Pulmonary ventilation is commonly referred to as breathing. It is the process of air flowing into the lungs during inspiration (inhalation) and out of the lungs during expiration (exhalation). Air flows because of pressure differences between the atmosphere and the gases inside the lungs.
Pulmonary Ventilation Pressure Relationships
Inspiration (or inhalation) and expiration (or exhalation) are dependent on the differences in pressure between the atmosphere and the lungs. In a gas, pressure is a force created by the movement of gas molecules that are confined. For example, a certain number of gas molecules in a two-liter container has more room than the same number of gas molecules in a one-liter container. In this case, the force exerted by the movement of the gas molecules against the walls of the two-liter container is lower than the force exerted by the gas molecules in the one-liter container. Therefore, the pressure is lower in the two-liter container and higher in the one-liter container. At a constant temperature, changing the volume occupied by the gas changes the pressure, as does changing the number of gas molecules. Boyle’s law describes the relationship between volume and pressure in a gas at a constant temperature. Boyle discovered that the pressure of a gas is inversely proportional to its volume: If volume increases, pressure decreases. Likewise, if volume decreases, pressure increases. Pressure and volume are inversely related (P = k/V). Therefore, the pressure in the one-liter container (one-half the volume of the two-liter container) would be twice the pressure in the two-liter container. Boyle’s law is expressed by the following formula:
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 V2, respectively. If the two- and one-liter containers were connected by a tube and the volume of one of the containers were changed, then the gases would move from higher pressure (lower volume) to lower pressure (higher volume).
Pulmonary ventilation is dependent on three types of pressure: 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 respiration, other pressure values are discussed in relation to atmospheric pressure. Therefore, negative pressure is pressure lower than the atmospheric pressure, whereas positive pressure is the 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 (intrapulmonary pressure) is the pressure of the air within the alveoli, which changes during the different phases of breathing. Because the alveoli are connected to the atmosphere via the tubing of the airways (similar to the two- and one-liter containers in the example above), the intrapulmonary pressure of the alveoli always equalizes with the atmospheric pressure.
Intrapleural pressure is the pressure of the air within the pleural cavity, between the visceral and parietal pleurae. Similar to intra-alveolar pressure, intrapleural pressure also changes during the different phases of breathing. However, due to certain characteristics of the lungs, the intrapleural pressure is always lower than, or negative to, the intra-alveolar pressure (and therefore also to atmospheric pressure). Although it fluctuates during inspiration and expiration, intrapleural pressure remains approximately –4 mm Hg throughout the breathing cycle.
Competing forces within the thorax cause the formation of 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. The surface tension of the alveolar fluid, which is mostly water, 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. Too much or too little pleural fluid would hinder the creation of the negative intrapleural pressure; therefore, the level must be closely monitored by the mesothelial cells and drained by the lymphatic system. Since the parietal pleura is attached to the thoracic wall, 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, and it determines the size of the lungs. A higher transpulmonary pressure corresponds to a larger lung.
Factors Affecting Pulmonary Ventilation: Surface Tension of Alveolar Fluid
The surface tension of alveolar fluid is regulated by pulmonary surfactant, allowing efficient respiration.
Key Points
Type II avleolar epithelial cells secrete pulmonary surfactant to lower the surface tension of water, which helps prevent airway collapse.
Reinflation of the alveoli following exhalation is made easier by pulmonary surfactant.
The surfactant reduces surface tension within all alveoli through hydrophilic and hydrophobic forces.
Insufficient pulmonary surfactant in the alveoli can contribute to atelectasis (collapse of part or all of the lung ).
Premature infants often don’t have the capacity to produce enough surfactant to survive on their own.
Key Terms
- atelectasis: The collapse of a part of or the whole lung caused by inner factors, rather than a pneumothorax.
- surfactant: A lipoprotein in the tissues of the lung that reduces surface tension and permits more efficient gas transport.
- Surface tension: The inward force created by films of molecules that can reduce the area of a surface.
EXAMPLES
Elective cesarean sections are becoming more common. One unfortunate consequence of this is that many of the infants delivered by this method are actually slightly physiologically premature. They lack sufficient surfactant to initiate proper breathing, and therefore, go into respiratory distress.
The alveoli are highly elastic structures in the parenchyma of the lungs that are the functional site of gas exchange. As the alveoli fill with air during inhalation they expand, and as air leaves the lung with exhalation, the alvoli return to their non-inflated size. The reason for the elasticity of the alveoli is a protein found in the extracellular matrix of the alveoli, called elastin, as well as the surface tension of water molecules on the alveoli themselves.
