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By Michael J. Light
American Academy of PediatricsCopyright © 2011 American Academy of Pediatrics
All rights reserved.
Anatomy of the Lung
Michael J. Light, MD
Knowledge of the development of the lungs helps us to understand congenital pulmonary anomalies. The lungs develop with the ultimate goal of sustaining life after delivery of the newborn. To sustain life, oxygen from the atmosphere is breathed into the lungs and carbon dioxide is excreted. Oxygen provides the fuel to allow the human body to function. Here we describe the gross anatomy of the lung, rather than microscopic anatomy.
Embryology of the Lungs
The 3 laws of development of the lungs according to Reid are as follows:
1. The bronchial tree is developed by the 16th week of intrauterine life.
2. Alveoli develop after birth, increasing in number until 5 to 8 years of age and increasing in size until growth of the chest wall finishes with adulthood.
3. The pre-acinar vessels (arteries and veins) follow the development of the airways; development of the intra-acinar vessels follows that of the alveoli. Muscularization of the intra-acinar arteries does not keep pace with the appearance of new arteries.
There are 5 phases or periods of lung development (Figure 1-1). Before 3 weeks of gestation a pouch arises from the primitive foregut, at which time the embryo is 3 mm in length. This period constitutes the embryonic phase. The lung bud divides into right and left, which will become the right and left lungs. By the end of the embryonic period there will be 5 additional branches, which are the major bronchi, and the lung buds will have elongated into primary lung sacs. Developmental anomalies at this stage will result in anomalies of the major airways, including atresia (closed or undeveloped) and tracheoesophageal fistula.
The glandular period (also called pseudoglandular) starts at the end of the 5th week and continues to the 16th week as the conducting airways are formed by dichotomous branching. It is called pseudoglandular because the airways are blind tubes lined by columnar or cuboidal epithelium. The terminal bronchioles are formed and primitive acinar (terminal airway) structures are developing. If there is a diaphragmatic hernia there is the potential for a reduction in the number of branches formed on the side of the hernia, with resultant hypoplastic lung.
The canalicular period is from the 17th week until the 24th week. During this period the terminal bronchioles will have divided to produce a number of respiratory bronchioles, and the capillary bed is forming so that toward the end of this stage gas exchange can occur and potentially life can be sustained, even though the alveoli have not yet formed.
The airways from the trachea to the 19th generation are the conducting airways and the gas-exchanging units are from the 20th to 27th generation and are the terminal respiratory units. From the major bronchi at the 8th generation to the 20th are the non-respiratory bronchioles, and the respiratory bronchioles are from 20th to 23rd generation (Figure 1-1).
The saccular period extends from the end of the canalicular phase until birth and overlaps with the alveolar period, which extends to 5 to 8 years of age. The terminal respiratory unit comprises the respiratory bronchiole and the alveolar ducts, including the alveoli, and the unit is also known as the acinus. Alveoli are lined by type I (95%) and type II pneumocytes. Type II pneumocytes are cuboidal and synthesize surfactant and divide during repair. Eventually most of them flatten out to form type I pneumocytes, which are supportive. The primitive airways, prior to delivery, contain lung fluid, which drains into the amniotic fluid.
In the postnatal period, alveoli continue to develop until 5 to 8 years of age and enlarge through adolescence. The term infant has between 20 to 50 million alveoli at birth, and this number increases to about 300 million at age 8 years. The alveolar surface area is approximately 2.8 square meters at birth, 32 square meters at 8 years of age, and 75 square meters at adulthood. This last number is often equated to the size of a tennis court.
During the embryonic and glandular periods, the development of the pulmonary arteries parallels that of the branching airways. During this same period the bronchial vessels are close to the pulmonary vessels. The bronchial arteries supply blood for the nutrition of the lung; they are derived from the thoracic aorta or from the upper aortic intercostal arteries. The conducting airways receive their blood supply from the bronchial vessels, and the terminal respiratory units receive their blood from the pulmonary vessels. The pulmonary veins form from the capillary network and join together to form the 4 main pulmonary veins, which drain oxygenated blood into the left atrium. The pulmonary artery pressures are high at birth and fall, in response to the higher oxygen levels, over the next days and weeks. The bronchial arterial circulation is at systemic pressures.
