Lab 4 Flashcards

1
Q

What is the equation for the PAO2?

A

This is the fraction of gas times the portal pressure the air (considering partial pressure of H2O)

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2
Q

What is the partial pressure of water?

A

H2O

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3
Q

What is the normal range for alveolar PAO2?

A

98-108 mmHg

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4
Q

What is the normal alveolar PACO2 range?

A

36 - 42 mmHg

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5
Q

How does the design of the Haldane-Priestley tube ensure that the sample of gas removed represents alveolar gas?

A

This is a long thin tube. This allows separation of dead space gas and alveolar gas.
There is a small surface area so there is slow diffusion which takes a while to do down the tube

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5
Q

How does the design of the Haldane-Priestley tube ensure that the sample of gas removed represents alveolar gas?

A

This is a long thin tube. This allows separation of dead space gas and alveolar gas.
There is a small surface area so there is slow diffusion which takes a while to do down the tube

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6
Q

Why are our values a bit smaller than the normal values of PAO2 and PACO2?

A

This could be due to experimental error (eg. take it out too early) so the gas taken out includes the dead space.
It could also be due to subject error: you could accidentally hyperventilate or hold you breath or not close the mouth piece correctly

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7
Q

What happened to the alveolar gases after the breath hold after normal breathing?

A

The PACO2 increased and the PAO2 decreased

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8
Q

What happened to the alveolar gases after deep inspiration in comparison to after a normal breath? Why is this?

A

The PACO2 in the alveolar gas was less after deep inspiration compared to after normal breath.
The PAO2 in the alveolar gas was increased after deep inspiration compared to after normal breath.
This is due to increased alveolar ventilation.

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9
Q

What happened to the length of the breath hold after deep inspiration in comparison to after a normal breath? Why is this?

A

The breath hold was longer after the deep inspiration.
This is because you are initially increasing the ventilation initially but the this decreases as we hold our breath. We are using O2 and producing CO2 so the PACO2 increases and PAO2 decreases

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10
Q

What is ventilation?

A

This is breathing fast and deeply

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11
Q

What happened to the alveolar gases after hyperventilation in comparison to after a normal breath?

A

The PACO2 has decreased from normal and the PAO2 has increased a lot from normal.

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12
Q

What happened to the length of the breath hold after hyperventilation in comparison to after a normal breath? Why is this?

A

The breath hold is much longer. This is because it takes a lot longer to reach the build up of CO2

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13
Q

PACO2 is a key regulator of blood pH BECAUSE CO2 is

buffered in the blood to form bicarbonate and H+ through the activity of carbonic anhydrase.

A

1) Both statements are true, and the second causes the first.

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14
Q

What could lengthen the duration of a breath hold?

1) Slow and shallow breathing before the breath hold
2) Rapid and shallow breathing before the breath hold
3) 3-4 practice breath holds immediately before the ‘real’ breath hold
4) Hyperventilating with deep, fast breathing before the breath hold

A

4) Hyperventilating with deep, fast breathing before the breath hold

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15
Q

What does you breath hold data tell you about the relative importance of arterial PO2 and arterial PCO2 in the control of normal breathing?

A

We know that CO2 is the primary modulator of normal restful ventilation. This is because the CO2 increases and this causes an increase in the [H+]. H+ ions in the CSF stimulate the central chemoreceptors to increase ventilation

16
Q

Ptp = what?

A

Palv - Pip

17
Q

The transpulmonary pressure increases during inspiration
BECAUSE during inspiration the intrapleural pressure
becomes more sub-atmospheric

A

1) Both statements are true, and the second causes the first.

18
Q

Which of the following is NOT associated with a

restrictive lung disease?

A

FEV1

/FVC ratio below 70%

18
Q

Which of the following is NOT associated with a

restrictive lung disease?

A

FEV1

/FVC ratio below 70%

19
Q

Expiration at rest:

  1. Is driven by an increase in transpulmonary pressure
  2. Is a passive process
  3. Requires the contraction of expiratory muscles
  4. Requires the thoracic cavity to increase in size
A
  1. Is a passive process
20
Q

Why are free-divers more likely to blackout as they win towards the surface?

A

As you swim down, the pressure increases so although the FO2 decreases, the PaO2 stays the same so you are fine. As you ascend, the pressure decreases and the FAO2 decreases so you decrease the PaO2 and this is very bad