3 - Lung Mechanics & Function Testing Flashcards

1
Q

What has to happen for breathing to be successful?

A

The lungs and thorax must move (due to action of diaphragm etc) and gas exchange must take place.

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2
Q

What is pleural fluid?

A

A thin layer of fluid between the visceral (attached directly to the lungs) and parietal (attached to the thoracic cavity; both are mesoderm derivatives) layers.

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3
Q

What are the functions of pleural fluid?

A

Ensure the lungs fill the thoracic cavity and that they change volume as the thorax does.

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4
Q

What is a pneumothorax?

A

Where the integrity of the pleural seal is lost (i.e. a hole in the pleura) - the lungs will tend to collapse if this occurs.

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5
Q

Breathing is about the balance of forces. How do the lungs, thoracic cage and diaphragm affect the balance?

A

Lungs pull in and up, Thoracic cage pulls out, Diaphragm (passive stretch - contracts on inspiration) pulls down.

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6
Q

At resting expiratory level what is the disturbance in the balance of the forces?

A

There is no disturbance - forces are balanced. If disturbed - e.g. in the process of breathing the lungs will return to this state.

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7
Q

What structures are involved in quiet inspiration? Is it active or passive?

A

It is an active process. The Diaphragm (contraction) and Intercostals

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8
Q

What structures are involved in quiet expiration? Is it active or passive?

A

It is a passive process. Nothing involved - muscles involved in inspiration will relax.

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9
Q

When quiet breathing, what process expends the most energy? Can this change?

A

The stretching of the lungs. This may not be the case if the diaphragm struggles to move into the abdomen (e.g. pregnancy, obesity)

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10
Q

What structures are involved in forced expiration? Is it active or passive? How is inspiration that follows it affected?

A

It is an active process - must breathe out beyond resting expiratory level. This requires force which is exerted by abdominal muscles. Inspiration following a forced expiration will be passive up to the resting expiratory level.

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11
Q

What is lung compliance?

A

A measure of the stretchiness of the lungs. This can be calculated through (change in volume / change in pressue).

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12
Q

What is the lung specific compliance? Why is this important?

A

Due to the fact compliance will be different depending on the starting lung capacity.

i.e. (volume change / pressure change) / starting volume of lungs.

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13
Q

If the lungs have a high compliance what will their stretchiness be like?

A

Great. They will have a low resistance to stretching.

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14
Q

What are the two main contributing factors to lung elasticity?

A

Surface Tension,
Surfactant.

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15
Q

What is surface tension? How does lung elasticity affect it?

A

Surface tension is the interactions between molecules at the surface of a liquid. This makes the surface resist stretching.

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16
Q

If the lungs have high surface tension what will their stretchiness be like?

A

Reduced. A high surface tension will mean there is an increased resistance to stretching.

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17
Q

What are surfactants? How do they affect surface tension?

A

They are a mixture of detergents that reduce surface tension by disrupting the interactions between surface molecules.

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18
Q

Molecularly, what does surfactant consist of?

A

A mix of phospholipids and proteins. The hydrophilic ends of these molecules lies in the alveolar fluid with the hydrophobic ends projecting into the alveolar gas. These molecules therefore float on the surface of the lining fluid disrupting interaction between surface molecules.

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19
Q

In the lungs what is surfactant produced by?

A

Type 2 alveolar cells.

20
Q

Does surfactant always affect surface tension the same way?

A

No it depends on how inflated the lungs are.

Deflated: reduces surface tension (therefore increasing compliance)

Fully inflated: does not affect surface tension

This means that breathing is easier initially and as the breaths get larger in volume, they become more difficult.

21
Q

What is hysteresis?

A

The energy needed to stretch a film of surfactant.is not all recovered when the film recoils. Energy is lost - being at its greatest when tidal volume is maximal - little breaths are better.

22
Q

What are bubbles?

A

They are formed when a film of fluid, surrounding gas, shrinks compressing gas until there is an equilibrium between tension and pressure.

23
Q

What is Laplace’s Law and its relevance to bubbles?

A

Pressure = 2 x surface tension / radius

Big bubbles have a low pressure; small bubbles have a high pressure.

24
Q

What is the ‘law of bubbles’? How does this apply to Laplace’s Law?

A

If bubbles are connected in series, air will flow from high pressure to low pressure, i.e. small bubbles to big bubbles. Therefore big bubbles eat small bubbles.

25
Q

Why does this law of bubbles not apply to the lungs?

A

Pressure = 2 x surface tension / radius

Surfactant affects the surface tension (more surfactant reduces surface tension) - it is less effective as alveoli get bigger, so in large alveoli surface tension and radius will be higher - pressure stays high.
Large alveoli will not eat small alveoli!

If large alveoli (low pressure) ate small alveoli (high pressure) then the lungs could not exist.

26
Q

What is respiratory distress syndrome?

A

It occurs in babies born prematurely, where too little surfactant is produced - decreasing compliance and there are few, large alveoli.

