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CVPR > CVPR Week 5: Mechanics of breathing > Flashcards

CVPR Week 5: Mechanics of breathing Flashcards

1
Q

Objectives

5 listed

A
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2
Q

Congenital central hypoventilation syndrome genetics

A

PHOX2B gene

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3
Q

Congenital central hypoventilation syndrome clinical features

A

if you fall asleep you stop breathing

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4
Q

Identify symbols

A
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5
Q

Identify

A
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6
Q

Identify

A
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7
Q

Identify

A
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8
Q

The lungs have how many attachments to the body?

A

1 . . . the Hilum

the lungs are otherwise free-floating in the pleural space

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9
Q

What is in between the chest wall and the lungs?

A

pleural membranes Parietal pleura of the chest wall and the visceral pleura of the lung

and

intrapleural fluid

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10
Q

Intrapleural fluid function

A

helps hold the parietal and visceral pleural membrane together providing surface tension and also lubricates them to ease sliding

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11
Q

Intrapleural fluid location

A

in between the visceral pleura of the lung and the parietal pleura of the chest wall

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12
Q

Gases move in and out of the lung by?

A

Bulk flow

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13
Q

How are CO2 and O2 exchanged in the lungs?

A

Diffusion

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14
Q

Gasses dissolved in the blood are transported via?

A

Bulk flow

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15
Q

How are CO2 and O2 exchanged in the tissues?

A

Diffusion

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16
Q

~ Surface area of the lung available for diffusion

A

about one half of a tennis court

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17
Q

Identify

A
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18
Q

Factors that influence the speed of diffusion

6 listed

A
  • surface area
  • distance traveled (thickness of membranes)
  • partial pressures
  • temperature
  • solvent density
  • mass of the solute
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19
Q

Identify

A

A = Alveoli

RB = Respiratory bronchioles

TB = Terminal bronchioles

AD = Alveolar ducts

Macrophage is here also

Type II pneumocytes make surfactant

C = capillary

PA = Pulmonary artery

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20
Q

Pulmonary function testing can measure?

A

Lung volumes and capacities

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21
Q

What is spirometry?

A

a pulmonary function test that measure volumes and capacities

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22
Q

What cannot be measured with simple spirometry?

3 listed

A
  • TLC
  • FRC
  • RV
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23
Q

TLC AKA

A

Total lung capactity

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24
Q

FRC AKA

A

Functional residual capacity

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25
Q

RV AKA

A

Residual volume

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26
Q

What is tidal volume

A
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27
Q

What is inspiratory reserve volume?

A
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28
Q

What is the expiratory reserve volume?

A
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29
Q

What is the residual volume?

A
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30
Q

What is the vital capacity?

A
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31
Q

What is the inspiratory capacity?

A
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32
Q

What is the functional residual capacity?

A
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33
Q

What is the total lung capacity?

A
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34
Q

Question 1

A

C)

Contraction of the diaphragm decreases Pip with increases the transmural pressure gradient, expanding the alveoli, the larger alveoli now has a subatmospheric pressure creating a gradient for air flow

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35
Q

What is the mechanism of normal quiet breathing?

A

Inspiration is from the contraction of the diaphragm creating a sub-atmospheric pressure change driving air in

Expiration is caused by the relaxation of the diaphragm pushing the air out

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36
Q

What is the transmural pressure gradient?

A

P alv - Ppl = transmural pressure

It is the pressure gradient and determines the volume of the lung (distending pressure of the alveoli)

Palv = alveolar pressure

Ppl = interpleural pressure

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37
Q

What is the pressure gradient driving air flow?

A

Palv - Pbs(ao) = the pressure gradient driving air flow

Palv = alveolar pressure

Pbs(ao) = body surface or atmospheric

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38
Q

PV = nRT therefore?

A

Pα = 1/V

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39
Q

What pressure gradient determines the volume of the alveoli?

