Editing Respiratory system (section)

==Mammals==
===Anatomy===
{{Main|Lung|Respiratory tract}}
[[File:Poumons2.jpg|thumb|left|300px|'''Fig. 1.''' Respiratory system]]
[[File:illu quiz lung05.jpg|thumb|180px|'''Fig. 2.''' The [[Respiratory tract#Lower respiratory tract|lower respiratory tract]], or "Respiratory Tree"{{ordered list |[[Vertebrate trachea|Trachea]] |[[Main bronchus|Mainstem bronchus]] |[[Secondary bronchus|Lobar bronchus]] |[[Tertiary bronchus|Segmental bronchus]] |[[Bronchiole]] |[[Alveolar duct]] |[[Pulmonary alveolus|Alveolus]]}}]]
In [[human]]s and other [[mammal]]s, the anatomy of a typical respiratory system is the [[respiratory tract]]. The tract is divided into an [[Respiratory tract#Upper respiratory tract|upper]] and a [[Respiratory tract#Lower respiratory tract|lower respiratory tract]]. The upper tract includes the [[nose]], [[nasal cavity|nasal cavities]], [[paranasal sinuses|sinuses]], [[pharynx]] and the part of the [[larynx]] above the [[vocal folds]]. The lower tract (Fig.&nbsp;2.) includes the lower part of the [[larynx]], the [[trachea]], [[bronchus|bronchi]], [[bronchiole]]s and the [[pulmonary alveolus|alveoli]].

The branching airways of the lower tract are often described as the [[Respiratory tract#Lower respiratory tract|respiratory tree]] or [[tracheobronchial tree]] (Fig.&nbsp;2).<ref name=gilroy>{{cite book|last1=Gilroy|first1=Anne M.|last2=MacPherson|first2= Brian R.|last3= Ross|first3=Lawrence M.|title= Atlas of Anatomy|publisher=Thieme|location=Stuttgart|date=2008|pages=108–111|isbn=978-1-60406-062-1}}</ref> The intervals between successive branch points along the various branches of "tree" are often referred to as branching "generations", of which there are, in the adult human, about 23. The earlier generations (approximately generations 0–16), consisting of the trachea and the bronchi, as well as the larger bronchioles which simply act as [[Conducting zone|air conduits]], bringing air to the respiratory bronchioles, alveolar ducts and alveoli (approximately generations 17–23), where [[gas exchange]] takes place.<ref name="Pocock">{{cite book|last1=Pocock|first1=Gillian|last2=Richards|first2=Christopher D.|title=Human physiology : the basis of medicine|date=2006|publisher=Oxford University Press|location=Oxford|isbn=978-0-19-856878-0|pages=315–317|edition=3rd}}</ref><ref name=tortora1 /> [[Bronchiole]]s are defined as the small airways lacking any [[cartilaginous]] support.<ref name=gilroy />

The first bronchi to branch from the [[trachea]] are the right and left main bronchi. Second, only in diameter to the trachea (1.8&nbsp;cm), these bronchi (1–1.4&nbsp;cm in diameter)<ref name="Pocock"/> enter the [[lung]]s at each [[Root of the lung|hilum]], where they branch into narrower secondary bronchi known as lobar bronchi, and these branch into narrower tertiary bronchi known as segmental bronchi. Further divisions of the segmental bronchi (1 to 6&nbsp;mm in diameter)<ref name="Kacmarek">{{cite book|last1=Kacmarek|first1=Robert M.|last2=Dimas|first2=Steven|last3=Mack|first3=Craig W.|title=Essentials of Respiratory Care - E-Book|url=https://books.google.com/books?id=FV9PAQAAQBAJ&pg=PA81|publisher=Elsevier Health Sciences|language=en|date=13 August 2013|isbn=9780323277785}}</ref> are known as 4th order, 5th order, and 6th order segmental bronchi, or grouped together as subsegmental bronchi.<ref name="Netter">{{cite book|last1=Netter|first1=Frank H.|title=Atlas of Human Anatomy Including Student Consult Interactive Ancillaries and Guides.|date=2014|publisher=W B Saunders Co|location=Philadelphia, Penn.|isbn=978-1-4557-0418-7|page=200|edition=6th}}</ref><ref>{{Cite book|last=Maton|first=Anthea|author2=Jean Hopkins|author3=Charles William McLaughlin|author4=Susan Johnson|author5=Maryanna Quon Warner|author6=David LaHart|author7=Jill D. Wright|title=Human Biology and Health|publisher=Prentice Hall|year=1993|location=wood Cliffs, New Jersey, US|url=https://archive.org/details/humanbiologyheal00scho|isbn=0-13-981176-1}}{{Page needed|date=September 2010}}</ref>

Compared to the 23 number (on average) of branchings of the respiratory tree in the adult human, the [[mouse]] has only about 13 such branchings.

The alveoli are the dead end terminals of the "tree", meaning that any air that enters them has to exit via the same route. A system such as this creates [[Dead space (physiology)|dead space]], a volume of air (about 150&nbsp;ml in the adult human) that fills the airways after exhalation and is breathed back into the alveoli before environmental air reaches them.<ref name=fowler1948 /><ref>{{cite web|title=anatomical dead space|url=http://medical-dictionary.thefreedictionary.com/anatomical+dead+space|website=TheFreeDictionary.com}}</ref> At the end of inhalation, the airways are filled with environmental air, which is exhaled without coming in contact with the gas exchanger.<ref name=fowler1948 />

===Ventilatory volumes===
[[File:Lungvolumes Updated.png|thumb|550px|'''Fig. 3''' Output of a 'spirometer'. Upward movement of the graph, read from the left, indicates the intake of air; downward movements represent exhalation.]]{{Main |Breathing|Lung volumes}}
The lungs expand and contract during the breathing cycle, drawing air in and out of the lungs. The volume of air moved in or out of the lungs under normal resting circumstances (the resting [[tidal volume]] of about 500&nbsp;ml), and volumes moved during maximally forced inhalation and maximally forced exhalation are measured in humans by [[spirometry]].<ref name=tortora8 /> A typical adult human spirogram with the names given to the various excursions in volume the lungs can undergo is illustrated below (Fig.&nbsp;3):

Not all the air in the lungs can be expelled during maximally forced exhalation ([[Expiratory reserve volume|ERV]]). This is the [[Lung volumes|residual volume]] (volume of air remaining even after a forced exhalation) of about 1.0–1.5&nbsp;liters which cannot be measured by spirometry. Volumes that include the residual volume (i.e. [[functional residual capacity]] of about 2.5–3.0&nbsp;liters, and [[total lung capacity]] of about 6&nbsp;liters) can therefore also not be measured by spirometry. Their measurement requires special techniques.<ref name=tortora8>{{cite book |last1= Tortora |first1= Gerard J. |last2=Anagnostakos|first2=Nicholas P.| title=Principles of anatomy and physiology |url= https://archive.org/details/principlesofanat05tort |url-access= registration |pages=[https://archive.org/details/principlesofanat05tort/page/570 570–572]|edition= Fifth |location= New York |publisher= Harper & Row, Publishers|date= 1987 |isbn= 0-06-350729-3 }}</ref>

The rates at which air is breathed in or out, either through the mouth or nose or into or out of the [[alveoli]] are tabulated below, together with how they are calculated. The number of breath cycles per minute is known as the [[respiratory rate]]. An average healthy human breathes 12–16 times a minute.

