Airway resistance and flow Flashcards

1
Q

What causes resistance to flow?

A

Lung tissue viscous resistance, 10-20%
Airway resistance, 80-90%

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2
Q

What is the formula for flow?

A

Flow = pressure gradient / resistance

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3
Q

What is the equation for airflow?

A

Airflow = pressure gradient/ resistance
Pressure gradient = alveolar pressure - atmospheric pressure
The tubes provide the resistance to flow.

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4
Q

How is airway resistance measured?

A

RAW = PB-PA/V
PB at sea level, 100kPa.
PA - measure with a plethysmograph
V - measure with a pneumotachometer

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5
Q

What is the distribution of airway resistance?

A

The total airway resistance is quite low.
The most resistance is at the larger airways of the system - pharynx/larynx, and airways with more than 2mm diameter.
Airway resistance is measured in cmH2O(L/s) because pressure is so low.

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6
Q

What is fluid movement similarities?

A

5L/min cardiac output
6L/min of minute ventilation.
The alveolar pressure only decreases 1kPa below atmospheric pressure, to produce a similar amount of fluid movement per min to the cardiovascular system.
Therefore can have similar fluid movement at a lower pressure gradient, so can have a lower resistance overall.

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7
Q

What are the types of airway resistance?

A

As the airways divide, the resistance is in series, so the resistance is added up to a total, and overall resistance is high.
As the airways become branched, the resistance is in parallel, so overall resistance decreases.

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8
Q

What are the determinants of airway resistance?

A

A smaller radius will produce a higher resistance.
At the top of the airway, there are few tubes, so the only factor is radius.
In the first few generations, resistance is increasing, because airway is decreasing in radius.
As there are more tubes in parallel, so the number of tubes have become the dominant effect, and resistance decreases.

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9
Q

How is resistance variable?

A

The larger airways have a constant radius, so have constant resistance.
As they move down, the diameter changes and the resistance becomes variable.

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10
Q

How does the structure of the upper airways affect resistance?

A

The upper airways have cartilage holding the trachea open.
If the pressure inside is greater than outside, the airway is open.
If the pressure outside is greater, the cartilage will hold the trachea open so it doesn’t collapse.
Cartilage is static, so gives a fixed radius, and therefore fixed resistance.

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11
Q

How does the structure of the lower airways affect resistance?

A

The airways lose cartilage, and instead smooth muscle supports the structure.
This can contract and relax, so resistance is variable.
The airway is embedded in the lung tissue, so what happens to the tissue affects the airway.

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12
Q

What is the effect of the terminal bronchioles?

A

The terminal bronchioles contribute a relatively small amount of resistance.
When respiratory disease begins, there is only a small amount of change in total resistance, so there is no noticeable change in breathing.
The disease can therefore get to a late stage before the effects are noticed, and treatment becomes harder.

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13
Q

What are the determinants of airway resistance?

A

Airway smooth muscle tone.
Mucus build up.
Lung volume.

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14
Q

What causes bronchodilation?

A

Sympathetic activity - although little evidence.
B-receptor agonists - salbutamol.
Adrenaline is potent but noradrenaline is weak.
Cholinergic antagonists - atropine.
Hypercapnia (high CO2)

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15
Q

How is bronchodilation not caused by sympathetic activity?

A

The B receptors are more receptive to circulating hormonal adrenaline rather than noradrenaline release from sympathetic stimulation.
So there are different nerves that cause bronchodilation, rather than sympathetic.

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16
Q

What causes bronchoconstriction?

A

Parasympathetic activity - 30% of resting tone, normally active.
Cholinergic agonists
B-receptor antagonists
Inflammatory mediators - histamine and leukotrienes (mast cells)
Hypocapnia (low CO2).

17
Q

How does the heart smooth muscle tone change?

A

There are B1 receptors on the SA node and ventricles.
When stimulated these increase Ca2+, so increase heart rate and force of contraction - ionotropic effect.
These are most potently stimulated by the hormone adrenaline.

18
Q

How do the airways smooth muscle change?

A

There are B2 receptors on the airways, which when stimulated, will cause relaxation of smooth muscles and bronchodilation.
In pharmacology, the drugs need to be B2 specific, because non-selective drugs will also affect the heart, and other things.

19
Q

What is the effect of mucus build up on airway resistance?

A

Mucus changes size of tube and therefore resistance.
Cells or signalling that causes inflammation cause mucus to be produced.
An anti-inflammatory drug or B2 agonist can reduce inflammation and therefore mucus.

20
Q

What is the effect of lung volume on airway resistance?

A

Increased lung volume from breathing in will make the pleural pressure more negative, which holds the airways open, and the pressure gradient increases.
As the lung volume increases, the airways get bigger, and resistance decreases.
During forced expiration, the pressure outside the lungs is greater than inside, so airways collapse and air no longer flows through.

21
Q

What is the effect of radial traction on airway resistance?

A

Airways are embedded in lung tissue.
Fibres act like a scaffold to keep the airways open.
During disease, where tissue structure or rigidity is lost, radial traction will be affected.

22
Q

What is the effect of radial traction and lung volume on resistance?

A

The trans-airway pressure (gradient) and radial traction hold the airways open at the highest lung volume, with the least resistance, so air flow is greatest.

23
Q

How can airway resistance change be measured?

A

Pulmonary function test by spirometry - measures the pressure difference, converts to flow then volume. Shows the residual volume.
Peak flow measurements - a faster flow causes the volume to change faster.
There is the lowest resistance at total lung volume, so peak flow should happen as soon as you start expiring.

24
Q

What is residual volume?

A

The air that cannot be expired because the airways are collapsed due to the decreased pressure.
This will change in disease and at what point the airways collapse.

25
Q

What are the determinants of peak expiratory flow?

A

Flow = pressure gradient / resistance.
When using elastic recoil of the lungs, there is the least airway resistance as embedded airways are open, and the biggest pressure gradient generated from total lung capacity.
So peak expiratory flow would start as soon as expiration begins.

26
Q

What happens to peak expiratory flow when determinants change?

A

When there is normal elastic recoil with increased airway resistance, there is decreased airflow.
If there is decreased elastic recoil, with normal airway resistance, there is decreased airflow.
Peak flow measures a change, but cannot distinguish between recoil and resistance.

27
Q

What is FEV1?

A

The peak expiratory flow happens at the start of the expiration.
Flow is how quickly the volume is changing.
So if peak flow is down, the volume in the first second of expiring will be decreased.
This measures the forced expiratory volume in the first second after maximal inspiration (FEV1).

28
Q

What is FVC?

A

Vital capacity can also be measured in spirometry - the total air expired.
Forced vital capacity is the maximum volume of air that a person can forcibly expire after a maximal inspiration.
This is expressed as a %.

29
Q

What is FER?

A

Forced expiratory ratio = FEV1 / FVC.
The % of total breaths that can be got out in the first second.
This changes with airway resistance.
The lower the ratio, the more likely it is that the airways are obstructed. A healthy person will have a ratio of 0.8 (80%) or more.

30
Q

How does airway resistance change FER?

A

If change airway resistance then obstructive disease.
If vital capacity decreased, then restrictive disease (reduction in size of lungs).
So can distinguish between these using spirometry.
A lower ratio indicates a slower rate of expiration, which may be caused by resistance in airways - asthma.

31
Q

What are some true statements about resistance?

A

Resistance is calculated from the pressure difference divided by flow rate.
The longer the tube, the greater the resistance to flow.
An increased air density increases resistance to airflow.