A

Transmural pressure

Palv - Pbs(ao) = the pressure gradient driving air flow

Palv = alveolar pressure

Pbs(ao) = body surface or atmospheric

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40
Q

The chest wall is always pulling in which direction?

A

out away from the lungs

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41
Q

The lung is always pulling in which direction?

A

inwards

when cadaver the association with the chest wall is gone and the lungs retract and recoil

42
Q

Increasing alveolar volume does what?

A

decreases Palv sucking air into the lung

43
Q

intrapleural pressure changes

A
  • 5 mmHg to -8mmHg …. etc should be more
44
Q

What defines these volumes?

TLC

FRC

RV

A

Mechanical recoil forces of the lung and chest wall establish these volumes

outward forces of the chest wall, muscles of inspiration

vs

how much inward recoil force of the lung

45
Q

How is the TLC defined?

A

When the total outward forces match those of the inward recoil force of the lung

(Force out = force in ) = TLC

46
Q

How is FRC defined?

A

Functional residual capacity is in between breaths

where the inward recoil of the lung is exactly equal and opposite the outward forces of the chest wall

47
Q

How is RV defined?

A

when the recoil of the lung is equal and opposite the forces of the muscles of expiration and chest wall

48
Q

When does the transmural pressure point become negative?

A

Just after the equal pressure point (EPP) the transmural pressure becomes negative

49
Q

Why do the pressures going away from the alveoli decrease?

A

because there is resistance to flow

50
Q

Pressures of passive expiration vs forced expiration

A

trachea cartilage holds it open

51
Q

Losing some recoil of the lung in?

A

Emphysema - you lose some elastic tissues so there’s less recoil force

also increasing resistance through a process called (lateral infraction?)

52
Q

Emphysema EPP

A

in ephysema, elastic tissues are lost so there is also loss of recoil of the lung

the EPP migrates closer to the alveoli and away from the cartilaginous rings so the air ways collapse

53
Q

Question 2

A

increase because the lung can collapse in emphysema

if it decreased then the lung would stiffen and probably not collapse

54
Q

Compliance curve of the lung

A

transpulmonary pressure vs volume

55
Q

ΔV / ΔP =

A

Compliance

56
Q

The steeper the compliance slope the. . .

A

easier it is to expand the lung

57
Q

Restrictive lung diseases

A

Interstitial fibrosis (“scar tissue”) make lungs stiffer - more muscular work

58
Q

Obstructive lung diseases

A

Diseases that destroy elastic tissue (e.g. emphysema) make the lung more compliant

59
Q

Compliance of restrictive lung diseases

A

greater changes in pressure are required to expand the lung

Requires more work

Also

FRC changes to breathe from smaller lung volumes (makes sense so they can do less work)

60
Q

Compliance of obstructive lung diseases

A

smaller changes in pressure are required to fill the lungs

less work is required to breath

FRC changes to a higher capacity (because exhaling is a passive process which requires the lung to be an elastic organ, so a higher capacity, also to facilitate expiration in the absence of elastic tissue)

61
Q

Lung volumes in obstructive and restrictive lung diseases

A
62
Q

Explain this graph

A

in the saline-filled lung, there is no air fluid interface so you don’t have to fight against the forces of surface tension in the lung

In the air-filled lung, there is an air-fluid interface so the surface tension forces must be overcome to inflate the lung

63
Q

La Place’s Law equation

A

P = 2T/r

64
Q

Explain La Place’s Law

A

helps us relate the pressure inside a sphere to the surface tension and the size of that sphere

smaller spheres would have higher pressure than larger alveoli

65
Q

Why don’t we just have 1 big alveolus due to smaller alveoli pushing their air into the larger

A

pulmonary surfactant allows us to have different sized-alveoli and avoid the collapsing alveoli problem

because the surface tension that is produced is area dependent

66
Q

What happens with surfactant deficiency?

A

requires a lot of pressure to open the lungs

67
Q

old term of surfactant deficiency

A

hyalin membrane disease

68
Q

Identify

A
69
Q

What is surfactant composed of?

