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Respiratory tract
Respiratory tract
Respiratory tract
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Respiratory tract
Conducting passages
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SystemRespiratory system
Identifiers
FMA265130
Anatomical terminology

The respiratory tract is the subdivision of the respiratory system involved with the process of conducting air to the alveoli for the purposes of gas exchange in mammals.[1] The respiratory tract is lined with respiratory epithelium as respiratory mucosa.[2]

Air is breathed in through the nose to the nasal cavity, where a layer of nasal mucosa acts as a filter and traps pollutants and other harmful substances found in the air. Next, air moves into the pharynx, a passage that contains the intersection between the oesophagus and the larynx. The opening of the larynx has a special flap of cartilage, the epiglottis, that opens to allow air to pass through but closes to prevent food from moving into the airway.

From the larynx, air moves into the trachea and down to the intersection known as the carina that branches to form the right and left primary (main) bronchi. Each of these bronchi branches into a secondary (lobar) bronchus that branches into tertiary (segmental) bronchi, that branch into smaller airways called bronchioles that eventually connect with tiny specialized structures called alveoli that function in gas exchange.

The lungs which are located in the thoracic cavity, are protected from physical damage by the rib cage. At the base of the lungs is a sheet of skeletal muscle called the diaphragm. The diaphragm separates the lungs from the stomach and intestines. The diaphragm is also the main muscle of respiration involved in breathing, and is controlled by the sympathetic nervous system.

The lungs are encased in a serous membrane that folds in on itself to form the pleurae – a two-layered protective barrier. The inner visceral pleura covers the surface of the lungs, and the outer parietal pleura is attached to the inner surface of the thoracic cavity. The pleurae enclose a cavity called the pleural cavity that contains pleural fluid. This fluid is used to decrease the amount of friction that lungs experience during breathing.

Structure

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Complete respiratory system

The respiratory tract is divided into the upper airways and lower airways. The upper airways or upper respiratory tract includes the nose and nasal passages, paranasal sinuses, the pharynx, and the portion of the larynx above the vocal folds (cords). The lower airways or lower respiratory tract includes the portion of the larynx below the vocal folds, trachea, bronchi and bronchioles. The lungs can be included in the lower respiratory tract or as separate entity and include the respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli.[3]

Adult and pediatric airway anatomy

The respiratory tract can also be divided into a conducting zone and a respiratory zone, based on the distinction of transporting gases or exchanging them.

The conducting zone includes structures outside of the lungs – the nose, pharynx, larynx, and trachea, and structures inside the lungs – the bronchi, bronchioles, and terminal bronchioles. The conduction zone conducts air breathed in that is filtered, warmed, and moistened, into the lungs. It represents the 1st through the 16th division of the respiratory tract. The conducting zone is most of the respiratory tract that conducts gases into and out of the lungs but excludes the respiratory zone that exchanges gases. The conducting zone also functions to offer a low resistance pathway for airflow. It provides a major defense role in its filtering abilities.

The respiratory zone includes the respiratory bronchioles, alveolar ducts, and alveoli, and is the site of oxygen and carbon dioxide exchange with the blood. The respiratory bronchioles and the alveolar ducts are responsible for 10% of the gas exchange. The alveoli are responsible for the other 90%. The respiratory zone represents the 16th through the 23rd division of the respiratory tract.

From the bronchi, the dividing tubes become progressively smaller with an estimated 20 to 23 divisions before ending at an alveolus.[1]

Upper respiratory tract

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Details of upper respiratory tract

The upper respiratory tract can refer to the parts of the respiratory system lying above the vocal folds, or above the cricoid cartilage.[4][5] The larynx is sometimes included in both the upper and lower airways.[6] The larynx is also called the voice box and has the associated cartilage that produces sound. The tract consists of the nasal cavity and paranasal sinuses, the pharynx (nasopharynx, oropharynx and laryngopharynx) and sometimes includes the larynx.

Lower respiratory tract

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Parts of the lower respiratory tract

The lower respiratory tract or lower airway is derived from the developing foregut and consists of the trachea, bronchi (primary, secondary and tertiary), bronchioles (including terminal and respiratory), and lungs (including alveoli).[7] It also sometimes includes the larynx.

The lower respiratory tract is also called the respiratory tree or tracheobronchial tree, to describe the branching structure of airways supplying air to the lungs, and includes the trachea, bronchi and bronchioles.[8]

At each division point or generation, one airway branches into two smaller airways. The human respiratory tree may consist on average of 23 generations, while the respiratory tree of the mouse has up to 13 generations. Proximal divisions (those closest to the top of the tree, such as the bronchi) mainly function to transmit air to the lower airways. Later divisions including the respiratory bronchiole, alveolar ducts, and alveoli, are specialized for gas exchange.

The trachea is the largest tube in the respiratory tract and consists of tracheal rings of hyaline cartilage. It branches off into two bronchial tubes, a left and a right main bronchus. The bronchi branch off into smaller sections inside the lungs, called bronchioles. These bronchioles give rise to the air sacs in the lungs called the alveoli.[10]

The lungs are the largest organs in the lower respiratory tract. The lungs are suspended within the pleural cavity of the thorax. The pleurae are two thin membranes, one cell layer thick, which surround the lungs. The inner (visceral pleura) covers the lungs and the outer (parietal pleura) lines the inner surface of the chest wall. This membrane secretes a small amount of fluid, allowing the lungs to move freely within the pleural cavity while expanding and contracting during breathing. The lungs are divided into different lobes. The right lung is larger in size than the left, because of the heart's being situated to the left of the midline. The right lung has three lobes – upper, middle, and lower (or superior, middle, and inferior), and the left lung has two – upper and lower (or superior and inferior), plus a small tongue-shaped portion of the upper lobe known as the lingula. Each lobe is further divided up into segments called bronchopulmonary segments. Each lung has a costal surface, which is adjacent to the ribcage; a diaphragmatic surface, which faces downward toward the diaphragm; and a mediastinal surface, which faces toward the center of the chest, and lies against the heart, great vessels, and the carina where the two mainstem bronchi branch off from the base of the trachea.

