Respiratory system

In humans and other mammals, the anatomy of a typical respiratory system is the respiratory tract. The tract is divided into an upper and a lower respiratory tract. The upper tract includes the nose, nasal cavities, sinuses, pharynx and the part of the larynx above the vocal folds. The lower tract includes the lower part of the larynx, the trachea, bronchi, bronchioles and the alveoli.

External respiration

External respiration is basically the transfer of gas between respiratory organs such as lungs and the outer environment. It takes place prior to internal respiration.

Internal Respiration

Internal Respiration an exchange of gases between the cells of the body and the blood by way of the fluid bathing the cells.

Inspiration

•       It is an active process.

•       Contraction of external intercostals muscles and relaxations and internal intercostals muscles occur.

•       Rib cages move forward and outward.

•       Diaphragm contracts and becomes flattened.

•       Increase in volume of thoracic cavity.

•       Air pressure in lungs is less than atmospheric pressure.

•       Intake of air into lungs.

Expiration

•       It is a passive process.

•       Relaxations of external intercostals muscles and Contraction of internal intercostals muscles occur.

•       Rib cages move downward and inward.

•       Diaphragm relaxes and becomes original dome shaped.

•       Decrease in volume of thoracic cavity.

•       Air pressure in lungs is higher than atmospheric pressure.

•       Expulsion of air from the lung

Structure of Respiratory System

Structurally the organs of the Respiratory track can be divided into two groups

 

The Upper Respiratory Track             The Lower Respiratory Track

Nose                                                     Larynx

Nasal Cavity                                        Trachea

Sinuses                                                 Bronchial Tree

Pharynx                                                Lungs

 

Ventilatory 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 ml), and volumes moved during maximally forced inhalation and maximally forced exhalation are measured in humans by spirometry.^[12] A typical adult human spirogram with the names given to the various excursions in volume the lungs can undergo is illustrated below (Fig. 3):

Fig. 3 Output of a 'spirometer'. Upward movement of the graph, read from the left, indicates the intake of air; downward movements represent exhalation.

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.^[12]

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.

Measurement	Equation	Description
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.

 

Mechanics of breathing

Fig. 6 Real-time magnetic resonance imaging (MRI) of the chest movements of human thorax during breathing

Main article: Breathing § Mechanics

The "pump handle" and "bucket handle movements" of the ribs

Fig. 4 The effect of the muscles of inhalation in expanding the rib cage. The particular action illustrated here is called the pump handle movement of the rib cage.

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.

Breathing

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 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 cause 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.

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.

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. 4. All the ribs slant downwards from the rear to the front (as shown in Fig. 4); but the lowermost ribs also slant downwards from the midline outwards (Fig. 5). 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. 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. The inflow of air into the lungs occurs via the respiratory airways (Fig. 2). 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.^[13][14]

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. 7) when the lungs contain their functional residual capacity of air (the light blue area in the right hand illustration of Fig. 7), which in the adult human has a volume of about 2.5–3.0 liters (Fig. 3).^[6]Resting exhalation lasts about twice as long as inhalation because the diaphragm relaxes passively more gently than it contracts actively during inhalation.

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 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.^[10][15] 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.^[6] 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).^[6]

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.^[6] 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.^[6]

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.^[16] 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

Mechanism of gas exchange

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.

Fig. 12 A diagrammatic histological cross-section through a portion of lung tissue showing a normally inflated alveolus (at the end of a normal exhalation), and its walls containing the 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 ml blood.

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 I epithelial cells (or type 1 pneumocytes). The two red objects labeled "RBC" are red blood cells in the pulmonary capillary blood.

