A complete, schematic view of the human respiratory system with their parts and functions.
The respiratory system (also respiratory apparatus, ventilatory system) is a biological system consisting of specific organs and structures used for gas exchange in animals and plants. The anatomy and physiology that make this happen varies greatly, depending on the size of the organism, the environment in which it lives and its evolutionary history. In land animals the respiratory surface is internalized as linings of the lungs. The lungs with their alveolar gas exchange units are sometimes referred to as the gas exchanger. These communicate with the external environment via a system of airways, or hollow tubes, of which the largest is the trachea, which branches into the two main bronchi. These "main" or "principal" bronchi enter the lungs where they branch into narrower and more numerous secondary, tertiary and progressively smaller bronchi that eventually gives rise to the millions of smallest tubes, called the bronchioles. In birds the bronchioles are termed parabronchi. The bronchioles, or parabronchi, generally open into microscopic air sacs called alveoli in mammals and atria in birds. Gas exchange takes place across the very large surface areas created by the many millions of these microscopic air sacs, which have a very rich blood supply. Air has to be pumped from the environment into the alveoli or atria by the process of breathing which involves the muscles of respiration.
In most fish, and a variety of other aquatic animals (both vertebrates and invertebrates) the respiratory system consists of gills, which are either partially or overtly external organs bathed in the watery environment. The water flows over the gills by a variety of active or passive means. Gas exchange takes place in the gills which consist of thin or very flat filaments and lammelae which expose a very large surface area of highly vascularized tissue to the watery environment.
Other animals, such as insects, have respiratory systems with very simple anatomical features, and in amphibians even the skin plays a vital role in gas exchange. Plants also have respiratory systems but the directionality of gas exchange can be opposite to that in animals. The respiratory system in plants includes anatomical features such as stomata, that are found in various parts of the plant.
The anatomy of a typical mammalian respiratory system, the respiratory tract, is often described as a respiratory tree or tracheobronchial tree (Fig. 1). Larger airways give rise to branches that are slighly narrower, but more numerous than the "trunk" airway that gives rise to the branches. The human respiratory tree may consist of, on average, 23 such branchings into progressively smaller airways, while the respiratory tree of the mouse has up to 13 such branchings. Divisions closest to the top of the tree, such as the trachea and bronchi, function mainly to transmit air to the lower airways. Later divisions such as the respiratory bronchioles, alveolar ducts and alveoli, are specialized for gas exchange.
The trachea and the first portions of the main bronchi are outside the lungs. The rest of the "tree" branches within the lungs, and ultimately extends to every part of the lungs. Above the illustrated "tree" (Fig. 1) is the upper respiratory tract, consisting of, in order moving upwards, the larynx, pharynx, the nasal passages ending in the nostrils.
The names given to the successive "generations" of airways, in order from largest to smallest are:
The alveoli are the dead end terminals of the "tree", meaning that any air that enters them has to exit via the same route it used to enter the alveoli. A system such as this creates dead space, a volume of air that fills the airways (the dead space) towards the end of inhalation, and is breathed out, unchanged, during the next exhalation, never having reached the alveoli.
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 ml), and volumes moved during maximally forced inhalation and maximally forced exhalation are measured in humans by spirometry. A typical adult human spirogram with the names given to the various excursions in volume the lungs can undergo is illustrated below (Fig. 3):
Note that not all the air in the lungs can be expelled during maximally forced exhalation. This is the residual volume of about 1.0-1.5 liters which cannot be measured by spirometry. Volumes that include the residual volume (i.e. functional residual capacity of about 2.5-3.0 liters, and total lung capacity of about 6 liters) can therefore also not be measured by spirometry. Their measurement requires special techniques.
Other volumes, not measured by means of spirometry include dead space ventilation (about 150 ml per breath), which is air that fills that airways after exhalation and is breathed back into the alveoli before environmental air reaches them. At the end of inhalation the airways are filled with environmental air, which is exhaled without coming in contact with the gas exchanger.
