What's physiological mechanism of this?? (CO2 and vessel constrict. in body vs head)

[cardsurgguy]

I was curious about the physiological mechanism of how something works...
This probably should go in a critical care medicine/pulmonary forum if there was one. But here is the most traveled residency forum anyways, so hopefully someone will satisfy my curiousity about this.

We had a kid the other day who had congenital heart surgery.
During the first night after surgery, blood gas came back and he had a PCO2 of lower 40's and a pH of 7.41 I think. The nurse said we got to increase his rate on the vent to get his PCO2 down and pH up since the pediatric cardiac surgeon wanted to keep the kid at around mid 7.4 range. So we did that and the blood gas after the vent change came back with a PCO2 of 35 I believe and a pH of 7.46-47.
I know how an increase in rate on the vent would get the PCO2 down and the pH up(via the bicarb-CO2 and H2O equilibrium, increase rate=less CO2=less H+=higher pH)

My question deals specifically with something else the nurse said. When I asked, she said that the reason why the PCO2 need to be kept low enough in these kids (ie not 40's) is because CO2 constricts blood flow through the pulmonary vasculature and therefore less bloodflow goes to the pulmonary bed. In this kid with a hypoplastic left heart, obviously this isn't ideal, so the CO2 needs to be kept low enough to not constrict bloodflow to the pulmonary bed.

Something else she said is what my question deals with. She said that CO2 constricts bloodflow pulmonary wise (and systemically) but CO2 has the direct opposite effect on the vessels in the brain. In the brain, CO2 dilates the vessels and hence a lack of CO2 would constrict the vessels in the brain.

My question is: How????

By what physiological mechanism can CO2, the same molecule, constrict blood vessels in the body and lungs, but dilate them in the head??

Does it have to do with different receptors on the blood vessels in each of the respective locations?

I've been really curious about this because it seems so awkward.

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[missdr]

you should post this on the anesthesiology forum..they love this kind of stuff!

ps. while nurses can be your best friends on the wards they are not always right... just beware

 

[new_avatar]

Slide 5: Factors affecting pulmonary vascular resistance
There’s lots of factors that can affect pulmonary vascular resistance. And it’s important that you be aware of them. The most important and the ones that you will see most routinely are alveolar hypoxia, acidemia, alveolar hypercarbia by leading to acidemia, blood viscosity in other words if a patients blood counts are very high, the viscosity and the turbulence in the small arteries is impaired and that will increase the pulmonary vascular resistance and specifically when we talk about the pulmonary vasculature, we’re talking about two specific cell types, and that’s the endothelial cells that’s lining the vascular surface, and the smooth muscle cell that’s around the endothelial cell. We find that in patients with pulmonary hypertension, endothelial cell dysfunction and smooth muscle cell hypertrophy occur and as a result of that and as a result of the altered hemodynamics inside the small vessels in the pulmonary circulation we get in situ thrombosis. And these are all either mechanisms or effects of increased pulmonary vascular resistance.

Alveolar hypoxia, acidemia and hypercarbia cause vasoconstriction, and by that mechanism they increase pulmonary vascular resistance. And I’d just like to spend on moment describing the mechanism by which alveolar hypoxia causes vasoconstriction, because its relevant in the pathophysiology of pulmonary hypertension, and its interesting to keep in mind when we think about these diseases.


Slide 6: Hypoxia
We know that hypoxia vasoconstricts the pulmonary vasculature. What does hypoxia do to the peripheral vasculature? Dilates, ok, so there’s another difference between the pulmonary and systemic circulation. Hypoxia will vasoconstrict pulmonary vasculature, whereas the peripheral circulation will vasodilate in response to hypoxemia. And why do you think that happens? If you have hypoxemia, you would like to continue to preserve oxygen delivery to your periphery and by vasodilating, you’re able to do that. However, if you have local hypoxemia in the lungs, you would like to limit the amount of hypoxemia and the amount of blood that is shunted to those hypoxemic areas, and therefore you have local vasoconstriction in the pulmonary circulation as opposed to the systemic.

Now, what we know and what we’ve identified is that hypoxia inhibits these voltage gated potassium channels that are located in the pulmonary artery smooth muscle cell. And that when your patient is hypoxemic these voltage gated channels open, they lead to a flux of calcium into the smooth muscle and this leads to vasoconstriction. So this is the mechanism by which hypoxia leads to the local vasoconstriction of the pulmonary circulation. What’s interesting, and the reason why I bring it up is because pulmonary hypertension is a disease that came into sort of the public consciousness sometime in the late 60’s when there were a whole slew of young women that had been taking diet pills that developed pulmonary hypertension. And the reason why these women developed pulmonary hypertension in this setting is because these drugs where affecting the potassium channel blockers. In fact, now that we know more about how hypoxia and some of these drugs and toxins affect vasoconstriction, we know that in primary pulmonary hypertension, there’s evidence of some genetic abnormalities in these potassium channels. So as we learn more and more about the pathophysiology about this disease. We are able to devise pathophysiological mechanisms of why they occur. And, also to try to combat them by developing drugs that will help alleviate the problem.

