Respiratory #12-1 Flashcards

1
Q

How long of an expiration is considered a full expiration?

A

6 seconds

In young individuals → get to no flow at end (before 6 seconds)
In older → might not get to no flow so 6 seconds = good estimate

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2
Q

Can athletes acquire larger TLC?

A

No, athletes may be genetically favoured by larger TLC, but can’t acquire larger TLC

*Helps with swimmer buoyancy

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3
Q

What is determined by inspiratory capacity?

A

The capacity to exercise
Ex: if lung disease pushed repiration closer to TLC, less capacity to exercise because smaller IC

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4
Q

What is the limit of the spirometer?
How does it work?

A

Can’t measure residual volume, can only measure relative volumes

Tube → Bell immersed in water ceil → bell moved up and down → movement recorded/marked on rotating drum

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5
Q

How does the body plethysmograph work?

A

Measure the change in volume at the chest wall during occluded breathing → changes the pressure in the closed chamber → Boyle’s law

For a fixed mass of gas: PV = k at constant temperature
Thoracic gas volume at the time of occlusion → Vtg = (∆V/∆P)
Patm

*Try to occlude at FRC to have volume at FRC, but can measure from any volume

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6
Q

How can thoracic gas volume be measured by helium dilution?

A

Setup: Helium = tracer gas + resident gas volume
By breathing in and out, He eventually equilibrates between 2 compartements → can calculate volume of thoracic compartement knowing the initial concentration of He

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7
Q

What bias is introduced in He dilution technique that is not in body plethysmograph

A

You assume all airways have free communication with the mouth

In cases of obstructive lung diseases → gas volumes behind closed airways will be under-estimated

Not a problem with body plethysmograph because changes in pressure are transmitted to obstructed airways just as well

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8
Q

What is the 1st application of spirometry vs the most common usage today?

A

1st usage → measure TLC / static volumes → allowed to conclude that men had larger lungs than female, tall people had larger lungs than shorter people

Most common usage → FEV1 and PEF (maximal expiratory flows)

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9
Q

What are the main determinants of expiratory flow?

A
  1. Airways resistance → faster decrease in pressure as air gets out of the alveoli
    - reduced cross-sectional airways lumen (broncoconstriction)
  2. Driving pressure = lung elastic recoil → greater gradient between pleural pressure outside the alveoli and inside
    - Elastic recoil of the lungs (emphysema, lung fibrosis)
    - Other factors: effort, neuromuscular disease (can generate enough positive pleural pressure)

Both act on the equal pressure point (and choke point which is just upstream)
*Waterfall effect → only upstream characteristics act on the choke point → on maximal flow

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10
Q

How does the maximal expired flow change at different lung volumes?

A

Increases with increased lung volume → Greater recoil of lungs at higher volumes → greater driving pressure (greater gradient vs outside of alveoli)

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11
Q

Why are we interested in expiratory maneuvers?
What are healthy reasonable values for FEV1?

A

Several respiratory diseases affect the ability to empty the lungs

FEV1 ~ 5.0 L
FVC ~ 6.0 L
FEV1/FVC = 0.83 → females tend to have higher ratios → relative size of airways is greater in females than males (even if males have larger lungs)

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12
Q

What is the FEF25-75%? Why is it useful?

A

It is the slope of theIt is the mid maximal expiratory flow (MEFR) → slope of expiration from 25% → 75% of expiration
Measures expiration on a lower lung volume range than FEV1 → more sensitive to conditions that augment obstruction at lower lung volumes

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13
Q

How can effort affect the expiratory flow?

A

There is a max expiratory flow line for each volume → The higher the volume the larger the max expiratory flow (not really effort dependent)

At high lung volumes, expiratory flow increases progressively with increasing effort (max flow is very high) → effort dependent
At intermediate/low lung volumes → max expiratory flow reached at only modest efforts, more effort does not increase flow (not effort dependent)

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14
Q

How does pleural pressure change with different lung volumes (for expiration)

A

There a certain amount of positive pleural pressure needed to generate different max expiratory flows

Higher lung volume → need more positive pleural pressure to go to max flow-volume envelop (more effort)
*At TLC → can’t generate enough positive pleural pressure to reach max expiratory flow (?)