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.
|Minute ventilation||tidal volume * respiratory rate||the total volume of air entering, or leaving, the nose or mouth per minute.|
|Alveolar ventilation||(tidal volume – dead space) * respiratory rate||the volume of air entering or leaving the alveoli per minute.|
|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.|
Ventilation of the lungs in mammals occurs via the respiratory centers in the medulla oblongata and the pons of the brainstem. These areas form a series of neural pathways which receive information about the partial pressures of oxygen and carbon dioxide in the arterial blood. This information determines the average rate of ventilation of the alveoli of the lungs, to keep these pressures constant. The respiratory center does so via motor nerves which activate the diaphragm and other muscles of respiration.
The breathing rate increases when the partial pressure of carbon dioxide in the blood increases. This is detected by central blood gas chemoreceptors on the anterior surface of the medulla oblongata. The aortic and carotid bodies, are the peripheral blood gas chemoreceptors that are also sensitive to the arterial partial pressure of CO2 though they respond more strongly to the partial pressure of O2. 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 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.
Exercise increases the breathing rate due to the extra carbon dioxide produced by their enhanced metabolism, though passive movements of the limbs also reflexly produce an increase in the breathing rate.
In mammals, inhalation at rest is primarily due to the contraction of the 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. 7) increasing the volume of the thoracic cavity. The contracting diaphragm pushes the abdominal organs downwards. But because the pelvic floor prevents the lowermost abdominal organs 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. 7). This entirely passive bulging (and shrinking during exhalation) of the abdomen during normal breathing is sometimes referred 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 only during forceful exhalation (see Fig. 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. 5. All the ribs slant downwards from the rear to the front (as shown in Fig. 5); but the lowermost ribs also slant downwards from the midline outwards (Fig. 6). Thus the rib cage's transverse diameter can be increased in the same way as the antero-posterior diameter is increase by the so-called pump handle movement shown in Fig. 5.
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. The inflow of air into the lungs occurs via the respiratory airways (Fig. 1). In health these airways (starting at the nose or mouth, and ending in the microscopic dead-end sacs called alveoli) are always open, though the diameters of the various sections can be changed by the sympathetic and parasympathetic nervous systems. The alveolar air pressure is therefore always close to atmospheric air pressure (about 100 kPa at sea level) at rest, with the pressure gradients that cause air to move in and out of the lungs during breathing rarely exceeding 2–3 kPa.
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 (right hand illustration in Fig. 7) when the lungs contain their functional residual capacity of air (see Fig. 3), which in the adult human has a volume of about 2.5–3.0 liters. Resting exhalation lasts about twice as long as inhalation because the diaphragm relaxes passively more gently than it contracts actively during inhalation.
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 ml per breath. At the end of exhalation the airways contain about 150 ml of alveolar air which is the first air that is breathed back into the alveoli during inhalation. This volume air that is breathed out of the alveoli and back in again is known as dead space ventilation, which has the consequence that of the 500 ml breathed into the alveoli with each breath only 350 ml (500 ml - 150 ml = 350 ml) is fresh warm and moistened air. Since this 350 ml of fresh air is thoroughly mixed and diluted by the air that remains in the alveoli after normal exhalation (i.e. the functional residual capacity of about 2.5–3.0 liters), it is clear that the composition of the alveolar air changes very little during the breathing cycle (see Fig. 9). The oxygen tension (or partial pressure) remains close to 13-14 kPa (about 100 mm Hg), and that of carbon dioxide very close to 5.3 kPa (or 40 mm Hg). This contrasts with composition of the dry outside air at sea level, where the partial pressure of oxygen is 21 kPa (or 160 mm Hg) and that of carbon dioxide 0.04 kPa (or 0.3 mmHg).
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 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 clavicles. 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 downwards (front and sides) (Fig. 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. 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.
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. 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.