So we’re going to get to the case now.

NYU website

 

[cardsurgguy]

you should post this on the anesthesiology forum..they love this kind of stuff!

ps. while nurses can be your best friends on the wards they are not always right... just beware

Oh yeah. I know

That's part of the reason I'm posting here. She didn't know the answer of why the two were different.

Even if she told me, I would ask anyways just to get a more detailed answer.

She's sharp though. As I'm sure you know, there's a large variance in the knowledge among nurses. Some are very sharp and some are not. She's good though. That's part of the reason she was on the congenital heart patient. There's only certain nurses that do them.

If nobody responds here, I'll go over to the anes. forum.

 

[cardsurgguy]

This article reports work done on sheep:

sheep article

seems to suggest alkalosis, whether respiratory or metabolic induces pulmonary vasoconstriction in newborn lambs.


Hyperventilation is used to control cerebral edema (along with steroids and mannitol), blood flow responds to CO2, which makes sense, in hypercapnic states more flow would ensure more exchange volume.

ICP control

Thanks, good stuff.

I just breezed over really quickly, since I'm doing other stuff.
But I couldn't find the physiological cause for the different effect cerebral vs. body.

Who knows, maybe it's one of those things that is just known to be the case, without the exact physiological mechanism for the difference actually known...

 

[SoCuteMD]

I was curious about the physiological mechanism of how something works...
This probably should go in a critical care medicine/pulmonary forum if there was one. But here is the most traveled residency forum anyways, so hopefully someone will satisfy my curiousity about this.

We had a kid the other day who had congenital heart surgery.
During the first night after surgery, blood gas came back and he had a PCO2 of lower 40's and a pH of 7.41 I think. The nurse said we got to increase his rate on the vent to get his PCO2 down and pH up since the pediatric cardiac surgeon wanted to keep the kid at around mid 7.4 range. So we did that and the blood gas after the vent change came back with a PCO2 of 35 I believe and a pH of 7.46-47.
I know how an increase in rate on the vent would get the PCO2 down and the pH up(via the bicarb-CO2 and H2O equilibrium, increase rate=less CO2=less H+=higher pH)

My question deals specifically with something else the nurse said. When I asked, she said that the reason why the PCO2 need to be kept low enough in these kids (ie not 40's) is because CO2 constricts blood flow through the pulmonary vasculature and therefore less bloodflow goes to the pulmonary bed. In this kid with a hypoplastic left heart, obviously this isn't ideal, so the CO2 needs to be kept low enough to not constrict bloodflow to the pulmonary bed.

Something else she said is what my question deals with. She said that CO2 constricts bloodflow pulmonary wise (and systemically) but CO2 has the direct opposite effect on the vessels in the brain. In the brain, CO2 dilates the vessels and hence a lack of CO2 would constrict the vessels in the brain.

My question is: How????

By what physiological mechanism can CO2, the same molecule, constrict blood vessels in the body and lungs, but dilate them in the head??

Does it have to do with different receptors on the blood vessels in each of the respective locations?

I've been really curious about this because it seems so awkward.

I'm not sure what the mechanism is, but the nurse is only partially right. An increase in pCO2 causes vasoconstriction in the pulmonary vasculature and vasodilation EVERYWHERE else.

CO2 causes constriction in the pulmonary vasculature because an increase in pC02 sends the message "there is damage/shunting here, sending blood here will not effectively oxygenate it" so blood is preferentially sent to a different part of the lung where it will receive better oxygenation. The problem comes when

In the non-pulmonary tissues, hypoxia is going to induce vasodilation so as to better perfuse the tissues.

However, I suppose if you had peripheral tissues, the brain, and the heart competing for a limited blood flow (such as in left heart failure), then blood flow would go preferentially to the heart and brain and decrease to peripheral tissues - sort of like the "diving" or "diving seal" reflex, minus the cold water!

 

[DeLaughterDO]

I'm not sure what the mechanism is, but the nurse is only partially right. An increase in pCO2 causes vasoconstriction in the pulmonary vasculature and vasodilation EVERYWHERE else.

CO2 causes constriction in the pulmonary vasculature because an increase in pC02 sends the message "there is damage/shunting here, sending blood here will not effectively oxygenate it" so blood is preferentially sent to a different part of the lung where it will receive better oxygenation. The problem comes when

In the non-pulmonary tissues, hypoxia is going to induce vasodilation so as to better perfuse the tissues.