The alveoli are tiny air sacs in the lungs where gas exchange takes place. The mean number of alveoli in a human lung is 480 million.[11] When the diaphragm contracts, a negative pressure is generated in the thorax and air rushes in to fill the cavity. When that happens, these sacs fill with air, making the lung expand. The alveoli are rich with capillaries, called alveolar capillaries. Here the red blood cells absorb oxygen from the air and then carry it back in the form of oxyhaemaglobin, to nourish the cells. The red blood cells also carry carbon dioxide (CO2) away from the cells in the form of carbaminohemoglobin and release it into the alveoli through the alveolar capillaries. When the diaphragm relaxes, a positive pressure is generated in the thorax and air rushes out of the alveoli expelling the carbon dioxide.

Microanatomy

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See also: Respiratory epithelium
Respiratory epithelium

The respiratory tract is covered in epithelium, which varies down the tract. There are glands and mucus produced by goblet cells in parts, as well as smooth muscle, elastin or cartilage. The epithelium from the nose to the bronchioles is covered in ciliated pseudostratified columnar epithelium, commonly called respiratory epithelium.[12] The cilia beat in one direction, moving mucus towards the throat where it is swallowed. Moving down the bronchioles, the cells get more cuboidal in shape but are still ciliated.

Glands are abundant in the upper respiratory tract, but there are fewer lower down and they are absent starting at the bronchioles. The same goes for goblet cells, although there are scattered ones in the first bronchioles.

Cartilage is present until the bronchioles. In the trachea, they are C-shaped rings of hyaline cartilage, whereas in the bronchi the cartilage takes the form of interspersed plates. Smooth muscle starts in the trachea, where it joins the C-shaped rings of cartilage. It continues down the bronchi and bronchioles, which it completely encircles. Instead of hard cartilage, the bronchi and bronchioles are composed of elastic tissue.

The lungs are made up of thirteen different kinds of cells, eleven types of epithelial cell and two types of mesenchymal cell.[13] The epithelial cells form the lining of the tracheal, and bronchial tubes, while the mesenchymal cells line the lungs.

  • Differences in cells along the respiratory tract
    Differences in cells along the respiratory tract
  • Transverse section of tracheal tissue. Note that image is incorrectly labeled "ciliated stratified epithelium" at upper right.
    Transverse section of tracheal tissue. Note that image is incorrectly labeled "ciliated stratified epithelium" at upper right.

Function

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Most of the respiratory tract exists merely as a piping system for air to travel in the lungs, and alveoli are the only part of the lung that exchanges oxygen and carbon dioxide with the blood.

Respiration

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Main article: Breathing

Respiration is the rhythmical process of breathing, in which air is drawn into the alveoli of the lungs via inhalation and subsequently expelled via exhalation. When a human being inhales, air travels down the trachea, through the bronchial tubes, and into the lungs. The entire tract is protected by the rib cage, spine, and sternum. In the lungs, oxygen from the inhaled air is transferred into the blood and circulated throughout the body. Carbon dioxide (CO2) is transferred from returning blood back into gaseous form in the lungs and exhaled through the lower respiratory tract and then the upper, to complete the process of breathing.

Unlike the trachea and bronchi, the upper airway is a collapsible, compliant tube. As such, it has to be able to withstand suction pressures generated by the rhythmic expansion of the thoracic cavity that sucks air into the lungs. This is accomplished by the contraction of upper airway muscles during inhalation, such as the genioglossus (tongue) and the hyoid muscles. In addition to rhythmic innervation from the respiratory center in the medulla oblongata, the motor neurons controlling the muscles also receive tonic innervation that sets a baseline level of stiffness and size.

The diaphragm is the primary muscle that allows for lung expansion and contraction. Smaller muscles between the ribs, the external intercostals, assist with this process.

Defences against infection

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Further information: Mucociliary clearance

The epithelial lining of the upper respiratory tract is interspersed with goblet cells that secrete a protective mucus. This helps to filter waste, which is eventually either swallowed into the highly acidic stomach environment or expelled via spitting. The epithelium lining the respiratory tract is covered in small hairs called cilia. These beat rhythmically out from the lungs, moving secreted mucus foreign particles toward the laryngopharynx upwards and outwards, in a process called mucociliary clearance, preventing mucus accumulation in the lungs. Macrophages in the alveoli are part of the immune system which engulf and digest any inhaled harmful agents.

Hair in the nostrils plays a protective role, trapping particulate matter such as dust.[14] These hairs, called vibrissae, are thicker than body hair and effectively block larger particles from entering the respiratory tract. They also increase the surface area for particle deposition, improving the nose's ability to filter pathogens.[15] The cough reflex expels all irritants within the mucous membrane to the outside. The airways of the lungs contain rings of muscle. When the passageways are irritated by some allergen, these muscles can constrict.

Clinical significance

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See also: Respiratory disease

The respiratory tract is a common site for infections.

Infection

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Upper respiratory infection

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Main article: Upper respiratory tract infection

Upper respiratory tract infections are probably the most common infections in the world.

The respiratory system is very prone to developing infections in the lungs. Infants and older adults are more likely to develop infections in their lungs because their lungs are not as strong in fighting off these infections. Most of these infections used to be fatal, but with new research and medicine, they are now treatable. With bacterial infections, antibiotics are prescribed, while viral infections are harder to treat but still curable.

The common cold, and flu are the most common causes of an upper respiratory tract infection, which can cause more serious illness that can develop in the lower respiratory tract.

Lower respiratory tract infections

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Main articles: Lower respiratory infection and Pneumonia

Pneumonia is the most common, and frequent lower respiratory tract infection. This can be either viral, bacterial, or fungal. This infection is very common because pneumonia can be airborne, and when you inhale this infection in the air, the particles enter the lungs and move into the air sacs. This infection quickly develops in the lower part of the lung and fills the lung with fluid, and excess mucus. This causes difficulty in breathing and coughing as the lower respiratory tract tries to get rid of the fluid in the lungs. You can be more prone to developing this infection if you have asthma, flu, heart disease, or cancer[16]

Bronchitis is another common infection that takes place in the lower respiratory tract. It is an inflammation of the bronchial tubes. There are two forms of this infection: acute bronchitis, which is treatable and can go away without treatment, or chronic bronchitis, which comes and goes, but will always affect one's lungs. Bronchitis increases the amount of mucus that is natural in your respiratory tract. Chronic bronchitis is common in smokers, because the tar from smoking accumulates over time, causing the lungs to work harder to repair themselves.[17]

Tuberculosis is one of many other infections that occurs in the lower respiratory tract. You can contract this infection from airborne droplets, and if inhaled you are at risk of this disease. This is a bacterial infection that deteriorates the lung tissue resulting in coughing up blood.[18] This infection is deadly if not treated.