Surface Tension in the Lung
Surface tension is the force exerted by water molecules on the surface of the lung tissue as those water molecules pull together. Water (H2O) is a highly polar molecule, so it forms strong covalent bonds with other water molecules. The force of these covalent bonds effectively creates an inward force on surfaces, such as lung tissue, with the effect of lowering the surface area of that surface as the tissue is pulled together. As the air inside the lungs is moist, there is considerable surface tension within the tissue of the lungs. Because the alveoli of the lungs are highly elastic, they do not resist surface tension on their own, which allows the force of that surface tension to deflate the alveoli as air is forced out during exhalation by the contraction of the pleural cavity.
Pulmonary Surfactant
The force of surface tension in the lungs is so great that without something to reduce the surface tension, the airways would collapse after exhalation, making re-inflation during inhalation much more difficult and less effective. The collapse of the lungs is called atelectasis. Fortunately, the type II epithelial cells of the alveoli continually secrete a molecule called surfactant that solves this problem.
A surfactant is a lipoprotein molecule that reduces the force of surface tension from water molecules on the lung tissue. The main reason that surfactant has this function is due to a lipid called dipalmitoylphosphatidylcholine (DPPC) which contains hydrophilic and hydrophobic ends. The hydrophilic ends are water-soluble and attach to the water molecules on the surface of the lungs. The hydrophilic ends are water-insoluble and face towards the air and pull away from the water. The net result is that the surface tension of the lungs from water is reduced so that the lungs can still inflate and deflate properly without the possibility of collapse from surface tension alone.
As unborn humans grow and develop in the womb, they receive oxygen from the mother, so their lungs aren’t fully functional right away. Of particular importance is the fact that they don’t produce surfactants until 24 weeks of development and usually don’t have enough built-up to prevent lung collapse until 35 weeks of development. Therefore prematurely born infants are at a high risk of respiratory distress syndrome from airway collapse, which can cause death if untreated. It is treated through pulmonary surfactant replacement therapy and mechanical ventilator treatment until the infant’s lungs are old enough to secrete enough surfactant to survive on their own. Other diseases may cause atelectasis, such as COPD, or any sort of lung trauma and inflammation that involves extensive damage to the pleural cavity or the lung parenchyma.
Diagram of an Alveoli: An alveoli with both cross-section and external views
Factors Affecting Pulmonary Ventilation: Compliance of the Lungs
Lung compliance refers to the magnitude of change in lung volume as a result of the change in pulmonary pressure.
Key Points
Low lung compliance would mean that the lungs would need a greater-than-average change in intrapleural pressure to change the volume of the lungs.
High lung compliance would indicate that little pressure difference in intrapleural pressure is needed to change the volume of the lungs.
Persons with low lung compliance due to obstructive lung diseases tend to take rapid shallow breaths and sit hunched over to make exhalation less difficult.
Persons with high lung compliance due to restrictive lung diseases tend to have difficulty expanding and deflating the lungs.
Two factors determine lung compliance: elasticity of the lung tissue and surface tensions at air-water interfaces.
Two factors determine lung compliance – elasticity of the lung tissue and surface tensions at air-water interfaces.
Key Terms
- Lung compliance: The ability of the lungs and pleural cavity to change in volume based on changes in pressure.
EXAMPLES
Low lung compliance can be the result of interstitial lung diseases resulting from the inhalation of particulate substances such as asbestos (asbestosis) and silicon (silicosis).
Compliance is the ability of the lungs and pleural cavity to expand and contract based on changes in pressure. Lung compliance is defined as the volume change per unit of pressure change across the lung and is an important indicator of lung health and function. Measurements of lung volumes differ at the same pressure between inhalation and exhalation, meaning that lung compliance differs between inhalation and exhalation. Lung compliance can either be measured as static or dynamic based on whether only volume and pressure (static) are measured or if their changes over time are measured as well (dynamic).
Compliance and Elastic Recoil of the Lung
Compliance depends on the elasticity and surface tension of the lungs. Compliance is inversely related to the elastic recoil of the lungs, so thickening of lung tissue will decrease lung compliance. The lungs must also be able to overcome the force of surface tension from water on lung tissue during inflation in order to be compliant, and greater surface tension causes lower lung compliance. Therefore, surfactant secreted by type II epithelial cells increases lung compliance by reducing the force of surface tension.
A low lung compliance means that the lungs are “stiff” and have a higher than normal level of elastic recoil. A stiff lung would need a greater-than-average change in pleural pressure to change the volume of the lungs, and breathing becomes more difficult as a result. Low lung compliance is commonly seen in people with restrictive lung diseases, such as pulmonary fibrosis, in which scar tissue deposits in the lung making it much more difficult for the lungs to expand and deflate, and gas exchange is impaired. Pulmonary fibrosis is caused by many different types of inhalation exposures, such as silica dust.
