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MD3001resp > Ventilation: Physics Of Breathing > Flashcards

Ventilation: Physics Of Breathing Flashcards

1
Q

What is the function of ventilation?

How is this achieved?

A

Function = to provide O2 to the tissues and remove CO2

Achieved by:
- pulmonary ventilation (movement of air from atmosphere to alveoli)
- regulation of ventilation
- matching of pulmonary blood flow to alveolar ventilation
- Movement of O2 and CO2 between alveoli and blood
- transport of O2 and CO2 in the blood and body fluids

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2
Q

What are the non-respiratory functions of ventilation?

A
  • expulsion of foreign body
  • defence against infection/disease
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3
Q

what does pulmonary ventilation do?

what is alveolar ventilation?

what happens to some of the air that we breathe in?

what is anatomical dead space?

A

1- pulmonary ventilation will renew the air in gas exchange areas

2- alveolar ventilation is the rate at which new air reaches these areas

3- not all of the air that we breathe in reaches alveolar ventilation areas because it fills the respiratory passage (anatomical dead space)

4- anatomical dead space is the total volume of the air in the conducting airway from nose to the terminal bronchioles.

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4
Q

equation for minute (total) ventilation rate?

equation for alveolar ventilation rate?

A

minute (total) ventilation rate (Ve) = Freq x Vt

alveolar ventilation rate (Va) = Freq x (Vt - Vd)

Va= volume of alveolar ventilation per minute
Freq= frequency of respiration per minute
Vt= tidal volume
Vd= dead space volume

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5
Q

what are the normal values for:

Frequency of breathes?
Vt (tidal volume)?
Vd (dead space volume)?
therefore…. using the alveolar ventilation rate equation, what is Va?

A

Frequency = 12 breathes/min
Vt= 500ml
Vd= 150ml

therefore Va= 12 x (500-150)
= 4200ml/min

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6
Q

what is alveolar ventilation one of the major determinants of?

A

alveolar ventilation is one of the major factors determine O2 and CO2 concentrations in alveoli

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7
Q

what are the 4 most important muscles in raising the rib cage?

A
  • external intercostals
  • sternocleidomastoid (lifts upwards on sternum)
  • anterior serrati (lift many ribs)
  • scaleni (lift first two ribs)
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8
Q

what are the 2 most important muscles that lower the rib cage? (forced expiration)

A
  • abdominal recti
  • internal intercostal
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9
Q

what are the 2 ways lungs can be expanded?

what way does normal quiet breathing use?

what happens during heavy breathing?

A

1- 1st way = downward and upward movement of diaphragm to lengthen or shorted chest cavity

2nd way = elevation and depression of the ribs to increase or decrease anteroposterior diameter of chest cavity

2- normal quiet breathing is entirely by 1st method.

3- during heavy breathing, the normal elastic recoil is not quick enough so we need contraction of abdominal muscles too.

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10
Q

what are the static properties of the lungs?

how do the lungs float ion the thoracic cavity?

describe how the suction effect of lungs held against the thoracic wall is achieved?

A
  • the lungs always want to contract when there is no force to keep them inflated (elastic recoil)
  • the ribs always want to be pulled out
  • lungs are not directly attached to chest wall
  • lungs float on the thoracic cavity surrounded by thin layer of pleural fluid that acts as a lubricant
  • lymphatic drainage of excess fluid between lung pleural membrane and pleural surface of thoracic wall leads to suction effect, lungs will be held against thoracic wall.
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11
Q

what happens if air gets into this space between the 2 pleural membrane layers?

will this effect both lungs?

A

you will get an increase in pressure which allows the lungs to move away from the chest wall = pneumothorax

this will not effect both lungs because they are in isolation of each other in their own membranes.

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12
Q

what happens to the recoil in flail chest?

A

we have lost the recoil of the lungs which will be seen in a pneumothorax as they move away from the chest wall.

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13
Q

what is intrapleural pressure?

how will it vary?

A
  • this is the pressure of fluid in thin space between lung pleura and chest wall pleura- slight negative pressure
  • it will vary over the length of the lungs
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14
Q

pressure changes during inspiration:

at the start of respiration, what will plural pressure be at?

what changes happen during inspiration?

what does this cause?

