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1

Describe airway resistance and outline relative contribution of forces to airway resistance. Explain why smallest airways don't create greatest resistanct to flow

Resistance to flow is R(aw) and its very small, compared to say smoking through a pipe which takes 250x more resistance and more faorce to generate.

Forces
1. Inertia (negligible)
2. Friction of
a. Lung and chest wall slide past each other
b. Airway gliding past each other
c. Frictional resistance of air flowing though airways (80% total resistance)
§ Upper 60,
Trachiobronchial tree 40.

As you travel down the tree, the diameters get smaller (exponential bifurcation to create 8 million airways), but since they're next to each other they actually end up making the total cross section LARGER. so there is less resistance. more paths for the air to take.
- by the parallel design.

In health: airway resistance is largest in medium sized bronchi
In airway disease by smoking, resistance largest in smaller airways. Silent zone, so must be measured by airflow rather than resistance.

2

How airway size is controlled by autonomic nervous system how this applies to drug treatment for asthma

Parasympathetic: smooth muscle contraction (bronchoconstriction) via ACh release from vagus nerve onto muscarinic m3 receptors. Dominant control

Sympathetic: relaxation of smooth muscle (bronchodilation) via adrenaline release from adrenal medula onto B2 receptors. not nerve innervation!

Asthma treatments consist of anti-cholergenic and sympathomimetic bronchodilator medications.
Running makes airways larger so that air can get in.

3

What are the causes of increased airway resistance and expiratory airflow limitation in the obstructive lung diseases?

Airway Narrowing
-impact maximal expiratory flow
- Increase limitation

1. Excess mucus production (making it narrower)
a. Asthma, bronchitis, cystic fibrosis
2. Inflammation of airways: asthsma, copd, bronchitis,
3. Bronchoconstriction: because smooth muscle is contracting it, (asthma copd)
4. Reduced elastic recoil, increased compliance, emphysema

Anything that narrows airway (1-3) increase maximum limitation during maneuver and it can be measured.

4

Explain impact of lung volume, tissue elastance and pulmonary surfactant on lung compliance.

1. Tissue elasticity: connective tissue surrounding the airways
- mechanical compliance.
Connective tissue fibres: have collagen and elastin
Collagen: high tensile strength but not stretchable
Elastin: low strength but stretchable.
If CONNECTIVE TISSUE is lost, and loss of ELASTIN, wrinkles and increased lung compliance (less elastic-floppy lugs) INFLATE EASILY DEFLATE POORLY.

2. Lung volume: the more the lung is filled the more pressure it takes to fill it. Compliance is lung volume dependant. Lung is less compliant when inflated.

3. Alveolar surface tension: water is attracted to each other, since there's no molecule on top it's attracted. Water covers the surface of the alveoli from humidified air, so they want to collapse.
- Type 2 cells release surfactant which reduces surface tension so that they are stable against collapse.
- not enough surfactant creates inward recoil and collapse "atelectasis" see NRSD

5

Outline key differences between the PV curve of lungs in health, empysema and pulmonary fibrosis

PV normal: baseline
Emphysema: high compliance, but FRC is higher and TLC is higher too. Steep slope (slope is compliance because its changing volume over changing pressure)
Pulmonary Fibrosis: lower compliance, so FRC is about the same and TLC is lower. Shallow slope

6

Describe role of pulmnary surfactant in 1) alveolar surface tension and 2) compliance of lungs and 3) NRDS.

Reduce surface tension, decreasing compliance of the lung (stiff lungs) hard to inflate because the surface tension is too high. This is life threatening, treated with surfactant and mother treated with corticosteroids as a growth hormone.

7

what do a smokers lungs look like?

dark with bullae holes: emphysema (destruction of alveolar walls)

8

How does pressure relate to driving pressure and resistance?

flow = change in pressure/resistance.
2cm/h20/L/second at peak flow is the resistance.
1cm/h20 is the difference in pressure.
change in pressure is the pressure gradient.

9

Describe how expiration works with pressures during different types of expiration.

1. Breathing out during normal breath
Negative pleural space
Positive pressure in airway relative to atmosphere (generated cause of elastic recoil of the lung, stopped breathing in, lung recoiled, volume changed, pressure gone up, creating driving pressure OUT)
2. Breathing out during exercise
Use your chest wall, abdominal, intercostals, contract and squeeze everything inwards (as well as elastic recoil) additional positive pleural pressure . Because you're squishing everything else.
- Increase rate of flow, by adding compression through compression of chest wall that increases pressures inside it
- Pressures + elastic recoil = positive pleural pressures and more other pressures. GREATER FLOW
3. Breathing out during forced expiration (forced vital capacity maneuver)- test to see if someone is diseased that impacts air moving out
Making largest flow/compression that you can
Largest positive pleural pressure
Added to elastic recoil of the lung
Sum = alveolar pressure and airflow out.
High pleural pressure where pleural pressure is GREATER THAN the airway pressure. (because it gets less towards the mouth) losing some to the atmosphere.
= pressure in less than pressure out. The top gets narrower. (flow limiting segment)
- Depending on narrowing, they will have less flow rate (disease) and depends on structure (if it's floppy)

10

Describe lung compliance and elastance:

inverse of each other.
Elastance: tendency to return to original form (how easy it is)
Compliance: how easy it is to stretch a lung.
Make an elastic band thicker increases elastance and decreases compliance.

11

Describe the differences betwenn PUlmonary fibrosis,
emphysema.

Emphysema: disappearing lung disease
- smoking
- genetic (a1 antitrypsin deficiency)
Destroyed alveolar wall
Lung compliance increases leading to floppy lungs. (easy to stretch not to empty) Elastance gone down.

Pulmonary Fibrosis:
Collagen depositon in response to lung injury (asbestosis) type 3 macrophages didn't do their job, lead to inflammation and scar formation, which decreases lung compliance leading to stiff lungs, harder to fill but easy to exhale.

12

Verginina Slim Q lecture 3 3nding.

go now hoe!