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Respiratory Flashcards

1
Q

What is ficks law

A

Diffusion = Surface area x (P1-P2) / distance

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2
Q

How much is the anatomical dead space and how do you measure it?

A

Fowler’s method aka nitrogen washout

150mL

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3
Q

Alveolar region = what capacity?

A

2.5-3L

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4
Q

Where does convection and where does diffusion occur?

A

Convection in conducting zone

Diffusion in respiratory zone

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5
Q

What is the mean pressure in the pulmonary artery?

A

15mmHg

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6
Q

What is capillary wall thickness?

A

0.3 micrometers

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7
Q

Define physiological dead space

A

Volume of gas which doesnt eliminate CO2 - around 150mL but greater in disease

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8
Q

Where is ventilation greatest?

A

Base

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9
Q

Where is perfusion greatest?

A

Base

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10
Q

Where is V/Q greatest?

A

Apex

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11
Q

What is average V/Q?

A

0.8

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12
Q

What is the commonest cause of RF?

A

Pathological V/Q inequality / decrease

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13
Q

Where does the control of ventilation stem from?

A

Rhythm generator in medulla oblongata

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14
Q

What affects respiration rate?

A

Peripheral (carotid and aortic bodies):

  • PaO2 primarily (also H+ and CO2)
  • very sensitive and rapid

Central (medulla)

  • PaCO2 and H+ mainly
  • very sensitive because the proteins in blood act as a buffer for pH but there is little (or no?) protein in CSF to bufer
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15
Q

Which three values can’t spirometry measure?

A

RV
TLC
FRC

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16
Q

What happens to FEV1/FVC in obstructive and restrictive disease? (and what is it normally?)

A

0.8 normally
Decreases in obstructive
Increases in restrictive

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17
Q

Volume of IC?

A

3.5L

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18
Q

Volume of TV?

A

500mL

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19
Q

Vol of TLC?

A

5-6L

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20
Q

Vol of VC?

A

80% of TLC = around 4.8L

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21
Q

How do you calculate IC?

A

IRV + TV

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22
Q

What is A-a gradient?

A

PAO2 - PaO2

Difference between PO2 in arteries and PO2 in alveoli

Normal is below 10

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23
Q

How do you calculate physiological dead space?

A

Bohr equation

Physiological dead space = the percentage of CO2 not expired by the lungs e.g. if PACO2 = 100 and PECO2 = 80, PACO2 - PECO2 = 20 and so % = 20. 20% of 500mL (TV) = 100mL physiological dead space

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24
Q

What is RQ in the alveolar gas equation?

A

0.8; CO2 eliminated / O2 consumed

Determined mainly by diet

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25
Q

What is the alveolar gas equation?

A

PAO2 = PIO2 - PaO2/R

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26
Q

What are the three zones of the lung?

A

Zone 1 = not common in health; just in haemorrhage / positive pressure. PA>Pa>Pv. PA causes collapse and so the area is dead space.

Zone 2 = STARLING RESISTOR / WATERFALL EFFECt. Pa>PA>Pv. Blood flows in pulses; pressure in the venous end prevents flow until Pa exceeds Pv in systole and then flow ceases again as capillary pressure drops.

Zone 3 = majority of lungs in health. Pa>Pv>PA. Blood flow is continuous. Vessels are stretched due to gravity and so resistance is lower and flow is higher.

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27
Q

What are the uses of the helium dilution test?

A

Helium dilution is used where spirometry can’t be used:

TLC
RV
FRC

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28
Q

What are examples that affect V and Q?

A

V = disease causing alveolar thickening e.g CF, fibrosis. or destruction of alveoli e.g. emphysema

Q = decreased RBCs e.g. anaemia, decreased CBV e.g. PE, capillary destruction e.g. emphysema

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29
Q

What is the PO2 and PCO2 of mixed venous blood?

A 
PO2 = 40
PCO2 = 45
30
Q

What is the PO2 of normal arterial blood?

A 
PO2 = 100
PCO2 = 40
31
Q

What is the PO2 of inspired air?

A 
PO2 = 150
PCO2 = 0
32
Q

Why does V/Q inequality affect PaO2 so much?

A

The V/Q ratio of the lung places it just at the top of the O2 dissociation curve plateau, so a decrease in V/Q causes it to fall down the slope dramatically, but an increase in V/Q affects the O2 very little

This is the basis of the A-a difference: there are bigger differences in alveolar ventilation than there are in arterial O2 and that means that mixed arterial PO2 is lower than mixed alveolar PO2. This is a small difference in health though, but drops dramatically in disease hence ABGs.

33
Q

What is hypoxaemia without CO2 increase?

34
Q

What is hypoxaemia with CO2 increase?

35
Q

What is the mechanism of CO poisoning?

A

CO binds Hb 240x stronger than O2:

PaO2 is normal
[Hb] is normal

but O2 carriage is dramatically reduced due to Hb being tied up with CO

Why is there a left shift of the curve?

36
Q

How is CO2 transported?

A
  1. CO2 dissolved in plasma = 10%
  2. MAJORITY IS AS CARBONATE: CO2 + H2O H2CO3 HCO3- + H+
  3. Carbamino compounds???
37
Q

What is the haldane effect?

