Anatomy , or "Respiratory Tree" 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 (Fig. 2.) includes the lower part of the
larynx, the
trachea,
bronchi,
bronchioles and the
alveoli. The branching airways of the lower tract are often described as the
respiratory tree or
tracheobronchial tree (Fig. 2). 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
air conduits, bringing air to the respiratory bronchioles, alveolar ducts and alveoli (approximately generations 17–23), where
gas exchange takes place. are known as 4th order, 5th order, and 6th order segmental bronchi, or grouped together as subsegmental bronchi. 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, a volume of air (about 150 ml in the adult human) that fills the 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. An average healthy human breathes 12–16 times a minute.
Mechanics of breathing (MRI) of the chest movements of human thorax during breathing {{Multiple image 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 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. 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. 8, and discussion below) and 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 increased 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,
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
begin with the nose. (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.) It ends in the microscopic dead-end sacs called
alveoli, which 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 because of lungs contraction and expansion 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 (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). 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. 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 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 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, across a very thin membrane (known as the
blood–air barrier), which forms the walls of the
pulmonary alveoli (Fig. 10). It consists 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 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 until 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 until 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. 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 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. The reaction can go in both directions depending on the prevailing partial pressure of CO2. compared to the concentration of oxygen in saturated arterial blood of about 9 mM (or 20 ml/100 ml blood). In addition, passive movements of the limbs also reflexively produce an increase in the breathing rate. 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). 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. 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. (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 the 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 (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.
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. 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.
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 the 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.
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
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 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
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.
Temperature control 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 Disorders of the respiratory system can be classified into several general groups: • Airway obstructive conditions (e.g.,
emphysema,
bronchitis,
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,
particulate pollutants) • Primary cancers (e.g.
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.
respiratory distress syndrome in pre-term babies) . Disorders of the respiratory system are usually treated by a
pulmonologist and
respiratory therapist. Where there is an inability to breathe or insufficiency in breathing, a
medical ventilator may be used. ==Exceptional mammals==