{| class="wikitable"
|-
! Measurement  !! Equation !! Description
|-
| [[Respiratory minute volume|Minute ventilation]] ||  tidal volume * respiratory rate|| the total volume of air entering, or leaving, the nose or mouth per minute or normal respiration.
|-
| Alveolar ventilation || (tidal volume – [[Dead space (physiology)|dead space]]) * respiratory rate || the volume of air entering or leaving the alveoli per minute.
|-
| [[Dead space (physiology)|Dead space ventilation]] || dead space * respiratory rate ||  the volume of air that does not reach the alveoli during inhalation, but instead remains in the airways, per minute.
|}

===Mechanics of breathing===
[[File:Real-time MRI - Thorax.ogv|thumb|right|'''Fig. 6''' Real-time [[magnetic resonance imaging]] (MRI) of the chest movements of human thorax during breathing]]

{{Main|Breathing#Mechanics}}
{{Multiple image
| direction = vertical
| align = left
| header = The "pump handle" and "bucket handle movements" of the ribs 
| width1 = 200
| image1 = ribcage during inhalation.jpg
| caption1 = '''Fig. 4''' The effect of the [[Muscles of respiration|muscles of inhalation]] in expanding the [[rib cage]]. The particular action illustrated here is called the [[pump handle movement]] of the rib cage.
| width2 = 200
| image2 = Costillas.png
| caption2 = '''Fig. 5''' In this view of the rib cage the downward slope of the lower ribs from the midline outwards can be clearly seen. This allows a movement similar to the "pump handle effect", but in this case, it is called the [[bucket handle movement]]. The color of the ribs refers to their classification, and is not relevant here. }}
{{Multiple image
| direction = horizontal
| align = top
| header = Breathing
| width2 = 200
| image2 = Forceful breathing.jpg
| caption2 = '''Fig. 8''' The muscles of forceful breathing (inhalation and exhalation). The color code is the same as on the left. In addition to a more forceful and extensive contraction of the diaphragm, the intercostal muscles are aided by the accessory muscles of inhalation to exaggerate the movement of the ribs upwards, causing a greater expansion of the rib cage. During exhalation, apart from the relaxation of the muscles of inhalation, the abdominal muscles actively contract to pull the lower edges of the rib cage downwards decreasing the volume of the rib cage, while at the same time pushing the diaphragm upwards deep into the thorax.
| width1 = 200
| image1 = Quiet breathing.jpg
| caption1 = '''Fig. 7''' The muscles of breathing at rest: inhalation on the left, exhalation on the right. Contracting muscles are shown in red; relaxed muscles in blue. Contraction of the [[Thoracic diaphragm|diaphragm]] generally contributes the most to the expansion of the chest cavity (light blue). However, at the same time, the intercostal muscles pull the ribs upwards (their effect is indicated by arrows) also causing the [[rib cage]] to expand during inhalation (see diagram on other side of the page). The relaxation of all these muscles during exhalation causes the rib cage and abdomen (light green) to elastically return to their resting positions. Compare with Fig. 6, the MRI video of the chest movements during the breathing cycle.
}}
In [[mammals]], inhalation at rest is primarily due to the contraction of the [[Thoracic diaphragm|diaphragm]]. This is an upwardly domed sheet of muscle that separates the thoracic cavity from the abdominal cavity. When it contracts, the sheet flattens, (i.e. moves downwards as shown in Fig.&nbsp;7) increasing the volume of the thoracic cavity in the antero-posterior axis. The contracting diaphragm pushes the abdominal organs downwards. But because the pelvic floor prevents the lowermost abdominal organs from moving in that direction, the pliable abdominal contents cause the belly to bulge outwards to the front and sides, because the relaxed abdominal muscles do not resist this movement (Fig.&nbsp;7). This entirely passive bulging (and shrinking during exhalation) of the abdomen during normal breathing is sometimes referred to as "abdominal breathing", although it is, in fact, "diaphragmatic breathing", which is not visible on the outside of the body. Mammals only use their abdominal muscles during forceful exhalation (see Fig.&nbsp;8, and discussion below). Never during any form of inhalation.

As the diaphragm contracts, the [[rib cage]] is simultaneously enlarged by the ribs being pulled upwards by the [[intercostal muscles]] as shown in Fig.&nbsp;4. All the ribs slant downwards from the rear to the front (as shown in Fig.&nbsp;4); but the lowermost ribs ''also'' slant downwards from the midline outwards (Fig.&nbsp;5). Thus the rib cage's transverse diameter can be increased in the same way as the antero-posterior diameter is increased by the so-called [[pump handle movement]] shown in Fig.&nbsp;4.

The enlargement of the thoracic cavity's vertical dimension by the contraction of the diaphragm, and its two horizontal dimensions by the lifting of the front and sides of the ribs, causes the intrathoracic pressure to fall. The lungs' interiors are open to the outside air and being elastic, therefore expand to fill the increased space, [[Pleural cavity|pleura fluid]] between double-layered pleura covering of lungs helps in reducing friction while lungs expand and contract. The inflow of air into the lungs occurs via the [[respiratory airways]] (Fig. 2). In a healthy person, these airways [[Obligate nasal breathing|begin with the nose]].<ref name=cc>{{cite web
|url=https://health.clevelandclinic.org/breathe-mouth-nose/
|title=Should You Breathe Through Your Mouth or Your Nose?
|access-date=2020-06-28
|last=Turowski
|first=Jason
|date=2016-04-29
|publisher=[[Cleveland Clinic]]
}}</ref><ref name="guardian">{{cite web|title=Your Nose, the Guardian of Your Lungs|url=https://www.bmc.org/otolaryngology-head-neck-surgery/resources/your-nose-guardian-your-lungs|access-date=2020-06-29|publisher=[[Boston Medical Center]]}}</ref> (It is possible to begin with the mouth, which is the backup breathing system. However, chronic [[mouth breathing]] leads to, or is a sign of, illness.<ref name=harmful>{{cite web
|url=https://www.nbcnews.com/healthmain/mouth-breathing-gross-harmful-your-health-1C6437430
|title='Mouth-breathing' gross, harmful to your health
|access-date=2020-06-28
|last=Dahl
|first=Melissa
|date=2011-01-11
|publisher=NBC News
}}</ref><ref name="role">{{cite web
|url=https://www.journal-imab-bg.org/issues-2018/issue1/JofIMAB-2018-24-1p1878-1882.pdf
|title=THE ROLE OF MOUTH BREATHING ON DENTITION DEVELOPMENT AND FORMATION
|access-date=2020-05-31
|last=Valcheva
|first=Zornitsa
|date=January 2018
|publisher=Journal of IMAB
}}</ref><ref name="nesnpr">{{cite web
|url=https://www.npr.org/transcripts/862963172
|title=How The 'Lost Art' Of Breathing Can Impact Sleep And Resilience
|access-date=2020-06-23
|last=Gross
|first=Terry
|date=2020-05-27
|publisher=[[NPR|National Public Radio (NPR)]]/[[Fresh Air]]
}}</ref>) It ends in the microscopic dead-end sacs called [[Pulmonary alveolus|alveoli]], which are always open, though the diameters of the various sections can be changed by the [[Sympathetic nervous system|sympathetic]] and [[parasympathetic nervous system]]s. The alveolar air pressure is therefore always close to atmospheric air pressure (about 100&nbsp;[[Pascal (unit)|kPa]] at sea level) at rest, with the pressure gradients because of lungs contraction and expansion cause air to move in and out of the lungs during breathing rarely exceeding 2–3&nbsp;kPa.<ref name="Chrisvan L 1995">{{cite journal |last1=Koen |first1=Chrisvan L. |last2=Koeslag |first2=Johan H. | title=On the stability of subatmospheric intrapleural and intracranial pressures |journal= News in Physiological Sciences | date=1995 |volume=10 |issue=4 |pages=176–178 |doi=10.1152/physiologyonline.1995.10.4.176}}</ref><ref name="Williams & Wilkins">{{cite book |last1=West |first1=J.B. |title=Respiratory physiology: the essentials. |location=Baltimore |publisher=Williams & Wilkins |date=1985| pages= 21–30, 84–84, 98–101 }}</ref>

