12.3 Pulmonary Ventilation

Rhythmic contraction and relaxation of the respiratory muscles enable inspiration and expiration. In order to fully understand how these activities of the respiratory muscles lead to ventilation, it is essential to understand the relationship between the volume of an pressure of a gas at a constant temperature.

Pressure-Volume Relationships

When referring to a gas, pressure is a force created by the movement of gas molecules that are confined. Increasing the number of gas molecules in a confined space will increase the pressure. At a constant temperature, changing the volume occupied by the gas changes the pressure, as does changing the number of gas molecules. Consider Figure 12.3.1, which shows two containers of different volume, each containing 13 molecules of a gas. The force exerted by the movement of the gas molecules against the walls of the larger container on the left is lower than the force exerted by the gas molecules in the container on the right. Therefore, the pressure is lower in the larger container and higher in smaller container.

Boyle’s law describes the relationship between the volume and pressure of a gas in a confined space. Specifically, the Law states that for a given mass of a gas in a confined space at a constant temperature, the product of the pressure and volume is also constant (“k” in the equation in Figure 12.3.1). Boyle’s Law is expressed by the following formula:

P₁V₁ = P₂V₂

In this formula, P₁ represents the initial pressure and V₁ represents the initial volume, whereas the final pressure and volume are represented by P₂ and V_2, respectively. In short, pressure and volume are inversely related. 

Respiratory Pressures

Pulmonary ventilation is dependent on three pressures: atmospheric, intra-alveolar, and intrapleural. Atmospheric pressure is the amount of force that is exerted by gases in the air surrounding any given surface, such as the body. Atmospheric pressure can be expressed in terms of the unit atmosphere, abbreviated atm, or in millimeters of mercury (mm Hg). One atm is equal to 760 mm Hg, which is the atmospheric pressure at sea level. Typically, for ventilation, other pressure values are discussed in relation to atmospheric pressure. Therefore, negative pressure is pressure lower than the atmospheric pressure, whereas positive pressure is pressure that it is greater than the atmospheric pressure. A pressure that is equal to the atmospheric pressure is expressed as zero.

Intra-alveolar pressure is the pressure of the air within the alveoli, which changes during the different phases of breathing (Figure 12.3.2). Because the alveoli are connected to the atmosphere via the airways, intra-alveolar pressure always equalizes with atmospheric pressure.

Intrapleural pressure (P_ip) is the pressure within the fluid-filled pleural cavity. Similar to intra-alveolar pressure, intrapleural pressure also changes during the different phases of breathing. Although it fluctuates during inspiration and expiration, intrapleural pressure is always less than atmospheric pressure and intra-alveolar pressure. P_ip remains approximately –4 mm Hg throughout the breathing cycle. P_ip results from the surface tension between the visceral and parietal pleura and the parietal pleura’s adhesion to the body wall and diaphragm. Competing forces within the thorax cause the formation of the negative intrapleural pressure. One of these forces relates to the elasticity of the lungs themselves—elastic tissue pulls the lungs inward, away from the thoracic wall. Alveolar surface tension also creates an inward pull of the lung tissue. This inward tension from the lungs is countered by opposing forces from the pleural fluid and thoracic wall: surface tension within the pleural cavity pulls the lungs outward and the natural elasticity of the chest wall opposes the inward pull of the lungs. Ultimately, the outward pull is slightly greater than the inward pull, creating the –4 mm Hg intrapleural pressure relative to the intra-alveolar pressure.

Transpulmonary pressure is the difference between the intrapleural and intra-alveolar pressures. Transpulmonary pressure is always positive in a healthy respiratory system; this is essential in allowing the lungs to stay open.

In summary, two main forces keeping the lungs open are pleural fluid surface tension and positive transpulmonary pressure.

Respiratory Muscles and Pulmonary Ventilation

Recall that the main determinant of ventilation is a difference in air pressure between the atmosphere (atmospheric pressure, P_atm) and inside the alveoli (intra-alveolar pressure, P_alv). The regular contraction and relaxation of the respiratory muscles cause this air pressure difference; specifically, P_alv changes as the respiratory muscles contract and relax.

Inspiration: Normal, Quiet Breathing

 In general, two muscle groups are used during normal, quiet inspiration: the diaphragm and the external intercostal muscles. Inspiration is active: it involves muscle contraction. When the diaphragm contracts, it moves inferiorly toward the abdominal cavity, creating a larger thoracic cavity. At the same time, contraction of the external intercostal muscles moves the ribs upward and outward, causing the rib cage to expand, which increases the volume of the thoracic cavity. Due to the surface tension of the pleural fluid, the expansion of the thoracic cavity forces the lungs to stretch and expand as well. This increase in volume leads to a decrease in intra-alveolar pressure, creating a pressure lower than atmospheric pressure. As a result, a pressure gradient is created that drives air into the lungs.

