Alveolus (singular) is the word used for hollow cavities in anatomy. Consequently, there are different types of alveoli (plural) found throughout the human body. However, alveoli are usually used to describe the small air sacs of the lungs of mammals, and are therefore known more specifically as the pulmonary alveoli. The pulmonary alveolus is a sac roughly 0.2 to 0.5 mm in diameter. These alveoli are located at the ends of air passageways in the lungs. Sometimes, people compare alveoli structures to the appearance of a raspberry or a “bunch of grapes.”
In the average adult lung, there is an average of 480 million alveoli (with a range of 274-790 million, coefficient of variation: 37%; although this number varies depending on total lung volume), with a total average surface area of around 75 square meters. Each alveolus is in turn surrounded by a nest of blood capillaries supplied by small branches of the pulmonary artery. A respiratory membrane creates the barrier between alveolar air and blood, and this membrane consists only of the squamous alveolar cell, squamous endothelial cell of the capillary, and their shared basement membrane. Membranes have a total thickness of only 0.5-micrometers, in contrast to the 7.5-micrometer diameter of the erythrocytes (blood cells) that pass through the capillaries.
The major cell type found on the alveolar surface, covering about 95% of the surface area, are thin, broad cells known as squamous (type I) alveolar cells. The thin walls of these cells allow for rapid gas diffusion between the air and blood, and therefore allow for gas exchange to occur. The other 5% of the surface area of an alveolus is covered by round to cuboidal great (type II) alveolar cells. Although type II alveolar cells cover less surface area, they greatly outnumber the squamous alveolar cells.
The type II alveolar cells have two functions: (1) to repair the alveolar epithelium when squamous cells are damaged, and (2) to secrete pulmonary surfactant. Surfactant is composed of phospholipids and protein, and coats the alveoli and smallest bronchioles, which prevents the pressure buildup from collapsing the alveoli when one exhales. Without surfactant, the walls of a deflating alveolus would tend to cling together like sheets of wet paper, and it would be very difficult to re-inflate them on the next inhalation.
However, the most numerous of all cells in the lung are the alveolar macrophages (dust cells), which drift through the alveolar lumens and the connective tissue between them clearing up debris through phagocytosis. These macrophages “eat” the dust particles that escape from mucus in the higher parts of the respiratory tract, as well as other debris that is not trapped and cleared out by your mucus. If your lungs are infected or bleeding, the macrophages also function to phagocytize bacteria and loose blood cells. At the end of each day, as many as 100 million of these alveolar macrophages will expire as they ride up the mucociliary escalator to be swallowed at the esophagus and digested—this is how debris from the lungs is removed.
When a breath is taken during inhalation, the concentration of the incoming oxygen is higher in the alveolus than in the red blood cells. For this reason, oxygen will leave the alveolus and enter the red blood cells.
During exhalation, the opposite occurs. The concentration of carbon dioxide is lower in the alveolus than in the red blood cells, thus, carbon dioxide leaves the red blood cell, enters the alveolus, and is exhaled.
Since gases are constantly required physiologically and produced are as a by-product of cellular and metabolic processes in the body, an efficient system for their exchange is extremely important. Respiration therefore serves an important regulatory role in gas exchange. To give an example, metabolic changes in patients with diabetic ketoacidosis (DKA) ultimately result in changes in respiration patterns. This is because DKA will result in metabolic acidosis, where the body will initially buffer the change with the bicarbonate buffering system. However, once the body is overwhelmed and can no longer compensate for the acidosis, one compensatory mechanism is then hyperventilation, in order to lower the blood carbon dioxide levels by blowing off the carbon dioxide through exhalation (extreme forms of this hyperventilation are known as Kussmaul respiration).
In the clinic, it is very important to prevent fluid accumulation in the alveoli, since gases diffuse too slowly through liquid to be able to sufficiently aerate the blood. Except for a thin film of moisture on the alveolar wall, the alveoli are kept dry by the absorption of excess liquid by the blood capillaries (dependent on hydrostatic and oncotic forces described by the Starling equation). Their mean blood pressure is only 10 mmHg and the oncotic pressure is 28 mmHg, which means that the osmotic uptake of water overrides filtration and keeps the alveoli free of fluid. In general, the lungs also have a more extensive lymphatic drainage than any other organ in the body since edema (buildup of fluid) can cause many pathophysiologies, some of which are often fatal. In addition, a low capillary blood pressure also prevents the rupture of the delicate respiratory membrane.