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RESP > Mechanics of breathing > Flashcards

Mechanics of breathing Flashcards

1
Q

1ᵒ function of respiratory system?

A

ventilate gas exchange surfaces by

moving air between alveoli + from atmosphere, via airways

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2
Q

Total Lung Capacity?

A

volume of air within lungs at end of max inspiration

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3
Q

Vital Capacity?

A

total volume of air an individual can breath in from max forced expiration to max forced inspiration

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4
Q

Tidal Volume?

A

air which enters + leaves lungs during normal breathing

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5
Q

Residual Volume?

A

volume of air remaining in the lungs after a maximum forced expiration

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6
Q

Expiratory Reserve Volume?

A

air that can be expired from the lungs by determined effort after normal expiration

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7
Q

Functional Residual Capacity?

A

volume of air within lungs at end of a resting/quiet expiration

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8
Q

Inspiratory Reserve volume?

A

-Volume of additional air that be forcibly drawn in at the end of normal tidal volume

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9
Q

What does total level of ventilation (total v of air inspired over time period) depend on?

A

v of air inspired

frequency of breathing per min(respiratory rate)

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10
Q

What’s V̇= Vt x f?

A

min v (mL) = tidal v (mL) x frequency (min⁻¹)

total v of air inhaled in all breaths over 1 min = v of air inhaled in each breath x number of breaths per min

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11
Q

What’s ‘dead space’ ?

A

air required to occupy the airways but doesn’t contribute to gas exchange

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12
Q

Why doesn’t 150ml of dead space air reach the alveoli?

A

1st to leave respiratory system at beginning of expiration

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13
Q

How do you calculate alveolar ventilation rate?

A

V̇a = (Vt - Vd) x f

Alveolar minute v(mL) = (tidal v - dead space v) x frequency per min

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14
Q

What’s alveolar minute v?

A

Total v of fresh air entering alveoli across all breaths over 1 min

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15
Q

What’s Boyle’s law?

A

P ∝ n/V

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16
Q

How’s movement of air between atmosphere + lungs achieved?

A

changing alveolar p

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17
Q

How’s alveolar p changes achieved?

A

contraction/relaxation of respiratory muscles

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18
Q

How’s the sealed pleural cavity stretched between the lungs + chest wall?

A

lungs recoil inwards + chest wall recoils outwards due to elastic properties

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19
Q

What happens if pleural cavity is stretched?

A

decrease p as greater volume but same number of molecules – gas or liquid cannot enter from adjacent area as the space is sealed

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20
Q

Why does the pleural cavity resist changes in v more?

A

filled w liquid

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21
Q

What’s negative p?

A

overall effect of the opposing recoil of the chest wall + lungs –> intrapleural p is naturally subatmospheric

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22
Q

What happens when there’s negative intrapleural p?

A

pull 2 pleura together - collapsing force

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23
Q

What happens when there’s positive intrapleural p?

A

pull 2 pleura apart - expanding force

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24
Q

What does chest wall recoil do?

A

pulls chest wall outwards + expand the thoracic

cavity

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25
Q

What does lung recoil do?

A

pull the visceral pleura inwards + compress lung

v

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26
Q

What forces determine if lungs expand or compress at

given time?

A

lung recoil
chest wall recoil
intrapleural p

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27
Q

When should the forces be equal?

A

between end of expiration + start of next inspiration

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28
Q

How inspiration begins?

A

-contraction of diaphragm
-pull parietal pleura outwards
-stretches pleural cavity
-decreasing intrapleural p –> negative
-force pulling 2 pleurae together increases > force
lung recoil
-visceral pleura pulled outward, expanding lung

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29
Q

How expiration begins?

A
  • relaxation of inspiratory respiratory muscles
  • decreased outward force acting on the parietal pleura -reduces force acting to stretch the pleural cavity,
  • increasing intrapleural p < lung recoil
  • visceral pleura pulled inward (along with the pleural cavity and parietal pleura)
  • decreasing lung v
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30
Q

How forced expiration begins?

A
  • abdominals actively contract to compress v of thoracic cavity
  • muscle contraction generates inward force on parietal pleura
  • compressing pleural cavity
  • more pronounced decline in lung v (speed + magnitude)
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31
Q

Inspiration?

A
  • diaphragm contract
  • increase in thoracic cavity v
  • more negative intrapleural p
  • outward force exerted on visceral pleura > inward recoil force
  • lungs expand increasing v
  • alveolar p < atmospheric p
  • air moves down p gradient via airways to alveoli
  • lungs expand
32
Q

Expiration?

A
  • diaphragm relax, lungs recoil
  • decrease in thoracic cavity v
  • increase in intrapleural p
  • lung v decreases
  • alveolar p > atmospheric p
  • air moves down p gradient into atmosphere deflating lungs
33
Q

When does the compression of lungs happen?

A

forced expiration

34
Q

What does the speed of airflow depend on?

A

p gradient

level of airway resistance

35
Q

How is intrapleural p naturally sub-atmospheric?

A

opposing recoil of chest wall + lungs

36
Q

Define pneumothorax

A

air entering pleural space

37
Q

Entry of air into the pleural cavity

A
  • loss of negative p
  • intrapleural p will increase until = atmospheric p
  • expansion of the pleural cavity which decreases lung v (collapses)
  • reduces intrapleural p changes during inspiration so lungs can’t expand
38
Q

What happens if there’s a loss of negative intrapleural p?

A

elastic recoil of chest wall + lungs no

longer resisted –>affected regions of lungs to collapse

39
Q

Ohm’s law?

A 
V = P/R
airflow = change in p/resistance
40
Q

What factors determine level of resistance?