A
  • -5cm H20
  • during inspiration, expansion of the chest cage pulls lungs outward so negative pressure increases to -7.5cm H20
  • air is sucked into lungs
  • process is reversed in expiration(-7.5 to -5 cmH2O)
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15
Q

what does the negativity of the intrapleural pressure do?

A

it stops the lungs from collapsing.

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16
Q

what is alveolar pressure?

what is the pressure like in the respiratory when the glottis is open and there is no air flowing? (we just have out mouth open)

how is this different to what happens during inspiration?

A

alveolar pressure = the pressure of the air inside he lung alveoli

  • when the glottis is open and no air is flowing, pressure in all parts of the respiratory tree is equal to atmospheric pressure (0 cmH20)
  • during inspiration and chest wall expansion, alveolar pressure decreases to about -1cm H20, pulling 500ml of air into the lungs
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17
Q

what happens to the alveolar pressure during expiration?

A

the alveolar pressure will increase from -1cm H20 to just above 0cm H20 (as diagram is pushing air out of the lungs) then it will move back down to 0cm H20

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18
Q

what is trans pulmonary pressure?

what is it a measure of?

A

this is the pressure difference between that in the alveoli and that on the outer surface of the lungs

it is a measure of the elastic recoil that tend to collapse the lungs (recoil pressure)

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19
Q

what is total volume?

what would a normal tidal volume be?

A

tidal volume = the volume of air inspired or expired with each normal breath

normal volume would be 500ml in expiration and 500ml in inspiration

20
Q

during inspiration, what will intraplueral pressure drop to?

what is the decrease in intra pulmonary pressure?

A

intra pleural pressure drop = approx -7 mmHg

decrease in intrapulmonary pressure by = approx -1 mmHg

21
Q

overview of quite expiration:

why type of movement is it?
how much does volume decrease by?

what happens to the intrapulmonary pressure?
what gradient does air move?

A
  • quite respiration is passive with no direct muscle action
  • relaxation of muscle contraction
  • elastic recoil (drives air out of lungs)
  • thoracic volume decreases by 500ml
  • intrapulmonary pressure increases
  • air moves down a pressure gradient
22
Q

describe muscle action on forced expiration?

A
  • contraction of abdominal walls
  • forces abdominal contents up against diaphragm and intercostals
  • pulls ribs down
23
Q

in dynamic lung mechanisms:

energy is required to do what?

A
  • contract the muscles of inspiration
  • stretch elastic elements
  • overcome airway resistance (mucus etc)
  • overcome frictional forces arising from the viscosity of the lung and chest wall
  • overcome inertia of the air and tissues
24
Q

what is the equation for air flow?

what does the equation for ir flow tell us tell us?

A

this equation tells us the amount of air that flows is determined by the change of pressure divided by resistance.

25
Q

what has the greatest effect on airway resistance?

what is the equation for Poiseuile Law?
what does it tell us?

A

airway radius

poiseuile law tells us that the airway radius has greatest effect on airway resistance, as radius it to the power of 4, meaning small changes in radius will drastically alter airway resistance.
smaller radius = more resistance to flow.

26
Q

where is turbulent flow likely to occur?

where is the greatest resistance to airflow found?

what is flow and resistance like in the smallest airways?
why is this?

A
  • turbulent flow is likely to occur with high velocities and larger diameter airways.
  • the greatest resistance to airflow is found in the segmental bronchi (cross sectional area relatively low and airflow high and turbulent
  • in the smallest airways, flow is laminar and resistance is small (there is a large cross sectional area due to a large umber of small airways combined)
27
Q

what is static compliance?

what does a high static compliance mean ?

A
  • static compliance = is the extent to which the lungs will expand for each unit increase in trans pulmonary pressure (given time to reach equilibrium)
  • a high static compliance means that the lungs will expand easier
28
Q

what is elastance?

A

The elastanse = the elastanse of the lungs (measure of the elastic recoil) is the reciprocal of the compliance (E=1/C)

High compliance means low elastic recoil.

29
Q

what are the 2 elastic forces that determine compliance?

