18 Lung Mechanics Flashcards

1
Q

Q: What’s the difference between obstructive and restrictive lung disease in terms of:

TLC?
VC?
Residual volume?
ERV?
IVR?
TV?
A

A: increases for O
decreases for R

decreases in both

greater in O
lower in R

last 3 decrease in both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Q: What happens in COPD? (5)

A

A: -narrowing of airways

  • break down of parenchyma
  • so the alveoli have less recoil
  • bronchi will close
  • and the air will be trapped distal to the upper airways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Q: What would happen hypothetically if you removed the chest wall and lungs?

A

A: The chest wall, if you take it out of the body, is going to have a larger volume than at FRC

The lung, if you take it out of the body, is going to shrink and have a smaller volume than at FRC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Q: What is FRC?

A

A: functional residual capacity

sum of Expiratory Reserve Volume (ERV) and Residual Volume (RV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Q: Draw a pressue (x) volume (y) graph (flow rate graph) for the chest wall, lungs and combined (transrespiratory system pressure).

  1. What happens if you apply pressure to either the lungs or chest wall at beginning?
  2. As you follow the curve up?
  3. When do you you get a greater change in volume per unit pressure?

Summary? (2)

A

A: REFER: Around the volumes in the middle of the graph, a small change in pressure will cause a large change in volume (the triangle is about as tall as it is wide)

  1. a small pressure change will result in a large change in volume to begin with
  2. it takes a more substantial pressure to bring about the same change in volume
  3. when you’re closer to the y axis (closer to FRC)
  • End of INSIPRATION = DECREASE in pleural pressure (MORE NEGATIVE)
  • End of EXPIRATION = FRC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Q: What is transrespiratory system pressure?

A

A: the lung and chest wall combined when they are stuck together and interacting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Q: How is lung tissue connected to the chest wall? movement?

A

A: lung tissue and the chest wall have a pleural membrane and in between the membranes there is a sealed volume of pleural fluid and the two layers work as if they are holding hands tightly - if one layer is pulled in a certain direction, it will pull the other layer as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Q: What does the tension between the pleural membrane layers change according to?

A

A: tension between the two layers will increase or decrease depending on whether there is a pulling force (end of inspiration/start of expiration) or a pushing force (end of expiration/start of inspiration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Q: Describe the relationship between the chest wall and lungs at FRC. Pressure? Air movement?

A

A: At FRC (zoom in on the top left lung schematic) the lungs are pulling in and the chest wall is pushing out the same amount so there is negative pressure in the middle because the pleural layers are being pulled in both directions and hence there is negative pressure (a little vacuum)

Because the Transrespiratory Pressure (between outside and inside) is ZERO, there is NO NET MOVEMENT OF AIR at FRC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Q: Describe the air movement at the end of tidal inspiration. Pleural pressure compared to FRC?

A

A: there is also no air movement because the transrespiratory system pressure is ZERO (like at FRC)

pleural pressure is MORE NEGATIVE than FRC because there is a greater recoil force on one side (the lung recoil inwards is greater than the chest recoil outwards)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Q: Why is expiration a passive process? What’s pleural pressure at the end?

A

A: due to the natural tendency of the lungs to recoil inwards to at the end of expiration, pleural pressure will return to the same pressure as it was at FRC (-5 mm Hg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Q: How can you make the pressure more positive than FRC?

A

A: if you do FORCED expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Q: Draw and describe how a pressure (x)-volume (y) graph (flow rate graph) changes when obstructive and restrictive.

A

A: REFER: similar shapes (obstructive is above normal and restrictive below)

The default point for restrictive lung disease is lower = all lower and need much more pressure to achieve more volume

The default point for obstructive lung disease is higher = all higher up and not as wide

  • apply small pressure and get larger volume
  • has lost compliance and recoil

The FRC is different in both restrictive (lower) and obstructive (higher)
-lost elasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Q: Draw a graph for volume and pressure (y) by time (x) for alveoli. Add pleural pressure line.

