Understanding Increase in Peripheral Resistance & Blood Pressure

[jaumzaum]

Hello guys, can anyone help me to understand why an increase in peripheral resistance causes an increase in the blood pressure?

If we assume the equation
Delta P = R times Q

If we assume Q is constant, the greater the resistance the greater the the decrease in pressure, so the pressure should be lower not higher

The only explanation I would have for the blood pressure to increase would be the heart trying to increase the aortic pressure so that the cava vein pressure (usually less than 4 mmHg) remains positive, and so the increase in blood pressure would be an indirect effect created because the heart itself begins to pump stronger. Is that right?

 

[DaveC426913]

Hello guys, can anyone help me to understand why an increase in peripheral resistance causes an increase in the blood pressure?

If we assume the equation
Delta P = R times Q

If we assume Q is constant, the greater the resistance the greater the the decrease in pressure, so the pressure should be lower not higher

The only explanation I would have for the blood pressure to increase would be the heart trying to increase the aortic pressure so that the cava vein pressure (usually less than 4 mmHg) remains positive, and so the increase in blood pressure would be an indirect effect created because the heart itself begins to pump stronger. Is that right?

I am no med student but I suspect you are misinterpreting the equation.

If we assume Q is constant, the greater the resistance the greater the the decrease in pressure,

Question this assumption.

Delta P = R times Q translates to
The difference in pressure** is proportional to the flow and to the resistance.

**specifically, the difference in pressure from the inlet of the vessel to the outlet

So - for a given flow - if resistance in the vessel increases, then pressure differential from one end to the other increases. Which makes intuitive sense, yes?

 

[pinball1970]

Hello guys, can anyone help me to understand why an increase in peripheral resistance causes an increase in the blood pressure?

If we assume the equation
Delta P = R times Q

If we assume Q is constant, the greater the resistance the greater the the decrease in pressure, so the pressure should be lower not higher

The only explanation I would have for the blood pressure to increase would be the heart trying to increase the aortic pressure so that the cava vein pressure (usually less than 4 mmHg) remains positive, and so the increase in blood pressure would be an indirect effect created because the heart itself begins to pump stronger. Is that right?

I'm not sure about your equation. One of the Phys guys may know.
Increase in blood pressure can be alleviated via, reduction in stroke volume, heart rate, vasodilator, volume.
So less power, less beats, greater area less fluid.
Peripheral resistance would be? From, vessel to capillaries to cells? If something is hindering that then pressure will build up.
Atherosclerosis, narrowing?
Edit. Analogy pump water at a constant rate through a pipe, same volume. Put a smaller volume at the end of the pipe the pressure will go up.
Reducing the pressure would involve slowing the rate down or reducing the volume if the area is permanently changed.

Is this what you are getting at? I cannot illustrate this quantitatively.
I need @jim mcnamara or @BillTre if you need something else

 

[jaumzaum]

I suspect you are misapplying the equation.

Delta P = R times Q translates to
The change in pressure is proportional to the flow and to the resistance.So - for a given flow - if resistance increases, then pressure increases.

The Delta P increases. But this Delta P is the pressure consumed, not the pressure gained. In a pipe for example, if the initial pressure is 100 mmHg, and Delta P is 90 mmHg, the final pressure is 10 mmHg.

 

[DaveC426913]

The Delta P increases. But this Delta P is the pressure consumed, not the pressure gained. In a pipe for example, if the initial pressure is 100 mmHg, and Delta P is 90 mmHg, the final pressure is 10 mmHg.

OK, I see your point. Assuming what you say is true, then it's non-intuitive.

Can you give us context from your textbook about pressure consumed v. gained?

 

[jaumzaum]

OK, I see your point. Assuming what you say is true, then it's non-intuitive.

Can you give us context from your textbook about pressure consumed v. gained?

The equation that relates pressure, resistance and flow can be written as:
Delta P = -RQ, where Delta P is final pressure minus initial pressure
Or, as many people prefer:
Delta P = RQ, where Delta P now is the initial pressure minus the final pressure.

When a fluid, that has some pressure, flows through a tube, because of friction the pressure decreases. That’s why the aortic pressure is 100 mmHg and because of the resistance of the vessels in the body only 5-10 mmHg arises at vena cava. 90-95 mmHg was consumed by the friction.

 

[pinball1970]

OK, I see your point. Assuming what you say is true, then it's non-intuitive.

Can you give us context from your textbook about pressure consumed v. gained?

Think I have the wrong end of the stick on this.

