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PHGY 312 > Respiratory #2-4 > Flashcards

Respiratory #2-4 Flashcards

1
Q

What are the 5 different stages of lung development?
What type of cell is found in each stage?

A
  1. Embryonic (directiculum) → Only progenitor cells
  2. Pseudoglandular →Progenito cells become Columnar cells
  3. Canicular → Ciliated cells (1st respiratory epithelial cells) + Columnar cells
  4. Saccular → Ciliated cells + Columnar cells differentiate into AT1, AT2 and basal cells
  5. Alveolar → Only AT1, AT2

*Epithelium gradually differentiates

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2
Q

Where do the lungs initially develop from?

A

Foregut
1. Respiratory diverticulum buds off early on → Gives rise to lungs

Respiratory system shares features that are similar to intestin (both derived from the gut) → Musclar walls in the aways (smooth muscles)

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3
Q

What are the Tracheo-esophageal ridges?

A

Longitudinal ridges that eventually fuse to separate trachea from esophagus

Failure in splitting keads to communication (fistula) between the 2 structures which requires surgical intervention
Infant would choke on milk if don’t dissociate

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4
Q

What is bronchopulmonary dysplasia?

A

Can occur in extreme cases of premature birth
- Reduced alveolarization
- Abnormalities of vascular development

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5
Q

What do the right and left lungs develop from?

A

Lung buds

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6
Q

What are basal cells?

A

Progenitors of airway epithelium
- Can differentiates into any cells (including cilliated cells) → repair the protective functions of the airway epithelium

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7
Q

What is the importance of type 2 alveolar cells in the alveolar phase and late?

A
  • Become the new progenitor cells
  • Replace dammaged AT1 and AT2 cells
  • Proliferate in the context of injury (specifically alveolar tissue damage)
  • Produce surfactant
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8
Q

What are the main respiratory muscles appart form the diaphragm?

A

External intercostals → mostly inspiratory in action (pull up the ribs to extend rib cage)
Internal intercostals → mostly expiratory in action
Parasternal area of internal intercostals → inspiration in action
Posterior of external → expiratory in action
*Required for proper diaphragmatic function

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9
Q

What are the main accessory muscles?

A
  • Sternocleidomastoid → elevates the strenum
  • Scalenes (anterior, middle, posterior) → elevates and fix upper ribs
  • Abdominal muscles (recits abdominis, oblic and transverse) → expiratory in action
  • *Tone in abdominal muscles prevents excessive diaphragm shortening
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10
Q

Why is it important to limit diaphragm shortening?

A

Diaphragm acts just like other skeletal muscles
Respiratory muscle has force-length relationship with optimal length (too much shortening → loss of force)
*By the time the muscle is at 60% of optimal length, lost ability to generate active force
Transdiaphragmatic pressure curve follows force-length relationship —> has optimal length of diaphragm for max Pdi
Velocity-force relationship:
The greater the load, the slower tha ability of the muscle to contract when maximally stimulated (Less load = faster contraction)

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11
Q

How can diaphragm force be assessed?

A

Placing ballon cathter in the stomach → measures intra-abdominal pressure + one in the lower esophagus → pleural pressure
Difference between both pressures = transdiaphragmatic pressure → declines with increasing lung volume (proves the force-length relationship)

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12
Q

What are the zones of aposition?

A

Where the diaphragm is in direct contact with the rib cage (no lung between them)

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13
Q

What is the effect of contraction of the diaphragm on the abdominal pressure and the pleural pressure?

A

Lowers pleural pressure
Increases abdominal pressure → not compressable → abdominal walls move outwards + pushing out the lower rib cage

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14
Q

What happens if diaphragm is only muscle to contract?

A

Upper part of rib cage would be pulled in (atm pressure > pleural pressure) without action of intercostal

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15
Q

What is bucket handles movement and pump handle movement?

A

Bucket handle = Contraction of the external intercostals raises the lateral part of the ribs causing a bucket handle motion that increases the transverse diameter of the thorax (rotation)

Pump handle = lateral movement of ribs, when sternum is lifted

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16
Q

How many generation of airways does an airway tree contain?