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,^[17] 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).^[18] 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^[18] (each between 75 and 300 µm in diameter) branching off from the respiratory bronchioles in the lungs, thus providing an extremely large surface area (approximately 145 m²) for gas exchange to occur.^[18]

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).^[6] 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.^[6]

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 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 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.^[19] 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 CO₂and, 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 and carotid bodies, as well as by 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.^[20]

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 hemegroups 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 bicarbonate ions (HCO₃⁻) 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.^[21] The reaction can go in both directions depending on the prevailing partial pressure of CO₂.^[6]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),^[22] compared to the concentration of oxygen in saturated arterial blood of about 9 mM (or 20 ml/100 ml blood).^[6]

 

Control of ventilation

Ventilation of the lungs in mammals occurs via the respiratory centers in the medulla oblongata and the pons of the brainstem.^[6] 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.^[6] The aortic and carotid bodies, are the peripheral blood gas chemoreceptors which are particularly sensitive to the arterial partial pressure of O₂ though they also respond, but less strongly, to the partial pressure of CO₂.^[6] 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.^[6]

Exercise increases the breathing rate due to the extra carbon dioxide produced by the enhanced metabolism of the exercising muscles.^[23] In addition passive movements of the limbs also reflexly produce an increase in the breathing rate.^[6][23]

Information received from stretch receptors in the lungs limits tidal volume (the depth of inhalation and exhalation).

 

Responses to low atmospheric pressures

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.

Fig. 14 A graph showing the relationship between total atmospheric pressure and altitude above sea level.

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.^[24] 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.^[25] 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).

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 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.^[26] 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.^[24] 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.^[13][14] 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.^[6] 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.^[6] 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.^[27] (This is the exact opposite of the corresponding reflex in the tissues, where low arterial partial pressures of O₂ 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 (often known only by its abbreviated form as EPO)^[28] into the blood.^[29] 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 hemoglobincontent 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.^[29][30]

 

Other functions of the lungs

Local defenses

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.^[6] 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.^[31]

Most of the respiratory system is lined with mucous membranes that contain mucosa-associated lymphoid tissue, which produces white blood cells such as lymphocytes.

Prevention of alveolar collapse

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.^[6] 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.^[6] 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.^[6] 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.^[6][32]

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.^[33] 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.^[34]

Contributions to whole body functions

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 prostaglandinsare 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.^[35] 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.

Effect of Exercise on the Respiratory system

1)      Increased Lung Volume-

lung volume is increased that means the total volume of air that can be voluntarily moved in one breath from full inspiration to maximum expiration as result increase vital capacity. A trained athlete may have 5-6 lit, and untrained person may have 3 to-4 lit.

2)      Respiratory rate

Breathing frequency is the number of breaths per minutes. Normally after training breathing frequency is decreased . A normal individual may have 12-20 breath/min but a trained athlete may have 7 to 8 breaths/per min.

Newborn-30-60 breaths/m

3)      Pulmonary ventilation

Minute ventilation is the volume of air, which is inspired or expired from a person’s lungs in one minute. It is normally increased after exercise .

4)      Tidal volume-

The tidal volume, which is the amount of air either inspired or expired in a normal breath is also increased as a result of training. A untrained person may have  500 mL/breath, or trained person may have 600/700 mL/ breath.

5)      Ventilator Efficiency-

Due to exercise ventilator efficiency gets better. That means 15 lit air is required to get one lit of O2 for a normal man, whereas for a trained athlete same amount of O2 can be acquired from 12 lit of air.

6)      Consumption of O2 –

During exercise the consumption of O2 by the tissues particularly the skeletal muscles is greatly increased due to more amount of blood flows through the muscles.

7)      Nature of second wind-

During severe exercise, initially a frequent feeling of distress is developed. But if the exercise is further continued, this sense of distress is relapsed by a sense of great relief. This sense is called second wind.

•       Inspiratory Reserve: Additional air that can be forcibly inhaled after inspiration of tidal volume. Can increase lung volume by up to 2900 mL

•       Expiratory reserve volume 1400 mL of air

•       Vital Capacity: The volume of air breathed out after the deepest inhalation. Total of tidal, inspiratory and expiratory reserve volumes.

•       Residual Volume: (about 100 ml) The amount of air that remains in a person’s lungs after maximum exhalation.