The lung alveoli are the microscopic, cup-shaped air sacs that form the functional core of the human respiratory system. Located at the very end of the respiratory tree, these tiny structures inflate with air during inhalation and deflate during exhalation. A typical pair of human lungs contains approximately 480 million alveoli, collectively providing a massive surface area for gas exchange, estimated to be between 70 and 80 square meters. This vast internal surface is necessary for the body to absorb the required amount of oxygen and to efficiently expel carbon dioxide. The alveoli are the dedicated site where the atmosphere and the bloodstream meet, performing the life-sustaining task of respiration.
Anatomy and Cell Types
The physical structure of the alveolus is designed for maximum efficiency, featuring extremely thin walls that minimize the distance gases must travel. Each alveolus is a hollow cavity surrounded by a dense network of pulmonary capillaries, forming a structure known as the alveolar-capillary membrane. This membrane is typically only 0.2 to 2 micrometers thick, which is a short diffusion distance that allows for rapid gas transfer.
The alveolar wall is primarily composed of two distinct cell types, known as pneumocytes. The Type I pneumocytes are flat, thin, and squamous cells that line over 95% of the alveolar surface, providing the primary structural component of the air-blood barrier. Their shape is optimized for facilitating the quick passage of gases across the membrane.
The second cell type, Type II pneumocytes, are smaller, more cuboidal cells that have an equally important role. They are responsible for producing and secreting pulmonary surfactant, a substance that prevents the collapse of the air sacs. Additionally, Type II pneumocytes possess the ability to differentiate and replace damaged Type I cells, which is a crucial function for alveolar repair. The alveoli also contain alveolar macrophages, which are mobile immune cells that engulf foreign particles, dust, and bacteria that reach the air sacs, acting as the lung’s internal cleanup crew.
The Process of Gas Exchange
The fundamental purpose of the alveoli is external respiration, the process of moving oxygen into the blood and carbon dioxide out of it. This gas exchange occurs passively through simple diffusion, which does not require the body to expend energy. The direction of movement is governed by the partial pressure gradient of each gas across the alveolar-capillary membrane.
Inhaled air gives the alveoli a high partial pressure of oxygen (pO2), while the deoxygenated blood arriving at the capillaries has a lower pO2. This pressure difference causes oxygen molecules to diffuse rapidly across the thin membrane and into the bloodstream, where they quickly bind to hemoglobin in red blood cells. Simultaneously, the blood arriving from the tissues has a high partial pressure of carbon dioxide (pCO2), a waste product of cellular metabolism.
The pCO2 in the blood is higher than the pCO2 in the alveolar air, which drives the carbon dioxide molecules to diffuse in the opposite direction, from the capillary blood into the alveolus. Once in the air sac, the carbon dioxide is expelled during exhalation. The efficiency of this exchange is enhanced because carbon dioxide is significantly more soluble in the blood than oxygen, allowing it to diffuse easily despite a smaller pressure gradient.
The Role of Pulmonary Surfactant
The inner surface of the alveoli is lined with a thin layer of fluid, which creates a force known as surface tension. Water molecules in this fluid are more attracted to each other than to the air, generating an inward-pulling force that would cause the small, wet air sacs to collapse completely, similar to a deflating balloon. Pulmonary surfactant is a lipoprotein mixture, primarily composed of a lipid called dipalmitoylphosphatidylcholine (DPPC), that counteracts this collapsing force.
Secreted by the Type II pneumocytes, surfactant reduces the surface tension at the air-liquid interface within the alveoli. The effect of the surfactant increases as the alveoli shrink, lowering the surface tension to near-zero levels at the end of exhalation. This mechanism ensures the air sacs remain slightly open, preventing a complete collapse, a condition known as atelectasis. Without sufficient surfactant, the effort required to re-inflate the lungs with every breath becomes enormous, a problem seen in premature infants with Infant Respiratory Distress Syndrome.
Diseases Caused by Alveolar Damage
Damage to the delicate alveolar structure underlies several serious respiratory conditions, each impairing the gas exchange process in a distinct way.
Emphysema
Emphysema, often linked to smoking, involves the permanent destruction of the alveolar walls and the surrounding capillary network. This damage leads to the merging of multiple small air sacs into fewer, larger, less efficient air spaces, drastically reducing the total surface area available for gas exchange. The loss of elastic tissue also causes air to become trapped, making exhalation difficult.
Pneumonia
Pneumonia is an infection that causes inflammation and the buildup of fluid, pus, or blood within the alveolar space. This accumulation of material effectively thickens the alveolar-capillary membrane, increasing the distance that oxygen and carbon dioxide must diffuse. The impaired diffusion and reduced air volume within the functional alveoli result in lower oxygen levels in the bloodstream.
Pulmonary Fibrosis
Pulmonary fibrosis involves the development of scarring and excess fibrous tissue around the alveoli. This process makes the lung tissue stiff and thickens the diffusion barrier, severely impeding the transfer of gases, especially oxygen.