Lung Anatomy

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The anatomy of the respiratory system can be divided into 2 major parts, airway anatomy and lung anatomy.

Airway anatomy can be further subdivided into the following 2 segments:

The extrathoracic (superior) airway, which includes the supraglottic, glottic, and infraglottic regions

The intrathoracic (inferior) airway, which includes the trachea, the mainstem bronchi, and multiple bronchial generations (which have as their main function the conduction of air to the alveolar surface)

Lung anatomy includes the lung parenchyma, which carries part of the conduction system but is mainly involved in the gas exchange at the alveolar level. The lung parenchyma is further subdivided into lobes and segments.

The purpose of this chapter is to provide a better understanding of the anatomy of the airways and lungs, which will help the health provider to recognize and manage different respiratory abnormalities.

The trachea is a cartilaginous and fibromuscular tube that extends from the inferior aspect of the cricoid cartilage (sixth cervical vertebra level) to the main carina (fifth thoracic vertebra level). Its length is 3 cm at birth and 10-12 cm in adults (of which 2-4 cm is extrathoracic and 6-9 cm intrathoracic). Tracheal diameters vary widely, ranging from 13 to 25 mm (coronal plane) in men. In women, the variability is still noted, with a range of 10-21 mm (coronal plane). The shape of the intrathoracic trachea changes during expiration as a result of invagination of the posterior wall, causing as much as a 30% reduction of the anteroposterior diameter as seen on dynamic CT scanning (see the images below). ^[1]

The tracheal wall has 4 different layers: mucosa, submucosa, cartilage or muscle, and adventitia. The posterior tracheal wall lacks cartilage and instead is supported by a thin band of smooth muscle.

The airways divide by dichotomous branching, with approximately 23 generations of branches from the trachea to the alveoli (see the images below).

Bronchi are composed of cartilaginous and fibromuscular elements; however, the distinction between these elements is less clear-cut in the bronchi than in the trachea, especially on the more distal airways. The wall thickness is approximately proportional to the airway diameter on airways distal to the segmental branches. For airways less than 5 mm in diameter, the wall should measure one sixth to one tenth of the diameter.

Different systems of nomenclature have been applied to the bronchial tree over the years. ^[2] In general usage, there are 2 mainstem bronchi (right and left) and 3 lobar bronchi (right), with a total of 10 segmental bronchi; 2 lobar bronchi are found on the left, with a total of 8 segmental bronchi. No accepted terminology for subsegmental bronchi exists. The terminal bronchioles, including respiratory bronchioles, alveolar ducts, and alveolar sacs, are discussed elsewhere (see Microscopic Anatomy section). Generally, the length and diameter of the central airways vary from right to left.

The vascular supply of the trachea and bronchial tree depends on branches from the inferior thyroid arteries, intercostal arteries, and bronchial arteries (aortic branches). These arteries (except the thyroid artery) form a peribronchial plexus that follows the bronchial tree deep into the lung parenchyma to supply blood also to the visceral pleura and the walls of the pulmonary arteries and veins (vasa vasorum).

Some symmetry exists between the right and the left lungs. Both lungs are divided into lobes (see the image below). The gross functional subunits of each lung are called segments and have a close relation with the segmental bronchi described above. The right lung comprises 10 segments: 3 in the right upper lobe (apical, anterior and medial), 2 in the right middle lobe (medial and lateral), and 5 in the right lower lobe (superior, medial, anterior, lateral, and posterior). The left lung comprises 8 segments: 4 in the left upper lobe (apicoposterior, anterior, superior lingula, and inferior lingula) and 4 in the left lower lobe (superior, anteromedial, lateral, and posterior).

Each lung is covered by the visceral pleura, which covers the surface of the lung and dips into lobar fissures. Near the hilum and mediastinum, it reflects and becomes parietal pleura, which covers the inner surface of the respective hemithorax, and thus creates a potential space (pleural space). The visceral pleura forms invaginations into both lungs, which are called fissures. There are 2 complete fissures in the right lung and 1 complete fissure with an incomplete fissure in the left (see the image below); these separate the different lung lobes. The pleura also forms the pulmonary ligament, which is a double layer of pleura that extends caudad along the mediastinum from the inferior pulmonary vein to the diaphragm.

A close relation exists between the bronchial tree and the anatomy of the pulmonary vasculature, composed mainly of the pulmonary arteries and veins (see the image below). The main pulmonary artery originates in the right ventricle and divides into 2 branches. The right pulmonary artery passes posterior to the aorta and the superior vena cava, emerging lateral to the atria and anterior and slightly inferior to the right mainstem bronchus. In contrast, the origin of the left pulmonary artery is situated anterior to the left mainstem bronchus. The arborization of the pulmonary arteries varies from right to left but mainly divides into truncal, lobar, segmental, and subsegmental arteries, which generally follow the branches of the bronchial tree.

