociliary transport (movement of mucus upward) is a primary defense mechanism of the tracheobronchial tree. Inhaled particles, bacteria, and macrophages are removed from the respiratory tract by ciliary clearance and the cough reflex. Ciliary function is impaired by smoking, alcohol ingestion, hypothermia, hyperthermia, cold air, low humidity, starvation, anesthetics, corticosteroids, noxious gases, the common cold, and increased mucus production.^2,3

The eustachian tube between the middle ear and the posterior nasopharynx maintains the air in the middle ear at atmospheric pressure. To prevent secretions or food from entering the middle ear during swallowing, the pharyngeal muscles close the eustachian tube briefly. The nasal end of the eustachian tube is surrounded by flexible cartilage arranged in a spiral configuration. The muscles surrounding the eustachian cartilage close the opening by pulling the cartilage tighter. Because the tube is shorter in children, the potential for otitis media (infection of the middle ear) is increased.2,3

After air passes through the nasal cavity or oral cavity into the pharynx, it moves into the larynx and finally into the tracheobronchial tree. The acinus (Figure 21-5) is located at the end of the tracheobronchial tree and is composed of bronchioles, alveolar ducts, and alveoli.

The larynx is the transition area between the upper and lower airways. Anatomically it is considered part of the lower airway, but functionally it is similar to the upper airway. The larynx contains the epiglottis, vocal cords, and cartilages. The anatomic arrangement of the larynx functions to prevent aspiration during swallowing and to assist in phonation and coughing. Each vocal cord is attached anteriorly to the thyroid cartilage and posteriorly to the arytenoid cartilage. Vibration of the cords leads to phonation. Food is prevented from entering the trachea during swallowing by closure of the epiglottis. If food or fluid should bypass the epiglottis and enter the tracheobronchial tree, the cough reflex is initiated. The majority of cough receptors lie at the carina. A cough reflex is produced when the epiglottis and vocal cords close tightly against air entrapped in the lungs. Occasionally, individuals cough hard enough to break a rib. When the expiratory muscles contract forcefully against the closed epiglottis and vocal cords, a pressure of approximately 100 mm Hg is created. When the cords and epiglottis suddenly open, the high-pressure buildup is allowed to escape. This reflex rapidly removes foreign matter from the tracheobronchial tree.2,3

The major cartilages of the larynx are the thyroid, cricoid, and arytenoid. The thyroid cartilage is a large shield-shaped cartilage often referred to as the Adam’s apple. Immediately below the thyroid cartilage is the site for emergency opening (cricothyroidotomy) of the tracheal passageway. The cricoid cartilage lies below the thyroid cartilage and is the narrowest point in the airway of a child. It is the only complete tracheal ring, and because of its narrowness in the small child’s airway, an endotracheal tube cuff is not necessary for required intubation of the airway.

The trachea, bronchi, and bronchioles make up the conducting airways that allow passage of gases to and from the gas exchange units (alveoli). These conducting airways comprise a proportionately larger amount of the total airway system in the infant and child than in the adult. The trachea (Figure 21-6) contains incomplete cartilaginous rings; it is approximately 11 to 13 cm long and lies between the cricoid cartilage and the carina (ridge located at the lower end of the trachea). Individual variations in tracheal shape include U, circular, D, C, triangular, and elliptical (Figure 21-7). Of 111 adult tracheas studied, the incidence of shapes in order of frequency was 48.6% C, 27% U, 12.6% D, 8.2% elliptical, 1.8% circular, and 1.8% triangular.⁴ These tracheal variations may affect ventilation of patients who have endotracheal tubes in their airways and require mechanical ventilation.

The trachea divides into two mainstem (primary) bronchi, which contain cartilage and smooth muscle. Viewing the body anteriorly, the carina is located at the angle of Louis, between the sternum and manubrium at the second intercostal space.

The small size of the conducting airway in the infant and child makes even a small decrease in the size of the lumen from an obstruction critical to airway conduction.5 Primary bronchi further divide into five (secondary) lobar branches, three to the right lung and two to the left lung. Each lobar branch enters a lobe of the lung and further divides into bronchopulmonary segments (10 segments in the right lung, 9 segments in the left lung) (Figure 21-8).^2,3 Each bronchopulmonary segment is composed of 50 or more terminal bronchioles (conducting airways), which branch into respiratory bronchioles, where gas exchange begins.

