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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
What does lung recoil do?
pull the visceral pleura inwards + compress lung | v
26
What forces determine if lungs expand or compress at | given time?
lung recoil chest wall recoil intrapleural p
27
When should the forces be equal?
between end of expiration + start of next inspiration
28
How inspiration begins?
-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
29
How expiration begins?
- 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
30
How forced expiration begins?
- 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)
31
Inspiration?
- 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
Expiration?
- 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
When does the compression of lungs happen?
forced expiration
34
What does the speed of airflow depend on?
p gradient | level of airway resistance
35
How is intrapleural p naturally sub-atmospheric?
opposing recoil of chest wall + lungs
36
Define pneumothorax
air entering pleural space
37
Entry of air into the pleural cavity
- 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
What happens if there's a loss of negative intrapleural p?
elastic recoil of chest wall + lungs no | longer resisted -->affected regions of lungs to collapse
39
Ohm's law?
``` V = P/R airflow = change in p/resistance ```
40
What factors determine level of resistance?
cross sectional area of airway lumen | airflow pattern
41
Hagen-Poiseuille + what does it show?
R ∝ 1/radius⁴ | As radius of an airway decreases, resistance increases dramatically --> airflow decreases dramatically
42
How does air flow in healthy airways?
laminar pattern
43
How does air flow in obstructed airways?
turbulent pattern
44
How does turbulence occur?
where high velocities of airflow are achieved (during forced breathing manoeuvres) sudden decrease in luminal area (obstructed airways)
45
What causes wheezing sound?
vibration generated by the turbulent airflow
46
Define airway patency
state of being open/unobstructed
47
What's open airways are maintained by?
elastic fibres within airway wall | radial traction
48
Why's airway obstruction more noticeable during expiration?
during expiration, lung tissue+airways compressed
49
What can reduce airway patency during forced expirations?
p differentials between the intrapleural space + airway
50
What's Spirometry + role?
measuring FEV₁/FVC ratio | quantifying airflow + level of airway obstruction present during breathing
51
What does measuring FEV₁/FVC involve?
producing a max forced expiration into a | spirometer- measures v of air passing through over time
52
What's FEV₁ + corresponds to?
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
Values of obstructive airway diseases?
reduction in FEV₁ (<80% expected value) | FEV₁/FVC ratio (<70%)
54
Values of restrictive lung diseases?
reduction in FEV₁ + FVC (<80% expected value) | relatively normal FEV₁/FVC ratio (>70%)
55
Why does restrictive lung diseases have a normal FEV₁/FVC ratio?
decrease in FEV₁ reflects an overall decrease in lung v rather than airway obstruction
56
Define transpulmonary p
Ptp = Palv – Pip | diff between p within alveoli + intrapleural space
57
Role of transpulmonary p?
determines level of force acting to expand/compress lungs
58
Define compliance
how easily lungs can be distended | compliance = change in v/change in p
59
What happens if there's a higher compliance + eg?
- less elastic recoil - less force required to inflate - ↑ v change per pressure change (↑gradient on v-p curve) - emphesyma (elastic degrades)
60
What happens if there's a lower compliance + eg?
- more elastic recoil - more force required to inflate - ↓v change per pressure change (↓ gradient on v-p curve) - pul fibrosis (scar, fibrosis, collagen)
61
Features of lung v-transpulmonary p curve?
- gradient = lung compliance | - measurements taken when no airflow 0 (STEEP) = static compliance
62
What's dynamic compliance?
measurements taken in presence of airflow - gradient between end tidal inspiratory + end tidal expiratory points on v-p curve
63
Features of v-p loops?
- gradient of overall line from end of expiration to end of inspiration = compliance - area within loop = proportional to level of airway resistance generated
64
Why would there be a greater area of v-p loop?
forced inspiration/expiration | airway obstruction
65
What are the structures affect lung compliance ?
chest wall mechanics ↑ alveolar surface tension ↓ elastic fibres ↓
66
How's bubble formed?
water-air interface formed between lining fluid + pseudo-spherical alveolar airspace
67
What happens within bubble?
surface tension due to H bonds between | water molecules --> collapsing force toward the centre of the bubble --> p
68
Law of Laplace + what does it show?
``` 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
Why would the inflation of the lungs be impossible?
p gradients that would be created between diff sized alveoli --> smaller alveoli collapsing into larger
70
How is smaller alveoli collapsing resolved by?
pulmonary surfactant: phospholipoprotein secreted by type II pneumocytes (alveolar cells)
71
Features of pulmonary surfactant + how they work?
-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
What does the surface tension at the air-liquid interface do?
- 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
Why does Neonatal Respiratory Distress Syndrome (NRDS) occur?
develop + produce insufficient pul surfactant | surfactant production at week 24-28
74
What does NRDS do?
-respiratory failure due to: alveoli collapsing, low lung compliance, alveolar oedema -hypoxia -pul vasoconstriction, endothelial damage, acidosis, pul + cerebral hemorrhage
75
How is NRDS treated?
-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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