The Mechanics of Breathing (Physiology)

Airway resistance is the opposition encountered by airflow as it moves through the airways.

Increased airway resistance leads to decreased airflow, while decreased resistance leads to increased airflow.

The level of airway resistance is determined by factors such as the diameter of the airways, the length of the airways, the viscosity of the air, and the density of the air.

When the pressure gradient increases, airflow increases.

Increased resistance leads to decreased airflow.

As resistance increases, airflow decreases.

The decrease in airflow due to increased resistance can be somewhat overcome by increasing the pressure difference between the two ends of the conduit.

The effort or force required to increase the pressure difference may not be able to be generated, or the airway might be completely obstructed, leading to limitations in overcoming increased resistance.

The level of airway resistance is determined by factors such as the diameter of the airways, the length of the airways, the viscosity of the air, and the density of the air.

The major variable factors within the airways are the cross-sectional area of the airway lumen and the airflow pattern.

The Hagen-Poiseuille equation describes the relationship between resistance and various properties of airways and airflow.

The Hagen-Poiseuille equation demonstrates that the resistance of a gas flowing through a pipe is inversely proportional to the cross-sectional radius raised to the power 4.

A relatively small decrease in radius results in a large increase in resistance and a dramatic decrease in airflow. For example, if the airway radius is halved, airway resistance increases by a factor of 16, accompanied by a resulting proportional decrease in airflow.

Contraction of airway smooth muscle, excessive mucus secretion, edema/swelling of the airway tissue, and damage to the integrity of the airway structure (loss of patency) all reduce the size of the airway lumen.

These pathological features increase airway resistance and decrease airflow by reducing the cross-sectional area of the airway lumen.

The pattern of airflow can increase airway resistance, particularly when airflow changes from a linear to a turbulent pattern.

Turbulence occurs when high velocities of airflow are achieved, such as during forced breathing maneuvers, or if there is a sudden decrease in luminal area, such as in obstructed airways.

The vibration generated by turbulent airflow is responsible for the wheezing sound produced in patients with obstructed airways.

Airway patency refers to the state of being open or unobstructed. A loss of patency results in closing or obstruction of the airways.

The open structure of the airways is maintained by elastic fibers within the airway wall and radial traction, which is the pulling force exerted on the airways by the surrounding lung tissue.

During inspiration, as the lungs expand, the lung tissue and airways contained within are stretched open.

Airway obstruction is often more noticeable during expiration because during expiration, the lung tissue and airways are compressed.

Positive intrapleural pressure during forced expirations can exert a collapsing force onto the airways, potentially reducing airway patency.

Lung compliance refers to how much force is required to expand the lungs.

Transpulmonary pressure, calculated as the difference between alveolar pressure and intrapleural pressure, determines the level of force acting to expand (if positive) or compress (if negative) the lungs.

Lung compliance describes how easily the lungs can be distended or expanded in response to changes in transpulmonary pressure.

Lung compliance describes the relationship between the change in lung volume and the change in transpulmonary pressure. Higher lung compliance means that less expansive force is required to inflate the lungs, resulting in a greater volume change per transpulmonary pressure change. Lower lung compliance means that more expansive force is required to inflate the lungs, resulting in a smaller volume change per transpulmonary pressure change.

Lung compliance can be affected by changes in the structure of lung tissue, particularly the density of elastic and structural fibers such as elastin and collagen.

Lung compliance is represented by the gradient or slope of volume-pressure curves. Higher lung compliance is indicated by a greater (steeper) gradient, while lower lung compliance is indicated by a lower (shallower/less steep) gradient.

Lung compliance is represented by the gradient or slope of the curve on a graph of lung volume vs. transpulmonary pressure.

Static compliance is measured when airflow is zero, and the steepest part of the curve is used for measurement.

Dynamic compliance is measured in the presence of airflow, and the gradient between the end tidal inspiratory and end tidal expiratory points is used for measurement.

The internal surfaces of alveoli are lined with fluid.

Surface tension within alveoli arises from the relative strength of hydrogen bonds between water molecules, exerting an overall collapsing force toward the centre of the alveolar bubble.

Pressure is generated within alveoli due to the collapsing force produced at the water-fluid interface.

The Law of Laplace describes the relationship between collapsing pressure, the radius of the bubble, and surface tension.

Pressure and bubble radius are inversely proportional, meaning that pressure increases as radius decreases. Smaller bubbles generate greater pressure than larger ones.

When bubbles of varying size are connected, such as different-sized alveoli connected by airways, the smaller bubble will empty into the larger ones due to the pressure gradient.

Pulmonary surfactant, secreted by type II pneumocytes (alveolar cells), reduces surface tension at the air-liquid interface in the alveoli. This reduces the collapsing pressure generated, preventing smaller alveoli from collapsing into larger ones.

Surfactant molecules are amphipathic, possessing hydrophilic head and hydrophobic tail regions, allowing them to naturally position themselves at the air-liquid interface.

Surfactant disrupts the attractive forces between water molecules, thereby reducing surface tension.

Pulmonary surfactant reduces surface tension at the air-liquid interface, which equalizes pressure between alveoli of varying sizes. During inflation, as alveolar size increases, the concentration of surfactant molecules at the interface decreases. This results in an increase in surface tension and pressure with increasing alveolar surface area.

With the presence of surfactant, air naturally flows from larger, more inflated alveoli to smaller ones, helping to distribute air across the lung during inspiration.

Surface tension at the air-liquid interface reduces hydrostatic pressure in the alveolar tissue. This pressure reduction pulls fluid out of the surrounding pulmonary capillaries and into the alveoli and interstitial tissue.

Pulmonary surfactant reduces surface tension, which helps prevent alveolar edema by reducing the excessive fluid pulled from capillaries into the alveoli and interstitial tissue.

Patients with insufficient levels of pulmonary surfactant may experience pathology related to alveolar oedema due to the inability to adequately reduce surface tension.

Neonatal Respiratory Distress Syndrome is a condition that occurs in infants born prematurely who produce insufficient levels of pulmonary surfactant. This deficiency leads to respiratory failure due to alveolar collapse, decreased lung compliance, and increased risk of alveolar oedema.

Insufficient pulmonary surfactant production in NRDS results in decreased lung compliance, making the lungs stiffer and more prone to collapse during inspiration. It also increases the likelihood of alveolar oedema, reducing the rate of gas exchange. Additionally, increased forces and pressures within the lungs can potentially damage alveoli and capillaries, further impairing respiratory function.

NRDS is treated by supplementing affected infants with artificial surfactant and/or administering glucocorticoids to mothers at high risk of premature birth. Glucocorticoids increase surfactant production by maturing type 2 pneumocytes.