However, I suppose if you had peripheral tissues, the brain, and the heart competing for a limited blood flow (such as in left heart failure), then blood flow would go preferentially to the heart and brain and decrease to peripheral tissues - sort of like the "diving" or "diving seal" reflex, minus the cold water!

This is correct - hypoxia and hypercarbia in the pulmonary vasculature causes vasoconstriction in an effort to better equalize the V/Q ratio and keep it as near 1 as possible (i.e. keep the areas getting oxygen flow matched with good blood flow), since localized hypoxia and hypercarbia mean there is altered gas flow.

In the peripheral vasculature (brain, heart, gut, skin, musculature...) localized hypercarbia and hypoxia cause vasodilation. This is due, in part, to other local mediators (ADP, lactate, H+), but those factors (hypoxia, hypercarbia) do have some independent effects.

In the case of generalized hypoxia and hypercarbia (i.e. shock, CHF), other mediators come into play. Renal hypoxia and decreased blood flow cause the release of renin with activation of the renin-angiotensin cascade, as well as the release of epinephrine and norepi via sympathetic activation. This causes more peripheral and gut vasoconstriction to shunt blood flow to the more important organs (brain, heart).

I'm sure I've forgotten some of this, but I haven't had physiology in a couple of years, but I think I've hit the main points.

jd

btw - socuteMD, don't forget to pay this back...

 

[14022]

I was curious about the physiological mechanism of how something works...
This probably should go in a critical care medicine/pulmonary forum if there was one. But here is the most traveled residency forum anyways, so hopefully someone will satisfy my curiousity about this.

We had a kid the other day who had congenital heart surgery.
During the first night after surgery, blood gas came back and he had a PCO2 of lower 40's and a pH of 7.41 I think. The nurse said we got to increase his rate on the vent to get his PCO2 down and pH up since the pediatric cardiac surgeon wanted to keep the kid at around mid 7.4 range. So we did that and the blood gas after the vent change came back with a PCO2 of 35 I believe and a pH of 7.46-47.
I know how an increase in rate on the vent would get the PCO2 down and the pH up(via the bicarb-CO2 and H2O equilibrium, increase rate=less CO2=less H+=higher pH)

My question deals specifically with something else the nurse said. When I asked, she said that the reason why the PCO2 need to be kept low enough in these kids (ie not 40's) is because CO2 constricts blood flow through the pulmonary vasculature and therefore less bloodflow goes to the pulmonary bed. In this kid with a hypoplastic left heart, obviously this isn't ideal, so the CO2 needs to be kept low enough to not constrict bloodflow to the pulmonary bed.

Something else she said is what my question deals with. She said that CO2 constricts bloodflow pulmonary wise (and systemically) but CO2 has the direct opposite effect on the vessels in the brain. In the brain, CO2 dilates the vessels and hence a lack of CO2 would constrict the vessels in the brain.

My question is: How????

By what physiological mechanism can CO2, the same molecule, constrict blood vessels in the body and lungs, but dilate them in the head??

Does it have to do with different receptors on the blood vessels in each of the respective locations?

I've been really curious about this because it seems so awkward.

This is strange. We had the same issue yesterday in our peds icu. First of all, what stage of his HLHS repair was he at? Did he receive a Glenn? If he was on the second stage of the repair and received a Glenn, our attending said that you are supposed to accept higher than normal CO2 levels and because of the mechanism you describe. When thinking about these mechanisms, you have to keep in mind that these hypoplast kids have extremely abnormal anatomy after their surgical repair, so you manage them much differently than you would other heart surgeries with "normal" anatomy (eg, VSD or AV canal repair, arterial switch for transposition, etc).

After a Norwood (stage 1 of 3 of HLHS repair) the right ventricle becomes the only source of forward flow, thus univentricular physiology. The patient has a single atrium (the atrial septum is removed) that leads into the single ventricle that connects to the aorta. To allow flow to the lungs, the patient will either have a BT shunt (subclavian artery to right pulmonary artery shunt) or Sano shunt (single ventricle to pulmonary artery shunt). During the second stage of the repair, the shunt is cut down and a Glenn is performed. This process separates the SVC from the heart and connects it to the side of the left pulmonary artery to allow flow to each lung. Since the IVC is connected to the single ventricle, the IVC sends its deoxygenated blood directly back to the body and skips the lungs. Therefore, the Glenn provides the only source of pulmonary blood flow, which is the venous return from the divided SVC into the pulmonary arteries. Therefore, the only way to get blood to the lungs is to get blood to the head first. By keeping a higher PCO2, the cerebral blood vessels dilate allowing more blood flow to the head, more flow into the SVC, and therefore more flow to the lungs. Lowering the CO2 by too much will cause cerebral vasoconstirction and push more flow from the head to the lower body, which will become blue blood, enter the IVC to the atrium into the single ventricle and back to the body without going to the lungs. Of course, if the PCO2 is too high, blood will go to the head but the pulmonary resistance will be too high so you will have elevated cerebral pressures without having optimal pulmonary flow.