A

Up to 23 generations, but path to final alveolar compartement can vary in number
Not perfect symmetrical dichotomous branching

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17
Q

Is the draphragm stimulated unilaterally or bilaterally

A

Normally stimulated bilaterally, but can be stimulated unilaterally (can breathe normally with 1 side of diaphragm if no lung disease)

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17
Q

What are the characteristics and effects of the airway smooth muscles?

A
  • Narrow the airways when activated
  • Same characteristics are skeletal muscles, but slower velocity of contraction and sustained contractions
  • Can get active force down to very very short lengths compared to skeletal muscles (not great, because can have closing of the airways)
  • have force-length and force-velocity properties
  • Innervated by cholinergic (ACh) system (Vagus nerve from CNS)
  • Irritant receptors in ariways react and send message through vagues to CNS, get response back
  • No dilation innervation (only constricting)
  • Spiral around the airways
    *No sympathetic innervation to airways (only to vasculature), no nerves dilate airways
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18
Q

How does the length of the diaphragm changes with increasing lung volume?

A

Diaphragm shortens at higher lung volume

Equilibrium between operating lung volume and operating length of diaphragm

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19
Q

What is the importance of abdominal muscles?

A
  • Role in posture
  • Optimizing function of diaphragm → resist descent of the diaphragm during inspiration (relaxation) → facilitate inspiration
  • When breathe out → push diaphragm back to resting position

*Maintain length of diaphragm for optimal length

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20
Q

What would hapen to someone with complete paralysis of diaphragm whilst laying down?

A

Can’t use gravity pull diaphragm down so can’t breathe

Could breathe standing up because gravity pulls diaphragm down and abdominal muscles pushes back

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21
Q

How does the cross-sectional area change across the respiratory system?

A

Cross-sectional area of repiratory zone/ terminal bronchioles = much greater than Conducting zone
*Exponential curve

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22
Q

Where in the respiraotry system, is the resistance to airflow the greatest?

A

In larger airways because their cross-sectional area is smaller

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23
Q

What are the layers of the airway tissue?

A

Surface → deeper
little foldings at the epithelium (with ciliated cells and their contractile apparatus) → basal cells (give rise to new epithelial cells if needed) → connective tissues → muscles

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24
Q

What occurs with airway narrowing?

A
  • More infolded epithelium
  • Airway recoil becomes outwards (instead of inwards)
  • Alveolar SEPTA → aiway walls can transmit negative pressure from the pleural space into the lungs to pull airways open
  • Some airways have cartilage which prevents narrowing
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25
Q

What are the function of lymphatics?

A

Remove excess fluid to keep alveolar compartements relatively dry

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26
Q

How do airways get nourishment?

A

Through bronchial circulation → Small shunt of blood that is not oxygenated
Bronchial also helps to heat (conservation of heat) and humidify the inspired air (add water vapour) → add on the way in, take back on the way out (take back the heat which makes water vapour condense)

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27
Q

What is an acinus?
What is the purpose of the holes in alveoli?

A

Functional unit of the peripheral lung

Holes allow air drift from 1 alveoli to another = Collateral ventilation → increase in number with age

28
Q

How is the internal surface area of the lung related to the height of a person?

A

The taller the person, the greater the total surface area of the lungs → not very strong correlation
Other determinants that relate to height that increase surface area

29
Q

What are the pressure of the systemic and peripheral circulation?

A

Pulmonary = 25/8 → mean = 15
Systemic = 120/80 → mean = 100

30
Q

What are lamellar bodies?

A

Part of the type 2 alveolar cells that produce surfactant

31
Q

What are the characteristics of type 1 alveolar cells?

A

Thin, flat cover most of the surface
Responsible for gas exchange
- important to permeability barrier function of alveolar membrane

32
Q

What are the characteristics of the right ventricle?

A
  • Thinner walled than left ventricle
  • Suited to increase in volume
  • Unsuited to increase in pressure acutely
  • Adapts to pressure chronically by hypertrophy
33
Q

What are characteristics of lymphatic flow?