A

DeoxyHb has higher pH so is a better H+ acceptor

If deoxyHb is higher due to low O2, it mops up H+

CO2 + H2O H2CO3 H+ + HCO3-

Mopping up H+ shifts the equilibrium to the right and CO2 is therefore taken up by deoxyHb

HALDANE EFFECT IS THE INCREASED CAPACITY OF Hb TO UPTAKE CO2 IN DEOXYGENATED BLOOD

This is obviously advantageous in peripheral tissues with low oxygen, where CO2 can be taken up and oxygen offloaded (bohr effect means curve shifts to right when CO2 builds up, and so O2 is offloaded easier)

38
Q

What is Henry’s law?

A

PO2 at the surface of fluid is the same as the concentration dissolved within the fluid

39
Q

What are the functions of globin?

A
  • Allows reversible oxygenation by sandwiching O2

- Makes haem bind oxygen cooperatively

40
Q

Mechanism of cooperative binding?

A

Deoxyhaemoglobin:

  • Tense configuration
  • Lots of salt bridges
  • Decreased O2 affinity

Oxyhaemoglobin:

  • Relaxed configuration
  • Much fewer salt bridges (or none?)
  • Increased O2 affinity

With every oxygen molecule that is added to deoxyhaemoglobin, the chance of it snapping into relaxed configuration (all salt bridges breaking at once) and the O2 affinity increasing dramatically, is increased. So oxygen binding increases the chance of more oxygen binding.

41
Q

What is the benefit of the plateau of the Hb oxygen curve?

A

It is a safety buffer; normal PAO2 is far along the plateau so a drop means it doesnt affect Hb affinity for oxygen

42
Q

What is the benefit of the steep slope of the Hb oxygen curve?

A

A small drop in oxygen concentration between around 20 and 50mmHg will vastly decrease the affinity of Hb for oxygen. This is useful in the peripheries where oxygen levels are low and oxygen unloading to tissues is needed.

43
Q

What is BPG and when is it increased?

A

End product of glycolysis

Anaemia or chronic hypoxemia -> increases O2 offloading (encourages adequate tissue perfusion in low O2)

44
Q

What shifts the curve to the right?

A

CO2
Heat
H+
BPG

45
Q

What is the structure of haemoglobin?

A

Heme; surrounded by globin

Globin = 2 alpha and 2 beta subunits (ab dimers)

46
Q

PP of CB

A

Increased mucus production and hypertrophy of mucus glands due to chronic inflammation process

Smoke / irritation causes:

  • epithelial cell irritation
  • inflammatory cell infiltration
  • mucus secretion
  • mucus gland / goblet cell hypertrophy
  • cilia stunning
  • all leads to blockage, air trapping, infections
47
Q

PP of SAD

A

“bronchiolitis”

Narrowing of lumen due to inflammation, mucus plugging and fibrosis (thicker walls)

Smoke/irritant causes:

  • epithelial irritation
  • mucus gland hypertrophy and hypersecretion
  • goblet cell…
  • increased neutrophils = increased elastase, increased MYOFIBROBLASTS and FIBROBLASTS = increased fibrosis
48
Q

PP of emphysema

A

Abnormal irreversible enlargement of airways distal to TBs without fibrosis

Smoking:

  • Nicotine causes increased neutrophils which release elastases and proteases which overwhelm alpha-1-antitrypsin
  • ROS cause cytokine release and alpha-1-antitrypsin inactivation

Elastin degrades alveolar wall
Proteases degrade collagen type IV (capillary thin side)

Less surface area = less gas exchange

49
Q

How does nicotine cause emphysema?

A

Its a neutrophil chemotractant so more elastases etc

50
Q

How do ROS cause emphysema?

A

Activate macrophages which release cytokines and this attracts neutrophils which release elastases etc

Also inactivate alpha-1-antitrypsin (and the rest is obvious…)

51
Q

What causes “pleural rub”

A

Stick slip of inflamed pleurae

52
Q

Distinguish peri from pleural rub

A

Pleural only on breathing

Peri 3 part

53
Q

Best biochemical marker for shock?

A

LACTIC ACID

54
Q

Vol inspirable after tidal volume

55
Q

Air inspired in normal breathing

56
Q

Volume that can be expired after normal breathing

57
Q

Max air in lungs

58
Q

Total amount which can be exhaled after fully inhaling

59
Q

Max amount which can be inspired (inc TV)

60
Q

Air left in lungs after normal exhal

61
Q

How could a COPD patient be helped with potential acute ex events?

A

Give a course of corticosteroids and ABx to have at home.

Start CS if SOB disrupts normal ADLs.
Start ABx if sputum becomes purulent.

62
Q

First investigation for suspected COPD in GP practice?

A

Spirometry

63
Q

First investigation for acutely unwell patient in hospital with acute exacerbation of COPD?

A

ABG then CXR

64
Q

What is stridor?

A

High pitched INSPIRITORY wheeze
Audible at distanced
Cuased by laryngeal oedema, vocal cord spasm, OBSTRUCTION

65
Q

What is wheeze?

A

Most prominant at EXPIRATION
Lightly touching bronchi walls oscillate in jet of air
Frequency is dependent on air velocity, not airway size

66
Q

Causes of monophonic wheeze?

A

Criritcal stenosis:

  • inhaled foreign body
  • bronchial tumour
67
Q

Causes of polyphonic wheeze?

A
  • COPD

- Asthma

68
Q

What are crackles caused by?

A

Airways closed in experiation snap open

69
Q

Early crackles suggest?

70
Q

Middle crackles suggest?

A

Bronchiectasis

71
Q

Late crackles suggest

March (13 decks)

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