The primary purpose of the respiratory system is the equilibration 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, across a very thin membrane (known as the blood–air barrier), which forms the walls of the pulmonary alveoli (Fig. 10). It consisting of the alveolar epithelial cells, their basement membranes and the endothelial cells of the alveolar capillaries (Fig. 10). This blood gas barrier is extremely thin (in humans, on average, 2.2 μm thick). It is folded into about 300 million small air sacs called alveoli (each between 75 and 300 µm in diameter) branching off from the bronchioles in the lungs, thus providing an extremely large surface area (approximately 145 m2) for gas exchange to occur.
The air contained within the alveoli has a semi-permanent volume of about 2.5-3.0 liters which completely surrounds the alveolar capillary blood (Fig. 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 kPa (100 mmHg), and a partial pressure of carbon dioxide of 5.3 kPa (40 mmHg) (i.e. the same as the oxygen and carbon dioxide gas tensions as in the alveoli). As mentioned in the section above, the corresponding partial pressures of oxygen and carbon dioxide in the ambient (dry) air at sea level are 21 kPa (160 mmHg) and 0.04 kPa (0.3 mmHg) respectively.
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 lung). This typically 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 liters, in the alveoli after exhalation), ensures that the composition of the alveolar air is only minimally disturbed when the 350 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 present-day ambient air. 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 homeostatically controlled. A rise in the arterial partial pressure of CO2 and, to a lesser extent, a fall in the arterial partial pressure of O2, will reflexly cause deeper and faster breathing till the blood gas tensions 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 till blood gas normality is restored.
Since the blood arriving in the alveolar capillaries has a partial pressure of O2 of, on average, 6 kPa (45 mmHg), while the pressure in the alveolar air is 13-14 kPa (100 mmHg), there will be a net diffusion of oxygen into the capillary blood, changing the composition of the 3 liters of alveolar air slightly. Similarly, since the blood arriving in the alveolar capillaries has a partial pressure of CO2 of also about 6 kPa (45 mmHg), whereas that of the alveolar air is 5.3 kPa (40 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 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, carotid bodies, and the 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 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 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 kPa (40 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 carbon dioxide and 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 H+ and HCO3− 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 CO2 from the blood into the outside air.
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 ferrous iron-containing heme groups per hemoglobin molecule. When all the heme groups carry one O2 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 HCO3− ions in the plasma. However the conversion of dissolved CO2 into HCO3− (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 cells. The reaction can go in both directions depending on the prevailing partial pressure of CO2. 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 CO2, and carbamino groups) in arterial blood (i.e. after it has equilibrated with the alveolar air) is about 26 mM (or 58 ml/100 ml), compared to the concentration of oxygen in saturated arterial blood of about 9 mM (or 20 ml/100 ml blood).
The 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 expansion of the lungs (through lowering of the diaphragm and expansion of the thoracic cage) the alveolar air now occupies a larger volume, and its pressure falls proportionally, causing air to flow in from the surroundings, through the airways, till the pressure in the alveoli is once again at the ambient air pressure. The reverse obviously happens during exhalation. This process (of inhalation and exhalation) is exactly the same at sea level, as on top of Mt. Everest, or in a diving chamber or decompression chamber.
However, as one rises above sea level the density of the air decreases exponentially (see Fig. 14), halving approximately with every 5500 m rise in altitude. Since the composition of the atmospheric air is almost constant below 80 km, as a result of the continuous mixing effect of the weather, the concentration of oxygen in the air (mmols O2 per liter of ambient air) decreases at the same rate as the fall in air pressure with altitude. 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).