Terminal bronchioles, which include the conducting airways, further subdivide into two or more respiratory bronchioles in which gas exchange begins. The respiratory bronchioles divide into two or more alveolar ducts, which in turn supply several alveoli.

Nervous system control of the bronchi and bronchioles is mediated by the autonomic nervous system. Stimulation of the parasympathetic nervous system via the vagus nerve leads to constriction (by means of acetylcholine receptors) of bronchial smooth muscle. Stimulation of the sympathetic nervous system leads to relaxation of bronchial smooth muscle. Sympathetic stimulation is mediated by β₂-adrenergic receptors, which are under the control of circulating catecholamines.5 (See the discussion in the Neurologic Control of Ventilation section later in this chapter for additional information.)

The lung is fully developed by the eighth year of life.^1,2 The large alveolar surface area in conjunction with pulmonary surfactant, a phospholipid produced by type II alveolar cells, lowers surface tension and facilitates gas exchange. Two other types of cells are found: type I alveolar cells (type I pneumocytes), which are the epithelial structural cells of the alveoli, and alveolar macrophages, which act as a defense mechanism by phagocytizing particles in the alveoli. Alveolar macrophages can be damaged by cigarette smoking and by inhalation of silica (SiO₂).

Adult lungs contain approximately 300 million alveoli, and the newborn lung contains one eighth to one sixth the adult number.^1–3 An elderly person may also have a reduction in the number of alveoli as part of the normal aging process, but many elderly people retain the same number of alveoli they had as a younger adult.

Gas exchange occurs in the alveolar units (see Figure 21-5) where oxygen (O₂) and carbon dioxide (CO₂) transfer across the alveolar-capillary membrane. The partial pressures of gases in the alveoli are termed PAO₂ for oxygen and Paco₂ for carbon dioxide. The partial pressures of gases in the blood are termed Pao₂ for oxygen and Paco₂ for carbon dioxide. Collateral alveolar ventilation can also occur through holes in the alveolar walls, called the pores of Kohn or canals of Lambert. A small child has less collateral ventilation, because of fewer pores of Kohn.⁶ The alveolar membrane is thicker in the neonate and reaches the adult thinness of 0.5 mm by the age of 8 years. This thinner membrane may allow increased transfer of O₂. The healthy older adult has very thin-walled, enlarged air sacs and fewer capillaries than a younger adult.^2,7 Respiratory system changes associated with normal aging are described in Geriatric Considerations: Changes in the Respiratory System.

GERIATRIC CONSIDERATIONS

Changes in the Respiratory System

With aging, the result of all pulmonary changes is an increase in the work of breathing. The lungs show a reduction in the amount of elastin and an increase in collagen concentration, leading to decreased elastic recoil and increased compliance. These changes lead to increased residual volume and early airway closure. The chest wall becomes stiffer or more rigid as a result of rib and cartilaginous calcification. The strength of the diaphragm, intercostal muscles, and accessory muscles declines. The stiff chest wall and diminished respiratory muscle strength cause other functional changes, including an increase in dead space and decreased expiratory flow rates and vital capacity.

There is a reduction in the number and motility of cilia, resulting in a decrease in respiratory clearance. There is an increase in and hypertrophy of bronchial mucous glands. The decreased respiratory muscle strength, increased mucus production, increased chest wall stiffness, and loss of cilia together reduce cough effectiveness.

Within the lungs, there is enlargement of alveoli and respiratory bronchioles with subsequent decreased surface area. The arterial blood flow through the pulmonary vessels decreases proportionally to changes in cardiac output. The loss of elastic recoil causes the enlarged respiratory bronchioles to collapse or close before the alveoli empty. Alveolar enlargement, along with reduced pulmonary artery blood flow and early airway closure, lowers diffusion capacity and the amount of gas exchange. It also increases air trapping and residual volume.

Because of chest wall stiffness and lung rigidity, apical ventilation increases in the elderly, whereas basilar ventilation decreases. Ventilation-perfusion mismatch occurs as a result of increasing apical ventilation with poor apical capillary blood flow. The result of these changes leads to reduced arterial oxygen pressure (Pao₂). Because of increased ventilation-perfusion mismatch, the Pao₂ may decrease when the elderly individual reclines.

Under normal resting conditions, some pulmonary capillaries are closed and not perfused (filled with blood). The pulmonary circulation has two mechanisms for lowering pulmonary vascular resistance, when vascular pressures are increased because of increased blood flow (Figure 21-9).^2,3,5 The first mechanism is recruitment, which allows opening of previously closed capillary vessels. The second mechanism is distention, which allows for widening of capillary vessels.

