Breathing


Breathing is the rhythmic process of moving air into and out of the lungs to enable gas exchange with the internal environment, primarily to remove carbon dioxide and take in oxygen.
All aerobic organisms require oxygen for cellular respiration, which extracts energy from food and produces carbon dioxide as a waste product. External respiration brings air to the alveoli where gases move by diffusion; the circulatory system then transports oxygen and carbon dioxide between the lungs and the tissues.
In vertebrates with lungs, breathing consists of repeated cycles of inhalation and exhalation through a branched system of airways that conduct air from the nose or mouth to the alveoli. The number of respiratory cycles per minute — the respiratory or breathing rate — is a primary vital sign. Under normal conditions, depth and rate of breathing are controlled unconsciously by homeostatic mechanisms that maintain arterial partial pressures of carbon dioxide and oxygen. Keeping arterial CO₂ stable helps maintain extracellular fluid pH; hyperventilation and hypoventilation alter CO₂ and thus pH and produce distressing symptoms.
Breathing also supports speech, laughter and certain reflexes and can contribute to thermoregulation.

Mechanics

The lungs do not inflate themselves; they expand only when the thoracic cavity volume increases. In mammals this expansion is produced mainly by contraction of the diaphragm and, to a lesser extent, by contraction of the intercostal muscles, which lift the rib cage. During forceful inhalation accessory muscles may augment the pump-handle and bucket-handle movements of the ribs to further increase chest volume. At rest exhalation is largely passive as inhalatory muscles relax and the elastic recoil of the lungs and chest wall returns the chest to its resting position. At this resting point the lungs contain the functional residual capacity.
During heavy breathing, such as with exercise, exhalation also involves active contraction of the abdominal muscles, which pushes the diaphragm upward and reduces end-exhalatory lung volume. Even at maximum exhalation a normal mammal retains residual air in the lungs.
Diaphragmatic breathing produces visible abdominal movement; use of accessory muscles with clavicular elevation is seen in labored breathing, for example during severe asthma or chronic obstructive pulmonary disease exacerbations.

Passage of air

Upper airways

Air is ideally inhaled and exhaled through the nose. The nasal cavities — divided by the nasal septum and lined with convoluted conchae — expose inhaled air to a large mucosal surface so it is warmed and humidified and particulate matter is trapped by mucus before reaching the lower airways. Some of the heat and moisture are recovered during exhalation when air passes back over cooler, partially dried mucus.

Lower airways

Below the upper airways the mammalian respiratory system is commonly described as a respiratory or tracheobronchial tree. Larger conducting airways branch repeatedly into smaller bronchi and bronchioles; in humans there are on average about 23 branching generations. Proximal divisions transmit air, while terminal divisions are specialized for gas exchange. The trachea and major bronchi begin outside the lungs and most branching occurs within the lungs until the blind-ended alveoli are reached. This arrangement produces anatomical dead space — the volume of conducting airways that does not participate in gas exchange.

Gas exchange

The primary purpose of breathing is to refresh alveolar air so gas exchange between alveolar air and pulmonary capillary blood can occur by diffusion. This diffusion of gases occurs through the utilization of the thin respiratory membrane, which is composed of alveolar epithelium, capillary endothelium and the basement membrane that come together to form a blood-gas barrier. After exhalation the lungs still contain the functional residual capacity; on a typical inhalation only a relatively small volume of new atmospheric air mixes with the FRC, so alveolar gas composition remains fairly constant across breaths. Pulmonary capillary blood therefore equilibrates with a relatively steady alveolar gas composition, and peripheral and central chemoreceptors sense gradual changes in dissolved gases rather than rapid swings. Homeostatic control of breathing thus centers on arterial partial pressures of CO₂ and O₂ and on maintaining blood pH.

Control

Breathing rate and depth are regulated by respiratory centers in the brainstem that receive input from central and peripheral chemoreceptors. Central chemoreceptors in the medulla are particularly sensitive to pH and CO₂ in the blood and cerebrospinal fluid; peripheral chemoreceptors in the aortic and carotid bodies are sensitive primarily to arterial O₂. Information from these receptors is integrated in the pons and medulla, which adjust ventilation to restore blood gas tensions. Motor nerves, including the phrenic nerves to the diaphragm, convey respiratory center outputs to the muscles of breathing. Although breathing is primarily automatic, it can be voluntarily modified for speaking, singing, swimming, or breath-holding training; conscious breathing techniques may promote relaxation. Reflexes such as the diving reflex alter breathing and circulation during submersion to conserve oxygen.

