Respiratory System: Mechanics of Breathing Flashcards

1
Q

Define airway resistance

A

Airway resistance = the force generated by gas molecules colliding with the airway surfaces, which opposes air flow.

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2
Q

What happens if airway resistance increases?

A

More resistance slows down flow. This can be overcome by increasing pressure gradient, but this has physical limitations, e.g. you can’t generate the force required to do so, or the airway might be completely obstructed.

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3
Q

If airflow is proportional to resistance, factors that then determine the level of resistance are…

A

..the cross sectional area of the airway lumen and the airflow pattern.
The Hagen-Poiseuille eqn shows that small decrease in radius will produce a large increase in resistance (and so dramatically decrease airflow).

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4
Q

What factors reduce the size of the airway lumen?

A
  • Contraction of airway smooth muscle
  • Oedema/swelling of the airway tissue
  • Damage to the integrity of the airways structure (loss of patency)
  • Excessive mucus secretion

These all reduce airway lumen size, increasing resistance and decreasing airflow

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5
Q

How does airflow pattern change airway resistance?

A

When airflow changes from a linear to a turbulent pattern, airway resistance increases.
Turbulence occurs in high velocities of airflow (e.g. during forced breathing manoeuvres) or in obstructed airways.
The vibration from turbulent airflow produces wheezing.

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6
Q

What is airway patency? What maintains it?

A
Airway patency (openness) also determines the degree of airway obstruction (‘loss of patency’ =obstruction)
Elastic fibres within the airway wall and radial traction maintain patency.
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7
Q

Why is airway obstruction more noticeable during expiration?

A

As lungs expand during inspiration, the lung tissue and airways are stretched upon. During expiration, the lung tissue and airways are compressed. This explains why airway obstruction is more noticeable during expiration.

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8
Q

What else can reduce airway patency?

A

When intrapleural pa becomes positive (eg during forced expiration), collapsing force is exerted onto the airways, reducing patency.
In healthy individuals, the structural airway integrity prevents collapse, but is problematic in diseases w impaired airway structure (e.g. COPD)

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9
Q

Define lung compliance and trans pulmonary pressure

A

A change in transpulmonary pressure produces a change in lung volume. This relationship= lung compliance. It describes how easily the lungs can be distended.
Transpulmonary pa= Pa difference between the alveoli and intrapleural space. It determines the level of force to expand or compress the lungs.

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10
Q

What does it mean if you have higher or lower lung compliance?

A

Higher lung compliance = less elastic recoil which means less force required to inflate the lungs. ↑ volume change per pa change (↑gradient on volume-pressure curve)

Lower compliance = more elastic recoil, so more force required to inflate the lungs. ↓volume change per pa change (↓ gradient on volume-pressure curve)

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11
Q

Use this graph to explain the difference between static and dynamic compliance

A

The steeper the curve, the higher the lung compliance. This is bc a more compliant lung needs less force acting on it to expand in volume.

Static compliance is when the patient stops inspiration briefly so that airflow falls to 0. To determine dynamic compliance a patient breaths normally at tidal volume. Dynamic compliance=gradient of the line from the end of expiration to the end of inspiration.

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12
Q

Using a graph, explain the effect of fibrosis and emphysema on lung compliance

A

Emphysema= degradation of elastin fibres making the lung less stiff and more complaint (but reducing recoil). Pulmonary fibrosis= scarring and deposition of structural fibres such as collagen, making the lung stiff and less compliant.

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13
Q

Why do alveoli generate inward collapsing pressure?

A

Alveoli are lined with fluid to enable gas exchange (the gas molecules dissolve into water before diffusing.)

H bonds between water molecules create surface tension, exerting a collapsing force toward the centre.
The collapsing forces generates pressure. The amount in a specific bubble is described by the Law of Laplace (see image)
Unless sufficient force resists this collapsing pressure, the alveoli will collapse and fail to inflate.

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14
Q

Smaller radius generates greater pressure within alveoli. So what would happen if 2 different sized alveoli were connected via airways?

A

Seria pressure gradients between the alveoli, so the smaller alveoli would empty into larger ones. This would make lung inflation extremely difficult
This is resolved by pulmonary surfactant, a phospholipoprotein secreted by type II pneumocytes (alveolar cells).

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15
Q

What is pulmonary surfactant? How does it reduce surface tension and collapsing pressure?

A

Pulmonary surfactant is a phospholipoprotein secreted by type II pneumocytes (alveolar cells).
Surfactant molecules disrupt the attractive forces between water molecules, reducing surface tension and collapsing pressure.

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16
Q

Pulmonary surfactant also equalises pressure between alveoli of varying size. How does it do this?

A

As alveolar size increases during inflation, surfactant molecule conc at the interface decreases.
So where pulmonary surfactant is present, surface tension (and so pa generated) increases with increasing alveolar surface area.
This means air will naturally flow from larger (more inflated) alveoli to smaller ones, distributing air across the lung during inspiration

17
Q

Pulmonary surfactant reduces surface tension. Why is this an advantage?

A

Surface tension produced at the air-liquid interface also reduces hydrostatic pa. This means less fluid is pulled out of surrounding capillaries and into the alveoli.
This prevents alveolar oedema.

18
Q

Describe neonatal respiratory distress syndrome

A

(NRDS) occurs in premature infants who don’t produce enough pulmonary surfactant.
This results in the alveoli collapsing, decreasing lung compliance, causing respiratory failure.
Alveolar oedema also reduces gas exchange. The increased pressures within the lung also damage alveoli and innervating capillaries.

19
Q

How is NDRS treated?

A
  • Supplementation of affected infants with artificial surfactant.
  • Administering glucocorticoids (which increase surfactant production via maturation of type 2 pneumocytes) to high risk mothers

(e.g. mothers with poor diabetic control – insulin affects pneumocyte maturation - or those at risk of premature birth).

20
Q

Draw a flow chart demonstrating the pathophysiology of neonatal respiratory distress syndrome

A
21
Q

How does compliance affect pressure-volume loops?

A

Compliance= the gradient of the overall line from end of expiration to end of inspiration.

22
Q

How does airway resistance affect pressure volume loops?

A

Airway resistance= loop area/fatness. It increases w forced in/expiration and airway obstruction. It decreases w slow inspiration and no airway obstruction.

23
Q

How do we know if hypoventilation or reduced oxygenation is the cause of hypoxaemia?

A

The alveolar gas eqn can interpret ABGs and determine if hypoxaemia is caused by hypoventilation and/or reduced oxygenation/perfusion.

If hypoventilation is the problem, then PaCO2 is >6KPa. If the problem is V/Q inequality or deficits in oxygenation (but sufficient ventilation to remove excess PaCO2), then PaCO2 will be lower.

24
Q

How do we know if the oxygen that reaches the alveoli is being exchanged into the blood adequately?

A

If PAO2 is much greater than PaO2 (excessive pa gradient) this shows issues w gas exchange and blood oxygenation (e.g. V/Q mismatch/diffusion defects).

Normally difference between PAO2 and PaO2 is 1.5 to 3kPa. If alveolar-arterial gradient is much >2kPa, this means the 02 reaching the alveoli isn’t diffusing into the blood efficiently.

25
Q

What is the alveolar gas eqn?

A