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15
Q

How is expiratory flow affected by obstructive lung disease?

A
  • Very slow increase in expiratory flow during inspiration
  • Rapid decline to very low flows at start of expiration
  • RV is much larger → breathe at much higher lung volumes
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16
Q

How can the lungs pressure-volume characteristics be measured?

A

Esophageal balloon + Gastric balloon → transdiaphragmatic pressure/volumes

Catether has holes → pressure within the balloon is the one of the compartement

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17
Q

Why is the maximal expiratory pressure greater than the muscle lung recoil?

A

Because of the lung recoil that also increase the expiratory pressure

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18
Q

Why does inspiration not exactly start at RV (in terms of volumes) ?

A

Because there is gas decompression before gas actually flows in, with opening of the rib cage

Same with expiration → starts at lower volume than VT because there is gas compression

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19
Q

How does respiratory muscle weakness affect flow-volume curve?

A

It is all blunted/rounded up (instead of being sharp peaks):
- Reduced peak flow
- Decreased slop of ascending limb
- Abrupt drop in expiratory flow
- Reduced inspiratory flow

*Max flow are dependent on muscle strength, but can loose muscle strength and still be able to reach max flow

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20
Q

How can diffusion capacity be tested?
(And alveolar volume)

A

CO used to replace O2, but doesn’t have background pressure in vessels + binds to Hb so no change in background pressure

Can measure in and out concentrations for 1 min to measure O2 uptake in a minute

Helium is used to calculate alveolar volume accessed by the CO → He dilution technique

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21
Q

What are the different purposes of exercise testing?

A
  • Assessment of exercise capacity
  • Evaluation of the physiological factors leading to exercise limitation
  • Assessment of unexplained dyspnea
  • Longitudinal assessment of progressive disease processes
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22
Q

What is the criteria for maximal exercise test? (For the test to be considered at max effort)

A
  1. Minute ventilation ~ FEV1 * 35
  2. Gas exchange → profound hypoxemia (criteria for stopping the test)
  3. Cardio response → reached predicted max HR (220-age)
  4. Metabolic parameter → respiraotry exchange ratio > 1.15 (lactic acid is being produced)
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23
Q

What is the maximal metabolic respiratory exchange ratio?

A

1 → (CO2 expired vs O2 consumed) → if only metabolising carbs

0.7 → only metabolizing gas
0.8 → normal metabolism

Anything over 1 means the body produced/expires more CO2 than the uptake in oxygen → bicarbonate is converted back to CO2 (take up H+ from lactate + carbonic acid)
*Indicator the person is producing lactic acid

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24
Q

What different parameters are measured during a maximal exercise test?

A

Ventilation:
1. Minute ventilation
2. Breathing pattern (Vt and frequency)
3. Dead space : Vt ratio

Gas exchange:
1. Oxygen saturation
2. End-tidal CO2

25
Q

How does the FEV1/FVC ratio of a fibrotic lung change?

A

It doesn’t change much, stays quite high because the lung still has a lot of recoil

Absolute volumes are smaller, but the ratio stays similar/high

26
Q

How is TLC different in a normal vs fibrotic vs emphysemic lung?

A

fibrotic&raquo_space; normal&raquo_space; emphysemic

27
Q

How is gas exchange different in a fibrotic lung vs normal lung (exposed to absestos)?

A

O2 inspired might be lower
Same for CO2 excretion

28
Q

What is the effect of asbestos on the lungs?

A

Causes fibrosis
Causes mesothelioma → bad condition of the pleural space

29
Q

How is a fibrotic lung different from a normal lung during exercise?

