The smallest air passages in the lungs, known as bronchioles, are delicate tubes that deliver air to the alveoli where gas exchange occurs. Their diameter, approximately one millimeter or less in terminal sections, presents a significant physiological challenge. These tiny airways are continuously threatened by collapse, especially during exhalation when internal lung pressure drops. The body employs two complementary mechanisms—one chemical and one mechanical—to ensure these soft-walled structures remain open throughout the respiratory cycle.
The Structural Vulnerability of Bronchioles
The larger airways, or bronchi, possess rigid structural support in the form of cartilage rings or plates embedded within their walls. This cartilage provides a firm scaffolding that prevents the bronchi from collapsing, regardless of pressure changes within the chest cavity. Bronchioles are defined by the point where this protective cartilage abruptly disappears, typically around the sixteenth generation of airway branching.
The absence of cartilage leaves the bronchiole walls soft and highly pliable, composed primarily of smooth muscle and elastic fibers. This structural difference makes bronchioles extremely susceptible to pressure changes during breathing. During exhalation, the surrounding pressure increases, creating a squeezing force that would otherwise seal them shut.
Internal Protection Through Surface Tension Reduction
One of the greatest internal threats to the stability of the small airways is surface tension. The inner lining of the bronchioles and alveoli is coated with a thin layer of water-based fluid. The cohesive forces between these water molecules create a strong inward-pulling tension, effectively pulling the small airways closed.
The body counters this collapsing force with pulmonary surfactant, a specialized lipoprotein complex produced by Type II alveolar cells. Surfactant acts as a chemical wedge, inserting itself between water molecules at the air-fluid boundary. The main lipid component, dipalmitoylphosphatidylcholine (DPPC), interrupts the strong water-water bonds, dramatically lowering the surface tension.
This reduction in tension makes it easier to inflate the airways during inhalation and prevents their collapse during exhalation. Surfactant’s ability to lower surface tension increases as the airway radius decreases. This means it is most effective precisely where needed, offering a dynamic defense against collapse in the smallest bronchioles and alveoli.
External Support Via Radial Traction
The second mechanism providing external support is a mechanical force called radial traction. This outward pulling force is generated by the natural elastic recoil of the entire lung tissue. The lungs are filled with elastic fibers that stretch during inhalation and naturally seek to snap back to a smaller size.
The walls of the small bronchioles are physically tethered by connective tissue fibers to the surrounding alveolar walls. As the lungs expand during inspiration, the stretching of the alveolar tissue exerts an outward pull on the bronchioles. This tethering acts like tiny guy wires, pulling the soft walls of the airways open and maintaining their diameter.
This mechanism ensures that as overall lung volume increases, the airways widen, minimizing resistance to airflow. The protective effect of radial traction is directly dependent on lung volume. The traction force is strongest when the lungs are fully inflated and weakest during maximal exhalation, when bronchioles are most vulnerable to collapse.