Cancer

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Main article: Lung cancer
3D still showing increased mucus

Some of these cancers have environmental causes such as smoking. When a tobacco product is inhaled, the smoke paralyzes the cilia, causing mucus to enter the lungs. Frequent smoking, over time, causes the cilia hairs to die and can no longer filter mucus. Tar from the smoke inhaled enters the lungs, turning the pink-coloured lungs black. The accumulation of this tar could eventually lead to lung cancer, or chronic obstructive pulmonary disease.[7]

COPD

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Main article: Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a common lower respiratory disease that can be caused by exposure to harmful chemicals, or prolonged use of tobacco. This disease is chronic and progressive, the damage to the lungs is irreversible and eventually fatal. COPD destroys the alveoli, and lung tissue which makes breathing very difficult, causing shortness of breath, hyperventilation, and raised chest. The decreased number of alveoli causes loss of oxygen supply to the lungs and an increased accumulation of carbon dioxide. There are two types of COPD: primary and secondary.[citation needed] Primary COPD can be found in younger adults. This type of COPD deteriorates the air sacs, and lung mass. Secondary COPD can be found in older adults who smoke or have smoked and have a history of bronchitis. [citation needed] COPD includes symptoms of emphysema and chronic bronchitis.[19]

Asthma

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Main article: Asthma
3D still showing constricted airways

The bronchi are the main passages to the right and left lungs. These airways carry oxygen to the bronchioles inside the lungs. Inflammation of the bronchii and bronchioles can cause them to swell up, which could lead to an asthma attack. This results in wheezing, tightness of the chest, and severe difficulty in breathing. There are different types of asthma that affect the functions of the bronchial tubes. Allergies can also set off an allergic reaction, causing swelling of the bronchial tubes; as a result, the air passage will swell up, or close up completely.[20]

Mouth breathing

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In general, air is inhaled through the nose. It can be inhaled through the mouth if it is not possible to breathe through the nose. However, chronic mouth breathing can cause a dry mouth and lead to infections.[21]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Respiratory tract

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from Grokipedia
The respiratory tract, also known as the , is the integrated network of organs and structures that enables the intake of oxygen and the expulsion of through the process of , primarily facilitating in the lungs. It is divided into the upper respiratory tract, which includes the , , , and , and the lower respiratory tract, encompassing the trachea, bronchi, bronchioles, and lungs. The system's core function is to conduct air from the external environment to the alveoli in the lungs, where oxygen diffuses into the bloodstream and is removed, while also providing , humidification, and warming of inhaled air to protect the body from pathogens and environmental irritants. The upper respiratory tract serves as the entry point for air, beginning with the nose and nasal cavity, which are lined with mucous membranes and cilia that trap dust, allergens, and microbes, while turbinates increase surface area for humidification and warming. Air then passes through the pharynx, a muscular tube divided into nasopharynx, oropharynx, and laryngopharynx, which aids in swallowing and directs air to the larynx, the voice box composed of cartilages like the thyroid, cricoid, and epiglottis that prevent food aspiration and enable vocalization via the vocal folds. These structures not only conduct air but also initiate immune defenses through mucus production and resident macrophages. In the lower respiratory tract, the trachea, a flexible tube reinforced by C-shaped cartilage rings, extends from the larynx to bifurcate into the right and left main bronchi at the carina, with the right bronchus being wider, shorter, and more vertical, making it more prone to aspiration. The bronchi branch into lobar and segmental bronchi, transitioning to cartilage-free bronchioles that further divide into respiratory bronchioles leading to alveolar ducts and sacs. The lungs, paired cone-shaped organs protected by the rib cage and pleura—a double-layered membrane with lubricating fluid—house approximately 480 million alveoli, where thin-walled type I pneumocytes form the air-blood barrier for efficient gas exchange, supported by type II pneumocytes that secrete surfactant to reduce surface tension and prevent alveolar collapse. The right lung has three lobes and the left has two, accommodating the heart's position, and the entire tract is innervated by the vagus nerve for parasympathetic control (promoting bronchoconstriction) and sympathetic fibers for dilation, ensuring regulated airflow.