The pulmonary veins originate in the alveoli and also receive drainage from the bronchial and pleural branches. After the confluence of the small branches into bigger ones, 2 pulmonary veins, superior and inferior, are formed on each side. These 4 veins typically join at or near their junction with the left atrium, and usually this common area is intrapericardial.

The lymphatic drainage of the lungs start with lymphatic vessels that first drain into intraparenchymal lymphatics and lymph nodes, then move to peribronchial (hilar) lymph nodes, and subsequently move to subcarinal, tracheobronchial, and paratracheal lymph nodes (see the images below). The lymphatics eventually communicate with the venous system via the bronchomediastinal lymphatic trunk and the thoracic duct or via the inferior deep cervical (scalene) lymph nodes. However, some variants of the lymphatic drainage are very important to consider overall in the dissemination of pulmonary neoplasms (see Pathophysiologic Variants).

The trachea has multiple layers (see the image below). The mucosa is composed of a ciliated pseudostratified columnar epithelium and numerous mucus-secreting goblet cells that rest on a basement membrane with a thin lamina propria (mainly collagenous). The submucosa contains seromucous glands. The adventitia contains cartilaginous rings interconnected by connective tissue. The hyaline cartilage rings have the form of the letter C and are opened posteriorly. The open ends are connected by fibroelastic tissue and a band of smooth muscle (the trachealis).

The epithelium of the bronchus is pseudostratified columnar ciliated epithelium, also with numerous goblet cells. This epithelium transitions first into a simple columnar ciliated epithelium and then into a cuboidal epithelium as it continues branching into smaller bronchioles. The cartilage support is eventually lost at the bronchiolar level (0.5-1.0 mm diameter). The muscle layer becomes the dominant structure and is composed of smooth muscle and elastic fibers (see the image below). At this level, the mucosa may be highly folded because of the loss of supporting structure.

The terminal bronchioles are considered the respiratory zone of the lungs (ie, the area where gas exchange occurs). They divide into respiratory bronchioles, which continue downstream as alveolar ducts that are completely lined with alveoli and alveolar sacs (see the image below). Over 300 million alveoli exist in the human lung, all of them covered by an extensive network of capillaries (branches from the pulmonary arteries). The respiratory zone constitutes most of the lung (2.5-3 L).

The epithelium of the respiratory bronchiole is primary cuboidal and may be ciliated; goblet cells are absent. The supporting thin layer is formed by collagenous and smooth muscle. Alveoli appear as small pockets that interrupt the main wall. The terminal portion of the respiratory duct gives rise to the alveolar sacs (composed of a variable number of alveoli). The alveoli are the smallest and most numerous subdivisions of the respiratory system. The interalveolar septum often contains 10-15 μ m openings between neighboring alveoli that help equalize air pressures among them.

The alveolar wall is very thin (25 nm) and formed by squamous epithelium (type I cells) covered by a thin film of surfactant fluid rich in hydrophilic phospholipid produced by type II cells (septal cells). This surfactant fluid keeps the alveoli open by reducing the surface tension of the interface between opposing alveolar surfaces, which reflects into reduced inspiratory work.

The respiratory epithelium is composed mainly of type I cells (98%), along with some type II cells. The basal lamina is in intimate contact with the capillaries from the pulmonary vascular system, favoring the transfer of oxygen to the red blood cells and the release and transfer of carbon dioxide to the alveolar airway.

As a human being develops from a fetus to a fully developed adult, several changes take place. Some of these changes follow regular patterns, and others either compensate for certain conditions or occur for unknown reasons.

Congenital anatomic variants of the lungs are present in the following forms:

Agenesis – A congenital complete absence of one or both lungs, the latter being incompatible with life (The condition is associated with other congenital abnormalities and is rare.)

Aplasia or hypoplasia – The presence of a rudimentary bronchus that ends in a blind pouch with no evidence of pulmonary vasculature or lung parenchyma

Accessory lobes, and fusion of lobes – Variations over the lung lobes that are mainly caused by the incomplete obliteration of the visceral pleural folds, result from the presence of abnormal vessels (creating extra lobes), or occur secondary to (completely or partially) fused lobes from obliteration of the normal lung fissures (See the images below.) ^[3]

Congenital anatomic variants of the airway are present in the following forms:

Bronchial variations – Variations in the patterns of the bronchial tree are predominantly due to displacement of segmental and subsegmental bronchi (reduction migration and selection theories) ^[4]  (Anatomic abnormalities of the bronchi may be the favored locales for deformities, chronic inflammations [see the image below], and bronchial neoplasms.)

