Pulmonary Gas Exchange Flashcards

1
Q

When is airflow turbulent?

A

Passing uneven surfaces/bifidcations (at branches and irregularities in the airways). Especially in the upper respiratory tract.

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2
Q

What is laminar air flow and where does this occur?

A

When its in straight lines, easy flow through. Mainly in tubular structures, eg bronchi down to cebntri-acinar region of perhiperal part of lung

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3
Q

What is the centriacinar region of the peripheral part of the lung

A

The area around the terminal bronchiole and 1st respiratory bronchiole. Big change in flow laminar to turbulent.

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4
Q

What is the “blood-air barrier”?

A

Basicallly the alveolar pneumocyte to the endothelial cell.

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5
Q

What is FIO2

A

The fraction on inspired air that is oxygen (eg. of air we breathe is 21%)

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6
Q

Hb leave lungs with what saturation and why?

A

98% oxygen saturation, because Hb is very efficient in picking up oxygen

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7
Q

Is it common or rare for CO2 transfer to be affected by disease and why?

A

Rare, due to the extremely high solubility of CO2 it can easily continue to equilibrilate (usually)

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8
Q

Normal PaO2 and PaCO2 (kPa)

A
PaO2 = 10.5 - 13.5kPa
PaCO2 = 4.8 - 6.0kPa
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9
Q

Type 1 vs Type 2 resp failure

A

Type 1 = hypoxia (PaO2 less than 8kPa) - PaCO2 normal or low

Type 2 = PaCO2 = >6.5kPa (O2 usually low)

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10
Q

4 mechanisms of abnormal pulmonary gas exchange

A

ventilation/perfusion mismatch (V/Q)
shunting
diffuse impairment (interstitial lung diseases)
Alveolar hypoventilation

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11
Q

v/q =? and what is normal v/q ratio?

A

Ventilation/perfusion ratio
Usually:
4L/5L = 0.8

as ventilation is approx 4L/min and perfusion is approx 5L/min.

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12
Q

low/high v/q commonest cause of hypoxeimia?

A

Low (reduction in ventilation)

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13
Q

will O2 help fix v/q mismatch?

A

Help. Usually the mismatch isn’t throughout the whole lung and so the increased oxygen won’t help the areas that are already performing well but by increasing the concentration of oxygen in areas with v/q mismatch it means that the haemoglobin are able to become more saturated with oxygen.

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14
Q

What is Shunt?

A

When blood goes from right ventricle to left atrium with NO opportunity for gas exchange (without contacting ventilated alveoli)

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15
Q

Normal % shunt?

A

2-4% in a normal person

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16
Q

What can cause shunts more?

A
AV malformations (Arteriovenous malformation) - when the artery just turns into the vein and back to the heart
Congenital Heart disease
Pulmonary disease (eg. complete consolidation of the lung in pneumonia)
17
Q

Do shunts improve with o2? Why?

A

No, because the blood still isn’t going past any opportunity for ventilation, and the blood leaving normal lung is already saturated with 98% O2.

18
Q

Pneumonia, why hypoxaemia?

A

Severe bronchopneumonia/lobar pattern with large areas of consolidation - get shunting

Bronchitis/Bronchopneumonia (Areas not fully consolidated) - decreased ventilation/perfusion ratio

19
Q

When does shunting occur in pneumonia?

A

When there has been large areas of consolidation

20
Q

What is hypoventilation?

A

When there is low ventilation, so not enough fresh air getting to the alveolar.

21
Q

Hypoventilation leads to what type of resp failure why?

A

Type 2,

CO2 still able to diffuse across, not enough fresh air coming into/leaving alveolar, so increase in PA CO2. Therefore decreasing the gradient for CO2 and leading to PaCO2 increasing. Due to the increased PACO2, the PAO2 will fall, and so will the PaO2.

The decrease in PaO2 can be corrected by raising FIO2.

22
Q

Hypovention improve with O2?

A

Yes

23
Q

Hypoventilation, why???

A

Usually affects ALL of the lngs.

Upper airway/tracheal obstruction

Skeletal - mechanical problems - chest wall damage
Muscular - eg paralysis/diaphragmatic damage
Neuro - ig nerve damage/CNS malfunction - eg Opiate posioning/COPD not responding - hypoxic drive

24
Q

What is a characteristic feature of opiate/herrorin overdose?

A

Suppresses the CNS and can lead to sometimes fatal alveolar hypoventilation

25
Q

COPD desensitised to what??

A

The increase in CO2 , therefore lives at a higher PaCO2 and lower level of PaO2 as reliant of hypoxic drive from peripheral chemoreceptors

26
Q

COPD patient hypoxaemia, why??

A

V/Q mismatch - airway obstructio (+/- bronchopneumonia)
Diffusion impairment (loss of alveolar surface area in emphysema
Alveolar Hypoventilation -reduced respiratory drive
Shunt - Only during acute exacerbation if pneumonia is enough

27
Q

What does gas diffusion depend on? And what can impair it?

A

Pressure of the gas - impaired diffusion if low pressure of gas
Thickness of membrane - thicker interstitium impairs diffusion
Surface area available - less surface area impairs diffusion

28
Q

why co2 easier diffusion? What effect does this have when there is impairment?

A

Greater solubility. It means when there is impairment, the PaCO2 may remain normal whilst PaO2 drops.

29
Q

What effect does diffusion impairment have on the time taken to adequately saturate the haemoglobin?

A

Increase

30
Q

Equilibration usually takes how long in normal cells? (length of time for Hb to become fully saturated)

A

0.25 seconds

31
Q

How long is capillary transit time?

A

0.75s at rest

32
Q

In disease how long may it take to get equilibrated?

A

More than 0.25s, up to and over the 0.75s threshold of time the Hb has going past the alveoli

33
Q

What happens to capillary transit time during exercise?

A

Decreases

34
Q

Increasing O2 conc has what effect on time taken to equilibrate?

A

Decreases