A

mostly DPPC lipid

also have proteins

70
Q

Where is surfactant made?

A

in the lung by type II pneumocytes

71
Q

Identify

A
72
Q

Surfactant protein SP-A/SP-D

A
  • Involved in the unraveling of lamellar bodies
  • host immune response
73
Q

Surfactant protein SP-B/SP-C

A

Optimize rapid absorption and spreading of phospholipids on the alveolar surface

74
Q

Surfactant small hydrophobic proteins

A

SP-B and SP-C

75
Q

Surfactant lung collectins

A

SP-A and SP-D

76
Q

Surfactant proteins and functions

A
77
Q

Regulation of surfactant secretion

4 listed

A
  • Gestational age
  • β-adrenergic and ATP-mediated activation of purinergic receptors
  • Signaling pathways involve changes in intracellular Ca2+ as well as activation of PKA and PKC
  • Mechanical distention (sigh and exercise)
78
Q

Question

A
79
Q

Total work in the lung

A

work to overcome recoil (elastic/surface tension) forces (lung and chest wall) + Resistive work (tissue and AIRWAYS) but also friction

friction between the lung and the chest wall (minimized by intrapleural fluid) + frictional resistance of air moving in airways (primary)

80
Q

Resistance of air moving in airways equation

A
81
Q

Where is the site of greatest resistance along the respiratory tree?

A

in the tertiary bronchi?

82
Q

Resistance along the respiratory tree

A
83
Q

Resistance is low in the terminal bronchioles because

A

parallel resistances and smaller lengths

84
Q

Lung volume and airway resistance and why?

A

as the lung is expanded airway resistance decreases

  • the transmural pressure gradient also affects smaller airways
  • lateral traction
    *
85
Q

Lateral traction

A

airway is surrounded by alveoli

when the alveoli expands it wants to return back to its original shape and pulls out on the airway causing lateral traction

this is partly why resistance is increased in emphysema because loss of tissue results in loss of these phenomenon

86
Q

Bronchial smooth muscle tone and airway resistance

A
87
Q

CO2 effect on bronchial smooth muscle

A

cause the bronchial dilation

88
Q

innervation bronchial smooth muscle

A

β2 adrenergic activation causes dilation

vagal cholinergic causes constriction

89
Q

bronchial smooth muscle reflex

A

chemical irritants, smoke, dust (reflex response) mediated by parasympathetic cholinergic pathways

90
Q

Question

A
91
Q

Question

A
92
Q

To inflate the lung you must over come these intrinsic forces

A
93
Q

What can modify airway resistance?

A

airway obstruction and reduced lateral traction

94
Q

Elastic work vs frictional work

A
95
Q

compliance curves in normal, fibrosis and asthma/chronic fibrosis

A
96
Q
A
97
Q

Functions of the respiratory system outside of breathing

4 listed

A
  • Vascular reservoir
  • Acid-base balance
  • Defense mechanisms
  • metabolic functions of the lung
98
Q

The lungs as a Vascular reservoir

A

can have fluctuations in CO without huge changes in pulmonary pressre

pulmonary arteries are thin walled and distensible and expand their radius to buffer an increase in pressure

also

not every single pulmonary artery are receiving blood so you can recruit or stop using some to buffer changing pulmonary arterial pressures

99
Q

The lungs in acid-base balance

A

bicarbonate buffer system to eliminate CO2

the lung eliminates CO2 returning the blood back to steady state pH

100
Q

The lungs defenses

A

Filtration

mechanical filter cough or sneeze them out

microcirculation (remove emboli)

Immune defense mechanisms (example is pulmonary alveolar macrophages)

101
Q

Metabolic functions of the lung

A

Activation of ACE

Inactivation thorugh Bradykinin (ACE) ET-1 (ETb receptors)

102
Q

Lungs in speech

A

need air around vocal cords to make sound

CVPR (93 decks)

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