During exhalation, the diaphragm and intercostal muscles relax. This returns the chest and abdomen to a position determined by their anatomical elasticity. This is the "resting mid-position" of the thorax and abdomen (Fig.&nbsp;7) when the lungs contain their [[functional residual capacity]] of air (the light blue area in the right hand illustration of Fig.&nbsp;7), which in the adult human has a volume of about 2.5–3.0&nbsp;liters (Fig.&nbsp;3).<ref name=tortora1>{{cite book |last1= Tortora |first1= Gerard J. |last2=Anagnostakos|first2=Nicholas P.| title=Principles of anatomy and physiology |url= https://archive.org/details/principlesofan1987tort |url-access= registration |pages=[https://archive.org/details/principlesofan1987tort/page/556 556–586]|edition= Fifth |location= New York |publisher= Harper & Row, Publishers|date= 1987 |isbn= 0-06-350729-3 }}</ref> Resting exhalation lasts about twice as long as inhalation because the diaphragm relaxes passively more gently than it contracts actively during inhalation.

[[File:Alveolar air.png|thumb|right|400 px|'''Fig. 9''' The changes in the composition of the alveolar air during a normal breathing cycle at rest. The scale on the left, and the blue line, indicate the partial pressures of carbon dioxide in kPa, while that on the right and the red line, indicate the partial pressures of oxygen, also in kPa (to convert kPa into mm Hg, multiply by 7.5).]]The volume of air that moves in ''or'' out (at the nose or mouth) during a single breathing cycle is called the [[tidal volume]]. In a resting adult human, it is about 500&nbsp;ml per breath. At the end of exhalation, the airways contain about 150&nbsp;ml of alveolar air which is the first air that is breathed back into the alveoli during inhalation.<ref name=fowler1948>{{cite journal | author = Fowler W.S. | year = 1948 | title = Lung Function studies. II. The respiratory dead space | journal = Am. J. Physiol. | volume = 154 | issue = 3| pages = 405–416 | doi=10.1152/ajplegacy.1948.154.3.405| pmid = 18101134 }}</ref><ref>{{cite journal|last=Burke |first=TV |author2=Küng, M |author3=Burki, NK |title=Pulmonary gas exchange during histamine-induced bronchoconstriction in asthmatic subjects. |journal=Chest |year=1989 |volume=96 |issue=4 |pages=752–6 |pmid=2791669 |doi=10.1378/chest.96.4.752|s2cid=18569280 }}</ref> This volume air that is breathed out of the alveoli and back in again is known as [[Dead space (physiology)|dead space]] ventilation, which has the consequence that of the 500&nbsp;ml breathed into the alveoli with each breath only 350&nbsp;ml (500&nbsp;ml – 150&nbsp;ml = 350&nbsp;ml) is fresh warm and moistened air.<ref name=tortora1 /> Since this 350&nbsp;ml of fresh air is thoroughly mixed and diluted by the air that remains in the alveoli after a normal exhalation (i.e. the [[functional residual capacity]] of about 2.5–3.0&nbsp;liters), it is clear that the composition of the alveolar air changes very little during the breathing cycle (see Fig. 9). The oxygen [[Partial pressure|tension]] (or partial pressure) remains close to 13–14&nbsp;kPa (about 100&nbsp;mm&nbsp;Hg), and that of carbon dioxide very close to 5.3&nbsp;kPa (or 40&nbsp;mm&nbsp;Hg). This contrasts with composition of the dry outside air at sea level, where the partial pressure of oxygen is 21&nbsp;kPa (or 160&nbsp;mm&nbsp;Hg) and that of carbon dioxide 0.04&nbsp;kPa (or 0.3&nbsp;mmHg).<ref name=tortora1 />

During heavy breathing ([[hyperpnea]]), as, for instance, during exercise, inhalation is brought about by a more powerful and greater excursion of the contracting diaphragm than at rest (Fig. 8). In addition, the "[[accessory muscles of respiration|accessory muscles of inhalation]]" exaggerate the actions of the intercostal muscles (Fig. 8). These accessory muscles of inhalation are muscles that extend from the [[cervical vertebrae]] and base of the skull to the upper ribs and [[sternum]], sometimes through an intermediary attachment to the [[clavicle]]s.<ref name=tortora1 /> When they contract, the rib cage's internal volume is increased to a far greater extent than can be achieved by contraction of the intercostal muscles alone. Seen from outside the body, the lifting of the clavicles during strenuous or labored inhalation is sometimes called [[clavicular breathing]], seen especially during [[asthma]] attacks and in people with [[chronic obstructive pulmonary disease]].

During heavy breathing, exhalation is caused by relaxation of all the muscles of inhalation. But now, the abdominal muscles, instead of remaining relaxed (as they do at rest), contract forcibly pulling the lower edges of the [[Rib cage#Function|rib cage]] downwards (front and sides) (Fig.&nbsp;8). This not only drastically decreases the size of the rib cage, but also pushes the abdominal organs upwards against the diaphragm which consequently bulges deeply into the thorax (Fig.&nbsp;8). The end-exhalatory lung volume is now well below the resting mid-position and contains far less air than the resting "functional residual capacity". However, in a normal mammal, the lungs cannot be emptied completely. In an adult human, there is always still at least 1 liter of residual air left in the lungs after maximum exhalation.<ref name=tortora1 />

The automatic rhythmical breathing in and out, can be interrupted by coughing, sneezing (forms of very forceful exhalation), by the expression of a wide range of emotions (laughing, sighing, crying out in pain, exasperated intakes of breath) and by such voluntary acts as speech, singing, whistling and the playing of wind instruments. All of these actions rely on the muscles described above, and their effects on the movement of air in and out of the lungs.