 

[jaumzaum]

I'm not sure about your equation. One of the Phys guys may know.
Increase in blood pressure can be alleviated via, reduction in stroke volume, heart rate, vasodilator, volume.
So less power, less beats, greater area less fluid.
Peripheral resistance would be? From, vessel to capillaries to cells? If something is hindering that then pressure will build up.
Atherosclerosis, narrowing?
Edit. Analogy pump water at a constant rate through a pipe, same volume. Put a smaller volume at the end of the pipe the pressure will go up.
Reducing the pressure would involve slowing the rate down or reducing the volume if the area is permanently changed.

Is this what you are getting at? I cannot illustrate this quantitatively.
I need @jim mcnamara or @BillTre if you need something else

Thanks @pinball1970, can you illustrate your example a little better?

 

[jim mcnamara]

Example: angiotensin II, and the vagus nerve do what you ask ( I guess here)

Angiotensin-converting enzyme decreases blood pressure. Inhibitors like this relax the veins and arteries to lower blood pressure. ACE inhibitors prevent production of angiotensin II, a hormone that narrows blood vessels.

BP regulation is a systemic set of biochemical processes that respond to other regulating hormones like cortisol - the so-called "fight or flight hormone". Or to vagus nerve input from the right atrium of the heart. (faster)

Secondary to the above are physical factors like standing up rapidly, especially after bending over. (Atrium thing)

I'm not getting what you are asking at all. BP control is NOT a merely simple hydrodynamics problem. As a wild hand-wavy guess I think an answer might be cortisol induced arterial contractions in response to low return blood pressure. Here is why:

Britannica

Special pressure sensors called baroreceptors (or venoatrial stretch receptors) located in the right atrium of the heart detect increases in the volume and pressure of blood returned to the heart. These receptors transmit information along the vagus nerve (10th cranial nerve) to the central nervous system.

The vagus nerve mediates changes in heart rate, and angiotensin II levels, to maintain enough blood pressure for the brain to keep going. Fainting can be a result of too low blood pressure to the brain, for example. Hypoglycemia (low blood sugar from no food ) gives a similar result sometimes. For the same reason -> feed the brain or else.

 

[pinball1970]

Thanks @pinball1970, can you illustrate your example a little better?

@Jim can answer your specifics if it's physiology based. I was just trying to give an example.
Hose pipe, constant rate and fixed volume until you squeeze the end with your fingers. The water sprays out with more force because you have just reduced the volume at the end. The pressure has built up, backed up (non technical language)

 

[jaumzaum]

Example: angiotensin II, and the vagus nerve do what you ask ( I guess here)

Angiotensin-converting enzyme decreases blood pressure. Inhibitors like this relax the veins and arteries to lower blood pressure. ACE inhibitors prevent production of angiotensin II, a hormone that narrows blood vessels.

BP regulation is a systemic set of biochemical processes that respond to other regulating hormones like cortisol - the so-called "fight or flight hormone". Or to vagus nerve input from the right atrium of the heart. (faster)

Secondary to the above are physical factors like standing up rapidly, especially after bending over. (Atrium thing)

I'm not getting what you are asking at all. BP control is NOT a merely simple hydrodynamics problem. As a wild hand-wavy guess I think an answer might be cortisol induced arterial contractions in response to low return blood pressure. Here is why:

BritannicaThe vagus nerve mediates changes in heart rate, and angiotensin II levels, to maintain enough blood pressure for the brain to keep going. Fainting can be a result of too low blood pressure to the brain, for example. Hypoglycemia (low blood sugar from no food ) gives a similar result sometimes. For the same reason -> feed the brain or else.

I will try to make my doubt clear.
Consider the image below:

The left ventricle pressure in a given moment is 100 mmHg. We measure the pressure at the brachial artery location, and because there are some resistance from the left ventricle to the brachial artery, the pressure will be a bit lower, let's consider it's 90 mmHg. When the blood gets to the vena cava (immediately before the right atrium) the pressure will be still lower, because the resistance from the left ventricle to the vena cava (systemic vascular resistance) is much greater. Consider the pressure there is 10 mmHg.

Now, for some reason, the resistance of any vessel in our body increases 10%. If we consider Q and the left ventricle pressure remains constant, then Delta P will increase, so that we would have the following:

This is a decrease in blood pressure, not an increase. That's why I'm confused, because all textbooks say there is an increase.

My theory is that the body senses the vena cava pressure drop and make the heart pump stronger, increasing the left ventricle pressure. So the constant thing there will not be the left ventricle pressure, but the vena cava pressure, and we would have the following:

And that is consistent with the textbooks, but I don't really know if this is right.