A
  • Increased by increased filtration pressure
  • Increased by altered pores sizes
  • Increased by reduced plasma oncotic pressure
34
Q

What does the static pressure-volume relationship of the respiratory system show?

A

S-curve
At extreme volumes → more pressure

35
Q

What are the different subdivisions of lung volume? (TLC, IC, FRC, IRV, Vt, ERV, RV, VC)

A

TLC = empty lungs → max insp. = FRC + IC
FRC = empty lungs → quiet exp.
IC = quiet exp. → max insp.
RV = empty lungs → max exp.
ERV = max exp. → quiet exp.
Vt = quiet exp. → quiet insp.
IRV = quiet insp. → max insp.
VC = max exp. → max insp. = ERV + Vt + IRV = TLC - RV

35
Q

What does the body plethysmograph allow?

A

Plethysmograph as a device measures flow → in respect to time → gives volume

Measures lung volume changes, changes in the chest wall volume

36
Q

What are the determinants of static lung volumes? (VC, TLC, RV)

A

VC is defined by max and min lung volume (TLC - RV)

Determinants of TLC = inspiratory muscle force (neuromusclar diseases) against chest wall and lung recoil forces (emphysema, lung fibrosis)

Determinants of RV = Expiratory muscle force (neuromusclar diseases) against outward recoil of forces of chest wall and airways resistances (obstructive airway diseases, aging)

37
Q

How is pleural pressure a bit different or similar to measured esophageal pressure?

A

Inspiration → negative side → pleural pressure = esophageal pressure

Expiratory → positive side → pleural pressure doesn’t quite follow the E.P. line as it can’t go as positive

38
Q

How can absolute volumes be measured?

A

With Boyle’s law: PV = kT
PV = (P + ∆P)(V - ∆V) where P = Patm and V = thoracic gas volume at point of occulsion of the airway opening
Patm*Vtg = (Patm + ∆P)(Vtg - ∆V) → Vtg = Patm(∆V/∆P)

39
Q

How are the elastic properties of the lungs different in inspiration vs expiration?

A

P-V curve not the same for insp. and exp.
- During inspiration, higher pressure for same volume than during expiration
- During inspiration, as get close to max inspiration → V(y)/P(x) curve flattens at the top
- Linear relationship over good range

Hysteresis = when pathway up and down are not the same

40
Q

What are the influences of the pressure volume relationship for the respiratory system (chest wall and lungs)

A

S-shaped
At very low volumes → chest wall outward recoil predominates (Plungs ~ 0, Pw ~ -40 cm H2O)
At very high volumes → The recoil of the lungs predominate (Plungs ~ + 40 cm H2O, Pw ~ + 10 cm H2O)

41
Q

What happens to abdominal compartement pressure at very low lung volumes?

A

It becomes negative as the diaphragm is higher up (max ~ -20 cm H2O), ~ 0 cm H2O at 40% of VC

trans-diaphragmatic pressure also becomes negative, ~ 0 cm H2O at 27% of VC (thoracic - abdominal)

42
Q

What is the effect of transpulmonary pressure on alveolar geometry?

A

At low transpulmonary pressure → alveolar ducts are narrow, interalveolar wall infolded

Pao = 10 cm H2O, alveolar duct is widened, collagen and elastin fiber system stretched
*Collagen and elastin in inter-alveolar septum controbutes to mechanical properties

Pressure responsible for inflation of lungs = Pleural pressure - alveaolar space pressure

43
Q

What is a major portion of the elastic recoil of the lungs attributable to?

A

Air-liquid surface tension
*Seen as lungs inflate a lot easier in saline solution because there is no air-liquid surface

44
Q

What is the importance of surfactant?
What is it disrupted by?