A

Doesn’t reach max HR → exercise is limited by ventilatory parameters more than cardio

Inflexion point:
- Decrease in O2 saturation
- Steeper increase in minute ventilation
- more CO2 produced than O2 consumed

Same as for normal lung, tidal volume 1st increase, then frequency increases, but tidal volume is very limited so more increase in frequency

30
Q

How does the fibrotic lung parameters change during exercise?

A
  • Very small decrease O2 saturation
  • Ventilation takes off almost vertically at very low VO2 → strong sense of being short of breath

Typical reaction of tidal volume and frequency of breathing

HR increases much more than expected → CO = SV*HR, but SV is limited in fibrotic lung (could be left or right function)

31
Q

What is the Oxygen pulse?

A

Amount of oxygen taken up with each heart beat

increase in O2 extraction + increase in SV → increase in O2 delivery/heart beat

32
Q

How did oxygen treating first arise in early organisms?

A
  1. Trough endosymbiosis → cyanobacteria were incorporated into larger eukaryotic cells (modern chloroplasts)
  2. a-proteobacteria were ingested by eukaryotic cells evolving into modern mitochondria
33
Q

When in history did the Great oxidation event occur?

A

2500 million years ago

34
Q

What changes leaded to mass extinctions?

A

Flunctuations in atmospheric oxygen

35
Q

How did O2 levels during evolution influenced organism development?

A
  1. Direct relationship between atm O2 level and max body size
  2. Correlation between lake O2 level and extant crustacean size
  3. Drosophila raised in hyperoxia → larger over generations (and inversely)
  4. In mammals → hypoxia → increase in structural dimension of the gas exchanger
36
Q

What are 4 historic events in respiratory system evolution?

A
  1. Oxygen forms on Earth → aerobic biochemistry
  2. Accretion of unicellular into multicellular organisms → higher energy needs, O2 delivery from far-removed cells
  3. Aquatic-terrestrial transition → Desiccating air systems, invagination of respiratory organs
  4. High energy lifestyles (endothermy; flight) → systemic/pulmonary circulation, buccal-force pump to suction breathing, uni-direcitonal airflow (birds)
37
Q

How is energy produced?

A

Fermentation/anaerobic respiration/glycolysis (not O2-dependent) = Sugar → Energy (2 ATP/glucose)

Oxydative phosphorylation (O2-dependent) = Sugar → Energy (36 ATP/glucose)

38
Q

What are the pros and cons of oxygen?

A

Pro → Oxygen greatly increases efficiency or energy extraction from glucose (aerobic metabolism)
*detoxifying process produces energy

Con → Oxidative stress at cellular level is toxic
Reactive oxygen species → oxidative damage to lipids, proteins, DNA

39
Q

How can we calculate easily the PCO2 and PO2 in the ambiant air?

A

PCO2 = [CO2]Pb = 0.04%760 mm Hg = 0.3 mm Hg
PO2 = [O2]*Pb = 20.9% * 760 mm Hg = 159 mm Hg

40
Q

What mechanism is responsible for moving O2 and CO2 from cell → envrionement (and inversely)?

A

Diffusion

41
Q

What laws govern diffusion?

A

Diffusion of gases:
Q(x)/t = ∆x(A/L)Dx
Q(O2)/t = ∆PO2/Pb(A/L)D(O2)

Diffusion of a gas in a liquid:
Q(O2)/t = ∆PO2/Pb(A/L)D(O2)*a(O2)

a(O2) → solubility coefficient
D(O2) → diffusion coefficient

42
Q

How does bulk transport of gas into and out of the lungs occur (equations)?

A

Convection of a gas by a medium

Q(O2)/t = V(carrier)/t * a(O2) * P(O2)

Convection necessitates the presence of a pumping mechanism, the work or which reqires energy consumption (not like diffusion)

43
Q

What is the difference in PO2 between Air, alveoli, end capillary, arterial blood, tissue capillary, cell, mitochondria

A

OXYGEN CASCADE:
Air PO2 = 150 mm Hg
Alveoli PO2 > End capillary > Arterila blood = 100 mm Hg
Tissue capillary = 35 mm Hg
Cell = 10 mm Hg
Mitochondria = 0.5-2.5 mm Hg

44
Q

What are the concepts behind the oxygen cascade?