Expiration: Normal, Quiet Breathing

The process of normal, quiet expiration is passive, meaning that energy is not required to push air out of the lungs. Instead, the elasticity of the lung tissue causes the lung to recoil, as the diaphragm and intercostal muscles relax following inspiration. In turn, the thoracic cavity and lungs decrease in volume, causing an increase in intra-alveolar pressure. The intra-alveolar pressure rises above atmospheric pressure, creating a pressure gradient that causes air to leave the lungs.

Inspiration and Expiration During Forced Breathing

During forced breathing, inspiration and expiration both occur due to muscle contractions. During periods of high ventilatory need (or drive), additional muscles can contribute to expansion of the rib cage during inspiration (Figure 12.3.4). These “accessory” muscles assist the external intercostals and include the sternocleidomastoids, the scalenes, and the pectoralis minor. All of these groups allow for a greater thoracic expansion and thus a greater lung volume. Recognizing that a patient is using these muscles to breathe is a useful clinical sign; use of these muscles during rest is highly indicative of a raised respiratory effort to cope with an underlying and probably significant problem.

During forced expiration, accessory muscles of the abdomen, including the obliques, contract, forcing abdominal organs upward against the diaphragm (Figure 12.3.5). This helps to push the diaphragm further into the thorax, pushing more air out. In addition, accessory muscles (primarily the internal intercostals) help to compress the rib cage, which also reduces the volume of the thoracic cavity.

Figure 12.3.8 – Transitional Flow

In reality, the vast majority of the airways are branching small tubes, so we see a mixture of the two above—mostly laminar flow but some turbulence generated at the branch (or transitional) points (Figure 12.3.8)

The following formula helps to describe the relationship between airway resistance and pressure changes or differences between two areas in the respiratory tract:

Where: F = gas flow; ∆P = pressure difference between atmosphere and alveoli; R = resistance

With diameter having such a powerful effect on airway resistance, we would expect that airway resistance would be a significant force to overcome during ventilation. However, in a person free of respiratory disease, airway resistance is insignificant. This is due to two main factors:

• In the first part of the conducting zone, airway diameters are huge relative to the low air viscosity.
• Although the airways get progressively smaller as we move through the bronchial tree, there are also progressively more airways; therefore despite the tiny diameters of bronchioles, there is an enormous number of them occurring in parallel which results in a large total cross-sectional area.

The greatest resistance to flow is actually in the medium-sized segmental bronchi (Figure 12.3.9).

There are a couple of clinically important points to make here:

1. If radius is reduced by disease, such as during inflammation of the airway wall or contraction of airway smooth muscle causing bronchoconstriction, then resistance is markedly increased, and to maintain flow, the pressure differential must be increased. Increasing this pressure differential means increasing the work of ventilation.
2. The vast total cross-sectional area of the lower airways means that a significant amount of damage can be done before symptoms arise. This “silent zone” means that a disease may be significantly established and be in a relatively late stage before the patient becomes symptomatic and goes to the physician.

Compliance

Compliance is the ability of the lungs to stretch, and therefore how easy they are to inflate. Compliance in healthy lungs is high. One factor that could make the lungs harder to inflate, i.e. less compliant, is the strong inward pull of the alveolar surface tension. However, recall that surfactant made by type II alveolar cells reduces the alveolar surface tension (see Section 12.1). In this way, surfactant production is one important factor keeping lungs compliant.

Compliance of the thoracic cavity is also important in facilitating proper ventilation. In order for inspiration to occur, the thoracic cavity must expand. The expansion of the thoracic cavity directly influences the capacity of the lungs to expand. If the tissues of the thoracic wall are not very compliant, more effort will be necessary to expand the thorax during breathing.

Respiratory Volumes and Capacities

In addition to the air that creates respiratory volumes, the respiratory system also contains anatomical dead space, which is air that is present in the airway that never reaches the alveoli and therefore never participates in gas exchange. The anatomical dead space totals about 150 mL (see Section 12.1.) Alveolar dead space involves air found within alveoli that are unable to function, such as those affected by disease or abnormal blood flow. Total dead space is the anatomical dead space and alveolar dead space together, and represents all of the air in the respiratory system that is not being used in the gas exchange process.

Pulmonary Function Tests

Spirometry is a method used to measure respiratory volumes and capacities. Spirometry alone cannot provide a specific diagnosis but it can help evaluate losses in respiratory function and can help a clinician distinguish between categories of respiratory diseases. In addition to being used to measure certain volumes and capacities, clinicians use spirometry to assess the rate at which air flows into and out of the lungs. For example, forced vital capacity (FVC) is the volume of air expired when a person takes a deep breath and then maximally exhales as quickly as possible. Forced expiratory volume (FEV) measures the amount of air forcefully expired during certain time intervals (e.g., FEV₁ is the volume of air expelled in one second).