Although not a form of breathing, the [[Valsalva maneuver]] involves the respiratory muscles. It is, in fact, a very forceful exhalatory effort against a tightly closed [[glottis]], so that no air can escape from the lungs.<ref name="taylor">{{cite journal |last=Taylor |first=D |title=The Valsalva Manoeuvre: A critical review |journal=South Pacific Underwater Medicine Society Journal |volume=26 |issue=1 |year=1996 |issn=0813-1988 |oclc=16986801 |url=http://archive.rubicon-foundation.org/6264 |access-date=14 March 2016 |archive-date=31 January 2010 |archive-url=https://web.archive.org/web/20100131114931/http://archive.rubicon-foundation.org/6264 |url-status=usurped }}</ref> Instead, abdominal contents are evacuated in the opposite direction, through orifices in the pelvic floor.  The abdominal muscles contract very powerfully, causing the pressure inside the abdomen and thorax to rise to extremely high levels. The Valsalva maneuver can be carried out voluntarily but is more generally a reflex elicited when attempting to empty the abdomen during, for instance, difficult defecation, or during childbirth. Breathing ceases during this maneuver.

===Gas exchange===
{{Main|Gas exchange}}
{{Multiple image
| direction         = vertical
| align             = right
| header            = Mechanism of gas exchange
| width1            = 250
| image1            = Gas exchange.jpg
| caption1          = '''Fig. 11''' A highly diagrammatic illustration of the process of gas exchange in the mammalian lungs, emphasizing the differences between the gas compositions of the ambient air, the alveolar air (light blue) with which the pulmonary capillary blood equilibrates, and the blood gas tensions in the pulmonary arterial (blue blood entering the lung on the left) and venous blood (red blood leaving the lung on the right). All the gas tensions are in kPa. To convert to mm Hg, multiply by 7.5.
| width2            = 250
| image2            = Alveolus.jpg
| caption2          = '''Fig. 12''' A diagrammatic histological cross-section through a portion of lung tissue showing a normally inflated [[Pulmonary alveolus|alveolus]] (at the end of a normal exhalation), and its walls containing the [[Pulmonary circulation|pulmonary capillaries]] (shown in cross-section). This illustrates how the pulmonary capillary blood is completely surrounded by alveolar air. In a normal human lung, all the alveoli together contain about 3 liters of alveolar air. All the pulmonary capillaries contain about 100{{nbsp}}ml of blood.
}}
 
[[File:Alveolar Wall.svg|thumb|300 px|left|'''Fig. 10''' A histological cross-section through an alveolar wall showing the layers through which the gases have to move between the blood plasma and the alveolar air. The dark blue objects are the nuclei of the capillary [[endothelial]] and alveolar type&nbsp;I&nbsp;[[epithelial]] cells (or type&nbsp;1&nbsp;[[pneumocyte]]s). The two red objects labeled "RBC" are [[red blood cell]]s in the pulmonary capillary blood.]]

The primary purpose of the respiratory system is the equalizing of the partial pressures of the respiratory gases in the alveolar air with those in the pulmonary capillary blood (Fig. 11). This process occurs by simple [[Diffusion#Diffusion vs. bulk flow|diffusion]],<ref>{{cite book|last1=Maton|first1=Anthea|first2=Jean Susan|last2= Hopkins|first3=Charles William|last3=Johnson|first4=Maryanna Quon|last4= McLaughlin|first5=David|last5=Warner|first6=Jill|last6= LaHart Wright|title=Human Biology and Health|publisher=Prentice Hall|year=2010 |location=Englewood Cliffs|pages= 108–118|isbn=978-0134234359}}</ref> across a very thin membrane (known as the [[blood–air barrier]]), which forms the walls of the [[pulmonary alveoli]] (Fig.&nbsp;10). It consists of the [[Pneumocytes|alveolar epithelial cells]], their [[basement membrane]]s and the [[Endothelium|endothelial cells]] of the alveolar capillaries (Fig.&nbsp;10).<ref name=grays>{{cite book |last1=Williams |first1=Peter L. |last2=Warwick |first2=Roger |last3=Dyson|first3=Mary |last4=Bannister |first4=Lawrence H. |title=Gray's Anatomy| pages=1278–1282 |location=Edinburgh|publisher=Churchill Livingstone | edition=Thirty-seventh |date=1989|isbn= 0443-041776 }}</ref> This blood gas barrier is extremely thin (in humans, on average, 2.2&nbsp;μm thick). It is folded into about 300 million small air sacs called [[Pulmonary alveolus|alveoli]]<ref name=grays /> (each between 75 and 300&nbsp;μm in diameter) branching off from the respiratory [[bronchiole]]s in the [[lung]]s, thus providing an extremely large surface area (approximately 145&nbsp;m<sup>2</sup>) for gas exchange to occur.<ref name=grays />

The air contained within the alveoli has a semi-permanent volume of about 2.5–3.0&nbsp;liters which completely surrounds the alveolar capillary blood (Fig.&nbsp;12). This ensures that equilibration of the partial pressures of the gases in the two compartments is very efficient and occurs very quickly. The blood leaving the alveolar capillaries and is eventually distributed throughout the body therefore has a [[partial pressure]] of oxygen of 13–14&nbsp;kPa (100&nbsp;mmHg), and a [[PCO2|partial pressure of carbon dioxide]] of 5.3&nbsp;kPa (40&nbsp;mmHg) (i.e. the same as the oxygen and carbon dioxide gas tensions as in the alveoli).<ref name=tortora1 /> As mentioned in [[#Mechanics of breathing|the section above]], the corresponding partial pressures of oxygen and carbon dioxide in the ambient (dry) air at sea level are 21&nbsp;kPa (160&nbsp;mmHg) and 0.04&nbsp;kPa (0.3&nbsp;mmHg) respectively.<ref name=tortora1 />

This marked difference between the composition of the alveolar air and that of the ambient air can be maintained because the [[functional residual capacity]] is contained in dead-end sacs connected to the outside air by fairly narrow and relatively long tubes (the airways: [[nose]], [[pharynx]], [[larynx]], [[trachea]], [[bronchi]] and their branches down to the [[bronchioles]]), through which the air has to be breathed both in and out (i.e. there is no unidirectional through-flow as there is in the [[Bird anatomy#Respiratory system|bird lung]]). This typical mammalian anatomy combined with the fact that the lungs are not emptied and re-inflated with each breath (leaving a substantial volume of air, of about 2.5–3.0&nbsp;liters, in the alveoli after exhalation), ensures that the composition of the alveolar air is only minimally disturbed when the 350&nbsp;ml of fresh air is mixed into it with each inhalation. Thus the animal is provided with a very special "portable atmosphere", whose composition differs significantly from the [[Great Oxygenation Event|present-day ambient air]].<ref>{{cite book |last1=Lovelock |first1=James | title=Healing Gaia: Practical medicine for the Planet|url=https://archive.org/details/healinggaiaprac00love |url-access=registration |pages=21–34, 73–88|location=New York |publisher=Harmony Books |date=1991|isbn= 0-517-57848-4}}</ref> It is this portable atmosphere (the [[functional residual capacity]]) to which the blood and therefore the body tissues are exposed – not to the outside air.

The resulting arterial partial pressures of oxygen and carbon dioxide are [[Homeostasis#Levels of blood gases|homeostatically controlled]]. A rise in the arterial partial pressure of CO<sub>2</sub> and, to a lesser extent, a fall in the arterial partial pressure of O<sub>2</sub>, will reflexly cause deeper and faster breathing until the [[blood gas tension]]s in the lungs, and therefore the arterial blood, return to normal. The converse happens when the carbon dioxide tension falls, or, again to a lesser extent, the oxygen tension rises: the rate and depth of breathing are reduced until blood gas normality is restored.

