Small airway disease

Small airway disease

Large airways are normally responsible for 45% of the total airway resistance and, of course, this can be greatly increased by obstruction due to foreign material or swelling of the upper airway. Resistance to gas flow is markedly affected by the patency of individual airways. The large airways (trachea and bronchi) have a significant amount of structural rigidity and are relatively large in diameter, depending mainly on transmural pressure gradients for their patency. In the normal lung resistance to airflow is equal throughout the pulmonary tree. In disease states, variances in the small resistances are a common cause of uneven distribution of ventilation.

Intrathoracic pressures

Elasticity is the property of matter that causes it to return to its resting state after being deformed by some external force. At the end of normal expiration there are chest wall elastic forces tending to expand the intrathoracic volume. Lung tissue elastic forces that tend to reduce intra thoracic volume balance these forces. The communication linking these two opposing forces is the pleura (its visceral layer is attached to the lung and its parietal layer is attached to the chest wall). The visceral and parietal layers are held together by a film of fluid in a similar manner to two glass microscope slides that are wet and stuck together. The slides readily move back and forth but resist being pulled apart. The pleural space is the potential space between the two layers of pleura, normally occupied by a small amount of fluid. The average resting intrapleural pressure is approximately 4 -5cm H20 less than atmospheric pressure. This subatmospheric pressure is a result of the opposing elastic forces of the thorax and the lung. The alveoli remain open at the end of expiration because of the distending pressure (the alveolar pressure is greater than the intra pleural pressures).