Structure and anatomy

Upper respiratory tract

The upper respiratory tract encompasses the anatomical structures responsible for the initial conduction, filtration, warming, and humidification of inspired air, extending from the external nares to the up to the level of the vocal folds. It includes the , , nasopharynx, oropharynx, laryngopharynx, and , serving as the extrathoracic portion of the airway that prepares air for entry into the lower respiratory tract without participating in . The boundary with the lower respiratory tract occurs at the , where the vocal folds mark the transition to the trachea. Key structures of the nasal cavity include the vestibule at the entrance, lined by with vibrissae for coarse , and the main chamber divided by the into two symmetric halves. The lateral walls feature three turbinates (inferior, middle, and superior conchae) that project into the cavity, creating meatuses that increase surface area for and direct airflow. The —air-filled extensions of the —comprise the (pyramidal, located in the above the orbits, draining into the middle meatus), (the largest, pyramidal in the below the orbits, draining into the middle meatus), ethmoid sinuses (multiple air cells between the orbits in the , with anterior cells draining to the middle meatus and posterior to the superior meatus), and (paired cavities in the body, draining into the sphenoethmoidal recess). These sinuses lighten the , resonate voice, and contribute to humidification. The , a muscular tube posterior to the nasal and oral cavities, divides into three regions: the nasopharynx (from the choanae to the , containing the pharyngeal and openings for ventilation), oropharynx (from the to the , including the palatine and serving both respiratory and digestive functions), and laryngopharynx (from the to the and , directing air to the and food to the ). The , positioned anterior to the laryngopharynx, consists of nine cartilages: the shield-shaped (forming the laryngeal prominence), ring-shaped (the only complete tracheal ring), leaf-like (covering the laryngeal inlet during ), paired arytenoid cartilages (for vocal fold attachment), and smaller corniculate and . The vocal folds, attached to the arytenoids, demarcate the and enable . Blood supply to the upper respiratory tract arises primarily from branches of the external and internal carotid arteries. The nasal cavity receives arterial blood via the sphenopalatine artery (from the maxillary artery), anterior and posterior ethmoidal arteries (from the ophthalmic artery), and superior labial and lateral nasal arteries (from the facial artery), with venous drainage into the facial vein and pterygoid plexus. The paranasal sinuses share this supply through their ostia connections to the nasal mucosa. The pharynx is supplied by the ascending pharyngeal, tonsillar (from the facial artery), and maxillary arteries, with venous drainage via pharyngeal veins to the internal jugular vein. The larynx obtains blood from the superior laryngeal artery (branch of the superior thyroid artery, supplying the supraglottic region and epiglottis) and inferior laryngeal artery (branch of the inferior thyroid artery, supplying the subglottic region and inferior vocal folds), with venous return to the thyroid veins and ultimately the internal jugular. Innervation of the upper respiratory tract involves sensory and motor components from cranial nerves, primarily for sensation, mucus secretion, and muscle control. The nasal cavity and paranasal sinuses receive sensory innervation from the ophthalmic (V1) and maxillary (V2) divisions of the trigeminal nerve (CN V), with olfactory sensation via the olfactory nerve (CN I) in the superior region. The nasopharynx is sensory-innervated by CN V2, the oropharynx by the glossopharyngeal nerve (CN IX), and the laryngopharynx by the internal branch of the superior laryngeal nerve (from the vagus nerve, CN X). Motor innervation to pharyngeal constrictor muscles comes from CN IX (stylopharyngeus) and CN X (other constrictors), while the larynx is supplied by the recurrent laryngeal nerve (CN X branch, innervating all intrinsic muscles except cricothyroid) and the external branch of the superior laryngeal nerve (for cricothyroid). Autonomic fibers from the vagus and facial nerves (CN VII) regulate vasomotor and secretory functions via parasympathetic pathways. In function, the upper respiratory tract conducts air from the external environment to the lower tract, filtering particulates via nasal hairs, turbinates, and (ciliated ), while vascular plexuses warm air to body temperature and mucous glands humidify it to near 100% relative humidity. This conditioning prevents and irritation of lower airway tissues, with no significant occurring here.

Lower respiratory tract

The lower respiratory tract begins inferior to the vocal folds and encompasses the structures responsible for conducting air to the gas exchange sites within the lungs. It includes the trachea, main bronchi, lobar and segmental bronchi, bronchioles, terminal and respiratory bronchioles, alveolar ducts, and alveoli. This tract extends from the thoracic inlet to the pulmonary , facilitating the distribution of inspired air while providing structural support against collapse during respiration. The trachea, a flexible tube approximately 10-12 cm long and 2-2.5 cm in diameter, is reinforced by 16-20 C-shaped rings that prevent collapse and maintain patency. These rings are incomplete posteriorly, allowing the to form a supportive band. At the carina, the trachea bifurcates into the right and left main bronchi, initiating the bronchial tree, which undergoes dichotomous branching for 16-23 generations to form an extensive network of progressively narrower airways. The right main bronchus is shorter, wider, and more vertical than the left, contributing to its higher susceptibility to aspiration. Lobar bronchi supply the three lobes of the right (upper, middle, and lower) and the two lobes of the left (upper and lower), with the lingula forming part of the left upper lobe, while segmental bronchi further divide into approximately 10 segments per . Bronchioles lack and rely on for tone, transitioning to terminal bronchioles (purely conductive) and respiratory bronchioles (with initial alveolar outpouchings), which lead to alveolar ducts and culminate in about 480 million alveoli across both lungs. The lungs are enveloped by pleural membranes: the visceral pleura adheres directly to the lung surface, while the parietal pleura lines the , with a thin between them containing lubricating . The blood supply to the lower respiratory tract is dual: the pulmonary arteries deliver deoxygenated blood to the alveolar capillaries for , while the bronchial arteries (branches of the ) provide oxygenated blood to nourish the airway walls, supporting metabolic needs of the and . Venous drainage from the pulmonary circuit returns oxygenated blood to the left atrium via pulmonary veins, whereas bronchial veins drain into the azygos or pulmonary veins. Innervation arises from the pulmonary plexus at the lung hilum, with parasympathetic fibers from the (cranial nerve X) promoting and glandular secretion via muscarinic receptors on and submucosal glands, and sympathetic fibers from the cervical and thoracic sympathetic chains inducing bronchodilation through beta-adrenergic receptors. Structural adaptations in the lower respiratory tract optimize air conduction and mechanical stability. Proximal airways feature prominent —complete C-shaped rings in the trachea transitioning to irregular plates in bronchi—for rigidity, which diminishes distally as bronchioles depend on elastic fibers and to resist compressive forces during expiration. This progressive reduction in cartilaginous support, combined with increasing mucosal folds and decreasing epithelial height, minimizes resistance while maximizing airflow distribution to the alveoli.

Microanatomy and histology

The microanatomy of the respiratory tract encompasses a specialized and supporting tissues that vary regionally to optimize air conduction, particle clearance, and . The lining the conducting portions—from the nasal passages through the bronchioles—consists primarily of pseudostratified ciliated columnar cells, interspersed with goblet cells and basal cells, which together form a protective barrier against inhaled particulates. In contrast, the alveolar regions of the respiratory zone are lined by simple squamous type I pneumocytes, which provide an expansive, thin surface for , and cuboidal type II pneumocytes, which serve as progenitors and secretory cells. Key supporting elements enhance these functions across the tract. Goblet cells within the pseudostratified epithelium secrete mucins to form a viscoelastic layer that traps microbes and . Cilia projecting from epithelial cells feature a 9+2 axonemal structure of , enabling metachronal beating that drives upward toward the . Submucosal glands, abundant in the trachea and larger bronchi, produce additional seromucous secretions to hydrate and lubricate the airway surface. Elastic fibers in the lamina propria and beyond impart elasticity for recoil during , while circumferential bundles in bronchi and bronchioles allow dynamic regulation of . Histologically, the tract divides into conducting and respiratory zones with distinct architectures. The conducting zone, spanning from the to terminal bronchioles, prioritizes and filtration without , featuring thicker , glands, and for structural support. The respiratory zone, including respiratory bronchioles, alveolar ducts, and alveoli, optimizes through a minimalist design: its blood-air barrier averages 0.2–1 μm in thickness, formed by fused basement membranes between type I pneumocytes and endothelial cells. Regional variations reflect adaptive specializations. The nasal vestibule is protected by keratinized , continuous with , to withstand mechanical irritation from air and particles. In the trachea and bronchi, incomplete rings or plates of embedded in the fibroelastic wall prevent collapse under pressure changes. Alveolar type II pneumocytes uniquely synthesize and release , primarily composed of dipalmitoylphosphatidylcholine, to minimize and prevent collapse.

