Resp Physiology Flashcards

1
Q

How is airflow obstruction defined on Lung function tests?

A

FEV1/FVC <5th percentile (Z score <-1.65)
- COPD definition has not yet incorporated the chenage to percentiles, instead obstruction in COPD is defined as FEV1/FVC <0.7

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2
Q

How is restriction defined in term of spirometry?

A

TLC <5th percentile (Z score <-1.65)

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3
Q

How is gas transfer impariment described in terms of spirometry?

A

DLCO <5th percentile (Z score <-1.65)

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4
Q

What is the flow volume curve features of obstruction? What does this represent?

A

Scaloping of the insp limb of the flow volume curve
THis means that for any given volume, the flow is not as good as a control

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5
Q

What is the flow volume curve features of restriction? What does this represent?

A

A taller but narrower insp loop compared to controls
- this is becasue the flow for any give volume is increased, the narrowness meas the overall volume is less

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6
Q

WHy do pts with COPD / asthma get dynamic airway colap[se on expiration whereas normal pts dont?

A

Dynamic airway collaspe is about the balance of intrapleural pressure to intraluminal pressure (aka the transpulmonary presure)
- If your intraluminal pressure is larger than your pleural pressure, then you will have a positive transpulmonary pressure. This pressure will keep the airways open
- If your intraluminal pressure is less than the intrapleural pressre then this will result in a negative transpulmonary pressure which will colapse airways

During expiration there is a high positive intrapleural pressure. There is a slightly higher intraluminal pressure
Air moves from the airways to the mouth because of the intraluminal positive pressure relative to atmosphere
By the time teh air gets to teh mouth it is at atmospheric pressure, therefore pressure disspiation ocurs as air traverses the airway to the mouth (due to tubulence etc)
At some point in this intrathorasic journry, the intraluminal pressure will fall below the intrapleural pressure and promote airway colapse. However for noraml people this occurs in the cartilagenous arways so dont colapse. In asthma pts, there is more fixed obstruction leading to fasdter intraluminal pressure disipation which meas that the point of positive transpulmonary pressure in the the non cartilagenous small aiurways causing colpse

This is gas trapping, this is why there is a sharp scalloping the insp loop of the flow volume curve

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7
Q

Why do pts with advanced COPD have an increased FRC/RV?

A

Gas trapping
- the main defect is due to incresed RV due to gas trapping and loculated air
- The RV can be increased such that the VC starts to decrease

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8
Q

Why are emphasematous pts cachectic? explain in terms of lung volume and work of breath?

A

FR increases due to gas trapping
THis eats into the ERV such that pts need to shift their tidal respirations higher up to have any room the breath out
In other words pt tidal respiration opccur at a much high volume compared to normal
This means more pressure is needed for tidal respirations because the muscles are not operating optimally (think of how hard it is to take a breath on top of a breath)
THis uses a lot of calories and hence cachexia

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9
Q

How are gas trapping and hyperinflation different

A

Gas trapping occurs early, hyperinflation is a long term change as a result of chronic gas trapping. It involves chest wall remodeling

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10
Q

What stage of respiration is energy used?

A

Inspiration
- exp is a passive process that uses the potential energy of lungs natural elastic recoil

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11
Q

Pts with advanced COPD or asthma exacerbation will have a reduced FEV1 (obstruction). THey can also have a reduced FVC. Why?

A

Dynamic gas trapping
- this can make an acute exacerbation of asthma look like a restrictive picture

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12
Q

Pt with lung problems has very high DLCO, what could be the cause?

A

Pulmonary haemorhage

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13
Q

WHy is CO used for DLCO rather than O2?

A

CO binds very strongly to red cells, therefore it is essentially diffusion limited.

Because O2 binds less strongly, it is diffusion and perfusion limited and so cannot isolate diffusion as a variable to be tested

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14
Q

What factors will affect DLCO?

A

Less available membrane for gas transfer
Harder to get through membrane
Less availible blood in pulmonary caps

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15
Q

What factors affect the diffusion of gas across a membrane (ie how hard it is to get through the membrane)?

A

Thickness of the membrane
Size of the molecule (mass)
solubility of the molecule
The Pressure gradient (vapor pressure gradient)

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16
Q

Why would a smoker have a decreased DLCO (even if they hypothetically had normal lungs)?

A

Cig smoke has CO in it, therefore smokers already have smoke CO in their blood. This decreases the partial pressure gradient during a DLCO test measing they wont take up as much and DLCO will be lower

17
Q

Pt with neuromuscular disorder has decreased DLCO. Why?

A

this is not due to an intrinsic lung condition. It is to do with the inability of the person to take up the gas into the lung (this effectivly reduces the amount of lung membrane that teh DLCO sees)

18
Q

When to use A-a Gradient?

A

Use for hypoxaemic pts

Used to distinguish between intrapulmoary and extrapulmoary causes of hypoxia

19
Q

What is the A-a gradient equasion?

A

A-a gradient = PAO2 - PaO2

PaO2 is from ABG
PAO2 is calculated using the alveolar gas equation

At STP (standard temp and pressure):
- PAO2 = 150 - (PaCO2/0.8)
OR alternatively
- PAO2 = 150 - (PaCO2 * 1.25)

20
Q

What is a normal A-a Gradient?

A

Normal A-a <15

21
Q

What defines hypoventilation?

A

Elevated PaCO2 = hypoventialtion or poor gas exchange

22
Q

What does an elevated A-a gradient represent?

A

Problem causing hypoxaemia is occuring in the lung / chest

For example high altitude as a cause of hypoxaemia will have a normal A-a gradient because this is an extra pulmonary cause

23
Q

Hypoxic pt. Normal A-a, high PaCO2. Dx?

A

Hypoventilation
- CNS depression, neuromuscular, obesity hypoventilation

24
Q

Hypoxic pt. Normal A-a, normal / low PaCO2. Dx?

A

Low FiO2
- Altitude

25
Q

Causes for an elevated A-a gradient?

A

V/Q mismatch (most common cause)
- Pneumonia, APO, ARDS, atalectasis
- Usually normal PaCO2
- Some area of the lung is being perfused, but there is reduced ventilation to that part

R->L shunt (this can occur with EXTREME V/Q mismatch)
- Usually low or normal PaCO2
- Anatomical shunt: PFO, ASD, Pul AVM, hepatorenal
- Physiological Shunt: massive atalectasis, Pul oedema, pneumothparx/effusion, ARDS (basically anything that takes out a significant portion of the lung)

Diffusion limited
- Rare. 1/3 of ILD pts have this. Extreme athletes during exercise
- Normal PaCO2

26
Q

What agents are used as direct and indirect challenge agent for airway constriction?

A

Methacoline, histamine

Indirect agents are hypertonic saline