Respiratory Physiology II (Mechanics of Breathing) Notes

Respiratory Physiology II (Mechanics of Breathing)

Learning Objectives

• Outline the relationships between the lungs, pleura, and chest wall.
• Define intrapleural pressure.
• Describe how intrapleural pressure changes during normal breathing and pneumothorax.
• Explain the balance between the elastic properties of the lung and chest wall.
• Draw the pressure-volume curve for the lung and state how it measures compliance.
• State the role of surface tension (and surfactant) in lung compliance.
• Understand the principles of airway resistance, the main sites of airway resistance, and factors that affect it.
• Describe what determines the work of breathing.

Pulmonary Ventilation (Breathing)

• The process of air flowing into the lungs during inspiration (inhalation) and out of the lungs during expiration (exhalation).
• Air flows due to pressure differences between the atmosphere and the gases inside the lungs.
• Air flows from a region of higher pressure to a region of lower pressure.
• Muscular breathing movements and recoil of elastic tissues create the pressure changes that result in ventilation.

Airflow into the Lungs

• Movement of air (in and out of the lungs) is due to pressure differences.
• Pressure at the beginning of the respiratory tract is atmospheric pressure (P_{atm}).
• Pressure inside the lungs is alveolar pressure (P_A).
• If P{atm} = PA, there is no airflow.
• If PA < P{atm}, air flows into the lungs.
• If PA > P{atm}, air flows out of the lungs.

Boyle's Law

• Boyle's Law: If the volume of a gas increases, the pressure exerted by the gas decreases.
• As alveoli expand, the pressure inside them decreases, and gas flows in from the conducting airways.
• Pressure differences are created by changes in thoracic volume.

Elastic Properties of the Lung

• Lungs are elastic and return to their original shape if a distorting force is removed.
• Elastic recoil produces a recoil pressure when air is prevented from escaping an inflated lung (balloon model).
• Lungs are inflated by reducing pressure outside, similar to a plunger in a syringe.

Elastic Properties of the Chest Wall

• The thoracic cage is also elastic.
• Under normal conditions, the chest wall tends to pull outwards, and the lungs tend to pull inwards, thus balancing each other.

Intrapleural Pressure (P_{pl})

• The lungs and chest wall are "locked together" by the intrapleural fluid in the intrapleural space.
• The intrapleural fluid functions as a lubricant, allowing the pleura to glide smoothly during exhalation and inhalation.
• At the end of expiration (complete relaxation), there is tension between the collapsing lungs and the outward-springing chest wall.
• This tension generates a pressure in the intrapleural space known as the intrapleural pressure (P_{pl}).
• Intrapleural pressure is usually negative with respect to atmospheric pressure and alveolar air pressure.

Changes in Intrapulmonary and Intrapleural Pressure

• Intrapulmonary pressure:
  • Pressure inside the lung decreases as lung volume increases during inspiration and increases during expiration.
• Intrapleural pressure:
  • Pleural cavity pressure becomes more negative as the chest wall expands during inspiration and returns to its initial value as the chest wall recoils.
• During each breath, pressure gradients move 0.5 liters of air into and out of the lungs.

Pneumothorax

• If the pleural cavity is damaged/ruptured, air enters the pleural space.
• The intrapleural pressure becomes equal to or exceeds atmospheric pressure, increasing pressure around the lungs, which may cause them to collapse.
• This condition is known as pneumothorax.

Lung Compliance (C_L)

• Lungs are elastic structures that return to their original shape and size when distorting forces are removed.
• Elasticity, measured as compliance, indicates how easily the lungs can be stretched.
• Compliance is the ease at which the lungs expand under pressure.
• Most lung diseases change lung compliance.
• Compliance is defined as the change in volume produced by a change in pressure: Compliance = "Change in volume" / "Change in pressure"
• This can be measured across the walls of the lungs (CL), chest wall (CW), or both (total compliance, C_{TOT}).

Measuring the Pressure-Volume Curve of the Lung

• Excised animal lung is cannulated and placed within a jar.
• Volume is measured using a spirometer.
• Pressure inside the jar is changed using a pump.
• The slope/gradient of the pressure-volume curve represents compliance (\Delta V / \Delta P).
• In the normal range, the lung is very compliant, but at high expanding pressures, it becomes stiffer and compliance decreases.
• Curves during inflation and deflation are different; at any given pressure, lung volume during inhalation is less than during exhalation.
• Even without expanding pressure, the lung always has some air due to airway closure, where small airways trap gas in alveoli. This increases with age and lung disease.

Diseases Affecting Compliance

• Diseases that affect either the chest wall or lung structure will affect compliance.

Reduced Compliance:

• Increase of fibrous tissue in the lung (pulmonary fibrosis).
• Collapse/closure of the lung (atelectasis).
• Increase in pulmonary venous pressure.

Increased Compliance:

• Age.
• Emphysema.

Effect of Disease on Lung Compliance: Emphysema

• In emphysema, there is destruction of the normal lung architecture, including elastic fibers and collagen.
• Impaired elastic recoil means lungs do not deflate easily.
• The lung is more easily distended, and compliance is increased.

Effect of Disease on Lung Compliance

• Normal: C = V/P = \Delta V / \Delta P
• Emphysema: Same amount of pressure results in it being easier to inflate.
• Fibrosis: Same amount of pressure results in it being harder to inflate.

Effect of Disease on Compliance of Chest Wall

• Structural changes in the thorax (e.g., kyphoscoliosis) will affect compliance.
• However, it's more usual for lung compliance to be affected.