Congenital anatomic variants of the diaphragm are present in the following forms:

Normal variations in the diaphragm are mainly consistent with different sites of insertion of the muscle that form the diaphragm, or due to congenital defect leading to communication from the abdominal to the chest cavity (eg, Bochdalek hernia, Morgagni hernia, diaphragmatic eventration) (see the image below)

Pathologic variants are related to changes in the structure of the airways, the lung parenchyma, or adjacent structures that lead to disruption of the normal anatomy of the respiratory system. The most common such variants are presented below.

Emphysema and chronic obstructive pulmonary disease are caused by an accumulation of inflammatory mucus that gives rise to a loss of elastic recoil resulting from lung tissue destruction or to an increase in the resistance of the conducting airways, leading to an abnormal permanent enlargement of air spaces distal to the terminal bronchioles (see the images below).

Pneumothorax, hemothorax, and hydrothorax are caused by a decrease in lung volume secondary to the presence of air, blood, or fluid between the visceral and parietal components of the pleura (see the images below).

Diaphragmatic hernia occurs when a defect in the diaphragm allows the abdominal contents to move into the chest cavity (see the image below). This could be congenital, traumatic, iatrogenic, or due to a weakness over the muscles forming the diaphragm.

Bronchial and tracheal stenosis occurs as a result of secondary and numerous malignant and benign processes and is also a consequence of surgical procedures and trauma (see the images and video below). The main defect is the obstruction or collapse of the airways at any level, which leads to changes in airflow that result in hypoxemia.

In most cases, paralysis or dysfunction of the vocal cords is caused by dysfunction of the recurrent laryngeal or vagus nerve innervating the larynx. Even when no real alteration of the anatomy is present, this condition may cause many of the same problems associated with bronchial and tracheal stenosis.

Infectious etiologies (eg, bacterial pneumonia and tuberculosis) include viral, fungal, and bacterial infections. They are characterized by consolidation of the affected part of the lung and filling of the alveolar air spaces with exudate, inflammatory cells, and fibrin, leading to a decrease in oxygen exchange (ventilation mismatch) and, in severe cases, to destruction of the lung parenchyma (see the images below).

Interstitial lung diseases include conditions caused by drugs, autoimmune processes, fibrotic diseases, organic and inorganic dust exposure, sarcoidosis, lymphangioleiomyomatosis (LAM), histiocytosis X, vasculitis, pulmonary alveolar proteinosis, and any other process that will cause reduced lung volumes due to an alteration in lung parenchyma leading to ventilation-perfusion mismatch (see the images below).

Malignancy is an uncontrolled cell growth of the tissue in the lungs or airways. Depending on the location and severity of the malignancy, it may lead to any of the above described anatomic changes.

Carden KA, Ernst A. Management of Tracheobronchomalacia. MJ Simoff, DH Sterman, A Ernst. Thoracic Endoscopy: Advances in Interventional Pulmonology. Malden, MA: Blackwell Futura; 2006. Vol 1: 344-51/Chap 24.

Dozaki T, Imai K, Mizukami S. [Biphasic (ulcer-forming and ulcer-preventing) effect of adrenaline in rats]. Nippon Yakurigaku Zasshi. 1975 Jul. 71(5):405-14. [Medline].

Meenakshi S, Manjunath KY, Balasubramanyam V. Morphological variations of the lung fissures and lobes. Indian J Chest Dis Allied Sci. 2004 Jul-Sep. 46(3):179-82. [Medline].

Gonlugur U, Efeoglu T, Kaptanoglu M, Akkurt I. Major anatomical variations of the tracheobronchial tree: bronchoscopic observation. Anat Sci Int. 2005 Jun. 80(2):111-5. [Medline].

Eduardo A Celis, MD Physician in Pulmonary and Critical Care Medicine, Interventional Pulmonology

Eduardo A Celis, MD is a member of the following medical societies: American Association for Bronchology and Interventional Pulmonology, American College of Chest Physicians, American College of Physicians, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Javier I Diaz-Mendoza, MD Senior Staff Physician, Interventional Pulmonology, Division of Pulmonary and Critical Care Medicine, Henry Ford Hospital

Javier I Diaz-Mendoza, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, American Association for Bronchology and Interventional Pulmonology

Disclosure: Nothing to disclose.

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women’s Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Lung Anatomy

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