Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Introduction to the Respiratory System
Learning Objectives
Upon completion of this chapter, the student should be able to answer the following questions:
- 1
What is the primary function of the upper airways? What is the primary function of the lower airways? What anatomical adaptations exist in the upper and lower respiratory systems to accomplish these functions?
- 2
How do the pulmonary and bronchial circulatory systems differ in blood flow, blood pressure, and anatomic distribution?
- 3
How does the autonomic nervous system regulate airway diameter, airway mucus production, and pulmonary circulation? Is regulation of bulk airflow an autonomic process?
- 4
What are the functional differences between the conducting airways and the respiratory units?
- 5
What is the response of the respiratory system to stimulation of the parasympathetic nervous system? What is the response of the respiratory system to stimulation of the sympathetic nervous system?
- 6
At what age is lung development complete?
The primary function of the lung is gas exchange, which consists of movement of oxygen (O 2 ) into the body and removal of carbon dioxide (CO 2 ) from the body. This chapter provides an overview of lung anatomical structure/function relationships (i.e., upper and lower airways, the bronchial and pulmonary circulatory systems, innervation, and muscles of respiration), lung development (at the embryonic stage and throughout life), and lung repair. This chapter is designed to provide a broad conceptual understanding of the respiratory system and is not intended to provide a comprehensive understanding of individual components.
Lung Anatomical Structure/Function Relationships
The lungs are contained in the thorax with a volume of approximately 4 L and provide a surface area for gas exchange that is roughly the size of a tennis court (≈85 m 2 ). This large surface area is composed of millions of independently functioning respiratory units. Unlike the heart, but like the kidneys, the lungs demonstrate functional unity; that is, each respiratory unit is structurally identical and functions like every other respiratory unit. The divisions of the lung and the sites of disease are designated by anatomic location (e.g., right upper lobe, left lower lobe) or radiographic location (e.g., right upper lung field, left lower lung field). It is essential to know pulmonary anatomy in order to understand respiratory physiology and pathophysiologic alterations caused by respiratory disease.
Upper Airways: Nose, Sinuses, and Pharynx
The respiratory system begins at the nose and ends in the most distal alveolus. Thus, the nasal cavity, the posterior pharynx, the glottis and vocal cords, the trachea, and all divisions of the tracheobronchial tree are included in the respiratory system. The upper airways include all structures from the nose to the vocal cords, including sinuses and the larynx, whereas the lower airways consist of the trachea, bronchial airways, and alveoli. The upper airways “condition” inspired air by adding humidity and bringing it to body temperature by the time air reaches the trachea and further into the lower airway. The nose also functions to filter, entrap, and clear inspired particles larger than 10 µm in size. The interior of the nose is lined by respiratory epithelial cells interspersed with surface secretory cells. These secretory cells produce important immunoglobulins, inflammatory mediators, and interferons, which are the first line of host respiratory defense.
The paranasal sinuses ( frontal , maxillary, sphenoid, and ethmoid) are lined by ciliated epithelial cells and surround the nasal passages ( Fig. 20.1 A ). The cilia facilitate the movement of mucus from the upper airways and clear the main nasal passages approximately every 15 minutes. The functions of the sinuses are (1) to lessen the weight of the skull; (2) to protect the brain from frontal trauma; and (3) to offer resonance to the voice. The fluid covering their surfaces is continually being moved from the sinuses into the nose. In some sinuses (e.g., the maxillary sinus ), the opening (ostium) is at the upper edge of the sinus cavity, which makes fluid drainage difficult. The ostia may be narrowed or entirely occluded by nasal edema (swelling). Retention of secretions can result, which may lead to secondary infection (sinusitis) .
The volume of the adult nose is approximately 15 to 20 mL, but the surface area is greatly increased by the nasal turbinates (a series of three continuous ribbons of tissue that protrude into the nasal cavity, see Fig. 20.1 B ) to approximately 160 cm 2 . The nose enables the sense of smell. Neuronal endings in the roof of the nose above the superior turbinate carry impulses through the cribriform plate to the olfactory bulb.
The pharynx is divided into three sections: the nasopharynx , oropharynx , and laryngopharynx. Important structures within these regions include the epiglottis, vocal cords, and arytenoid cartilage that is attached to the vocal cords (see Fig. 20.1 C ). The nasopharynx (2–3 cm wide and 3–4 cm long) is the most anterior and lies behind the nose. It contains small masses of lymphoid tissue (adenoids), also known as pharyngeal tonsils, which are a part of the immune system. They represent a drainage pathway of lymphatic fluid between the throat, nose, and ears. This network of structures provides a means of fighting infections but also is a common location for infectious symptoms.
