The alveolus is a microscopic, air-filled sac located at the end of the respiratory tree within the lungs. These structures, often compared to tiny balloons, are the final destination for inhaled air. The primary function of the approximately 300 to 500 million alveoli in the human lungs is to serve as the specialized interface for gas transfer. This delicate, thin-walled structure creates an immense surface area, estimated between 50 and 75 square meters, which is necessary for efficient respiration.
The Specialized Structure of the Alveolus
The architecture of the alveolus is built from three main cell types. The majority of the alveolar wall is lined by Type I pneumocytes, which are extremely thin, flat squamous cells covering over 95% of the internal surface area. Their minimal thickness minimizes the distance gases must travel during exchange. These cells form a continuous, thin epithelial lining fused to the basement membrane of the adjacent capillary.
Interspersed among the Type I cells are the cuboidal Type II pneumocytes, which produce pulmonary surfactant. Surfactant is a lipoprotein mixture that reduces the high surface tension created by water on the moist inner surface. Without this coating, the small air sacs would collapse entirely upon exhalation, making re-inflation extremely difficult. Type II cells can also divide and differentiate into new Type I cells, providing a repair mechanism for damaged alveolar walls.
The third residents of this space are alveolar macrophages, mobile immune cells often called “dust cells.” These macrophages patrol the inner surface, engulfing inhaled pathogens, dust, and cellular debris. This action maintains a clean environment necessary for gas exchange.
The Mechanism of Gas Exchange
Gas transfer across the alveolar surface relies entirely on the principle of passive diffusion, a process requiring no energy. This exchange occurs across the respiratory membrane, an incredibly thin layer formed by the combined walls of the Type I pneumocyte and the adjacent pulmonary capillary endothelium. The thickness of this barrier is remarkably slight, often less than 0.5 micrometers, which facilitates the rapid movement of gas molecules.
Gas movement is determined by the partial pressure gradient, which is the difference in concentration for each gas between the alveolar air and the blood. In the alveolus, the partial pressure of oxygen (\(P_{O2}\)) is high, typically around 104 mmHg. The deoxygenated blood arriving via the pulmonary artery has a much lower \(P_{O2}\) of approximately 40 mmHg.
This steep pressure difference causes oxygen to rapidly diffuse from the alveolus, across the respiratory membrane, and into the capillary blood. Simultaneously, carbon dioxide moves in the opposite direction, driven by its pressure gradient. The carbon dioxide partial pressure (\(P_{CO2}\)) in the arriving blood is higher (around 45 mmHg) compared to the lower \(P_{CO2}\) (40 mmHg) in the alveolar air.
Carbon dioxide readily diffuses out of the blood and into the alveolus for exhalation. This movement is aided because carbon dioxide is significantly more soluble in the respiratory membrane than oxygen, diffusing about 20 to 25 times faster. Constant ventilation of the alveoli with fresh air and continuous blood flow through the capillaries ensure these pressure gradients are maintained, allowing efficient gas exchange at all times.
Common Conditions Affecting Alveoli
Disruption to the delicate alveolar structure or function can severely impair gas exchange, leading to respiratory dysfunction. Emphysema is characterized by the progressive destruction of the alveolar walls. This breakdown causes many small air sacs to merge into fewer, larger, and irregularly shaped air spaces.
The net effect of this structural damage results in a significant reduction in the total surface area available for gas exchange. This loss hinders the movement of oxygen into the bloodstream, even when pressure gradients are normal. Pneumonia is another common condition, involving an infection that causes inflammation and fluid accumulation within the alveoli.
The presence of inflammatory fluid and cells within the air sac dramatically increases the thickness of the respiratory membrane. This increased diffusion distance significantly slows the rate at which oxygen enters the blood, making breathing difficult. In premature infants, Infant Respiratory Distress Syndrome (RDS) occurs due to the immaturity of the Type II pneumocytes.
When these cells cannot produce sufficient pulmonary surfactant, the high surface tension causes the alveoli to collapse with each breath. The lack of stable air sacs prevents meaningful gas exchange, requiring immediate medical intervention to provide external surfactant and maintain open airways. These conditions demonstrate how precise structural integrity is required for the alveolus to function as the body’s respiratory exchange unit.