Week 1- Mechanics of breathing Flashcards

1
Q

What determines lung volume?

A
  • The interaction between the opposing forces of chest wall expansion and inwards elastic recoil of the lungs determines lung volume.
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2
Q

Describe the elastic recoil of the thoracic cage and the lungs

Which direction is the recoil of each?

What is lung volume is determined when these forces reach equilibrium and define it.

A

The lungs and chest wall both have static elastic recoil, however these forces are in opposing directions:

The lungs tend to recoil inwards

The chest wall tends to recoil outwards

At equilibrium these forces balance each other and ends expiration with the FRC

FRC= the volume of air remaining in the lungs after passive expiration during normal quiet breathing.

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3
Q

What is inbetween the lungs and the thoracic cage that allows them to interact?

What layers form this structure?

What is inbetween the layers and what does this allow?

What pressure is in this space formed by these two layers?

A
  • The interaction between the lungs and chest wall is via the intrapleural space
  • The intrapleural space is in between the parietal and visceral layers of pleura
  • The space is filled with a thin layer of pleural fluid that helps to lubricate the lungs and allows transfer of expansile forces to the lungs where muscles pull on the parietal pleura which pulls the lungs up and out.
  • There is negative intrapleural pressure due to the outwards recoil of the chest wall vs the inwards elastic recoil of the lungs. They pull away from each other which creates a relative vacuum which allows expansion of the lungs into this space when the volume of the thoracic cage increases.
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4
Q

How is air moved into the lungs?

What creates resistance to flow?

What opposes lung expansion?

A
  • Air is moved into the lungs by bulk flow of air down a pressure gradient from more postive atmospheric pressure to more negative pressure in the peripheral airways.
  • This is created by the expansion of the thoracic cage and lung volume which by Boyle’s law decreases pressure within the lungs such that is becomes less than atmospheric pressure
  • Air moves into the lungs by bulk flow.
  • Resistance to flow is provided by the airway diameter and contents
  • Lung expansion is opposed by inherent elastic recoil of the lungs
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5
Q

Describe quiet respiration

What is required for inspiration? What forces are overcome?

What is required for expiration?

What lung volume is left after expiration?

How does this change during forced respiration with increased tidal volume?

A
  • During normal quiet respiration- inspiration:
    • requires muscular work which pulls the thoracic cage outwards
    • Pulls the parietal pleura which pulls on the lungs to pull them outwards
    • Lung expansion, drop in pressure, air moves in by bulk flow
    • overcomes the opposing elastic recoil and resistance to flow by the airways
  • During quiet expiration:
    • Expiration is passive requires only passive elastic recoil of the lungs
  • The FRC is left after expiration and is determined by an equilibrium being reached by outward elastic recoil of thoracic cage and inwards elastic recoil of the lungs
  • FRC = Volume of air present in the lungs at end of passive expiration
  • During forced inspiration with increased tidal volume (exercise) use of accessory muscles during inspiration and muscular work is required for expiration.
  • Muscles required for expiration to push increased lung volume out of the lungs to reach the same FRC in the same 2/3s of the respiratory cycle.
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6
Q

What muscles are required during quiet inspiration?

A
  • Main muscle on quiet inspiration is the diaphragm which when it contracts flattens and moves down, forces abdominal contents down and increasing the volume of the thoracic cavity.
  • Diaphragm is innervated by C3/4/5
  • Quiet inspiration also aided by the external intercostals (innervated by intercostal nerves) which elevate the ribs and sternum upwards and outwards by a bucket handle effect
  • Remeber quiet expiration is entirely passive requires only elastic recoil
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7
Q

What muscles are required during forced respiration?

Inspiration vs expiration

A

Forced inspiration requires:

  • Both diaphragm and external intercostals as in quiet inspiration
  • Scalenes which elevate the 1st and 2nd rib
  • Sternocleidomastoid muscle which elevates the sternum
  • Internal intercostal muscles (the portions that elevate the ribs only- intercartilaginous portion)

Forced expiration requires:

  • The internal intercostals (portion that depresses the ribs- extracartilaginous portion)
  • Innermost intercostals which depress the ribs
  • Abdominal muscles contract and compress the abdominal contents which pushes the diaphragm up.
  • Abdominal muscles : rectus abdominus, external oblique, internal oblique and transversus abdominis.
  • Pectoral girdle muscles
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8
Q

Define and explain the term “work of breathing”

A

Work of breathing = the energy expended during respiration (inspiration and expiration).