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 nose passages and pharynx. Saturated water vapor pressure is dependent only on temperature. At a body core temperature of 37 °C it is 6.3 kPa (47.0 mmHg), irrespective of any other influences, including altitude. Thus at sea level, where the ambient atmospheric pressure is about 100 kPa, the moistened air that flows into the lungs from the trachea consists of water vapor (6.3 kPa), nitrogen (74.0 kPa), oxygen (19.7 kPa) and trace amounts of carbon dioxide and other gases (a total of 100 kPa). In dry air the partial pressure of O2 at sea level is 21.0 kPa (i.e. 21% of 100 kPa), compared to the 19.7 kPa of oxygen entering the alveolar air. (The tracheal partial pressure of oxygen is 21% of [100 kPa – 6.3 kPa] = 19.7 kPa). At the summit of Mt. Everest (at an altitude of 8,848 m or 29,029 ft) the total atmospheric pressure is 33.7 kPa, of which 7.1 kPa (or 21%) is oxygen. The air entering the lungs also has a total pressure of 33.7 kPa, of which 6.3 kPa is, unavoidably, water vapor (as it is at sea level). This reduces the partial pressure of oxygen entering the alveoli to 5.8 kPa (or 21% of [33.7 kPa – 6.3 kPa] = 5.8 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 kPa vs. 7.1 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 kPa) results in an intrapulmonary air pressure of 50 kPa. Doing the same at 5500 m, where the atmospheric pressure is only 50 kPa, the intrapulmonary air pressure falls to 25 kPa. Therefore, the same change in lung volume at sea level results in a 50 kPa difference in pressure between the ambient air and the intrapulmonary air, whereas it result in a difference of only 25 kPa at 5500 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 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 kPa. A doubling or more of these small pressure differences could be achieved by only very minor adjustments to 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 blood gas homeostat, which regulates the partial pressures of oxygen and carbon dioxide in the arterial blood. This homeostat prioritizes the regulation of the arterial partial pressure of carbon dioxide over that of oxygen at sea level. That is to say, at sea level the arterial partial pressure of CO2 is maintained at very close to 5.3 kPa (or 40 mmHg) under a wide range of circumstances, at the expense of the arterial partial pressure of O2, 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 O2 in the ambient air) falls to below 50-75% of its value at sea level, oxygen homeostasis is given priority over carbon dioxide homeostasis. This switch-over occurs at an elevation of about 2500 m (or about 8000 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 consequent rise in the pH of the arterial plasma. This is one contributor to high altitude sickness. On the other hand, if the switch to oxygen homeostasis is incomplete, then hypoxia may complicate the clinical picture with potentially fatal results.
There are oxygen sensors in the smaller bronchi and bronchioles. In response to low partial pressures of oxygen in the inhaled air these sensors reflexly cause the pulmonary arterioles to constrict. (This is the exact opposite of the corresponding reflex in the tissues, where low arterial partial pressures of O2 values cause arteriolar vasodilation.) At altitude this causes the 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 the tops of the lungs receive far less blood than the bases, which are relatively over-perfused with blood. It is only in middle of the lungs that the 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 acclimatatization to high altitudes and low oxygen pressures.
The kidneys measure the oxygen content (mmol O2/liter blood, rather than the partial pressure of O2) 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 (commonly known as "EPO") into the blood. This hormone stimulates the 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 O2, 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.
Irritation of nerve endings within the nasal passages or airways, can induce a cough reflex and sneezing. These responses cause air to be expelled forcefully from the 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. 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 immunoglobulins (IgA), collectins, defensins 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 chemokines and cytokines are also secreted that recruit the traditional immune cells and others to site of infections.
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.
The lungs make a surfactant, a surface-active lipoprotein complex (phospholipoprotein) formed by 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. 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 the greater the tendency for the alveolus to collapse. 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 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 greater tendency to collapse (i.e. cause atelectasis) at the end of exhalation that 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. 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.
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 respiratory distress syndrome, is fatal. Basic scientific experiments, carried out using cells from chicken lungs, support the potential for using steroids as a means of furthering development of type II alveolar cells. In fact, once a 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.
The lung vessels contain a fibrinolytic system that dissolves 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 prostaglandins 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 arteriolar walls, causing arteriolar vasoconstriction, and consequently a rise in arterial blood pressure. Large amounts of the angiotensin-converting enzyme responsible for this activation are located on the surface 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.