Development and embryology

Embryonic development

The embryonic development of the respiratory tract originates from the ventral wall of the during the fourth week of , when the respiratory emerges as a laryngotracheal that elongates caudally to form the initial respiratory tube. This gives rise to the trachea, buds, and associated structures, with the separation of the respiratory tube from the beginning through the formation of tracheoesophageal ridges that fuse to create a by the end of week 5. Incomplete separation during this process can lead to congenital anomalies such as , where an abnormal connection persists between the trachea and , often associated with disruptions in signaling pathways like Sonic Hedgehog (SHH). Branching morphogenesis commences in week 5 as the primary lung buds form and penetrate the surrounding splanchnopleuric , generating secondary bronchi (two on the left and three on the right) by the end of that week, followed by tertiary buds that establish the bronchopulmonary segments by week 6. This process continues into the pseudoglandular stage (weeks 5–17), during which approximately 20 generations of airways develop through iterative epithelial-mesenchymal interactions driven by factors such as fibroblast growth factor 10 (FGF10) and bone morphogenetic protein 4 (BMP4), outlining the basic bronchial tree structure by week 16. Cellular contributions are multifaceted: the provides the epithelial lining of the airways, the differentiates into , , , and vasculature, while cells migrate to contribute to innervation and certain laryngeal cartilages. Key milestones include the separation of the and from the trachea by week 7 via laryngotracheal sulci, the establishment of the pleural cavities from mesodermal invaginations between weeks 5 and 7, and the initial formation of acinar precursors at the distal ends of the branching airways by the close of the pseudoglandular phase. These early events lay the foundational architecture for the respiratory tract, with further maturation occurring in subsequent fetal stages.

Fetal and postnatal maturation

The fetal respiratory tract undergoes significant maturation during the later stages of , transitioning from the canalicular phase (approximately weeks 16 to 26) where extensive vascularization occurs and primitive airspaces form, enabling initial potential for . During this period, the develops cuboidal lining the future airspaces, and capillaries closely approximate the epithelium to support oxygenation. This is followed by the saccular stage (weeks 24 to 36), characterized by the expansion of terminal sacs that give rise to primitive alveoli, with thinning of the and increased epithelial differentiation to prepare for air . The alveolar stage begins around week 36 and extends through term, during which mature alveoli form with type I epithelial cells flattening to optimize diffusion surfaces, though substantial alveolarization continues postnatally. Pulmonary surfactant, essential for reducing and preventing alveolar collapse, is produced by maturing type II alveolar cells that begin differentiating around week 24 of . secretion starts in small amounts at this time but ramps up progressively, reaching levels sufficient to stabilize alveoli and avert by approximately week 32. This lipid-protein complex, primarily composed of dipalmitoylphosphatidylcholine, is stored in lamellar bodies within type II cells and released in response to fetal movements, which emerge around week 20 to promote lung fluid dynamics. Following birth, postnatal lung growth involves rapid alveolar multiplication, with estimates indicating around 50 million alveoli present at birth, expanding to approximately 300 million by age 8 through septation of existing saccules. This process occurs exponentially in the first two years, followed by a slower increase, while overall lung volume grows proportionally to body size, reaching adult proportions by . Alveolar dimensions stabilize during this period, but the total surface area expands dramatically to meet rising metabolic demands. Prematurity poses significant risks to respiratory maturation, particularly before week 32 when production is inadequate, leading to respiratory distress syndrome characterized by alveolar collapse and impaired in neonates. Environmental exposures in early life, such as prenatal or postnatal tobacco smoke and , can influence airway caliber development by promoting and reduced luminal diameter in children. These factors may alter early , potentially limiting maximal even in otherwise healthy individuals. Lung function peaks during early adulthood, typically in the 20s, with maximal and achieved by age 25, after which a gradual decline begins around age 30 due to loss of parenchymal elasticity and weakened respiratory muscles. This age-related reduction in and capacity proceeds at about 1% per year, influenced by cumulative environmental insults but remaining minimal in non-smokers until later decades.

Function and physiology

Breathing mechanics

Breathing mechanics encompass the physical processes that drive the movement of air into and out of the lungs, known as ventilation, through coordinated changes in thoracic volume and pressure gradients. The ventilation cycle consists of inspiration, the active phase where air enters the lungs, and expiration, which is typically passive at rest. During inspiration, the primary muscle, the diaphragm, contracts and flattens, increasing the vertical dimension of the , while the elevate the ribs, expanding the anteroposterior and transverse dimensions. This enlargement of thoracic volume reduces from approximately -5 cmH₂O at rest to -7.5 to -10 cmH₂O, creating a subatmospheric pressure in the alveoli (around -1 cmH₂O during quiet ) that draws air in according to , which states that the pressure and volume of a gas are inversely proportional at constant : P1V1=P2V2P_1 V_1 = P_2 V_2. Expiration during quiet breathing relies on passive elastic recoil of the and chest wall, as the diaphragm and external intercostals relax, decreasing thoracic volume and raising alveolar to about +1 cmH₂O, expelling air until equilibrium with is reached. In forced expiration, such as during exercise, accessory muscles including the internal intercostals and abdominal muscles (e.g., rectus abdominis) contract to further reduce thoracic volume and increase expiratory . These muscle actions maintain the negative throughout the cycle, preventing collapse. The overall process is governed by the compliance of the lower respiratory tract, where —typically 0.2 L/cmH₂O—allows volume changes for a given alteration, reflecting the elastic properties of tissue and that minimize in alveoli. Lung volumes, measured via , quantify the mechanics of ventilation and vary with muscle effort. , the air moved in a normal breath, is approximately 500 mL in adults. Inspiratory reserve volume, the additional air that can be inhaled beyond , is about 3000 mL, while expiratory reserve volume, the extra air exhaled after a normal breath, is around 1100 mL. , the maximum air that can be exhaled after maximum (tidal volume + inspiratory reserve + expiratory reserve), totals roughly 4600 mL, providing a measure of overall ventilatory capacity. Airflow through the respiratory tract is influenced by resistance, particularly in narrower airways, where Poiseuille's describes : Q=πr4ΔP8ηLQ = \frac{\pi r^4 \Delta P}{8 \eta L}, with Q as flow rate, r as , ΔP as difference, η as , and L as length; resistance increases dramatically with reduced (inversely proportional to r⁴). The upper respiratory tract, including the and , accounts for about 50% of total due to its narrower passages and turbulent flow potential, while the lower tract's branching structure reduces resistance through parallel pathways despite smaller individual diameters.