A

cross sectional area of airway lumen

airflow pattern

41
Q

Hagen-Poiseuille + what does it show?

A

R ∝ 1/radius⁴

As radius of an airway decreases, resistance increases dramatically –> airflow decreases dramatically

42
Q

How does air flow in healthy airways?

A

laminar pattern

43
Q

How does air flow in obstructed airways?

A

turbulent pattern

44
Q

How does turbulence occur?

A

where high velocities of airflow are achieved (during forced breathing manoeuvres)
sudden decrease in luminal area (obstructed airways)

45
Q

What causes wheezing sound?

A

vibration generated by the turbulent airflow

46
Q

Define airway patency

A

state of being open/unobstructed

47
Q

What’s open airways are maintained by?

A

elastic fibres within airway wall

radial traction

48
Q

Why’s airway obstruction more noticeable during expiration?

A

during expiration, lung tissue+airways compressed

49
Q

What can reduce airway patency during forced expirations?

A

p differentials between the intrapleural space + airway

50
Q

What’s Spirometry + role?

A

measuring FEV₁/FVC ratio

quantifying airflow + level of airway obstruction present during breathing

51
Q

What does measuring FEV₁/FVC involve?

A

producing a max forced expiration into a

spirometer- measures v of air passing through over time

52
Q

What’s FEV₁ + corresponds to?

A

max v that’s expired during 1st second of a max forced expiration
how quickly air can pass via airways, reflects airway function + health

53
Q

Values of obstructive airway diseases?

A

reduction in FEV₁ (<80% expected value)

FEV₁/FVC ratio (<70%)

54
Q

Values of restrictive lung diseases?

A

reduction in FEV₁ + FVC (<80% expected value)

relatively normal FEV₁/FVC ratio (>70%)

55
Q

Why does restrictive lung diseases have a normal FEV₁/FVC ratio?

A

decrease in FEV₁ reflects an overall decrease in lung v rather than airway obstruction

56
Q

Define transpulmonary p

A

Ptp = Palv – Pip

diff between p within alveoli + intrapleural space

57
Q

Role of transpulmonary p?

A

determines level of force acting to expand/compress lungs

58
Q

Define compliance

A

how easily lungs can be distended

compliance = change in v/change in p

59
Q

What happens if there’s a higher compliance + eg?

A
  • less elastic recoil
  • less force required to inflate
  • ↑ v change per pressure change (↑gradient on v-p curve)
  • emphesyma (elastic degrades)
60
Q

What happens if there’s a lower compliance + eg?

A
  • more elastic recoil
  • more force required to inflate
  • ↓v change per pressure change (↓ gradient on v-p curve)
  • pul fibrosis (scar, fibrosis, collagen)
61
Q

Features of lung v-transpulmonary p curve?

A
  • gradient = lung compliance

- measurements taken when no airflow 0 (STEEP) = static compliance

62
Q

What’s dynamic compliance?

A

measurements taken in presence of airflow - gradient between end tidal inspiratory + end tidal expiratory points on v-p curve

63
Q

Features of v-p loops?

A
  • gradient of overall line from end of expiration to end of inspiration = compliance
  • area within loop = proportional to level of airway resistance generated
64
Q

Why would there be a greater area of v-p loop?

A

forced inspiration/expiration

airway obstruction

65
Q

What are the structures affect lung compliance ?

A

chest wall mechanics ↑
alveolar surface tension ↓
elastic fibres ↓

66
Q

How’s bubble formed?

A

water-air interface formed between lining fluid + pseudo-spherical alveolar airspace

67
Q

What happens within bubble?

A

surface tension due to H bonds between

water molecules –> collapsing force toward the centre of the bubble –> p

68
Q

Law of Laplace + what does it show?

A 
amount of p within bubble 
P = 2T/r
if T is constant surface tension of water 0.075N/m
P ∝ 1/r
smaller alveoli = larger p
69
Q

Why would the inflation of the lungs be impossible?

A

p gradients that would be created between diff sized alveoli –> smaller alveoli collapsing into larger

70
Q

How is smaller alveoli collapsing resolved by?

A

pulmonary surfactant: phospholipoprotein secreted by type II pneumocytes (alveolar cells)

71
Q

Features of pulmonary surfactant + how they work?

A

-amphipathic = hydrophilic head + hydrophobic tail regions
-disrupt H-bonds between water molecules, reducing
surfacing tension: decreases collapsing p + prevent alveolar oedema due to excessive fluid being pulled from capillaries
-equalise p between diff alveoli sizes:
as alveoli expand, conc of pul surfacant decreases, increasing surface tension –> larger alveolar collapse into smaller –> consistent inflation

72
Q

What does the surface tension at the air-liquid interface do?

A
  • increases collapsing p –> inconsistent inflation
  • reduces hydrostatic p in alveolar tissue so pull fluid out surrounding pulmonary capillaries into alveoli + interstitial tissue –> alveolar oedema
73
Q

Why does Neonatal Respiratory Distress Syndrome (NRDS) occur?

A

develop + produce insufficient pul surfactant

surfactant production at week 24-28

74
Q

What does NRDS do?

A

-respiratory failure due to:
alveoli collapsing, low lung compliance, alveolar oedema
-hypoxia
-pul vasoconstriction, endothelial damage, acidosis, pul + cerebral hemorrhage

75
Q

How is NRDS treated?

A

-HIGH RISK MOTHERS:maternal diabetes(insulin affect pneumocyte maturation) + premature birth
-supplementation of affected infants w artificial surfactant and/or administering glucocorticoids (increase surfactant production via
maturation of type 2 pneumocytes)

RESP (11 decks)

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