A

A: REFER

  • volume is normal distribution curve (volume change)
  • pressure is a trig graph starting at mid going down (flow rate matches this graph)

REFER (inhale and gets more neg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Q: What does alveolar pressure follow? why?

A

A: the flow rate because the flow rate is dictated by two pressures (atmospheric (which we can’t change) and alveolar pressure) - so to ventilate we either need to create positive outside pressure or negative inside pressure

Therefore, the flow changes depending on how WE change alveolar pressure

NOTE:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Q: Does change in alveolar pressure cause the change in flow rate or does change in flow rate change alveolar pressure?

A

A: change in alveolar pressure CAUSES the change in flow rate, not the other way around

17
Q

Q: Describe how alveolar pressure and volume changes in a breath. (4)

A

A: -begin with pressure at 0 mm Hg and a comfortable volume

  • respiratory muscles work to expand chest wall and increase capacity of thoracic cavity -> create NEGATIVE pressure inside which makes air flow in
  • alveoli fill up with gas -> return to equilibrium (third image) so there is no pressure difference (this is what happens when you take a deep breath in and hold in)
  • at start of expiration, you release tension in inspiratory muscles that were being used to hold your breath - it compresses gas molecules (fourth image) and creates a positive pressure which forces the air out and then you’re back where you started
18
Q

Q: Name 2 structural properties of lung tissue. Define. Eqn?

A

A: Compliance = willingness of a structure to change shape when pressure is applied (tendency to distort under pressure (change in vol over change in pressure)

Elastance is the OPPOSITE = tendency of something to recoil to its original volume (change in pressure over change in vol)

elastance graph has steeper balloon (vol is x axis)
compliance graph has steeper condom (pressure is x)

19
Q

Q: What is the difference between air filled and fluid filled lungs in terms of:

inflation?
compliance?
reason?

A

A: -harder to INFLATE (more pressure needed) than to deflate fluid filled lungs

-When lungs are fluid-filled they are much more compliant than when air-filled

EXPLANATION: There is a small amount of water lining the lungs (surfactant) and the air-water interface exhibits SURFACE TENSION whereas the fluid-water interface does NOT exhibit surface tension

20
Q

Q: In terms of a pressure volume graph, how do air filled and fluid filled lungs differ? Draw. What did this lead to?

A

A: for fluid filled: changes in pressure in relation to volume for inflation and deflation do NOT overlap

REFER (anticlockwise)

fluid filled lungs require less pressure to change volume

Fluid filled lungs are more compliant than airfilled lungs
-possibly due to surface tension

21
Q

Q: What creates surface tension? (3)

A

A: The water molecules all interact

At the top layer, there is air on one side so there is no matching force on one side

This makes some of the upper water molecules disappear down and causes a tension across the top - the molecules come under strain

22
Q

Q: Describe surface tension in alveoli. (2) Small alveolus?

A

A: Because of the shape of the alveoli, the distribution of water is more dense around the outside

On the inside, the water molecules are all attracted across the alveolar space to water molecules on the opposite side

This means that if the alveolus is too small, these forces will pull the alveoli together and collapse them

23
Q

Q: What produces surfactant? function? how? What’s it made of? (3)

A

A: Type II Pneumocytes produce SURFACTANT which breaks up the surface tension

surfactant splits the water molecules on the surface and reduces the surface tension between them

80% polar phospholipids; 10% non-polar lipids; 10% protein

24
Q

Q: 3 advantages of surfactant. Eqn.

A

A: prevents collapse of small airways

INCREASES COMPLIANCE (it changes the change in volume you achieve per unit change in pressure)

reduces work of ‘breathing’

law of laplace: pressure= 2T/r

25
Q

Q: Describe airflow in obstructive lung diseases. What volume is the lung operating at? Chronic causes? (3) Acute cause? How has residual volume changed?

