L07 Respiratory Physiology 3 Mechanics of breathing

Overview

This lecture covers the mechanics of breathing: how pressure gradients are generated to move air into and out of the lungs, the muscular and pressure changes underlying inspiration and expiration, the intrapleural pressure relationship between lung and chest wall, positive- and negative-pressure ventilation, the work of breathing (elastic recoil and airways resistance), lung compliance, the role of surfactant in overcoming alveolar surface tension, and the factors determining airways resistance.

Principles of ventilation

• Ventilation delivers O2 to, and removes CO2 from, the alveolar-capillary membrane.
• For airflow to occur, a pressure gradient must exist between the alveoli and the atmosphere.
• The gradient is generated by changing the volume of the respiratory system, which must expand above and then return to its resting volume.
• Air always moves from an area of high pressure to an area of low pressure.
• Boyle’s law: at constant temperature, gas volume varies inversely with absolute pressure ($P_1{V}_1=P_2{V}_2$); halving volume doubles pressure.
• Causal chain: change in lung volume -> change in alveolar pressure (relative to atmosphere) -> gas flow and pressure equalisation.
• Airflow requires overcoming two things, together termed the work of breathing:
  1. Elastic recoil of the lung and chest wall (to change volume)
  2. Airways resistance (friction, to get airflow)

A slide (repeated three times) shows "high(er)/low(er)" pressure body diagrams with red "er" suffixes that appear to be an in-lecture fill-in-the-blank exercise (building "higher"/"lower" from "high"/"low") rather than separate content.

Inspiration

• Diaphragm and external intercostal muscles contract.
• Thoracic volume increases.
• Lungs expand, lung volume increases and pressure decreases.
• Air moves into the lungs.
• Sequence: diaphragm and inspiratory intercostals contract -> thorax expands -> intrapleural pressure ($P_{ip}$) becomes more subatmospheric -> transpulmonary pressure increases -> lungs expand -> alveolar pressure ($P_{alv}$) becomes subatmospheric -> air flows into the alveoli.

A chest X-ray with lung/diaphragm borders traced does not state whether it shows inspiration or expiration; a further zoomed detail slide has no caption, and its exact relationship to the first X-ray is not stated.

Expiration

• Expiration is normally passive, driven by elastic recoil of the respiratory system, but can be forced.
• Inspiratory muscles relax.
• Diaphragm moves upward.
• Thoracic volume (and hence lung volume) decreases.
• Alveolar pressure increases.
• Air moves out of the lungs.
• Recoil back to resting volume (FRC) raises alveolar pressure and drives exhalation.
• Accessory muscles can augment expiration (generate more pressure), which may become necessary when airways resistance is very high.
• Sequence: diaphragm and inspiratory intercostals stop contracting -> chest wall recoils inward -> intrapleural pressure moves back toward its pre-inspiration value -> transpulmonary pressure moves back toward its pre-inspiration value -> lungs recoil toward pre-inspiration size -> air in the alveoli is compressed -> alveolar pressure exceeds atmospheric pressure -> air flows out of the lungs.

Intrapleural pressure and the lung-chest wall relationship

• The lung and chest wall are separated by the intrapleural space.
• The lung tends to recoil inward while the chest wall tends to expand outward, so they pull away from each other.
• As a result, intrapleural pressure is subatmospheric.
• At the point where these opposing forces are in equilibrium (functional residual capacity, FRC), intrapleural pressure is approximately -5 cm H2O (alveolar and lateral chest-wall pressures are 0 at this point).

Positive- and negative-pressure ventilation

• The same principle (only a pressure difference is needed) can be exploited by changing the outside pressure rather than only lung volume.
• Positive-pressure examples: bag-valve-mask (BVM) resuscitation, endotracheal intubation, and mechanical ventilators, which apply pressure via a gas cylinder, gauge/valve and mask/hose system.
• Negative-pressure ventilation (historical): the “iron lung” encloses the patient’s body, head protruding, in a tank; a leather diaphragm and positive/negative pressure valves change the pressure around the chest to drive breathing. Iron lungs were historically used on wards in large numbers.
• Pneumothorax, illustrated on chest X-ray by a visible pleural line/edge of a collapsed lung, is a clinical example where the normal lung-chest wall pressure relationship is disrupted.