Constitutes 5% total energy expenditure at rest but can massively increase during exercise.

Has 3 components:

  1. Elastic work or Compliance= energy required to overcome elastic recoil of lung and chest wall
  2. Tissue resistance work = energy required to overcome viscosity of lung and chest wall structures
  3. Airways resistance work = energy required to overcome resistance to airflow through respiratory tract during inspiration and expiration, depends on airway diameter and type of flow (either turbulent or laminar).
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9
Q

Why does expansion of the chest wall (and depression of the diaphragm) lead to expansion of the lung?

A
  • Due to the pleural seal created by the parietal and visceral pleural layer and the thin layer of pleural fluid between them.
  • As chest wall and lungs recoil in opposite directions this tends to pull the pleural layers away from each other, creating negative intrapleural pressure and a relative vacuum/ pleural seal.
  • When the chest wall expands due to muscle contraction, this pulls the chest wall and parietal pleura outwards, intrapleural pressure becomes even more negative and creates a suction which pulls the visceral pleura (and attached lung) outwards.
  • Forces of elastic recoil are exceeded by the pleural suction.
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10
Q

What is the most common cause of lung collapse?

A

The most common cause of lung collapse is a pneumothorax- where air enters the pleural cavity either due to lung puncture or chest wall puncture.

Air entering the pleural space leads to loss of negative intrapleural pressure and the pleural space. Loss of pleural suction on the parietal pleura means there are no forces opposing elastic recoil of the lung and the lung collapses inwards.

Chest Xray shows left sided pneumothorax- black due to air in pleural cavity, loss of hilar shadow, collapsed mass, depressed diaphragm.

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11
Q

Define compliance

Define elastance

A

Compliance is the change in lung volume that occurs per unit of force/pressure applied. It is a measure of the ability of the lung to stretch and expand in response to pressure.

Compliance= △V/△P

Elastance = the inherent ability of the lungs to return to resting position due to elastic recoil.

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12
Q

Describe the lung inflation curve- what are the differences between inspiration and expiration?

(Transplumonary pressure X axis, plotted against lung volume Y axis)

What does this plot show?

A

Lung inflation curve is a plot of the transpulmonary pressure plotted against lung volume and therefore shows the compliance of the lung (△V/△P = compliance).

On inspiration the curve has much lower compliance than the expiration curve. For each change in transpulmonary pressure the change in lung volume is lower compared to inspiration.

This is due to the increased force required to 1) firstly overcome the resistance of the airways and open them and 2) secondly to overcome the surface tension of alveoli.

The compliance during inspiration is very low at low lung volumes, need high pressure to get the lungs to open initially. Compliance increases around the FRC up to TLC where compliance decreases again. At high lung volumes compliance decreases again as you need to overcome the surface tension of the alveoli at this point.

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13
Q

What is Hooke’s law?

How does this relate to the lungs?

A

Hooke’s law describes the pressure required to stretch or compress a spring is directly proportional to its length- constant factor is its stiffness/ compliance.

Lungs are not a perfect spring but are stiffer at low lung volumes (need to overcome resistance and open airways) and stiffer at high volumes (need to overcome surface tension of alveoli).

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14
Q

What is the effect of emphysema on compliance?

What is the effect of fibrosis on compliance?

A
  • During emphysema, there is a destruction of alveolar walls and elastic tissue leading to a loss of elastic recoil and an expansion of airspaces due to tissue loss. This means there is increased compliance (less elastic recoil opposing expansion and less tissue to expand).
  • Fibrosis is a condition in which there is scarring of lung tissue, increasing lung rididity. Lung tissue is harder to expand which decreases its compliance.
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15
Q

What is the effect of emphysema on FRC?

What is the effect of fibrosis on FRC?

A
  • Emphysema leads to an increase in FRC due to loss of elastic tissue and elastic recoil. Loss of equilibrium between expansile chest wall and inwards recoil of lungs, favours chest expasion and higher FRC.
  • Fibrosis and scarring of lungs increases rigidity of the lungs, they become harder to expand. With less air volume in and less chest expansion, the equilibrium is pushed towards elastic recoil forces- lowering FRC.
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16
Q

What is surface tension?

Define it

Explain the science behind it and how this relates to expansion of alveoli.

A

Surface tension is a measure of the forces acting to pull a liquid’s surface molecules together at an air- liquid interface.