Gas exchange

Gas exchange in the respiratory tract occurs primarily in the alveoli and to a lesser extent in the respiratory bronchioles. This process relies on the thin blood-air barrier, composed of type I alveolar epithelial cells, a shared , and endothelial cells, which collectively form a trilamellar structure optimized for . Diffusion of gases across this barrier is driven by partial pressure gradients: oxygen moves from the alveolar air (partial pressure of 104 mmHg) into deoxygenated pulmonary blood (40 mmHg), while diffuses in the opposite direction from (46 mmHg) to alveolar air (40 mmHg). The rate of this diffusion is governed by Fick's law, expressed as V=DAΔPT,V = \frac{D A \Delta P}{T}, where VV is the diffusion rate, DD is the diffusion coefficient of the gas, AA is the surface area (approximately 70 m² in adults), ΔP\Delta P is the partial pressure difference, and TT is the barrier thickness (typically 0.2–0.6 μm). The large surface area and minimal thickness ensure efficient transfer, with oxygen equilibrating within 0.75 seconds of capillary transit time under normal conditions. Once diffused, oxygen binds to in red blood cells, forming oxyhemoglobin; this binding is characterized by the sigmoid-shaped oxyhemoglobin dissociation curve, where the P50 value—the at which is 50% saturated—is 26 mmHg at standard conditions ( 7.4, 37°C, PCO₂ 40 mmHg). , conversely, is transported mainly as ions (about 70% of total), facilitated by the enzyme in erythrocytes, which catalyzes the reversible reaction \ceCO2+H2O⇌[CA]H2CO3⇌H++HCO3−.\ce{CO2 + H2O ⇌[CA] H2CO3 ⇌ H+ + HCO3-}. The bicarbonate is exchanged for chloride ions across the red blood cell membrane (Hamburger shift), maintaining electroneutrality. For optimal efficiency, alveolar ventilation must match pulmonary perfusion, yielding an ideal ventilation-perfusion (V/Q) ratio of 0.8 globally (ventilation of 4 L/min to perfusion of 5 L/min); regional mismatches, such as high V/Q (dead space) or low V/Q (shunt), impair gas exchange and can cause hypoxemia by reducing arterial oxygen saturation. Pulmonary surfactant, a phospholipid-protein secreted by type II alveolar cells, minimizes at the air-liquid interface to prevent alveolar collapse, as described by the law of Laplace: P=2Tr,P = \frac{2T}{r}, where PP is the required to keep alveoli open, TT is , and rr is alveolar radius; reduces TT up to 15-fold, stabilizing smaller alveoli during expiration. Additionally, the modulates oxygen delivery: decreased (from CO₂ accumulation or metabolic acids) shifts the oxyhemoglobin dissociation curve rightward, lowering hemoglobin's oxygen affinity and promoting unloading in tissues.

Protective and sensory roles

The respiratory tract serves critical protective functions beyond , primarily through mechanical, cellular, and humoral defenses that prevent entry and remove inhaled particles. The mucociliary , a key innate defense mechanism, involves coordinated beating of cilia on epithelial cells lining the airways, which propel mucus-trapped particles toward the oropharynx at frequencies of 10-20 Hz, facilitating clearance without inflammation. Alveolar macrophages, resident phagocytes in the , engulf and destroy inhaled microbes and debris via , constituting the first line of cellular immunity in the alveoli. Secretory (IgA), abundant in airway surface liquid, neutralizes pathogens by preventing their adhesion to epithelial surfaces and promoting their expulsion. Reflexive responses, such as the and , further enhance protection; the , triggered by irritants in the lower airways, generates high-velocity airflow to expel material, while the sneeze reflex rapidly clears the nasal passages of foreign substances. Sensory roles in the respiratory tract enable detection of environmental threats and facilitate olfaction. The , located in the superior , contains approximately 400 types of neurons that detect odorants through G-protein-coupled receptors, with axons projecting through the to the for central processing. Irritant detection occurs via endings in the nasal and upper airway mucosa, which respond to chemical and mechanical stimuli, eliciting protective reflexes, and pulmonary J-receptors (juxtacapillary endings), vagal C-fibers sensitive to interstitial changes and irritants, which trigger sensations of breathlessness or to avert deeper of hazards. Phonation, a sensory-motor function, relies on the for sound production essential to communication. Vibration of the vocal folds during expiration generates voiced sounds, with fundamental frequencies typically ranging from 100-200 Hz in adult speech, modulated by tension and length adjustments via laryngeal muscles to produce pitch variation. Additional protective mechanisms include conditioning of inspired air and maintenance of optimal mucosal conditions. The upper respiratory tract warms and incoming air to near body temperature (37°C) and 100% relative humidity, preventing desiccation of the and enhancing mucociliary function. Airway pH regulation, primarily through epithelial ion transporters like CFTR and SLC26A9, maintains surface liquid acidity ( ~6.5-7.0) to optimize antimicrobial peptide activity and ciliary motility. These functions are integrated via modulation, where parasympathetic activation stimulates mucus secretion from submucosal glands to bolster barrier integrity, while sympathetic input can inhibit it during stress, fine-tuning responses to environmental demands.