The movement of gas through the larynx, pharynx and mouth allows humans to speak, or phonate. Vocalization, or singing, in birds occurs via the 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.
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).
Disorders of the respiratory system can be classified into several general groups:
Where there is an inability to breathe or an insufficiency in breathing a medical ventilator may be used.
Horses are obligate nasal breathers which means that they are different from many other mammals because they do not have the option of breathing through their mouths and must take in air through their noses.
The elephant is the only mammal known to have no pleural space. Rather, the parietal and visceral pleura are both composed of dense connective tissue and joined to each other via loose connective tissue. This lack of a pleural space, along with an unusually thick diaphragm, are thought to be evolutionary adaptations allowing the elephant to remain underwater for long periods of time while breathing through its trunk which emerges as a snorkel.
In the elephant the lungs are attached to the diaphragm and breathing relies mainly on the diaphragm rather than the expansion of the ribcage.
The respiratory system of birds differs significantly from that found in mammals. Firstly they have rigid lungs which do not expand and contract during the breathing cycle. Instead an extensive system of air sacs distributed throughout their bodies act as the bellows drawing environmental air into the sacs, and expelling the spent air after it has passed through the lungs. Birds also do not have diaphragms or pleural cavities. Fresh air is drawn into the air sacs in the abdomen during inhalation, at the same time as spent air in the lungs is drawn into anterior air sacs in the thorax. Air from the posterior air sacs is forced, during exhalation, through a set of airways in the lungs, the narrowest of which are a millions of parallel running air capillaries or parabronchi. Microscopic sacs bud radially off from the parabronchi, called "atria", which are the main site of gas exchange. The blood flow through the bird lung is at right angles to the flow of air through the parabronchi, forming a cross-current flow exchange system (see Fig. 15). The partial pressure of O2 in the parabronchi declines along their length as O2 diffuses into the blood. The capillaries leaving the exchanger near the entrances of airflow take up more O2 than capillaries leaving near the exit ends of the parabronchi. When the contents of all capillaries mix, the final partial pressure of oxygen of the mixed pulmonary venous blood is higher than that of the exhaled air, but lower than that of the inhaled air.
During exhalation, while fresh air from the posterior air sacs is forced though the lungs, the air in the anterior air sacs joins the air exiting from the lungs, to be expelled through the trachea into the environment. A sequence of localized bronchoconstrictions in the bronchial system ensures that the inflow and outflow of air during the breathing cycle take the paths described above.
The anatomical structure of the lungs is less complex in reptiles than in mammals, with reptiles lacking the very extensive airway tree structure found in mammalian lungs. Gas exchange in reptiles still occurs in alveoli however. Reptiles do not possess a diaphragm. Thus, breathing occurs via a change in the volume of the body cavity which is controlled by contraction of intercostal muscles in all reptiles except turtles. In turtles, contraction of specific pairs of flank muscles governs inhalation and exhalation.
Both the lungs and the skin serve as respiratory organs in amphibians. The ventilation of the lungs in amphibians relies on positive pressure ventilation. Muscles lower the floor of the oral cavity, enlarging it and drawing in air through the nostrils into the oral cavity. With the nostrils and mouth closed, the floor of the oral cavity is then pushed up, which forces air down the trachea into the lungs. The skin of these animals is highly vascularized and moist, with moisture maintained via secretion of mucus from specialised cells, and is involved in cutaneous respiration. While the lungs are of primary organs for gas exchange between the blood and the environmental air (when out of the water), the skin's unique properties aid rapid gas exchange when amphibians are submerged in oxygen-rich water. Some amphibians have gills, either in the early stages of their development (e.g. tadpoles of frogs), while others retain them into adulthood (e.g. some salamanders).
In most fish, respiration takes place through gills. Lungfish, however, do possess one or two lungs. The labyrinth fish have developed a special "labyrinth organ", which is a much-folded suprabranchial accessory breathing organ that allows them to take advantage of the oxygen of the air, to supplement the oxygen taken up from their watery environment by the gills. Thus labyrinth fish can survive for a short period of time out of water, as they can inhale the air around them, provided they stay moist.