The lymphatics draining from the lung comprise lymph ducts, lymph nodes, and the thoracic duct. At birth the pulmonary lymphatics are vital to the removal of lung liquid. There are 2 lymphatic networks: the pleural network and the parenchymal network. Most drainage is toward the hilum and, because of the valves in the lymph channels, the flow moves in one direction. Fully formed lymph nodes are not seen until birth and develop further in infancy. The main right lymphatic ducts follow the right side of the trachea, joining the venous system at the junction of the right jugular and subclavian veins. On the left side the veins follow the trachea and empty into the thoracic duct, which drains into the veins on the left side of the neck. Pulmonary lymphatic drainage is complex and is very variable from individual to individual.
The nerve supply of the lungs is from branches of the thoracic sympathetic ganglia and the vagus nerve. The upper 3 to 5 branches of the sympathetic ganglia supply the lungs and the lower supply the intercostal nerves. Almost all of the afferent (sensory) pathways are through the vagus nerve. Figure 1-2 shows the efferent or motor component. The efferent fibers control the caliber of the conducting airways, the activity of bronchial glands, and the state (constricted or dilated) of the pulmonary vessels. The parietal pleura is richly innervated with pain fibers. The visceral pleura has no pain fibers. The phrenic nerves supply the diaphragm, originating from the third to fifth cervical roots (Figure 1-2).
Gross Anatomy of the Lung
The lungs are within the thoracic cavity, separated by the heart and mediastinum (Figures 1-3 and 1-4). The airways terminate in the acinus where gas exchange occurs. The whole lung is sponge-like and pink in the early years, gradually becoming grayer with age. The apex extends into the root of the neck, and the base is concave resting on the convexity of the diaphragm. The right lung has 3 lobes and 2 fissures, the left lung has 2 lobes and one fissure (Figure 1-5). The lobes of the lung are further divided into segments, and these are shown diagrammatically in Figures 1-6 and 1-7.
The lungs are covered by the visceral pleura (also called pulmonary pleura), and this membrane extends into the fissures. The parietal pleura lines the inner surface of the thoracic cavity, and the visceral and parietal pleurae join at the root of the lung (hilum). There is an expandable space between the 2 layers that contains a small amount of fluid.
The mediastinum lies within the thoracic cavity between the pleurae of the 2 lungs with the anterior boundary of the sternum and posterior border of the vertebral column. The superior mediastinum is above the pericardium, while below the pericardium there are 3 parts. In front of the pericardium is the anterior mediastinum, the heart and pericardium are in the middle mediastinum, and the posterior mediastinum is behind the heart. The superior mediastinum has the thymus, trachea, esophagus, thoracic duct, and the upper great vessels including the arch of the aorta (Figure 1-3).
The hila of the lungs are where the structures of the lung enter from the mediastinum. The usual level of the hilum is anteriorly the third to fourth costal cartilage and posteriorly the fifth to seventh thoracic vertebrae.
Intercostal Muscles and Diaphragm
The muscles of respiration are the intercostals and the diaphragm. The anatomy of the diaphragm is shown in Figure 1-8. The right diaphragm overlies the liver and is higher than the left diaphragm, which overlies the stomach and spleen. The 3 major openings are the inferior vena cava at thoracic vertebral level (T) 12, esophagus (T10), and aorta (T12). The opening of the anterior diaphragm is the foramen of Morgagni and of the posterior diaphragm is the foramen of Bochdalek. These 2 foramina are the sites of diaphragmatic hernia, with the Bochdalek hernia being the most common and known as the posterolateral diaphragmatic hernia, mostly (80%–85%) on the left.
It is important to understand the surface anatomy of the lungs, and this is shown in the Figure 1-9. Knowing the area of the lung below the surface while percussing and auscultating the lungs is important in localizing the pathology. The diaphragm is attached to the lower costal margin and the leaves are dome-shaped. With inspiration, the diaphragm flattens and the lower border of the lungs correspondingly descend. This will result in a different level of the lower lung border, which changes by several centimeters during deep breathing.CHAPTER 2
Pnina Weiss, MD
The function of the respiratory system is to provide oxygen to arterial blood to nourish the body's tissues and to remove carbon dioxide from the returning venous blood. Gas exchange takes place at the level of the alveoli surrounded by a network of thin capillaries. Oxygen and carbon dioxide move between the air and blood by a process of diffusion. Air is brought to the alveoli by branching bronchi and bronchioles. The muscles of respiration act as a pump to move air in and out of the lungs. Elastic properties of the lung and chest wall and airway resistance affect the work and efficiency of the system. Disease processes that alter these relationships can lead to respiratory failure that is defined as failure of the lungs to oxygenate and ventilate adequately.