Diseases and disorders

Infections of the upper tract

Infections of the upper respiratory tract primarily involve the , , , and , and are most often caused by viral pathogens leading to self-limiting illnesses such as the . These infections typically manifest as acute conditions with symptoms including , , , , and low-grade fever, though bacterial involvement can occur in specific sites like the pharynx. Common viral pathogens include rhinoviruses, which account for 50% to 80% of cases, coronaviruses (responsible for 10-15% of colds), viruses (causing seasonal epidemics with up to 1 billion global cases annually), and parainfluenza viruses. Bacterial pathogens, such as ( ), are notable for causing acute , accounting for 15-30% of cases in children and over 600 million upper respiratory infections worldwide each year. Post-2020, variants have also contributed to upper tract involvement, often presenting with symptoms overlapping those of other viral infections. Specific acute infections include (middle ear inflammation often complicating viral upper infections), (inflammation of the ), and (laryngeal inflammation leading to hoarseness and voice changes). Symptoms vary by site: presents with severe and , while may cause in severe pediatric cases like . These conditions are differentiated from lower tract infections by their localization above the and generally milder, non-systemic course. Epidemiologically, upper respiratory infections impose a substantial global burden, with approximately 12.8 billion episodes reported in 2021, predominantly affecting children under 5 years who experience 6-10 colds annually compared to 2-3 in adults. Risk factors include environmental exposures like , which impairs mucosal defenses and increases infection susceptibility, and allergens, which exacerbate symptoms in individuals with or . The incidence is highest in young children due to immature immunity and close-contact settings like daycare. Transmission occurs primarily through respiratory droplets, airborne particles, and direct contact with contaminated surfaces or secretions, with an of 1-4 days for most viral agents like rhinoviruses. Hand hygiene and avoiding close contact reduce spread effectively. Complications are uncommon but can include secondary bacterial (affecting up to 30% of upper infections in children) or rare progression to ; spread to the lower tract occurs infrequently due to anatomical barriers.

Infections of the lower tract

Infections of the lower respiratory tract, which encompasses the trachea, bronchi, bronchioles, and alveoli, represent a significant burden due to their potential to cause severe , impaired , and systemic complications. These infections typically arise when pathogens bypass upper airway defenses and invade deeper structures, often leading to conditions that require medical intervention and hospitalization. Unlike upper tract infections, which are frequently self-limiting, lower tract involvement can result in hypoxia and long-term sequelae, particularly in vulnerable populations. Common pathogens include bacteria such as , the leading cause of , and , frequently implicated in . Viral agents like (RSV) predominate in infants, causing over 3.6 million hospitalizations annually worldwide for and , though new vaccines and monoclonal antibodies approved in 2023-2024 may reduce this burden.) Additionally, Mycobacterium tuberculosis drives tuberculosis (TB), with an estimated 10.8 million new cases in 2023, primarily affecting the lungs and contributing to chronic lower tract pathology. The primary types of lower tract infections are , , and . Acute involves inflammation of the bronchi, often viral but sometimes bacterial, leading to production and airway ; chronic , a component of , features persistent cough and recurrent exacerbations. manifests as lobar consolidation from uniform alveolar filling, typically bacterial, or bronchopneumonia with patchy distribution around bronchi, more common in viral or mixed etiologies. , primarily affecting small airways in young children, causes obstruction and wheezing, most often due to RSV during winter seasons. Epidemiologically, lower respiratory infections (LRIs) accounted for approximately 2.5 million deaths globally in 2021, remaining the leading infectious cause of mortality and disproportionately affecting children under 5 and adults over 70, as well as those in low- and middle-income countries. Incidence is higher in low-income settings, where limited access to vaccines and antibiotics exacerbates outcomes; post-COVID-19, survivors face elevated risks of persistent and recurrent infections, with studies showing up to 30% experiencing ongoing lung abnormalities one year later. Symptoms commonly include dyspnea, a productive cough with purulent sputum, and fever exceeding 38°C, reflecting inflammatory responses in the lower airways. Chest X-rays often reveal infiltrates or consolidations, aiding diagnosis of , while wheezing and signal . Key risk factors encompass aspiration, particularly in the elderly or those with disorders, and immunosuppression from conditions like or , which impair clearance. Environmental exposures, including and , heighten susceptibility, while is expanding vector-borne fungal infections such as , with projections of millions more at risk due to warming temperatures favoring fungal growth.

Obstructive lung diseases

Obstructive lung diseases encompass a group of chronic respiratory conditions characterized by persistent airflow limitation that is not fully reversible, primarily affecting the lower respiratory tract and leading to symptoms such as dyspnea, , and wheezing. These disorders result from abnormalities in the airways and , distinguishing them from restrictive diseases by the hallmark reduction in the ratio of forced expiratory volume in one second to forced (FEV1/FVC < 0.7 on after administration). The two most common obstructive lung diseases are and (COPD), which together impose a significant burden through reduced and increased mortality. Asthma is defined as a heterogeneous characterized by chronic airway and , resulting in recurrent episodes of wheezing, breathlessness, chest tightness, and , particularly at night or early morning, with variable expiratory airflow limitation that is often reversible spontaneously or with treatment. Common triggers include allergens such as or dust mites, exercise, cold air, and respiratory infections, which provoke and in susceptible individuals. Globally, asthma affects an estimated 262 million people as of , with prevalence continuing to rise in many regions due to environmental and factors. Diagnosis typically involves demonstrating reversible airway obstruction on , where an increase in FEV1 of at least 12% and 200 mL after administration confirms variability, alongside peak flow monitoring showing diurnal variability greater than 10% in symptomatic patients. In contrast, COPD represents a progressive, largely irreversible condition defined by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities, usually caused by significant exposure to noxious particles or gases. It encompasses two main pathological phenotypes: , involving destruction of alveolar walls and loss of elasticity, and chronic , marked by and production for at least three months in two consecutive years. is the primary , accounting for approximately 80-90% of cases in high-income countries, with additional contributions from biomass fuel exposure and in low- and middle-income settings. COPD caused 3.5 million deaths worldwide in 2021, ranking as the fourth leading and underscoring its impact. Severity is classified using the Global Initiative for Chronic Obstructive Disease (GOLD) stages based on post-bronchodilator FEV1 percentage of predicted value: mild (≥80%), moderate (50-79%), severe (30-49%), and very severe (<30%). The of obstructive diseases involves shared mechanisms, including chronic leading to airway remodeling—such as smooth muscle and subepithelial — hypersecretion from , and, in COPD, proteolytic destruction of elastic fibers causing loss of . In , predominates with eosinophilic infiltration and IgE-mediated responses, while COPD features neutrophilic and exacerbating tissue damage. These changes narrow the airways, increase resistance, and impair , with plugs further obstructing during exacerbations. Diagnosis of obstructive lung diseases relies on clinical history, physical examination, and confirmatory pulmonary function tests, with spirometry as the gold standard to establish airflow limitation (FEV1/FVC < 0.7 post-bronchodilator). For , documentation of reversibility or variability distinguishes it from COPD, where obstruction persists despite treatment; additional tests like fractional exhaled may support an eosinophilic asthma phenotype. variability over time aids in monitoring asthma control at home. Management of obstructive lung diseases focuses on symptom relief, reducing exacerbations, and improving function, tailored to the specific condition. For both asthma and COPD, inhaled therapies are cornerstone, including short-acting beta-agonists (e.g., albuterol) for acute relief and long-acting beta-agonists (e.g., salmeterol) combined with inhaled corticosteroids (e.g., ) to reduce and hyperresponsiveness. In asthma, step-wise escalation per GINA guidelines prioritizes controller medications to achieve symptom control and minimize future risks. For COPD, GOLD recommends bronchodilators as initial therapy, with as the most effective intervention to slow disease progression and reduce mortality by up to 50% in quitters. and vaccinations further support long-term management.

