Porth's Essentials of Pathophysiology, 4e
525
Control of Respiratory Function
C h a p t e r 2 1
another, and change their velocities. Whether turbulence develops depends on the radius of the airways, the inter- action of the gas molecules, and the velocity of airflow. It is most likely to occur when the radius of the airways is large and the velocity of flow is high. Turbulent flow occurs regularly in the trachea. Turbulence of airflow accounts for the respiratory sounds that are heard dur- ing chest auscultation (i.e., listening to chest sounds using a stethoscope). Airway Compression During Forced Expiration. Airway resistance does not change considerably during normal quiet breathing, but is significantly increased during forced expiration, such as occurs during vigor- ous exercise. The marked changes that occur during forced expiration are the result of airway compres- sion. Airflow through the collapsible airways in the lungs depends on the distending airway (intrapulmo- nary) pressures that hold the airways open and the external (intrathoracic) pressures that surround and compress the airways. The difference between these two pressures (airway minus intrathoracic pressure) is called the transpulmonary pressure. For airflow to occur, the distending pressure inside the airways must be greater than the compressing pressure outside the airways. During forced expiration, the transpulmonary pres- sure is decreased because of a disproportionate increase in the intrathoracic pressure compared with airway pressure. The resistance that air encounters as it moves out of the lungs causes a further drop in airway pres- sure. If this drop in airway pressure is sufficiently great, the surrounding intrathoracic pressure will compress the collapsible airways that lack cartilaginous support, causing airflow to be interrupted and air to be trapped in the terminal airways (Fig. 21-14).
Although this type of airway compression usually is seen only during forced expiration in persons with nor- mal respiratory function, it may occur during normal breathing in persons with lung diseases. For example, in conditions that increase airway resistance, such as asthma or chronic obstructive lung disease, the pres- sure drop along the smaller airways is magnified, and an increase in intra-airway pressure is needed to maintain airway patency. Measures such as pursed-lip breathing increase airway pressure and improve expiratory flow rates in persons with obstructive lung diseases (discussed in Chapter 23). This is also the rationale for using posi- tive end-expiratory pressure in persons who are being mechanically ventilated. Infants who are having trouble breathing often grunt to increase their expiratory air- way pressures and keep their airways open. Lung volumes, or the amount of air exchanged during ventilation, can be subdivided into three components: (1) the tidal volume, (2) the inspiratory reserve volume, and (3) the expiratory reserve volume. The tidal volume (TV), usually about 500 mL, is the amount of air that moves into and out of the lungs during a normal breath (Fig. 21-15). The inspiratory reserve volume (IRV) is the maximum amount of air that can be inspired in excess of the normal TV, and the expiratory reserve volume (ERV) is the maximum amount that can be exhaled in excess of the normal TV. Approximately 1200 mL of air remains in the lungs after forced expiration; this air is the residual volume (RV). The RV increases with age because there is more trapping of air in the lungs at the end of expiration. Lung Volumes and Pulmonary Function Studies
Oral airway pressure
Area of airway collapse
FIGURE 21-14. Mechanism that limits maximal expiratory flow rate. (A) Airway patency and airflow in the nonrigid airways of the lungs rely on a transpulmonary pressure gradient in which airway pressure is greater than intrapleural pressure. (B) Airway resistance normally produces a drop in airway pressure as air moves out of the lungs.The increased intrapleural pressure that occurs with forced expiration produces airway collapse in the nonrigid airways at the point where intrapleural pressure exceeds airway pressure.
Airway resistance
Forced expiration
Intrapleural pressure
Nonrigid airways
B
Airway pressure
A
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