30. Ventilation

Total ventilation (VT, minute ventilation) is the total gas flow into the lungs per minute. It is equal to the tidal volume (VT) x the respiratory rate (n). Total ventilation is the sum of dead space ventilation and alveolar ventilation.

Anatomic dead space is equivalent to the volume of the conducting airways (150 mL in normal individuals), i. e., the trachea and bronchi up to and including the terminal bronchioles. Gas exchange does not occur here. Physiologic dead space is the volume of the respiratory tract that does not participate in gas exchange. It includes the anatomic dead space and partially functional or nonfunctional alveoli (e. g., because of a pulmonan embolus preventing blood supply to a region of alveoli). In normal individuals, anatomic and physiologic dead space are approximately equal. Physiologic dead space can greatly exceed anatomic dead space in individuals with lung disease.

Dead space ventilation is the gas flow into dead space per minute. Alveolar ventilation is the gas flow entering functional alveoli per minute.

Alveolar ventilation: It is the single most important parameter of lung function. It cannot be measured directly. It must be adequate for removal of the CO₂ produced by tissue metabolism whereas the partial pressure of inspired O₂ is 150 mmHg, the partial pressure of O₂ in the alveoli is typically 100 mmHg because of the displacement of O₂ with CO₂. PAo2 cannot be measured directly.

total – общее количество

ventilation – вентиляция

flow – поток

per minute – в минуту

equal – равный

airways – воздушные пути

exchange – обмен

tract – трактат

to be measured – быть измеренным

directly – непосредственно

displacement – смещение

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. Intrapleural pressure decreases, causing 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 resistance. 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 anaphylaxis (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 volumes 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 volumes, bronchioles may collapse. The viscosity or density of inspired gases can affect airway resistance. The density of gas increases with deep sea diving, 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 expiration in normal subjects, this limited flow can be seen during 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