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Pulmonary Week 1 > Waters II > Flashcards

Waters II Flashcards

1
Q

What is the major muscle of inspiration?

A

the diaphragm

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2
Q

How much does the diaphragm move during tidal inspiration?

A

1cm down

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3
Q

How much does the diaphragm move during forced inspiration?

A

up to 10cm

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4
Q

What nerve innervates the diaphragm?

A

the phrenic nerve

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5
Q

What accessory muscles help in inspiration?

A
  • External intercostals (I for E and E for I),
  • Scalenes, and
  • SCM
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6
Q

How does expiration occur normally?

A

passive (no muscles)

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7
Q

How does forced expiration occur (what muscles?)?

A

abdominal muscles (rectus abdominus, internal and external obliques, transverse abdominus) and internal intercostals work

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8
Q

What happens to intra-pleural pressure during inspiration?

A

it becomes more negative and transpulmonary pressure increases

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9
Q

What is transpulmonary pressure?

A

Palveolar-Pintrapleural

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10
Q

What does an increase in transpulmonary pressure cause?

A

increased lung expansion

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11
Q

How does lung expansion affect Palveolar?

A

it becomes sub-atmospheric

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12
Q

What happens when Palveolar becomes sub-atmospheric?

A

air flows into alveoli

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13
Q

T or F. Pintrapleural becomes less negative during inspiration

A

F. It becomes more negative

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14
Q

When is Palveolar most negative?

A

Mid-inspiration

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15
Q

When is Palveolar most positive?

A

Mid expiration

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16
Q

What happens with Palv- Patm is negative?

A

inspiration

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17
Q

Why is Pintrapleural negative?

A

There is a natural tendency for the chest wall to pull out and for the lung tissue to collapse

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18
Q

The degress to which transpulmonary pressure (Palv- Pip) leads to lung expansion depends on ____ of the lung.

A

compliance (compliance= 1/elasticity)

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19
Q

T or F. Compliance changes during parts of inspiration (and expiration)

A

T. It is not constant or linear, nor is compliance the same during inspiration as it is during expiration

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20
Q

Why do compliance patterns differ from inspiration to expiration?

A

hysteresis (surfactant properties control this)

21
Q

What pathologies can decrease compliance of the lungs (this is considered ‘restrictive’)?

A
  • fibrosis
  • pulmonary edema

these patients have trouble getting air IN to the lungs and EXPANDING them

22
Q

What pathologies can increase compliance of the lungs (‘this is considered obstructive’)?

A
  • emphysema
  • some in normal aging

these patients have trouble getting air OUT of the lungs

23
Q

When compliance increases, ____ becomes more likely

A

lung collapse

24
Q

T or F. Restrictive lung patients have decreases capacities and volumes (FVC, TLC, RV, FRC)

A

T.

25
Q

T or F. Obstructive lung patients have decreases capacities and volumes (FVC, TLC, RV, FRC)

A

F. Increases FRC, TLC, FEV1 and RV, but normal or reduced FVC

26
Q

What does the term COPD encompass?

A

emphysema or chronic bronchitis

27
Q

80-90% of COPD cases are caused by what?

A

smoking

28
Q

What happens in emphysema?

A

destruction of alveolar walls due to loss of elastic material (increased compliance) and enlargement of alveolar air spaces which decreases surface area for gas exchange

29
Q

What happens when elastic material is lost from lung tissue?

A

the lungs struggle to stay open during forced expiration

30
Q

What causes chronic bronchitis?

A

inflammation where the airways become obstructed due to excessive mucus production

31
Q

What changes are seen in Pip at the end of inspiration in emphysema patients?

A

less negative Pip than normal due to loss of elastic fibers

32
Q

Lung compliance is determined by what main factors?

A
  • tissue properties

- surface forces

33
Q

What is interdependence?

A

The fact that adjacent alveoli share a wall prevents them from collapsing

34
Q

Tissue properties (collagen, elastin, etc.) account for approx. ___ of the compliance of the lung

A

1/3

35
Q

What is the role of pulmonary surfactant?

A

It acts as a detergent to reduce water molecule surface tension that tends to act to promote collapse of alveoli.

NOTE: Surface tension must also be overcome to expand the lungs

36
Q

What produces surfactant?

A

Type II pneumocytes

37
Q

What stimulates surfactant production?

A

large expansion of the lungs

38
Q

What happens in respiratory distress syndrome (RDS) of newborns?

A

reduced surfactant production (which occurs late in gestation) makes lung inflation difficult

39
Q

T or F. Compliance is increased in RDS

A

F.

40
Q

What is another potential consequence of RDS

A

Alveoli tend to collapse upon expiration (aka atelectasis)

41
Q

How is RDS treated?

A

mechanical ventilation and surfactant replacement therapy

42
Q

What is the transmural pressure needed to keep an alveoli open?

A

2*Tension/radius of sphere

Laplace’s law

43
Q

Atelectasis is a common complication of anesthesia, why?

A

it reduced surfactant function

44
Q

Resistance to air flow decreases drastically in the respiratory airways compared to conducting airways even though radius decreases substantially. Why?

A

Because the cumulative radius is higher

45
Q

What is lateral traction?

A

elastic connective tissue fibers attach to airways exterior and pull outward, tending to open airways

46
Q

What happens in asthma?

A

bronchioles constrict via inflammation

47
Q

Where is Pip most negative in the lung?

A

at the apical parts

48
Q

Where is resistance to flow highest in the lungs?

A

medium-sized bronchi, even as radii decrease moving toward alveoli, the flow becomes more laminar

Pulmonary Week 1 (17 decks)

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