The tensions or pressures of dissolved oxygen or carbon dioxide in the blood are designated as Po2 and Pco2 (individual partial pressures of the gases), respectively. Table 2-1 shows the partial pressures of gases in the atmosphere and the lung. Dry atmospheric air is composed primarily of nitrogen. Oxygen constitutes 20.93% of the atmosphere; there is a minimal amount of carbon dioxide.
Dry atmospheric air is humidified as it travels down the airways into the lungs. The Po2 in the alveoli is determined by the balance between the amount that flows in and the amount that is removed by the pulmonary capillaries. It will be decreased if barometric pressure is low (ie, high altitude), if there is no fresh supply of air (ie, atelectasis), or if Pco2 is elevated (ie, hypoventilation).
As gas moves in and out of the alveolus, blood flows through the pulmonary capillary vessels, which provide a large surface for gas exchange. Figure 2-1 depicts how gas exchange occurs in the alveolus. The driving force for gas exchange is the difference in pressures of Po2 and Pco2 between the venous blood and alveoli. Under normal conditions, the gases equilibrate fully and the Po2 and Pco2 of pulmonary capillary blood equals that of the alveoli.
Oxygen Consumption and Carbon Dioxide Production
The total amount of oxygen that is taken up by the body in 1 minute is called the oxygen consumption (Vo2) and the amount of carbon dioxide produced is the carbon dioxide production (Vco2). Oxygen consumption and carbon dioxide production are increased with exercise. The ratio between the two is known as the respiratory quotient and is usually 0.8. The respiratory quotient rises (ie, more carbon dioxide is produced for each molecule of oxygen consumed) on a high carbohydrate diet. For patients in respiratory failure, low carbohydrate and high lipid formulas are suggested in order to decrease the respiratory quotient and decrease carbon dioxide production.
The process of ventilation brings air in and out of the lungs. During inspiration, the size of the thoracic cavity increases and air moves into the lungs. The fresh air is carried through conducting airways to the alveoli, which are responsible for gas exchange.
Alveolar and Dead Space Ventilation
The volume of a breath is known as the tidal volume. However, only part of the breath is used for gas exchange. Only the air that reaches the alveolus is involved in gas exchange; this is known as alveolar volume and is shown in Figure 2-2. The conducting airways are not involved in gas exchange and the volume of air in them is known as dead space. About 30% of each breath ends up in dead space. In some disease processes, the dead space volume increases and less air is available in each breath for gas exchange.
Total ventilation is the total volume of fresh air that reaches the lung each minute. It is determined by the volume of each breath, multiplied by the number of breaths per minute. The relationship between tidal volume, respiratory rate, and total ventilation is shown in Figure 2-3. If a child has a tidal volume of 100 mL and is breathing 15 breaths/min, then the total ventilation is 1,500 mL/min. Alveolar ventilation is the total volume of air that reaches the alveoli and is available for gas exchange each minute. Thus, if a disease process decreases the respiratory rate and/or the volume of each breath or increases the dead space, it will decrease the effective ventilation. Total ventilation is easy to quantify since tidal volume is easily measured; alveolar ventilation is more difficult since dead space is more difficult to measure.
Relationship of Ventilation to Arterial Pco2
The removal of carbon dioxide from the blood depends on alveolar ventilation. If alveolar ventilation increases, then the elimination of carbon dioxide increases and its concentration in the arterial blood decreases. This relationship is shown in Figure 2-4. If alveolar ventilation decreases, then the elimination of carbon dioxide decreases and it accumulates in the arterial blood. There is a direct relationship between the alveolar ventilation and the arterial carbon dioxide concentration: If alveolar ventilation doubles, the arterial carbon dioxide concentration is halved. If the alveolar ventilation decreases by 50%, then the arterial carbon dioxide concentration doubles.
