Several physiologic factors are also important in determining airway resistance, in addition to the physical factors discussed earlier. Tissue resistance requires additional changes in Ppl to generate a given flow rate. The elastic behavior of the chest wall and the network of elastin and collagen in the lungs create a resistance to volume changes during ventilation. This resistance can be measured by getting a true measure of PA with a plethysmograph by independently solving Boyle's law for pressure instead of volume (as described in Chapter 18, Fig. 8). Tissue resistance is typically only 20% of pulmonary resistance, where pulmonary resistance is the term used to distinguish total resistance from airway resistance.
Lung volume is another important determinant of airway resistance. As lung volume increases from RV to TLC, airway resistance decreases nonlinearly from 4.0 to 0.5 (cm H2O sec)/L. Airway conductance is the inverse of airway resistance, and it increases linearly over the same volume range from near 0 to almost 2 L/(sec cm H2O). This decrease in resistance with increasing volume occurs because radial traction pulls the airways open as lung volume increases. The opposite occurs at low lung volumes, and small airways may even collapse, at the bottom of the lung.
Bronchial smooth muscle is also important in determining airway caliber and resistance. Smooth muscle in the airways is tonically active and is under the control of the autonomic nervous system, as described in Chapter 22. Histamine released from mast cells in the airways, or even reaching the lungs through the pulmonary circulation, causes powerful bronchoconstriction. Alveolar PCO2 also affects airway resistance. Decreased PCO2 causes bronchoconstriction by a direct effect on smooth muscle, and this tends to divert ventilation to other parts of the lung that are not receiving as much ventilation.
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