Since the blood arriving in the alveolar capillaries has a partial pressure of O<sub>2</sub> of, on average, 6&nbsp;kPa (45&nbsp;mmHg), while the pressure in the alveolar air is 13–14&nbsp;kPa (100&nbsp;mmHg), there will be a net diffusion of oxygen into the capillary blood, changing the composition of the 3&nbsp;liters of alveolar air slightly. Similarly, since the blood arriving in the alveolar capillaries has a partial pressure of CO<sub>2</sub> of also about 6&nbsp;kPa (45&nbsp;mmHg), whereas that of the alveolar air is 5.3&nbsp;kPa (40&nbsp;mmHg), there is a net movement of carbon dioxide out of the capillaries into the alveoli. The changes brought about by these net flows of individual gases into and out of the alveolar air necessitate the replacement of about 15% of the alveolar air with ambient air every  5&nbsp;seconds or so. This is very tightly controlled by the monitoring of the arterial blood gases (which accurately reflect composition of the alveolar air) by the [[Aortic body|aortic]] and [[Carotid body|carotid bodies]], as well as by the [[Central chemoreceptors|blood gas and pH sensor]] on the anterior surface of the [[medulla oblongata]] in the brain. There are also oxygen and carbon dioxide sensors in the lungs, but they primarily determine the diameters of the [[bronchioles]] and [[Pulmonary circulation|pulmonary capillaries]], and are therefore responsible for directing the flow of air and blood to different parts of the lungs.

It is only as a result of accurately maintaining the composition of the 3&nbsp;liters of alveolar air that with each breath some carbon dioxide is discharged into the atmosphere and some oxygen is taken up from the outside air. If more carbon dioxide than usual has been lost by a short period of [[hyperventilation]], respiration will be slowed down or halted until the alveolar partial pressure of carbon dioxide has returned to 5.3&nbsp;kPa (40&nbsp;mmHg). It is therefore strictly speaking untrue that the primary function of the respiratory system is to rid the body of carbon dioxide "waste". The carbon dioxide that is breathed out with each breath could probably be more correctly be seen as a byproduct of the body's extracellular fluid [[Homeostasis#Levels of blood gases|carbon dioxide]] and  [[Homeostasis#Blood pH|pH homeostats]]
 
If these homeostats are compromised, then a [[respiratory acidosis]], or a [[respiratory alkalosis]] will occur. In the long run these can be compensated by renal adjustments to the [[Acid-base homeostasis|H<sup>+</sup> and HCO<sub>3</sub><sup>−</sup> concentrations in the plasma]]; but since this takes time, the [[hyperventilation syndrome]] can, for instance, occur when agitation or anxiety cause a person to breathe fast and deeply thus causing a distressing [[respiratory alkalosis]] through the blowing off of too much CO<sub>2</sub> from the blood into the outside air.<ref>{{cite journal|last=Shu|first=BC |author2=Chang, YY |author3=Lee, FY |author4=Tzeng, DS |author5=Lin, HY |author6=Lung, FW|title=Parental attachment, premorbid personality, and mental health in young males with hyperventilation syndrome.|journal=Psychiatry Research|date=2007-10-31|volume=153|issue=2|pages=163–70|pmid=17659783|doi=10.1016/j.psychres.2006.05.006|s2cid=3931401 }}</ref>

Oxygen has a very low solubility in water, and is therefore carried in the blood loosely combined with [[hemoglobin]]. The oxygen is held on the hemoglobin by four [[Iron(II) oxide|ferrous iron]]-containing [[heme]] groups per hemoglobin molecule. When all the heme groups carry one O<sub>2</sub> molecule each the blood is said to be "saturated" with oxygen, and no further increase in the partial pressure of oxygen will meaningfully increase the oxygen concentration of the blood. Most of the carbon dioxide in the blood is carried as bicarbonate ions (HCO<sub>3</sub><sup>−</sup>) in the plasma. However the conversion of dissolved CO<sub>2</sub> into HCO<sub>3</sub><sup>−</sup> (through the addition of water) is too slow for the rate at which the blood circulates through the tissues on the one hand, and through alveolar capillaries on the other. The reaction is therefore catalyzed by [[carbonic anhydrase]], an [[enzyme]] inside the [[red blood cell]]s.<ref name="pmid10854618">{{cite journal | vauthors = Henry RP, Swenson ER | title = The distribution and physiological significance of carbonic anhydrase in vertebrate gas exchange organs | journal = Respiration Physiology | volume = 121 | issue = 1 | pages = 1–12 | date = June 2000 | pmid = 10854618 | doi = 10.1016/S0034-5687(00)00110-9}}</ref> The reaction can go in both directions depending on the prevailing partial pressure of CO<sub>2</sub>.<ref name=tortora1 /> A small amount of carbon dioxide is carried on the protein portion of the hemoglobin molecules as [[carbamino]] groups. The total concentration of carbon dioxide (in the form of bicarbonate ions, dissolved CO<sub>2</sub>, and carbamino groups) in arterial blood (i.e. after it has equilibrated with the alveolar air) is about 26&nbsp;mM (or 58&nbsp;ml/100 ml),<ref name=ciba>{{cite book |last1=Diem |first1=K. | last2=Lentner |first2=C. | chapter= Blood – Inorganic substances| title= in: Scientific Tables | edition= Seventh |location=Basle, Switzerland |publisher=CIBA-GEIGY Ltd. |date=1970 |page=571}}</ref> compared to the concentration of oxygen in saturated arterial blood of about 9&nbsp;mM (or 20&nbsp;ml/100 ml blood).<ref name=tortora1 />

===Control of ventilation===
{{Main|Control of ventilation}}
Ventilation of the lungs in mammals occurs via the [[respiratory center]]s in the [[medulla oblongata]] and the [[pons]] of the [[brainstem]].<ref name=tortora1 /> These areas form a series of [[neural pathway]]s which receive information about the [[Blood gas tension|partial pressures of oxygen and carbon dioxide]] in the [[arterial blood]].  This information determines the average rate of ventilation of the [[Pulmonary alveolus|alveoli]] of the [[lungs]], to keep these [[Homeostasis#Levels of blood gases|pressures constant]]. The respiratory center does so via [[Motor neuron|motor nerves]] which activate the [[Thoracic diaphragm|diaphragm]] and other [[muscles of respiration]].

The breathing rate increases when the [[PCO2|partial pressure of carbon dioxide]] in the blood increases. This is detected by [[Central chemoreceptors|central blood gas chemoreceptors]] on the anterior surface of the [[medulla oblongata]].<ref name=tortora1 /> The [[Aortic bodies|aortic]] and [[carotid body|carotid bodies]], are the [[Peripheral chemoreceptors|peripheral blood gas chemoreceptors]] which are particularly sensitive to the arterial [[Pulmonary gas pressures|partial pressure of O<sub>2</sub>]] though they also respond, but less strongly, to the partial pressure of [[Carbon dioxide|CO<sub>2</sub>]].<ref name=tortora1 /> At sea level, under normal circumstances, the breathing rate and depth, is determined primarily by the arterial partial pressure of carbon dioxide rather than by the arterial [[blood gas tension|partial pressure of oxygen]], which is allowed to vary within a fairly wide range before the respiratory centers in the medulla oblongata and pons respond to it to change the rate and depth of breathing.<ref name=tortora1 />

[[Physical exercise|Exercise]] increases the breathing rate due to the extra carbon dioxide produced by the enhanced metabolism of the exercising muscles.<ref name= ritchisong>{{cite web|title=Respiration|url=http://people.eku.edu/ritchisong/301notes6.htm|publisher=Harvey Project|access-date=27 July 2012}}</ref> In addition, passive movements of the limbs also reflexively produce an increase in the breathing rate.<ref name=tortora1 /><ref name= ritchisong />

Information received from [[stretch receptor]]s in the lungs' limits [[tidal volume]] (the depth of inhalation and exhalation).