A

Respiraotry system becomes series of finely tuned resistances → enough but not too much O2:
- Convection and diffusion in the lungs
- Chemical binding to metalloproteins (Hb)
- Distribution via cardiovascular regulation
- Dissociation form Hb in tissues
- Diffusion into peripheral cells

Effectively creating promodial (millions years ago) hypoxic conditions of Earth inside host cells → very low PO2 in mitochondria
- Increasing O2 above this level impairs muscle function

45
Q

What are respiratory strategies found in nature?

A

Gas exchanger → barrier across which a flux of oxygen and CO2 occur under a gradient

Type of gas exchangers → cell wall, cutaneous, gills, tracheae, lungs

46
Q

What are common gas exchanger features?

A
  1. Evagination/invagination from the body surface
  2. Maximization of surface area
  3. Thin partitioning of internal and external envrionment to facilitate gas flux
  4. Vascularization to facilitate blood exposure to external environment
    → Proteins take up O2 → keeping gradient to a minimum
47
Q

What organisms have cutaneous gas exchange mechanisms?

A

Amphibians (salamander, frogs, etc.) → major source of gas exchange
Fish, reptiles, mammals → minor source of cutaneous gas exchange

48
Q

Why are gills poorly designes for air breathing?

A
  • Large surface area, thin, closely packed
  • Dry out, collapse, adhere
  • Hypoxia, hypercapnia despite higher oxygen content of air by volume

Nevertheless some aquatic species are co-adapted for terrestrial living (~500 fish species can breathe air by primitive lung)

49
Q

At what level does gas exchange happen in insects?

A

At the level of tracheoles / Tracheae system → Invaginated tubular network

  • Spiracles on exoskeleton surface allow air entry into tracheae → Tracheae branch into tracheoles → Gas exchange occurs between tracheoles and tissues
    *Air sacs store gas, but do NOT contribute to gas exchange
    In a very dry environment, insects might close their spiracle so the system doesn’t dry out
50
Q

What is the structure of lungs?

A

Fish heart lacks coronary circulation → lungs evolved to supply the heart with oxygen
Spongy myocardium relies on luminal oxygen

Structure:
Gills → muscle and lungs → heart → gills
Developped to a 2 chamber heart:
Lung → left heart → muscles → right heart → gills → lung

51
Q

How did terrestrial lungs emerge from fish respiratory system?

A

Lungs evolved to cope with hypoxic habitat:
- Rivers subject to seasonal drought (dry)
- Fresh water swamps with oxygen consuming microbes
- High salt estuaries that lower O2 solubility → salt reduces solubility of O2 in H2O

52
Q

What are 2 types of lungs?

A

Alveolar lungs: (mammals)
- Bi-directional air flow → air comes in by the same system as it comes out
- Internl sub-divisions (increase in surface area)

Avian lungs:
- Unidirectional air flow (enter → airway → abdominal sac → parabronchi → anterior air sac → out)
- Cross-current circulation
- Better efficiency

53
Q

What is the proportion of type 1 cells in human lungs?

A

Human type 1 cells ~ 8% of lung cells, but cover 93% of the alveolar surface

54
Q

What was the original function of respiratory proteins?
What is another important actual function?

A

Related to protection against the toxicity of oxygen → appeared un nature more the 1000 millin years ago

By binding to oxygen in RBC, Hb helps maintain the gradient for diffusion (Hb saturation)

55
Q

What does oxygen bind to on Hb?

A

Binds to ferrous ions

56
Q

What is Hemocyanin?

A

It is a respiratory protein → same function in invertebrates based on binding of oxygen to copper

57
Q

What are the different barriers to diffusion? (from alveolar to RBC)

A

Alveolar-capillary membrane → plasma → RBC membrane → red cell interior → binds to Hb

58
Q

What is the value of TLC in a deathly subject?

A

6.0 Liters