A

1- elastic forces of the lung itself
- determines mainly by elastin and collagen fibres among lung parenchyma
- deflated lungs, fibres are contracted and kinked
- expanded lungs, fibres become stretched and unkinked

2- elastic forces caused by surface tension of fluid that lines alveoli.

30
Q

what are 3 lung conditions that effect compliance?

A

1- pulmonary fibrosis (compliance is reduced due to a lot of fibrous tissue so more difficult to inflate lungs)

2- Emphysema (broken down elastic tissue in the lungs, no elastic recoil)

3- COPD

31
Q

explain compliance changes in Pulmonary fibrosis?

A
  • disease process that causes deposition of fibrous tissue, so lungs become stiff
  • lung compliance is decreased, resulting in smaller than normal changes in lung volume for small changes in trans pulmonary pressure.
  • patients breathe more shallowly and rapidly
  • decreased Residual volume
    decreased functional residual capacity
    decreased total lung capacity
32
Q

explain the complaint changes in emphysema?

A
  • common consequence of smoking
  • alveolar and capillary walls progressively destroyed, particularly elastic tissue
  • lung compliance is increased, resulting in larger the normal changes in lung volume for small changes in transpulmonary pressure
  • as airways tend to collapse on expiration airway resistance is also increased
  • patients breathe more slowly and deeply

increased residual volume
increased functional residual volume
increased total lung capacity

33
Q

describe the changes in compliance of chronic bronchitis?

A
  • mucus and airway inflammation produce an increase in airway resistance
  • increase in residual volume
    increase in functional residual volume
    increase in total lung capacity
    HOWEVER ,,
    compliance is normal
34
Q

spirometry?

A

spirometry is a method for studying pulmonary ventilation

35
Q

inspiration reserve volume?

A

inspiration reserve volume is extra volume of air that can be inspired over and above tidal volume (2500ml)

36
Q

expiratory reserve volume?

A

expiration volume is max extra volume of air that can be expired by forceful expiration after end of normal tidal expiration (1100ml)

37
Q

residual volume?

A

residual volume is the volume of air remaining in lungs after most forceful expiration (1200ml)

38
Q

what is surface tension a measure of?

in the lungs, what will surface tension result in?

A

surface tension is a measure of the force acting to pull a liquid’s surface molecules together at an air-liquid interface.

  • in the lungs this results in the alveoli trying to force the air out of them so the smaller alveoli will collapse
39
Q

what is LaPlaces law?

how does this work in 2 connected alveoli of different diameters?

A
  • Law of LaPlace states that the pressure (P) within a vessel is proportional to the tension divided by the radius
    (air will move from smaller to larger diameter due to surface tension)
    P= T/R
  • therefore if there are 2 connected alveoli with different diameters, air will move into the larger alveoli from the smaller one.
40
Q

how are smaller alveoli stopped from collapsing?

A

because the body produced Surfactant.

41
Q

what is th main role of surfactant?

how does it decrease surface tension?

how does this effect compliance of alveoli?

A
  • reduce surface tension of H20
  • increasing compliace, making it easier to inflate the lungs.
  • by reducing surface tension you will be minimising fluid accumulation in the alveoli.
  • surfactant will help tokeep the alveoli uniform throughout the cycle
  • reduces atelactasis (alveolar collapse)
42
Q

how is surfactant produced?

A

1- lipid components enter type 2 from blood stream
2- surfactant will then be secreted by these type 2 alveolar epithelial cells

43
Q

what are the 2 types of lung epithelial cells?

A

type 1alveolar cell = permits diffusion

type 2 alveolar cell = produces surfactant that reduces the tendency for pulmonary alveoli to collapse

44
Q

how what surfactant a mixture of?

A

1- it is a complex mixture of phospholipids:
- DPPC
- proteins (surfactant apoproteins, SP-A, SP-B, SP-C, SP-D)
- ions (calcium)

45
Q

how does surfactant get taken up into the cells?

how is surfactant degraded and recycled?

A

part of the DPPC molecule dissolves in fluid while the rest spreads over surface of fluid

  • alveolar macrophages help in degrading surfactant
  • type 2 cells take up particles and recycle or destroy it.

MD3001resp (41 decks)

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