The nasopharynx is connected to the middle ear cavity via the Eustachian tubes. These aid in equalizing pressure between the middle ear and the atmospheric (by way of the pharynx). If there is inflammation in the nasopharynx, the Eustachian tubes may become narrowed or blocked. As a result, fluid drainage and air pressure equalization may be impaired, leading to symptoms of Eustachian tube dysfunction.
The soft palate separates the nasopharynx and the oropharynx. The oropharynx ends at the epiglottis. The laryngopharynx begins at the epiglottis and ends at the esophagus. The major role of the laryngopharynx is to help regulate the passage of food into the esophagus and air into the lungs. With some infections or repeated insults, these structures can become edematous and contribute significantly to airflow resistance. The epiglottis and arytenoid cartilage (attached to the vocal cords) cover or act as a hood over the vocal cords during swallowing. Thus, under normal circumstances, the epiglottis and arytenoid cartilage function to prevent aspiration of food and liquid into the lower airway. The act of swallowing food after mastication (chewing) usually occurs within 2 seconds, and it is closely synchronized with muscle reflexes that coordinate opening and closing of the airway. Air is allowed to enter the lower airway, while food and liquids are kept out. Patients with some neuromuscular diseases have altered muscle reflexes and can lose this coordinated swallowing mechanism. Prescription and recreational drugs may also impair these muscle reflexes. Impairment of this coordinated swallow mechanism increases the risk for aspiration of food and liquid and poses a risk for infection of the lung ( pneumonia ) or lung inflammation ( pneumonitis ).
Lower Airway: Trachea, Bronchi, Bronchioles, and Respiratory Unit
The right lung, located in the right hemithorax, is divided into three lobes (upper, middle, and lower) by two interlobular fissures (oblique, horizontal). The left lung, located in the left hemithorax, is divided into two lobes (upper, including the lingula, a tongue-like projection of the anterior aspect of the upper lobe , and lower) by an oblique fissure ( Fig. 20.2 ). Both the right and left lungs are covered by a thin membrane called the visceral pleura. The interior wall of the chest cavity is lined by another membrane called the parietal pleura. The interface of the visceral and parietal pleura allows for smooth gliding of the lung as it expands and contracts in the chest and produces a potential space. Normally this pleural space contains less than 5 mL of lubricating pleural fluid . Fluid can enter this space by a variety of pathologic mechanisms and create a pleural effusion or, if the fluid becomes infected, an empyema. Air can also enter the pleural space between the visceral and parietal pleura due to surgery, trauma, or spontaneous rupture of a group of alveoli. Air in the pleural space is called a pneumothorax. In either pneumothorax or pleural effusion, the muscles of respiration cannot efficiently create a negative intrathoracic pressure gradient, and work of breathing increases. In severe cases, respiratory distress or respiratory failure may occur.
The trachea branches into two mainstem bronchi ( Fig. 20.3 ). These mainstem bronchi then divide (like the branches of a tree) into lobar bronchi (one for each lobe), which in turn divide into segmental bronchi ( Fig. 20.4 ; see also Fig. 20.3 ) and then into smaller and smaller branches (bronchioles) until ending in the alveolus ( Fig. 20.5 ). Bronchi and bronchioles differ not only in size but also by the presence of cartilage, the type of epithelium, and their blood supply ( Table 20.1 ). Beyond the segmental bronchi, the airways divide in a dichotomous or asymmetrical branching pattern. Bronchi, distinguished by their size and the presence of cartilage, eventually become terminal bronchioles, which are the smallest airways without alveoli. Each branching of an airway results in an increase in the number of airways with smaller diameters; as a result, the total surface area for the next generation of branches increases. Terminal bronchioles end in an opening (duct) to a group of alveoli and are called respiratory bronchioles.
TABLE 20.1
Anatomical Characteristics of Bronchi and Bronchioles
| Anatomical Site | Cartilage | Diameter (mm) | Epithelium | Blood Supply | Alveoli | Volume (mL) |
|---|---|---|---|---|---|---|
| Bronchi | Present | >1 | Pseudostratified Columnar |
Bronchial | Absent | — |
| Terminal bronchioles | Absent | <1 | Cuboidal | Bronchial | Absent | >150 |
| Respiratory bronchioles | Absent | <1 | Cuboidal/alveolar | Pulmonary | Present | 2500 |
The region of the lung supplied by a segmental bronchus is called a bronchopulmonary segment and is the functional anatomical unit of the lung. Because of their structure, bronchopulmonary segments that have become irreversibly diseased can easily be removed surgically. The basic physiological unit of the lung is the gas-exchanging unit (respiratory unit), which consists of the respiratory bronchioles, the alveolar ducts, and the alveoli (see Figs. 20.4 and 20.5 ). The bronchi, which contain cartilage, and the terminal bronchioles (i.e., lacking alveoli), in which cartilage is absent, serve to move gas from the airways to the alveoli and are referred to as the conducting airways. This area of the lung (≈150 mL in volume) does not participate in gas exchange and is referred to as anatomical dead space . This region may further condition inspired air if the capacity of the upper airway to do so is exceeded. The area beginning with the respiratory bronchioles extending to the alveoli is where all gas exchange occurs. This region is only approximately 5 mm long, but it is the largest volume of the lung, at a volume of approximately 2500 mL and with a surface area of 70 m 2 when the lung and chest wall are at the resting volume (see Table 20.1 ).