Composition

Inhaled air is by volume 78% nitrogen, 20.95% oxygen and small amounts of other gases including argon, carbon dioxide, neon, helium, and hydrogen.
The gas exhaled is 4% to 5% by volume of carbon dioxide, about a hundredfold increase over the inhaled amount. The volume of oxygen is reduced by about a quarter, 4% to 5%, of total air volume. The typical composition is:
In addition to air, underwater divers practicing technical diving may breathe oxygen-rich, oxygen-depleted or helium-rich breathing gas mixtures. Oxygen and analgesic gases are sometimes given to patients under medical care. The atmosphere in space suits is pure oxygen. However, this is kept at around 20% of Earthbound atmospheric pressure to regulate the rate of inspiration.

Effects of ambient air pressure

Breathing at altitude

decreases with the height above sea level and since the alveoli are open to the outside air through the open airways, the pressure in the lungs also decreases at the same rate with altitude. At altitude, a pressure differential is still required to drive air into and out of the lungs as it is at sea level. The mechanism for breathing at altitude is essentially identical to breathing at sea level but with the following differences:
The atmospheric pressure decreases exponentially with altitude, roughly halving with every rise in altitude. The composition of atmospheric air is, however, almost constant below 80 km, as a result of the continuous mixing effect of the weather. The concentration of oxygen in the air therefore decreases at the same rate as the atmospheric pressure. At sea level, where the ambient pressure is about 100 kPa, oxygen constitutes 21% of the atmosphere and the partial pressure of oxygen is 21 kPa. At the summit of Mount Everest,, where the total atmospheric pressure is 33.7 kPa, oxygen still constitutes 21% of the atmosphere but its partial pressure is only 7.1 kPa. Therefore, a greater volume of air must be inhaled at altitude than at sea level in order to breathe in the same amount of oxygen in a given period.
During inhalation, air is warmed and saturated with water vapor as it passes through the nose and pharynx before it enters the alveoli. The saturated vapor pressure of water is dependent only on temperature; at a body core temperature of 37 °C it is 6.3 kPa, regardless of any other influences, including altitude. Consequently, at sea level, the tracheal air consists of: water vapor, nitrogen, oxygen and trace amounts of carbon dioxide and other gases, a total of 100 kPa. In dry air, the at sea level is 21.0 kPa, compared to a of 19.7 kPa in the tracheal air. At the summit of Mount Everest tracheal air has a total pressure of 33.7 kPa, of which 6.3 kPa is water vapor, reducing the in the tracheal air to 5.8 kPa, beyond what is accounted for by a reduction of atmospheric pressure alone.
The pressure gradient forcing air into the lungs during inhalation is also reduced by altitude. Doubling the volume of the lungs halves the pressure in the lungs at any altitude. Halving the sea level air pressure results in a pressure gradient of 50 kPa but doing the same at 5500 m, where the atmospheric pressure is 50 kPa, a doubling of the volume of the lungs results in a pressure gradient of the only 25 kPa. In practice, because we breathe in a gentle, cyclical manner that generates pressure gradients of only 2–3 kPa, this has little effect on the actual rate of inflow into the lungs and is easily compensated for by breathing slightly deeper. The lower viscosity of air at altitude allows air to flow more easily and this also helps compensate for any loss of pressure gradient.
All of the above effects of low atmospheric pressure on breathing are normally accommodated by increasing the respiratory minute volume, and the mechanism for doing this is automatic. The exact increase required is determined by the respiratory gases homeostatic mechanism, which regulates the arterial and. This homeostatic mechanism prioritizes the regulation of the arterial over that of oxygen at sea level. That is to say, at sea level the arterial is maintained at very close to 5.3 kPa under a wide range of circumstances, at the expense of the arterial, which is allowed to vary within a very wide range of values, before eliciting a corrective ventilatory response. However, when the atmospheric pressure falls to below 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. If this switch occurs relatively abruptly, the hyperventilation at high altitude will cause a severe fall in the arterial with a consequent rise in the pH of the arterial plasma leading to respiratory alkalosis. 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.