Mechanisms of Breathing Flashcards

1
Q

What do changes in lung volume induce?

A

→ Changes in alveolar pressure which generate pressure gradients between alveoli & atmosphere, causing air to flow.

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2
Q

why any differences in pressure between the alveoli and atmosphere not instantly negated by the movement of air?

A

There is a delay due to the time taken for air to move.

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3
Q

What does rate of airflow depend on?

A

pressure gradient & level of airway resistance

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4
Q

Ohm’s law…

A

𝐴𝑖𝑟𝑓𝑙𝑜𝑤 (𝑉) =(Δ𝑃𝑟𝑒𝑠𝑠𝑢𝑟𝑒 (𝑃))/(𝑅𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 (𝑅)

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5
Q

Hagen-Poiseuille equation…

A

𝑅𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 (𝑅) ∝ 1/𝑟𝑎𝑑𝑖𝑢𝑠^4

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6
Q

What happens to resistance as airway radius increase?

A

→the resistance increases (and the airflow decreases) dramatically

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7
Q

What are some causes of reduced airway lumen?

A

→Contraction of airway smooth muscle, →excessive mucus secretion, →oedema/swelling of the airway tissue, →damage to the integrity of the airways structure (i.e. loss of patency

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8
Q

When does turbulent airflow occur?

A

→where high velocities of airflow are achieved (e.g. during forced breathing manoeuvres)
→if there is a sudden decrease in luminal area such as in obstructed airways.

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9
Q

What produces the wheezing sound?

A

The vibration generated by the turbulent airflow

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10
Q

What is patency?

A

the state of being open or unobstructed; a ‘loss of patency’ = closing/obstruction

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11
Q

How are open structures maintained?

A

by elastic fibres within the wall of the airway and radial traction.
→the airways are pulled open by their connections to the surrounding tissue

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12
Q

How can intrapleural space reduce airway patency?

A

When intrapleural pressure becomes positive (as can occur during forced expiration), collapsing force will be exerted onto the airways
→In healthy individuals, the structural integrity of the airways is sufficient to prevent collapse

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13
Q

Why is decreased structural integrity of the airways problematic in COPD?

A

the simultaneous loss of elastic recoil within the lung tissue means that both radial traction of the airways and lung recoil and reduced.
→greater force is required to compress the lungs during expiration,
→however the more force that is exerted to maintain ventilation and airflow, the more obstructed the patient’s airways will become

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14
Q

How is transpulmonary pressure calculated?

A

(Ptp = Palv – Pip)

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15
Q

What is lung compliance?

A

→relationship between the change in lung volume produced by a particular changed in transpulmonary pressure
→describes how easily the lungs can be distended

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16
Q

What does high and low compliance mean for elastic recoil and force required to inflate, and volume change?

A

Higher lung compliance = less elastic recoil = less force required to inflate = ↑ volume change per pressure change (↑gradient on volume-pressure curve)

Lower compliance = more elastic recoil = more force required to inflate = ↓volume change per pressure change (↓ gradient on volume-pressure curve)

17
Q

Equation for compliance

A

volume/pressure

18
Q

How do you calculate lung compliance from a graph?

A

by a graph of lung volume vs. transpulmonary pressure,

→as lung compliance = the gradient of the curve

19
Q

What is the difference between static and dynamic compliance?

A

static= measurements taken whilst airflow =0, the steepest part of the curve is used

dynamic=measurements taken in the presence of airflow, the gradient between the end tidal inspiratory and end tidal expiratory points is used

20
Q

How does scoliosis affect compliance?

A

reduction

→ through chest wall mechanics

21
Q

How does neonatal respiratory distress syndrome affect compliance?

A

reduction

→ through alveolar surface tension

22
Q

How does fibrosis and COPD affect compliance?

A

reduction
→ through collagen deposition

COPD:
increases compliance

23
Q

What is emphysema?

A

involves degradation of elastin fibres making the lung less stiff and more complaint but reducing recoil

24
Q

What is pulmonary fibrosis?

A

scarring and deposition of structural fibres such as collagen making the lung stiff and less compliant.

25
Q

How is a bubble created?

A

The water-air interface formed between the lining fluid and pseudo-spherical alveolar airspace

26
Q

How does surface tension arise within a bubble?

A

due to the relative strength of hydrogen bonds between water molecules combining to exert an overall collapsing force toward the centre of the bubble.

27
Q

What is Laplace’s law and how is it associated with pressure?

A

The amount within a specific bubble is described by the Law of Laplace

→𝑃 =2𝑇/𝑟
Pressure
→Surface tension (e.g. water = 0.075N/m)
Radius of bubble (i.e. alveoli)
→(The smaller the alveoli, the larger the pressure generated)
28
Q

Q: What would happen if 2 bubbles of different radius were connected to each other (e.g. different size alveoli connected via airways)?

A

Pressure gradients would be created between different sized alveoli, resulting in smaller alveoli emptying into larger ones
→This would thus make inflation of the lung very difficult

29
Q

How is the potential problem of smaller bubbles lowering into larger ones resolved?

A

→by the presence of pulmonary surfactant
→acts to disrupt the attractive forces between water molecules, reducing surfacing tension and the collapsing pressure generated

30
Q

What are surfactants?

A

→phospholipoprotein secreted by type II pneumocytes (alveolar cells
→amphipathic, will naturally position themselves at the air-liquid interface.

31
Q

How do surfactants equalise pressure between varying alveoli sizes?

A

→As alveolar size increases during inflation, the concentration of surfactant molecules at the interface decrease
→surface tension (and thus pressure generated) increases with increasing alveolar surface area.
→air will naturally flow from larger (more inflated) alveoli to smaller ones, helping to distribute air across the lung during inspiration

32
Q

How does surfactants tension reduce alveolar oedema?

A

→reduces hydrostatics pressure in the alveolar tissue.
→acts to pull fluid out of the surrounding pulmonary capillaries and into the alveoli and interstitial tissue. →By reducing surface tension, pulmonary surfactant helps to prevent alveolar oedema due to excessive fluid being pulled from capillaries

33
Q

What is the neonatal respiratory distress syndrome?

A

→Premature birth, maternal diabetes, congenital developmental issues
→Insufficient surfactant production
→Stiff (low compliance) lungs, alveolar collapse, oedema
→Respiratory failure
→Hypoxia
→Pulmonary vasoconstriction, endothelial damage, acidosis, pulmonary + cerebral haemorrhage.
→innervating capillaries

34
Q

How is NRDS treated?

A

→supplementation of affected infants with artificial surfactant
→ maternal administering glucocorticoids (which increase surfactant production via maturation of type 2 pneumocytes) t

35
Q

What happens with saline filled lungs ex vivo?

A

lungs required less pressure to inflate (↑ compliance)

36
Q

What happens with washed lungs then inflation?

A

produced lungs that required more pressure to inflate (↓ compliance).