Respiratory tract cancers

Respiratory tract cancers encompass malignant neoplasms arising from the epithelial lining of the upper and lower respiratory pathways, with predominating due to its high incidence and mortality. The primary types include non-small cell (NSCLC), which accounts for approximately 85% of and is subdivided into , , and large cell carcinoma; small cell (SCLC), comprising about 15% of cases and characterized by rapid growth; , predominantly originating in the or supraglottis; and rare upper tract malignancies such as sinonasal cancers, which represent less than 1% of head and neck tumors with an incidence below 1 per 100,000 population. Approximately 85% of are attributable to , underscoring its role as the leading modifiable risk factor. Globally, , the most common respiratory tract malignancy, resulted in about 2.5 million new cases and 1.8 million deaths in 2022, according to estimates from the International Agency for Research on Cancer (IARC). The overall 5-year survival rate for remains low at around 20%, reflecting late-stage diagnoses in most patients. Beyond , key environmental risks include exposure, responsible for up to 15% of cases worldwide, particularly in never-smokers, and , which contributes to roughly 4% of cases and synergistically amplifies risk in smokers. Laryngeal cancers, while less frequent (about 180,000 cases annually), share and alcohol as primary risks, with sinonasal tumors linked to occupational exposures like wood dust. Pathogenesis involves oncogenic driver mutations, notably in where EGFR mutations occur in 10-30% of cases, often as exon 19 deletions or L858R substitutions, and mutations in 15-30%, primarily at codons 12 or 13, leading to uncontrolled . SCLC frequently harbors TP53 and RB1 alterations, promoting aggressive behavior. These cancers metastasize primarily via lymphatic channels to regional nodes and distant sites like the or bones, with hematogenous spread also common in advanced stages. Staging for NSCLC employs the TNM system (8th edition, American Joint Committee on Cancer), classifying tumors as stage I (localized, T1-2 N0 M0) to stage IV (metastatic, any T/N M1), informed by imaging modalities such as computed (CT) and (PET) for precise assessment. Treatment modalities vary by stage and histology: early-stage NSCLC is amenable to surgical resection (lobectomy or pneumonectomy), often curative with 5-year survival exceeding 60% for stage I. Advanced cases receive , including (platinum-based regimens like cisplatin-gemcitabine) and radiotherapy, with SCLC responding well initially to chemoradiation but prone to relapse. Targeted therapies have advanced post-2020, particularly immune checkpoint inhibitors targeting , such as pembrolizumab, approved for first-line use in -positive (≥50%) metastatic NSCLC based on KEYNOTE-024 trial results showing improved overall survival. For driver-mutated tumors, EGFR inhibitors like osimertinib provide benefits in EGFR-mutant . Laryngeal cancers are managed with , radiation, or chemoradiation, achieving voice preservation in select cases, while sinonasal tumors often require multidisciplinary approaches including surgery and due to anatomical constraints.

Other conditions

Mouth breathing often serves as a compensatory mechanism for habitual nasal obstruction, leading to altered airflow through the oral cavity instead of the nasal passages. This habit can result in dry mouth, or , due to reduced salivary flow and exposure of oral tissues to unfiltered air, increasing the risk of dental caries and oral infections. Additionally, chronic in children is associated with orthodontic issues, such as and altered mandibular posture, as it influences dentofacial development by promoting a forward head position and open-mouth posture. It also links to sleep-disordered breathing, including , where exacerbates airway collapse during sleep and worsens symptoms like . Congenital anomalies of the respiratory tract encompass structural defects present at birth that impair airway patency or function. involves a bony or membranous blockage of the posterior nasal choanae, leading to partial or complete nasal obstruction; bilateral cases cause immediate respiratory distress in newborns, who are obligate nasal breathers, potentially resulting in and requiring urgent intervention. is characterized by weakness or immaturity of the tracheal cartilage rings, causing dynamic collapse of the airway during expiration and symptoms such as , wheezing, and recurrent respiratory infections. , arising from mutations in the CFTR gene, disrupts chloride ion transport across epithelial cells, leading to dehydrated, viscous mucus accumulation in the airways; this impairs , fosters chronic infections, and causes progressive lung damage. Trauma to the respiratory tract includes acute injuries from external insults that compromise airway integrity. injury occurs when hot gases, smoke particulates, or chemical irritants damage the mucosal lining, resulting in , , and impaired ; , for instance, combines thermal and toxic effects, often complicating burns and increasing mortality risk. involves the inadvertent of objects into the , trachea, or bronchi, causing partial or complete obstruction, , and potential complications like or if not promptly removed. Environmental factors, particularly those intensified by , contribute to respiratory tract morbidity through increased exposure to airborne irritants. Wildfire smoke, driven by rising temperatures and prolonged droughts, exacerbates conditions like and by depositing fine particulate matter (PM2.5) deep into the lungs, triggering and acute respiratory events. Projections indicate that could lead to approximately 250,000 additional deaths annually between 2030 and 2050, with a substantial portion attributable to respiratory impacts from events like intensified wildfires and heatwaves. Globally, respiratory diseases impose a significant burden, accounting for about 7% of all deaths when considering chronic forms like COPD, which alone caused 3.5 million fatalities as of 2021. Disparities are pronounced in low-resource settings, where limited access to diagnostics, treatments, and clean air heightens vulnerability to early-life insults and environmental pollutants, resulting in higher prevalence and poorer outcomes compared to high-income regions.

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