Pulmonary Fibrosis: Pulmonary fibrosis stiffens the lungs through deposits of scar tissue, decreasing low compliance and making it more difficult for the lungs to inflate and deflate.
A high lung compliance means that the lungs are too pliable and have a lower than normal level of elastic recoil. This indicates that little pressure difference in pleural pressure is needed to change the volume of the lungs. Exhalation of air also becomes much more difficult because the loss of elastic recoil reduces the passive ability of the lungs to deflate during exhalation. High lung compliance is commonly seen in those with obstructive diseases, such of emphysema, in which destruction of the elastic tissue of the lungs from cigarette smoke exposure causes a loss of elastic recoil of the lung. Those with emphysema have considerable difficulty with exhaling breaths and tend to take fast shallow breaths and tend to sit in a hunched-over position in order to make exhalation easier.
Factors Affecting Pulmonary Ventilation: Airway Resistance
Airway resistance refers to resistance in the respiratory tract to airflow.
Key Points
Airway resistance is a concept in respiratory physiology that describes the resistance of the respiratory tract to airflow during inspiration and expiration.
Airway resistance can be indirectly measured with body plethysmography.
A two-fold change in the radius/diameter of an airway causes a 16-fold change in air resistance in the opposite direction (an inverse relationship).
Diseases affecting the respiratory tract can increase airway resistance.
Laminar flow is orderly and has low resistance while turbulent flow is disorganized and has high resistance.
Key Terms
- Airway resistance: Airway Resistance is a concept in respiratory physiology that describes the resistance of the respiratory tract to airflow during inspiration and expiration.
- plethysmography: The diagnostic use of a plethysmograph to measure changes in volume within an organ or whole body.
- Turbulent flow: Air with disorganized layers that have higher resistance. It is often located in areas where the airways branch or diverge.
EXAMPLES
Airway resistance can change over time, especially during an asthma attack when the airways constrict causing an increase in airway resistance.
Airway Resistance
Airway resistance is the resistance to the flow of air caused by friction with the airways, which includes the conducting zone for air, such as the trachea, bronchi, and bronchioles. The main determinants of airway resistance are the size of the airway and the properties of the flow of air itself.
Size of the Airway
Resistance in an airway is inversely proportional to the radius of the airway. However, the ratio for this relationship is not 1:1. Below is the equation for calculating airway resistance (R).
- R=8(Length×Gas Viscosity)(πr4)
The most important part of this formula is the radius of the airway (r). A common example is that if one were to double the diameter of an airway (thus doubling the radius as well) the resistance of the airway would drop by a factor of 16. This mathematical property between radius and resistance is consistent for all tubes and is often applied to the blood vessels in the cardiovascular system.
The radius of the airways of the conducting zone becomes smaller as air goes deeper into the lungs. Therefore the resistance to air in the bronchi is greater than the resistance to air in the trachea. The number of airways also plays a large role in the resistance to air, with more airways reducing resistance because there are more paths for the air to flow into. Therefore, despite the fact that the terminal bronchioles are the smallest airway in terms of radius, their high number compared to the larger airways means that the bronchi actually have greater resistance because there are fewer of them compared to the terminal bronchioles. Another important fact is that airway resistance is inversely related to lung volumes because the airways expand a bit as they inflate, so the airways in a fully inflated lung will have lower resistance than a lung after exhalation.
Airway resistance can be indirectly measured with body plethysmography, which is an instrument used for measuring changes in volume within a structure, such as the airways. The resistance of the airways is an important indicator of lung health and function and can be used to diagnose lung diseases.
The size of the airways, and thus the resistance can change based on the health and conditions of the lungs. Most lung diseases increase airway resistance in many different ways. For example, in asthma attacks the bronchioles spasm and constrict, which increases resistance. Emphysema also increases airway resistance because the lung tissue becomes too pliable and it the airways become more difficult to hold open by the flow of air.
Flow of Air
The air that flows through the lungs varies considerably in the properties of the flow of air. The airflow can either be turbulent, transitional, or laminar based on the airway. Laminar flow involves an orderly and concentric distribution of layers of air particles and tends to occur in smaller airways, and has lower resistance. Turbulent flow is the disorganized distribution of the layers of air and tends to occur in larger airways and places where the airways branch, and has a higher resistance. Transitional flow occurs in places that branch within smaller airways, in which the airflow becomes in between laminar and turbulent flow and has moderate resistance. The relationship between resistance and type of airflow is difficult to measure and apply, but some mathematical models (such as Reynold’s number) can provide a rough estimate.
Laminar and Turbulent Flow: Laminar flow (a) has orderly layers and low resistance. Turbulent flow (b) has disorganized layers and high resistance.