Another factor influencing pulmonary circulation is the fluid balance of the lung tissues. Fluid balance is regulated by the hydrostatic pressure, colloid osmotic pressure, and capillary permeability. When capillary hydrostatic pressure exceeds colloid osmotic pressure, fluid moves from the capillary to the interstitium. If the fluid shift is not controlled, the fluid volume will continue to increase until fluid is moved into the alveoli. Alveolar edema is more serious than interstitial edema (fluid in the interstitial space), because of its negative effects on gas exchange. Pulmonary interstitial and alveolar edema is common in disease processes such as congestive heart failure and infectious diseases of the lung. Other disease processes that also increase capillary permeability are acute respiratory distress syndrome (ARDS) and infant respiratory distress syndrome. (See Chapter 23 for further discussion.)

Structural and physiologic variations occur at each end of the age continuum. A summary of anatomic and physiologic respiratory variations by age group is presented in Table 21-1.⁸Pediatric considerations are shown in the box below.

PEDIATRIC CONSIDERATIONS

Changes in Respiratory System in Children

The respiratory system in children is very different than that of the adult, which makes the child susceptible to airway obstruction, aspiration, and infection. The trachea in the infant has more mucus-producing glands, which can create an overproduction of mucus in the infant. The trachea lumen, bronchi, and bronchioles are also smaller with a more narrow diameter. The excess mucus and more narrow respiratory structures increase the risk of airway obstruction in the child. The positioning of respiratory structures in the infant increases the chance of aspiration. The glottis is higher in the throat of an infant compared to a 5-year-old child (MacGregor, 2008). The trachea bifurcates at the third thoracic vertebra compared to the sixth in adults (MacGregor, 2008) and the larynx is located higher in the neck of the infant. Aspiration can lead to infection in the child and increase the work of breathing.

The infant has to work harder for ventilation of the lungs because of several factors. The more narrow diameter of bronchi and bronchioles creates a higher resistance to volume of air on inspiration. The large volume of dead space in the lungs requires the infant to breathe faster to meet oxygen demands. Compared to an adult, the alveoli are smaller and immature, which decreases the area for gas exchange to occur in the lungs. The number of alveoli and the size increase as the child ages. The flexible ribcage is unable to support the lungs adequately because it has less elastic recoil. The intercostal muscles of the ribcage also work inefficiently. The external intercostal muscles elevate the ribs for inspiration, whereas the internal intercostal muscles cannot lift the chest wall and do not help with inspiration. The infant depends on the diaphragm and abdomen for ventilation to compensate for the lack of intercostal muscle strength. All of these factors increase the work of breathing required for ventilation and the infant compensates by increasing his or her respiratory rate. By age 8 years the lungs are fully developed and the child’s respiratory system begins to resemble the adult’s respiratory system (MacGregor, 2008).

From MacGregor J: Introduction to the anatomy and physiology of children: a guide for students of nursing, child care and health, ed 2, New York, 2008, Routledge.

Ventilation is the process of moving air into the lungs and distributing air within the lungs to gas exchange units (alveoli) for maintenance of oxygenation and removal of carbon dioxide (CO₂).5 Measures of ventilation (amount of air moved) include four lung volumes and four lung capacities. Figure 21-10 schematically presents the various lung volumes and capacities; Table 21-2 defines each term and provides further details.

Lung volumes and capacities vary according to the individual’s body size, age (decreased in the neonate, young child, and the elderly),7–9 and body position (supine versus upright). Testing of pulmonary function to measure these volumes and capacities is covered under the Diagnostic Tests section in Chapter 22. Other measures important to ventilation are dead space, minute ventilation, and alveolar ventilation.

Dead space includes three dimensions: anatomic dead space, alveolar dead space, and physiologic dead space. Anatomic dead space includes the volume of gas (not used in gas exchange) in the conducting airways from the nose to the respiratory bronchioles.5,10,11 Generally, in adults this area is equal to 1 ml per pound of ideal body weight, or approximately 150 ml. In newborns and young children, the anatomic dead space is proportionately larger for their size.⁶ The anatomic dead space of elderly persons may increase slightly over that of healthy young adults because of the loss of alveolar sacs. Alveolar dead space is composed of ventilated, but unperfused areas of the lung, and is often referred to as wasted ventilation.⁵ Physiologic dead space (functional dead space) is the sum of the anatomic dead space and alveolar dead space.^7,11 Approximately one third of each breath occupies dead space.