A slide shows elephants swimming while breathing through their trunks, without stating how the example connects to the surrounding content; it is presumed, but not stated, to illustrate breathing against an external pressure or resistance, analogous to the adjacent "increase outside pressure" point.

Work of breathing (pressure-volume loop)

• The fall in intrapleural pressure during inspiration equates with the work done to move air, and has two components:
  1. A fall in pressure from the elastic pull of the lungs during inflation.
  2. A further fall in pressure needed to overcome airway resistance (from airflow and the friction of the expanding lungs).
• Work of breathing = work to expand the lungs (elastic recoil/compliance) + work to move air (airways resistance).
• On a tidal-volume vs intrapleural-pressure loop, the inspiration and expiration limbs diverge; the hatched area between them represents the extra work needed to overcome airway resistance.
• A time trace over inspiration, expiration and pause shows: intrapleural pressure falling (about -5 to -8 cm H2O) during inspiration and returning toward -5 during expiration; lung volume (change from FRC) rising to 0.5 L during inspiration and returning to 0; alveolar pressure dipping negative during inspiration and rising to about +2 cm H2O during expiration, returning to 0 at pause; airflow positive (inflow) during inspiration, negative (outflow) during expiration, and zero during the pause.

Compliance

• Lung compliance ($C_L$) measures the elastic properties (“stiffness”) of the lung: $C_L=\Delta V/\Delta P$, the slope of the pressure-volume graph.
• $C_L$ varies with:
  • Lung volume: as the lung is stretched it becomes harder to stretch further.
  • Disease: fibrosis or loss of elastic tissue.
  • Age: lungs become more compliant with age, but the chest wall becomes stiffer and respiratory muscles weaker, decreasing vital capacity.
  • Alveolar surface tension.
• Fibrosis makes the lung non-compliant (“stiff”): for a given pressure change, the volume change is less than normal.
• Emphysema destroys elastic tissue, making the lung more compliant: for a given pressure change, the volume change is more than normal.
• On a vital-capacity vs pressure graph, the curves rank from steepest (most volume per pressure) to flattest (least): emphysema, normal, fibrosis.

Surface tension and surfactant

• Fluid lining the alveoli exerts surface tension, causing the alveoli to contract and resist expansion; this force must be overcome to expand the lung.
• Surface tension is reduced by surfactant.
• Surfactant is a phospholipid produced by alveolar type II cells.
• It lowers surface tension by becoming interspersed between water molecules, reducing hydrogen-bonding attractive forces; this increases lung compliance.
• Lack of surfactant causes “stiff” lungs, seen in neonates and in ARDS.
• Relevant alveolar structure: basal lamina, surfactant lining the alveolar surface, the alveolar lumen, a macrophage, a type II alveolar cell (which produces surfactant), capillary endothelium with red blood cells, and a type I alveolar cell.

Airways resistance

• During quiet breathing, airflow is mainly laminar.
• Resistance is determined by Poiseuille’s law: $R=8\eta l/\pi r^4$, where $\eta$ = viscosity, $l$ = length, $r$ = radius.
• Resistance is inversely proportional to $r^4$: halving the radius increases resistance 16-fold.
• Bronchoconstriction and bronchodilation are therefore important determinants of airways resistance (e.g. in asthma).
• Most airway resistance arises in the upper airway and the first 6 generations of the lower airway, mainly the bronchi; the small airways contribute very little because of their large total cross-sectional area.
• Airway generations (branching tree): trachea (generation 0, conducting zone), bronchi (1-3), bronchioles (4), terminal bronchioles (5-16, end of conducting zone), then the transitional/respiratory zone: respiratory bronchioles (17-19), alveolar ducts (20-22), alveolar sacs (23).
• Factors determining airway resistance:
  • Bronchoconstriction: vagal parasympathetic activity (reflex from irritant and cough receptor stimulation in the airways); local chemical mediators (histamine, leukotrienes).
  • Bronchodilation: activation of ${\beta }_2$-adrenoceptors via circulating adrenaline or sympathomimetic drugs (e.g. isoprenaline, salbutamol).
  • Dynamic compression of airways.