===Responses to low atmospheric pressures===

The [[Pulmonary alveolus|alveoli]] are open (via the airways) to the atmosphere, with the result that alveolar air pressure is exactly the same as the ambient air pressure at sea level, at altitude, or in any artificial atmosphere (e.g. a diving chamber, or decompression chamber) in which the individual is breathing freely. With [[Thoracic diaphragm#Function|expansion of the lungs]] the alveolar air occupies a larger volume, and its [[Boyle's law|pressure falls proportionally]], causing air to flow in through the airways, until the pressure in the alveoli is again at the ambient air pressure. The reverse happens during exhalation. This ''process'' (of inhalation and exhalation) is exactly the same at sea level, as on top of [[Mount Everest|Mt. Everest]], or in a [[diving chamber]] or [[Diving chamber|decompression chamber]].
[[File:Altitude and air pressure & Everest.jpg|thumb|right|400 px|'''Fig. 14''' A graph showing the relationship between total atmospheric pressure and altitude above sea level]]  
However, as one rises above sea level the [[Atmosphere of Earth|density of the air decreases exponentially]] (see Fig.&nbsp;14), halving approximately [[Atmosphere of Earth#Pressure and thickness|with every 5500&nbsp;m rise in altitude]].<ref name=altitude>{{cite web|url=http://www.altitude.org/calculators/air_pressure.php|title=Online high altitude oxygen calculator|publisher=altitude.org|access-date=15 August 2007|url-status=dead|archive-url=https://archive.today/20120729214053/http://www.altitude.org/calculators/air_pressure.php|archive-date=29 July 2012}}</ref> Since the composition of the atmospheric air is almost constant below 80&nbsp;km, as a result of the continuous mixing effect of the weather, the concentration of oxygen in the air (mmols O<sub>2</sub> per liter of ambient air) decreases at the same rate as the fall in air pressure with altitude.<ref>{{cite book |last1=Tyson |first1=P.D.|last2=Preston-White|first2=R.A. |title=The weather and climate of Southern Africa. |location=Cape Town |publisher=Oxford University Press |date=2013| pages= 3–10, 14–16, 360|isbn=9780195718065 }}</ref> Therefore, in order to breathe in the same amount of oxygen per minute, the person has to inhale a proportionately greater volume of air per minute at altitude than at sea level. This is achieved by breathing deeper and faster (i.e. [[hyperpnea]]) than at sea level (see below).

[[File:Mount_Everest_as_seen_from_Drukair2_PLW_edit.jpg|thumb|left|300 px|'''Fig. 13''' Aerial photo of [[Mount Everest]] from the south, behind Nuptse and Lhotse]] 
There is, however, a complication that increases the volume of air that needs to be inhaled per minute ([[respiratory minute volume]]) to provide the same amount of oxygen to the lungs at altitude as at sea level. During inhalation, the air is warmed and saturated with water vapor during its passage through the [[nasal cavity|nose passages]] and [[pharynx]]. [[Vapour pressure of water|Saturated water vapor pressure]] is dependent only on temperature. At a body core temperature of 37&nbsp;°C it is 6.3&nbsp;[[Pascal (unit)|kPa]] (47.0&nbsp;mmHg), irrespective of any other influences, including altitude.<ref>{{cite book |last1=Diem |first1=K. |last2=Lenter| first2= C.|title=Scientific Tables| location=Basle, Switzerland|publisher=Ciba-Geigy |date=1970|edition= Seventh| pages= 257–258 }}</ref> Thus at sea level, where the ambient atmospheric pressure is about 100&nbsp;kPa, the moistened air that flows into the lungs from the [[trachea]] consists of water vapor (6.3&nbsp;kPa), nitrogen (74.0&nbsp;kPa), oxygen (19.7&nbsp;kPa) and trace amounts of carbon dioxide and other gases (a total of 100&nbsp;kPa). In dry air the [[partial pressure]] of O<sub>2</sub> at sea level is 21.0&nbsp;kPa (i.e. 21% of 100&nbsp;kPa), compared to the 19.7&nbsp;kPa of oxygen entering the alveolar air. (The tracheal partial pressure of oxygen is 21% of [100&nbsp;kPa – 6.3&nbsp;kPa] = 19.7&nbsp;kPa).  At the summit of [[Mount Everest|Mt. Everest]] (at an altitude of 8,848&nbsp;m or 29,029&nbsp;ft), the total [[Mount Everest#Death zone|atmospheric pressure is 33.7&nbsp;kPa]], of which 7.1&nbsp;kPa (or 21%) is oxygen.<ref name=altitude /> The air entering the lungs also has a total pressure of 33.7&nbsp;kPa, of which 6.3&nbsp;kPa is, unavoidably, water vapor (as it is at sea level). This reduces the partial pressure of oxygen entering the alveoli to 5.8&nbsp;kPa (or 21% of [33.7&nbsp;kPa – 6.3&nbsp;kPa] = 5.8&nbsp;kPa). The reduction in the partial pressure of oxygen in the inhaled air is therefore substantially greater than the reduction of the total atmospheric pressure at altitude would suggest (on Mt Everest: 5.8&nbsp;kPa ''vs.'' 7.1&nbsp;kPa).

A further minor complication exists at altitude. If the volume of the lungs were to be instantaneously doubled at the beginning of inhalation, the air pressure inside the lungs would be halved. This happens regardless of altitude. Thus, halving of the sea level air pressure (100&nbsp;kPa) results in an intrapulmonary air pressure of 50&nbsp;kPa. Doing the same at 5500&nbsp;m, where the atmospheric pressure is only 50&nbsp;kPa,  the intrapulmonary air pressure falls to 25&nbsp;kPa. Therefore, the same change in lung volume at sea level results in a 50&nbsp;kPa difference in pressure between the ambient air and the intrapulmonary air, whereas it result in a difference of only 25&nbsp;kPa at 5500&nbsp;m. The driving pressure forcing air into the lungs during inhalation is therefore halved at this altitude. The ''rate'' of inflow of air into the lungs during inhalation at sea level is therefore twice that which occurs at 5500&nbsp;m. However, in reality, inhalation and exhalation occur far more gently and less abruptly than in the example given. The differences between the atmospheric and intrapulmonary pressures, driving air in and out of the lungs during the breathing cycle, are in the region of only 2–3&nbsp;kPa.<ref name="Chrisvan L 1995"/><ref name="Williams & Wilkins"/> A doubling or more of these small pressure differences could be achieved only by very major changes in the breathing effort at high altitudes.

