Air moves from areas of higher pressure to areas of lower pres sure just as fluids do. A pressure gradient needs to be established to move air.
Alveolar pressure becomes less than atmospheric pressure when the muscles of inspiration enlarge the chest cavity, thus lowering the intrathoracic pressure. In—trapleural pressure decreases, caus ing expansion of the alveoli and reduction of intra—alveolar pressure. The pressure gradient between the atmosphere and the alveoli drives air into the airways. The opposite occurs with expiration.
Air travels in the conducting airways via bulk flow (mL/min). Bulk flow may be turbulent or laminar, depending on its velocity. Velocity represents the speed of movement of a single particle in the bulk flow. At high velocities, the flow may be turbulent. At lower velocities transitional flow is likely to occur. At still lower velocities, flow may be laminar (streamlined). Reynold's number predicts the air flow. The higher the number, the more likely the air will be turbulent. The velocity of particle movement slows as air moves deeper into the lungs because of the enormous increase in cross—sectional area due to branching. Diffusion is the primary mechanism by which gas moves between terminal bronchioles and alveoli (the respiratory zone).
Airway resistance: The pressure difference necessary to produce gas flow is directly related to the resistance caused by friction at the airway walls. Medium—sized airways (> 2 mm diameter) are the major site of airway resistance. Small airways have a high individual resis tance. However, their total resistance is much less because resistances in parallel add as reciprocals.
Factors affecting airway resistance: Bronchocon—striction (increased resistance) can be caused by parasympathetic stimulation, histamine (immediate hyper—sensitivity reaction), slow—reacting substance of anaphyla—xis (SRS—A = leukotrienes C4, D4, E4; mediator of asthma), and irritants. Bronchodilation (decreased resistance) can be caused by sympathetic stimulation (via beta–2 receptors). Lung volume also affects airway resistance. High lung vol umes lower airway resistance because the surrounding lung parenchyma pulls airways open by radial traction. Low lung volumes lead to increased airway resistance because there is less traction on the airways. At very low lung vol umes, bronchioles may collapse. The viscosity or density of inspired gases can affect airway resistance. The density of gas increases with deep sea div ing, leading to increased resistance and work of breathing. Low—density gases like helium can lower airway resistance During a forced expiration, the airways are compressed by increased intrathoracic pressure. Regardless of how forceful the expiratory effort is, the flow rate plateaus and cannot be exceeded. Therefore, the air flow is effort—independent; the collapse of the airways is called dynamic compression. Whereas this phenomenon is seen only upon forced expira tion in normal subjects, this limited flow can be seen dur ing normal expiration in patients with lung diseases where there is increased resistance (e. g., asthma) or increased compliance (e. g., emphysema).
intrapleural – внутриплевральный
intra—alveolar – внутриальвеолярный
collapse – коллапс
viscosity – вязкость
density – плотность