Mechanics of Ventilation

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Mechanics of Ventilation

The Lung-Thorax System

As described in Chapter 4, the lung and the thorax are lined by thin connective tissues sheets: the parietal pleura on the inside of the thoracic cage and the visceral pleura on the outside of the lung and mediastinum.

These two pleurae are in contact with each other, separated by only a thin film of fluid.

Because the lungs have a tendency to contract inward and the thorax expands outward during normal breathing, a negative (subatmospheric) pressure is maintained between the pleurae (Figure 5-1).

A convenient way of viewing the lung-thorax system is to consider it a two-spring system held together by the pleura (Figure 5-2). The thorax can be conceptualized as a band spring tending to expand outward, and the lung can be described as a coil spring tending to contract inward.

If the sternum is split and the pleura separated but not opened, the lung and thorax move to their independent resting positions (see Figure 5-1).

If air is allowed to enter the potential pleural space, a pneumothorax develops.

Any interference with the integrity of the pleura can interfere with ventilation.

II Pulmonary Pressures and Gradients

Six pressures are frequently referred to when discussing ventilation:

When the mechanics of breathing are discussed, four pressure gradients are commonly defined (Figure 5-3):

1. Transpulmonary pressure (Pl): The pressure difference across the lung (alveolar-pleural pressure, Pl = Palv − Ppl).

2. Transthoracic pressure (PW): The pressure difference across the thorax (pleural-body surface pressure, Pw = Ppl − Pbs).

3. Transrespiratory pressure (Prs): The pressure difference across the lung-thorax system; also referred to as the transairway pressure (alveolar-body surface pressure, Prs = Palv − Pbs).

4. Transdiaphragmatic pressure (Pdi): The pressure difference across the diaphragm (abdominal-pleural pressure, Pdi = Pab − Ppl).

III Inspiration

Figures 5-4 and 5-5 depict the intrapleural (intrathoracic) and intrapulmonary pressure curves during normal resting ventilation.

At functional residual capacity (FRC) level or resting exhalation, the intrapleural pressure is approximately −5 cm H2O, whereas the intrapulmonary pressure is zero (atmospheric; Figure 5-6).

Because the lung is a valveless pump, when gas flow stops and the glottis is open, intrapulmonary and atmospheric pressures are equal (i.e., the transrespiratory pressure gradient is zero).

Pressure gradients causing inspiration are established by contraction of the diaphragm, intercostals, and scalene muscles.

With inspiratory muscle contraction, the thoracic cavity expands, causing the intrapleural pressure to become more negative (approximately −9 cm H2O).

This pressure decrease increases the volume of the lung. Because of the relationship of the two pleura, the lungs must expand as the thorax expands.

The expansion of the lung decreases the intrapulmonary pressure to approximately −3 cm H2O.

The decreased intrapulmonary pressure establishes a pressure gradient with atmosphere, causing gas to enter the lung.

Once the intrapulmonary pressure is returned to normal by gas entering the lung, inspiration stops.

Boyle’s law explains all of the pressure-volume changes described in breathing.

IV Exhalation

Resistance to Ventilation

Ventilation is opposed by three major factors:

Elastic resistance is a result of distortion of pulmonary elastic tissue. Elastic resistance is established based on:

Nonelastic resistance is primarily the resistance to gas flow. It is equivalent to the frictional resistance of solids moving across each other. Overall nonelastic resistance is the combined effect of:

Inertia is the tendency of a body in motion to stay in motion and a body at rest to stay at rest.

VI Surface Tension

Surface tension is the force occurring at the interface between a liquid and another liquid or a gas that tends to cause the liquid to occupy the smallest volume possible (see Chapter 2).

Surface tension causes alveoli to decrease in size and would cause collapse were it not for the presence of a pulmonary surfactant secreted by type II alveolar cells.

The volume of surfactant produced by the respiratory tract is relatively constant. As a result, the effect the surfactant exerts is indirectly related to the surface area it covers.

At FRC there is a large amount of surfactant applied per unit area. This causes a significant reduction in pressure as a result of surface tension, with the following results:

At maximum inspiration, a small volume of surfactant is applied per unit area. Thus, the pressure as a result of surface tension tending to collapse the alveoli is great. This pressure assists in normal passive exhalation.

Pressures as a result of surface tension:

As a result the pressure-volume relationship of the lung is different during inspiration and expiration; a hysteresis exists (Figure 5-7). Greater volume is maintained in the lung for a given pressure during exhalation than during inspiration.

If the lung is filled with saline instead of air, much less pressure is needed to expand it with saline because the effect of surface tension is eliminated and the hysteresis disappears (see Figure 5-7).

The effect of surface tension cannot be evaluated directly. Changes in surface tension cause a change in compliance or elastance of the lung.

An increase in surface tension increases elastic resistance to ventilation and is reflected in a decrease in compliance, causing an increase in the work of breathing.

VII Compliance

Compliance is the ease of distention of the lung-thorax system and is inversely related to elastance (see Chapter 2).

Compliance is normally a static measurement so as to eliminate the effects of nonelastic resistance.

Compliance is determined by comparing the change in volume in a system with the pressure necessary to maintain the volume change:

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In the respiratory system, there are basically three types of compliance (Figure 5-8):

In the lung-thorax system, the tendency of the lung is to collapse to its resting position, and the tendency of the thorax is to expand to its resting position.

The FRC is that volume maintained in the lung at the resting expiratory position as a result of the equal and opposing effects of pulmonary (lung) and thoracic (chest wall) compliance.

Total compliance of the lung-thorax system is a result of the interaction of pulmonary and thoracic compliance (see Figure 5-8).

Compliance is linear only at relatively normal tidal volumes. As the lung volume exceeds or falls below tidal levels, compliance decreases. Thus, the total compliance curve is significantly distorted as lung volume approaches residual volume (RV) or total lung capacity (TLC; see Figure 5-8).

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