 

[pinball1970]

I will try to make my doubt clear.
Consider the image below:

View attachment 299839

The left ventricle pressure in a given moment is 100 mmHg. We measure the pressure at the brachial artery location, and because there are some resistance from the left ventricle to the brachial artery, the pressure will be a bit lower, let's consider it's 90 mmHg. When the blood gets to the vena cava (immediately before the right atrium) the pressure will be still lower, because the resistance from the left ventricle to the vena cava (systemic vascular resistance) is much greater. Consider the pressure there is 10 mmHg.

Now, for some reason, the resistance of any vessel in our body increases 10%. If we consider Q and the left ventricle pressure remains constant, then Delta P will increase, so that we would have the following:

View attachment 299841

This is a decrease in blood pressure, not an increase. That's why I'm confused, because all textbooks say there is an increase.

My theory is that the body senses the vena cava pressure drop and make the heart pump stronger, increasing the left ventricle pressure. So the constant thing there will not be the left ventricle pressure, but the vena cava pressure, and we would have the following:

View attachment 299842

And that is consistent with the textbooks, but I don't really know if this is right.

There is a huge amount that happens between those main two vessels. Veins have some smooth muscle help to move things along because the pressure is reduced.

 

[pinball1970]

Thanks @pinball1970, can you illustrate your example a little better?

I still don't know if this is physics question or medical question. I think the answer will be guided by that.

 

[BillTre]

Its a medical question, in a biophysics kind of way.
Its taught in some physiology courses.

I find the way this question was presented annoying. The question was poorly posed.
It took a long time to get through the thread to get see what your abbreviations were for (I don't remember them from long ago).
Also you took a long time to indicate between which two points the delta P was measured. It seems you mean branchial artery to vena cava (big vein).
@pinball1970 is right when he says:

There is a huge amount that happens between those main two vessels.

All other things being equal, if the resistance goes up between two points, the pressure downstream will go down.
Just to go through things that could affect the resistance between those two places:

• start at branchical artery
• a main point of control is in arterioles before the blood gets to the capillaries, but there could be more control point (by constriction) probably at branch points.
• the capillaries: these are the smallest blood vessels. Not all of them have big flows all the time. Some of the controls would be at the upstream end of the capillaries, but I think its mostly at the arterioles.
• Veins (which lead back to the vena cava) are low pressure after coming out of the capillaries. They have valves to prevent back flow and local pressure can be produced by body movements and muscles squeezing specific veins. In addition, veins can be quite floppy (looseness controlled by nerves and hormones of various kinds), so they can dilate. this means they can have a lot of blood flowing in and don't have to have the equivalent volume flowing out very soon. (Often times blood flow and pressure can be though of in terms of electrical circuits: blood flow is like current flow, blood pressure is like electrical potential (or voltage) (its the drive force), and resistance to blood flow is like electrical resistance. The compliance of veins (its ability to strech out and absorb blood volume) is like a capacitor in a circuit, with can store of charge.)

Getting back to your initial question:

why an increase in peripheral resistance causes an increase in the blood pressure?

Just in the simplest interpretation, an increase in the resistance will produce produce a larger drop in pressure along long single vessel.
An addition, the vascular system is branched with flows being directed to different parts of the body, as is appropriate for different conditions. Different areas you measure at can therefore receive a lot fo flow or not. For example, if you are cold blood flow will be internalized to prevent loss of precious body heat.
This stuff can get really complicated. You should take a physiology course to get a better understanding of it.

The choice the vena cava to measure a pressure difference from the starting blood pressure form is not a good choice for developing an understanding of the process. As @pinball1970 said:

There is a huge amount that happens between those main two vessels.

 

[Tom.G]

Lets try this approach:

A single beat of the heart expels an essentially constant volume (assuming a healthy heart). This volume is limited by the volume change of the heart chambers during filling and expulsion.

Given the (mostly) constant-volume situation, if there is a constriction in the blood vessels that impedes flow, the pressure upstream of the constriction will be higher. Likewise, the pressure downstream of the constriction will be lower.

The blood pressure is typically measured in the upper left arm in Humans. The left arm is chosen because, plumbing-wise, it is the closest accessible point to the heart; as such it is the least likely point to have a blockage and the pressure will be close to the pressure at the heart output.

The blood vessels walls are slightly elastic and the vessels expand and contract with each heartbeat. That's why you can feel your pulse in your wrist and neck, where the arteries are close to the surface. A persons blood pressure often goes up with age because the vessels lose their elasticity as they age, the vessels don't expand thereby increasing the friction to flow.

You may find this site interesting:
https://my.clevelandclinic.org/health/body/21775-circulatory-system

Hope this helps!

