Airway resistance refers to degree of resistance to the flow of air through the respiratory tract during inspiration and expiration. The degree of resistance depends on many things, particularly the diameter of the airway and whether flow is laminar or turbulent. Alveolar expansion is also dependent on surfactant, so we will consider the physiology and importance of this substance.
In this article, we shall consider how these factors affect flow, and consider some clinical conditions in which airway resistance is affected.
Determinants of Airway Resistance
Certain equations can be used to determine airway resistance.
Ohm’s law usually refers to electrical circuits, in which current = voltage/resistance. However, it can be applied to describe the relationship between airflow, pressure gradient and resistance.
The equation is: Flow = Pressure gradient / Resistance
This demonstrates that as resistance increases, the pressure gradient must also increase to maintain the same airflow to the alveoli.
Poiseuille’s Law, also known as the Hagen-Poiseuille equation, gives us the relationship between airway resistance and the diameter of the airway. The equation is given below in Figure 1 (R = resistance, n = substance viscosity, l = length of tube and r= radius of tube).
In the context of the respiratory system, the components of this equation are very hard to measure accurately, and the law only applies when there is laminar flow. However, it shows that the airway resistance is inversely proportional to the radius (to the power of 4). Hence a small change in diameter has a huge effect on the resistance of an airway e.g. halving the radius of an airway would cause a 16-fold increase in resistance.
Therefore, smaller airways such as bronchioles and alveolar ducts all individually have much higher flow resistance than larger airways like the trachea. However, the branching of the airways means that there are many more of the smaller airways in parallel, reducing the total resistance to air flow. So due to the vast number of bronchioles that are present within the lungs running in parallel, the highest total resistance is actually in the trachea and larger bronchi.
Nervous System Control
Airway diameter is usually determined by the autonomic nervous system. Sympathetic innervation causes relaxation of bronchial smooth muscle via beta-2 receptors, which increases diameter to allow more airflow. This is useful in situations such as exercise, as sympathetic nerve stimulation triggers airway muscle relaxation, increasing the diameter to allow more air into the lungs. This increases the rate of gas exchange at alveolar level compared to normal breathing.
Parasympathetic innervation works on muscarinic (M3) receptors to increase smooth muscle contraction and reduce diameter, as when resting it is not necessary to have an increased airflow to the lungs.
Inspiration vs Expiration
Resistance differs between inspiration and expiration due changes in the diameter of the airways. On inspiration, the positive pressure within the alveoli and small airways causes their diameter to increase, and therefore resistance to decrease. The opposite is true for expiration, as airways narrow due to the reduced pressure, thus increasing resistance.
In forced expiration, the thoracic cavity further reduces in size compared to quiet expiration, leading to a greater degree of compression of the lungs. This leads to the small airways becoming narrowed to the extent that the resistance is sufficient to trap some air in the alveoli which cannot be expelled – this volume of air is known as the residual volume.
Turbulent vs Laminar Flow
Laminar flow refers to the state of flow in which air moves through a tube in parallel layers, with no disruption between the layers, and the central layers flowing with the greatest velocity.
Turbulent flow refers to when air is not flowing in parallel layers, and direction, velocity and pressure within the flow of air become chaotic. If airflow becomes turbulent, the pressure difference required to maintain airflow will need to be increased, which in turn would increase turbulence and therefore resistance.
This means that turbulence leads to a need for a much greater difference in pressure to move the air. In physiological terms this means the pressure difference between the outside air and within the lungs would need to be increased, so the intercostal muscles and diaphragm would need to work harder to expand and contract the lungs.
Surface Tension and Surfactant
Lungs contain large amounts of elastic tissue, so in the absence of water they would be very stretchy. However, the humidity of the airways means that the alveoli are lined by fluid. As a result, the elasticity of lung tissue is limited by surface tension.
Surface tension refers to the tendency of fluid to shrink to the smallest possible volume. Fluid lines the alveolar surface, thus resisting stretching of the alveoli. The higher the surface tension, the harder it is for the lungs to stretch. However, this effect is overcome by respiratory surfactant.
Surfactant is secreted by type II alveolar cells, and associates equally with air and water. By doing so, it helps to overcome surface tension and allows the alveoli to expand. It is essential to note that surfactant is most effective at low alveolar volumes when the surfactant molecules are closest together.
At higher alveolar volumes, surfactant molecules are further apart and become less effective at reducing surface tension. Therefore, further expansion of the alveoli is resisted. This explains why once the lungs are mostly filled, it is harder to expand the lungs further to allow the entry of additional air.
Clinical Relevance – Asthma
In an asthma exacerbation, the already narrowed airways (due to mucosal inflammation and smooth muscle hypertrophy) are further constricted due to increased smooth muscle tone.
This can decrease the diameter of the airways significantly, causing resistance to airflow to become very high. This means the patient must put much more effort into breathing to overcome the resistance experienced within the airways. This can lead to turbulent flow within the airways, causing the characteristic wheeze of an asthma attack.
In order to reverse the constriction, beta-receptor agonists such as salbutamol can be given. This acts on beta-2 receptors in the airway, acting on Gs G-proteins to open potassium channels. Allowing potassium channels to open hyperpolarises the cell, making contraction of the smooth muscle less likely and effectively causing bronchodilation.