(Large bubbles = ineffective surfactant; change is in Small bubbles = ineffective surfactant. The law of bubbles applies and large alveoli eat small alveoli).

27
Q

What does Poiseulles’ law imply about air movement in airways?

A

Small radius = high flow resistance.

Therefore in small tubes (most parts of the airways) there is a very high resistance and gas exchange would be difficult.

28
Q

Why does Poiseulles’ law not impact movement of air as much as you would expect?

A

There are a lot of small airways in the airways… but they are connected in PARALLEL.

Air resistance is then highest in the trachea and lowest in the smallest airways (terminal bronchioles) - breathing is easy.

29
Q

Why is forced expiration still difficult however?

A

When the lung is compressed (against the thoracic wall) the small airways narrow and resistance increases dramatically - trapping air in the alveoli.

Also decreased compliance of the lung when it is fully inflated (due to less effective surfactant - higher surface tension).

30
Q

What happens to resistance in the airways in Obstructive Airway Disease?

A

In Obstructive Airway Disease (asthma, chronic bronchitis) where the small airways are narrowed, resistance increases much earlier in expiration - making breathing out very difficult.

31
Q

What does lung function testing assess?

A

Mechanical condition of the lungs,
Resistance of airways,
Gas exchange at alveolar membrane.

32
Q

How is lung function assessed non-invasively?

A

It may be inferred from measurement of volumes, pressures/flows and composition at the mouth.

33
Q

What is vital capacity - what affects it?

A

The difference in volume between maximum inspiration and maximum expiration.

Maximum inspiration: compliance of lungs; force of inspiratory muscles.

Maximum expiration: increasing airway resistance as airways are compressed.

34
Q

How can we predict vital capacity?

A

From tables (nomograms) which use age, gender and height to estimate.

35
Q

How can we measure forced vital capacity (FVC)? In what form are these results normally presented?

A

Single breath spirometry: subject undertakes forced inspiration before expiring as far and fast as possibly through a spirometer.

Vitalograph trace a plot of volume expired vs time.

36
Q

What is FVC normally?

A

~5L, will vary though so check nomograms.

37
Q

What is FEV1.0? What is it affected by?

A

The volume expired in the first second.

The resistance in the airways - less if airways are narrowed.

38
Q

What is the FEV1.0/FVC ratio normally? What is the significance of this ratio?

A

>70%.

If <70% this may be due to an obstructive deficit (asthma, chronic bronchitis).

If >70% patient may still have lung problems if FVC is impaired - restrictive deficit (lung fibrosis).

39
Q

Why do restrictive airway diseases cause FEV1.0/FVC to be >70%?

A

If lungs are difficult to fill (stiff, weak accessory muscles, problem with chest wall) they will start less full (impaired maximum inspiration).

FVC will be reduced, but FEV1.0 will be normal - air exits the airways as normal.

40
Q

Why do obstructive airway diseases cause FEV1.0/FVC to be <70%?

A

If airways narrow lungs are still easy to fill. However resistance increases in expiration.

Air comes out more slowly - FEV1.0 impaired - but FVC can still be normal (albeit slower to reach).

41
Q

What are flow volume curves? How can we produce these? What are their benefits over vitalographs?

A

A measure of volume expired against flow rate derived from a vitalograph trace.

They are a more sensitive indicator of airway narrowing and can discriminate between large and small airway narrowing.

42
Q

On a flow volume curve when will flow rate be at its maximum? What is this also known as?

A

Maximum flow rate when lungs are full: little air expired; the airways are stretched so that resistance is at a minimum.

Peak expiratory flow volume (PEFR).

43
Q

What will happen to a flow volume curve when lungs are compressed (e.g. chronic bronchitis)?

A

More air is expired; airways narrow as resistance increases. Thus flow rate volume will fall.

Flow rate volume will fall more if the airways are narrower to start with.

44
Q

What devices do asthmatics frequently use to help them manage their condition?

A

A peak flow - measuring peak flow expiratory rate.
It is a cheap device but insensitive.

45
Q

How can you measure residual volume? How is this done?

A

Helium dilution (not possible by spirometry). Helium is not present in air and not soluble in blood.

Patient starts at functional residual capacity (volume in lungs at end of quiet expiration).
Breathes in known [Helium].
Breathe out and measure concentration of expired air (how much [Helium] has been reduced by air already in lungs).

46
Q

What is nitrogen washout?

A

It measures serial dead space and can be used to measure ventilation-perfusion matching.

Subject breathes in pure O2,
Breathes out via meter measuring % Nitrogen,
Initially only O2 expired,
Then mixture of O2 and air (incluing Nitrogen) from alveoli,
Volume expired at ‘transition’ = serial dead space.

47
Q

What is diffusion conductance? How do you measure it?

A

How easily gas diffuses from alveolar air to blood.

CO is used because the high affinity-binding to Hb means it will not dissociate: no partial pressure in mixed venous blood.