A

Reduces surface tension within lungs from 70 dyn/cm → <10 dye/cm
- Polar head (interacts with liquid), non-polar tail
- Principal component = dipalmitoyl-3-sn-phosphatidylcholine
- Surfactant proteins B and C → important for integration in the surface layer
- When surface increase, surfactant is recruited from reservoir, when decrease surfactant is squeezed out
- Small aggregates of surfactant are recycled via endocytosis inside the AT2 cells and re-cycled

Disrupted that cause leaking of plasma proteins into alveolar compartement disrupt surfactant’s function, also damaged by high O2 tensions

45
Q

What happens to 2 close alveoli without surfactant?

A

The smaller (greater surface tension) one will recoil and poor into the larger one
Because they all have the same tension T, but different radius
P = 2T/r
Surfactant reduces T to a greater extent in smaller alveoli

46
Q

What are the 4 major surfactant proteins and their roles?

A

A → activates macrophages → elicit uterine contractions + cause pro-inflammatory reactions
SPB → organizes into tubular structures that are much more efficient at reducing surface tension (specific deficiency in surfactant B → respiratory distress)
SPC → enhances function of surfactant phospholipids
SPD → important in host defense

47
Q

What are the effects of prematurity on lungs?

A
  • Lack of surfactant → respiratory distress syndrome (surfactant administration works, only natural surfactant and need presence of SPB and SPC for speading in vivo)
  • Inadequately developped alveolar spaces
  • Oxygen toxicity + mechanical ventilation → bronchopulmonary dysplasia (arrested dev. of the airways and all tissues)
48
Q

How are the pressure-volume curves affected by Emphysema and Fibrosis?

A

Emphysema = loss of recoil → higher TLC, faster increase in volume of lungs with less increase in pressure (steeper slope)
Fibrosis = increased recoil → lower TLC, more increase in pressure needed for same increase in volume

49
Q

What equations can give us the transpulmonary pressure?

A

*See the lung as 1 single big compartement from mouth to alveoli
PL = Pao - Ppl = Pfr + Pel = Vt/Cl + RawV’

Pfr = Pao + Pa = pressure drop across the airways = pressure needed to overcome flow resistance
Pel = Pa - Ppl = press difference between alveoli and pleural space (el for elastance on alveoli)

Raw = airway resistance = Pfr/V’ (V’ = flow)
Pel = C(L)/V(T)

50
Q

What are the relationships between flow, volume and pressures?

A

Flow = insp → +, exp → -
Volume = increase during insp. decreases during exp.
Pfr = same as flow
Pel = same as volume
P total = offset from Pel curve because of Pfr
P L = P total = Pel + Pfr = Pao - Ppl

51
Q

What equation measures dynamic lung mechanics? (not elastic work + dynamic work, but similar)

A

Single compartement model:
P lungs = transpulmonary pressure = ResFlow + Elastance(1/compliance)Volume

52
Q

What is the equation/variables of passive emptying of the lungs?

A

Happens as the lungs don’t exactly behave as a homogenous unit
V = V0 e^(-T/τ) where τ = R*C
Different τ → different rates of filling and emptying
- Stiff compartements (lower C) will empty faster
- Lower resistance will lead to faster filling and emptying
*2 alveoli that empty at different rates will join in a common airway and travel at the same speed from that point on

53
Q

How does dynamic compliance differ at different breathing frequencies?

A

For healthy subjects → constant ratio between dynamic and static compliance ~ 100% to quite high frequencies

Asthmatic subjects → dynamic compliance falls with increase frequency of breathing (static stays cste) → Heterogenous airway narrowing meaning that in the time avaliable alveoli don’t fill equally/inadequate filling of some airways (can be helped by collateral channels)

Dynamic compliance = difference between transpumonary pressure in inpiration and expiration vs static compliance = pressure at different volumes

54
Q

What is collateral ventilation?

A

Prevents areas of lung collapsing when airways are obstructed → alveoli at the end of an airways that is obstructed can still get air and participate in ventilation through other airways
- Increases with age and disease

55
Q

How is lung volume dependent on resistance?

A

Closer to TLC, resistance is at its lowest → as lung volume decrease, resistance increases exponentially (mostly after FRC) because airways narrow at lower lung volumes, elastic recoil will pull inwards (no negative pleural pressure to pull outwards)

*Resistive cost higher at lower lung volumes

Airways collapse before reaching RV
That’s why its not advantageous to try to breathe close to RV → takes much more energy

56
Q

How is work of breathing measured/calculated?