Self-test

1. Define lung compliance and give the equation that expresses it.
2. State Boyle’s law and describe what happens to pressure if lung volume is halved.
3. Describe the sequence of events, from muscle contraction to airflow, that occurs during inspiration.
4. Describe the sequence of events, from cessation of inspiratory muscle contraction to airflow out, that occurs during expiration.
5. Explain why intrapleural pressure is subatmospheric, and state its approximate value at FRC.
6. List the two components that make up the “work of breathing” and explain what each represents on a pressure-volume loop.
7. Distinguish the effect of fibrosis from the effect of emphysema on the lung’s pressure-volume (compliance) curve.
8. Explain how surfactant reduces alveolar surface tension and increases lung compliance. Which cells produce it, and in which two clinical situations is a lack of surfactant seen?
9. State Poiseuille’s law and explain, using the equation, why a small reduction in airway radius produces a large increase in resistance.
10. Where in the airway tree does most airway resistance arise, and why do the small airways contribute so little?
11. List the mechanisms that cause bronchoconstriction and those that cause bronchodilation.
12. Give two clinical/historical examples of positive-pressure ventilation and one example of negative-pressure ventilation, and describe how each changes the pressure gradient driving airflow.
13. Using the concepts of compliance and airways resistance, explain why both are needed to fully account for the total work of breathing.

Answers

Reveal answers

1. $C_L=\Delta V/\Delta P$, the slope of the pressure-volume graph; it measures the elastic “stiffness” of the lung.
2. At constant temperature $P_1{V}_1=P_2{V}_2$; halving the volume doubles the pressure (e.g. 1.0 L at 100 mmHg becomes 0.5 L at 200 mmHg).
3. Diaphragm and inspiratory intercostals contract -> thorax expands -> intrapleural pressure becomes more subatmospheric -> transpulmonary pressure increases -> lungs expand -> alveolar pressure becomes subatmospheric -> air flows into the alveoli.
4. Diaphragm and inspiratory intercostals stop contracting -> chest wall recoils inward -> intrapleural pressure moves back toward its pre-inspiration value -> transpulmonary pressure moves back toward its pre-inspiration value -> lungs recoil toward pre-inspiration size -> air in the alveoli is compressed -> alveolar pressure exceeds atmospheric pressure -> air flows out.
5. The lung recoils inward while the chest wall expands outward, so they pull away from each other, making the intrapleural space subatmospheric; at FRC, where these opposing forces balance, intrapleural pressure is about -5 cm H2O.
6. (1) A fall in pressure from the elastic pull of the lungs during inflation (compliance-related work); (2) a further fall in pressure needed to overcome airways resistance. On the loop, the hatched area between the inspiration and expiration limbs represents the extra work done to overcome airway resistance.
7. Fibrosis: the lung is non-compliant/stiff, so a given pressure change produces a smaller volume change (flattest curve). Emphysema: destruction of elastic tissue makes the lung more compliant, so a given pressure change produces a larger volume change than normal (steepest curve).
8. Surfactant, a phospholipid made by alveolar type II cells, interposes between water molecules to reduce hydrogen-bonding attractive forces, lowering surface tension and increasing compliance. A lack of surfactant causes stiff lungs in neonates and in ARDS.
9. $R=8\eta l/\pi r^4$; resistance is inversely proportional to the fourth power of the radius, so halving the radius increases resistance 16-fold.
10. Most resistance arises in the upper airway and the first 6 generations of the lower airway (mainly the bronchi); the small airways contribute little because their combined total cross-sectional area is very large.
11. Bronchoconstriction: vagal parasympathetic activity (reflex from irritant/cough receptor stimulation), local chemical mediators (histamine, leukotrienes). Bronchodilation: ${\beta }_2$-adrenoceptor activation via circulating adrenaline or sympathomimetics (isoprenaline, salbutamol).
12. Positive pressure: bag-valve-mask ventilation and mechanical ventilation (via endotracheal tube) apply pressure from outside to push air in. Negative pressure: the iron lung reduces the pressure around the chest/body, via a leather diaphragm and valves, to expand the chest and draw air in.
13. Compliance accounts for the elastic work needed to expand the lung and chest wall against their recoil, while airways resistance accounts for the frictional work needed to move air through the airways; both must be overcome for airflow to occur, so together they make up the total work of breathing represented by the pressure-volume loop.