V/Q mismatch

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phd89

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i can't seem to understand V/Q mismatch what do the Pa > PA > Pv values mean at each of the levels? i've never been able to understand this concept do the values relate to PAO2 and PaO2 and PA CO2 PaCO2 in any way or is that different

At the apex---PA is greater than Pa so it collapases the arteries is that why V/Q is 3 at the apex don't understand this need help here
 
PA = intra-alveolar pressure

So if PA > Pa, the vasculature is not as patent because the alveoli are compressing the vessels.

If Pa > PA, the pressure within the vasculature exceeds that of the alveoli, so the vessels can stay open.

A few big things to know (what I've encountered through 9500 practice questions so far [excluding Kaplan and UWorld]):

1) Ventilation AND perfusion increase while going apices --> base, but perfusion increases proportionally greater than ventilation, so we get V/Q = 3 at the apices and 0.6 at the base. Perfusion increases because of gravity. Ventilation increases because the alveoli at the base are closer to the diaphragm, so they experience a greater compliance than those at the apices, so ventilation is enhanced per unit change in pressure.

2) Heavy exercise allows the V/Q distribution to approach 1 throughout the lung.

3) At the base, since Pa > Pv > PA, this is the zone (III) where flow is determined by the arterial-venous pressure gradient. I've seen this in several questions.

4) Zone I lung can be "created" if haemorrhage occurs or if PEEP is utilized. This is because haemorrhage would cause Pa to fall below PA; with PEEP, PA would be forced to exceed Pa.

5) If V/Q = 0, then PaO2 = 40 mm Hg and PaCO2 = 46 mm Hg. If V/Q = oo (infinity), then PaO2 = 150 mm and PaCO2 = 0 mm Hg.

6) Since PA is proportionally greater at the apices and pa is proportionally lower, pO2 is also greatest there and pCO2 the lowest. At the base, pO2 is lower and pCO2 greater.

7) Airway resistance is lowest at the apices because transmural pressure is greatest there (i.e. the difference between intra-alveolar and -pleural pressures) because gravity pulls the lung inferiorly, so the intra-pleural pressure must be most negative superiorly.

8) The A-a gradient is normal in opioid-induced hypoventilation (think about it).

9) When supine, blood flow spreads evenly, so the 3.0 --> 0.6 V/Q gradient is eliminated.
 
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Shouldnt it be PA02 =150 mm? I think you made a typo mate.

Both PAO2 and PaO2 would be 150 mm Hg.

PaO2 = 150 mm Hg because PAO2 is able to "achieve" 150 mm Hg when V/Q = oo, since no reduction of the oxygen partial pressure occurs due to mixing of gases.

I'm fairly sure the partial pressure due to water is ~47 mm Hg, and in conjunction with gas-mixing, PAO2 never normally reaches 150 mm Hg. However in the V/Q = oo state, it can. I would also then assume that respiration would still be perfusion-limited, but the higher O2 gradient would just mean equilibration further along the capillaries.
 
I've seen that too.

Why do you think that's the case?

Off the top of my hat I'd say its similar to arterioles.

Trachea is like the aorta, large bronchi like medium sized arteries, respiratory bronchioles/alveoli are like the capillaries (they actually branch off into grapelike clusters opening them up). That leaves us medium sized bronchi which are like arterioles.

I would also assume it is in medium sized bronchi you will find smooth muscle reacting to Beta stimulation.

These are all guesses, they make logical sense but may be totally wrong. :xf:
 
My guess would be that they are the location where the surface area to compliance ratio is the greatest.

Moving distally, surface area increases, but so does compliance. The bronchi develop greater surface area but are still inflexible due to cartilage. I would reason that the "smaller" bronchi must have a fibrocartilage model, rather than a strict cartilage one, that enables increased compliance relative to the medium-sized bronchi. The only reason I assume the latter is because the bronchiobronchiolar transition is marked by a shift from cartilage to fibrous connective tissue, so there must be a mid-point. This increased compliance would explain why the alveoli and smaller bronchi, despite having higher surface area, are not the source of greatest resistance.

As far as arterioles are concerned, I've seen in a practice question somewhere that they have the greatest resistance because they have the greatest wall thickness to lumen ratio (not the thickest walls, just the greatest ratio compared to the lumen). This implies greater capacity to alter lumen size per change in SNS stimulation.
 
My guess would be that they are the location where the surface area to compliance ratio is the greatest.

Moving distally, surface area increases, but so does compliance. The bronchi develop greater surface area but are still inflexible due to cartilage. I would reason that the "smaller" bronchi must have a fibrocartilage model, rather than a strict cartilage one, that enables increased compliance relative to the medium-sized bronchi. The only reason I assume the latter is because the bronchiobronchiolar transition is marked by a shift from cartilage to fibrous connective tissue, so there must be a mid-point. This increased compliance would explain why the alveoli and smaller bronchi, despite having higher surface area, are not the source of greatest resistance.

As far as arterioles are concerned, I've seen in a practice question somewhere that they have the greatest resistance because they have the greatest wall thickness to lumen ratio (not the thickest walls, just the greatest ratio compared to the lumen). This implies greater capacity to alter lumen size per change in SNS stimulation.

Correct, my thinking was however not related to compliance although that makes sense.

My thinking was that the bronchioles are like arterioles, they have smooth muscle that can constrict and dilate and change airway resistance in the same manner as arterioles change peripheral resistance to blood flow.
 
Both PAO2 and PaO2 would be 150 mm Hg.

PaO2 = 150 mm Hg because PAO2 is able to "achieve" 150 mm Hg when V/Q = oo, since no reduction of the oxygen partial pressure occurs due to mixing of gases.

I'm fairly sure the partial pressure due to water is ~47 mm Hg, and in conjunction with gas-mixing, PAO2 never normally reaches 150 mm Hg. However in the V/Q = oo state, it can. I would also then assume that respiration would still be perfusion-limited, but the higher O2 gradient would just mean equilibration further along the capillaries.

That makes sense, but:

In V/Q = infinite, there is zero perfusion by definition.
How will the gas exchange even take place if there's no blood to equlilibrate?

BRS Costanzo has a chart on it actually; she states:
In Pulm Embolus when V/Q = infinite
PAO2 = 150, PACO2 = 0,
PaO2 and PaCO2= -

I can only imagine that to mean that there is no gas exchange taking place.

I am sure you are not wrong though, what I'm not understanding is; how can the arterial Oxygen reach 150, when there is no perfusion taking place?
 
I guess my logic isn't consonant with reality then. I was thinking in terms of ventilation being infinite concurrent to a non-zero perfusion. In that case, V/Q would still be infinity and alveolar should equal arterial pressure, since the oxygen partial pressure reduction due to mixing/water would become irrelevant. However, in terms of real life, you're right that the only way V/Q would be infinite is if perfusion is eliminated. I'm not really sure what the " - " means for PaO2 and CO2 though. Perhaps you could elaborate?
 
If V/Q = 0, then PaO2 = 40 mm Hg and PaCO2 = 46 mm Hg. If V/Q = oo (infinity), then PaO2 = 150 mm and PaCO2 = 0 mm Hg.

If V/Q is infinity, doesn't this mean that we're perfusion-limited and can't readily exhale all the CO2 -> hypercapnia? If that's the case, why would PaCO2 be 0 mmHg?

Thanks for the HY facts!
 
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