Cheers,
Tom

 

[Fra]

A physicists take on this, ignoring the pulsations, "Ohms law" for the heart goes like this

"Pump pressure" = MAP – CVP = SVR * CO

MAP = mean arterial pressure
CVP = Central venous pressure
SVR = Systemic vascular resistance
CO = Cardiac output (flow), which is turn is = HR * SV (HeartRate x StrokeVolume)

If the peripheral vessels constrict, then it means SVR increase and the pressure in the heart increases, unless the HR is downregulated.

Several of these parameters are subject to autonomous regulation, and may change at the same time. To know what happens one probably need to ask what the reason for the peripheral construction, as other autoregulations make take place at the same time. This can happen due to cold shock, or mental stress. Typically SVR and BP goes up during stress, but in different ratios dependeing on if it's a challenge or threat, as the process involves also stress hormones that modulate the parameters in the equation as well.

Chapter 8 in handbook of psychophysiology
https://www.cambridge.org/core/book...hophysiology/CAB9D08704751D5A26A58C442B3F2BB8

/Fredrik

 

[russ_watters]

I am no med student but I suspect you are misinterpreting the equation.

Question this assumption.

Delta P = R times Q translates to
The difference in pressure** is proportional to the flow and to the resistance.

**specifically, the difference in pressure from the inlet of the vessel to the outlet

So - for a given flow - if resistance in the vessel increases, then pressure differential from one end to the other increases. Which makes intuitive sense, yes?

The Delta P increases. But this Delta P is the pressure consumed, not the pressure gained. In a pipe for example, if the initial pressure is 100 mmHg, and Delta P is 90 mmHg, the final pressure is 10 mmHg.

OK, I see your point. Assuming what you say is true, then it's non-intuitive.

Can you give us context from your textbook about pressure consumed v. gained?

I'm pretty sure you had it right the first time, Dave. This is a basic fluid system problem: The pressure gained at the pump (the heart) must sum to zero with the pressure loss of the system. If you increase the resistance, the pressure loss is larger in the system so the pressure gain provided by the pump must increase to maintain the same flow rate.

The Ohm's law/circuit analogy also works: voltage gain at the battery equals (sums to zero with) the voltage drop in the circuit.

 

[.Scott]

If you will allow a software engineer with ample experience with PID Loops and SCADA systems to attempt to address this issue:

One main objective of the circulatory system is the transport of "stuff" to and from all organs of the body. I wouldn't be surprised if a minimal pressure is also required - I'll leave that possibility to other.

In a situation where there is a fixed demand for the delivery rate of O2, CO2, nutrients, and whatever, you want a system that meets that demand. The best system design is one that will regulate heart rate and blood pressure based on the actual performance of the system. So if you are "starved" for whatever, you would hope that this regulatory system would respond by increasing or decreasing whatever it needs to fix the situation - to reach the delivery goals of whatever you are lacking.

You should expect any such regulated system to compensate for obstructed arteries, surge in demand, or any similar challenges. The most obvious compensation method would be to increase the heart rate in an attempt to maintain the flow rate even against the higher resistance. A secondary method might be to increase the volume and/or minimum pressure of the fluid system as a strategy to increase the average diameter of the tubing in an elastic system.

 

[Fra]

The dynamics of the regulation is complex indeed. The ohms law analogy is a nice simple overall view, but all the parameters in it are subject to regulation, and arent fixed like the resistor in an elecrtical circuit. Regulations can be classified as both systemic(usually controlled by ANS) vs local(local autoregulatory mechanisms), and quick(typically ANS) vs slow(typically hormones).

Slow responses are often mediated by hormones that affects the heart muscles, salt balance etc, this can regulate the blood volume etc, this is more economical for the body.

But in a actue stress situations the hormonal regulation are just way too slow, the ANS which have direct wires to the heart SA node pacemaker cells, can regulate the HR immediately if required. One of the quickest reflexes is the baroreflex, which downregulates the HR in response to pressure peaks. This is the famous mechanism behind the neck karate chop, it activates baroreflexes that can cause close to stopped heartbeat and fainting. The acute stress responses may be very costly in long term though for the body. The density of baroreceptor cells are particutlary high in the neck. Stimulating this reflexes is also a potential therapy that is alternative to blood pressure medicine
https://www.dicardiology.com/product/fda-approves-pacemaker-device-treat-heart-failure.

Local autonomous regulations also exists, for example NO is a local vasodilator and can be activated in local tissue from high pressure.

When all these regulations take place in concert modelling it becomes non-trivial, and implies modelling also the brains stress responses, where different subjects respond slitghtly differently to the same input.

/Fredrik