West's zone 2 starling resistor respiratory physiology

[coolia]

I posted this question in the physics forum with no luck, the concept has to do with physics but it's applications is within the body. It is found in the lung and also in venous return curves, when central venous pressure drops below 0. Basically, I am asking how the concept of zone 2 in the lung works, where the effective driving pressure is given by the difference between arterial pressure and alveolar pressure and not venous pressure. In fact, they say venous pressure has no effect on flow. I am confused on how this works so if anyone could give me an explanation that would be helpful. Below is my original post that gives my thoughts about and an image.

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My question is in regards to a starling resistor. A starling resistor is where a flexible tube passes through a box that can have it's pressure changed. If fluid passes through the tube then flow through the box will be determined by the pressure differences from the two sides of the box provided the pressure on both sides of the tube outside the box are greater than the pressure in the box.

If pressure in the box becomes greater than the downstream pressure of the tube coming out of the box then flow will be determined by the difference between the upstream pressure and the pressure in the box. The tube will collapse at a point where the pressure in the tube becomes less than the pressure in the box (this is a pressure of 6 in the diagram below). The downstream pressure will not affect flow through the tube. I attached an image that goes along with the above explanation. Pa(arterial)=upstream pressure, Pv(venous)=downstream pressure and PA(alveolar)=pressure in the box. The above occurs physiologically in bodies most popularly in the capillaries of the lungs (zone 2). My question is how is the upstream pressure - pressure in the box the driving pressure (as they say it is) when the pressure driving flow through a tube should be difference between the pressure at the two ends of the tube? Does the collapse occur gradually, in other words is end closest to the box a smaller opening than more upstream. Also, I'm assuming the resistance increases in the tube because of the collapse and this would be the cause of the decreased flow and not a change in pressure because the downstream and upstream pressure are the same. There would also be a greater drop in pressure from the collapsed ends than from the open ends, due to the collapsed ends having a greater resistance. Is this correct?
Thank you.

 

[Moonbear]

Respiratory physiology was never my strongest area, but here are some thoughts that might help. First, venous pressure won't have an effect on flow if it is a direct effect OF the flow. The only situation where something going on downstream would be a limiting factor for flow would be if there was a blockage of some sort.

I don't think collapse needs to be gradual, but it could be. At any time that the pressure inside a vessel is exceeded by the pressure of the surrounding tissue, you can get a collapse.

One thing to remember in physiology is that you're usually dealing with a closed system. Blood flowing out of the arteries returns through the veins in a continuous loop, unless you have a huge wound that's bleeding rapidly.

I don't know if I've helped at all though, because I'm having difficulty sorting through your post and explanation to really pinpoint what exactly your question or confusion is.

 

[coolia]

Thanks for the reply, I'll try to be more succint. When alveolar pressure is greater than venous pressure in the lungs (but not greater than arterial pressure), the capillary at the downstream end would collapse. They say that the pressure driving the flow is Arterial pressure - Alveolar pressure. My question is why isn't the effective driving pressure arterial pressure-venous pressure? Basically everything above is my explanation for why this occurs but I don't know if it is correct.

The same mechanism occurs in forced expiration, where the intrapleural pressure collapses the downstream airways, limiting airflow.

 

[Moonbear]

Can you think of a normal physiological situation (not pathological) when the example you provide could actually happen? I.e., a precipitous drop in venous pressure that is not accompanied by a drop in arterial pressure? I can only think of pathological examples, such as a clot obstructing flow from getting to the venous side of the capillary.

 

[coolia]

Sorry, can't think of an example where a precipitous drop in venous pressure is not accompanied by a drop in arterial pressure. But I do know if this where to occur in the situation described, if both arterial pressure and venous pressure dropped by the same amount the flow would decrease because the pressure outside the vessel has not changed but the effective driving pressure is arterial pressure-pressure outside vessel.

 

[Moonbear]

Sorry, can't think of an example where a precipitous drop in venous pressure is not accompanied by a drop in arterial pressure. But I do know if this where to occur in the situation described, if both arterial pressure and venous pressure dropped by the same amount the flow would decrease because the pressure outside the vessel has not changed but the effective driving pressure is arterial pressure-pressure outside vessel.

Right, which I think is why they say the arterial pressure is the driving force. We're talking about normal physiological situations. If you're dealing with pathology, all bets are off.

 

[coolia]

Hi, I think I found the answer. I have two theories both are similar. Firstly, Pousielle's law still applies, Pa-Pv=Resistance * Flow rate. To recap the condition, the alveolar pressure (or pressure outside the vessel ) is greater than the venous pressure but less than arterial. So, even though Pv decreases flow does not decrease, the only way to explain this with the above formula to still hold, the resistance has to increase proportionately. How does this occur, let me explain. As blood flow through a vessel (or any fluid) the pressure drops across the vessel, if the resistance is teh same throughout that vessel it drops in equal increments. There will be a point where the pressure in teh vessel will drop so taht it equals the outside pressure at this point the vessel will collapse, because transmural pressure is 0 or less than 0. When this happens everything downstream would collapse as well. However, the vessel would not completely collapse, the reason for this is because the pressure in teh vessel upstream from the point of collapse is greater than the outside pressure. This side is not collapsed and is holding the downstream side from complete collapse. it is like a flextible tube, where the only way to completely close the tube is to collapse it's entire length. If you try squeezing from only one side, that side would not collapse all the way.

So, how does venous pressure not affect blood flow. First, the point of collapse moves to the end of the tube the reason for that is because the pressure drop increases acroos this segment. REmember, the pressure drop acroos the entire segment has to equal the difference in pressure between upstream and downstream. So the segment that is collapsed decreases in size. Now here are where my two theories come in: If venous pressure were to drop, the effective length of this segment would either increase to account for the increased resistance to maintain the same flow. The second theory is that the length stays teh same but the resistance increases because the collapsed segment collapses by a greater amount, in other words the size of the opening decreases.

Here is an image:

 

[denverdoc]

Just catching up on some threads this morning. I love threads like these that really try to understand the physics of physiology. I think your answer makes sense given the assumptions of West. The last I have read on the subject is that Starling resistance is a real phenomenon but likely occurs upstream of the capillaries. This may help to explain why West's models don't seem to explain the non-homogeneity of blood flow within any particular zone either when measured in various experimental animal surgical preps or by fMRI in intact subjects. There does seem to be a critical pressure in various vascular preps which must be overcome where zero or low flow conditions despite an overall positive pressure gradient. This is the whole notion of the starling resistor.

A good mathematical treatment can be found http://www.biomatematica.it/urbino2002/programmi/oejnotes.pdf" and as you can see, the kind of simple current through a wire model becomes a richly complex, non-linear and chaotic system.

Regarding the other issue of venous return versus cvp, the following discussion may be of value as it is very easy to confuse http://faculty.washington.edu/brengelm/COvsVR/pg5.html" .