Minute ventilation is the product of tidal volume (milliliters of air inhaled with each breath) times respiratory rate per minute. For example, a person with a tidal volume of 500 ml who is breathing at a rate of 15 breaths/minute has a minute ventilation of 7500 ml (see Table 21-2 for typical volumes).

By comparison, alveolar ventilation (V˙A ) equals the difference between tidal volume (V_T) and anatomic dead space volume (V_D) multiplied by the respiratory rate (RR) per minute.10

Alveolarventilation(V˙A )=(VT −VD )×RR

Because alveolar ventilation is affected by both the anatomic dead space and the respiratory rate, slow deep breathing yields greater alveolar ventilation than rapid shallow respiration. The patient breathing 25 times/minute at a V_T of 200 ml would have alveolar ventilation as follows:

(200ml−150ml[anatomicdeadspace])×25breaths/minute=1250ml

A patient breathing 10 times/minute at a V_T of 600 ml would have an alveolar ventilation of

(600ml−150ml)×10=4500ml

The partial pressure of oxygen in the alveoli (Pao₂) is the driving force to move O₂ into the blood and is estimated with the following equation:

PAO2=FIO2(PB −47)−(PaCO2÷0.8)

where FIO₂ is the fraction of inspired oxygen, P_B is the barometric pressure, 47 is the constant for water vapor pressure (mm Hg), 0.8 is the respiratory quotient, and Paco₂ is the laboratory measurement of arterial CO₂ pressure (mm Hg).

The value for PAO₂ is normally very close to that for PaO₂. The difference between alveolar and arterial oxygen tensions is called the Alveolar-arterial Difference in oxygen (A − aDO₂). A large A − aDO₂ value indicates poor matching of alveolar ventilation with alveolar blood flow (V˙A /Q˙ matching)

For example, the calculation of A − aDO₂ for a person at sea level (P_B = 760 mm Hg) breathing room air (FIO₂ = 0.21) with Pao₂ = 75 mm Hg and Paco₂ = 40 mm Hg is

PAO2=0.21(760−47)−(40/0.8)=150−50=100

Therefore, using the arterial blood gas value obtained for the PaO₂ and the calculated PAO₂ of 100, a difference of 25 mm Hg is determined:

A−aDO2 =100−75=25mmHg

This large of a difference indicates a significant problem with gas exchange.

In critical care settings, it is useful to calculate the A − aDO₂ value to monitor the efficacy of oxygen exchange across the lung. The normal A − aDO₂ gradient in a normal, healthy young adult is less than 10 mm Hg at room air, but it increases with age and increasing FIO₂. A rising A − aDO₂ value indicates worsening lung function, even though hypoxemia (PaO₂ lower than 80 mm Hg at sea level) may not necessarily be present.

Hypoxemia that is primarily caused by hypoventilation suggests that the lung is normal, and treatment that increases ventilation will remedy the problem. This type of hypoxemia is characterized by a normal A − aDO₂ value.

A simple method of calculating expected PAO₂ is the “law of 5’s.” By multiplying the FIO₂ (%) by 5, the care provider has an estimate of what the oxygen level should be under normal, healthy conditions (e.g., 5 × 21% room air = 105).

The lungs have a natural recoil tendency, whereas the chest wall favors the expanded state. During inspiration, the chest wall muscles (external intercostals) contract, elevating the ribs as the diaphragm moves downward. These two actions create a negative intrapleural pressure that causes the lung to expand. During expiration, the lung deflates passively because of the elastic recoil (elastic fibers in the lung tissue) and relaxation of the diaphragm. During heavy breathing, as seen with exercise, the elastic forces are not strong enough to cause the necessary rapid expiration, so abdominal muscles contract, pushing the abdominal contents upward, compressing the lungs.3 Figure 21-11 shows the interaction of lung forces during inspiration and expiration. In the normal, healthy resting individual, expiration is accomplished almost entirely by relaxation of the diaphragm.⁵ At the end of a normal expiration, the alveoli still contain some air volume, known as the functional residual capacity. If the alveoli were allowed to empty completely, the high surface tension in the alveoli would make it more difficult to reinflate them and add significantly to the work of breathing. In the absence of surfactant, which reduces alveolar surface tension, the alveoli tend to collapse—a condition called atelectasis. Excessive surface tension can increase the work of breathing so much that mechanical ventilation may be required. This is often the case in ARDS and in infant respiratory distress syndrome (see Chapter 23).

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