  • Water molecules are attracted to each other more than they are attracted to air molecules due to Hydrogen bonds between them.
  • Water molecules are pulled in all directions except up at an air/liquid interface. Instead they move down into the bulk water phase
  • This creates an opposing force at the surface known as the surface tension
  • Water molecules have high surface tension, which tends to collapse alveoli
  • Need surfactant to overcome surface tension and open alveoli.
17
Q

Explain principles underlying laplace’s law

What is laplace’s law?

How does this relate to the alveoli?

A
  • Unbalanced forces acting on the surface water molecules within an alveolus tends to collapse the alveoli, acting like a belt tightening that reduces the size of the alveoli but increases the pressure within them.
  • At equilbrium the surface tension acting to collapse alveoli and the pressure within them acting the keep alveoli open balance.
  • Laplace’s equation describes the relationship between Pressure, surface tension and the radius of bubbles. P = 4T/ r
  • As in alveoli there is only 1 air-gas interface it becomes P = 2T/ r where P= pressure within alveolus/ pressure required to keep alveolus open T= surface tension r= radius of the alveoli.
  • At constant surface tension, smaller alveoli have a smaller radius and therefore have a higher pressure within them. This tends to force air out into the larger alveoli and leads towards alveolar collapse. Therefore these alveoli require a higher pressure to keep them open.
  • This means smaller alveoli have a tendency to collapse into larger alveoli
  • Surfactant is required to reduce the surface tension and keep smaller alveoli open.
18
Q

What cells secrete surfactant? What happens in disease?

Describe the nature of surfactant

How does its composition reflect is function?

A
  • Type ii pneuomcytes secrete surfactant, they have a high turnover, if lung damage occurs this can reduce surfactant secretion and lung expansion.
  • Surfactant composition:
    • Phospholipid (80%) - mainly dipalmitoyl phosphatidylcholine - hydrophobic tail interacts with gas phase, charged head interacts with water molecules.
    • Surfactant proteins (10%) : SP-A, SP-B, SP-C, SP-D
    • Neutral lipids (10%) - cholesterol
  • Surfactant function:
    • Reduces surface tension, increase compliance,reduce work of respiration
    • Stabilises alveoli and lung structure
    • Prevents tissue fluid exudation into alveolus
    • SP-A and SP-D bind pathogens and can activate macrophages/neutrophils- protection from infection
    • Lipid component has antioxidant properties
19
Q

If airflow is laminar what law determines resistance?

A

Posieulle’s law: R= 8nl/ π r4

20
Q

Under normal circumstances, where is the highest resistance in the airways?

What flow tends to occur in the larger airways?

A
  • According to poiseulles law, resistance may be expected to be highest in the smaller airways.
  • Under normal physiological conditions this is not the case as the smaller airways are many in number and provide many parallel pathways. Collectively they have the lowest resistance. (remember resistance in series is additive, resistance in parallel is r1 x r2/ r1 + r2)
  • The highest resistance is actually in the medium size bronchioles due to smaller radius and less parallel pathways being present.
  • Turbulent flow tends to occur in the larger airways rather than smaller airways.
21
Q

What is a bedside test of lung function and airways resistance?

A

Peak expiratory flow rate

22
Q

Describe factors that affect airways resistance

A
  • Autonomic NS:
    • Parasympathetic NS releases Ach, acts on muscarinic receptors inducing SMC contraction, reduction of airway diameter and increased resistance.
    • Sympathetic NS release noradrenaline and adrenaline, acts on B2 adrenoreceptors on SMC promotes relaxation, increase airway diameter, decrease resistance.
  • Lung volume:
    • Increasing lung volume tends to increase the airway radius which reduces airways resistance.
  • Turbulent vs Laminar flow: Turbulent flow has higher resistance and tends to occur in larger airways vs laminar flow in smaller airways
23
Q

What is the closing volume of the lung?

A

The closing volume of the lung describes the lung volume at which smaller airways and alveoli start to collapse. In a normal healthy individual closing volume makes up part of the residual volume and tends to always be below that of the FRC such that small airways are kept open during expiration.

Normal individual closing volume = 10% of vital capacity

In older individual closing volume = 40% vital capacity

As we age, the closing volume increases and can start to match FRC, meaning smaller airways start to collapse on expiration. This increases resistance to airflow as increased pressure is required to open up the smaller airways.