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Airway Resistance

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Original Author(s): Will Woodward
Last updated: 27th October 2021
Revisions: 25

Original Author(s): Will Woodward
Last updated: 27th October 2021
Revisions: 25

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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 rate of into the alveoli.

Diameter

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). 

Fig 1 – The Hagen-Poiseuille equation

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. Therefore, 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, individually, the smaller airways have much higher resistance than larger airways like the trachea. However, the significant downstream branching of the airways means that there are many 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 causes an increase in airway diameter to allow more airflow. This is useful in situations such as exercise, when sympathetic stimulation triggers airway muscle relaxation to allow more air into the lungs.

Conversely, parasympathetic innervation works on muscarinic (M3) receptors to increase smooth muscle contraction and reduce diameter.

Inspiration vs Expiration

Boyle’s Law states that the pressure of a gas is inversely proportional to its volume. During inspiration, contraction of the diaphragm and external intercostal muscles causes the thoracic cavity to increase in volume. As the volume of the alveoli and bronchioles increases, intrapulmonary pressure is reduced. As external pressure now exceeds internal pressure, air enters the lungs down the pressure gradient.

With the increased volume, the intrathoracic pressure surrounding the smaller airways is also reduced, allowing the airways to expand. As the radius of the airways increases, resistance to airflow is lower during this inspiratory phase.

Conversely, in expiration, the intrathoracic pressure increases due to the lower volume of the thoracic cavity. This pressure leads to narrowing of the smaller airways, so resistance is higher during expiration. In healthy lung tissue, the elastic fibres of the surrounding alveoli pull on the walls of small airways to hold them open – this force is called radial traction.

The higher the elastic recoil of the lungs, the greater the radial traction will be. Radial traction helps to prevent airway collapse in expiration.

Fig 2 – Elastic recoil of surrounding alveoli holding open a bronchiole in expiration

In forced expiration, the intrathoracic pressure becomes so high that it causes some smaller airways to collapse. Collapsed airways have an exponentially high resistance, so air which cannot be expelled is trapped in the alveoli – this volume of air contributes to 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.

Fig 3 – Diagram comparing laminar and turbulent flow through vessels.

Surface Tension and Surfactant

Lungs contain large amounts of elastic tissue, so in the absence of water they would be very stretchy (compliant). However, the humidity of the airways means that the alveoli are lined by fluid. As a result, the compliance of lung tissue is limited by surface tension.

Surface tension refers to the tendency of fluid to shrink to the smallest possible volume. In water, surface tension is generated by hydrogen bonds pulling the molecules together. 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. It has a hydrophilic component which lies in the alveolar fluid, and a hydrophobic component which associates with the alveolar gas. This causes surfactant molecules to rise to the surface of the fluid (the gas/fluid interface). The surfactant molecules disrupt the hydrogen bonds between water molecules on the surface. 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.

Fig 4 – Surfactant molecules reducing surface tension

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 work harder to overcome the increased resistance. This can lead to turbulent flow, 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.

Clinical Relevance – Emphysema

In emphysema, there is destruction of elastin fibres within alveoli. Therefore, there is less elastic recoil holding open the smaller airways, and thus radial traction is reduced. This means that during expiration, when the intrathoracic pressure is greater, the smaller airways collapse very easily, trapping an increased volume of air.

The airway obstruction is compounded in Chronic Obstructive Pulmonary Disease (COPD) by the additional narrowing of airway lumens by chronic bronchitis. People with COPD often exhale through pursed lips in an effort to keep their intrapulmonary pressure high and prevent premature collapse of the small airways.

 

 

 

 

 

 

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