Elastic Properties of the Lungs

• The elastic properties of the lungs are generated by:
  • Elastic fibers and collagen.
  • Surface tension forces.

Elastic Fibers in the Lungs

• Elastic fibers form the bulk of the connective tissue in the walls of the alveoli.
• Elastin fibers act like a stocking when stretched.

Surface Tension

• Cohesive forces between liquid molecules at the surface are responsible for surface tension.
• Molecules at the surface do not have other like molecules on all sides and cohere more strongly to those directly associated with them on the surface.
• This forms a surface "film," making it more difficult to move an object through the surface than when it is completely submerged.
• Water molecules on the boundary have a strong attraction for one another, causing the water surface to contract.

Surface Tension in Alveoli

• On the inner surface of alveoli, the water surface also tries to contract.
• This causes the alveoli to try to collapse, forcing air out through the bronchi.
• The net effect generates an elastic contractile force throughout the entire lungs, known as the surface tension elastic force.

Laplace's Law

• P = 2T/r
  • P = Pressure within the bubble
  • T = Surface tension
  • r = Radius
• The smaller the bubble, the greater the internal pressure required to keep it inflated.

Lung Surface Tension & Surfactant

• Surfactant stabilizes alveoli pressure = 2T/r (Law of Laplace). Without surfactant, pressure would be greater in smaller alveoli.
• Surfactant lowers surface tension more in smaller alveoli.

Action of Surfactant on Surface Tension

• Surfactants greatly reduce surface tension and, thus, reduce surface tension elastic forces.
• Pulmonary surfactant is a complex mixture of lipids and proteins.
• A major component (approx. 50%) is the phospholipid Dipalmitoylphosphatidylcholine (DPPC).
• It has an amphipathic character (hydrophilic and hydrophobic parts).

Surfactant Secretion

• Surfactant is secreted by type II alveolar epithelial cells.
• Assembly of surfactant occurs in the lamellar bodies, and it is secreted into alveolar fluid to form a surfactant layer at the water-air interface.

Infant Respiratory Distress Syndrome (IRDS)

• Caused by developmental insufficiency of surfactant production and structural immaturity in the lungs.
• Most babies produce enough surfactant to breathe normally by week 34.
• Premature babies may not produce enough surfactant, causing the lungs to collapse.

Airway Resistance (R_{aw})

• Air must be moved into and removed from the lungs (breathing).
• Airway resistance (R_{aw}) is the resistance to the flow of gas within the airways of the lung.
• Asthma increases airway resistance due to a reduction in airway diameter because of smooth muscle contraction, swelling due to inflammation, and/or mucus production.

Airway Flow

• The pattern of fluid flowing through a tube (e.g., airway or blood vessel) varies with the velocity and physical properties of the fluid.
• Two types of flow: laminar and turbulent.
• In laminar flow, the movement is orderly; in turbulent flow, it is chaotic.
• In most circumstances, flow can be considered laminar as a first approximation.

Poiseuille’s Law

• Laminar flow is described by Poiseuille’s law, which relates driving pressure and flow.
• The equation can be roughly applied to breathing.
• The most important factor is the radius of the tube (r^4).
• Small changes in airway diameter lead to relatively big changes in flow.

Example:

• Airway radius dilates from 4 units to 5 units.
  • Percentage increase in radius: ((5-4)/4) * 100 = 25\%
  • Percentage increase in airflow: r = 4, r^4 = 256 and r = 5, r^4 = 625; ((625-256)/256) * 100 = 144\%.
• Relatively small changes in airway diameter lead to big changes in flow.

Sites of Airway Resistance

• Just under half of the resistance to airflow is in the upper respiratory tract (nose, pharynx, and larynx).
• Significant resistance occurs in the nose (e.g., during inflammation and cold).
• Resistance reduces when breathing through the mouth (e.g., during exercise).

Sites of Airway Resistance: Lower Respiratory Tract

• Half of the resistance to airflow resides in the lower respiratory tract.
• Assuming laminar flow, Poiseuille’s law would predict major resistance in airways with smaller radii.
• However, the total cross-sectional area increases as you go down the tracheobronchial tree; although the diameter of each airway is small, there are a large number of them.

Sites of Airway Resistance: Small Bronchi and Bronchioles

• The most important part of the bronchial tree in terms of physiological control of airway resistance are small bronchi and bronchioles.
• Resistance is variable and under the influence of neuronal and hormonal factors.

Autonomic Control of Bronchial Smooth Muscle Tone

• Parasympathetic: Stimulate muscarinic receptors, causing smooth muscle constriction and bronchoconstriction.
• Sympathetic: Activate adrenergic receptors, causing smooth muscle relaxation and bronchodilation.

Other Factors Contributing to Bronchomotor Tone

• Mediator release (e.g., histamine): mast cell degranulation, neutrophils, and eosinophils are important in various stages of asthma.
• Rapidly adapting pulmonary receptors (irritant or cough receptors).
• Slowly adapting/stretch pulmonary receptors: activity reduces bronchomotor tone.

The Work of Breathing

• Performed by the respiratory muscles to overcome:
  • Resistance to airflow.
  • Elastic recoil of the lungs.
• Relationship between work (W) done to change a volume (∆V) of gas at constant pressure: W = P * \Delta V (measured in joules).
• Normally, respiration is very efficient and represents a small fraction of the total cost of metabolism, but this changes in disease.
• Changes in compliance and/or airway resistance may lead to increased workload.