A

A: The flow of air into and out of the lung is OBSTRUCTED

Lungs are operating at higher volumes
Chronic causes:
COPD
  Emphysema
  Bronchitis

Acute causes:
Asthma

RV increases due to air trapping and bronchitis, inflation

26
Q

Q: Describe airflow in restrictive lung diseases. What volume is the lung operating at? Chronic causes? (2) Acute causes? (2) How has residual volume changed?

A

A: Infaltion/deflation of the lung or chest wall is restricted

Lungs are operating at lower volumes

Pulmonary causes:
Lung fibrosis
Interstitial lung disease

Extrapulmonary causes
Obesity
Neuromuscular disease

much lower (all volumes have increased by around 60/70%)

27
Q

Q: How does pleural pressure change if you expire more? inspire more?

A

A: less negative

more negative

28
Q

Q: How does ventilation vary in a lung? Describe the alveoli, pleural pressure, transmural pressure.

A

A: upper part
P(PL)(pleural pressure) is more negative (-8 cmH2O)
Greater transmural pressure gradient (0 vs. -8)
Alveoli larger and less compliant
Less ventilation

lower
PPL is less negative (-2 cmH2O)
Smaller transmural pressure gradient (0 vs. -2)
Alveoli smaller and more compliant
More ventilation
29
Q

Q: How does perfusion vary in a lung? Describe the intravascular pressure, recuitment, resistance and flow rate.

A

A: upper part
Lower intravascular pressure (gravity effect)
Less recruitment (has more capacity for it)
Greater resistance
Lower flow rate

lower
Higher intravascular pressure (gravity effect)
More recruitment
Less resistance
Higher flow rate
30
Q

Q: What does conductance refer to? Show a 3 axis graph.

A

A: how willing a set of tubes is to carry a volume of air

x= volume, y on left is compliance and on right is resistance

resistance line goes down in curve

conductance is straight x=y line less steep

31
Q

Q: What does patent mean? Comparing pressures in collapsible airways.

Preinspiration.
Midinspiration.
End inspiration.
Forced expiration.

Hence?

A

A: means open-> air can travel through (describes airways)

o -5 pleural= +5 -> patent airway
o -8 pleural (being pulled out) compared to -2 in airway transmural = 6 -> patent
o -8 and 0= 8 -> patent

o +22 pleural and +20 transmural -> collapsed
=> hence airways have cartilage support

32
Q

Q: What is resistance equal to?

A

A: inversely to r^4

33
Q

Q: What is ventilation caused by? by? (2)

Differentiate the determinants of ventilation between fluid- and air- filled lungs.

A

A: ventilation is caused by a pressure gradient between the atmosphere and alveoli, caused either by external positive pressure or internal negative pressure

inflation and deflation require less pressure in fluid-filled lungs due to elimination of air-water interface

34
Q

Q: Explain the pressure-volume relationship for inspiration and expiration in a healthy individual and patients with obstrucuive/ restrictive disease.

A

A: the pressure volume curve is sigmoid-shaped; large changes in volume per unit pressure at middle volumes and small changes in volume per unit pressure towards RV and TLC

obstructive diseases operate at higher volumes, and greater changes per unit change in pressure

restrictive diseases operate at lower volumes and involve considerably higher pressures to inflate lungs (especially at high volumes)

35
Q

Q: Explain the role of surfactant in ventilation and lung structure.

A

A: surface tension of pulmonary fluid is a contributor to the recoil of the lung (and resistance to expansion) surfactant helps to reduce surface tension and increases compliance of the lung

36
Q

Q: Explain the concept of airway resistance in the lung.

A

A: resistance is highest in the medium-sized airways

airway resistance is lower at higher volumes because the airways also dilate

37
Q

Q: Explain how flow in collapsible tubes influences pulmonary function.

A

A: excessive intrapleural pressures can collapse bronchial structures largest airways supported by cartilage, smaller airway collapse has fewer effects