The effect of changes in respiratory rate, tidal volume, and dead space on ventilation and arterial carbon dioxide level are depicted in Table 2-2. Decreased alveolar ventilation with an increase in arterial carbon dioxide tension (Pco2) can be caused by a wide variety of factors. A decrease in respiratory rate or tidal volume can result from drugs such as opiates, benzodiazepines, or alcohol; central nervous system infection; trauma; seizures; or sepsis. Premature infants can have cessation of breathing, or apnea of prematurity. In congenital central hypoventilation syndrome, children have a decreased central drive to breathe and, consequently, hypoventilation. In children with obstructive sleep apnea, there is a relative decrease in their tidal volume because they can't get an effective breath in. Chest wall trauma or deformity, neuromuscular weakness, and lung disease can also decrease the tidal volume and impair ventilation. Disease processes, such as acute respiratory distress syndrome, scoliosis, pulmonary embolus, or general anesthesia, can increase the dead space and thus impair the proportion of effective ventilation.
Increased alveolar ventilation results in a decrease in Pco2. Causes for increasing respiratory rate and tidal volume are depicted in Table 2-2. The most common etiologies include metabolic acidosis, salicylate ingestion, anxiety, central nervous system disorders, and pain. There are also some instances in which the dead space can be decreased.
Regulation of Arterial Pco2
The arterial carbon dioxide concentration reflects a balance between carbon dioxide production and elimination. More carbon dioxide is produced when the metabolic rate is increased. Fever or increased muscle activity (shivering, seizures) produce more carbon dioxide and can produce elevations in arterial carbon dioxide levels unless ventilation is increased.
Ventilation is controlled by sensors called chemoreceptors that are located in the brain and the carotid bodies, which lie at the bifurcation of the carotid arteries. These receptors sense changes in arterial carbon dioxide concentration. They respond by activating effectors that alter ventilation to keep arterial carbon dioxide concentration normal.
Excerpted from Pediatric Pulmonology by Michael J. Light. Copyright © 2011 American Academy of Pediatrics. Excerpted by permission of American Academy of Pediatrics.
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Table of Contents
Foundation 1 Anatomy of the Lung 2 Pulmonary Physiology 3 Applied Pulmonary Physiology 4 Taking a Pulmonary History 5 The Pulmonary Physical Examination 6 Pulmonary Function Testing 7 Pulmonary Imaging 8 Bronchoscopy Allergic Conditions 9 Allergic Bronchopulmonary Aspergillosis 10 Hypersensitivity Pneumonitis 11 Eosinophilic Pneumonia 12 Asthma 13 Congenital Anomalies of the Upper Airway 14 Congenital Lung Anomalies 15 Chest Wall and Spinal Deformities 16 Croup, Epiglottitis, and Bacterial Tracheitis Lower Airway Infections 17 Bronchiectasis 18 Bronchiolitis 19 Pneumonia 20 The Complications of Pneumonia 21 Recurrent Pneumonia 22 Tuberculosis 23 Nontuberculous Mycobacteria 24 Atelectasis 25 Rheumatic and Granulomatous Diseases 26 Interstitial Lung Disease 27 Bronchopulmonary Dysplasia 28 Pleural Effusion (Nonbacterial) 29 Pneumothorax and Pneumomediatstinum 30 Pulmonary Hemorrhage Other Pulmonologic Issues 31 Apparent Life-Threatening Events 32 Aspiration (Foreign Body, Food, Chemical) 33 Lung Transplantation 34 Pulmonary Disorders Associated With Obesity 35 Functional Respiratory Disorders 36 Sleep-Disordered Breathing Genetic Disorders 37 Cystic Fibrosis 38 Primary Ciliary Dyskinesia and Other Genetic Lung Diseases Lung Diseases Associated With Systemic Disorders 39 Respiratory Considerations in Children With Cardiac Disease 40 Lung Disease Associated With Endocrine Disorders 41 Pulmonary Complications of Gastrointestinal Diseases 42 Pulmonary Complications of Sickle Cell Disease 43 Pulmonary Manifestations of Oncologic Disease and Treatment 44 Pulmonary Complications of Immunologic Disorders 45 Pulmonary Complications of Neuromuscular Disorders Treating and Managing Pulmonary Disease 46 Airway Clearance Techniques 47 Aerosol Delivery of medication 48 Bronchodilators 49 Antibiotics of Pulmonary Conditions 50 Nutritional Aspects of Pulmonary Conditions 51 Oxygen Therapy 52 Secondhand Tobacco Smoke Exposure and Active Smoking in Childhood and Adolescence 53 Treating Tobacco Dependence 54 Home Apnea Monitoring 55 Tracheostomies 56 Home Ventilation