The alveoli are polygonal in shape and approximately 250 µm in diameter. Alveolar spaces are responsible for most of the lung volume; these spaces are divided by tissue known collectively as the interstitium. The interstitium is composed primarily of lung collagen fibers and is a space in which fluid and cells can potentially accumulate. An adult has approximately 5 × 10 8 alveoli ( Fig. 20.6 ), which are composed of type I and type II epithelial cells. Under normal conditions, type I and type II cells exist in a 1:1 ratio.
The type I cell occupies 96% to 98% of the surface area of the alveolus, and it is the primary site for gas exchange. The thin cytoplasm of type I cells is ideal for optimal gas diffusion. In addition, the basement membrane of type I cells and the capillary endothelium are fused, which minimizes the distance for gas diffusion and thereby facilitates gas exchange.
Type II cells are cuboidal and usually found in the “corners” of the alveolus, where they occupy 2% to 4% of the surface area. During embryonic development, the alveolar epithelium is composed entirely of type II cells, and only very late in gestation do they differentiate into type I cells and form the “normal” alveolar epithelium for optimal gas exchange. Also, type II cells synthesize pulmonary surfactant (see Chapter 21 ). Pulmonary surfactant reduces alveolar surface tension, decreasing fluid cohesive forces that would otherwise lead to deaeration and collapse of the alveoli. Gas exchange occurs in the alveoli through a dense mesh-like network of capillaries and alveoli called the alveolar-capillary network. The barrier between gas in the alveoli and the red blood cell is only 1 to 2 µm thick and consists of type I alveolar epithelial cells, capillary endothelial cells, and their respective basement membranes. O 2 and CO 2 passively diffuse across this barrier. Oxygen diffuses into blood and subsequently into red blood cells (see Chapter 24 ) where it can bind with hemoglobin. Red blood cells pass through the network in 0.75 to 1.0 second, which is sufficient time for CO 2 and O 2 gas exchange. In conditions shortening capillary transit time (e.g., increased cardiac output) or conditions impairing function of the alveolar-capillary network (e.g., emphysema, interstitial lung disease) the transit time may be insufficient for adequate oxygen diffusion.
IN THE CLINIC
The conducting airways are involved in several major pulmonary diseases collectively referred to as obstructive pulmonary disease. Obstructive pulmonary diseases include asthma, bronchiolitis, chronic bronchitis, cystic fibrosis, and emphysema. Obstruction of airflow through the airways is commonly caused by increased amounts of mucus, airway inflammation, and smooth muscle constriction. Loss of cartilaginous support may also occur. Asthma is a chronic inflammatory disease of the large and small airways, mediated predominantly by lymphocytes and eosinophils. Asthma is associated with increased amounts of mucus in the airways and with reversible constriction of the airway smooth muscle (bronchospasm). Bronchiolitis is a disease of the bronchioles that usually occur in young infants and is caused by viruses, primarily respiratory syncytial virus. Chronic bronchitis, a disease typically of people who smoke, is associated with an increased number of mucus-secreting cells in the airways, an increase in mucus production, and recurrent airway infections. Cystic fibrosis is an autosomal recessive genetic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene that codes for a chloride ion channel. Mutations in the CFTR gene cause a reduction in chloride and water secretion into the mucus overlying the epithelia cells, which increases the viscosity of mucus. This situation results in mucus accumulation and chronic pulmonary infections, primarily by Pseudomonas aeruginosa.
Not every important obstructive lung disease involves the airways directly. Emphysema is an irreversible, obstructive lung disease. It is strongly linked to cigarette smoke inhalation. The pathogenesis involves a progressive destruction of the elastic tissues in the lung with a loss of alveolar/capillary structure. The mechanisms of tissue destruction are unclear but may involve proteolytic enzymes released by activated inflammatory cells and by toxic compounds present in cigarette smoke. Emphysema can occur in nonsmoking individuals with occupational or environmental exposures to lung irritants. Individuals with the genetic disorder α 1 -antitrypsin deficiency may also develop emphysema due to reduced tissue breakdown of proteolytic enzymes, such as elastase.
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here