Alveoli
Introduction
Alveoli are the tiny air sacs in the lungs where the exchange of oxygen and carbon dioxide occurs. They play a critical role in respiration by providing a large surface area for efficient gas exchange. Understanding their structure and function is essential for appreciating normal pulmonary physiology and various respiratory disorders.
Anatomy of Alveoli
Structure and Morphology
Alveoli are small, balloon-like structures located at the terminal ends of the respiratory tree. They cluster together in alveolar sacs connected by alveolar ducts, creating a network that maximizes the surface area available for gas exchange. The thin walls of alveoli, typically one cell layer thick, facilitate rapid diffusion of gases.
- Shape and size of alveoli: roughly spherical with diameters ranging from 200 to 300 micrometers.
- Alveolar sacs and ducts: alveoli are grouped into sacs connected by ducts that branch from the bronchioles.
- Surface area considerations: the combined alveolar surface area in human lungs is approximately 70 square meters, enhancing gas exchange efficiency.
Cell Types
Alveoli consist of several specialized cell types, each serving a distinct function in maintaining pulmonary health and facilitating gas exchange.
- Type I alveolar cells (pneumocytes): thin, flat cells covering about 95% of the alveolar surface, essential for gas diffusion.
- Type II alveolar cells (surfactant-producing cells): cuboidal cells that produce pulmonary surfactant, which reduces surface tension and prevents alveolar collapse.
- Alveolar macrophages: immune cells that reside within the alveolar lumen to ingest and remove pathogens, dust, and debris.
Capillary Network
Each alveolus is surrounded by a dense network of capillaries that enables efficient gas exchange between the alveolar air and blood. The close proximity of alveoli and capillaries creates the alveolar-capillary interface, where oxygen diffuses into the blood and carbon dioxide diffuses into the alveolar air for exhalation.
- Alveolar-capillary interface: thin barrier of approximately 0.2 to 0.5 micrometers between alveolar air and blood.
- Role in gas exchange: the extensive capillary network ensures a continuous flow of blood to maintain the diffusion gradient for oxygen and carbon dioxide.
Physiology of Alveoli
Gas Exchange
The primary function of alveoli is the exchange of gases between the lungs and the blood. Oxygen from inhaled air diffuses through the alveolar walls into the blood, while carbon dioxide from venous blood diffuses into the alveoli to be exhaled.
- Mechanism of oxygen diffusion: driven by partial pressure differences, oxygen moves from alveoli into capillary blood.
- Mechanism of carbon dioxide diffusion: carbon dioxide moves from blood, where its partial pressure is higher, into alveoli for exhalation.
- Factors affecting diffusion: thickness of the alveolar-capillary barrier, total surface area, and partial pressure gradients influence gas exchange efficiency.
Surfactant Function
Type II alveolar cells secrete pulmonary surfactant, a mixture of lipids and proteins that plays a crucial role in reducing surface tension within the alveoli. This prevents alveolar collapse during exhalation and contributes to lung compliance, facilitating breathing.
- Composition and production by type II cells: surfactant consists mainly of phospholipids and surfactant proteins.
- Role in reducing surface tension: prevents alveoli from collapsing by lowering the attractive forces between water molecules on the alveolar surface.
- Importance in preventing alveolar collapse (atelectasis): ensures alveoli remain open for continuous and efficient gas exchange.
Development and Aging
Alveolar Development
Alveolar formation begins during fetal development and continues after birth. Proper development is essential for establishing sufficient surface area and functional capacity for effective gas exchange throughout life.
- Embryonic and fetal development stages: initial formation of the respiratory diverticulum, branching of bronchioles, and emergence of primitive alveolar structures.
- Postnatal alveolar growth: alveoli increase in number and complexity after birth, with septation processes expanding the surface area significantly during early childhood.
Aging and Structural Changes
With advancing age, alveolar structure undergoes changes that can affect respiratory efficiency. These changes may contribute to decreased lung function and increased susceptibility to pulmonary diseases in older adults.
- Decrease in elasticity: the alveolar walls and surrounding lung tissue lose elastic recoil, making exhalation less efficient.
- Changes in surface area: some alveolar walls may degrade, reducing total surface area for gas exchange.
- Impact on respiratory efficiency: reduced elasticity and surface area can lead to decreased oxygen uptake and a higher risk of hypoxemia under stress or illness.
Pathophysiology
Infectious Conditions
Alveoli are susceptible to infections that can impair gas exchange and lead to respiratory illness. Infections often cause inflammation, fluid accumulation, and cellular damage.
- Pneumonia and alveolar inflammation: bacterial, viral, or fungal infections can fill alveoli with fluid and immune cells, impairing oxygen transfer.
- Tuberculosis affecting alveoli: Mycobacterium tuberculosis primarily targets alveolar tissue, leading to granuloma formation and potential tissue destruction.
Chronic Conditions
Long-term diseases can progressively damage alveolar structure and function, resulting in reduced lung capacity and impaired gas exchange.
- Chronic obstructive pulmonary disease (COPD) and emphysema: destruction of alveolar walls leads to enlarged air spaces and decreased surface area for gas exchange.
- Interstitial lung disease: fibrosis and scarring of alveolar walls thickens the diffusion barrier, reducing oxygen transfer efficiency.
Acute Conditions
Certain acute disorders can rapidly compromise alveolar function, requiring urgent medical attention to restore adequate oxygenation.
- Acute respiratory distress syndrome (ARDS): widespread alveolar injury causes fluid leakage, reduced lung compliance, and severe hypoxemia.
- Pulmonary edema: accumulation of fluid in alveoli, often due to cardiac failure or injury, disrupts normal gas exchange and oxygenation.
Clinical Significance
Diagnostic Imaging
Evaluation of alveolar structure and function often relies on imaging techniques that reveal abnormalities in lung tissue and air spaces.
- Chest X-ray findings: may show areas of consolidation, fluid accumulation, or hyperinflation affecting alveoli.
- CT scan features: provides detailed cross-sectional images to detect alveolar thickening, fibrosis, or small lesions not visible on standard X-rays.
Therapeutic Considerations
Treatment strategies often aim to support alveolar function, enhance gas exchange, and prevent complications from alveolar injury.
- Oxygen therapy: supplemental oxygen increases the gradient for diffusion, improving blood oxygenation in compromised alveoli.
- Ventilatory support strategies: mechanical ventilation or positive pressure ventilation can help maintain alveolar expansion and optimize gas exchange.
- Surfactant replacement therapy: administered in conditions such as neonatal respiratory distress syndrome to restore alveolar stability and prevent collapse.
References
- West JB. Respiratory Physiology: The Essentials. 10th ed. Philadelphia: Wolters Kluwer; 2020.
- Costanzo LS. Physiology. 7th ed. Philadelphia: Elsevier; 2018.
- Guyton AC, Hall JE. Textbook of Medical Physiology. 14th ed. Philadelphia: Elsevier; 2021.
- Weibel ER. Morphometry of the Human Lung. Berlin: Springer; 1963.
- Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1334-49.
- Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury. N Engl J Med. 2005;353(16):1685-93.
- King TE Jr, Pardo A, Selman M. Idiopathic pulmonary fibrosis. Lancet. 2011;378(9807):1949-61.
- Ballard PL, Ballard RA. Scientific basis and therapeutic regimens for surfactant replacement therapy. Pediatr Res. 1995;38(4):525-32.
- Hogg JC, Timens W. The pathology of chronic obstructive pulmonary disease. Annu Rev Pathol. 2009;4:435-59.
- Fishman AP. Fishman’s Pulmonary Diseases and Disorders. 5th ed. New York: McGraw-Hill; 2015.