All of the above influences of low atmospheric pressures on breathing are accommodated primarily by breathing deeper and faster ([[hyperpnea]]).  The exact degree of hyperpnea is determined by the [[Homeostasis#Levels of blood gases|blood gas homeostat]], which regulates the [[partial pressure]]s of oxygen and carbon dioxide in the arterial blood. This [[Homeostasis|homeostat]] prioritizes the regulation of the arterial [[partial pressure]] of carbon dioxide over that of oxygen at sea level.<ref name=tortora1 /> That is to say, at sea level the arterial partial pressure of CO<sub>2</sub> is maintained at very close to 5.3&nbsp;kPa (or 40&nbsp;mmHg) under a wide range of circumstances, at the expense of the arterial partial pressure of O<sub>2</sub>, which is allowed to vary within a very wide range of values, before eliciting a corrective ventilatory response.  However, when the atmospheric pressure (and therefore the partial pressure of O<sub>2</sub> in the ambient air) falls to below 50–75% of its value at sea level, oxygen [[homeostasis]] is given priority over carbon dioxide homeostasis.<ref name=tortora1 /> This switch-over occurs at an elevation of about 2500&nbsp;m (or about 8000&nbsp;ft). If this switch occurs relatively abruptly, the hyperpnea at high altitude will cause a severe fall in the arterial partial pressure of carbon dioxide, with a [[Homeostasis#Blood pH|consequent rise in the pH of the arterial plasma]]. This is one contributor to [[Altitude sickness|high altitude sickness]]. On the other hand, if the switch to oxygen homeostasis is incomplete, then [[Hypoxia (medical)|hypoxia]] may complicate the clinical picture with potentially fatal results.

There are oxygen sensors in the smaller [[Bronchus|bronchi]] and [[bronchiole]]s. In response to low partial pressures of oxygen in the inhaled air these sensors reflexively cause the pulmonary arterioles to constrict.<ref>{{cite journal |last1= Von Euler |first1=U.S. |last2= Liljestrand |first2=G. | title= Observations on the pulmonary arterial blood pressure in the cat |journal= Acta Physiologica Scandinavica | date=1946 |volume=12 |issue=4 |pages=301–320 |doi=10.1111/j.1748-1716.1946.tb00389.x}}</ref> (This is the exact opposite of the corresponding reflex in the tissues, where low arterial partial pressures of O<sub>2</sub> cause arteriolar vasodilation.) At altitude this causes the [[Hypoxic pulmonary vasoconstriction|pulmonary arterial pressure to rise]] resulting in a much more even distribution of blood flow to the lungs than occurs at sea level. At sea level, the pulmonary arterial pressure is very low, with the result that [[Ventilation/perfusion ratio#Physiology|the tops of the lungs receive far less blood than the bases]], which are relatively over-perfused with blood. It is only in the middle of the lungs that the [[Ventilation/perfusion ratio#Physiology|blood and air flow to the alveoli are ideally matched]]. At altitude, this variation in the [[ventilation/perfusion ratio]] of alveoli from the tops of the lungs to the bottoms is eliminated, with all the alveoli perfused and ventilated in more or less the physiologically ideal manner. This is a further important contributor to the [[Effects of high altitude on humans#Acclimatization|acclimatatization to high altitudes]] and low oxygen pressures.

The kidneys measure the oxygen ''content'' (mmol&nbsp;O<sub>2</sub>/liter blood, rather than the partial pressure of O<sub>2</sub>) of the arterial blood. When the oxygen content of the blood is chronically low, as at high altitude, the oxygen-sensitive kidney cells secrete [[erythropoietin]] (EPO) into the blood.<ref>{{cite web|url=https://www.wada-ama.org/en/questions-answers/epo-detection|title=EPO Detection |date=December 2014 | publisher=World Anti-Doping Agency|access-date=7 September 2017}}</ref><ref name=tortora>{{cite book |last1= Tortora |first1= Gerard J. |last2=Anagnostakos|first2=Nicholas P.| title=Principles of anatomy and physiology |url= https://archive.org/details/principlesofanat05tort |url-access= registration |pages=[https://archive.org/details/principlesofanat05tort/page/444 444–445]|edition= Fifth |location= New York |publisher= Harper & Row, Publishers|date= 1987 |isbn= 0-06-350729-3 }}</ref> This hormone stimulates the [[Bone marrow|red bone marrow]] to increase its rate of red cell production, which leads to an increase in the [[hematocrit]] of the blood, and a consequent increase in its oxygen carrying capacity (due to the now high [[hemoglobin]] content of the blood). In other words, at the same arterial partial pressure of O<sub>2</sub>, a person with a high hematocrit carries more oxygen per liter of blood than a person with a lower hematocrit does. High altitude dwellers therefore have higher hematocrits than sea-level residents.<ref name=tortora /><ref name=Fisher1996>{{cite journal |vauthors=Fisher JW, Koury S, Ducey T, Mendel S |title=Erythropoietin production by interstitial cells of hypoxic monkey kidneys |journal=British Journal of Haematology |volume=95 |issue=1 |pages=27–32 |year=1996 |pmid=8857934 |doi=10.1046/j.1365-2141.1996.d01-1864.x |s2cid=38309595 }}</ref>

===Other functions of the lungs===
====Local defenses====
Irritation of nerve endings within the [[nasal cavity|nasal passages]] or [[airway]]s, can induce a [[cough reflex]] and [[sneezing]]. These responses cause air to be expelled forcefully from the [[Vertebrate trachea|trachea]] or [[nose]], respectively. In this manner, irritants caught in the [[mucus]] which lines the respiratory tract are expelled or moved to the [[mouth]] where they can be [[swallowed]].<ref name=tortora1 /> During coughing, contraction of the smooth muscle in the airway walls narrows the trachea by pulling the ends of the cartilage plates together and by pushing soft tissue into the lumen. This increases the expired airflow rate to dislodge and remove any irritant particle or mucus.

[[Respiratory epithelium]] can secrete a variety of molecules that aid in the defense of the lungs. These include secretory [[immunoglobulin]]s (IgA), [[collectin]]s, [[defensin]]s and other peptides and [[proteases]], [[reactive oxygen species]], and [[reactive nitrogen species]]. These secretions can act directly as antimicrobials to help keep the airway free of infection. A variety of [[chemokine]]s and [[cytokine]]s are also secreted that recruit the traditional immune cells and others to the site of infections.

[[Pulmonary surfactant|Surfactant]] immune function is primarily attributed to two proteins: SP-A and SP-D. These proteins can bind to sugars on the surface of pathogens and thereby [[opsonize]] them for uptake by phagocytes. It also regulates inflammatory responses and interacts with the adaptive immune response. Surfactant degradation or inactivation may contribute to enhanced susceptibility to lung inflammation and infection.<ref>{{cite journal |doi=10.1159/000078172 |pmid=15211087 |title=Host Defense Functions of Pulmonary Surfactant |journal=Biology of the Neonate |volume=85 |issue=4 |pages=326–32 |year=2004 |last1=Wright |first1=Jo Rae |s2cid=25469141 }}</ref>

Most of the respiratory system is lined with mucous membranes that contain [[mucosa-associated lymphoid tissue]], which produces [[white blood cell]]s such as [[lymphocyte]]s.

