The upper respiratory tract includes the nose, pharynx and larynx; the lower respiratory tract starts at the trachea (Fig. 25a). The two lungs are enclosed within the thoracic cage, formed from the ribs, sternum and vertebral column, with the dome-shaped diaphragm separating the thorax from the abdomen. The left lung has two lobes, the right three. The airways, blood vessels and lymphatics enter each lung at the lung root or hilum, where the pulmonary nerve plexus receives autonomic nerves from the vagus and sympathetic trunk. The vagus contains sensory afferents from lung receptors (Chapter 29) and bronchoconstrictor parasympathetic efferents leading to the airways; sympathetic nerves are bronchodilatory (Chapter 7). Each lung lobe is made up of several wedge-shaped bronchopulmonary segments supplied by their own segmental bronchus, artery and vein. The lungs are covered by a thin membrane (visceral pleura), continuous with the parietal pleura that lines the inside surface of the thoracic cage. The tiny space between the pleura is filled with lubricating pleural fluid.
Airways (Fig. 25a)
The trachea divides into two main bronchi; their walls contain U-shaped cartilage segments linked by smooth muscle. On entering the lung, the bronchi divide repeatedly into lobar, segmental (generations 3 and 4) and small (generations 5–11) bronchi, the smallest having a diameter of ∼1 mm. These all have irregular cartilaginous plates and helical bands of smooth muscle. Bronchioles (generations 12–16) lack cartilage and are held open by surrounding lung tissue. The smallest (terminal) bronchioles lead to respiratory bronchioles (generations 17–19), and thence to alveolar ducts and sacs (generation 23), the walls of which form alveoli and contain only epithelial cells (Fig. 25c,d). Small pores (alveolar pores, pores of Kohn) allow pressure equalization between alveoli. Adult human lungs contain ∼17 million branches and ∼300 million alveoli, providing an exchange surface of ∼85 m2. The bronchial circulation supplies airways down to the terminal bronchioles; respiratory bronchioles and below obtain nutrients from the pulmonary circulation (Chapter 16).
Epithelium and airway clearance
The airways from the trachea to the respiratory bronchioles are lined with ciliated columnar epithelial cells. Goblet cells and submucosal glands secrete a 10–15-µm thick, gel-like mucus that floats on a more fluid sol phase (Fig. 25b). Synchronous beating of the cilia moves the mucus and associated debris to the mouth (mucociliary clearance). Factors that increase the thickness or viscosity of the mucus (e.g. asthma, cystic fibrosis) or reduce cilia activity (e.g. smoking) impair mucociliary clearance and lead to recurrent infections. Mucus contains substances that protect the airways from pathogens (e.g. antitrypsins, lysozyme, immunoglobulin A).
Epithelial cells forming the walls of the alveoli and alveolar ducts are unciliated, and largely very thin type I alveolar pneumocytes (alveolar cells; squamous epithelium) (Fig. 25d). These form the gas exchange surface with the capillary endothelium (alveolar–capillary membrane). A few type II pneumocytes secrete surfactant which reduces the surface tension and prevents alveolar collapse (Chapter 26). Macrophages (mobile phagocytes) in the airways ingest foreign materials and destroy bacteria; in the alveoli, they take the place of cilia by clearing debris.
The main respiratory muscles are inspiratory, the most important being the diaphragm; contraction pulls down the dome, reducing pressure in the thoracic cavity, and thus drawing air into the lungs. The external intercostal muscles assist by elevating the ribs and increasing the dimensions of the thoracic cavity. Quiet breathing is normally diaphragmatic; accessory inspiratory muscles (e.g. scalene, sternomastoids) aid inspiration if airway resistance or ventilation is high. Expiration is achieved by passive recoil of the lungs and chest wall, but, at high ventilation rates, this is assisted by the contraction of abdominal muscles which speed recoil of the diaphragm by raising abdominal pressure (e.g. exercise).
Lung volumes and pressures (Fig. 25e)
The tidal volume (TV) is the volume of air drawn into and out of the lungs during normal breathing; the resting tidal volume is normally
∼500 mL but, like all lung volumes, is dependent on age, sex and height. The vital capacity (VC) is the maximum tidal volume, when an individual breathes in and out as far as possible. The difference in volume between a resting and maximum expiration is the expiratory reserve volume (ERV); the equivalent for inspiration is the inspiratory reserve volume (IRV). The volume in the lungs after a maximum inspiration is the total lung capacity (TLC), and that after a maximum expiration is the residual volume (RV).
The functional residual capacity (FRC) is the volume of the lungs at the end of a normal breath, when the respiratory muscles are relaxed. It is determined by the balance between outward elastic recoil of the chest wall and inward elastic recoil of the lungs. These are coupled by the fluid in the small pleural space, which therefore has a negative pressure (intrapleural pressure: –0.2 to –0.5 kPa). Perforation of the chest therefore allows air to be sucked into the pleural space, and the chest wall expands while the lung collapses (pneumothorax). Dis- eases that affect lung elastic recoil alter FRC; fibrosis increases recoil and therefore reduces FRC, whereas in emphysema, where lung structure is lost, recoil is reduced and FRC increases.
During inspiration, the expansion of the thoracic cavity makes the intrapleural pressure more negative, causing the lungs and alveoli to expand, and reducing the alveolar pressure. This creates a pressure gradient between the alveoli and the mouth, drawing air into the lungs. During expiration, intrapleural and alveolar pressures rise, although, except during forced expiration (e.g. coughing), the intrapleural pressure remains negative throughout the cycle because expiration is normally passive.
The dead space refers to the volume of the airways that does not take part in gas exchange. The anatomical dead space includes the respiratory tract down to the terminal bronchioles; it is normally ∼150 mL. The alveolar dead space refers to alveoli incapable of gas exchange; in health, it is negligible. The physiological dead space is the sum of the anatomical and alveolar dead spaces.