A

In a fluid system → W = P*V = force over a certain length
Total work = Elastic work + Dynamic work

Dynamic work = needed to overcome resistance of airways
Elastic work = work against elastic recoil of the lungs → helped by outward recoil of the chest wall = space between static pressure-volume curve of lungs and of the chest-wall

57
Q

What is the effect of Histamine?

A

Released during allergic reaction → broncho-constrictor
When given to subject → breathing frequency increases → FRC rises gradually → hyperinflation (lungs being pushed to higher volume)
*Increase the work of breathing (elastic work part)

Volume of rib cage increases, Volume of the abdomen (not actual volume, but displacement of abdominal walls) also pushed out

58
Q

How does work of breathing changes as the lung gets closer to TLC? (During an asthma attack)

A
  • Increase in FRC, higher general lung volume
  • Greater swings in pleural pressure for same change in volume → Need greater work

As we get closer to TLC, chest wall starts having positive recoil so elastic work = Pcw + P lungs → much greater
Inspire at much more negative pressures, but expire around the same pressures

59
Q

What happens to the diaphragm when the abdominal antero-posterior dimension increases?

A

Diaphragm length is inversly proportional to abdominal volume → increase in abd volume (with asthma for example) → less force from can be generated by diaphragm as it shortens (at 60% of optimal length, can’t generate any force)
Conclusion: maximal transdiaphragmatic pressure declines with shortening of diaphragm
*Force-length curve for skeletal muscle

60
Q

What physiological circumstances would cause someone to breathe at lower lung volume?

A

When you lie down, FRC falls, breathe closer to RV. In healthy subject, not a problem

When exercise → breathe out below FRC but mean liung volume is still more elevated (NOT that)
Fibrotic lung → but not physiological

61
Q

How does the Dynamic pressure-volume loop change with more rapid breathing?

A

It becomes larger as you need more transpulmonary pressure to overcome the resistance

*Loop around the static pressure-volume curve of the lung

62
Q

How is work rate optimized?

A

It is optimized/minimized to different tidal volumes and frequencies at fixed alveolar ventilation and dead space → rate and depth of breathe chosen to minimize the work rate

Total work = Dynamic (resistive, viscous) work + elastic work
Work rate = work/breath * frequency

With high frequency → elastic work goes down and viscous work goes up
Optimized ~ 15 breaths/min

If more shallow breating → dead space takes greater proportion of ventilation → total ventilation must be higher)
If deep breathes → more elastic recoil at higher volumes for each breath (higher muscular cost) → more elastic work

*Optimization seen across different species

63
Q

How is the work of breathing during asthma?

A

Work rate increases substantially
- FEV1 falls with more narrow airways
- Different persons experience different degrees of energy expenditure

64
Q

How does the dynamic collapse of airways lead to limitation of flow?

A

When pleural pressure becomes very positive → equal pressure point after which aways collapse (pressure goes down gradually from alv → mouth during exp. because of resistance)
This point determines maximal expiratory flow
*Same gradient of pressure between alveolar compartement and choke point no matter the pleural pressure

*Happens even if alveolar pressure increases also in response to higher alveolar pressure

65
Q

What determines maximal expiratory flow?

A
  1. Airway resistance upstream from choke point
  2. Recoil of the lungs

Dynamic collapse of the lungs → same no matter the pleural pressure
Also the properties of the lungs following this equation:
V max = Area of airways* srqt(A/gas density * transmural pressure difference/change in airway area (airway stiffness))
*Comes down to elastic recoil of the lungs

Choke point = area of airways where smallest expiratory flow is allowed

66
Q

What are difference between male and femal for lung volume ratios?

A

Women generally have bigger airway:lung volume ratios → higher predicted FEV1/FVC

67
Q

What is the typical value of tidal volume?

A

~ 500 mL

PHGY 312 (14 decks)

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