====Prevention of alveolar collapse====
{{Main|Pulmonary surfactant}}
The lungs make a [[pulmonary surfactant|surfactant]], a surface-active [[lipoprotein]] complex (phospholipoprotein) formed by [[Type II pneumocyte|type II alveolar cells]]. It floats on the surface of the thin watery layer which lines the insides of the alveoli, reducing the water's surface tension.

The surface tension of a watery surface (the water-air interface) tends to make that surface shrink.<ref name=tortora1 /> When that surface is curved as it is in the alveoli of the lungs, the shrinkage of the surface decreases the diameter of the alveoli. The more acute the curvature of the water-air interface [[Pulmonary surfactant#Function|the greater the tendency for the alveolus to collapse]].<ref name=tortora1 /> This has three effects. Firstly, the surface tension inside the alveoli resists expansion of the alveoli during inhalation (i.e. it makes the lung stiff, or non-compliant). Surfactant reduces the surface tension and therefore makes the lungs more [[Pulmonary compliance|compliant]], or less stiff, than if it were not there. Secondly, the diameters of the alveoli increase and decrease during the breathing cycle. This means that the alveoli have a [[Pulmonary surfactant#Compliance|greater tendency to collapse]] (i.e. cause [[atelectasis]]) at the end of exhalation than at the end of inhalation. Since surfactant floats on the watery surface, its molecules are more tightly packed together when the alveoli shrink during exhalation.<ref name=tortora1 /> This causes them to have a greater surface tension-lowering effect when the alveoli are small than when they are large (as at the end of inhalation, when the surfactant molecules are more widely spaced). The tendency for the alveoli to collapse is therefore almost the same at the end of exhalation as at the end of inhalation. Thirdly, the surface tension of the curved watery layer lining the alveoli tends to draw water from the lung tissues into the alveoli. Surfactant reduces this danger to negligible levels, and keeps the alveoli dry.<ref name=tortora1 /><ref>{{cite book|author=West, John B.|title=Respiratory physiology-- the essentials|publisher=Williams & Wilkins|location=Baltimore|year=1994|pages=[https://archive.org/details/respiratoryphysi00west/page/21 21–30, 84–84, 98–101]|isbn=0-683-08937-4|url=https://archive.org/details/respiratoryphysi00west/page/21}}</ref>

[[Premature birth|Pre-term babies]] who are unable to manufacture surfactant have lungs that tend to collapse each time they breathe out. Unless treated, this condition, called [[Infant respiratory distress syndrome|respiratory distress syndrome]], is fatal. Basic scientific experiments, carried out using cells from chicken lungs, support the potential for using [[steroid]]s as a means of furthering the development of type II alveolar cells.<ref>{{cite journal|pmid=11506991 |year=2001|last1=Sullivan|first1=LC|last2=Orgeig|first2=S|title=Dexamethasone and epinephrine stimulate surfactant secretion in type II cells of embryonic chickens|volume=281|issue=3|pages=R770–7|journal=American Journal of Physiology. Regulatory, Integrative and Comparative Physiology|doi=10.1152/ajpregu.2001.281.3.r770|s2cid=11226056 }}</ref> In fact, once a [[Preterm birth|premature birth]] is threatened, every effort is made to delay the birth, and a series of [[steroid]] injections is frequently administered to the mother during this delay in an effort to promote lung maturation.<ref>[https://web.archive.org/web/20070604020429/http://www.pregnancy-facts.com/articles/childbirth/premature-babies.php Premature Babies, Lung Development & Respiratory Distress Syndrome]. Pregnancy-facts.com.</ref>

====Contributions to whole body functions====
The lung vessels contain a [[Fibrinolysis|fibrinolytic system]] that dissolves [[Blood clots|clots]] that may have arrived in the pulmonary circulation by [[embolism]], often from the deep veins in the legs. They also release a variety of substances that enter the systemic arterial blood, and they remove other substances from the systemic venous blood that reach them via the pulmonary artery. Some [[prostaglandin]]s are removed from the circulation, while others are synthesized in the lungs and released into the blood when lung tissue is stretched.

The lungs activate one hormone. The physiologically inactive decapeptide [[angiotensin I]] is converted to the [[aldosterone]]-releasing octapeptide, [[angiotensin II]], in the pulmonary circulation. The reaction occurs in other tissues as well, but it is particularly prominent in the lungs. Angiotensin II also has a direct effect on [[Arteriole|arteriolar walls]], causing arteriolar [[vasoconstriction]], and consequently a rise in [[arterial blood pressure]].<ref>{{Cite journal|title = Cellular Mechanism of Vasoconstriction Induced by Angiotensin II It Remains To Be Determined|journal = Circulation Research|date = 2003-11-28|issn = 0009-7330|pmid = 14645130|pages = 1015–1017|volume = 93|issue = 11|doi = 10.1161/01.RES.0000105920.33926.60|language = en|first1 = Hideo|last1 = Kanaide|first2 = Toshihiro|last2 = Ichiki|first3 = Junji|last3 = Nishimura|first4 = Katsuya|last4 = Hirano|doi-access = free}}</ref> Large amounts of the [[angiotensin-converting enzyme]] responsible for this activation are located on the surfaces of the [[endothelial cells]] of the alveolar capillaries. The converting enzyme also inactivates [[bradykinin]]. Circulation time through the alveolar capillaries is less than one second, yet 70% of the angiotensin I reaching the lungs is converted to angiotensin II in a single trip through the capillaries. Four other peptidases have been identified on the surface of the pulmonary endothelial cells.

====Vocalization====
The movement of gas through the [[larynx]], [[pharynx]] and [[Human mouth|mouth]] allows humans to [[speech|speak]], or ''[[phonation|phonate]]''. Vocalization, or singing, in birds occurs via the [[Bird anatomy#Respiratory system|syrinx]], an organ located at the base of the trachea. The vibration of air flowing across the larynx ([[vocal cords]]), in humans, and the syrinx, in birds, results in sound. Because of this, gas movement is vital for [[communication]] purposes.

====Temperature control====
[[Thermoregulation|Panting]] in dogs, cats, birds and some other animals provides a means of reducing body temperature, by evaporating saliva in the mouth (instead of evaporating sweat on the skin).

===Clinical significance===
[[Respiratory disease|Disorders of the respiratory system]] can be classified into several general groups:
* Airway obstructive conditions  (e.g., [[emphysema]], [[bronchitis]], [[Allergic asthma|asthma]])
* Pulmonary restrictive conditions  (e.g., [[fibrosis]], [[sarcoidosis]], alveolar damage, [[pleural effusion]])
* Vascular diseases  (e.g., [[pulmonary edema]], [[pulmonary embolism]], [[pulmonary hypertension]])
* Infectious, environmental and other "diseases" (e.g., [[pneumonia]], [[tuberculosis]], [[asbestosis]], [[air pollution#Pollutants|particulate pollutants]])
* Primary cancers (e.g. [[Lung cancer|bronchial carcinoma]], [[mesothelioma]])
* Secondary cancers (e.g. cancers that originated elsewhere in the body, but have seeded themselves in the lungs)
* Insufficient surfactant (e.g. [[Infant respiratory distress syndrome|respiratory distress syndrome]] in pre-term babies) .

Disorders of the respiratory system are usually treated by a [[pulmonology|pulmonologist]] and [[Respiratory therapy|respiratory therapist]].

Where there is an inability to breathe or insufficiency in breathing, a [[medical ventilator]] may be used.