Some species of crab use a respiratory organ called a branchiostegal lung. Its gill-like structure increases the surface area for gas exchange which is more suited to taking oxygen from the air than from water. Some of the smallest spiders and mites can breathe simply by exchanging gas through the surface of the body. Larger spiders, scorpions and other arthropods use a primitive book lung.
Most insects breath passively through their spiracles (special openings in the exoskeleton) and the air reaches every part of the body by means of a series of smaller and smaller tubes called 'trachaea' when their diameters are relatively large, and 'tracheoles' when their diameters are very small. The tracheoles make contact with individual cells throughout the body. They are partially filled with fluid, which can be withdrawn from the individual tracheoles when the tissues, such as muscles, are active and have a high demand for oxygen, bringing the air closer to the active cells. This is probably brought about by the build up of lactic acid in the active muscles causing an osmotic gradient, moving the water out of the tracheoles and into the active cells. Diffusion of gases is effective over small distances but not over larger ones, this is one of the reasons insects are all relatively small. Insects which do not have spiracles and trachaea, such as some Collembola, breathe directly through their skins, also by diffusion of gases.
The number of spiracles an insect has is variable between species, however they always come in pairs, one on each side of the body, and usually one pair per segment. Some of the Diplura have eleven, with four pairs on the thorax, but in most of the ancient forms of insects, such as Dragonflies and Grasshoppers there are two thoracic and eight abdominal spiracles. However, in most of the remaining insects there are fewer. It is at the level of the tracheoles that oxygen is delivered to the cells for respiration.
Insects were once believed to exchange gases with the environment continuously by the simple diffusion of gases into the tracheal system. More recently, however, large variation in insect ventilatory patterns have been documented and insect respiration appears to be highly variable. Some small insects do not demonstrate continuous respiratory movements and may lack muscular control of the spiracles. Others, however, utilize muscular contraction of the abdomen along with coordinated spiracle contraction and relaxation to generate cyclical gas exchange patterns and to reduce water loss into the atmosphere. The most extreme form of these patterns is termed discontinuous gas exchange cycles.
Molluscs generally possess gills that allow gas exchange between the aqueous environment and their circulatory systems. These animals also possess a heart that pumps blood containing hemocyanin as its oxygen-capturing molecule. Hence, this respiratory system is similar to that of vertebrate fish. The respiratory system of gastropods can include either gills or a lung.
Plants use carbon dioxide gas in the process of photosynthesis, and exhale oxygen gas as waste. The chemical equation of photosynthesis is 6 CO2 (carbon dioxide) and 6 H2O (water), which in the presence of sunlight makes C6H12O6 (glucose) and 6 O2 (oxygen). Photosynthesis uses electrons on the carbon atoms as the repository for the energy obtained from sunlight. Respiration is the opposite of photosynthesis. It reclaims the energy to power chemical reactions in cells. In so doing the carbon atoms and their electrons are combined with oxygen forming CO2 which is easily removed from both the cells and the organism. Plants use both processes, photosynthesis to capture the energy and oxidative metabolism to use it.
Plant respiration is limited by the process of diffusion. Plants take in carbon dioxide through holes that can open and close on the undersides of their leaves and other parts, known as stomata or pores. Most plants require some oxygen for catabolic processes (break-down reactions that release energy). But the quantity of O2 used per hour is small as they are not involved in activities that require high rates of aerobic metabolism. Their requirement for air, however, is very high as they need CO2 for photosynthesis, which constitutes only 0.04% of the environmental air. Thus, to make 1 g of glucose requires the removal of at least all the CO2 from 18.7 liters of air at sea level. But inefficiencies in the photosynthetic process cause considerably greater volumes of air to be used.
|The Wikibook Human Physiology has a page on the topic of: The respiratory system|
|The Wikibook Anatomy and Physiology of Animals has a page on the topic of: Respiratory System|
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