Hear are the articles supporting this.

http://www.ncbi.nlm.nih.gov/entrez/...t_uids=9852929&query_hl=2&itool=pubmed_docsum

http://www.ncbi.nlm.nih.gov/entrez/..._uids=14566243&query_hl=4&itool=pubmed_docsum

 

[cardsurgguy]

This is strange. We had the same issue yesterday in our peds icu. First of all, what stage of his HLHS repair was he at? Did he receive a Glenn? If he was on the second stage of the repair and received a Glenn, our attending said that you are supposed to accept higher than normal CO2 levels and because of the mechanism you describe. When thinking about these mechanisms, you have to keep in mind that these hypoplast kids have extremely abnormal anatomy after their surgical repair, so you manage them much differently than you would other heart surgeries with "normal" anatomy (eg, VSD or AV canal repair, arterial switch for transposition, etc).

After a Norwood (stage 1 of 3 of HLHS repair) the right ventricle becomes the only source of forward flow, thus univentricular physiology. The patient has a single atrium (the atrial septum is removed) that leads into the single ventricle that connects to the aorta. To allow flow to the lungs, the patient will either have a BT shunt (subclavian artery to right pulmonary artery shunt) or Sano shunt (single ventricle to pulmonary artery shunt). During the second stage of the repair, the shunt is cut down and a Glenn is performed. This process separates the SVC from the heart and connects it to the side of the left pulmonary artery to allow flow to each lung. Since the IVC is connected to the single ventricle, the IVC sends its deoxygenated blood directly back to the body and skips the lungs. Therefore, the Glenn provides the only source of pulmonary blood flow, which is the venous return from the divided SVC into the pulmonary arteries. Therefore, the only way to get blood to the lungs is to get blood to the head first. By keeping a higher PCO2, the cerebral blood vessels dilate allowing more blood flow to the head, more flow into the SVC, and therefore more flow to the lungs. Lowering the CO2 by too much will cause cerebral vasoconstirction and push more flow from the head to the lower body, which will become blue blood, enter the IVC to the atrium into the single ventricle and back to the body without going to the lungs. Of course, if the PCO2 is too high, blood will go to the head but the pulmonary resistance will be too high so you will have elevated cerebral pressures without having optimal pulmonary flow.

Hear are the articles supporting this.

http://www.ncbi.nlm.nih.gov/entrez/...t_uids=9852929&query_hl=2&itool=pubmed_docsum

http://www.ncbi.nlm.nih.gov/entrez/..._uids=14566243&query_hl=4&itool=pubmed_docsum

I think this patient was at the Hemi-Fontan stage (ie Glenn)

I could see both ways, the more blood to the head due to more blood through the SVC argument which would argue for a higher PCO2 and keeping the patient a little on the acidodic side

and also the argument I presented, which was the more blood to the pulmonary bed and keeping pulmonary resistance down argument which would argue for a lower PCO2 and keeping hte patient a little on the alkolodic side

I could see the logic behind either, and definitely could see the need to keep balance

who knows, maybe I have things mistaken or switched around, it's been known to happen before

or maybe the patient I'm talking about had a Fontan (the full Fontan, ie 3rd out of 3 operations)

All I'm sure about is that I love this stuff...

 

[14022]

I think this patient was at the Hemi-Fontan stage (ie Glenn)

I could see both ways, the more blood to the head due to more blood through the SVC argument which would argue for a higher PCO2 and keeping the patient a little on the acidodic side

and also the argument I presented, which was the more blood to the pulmonary bed and keeping pulmonary resistance down argument which would argue for a lower PCO2 and keeping hte patient a little on the alkolodic side

I could see the logic behind either, and definitely could see the need to keep balance

who knows, maybe I have things mistaken or switched around, it's been known to happen before

or maybe the patient I'm talking about had a Fontan (the full Fontan, ie 3rd out of 3 operations)

All I'm sure about is that I love this stuff...

hemi fontan and glenn are very similar, but not exactly the same thing...they are hemodynamically similar but a different surgical technique...only one or the other, never both, will be performed on the patient

the age of the patient will tell you what stage they are at

stage 1- Norwood- done in the first month of life, often the first week or two
stage 2- glenn or hemi-fontan- done at 5-7 months
stage 3- fontan- done at 35-50 pounds (around 3-5 years old)

 

[cardsurgguy]

hemi fontan and glenn are very similar, but not exactly the same thing...they are hemodynamically similar but a different surgical technique...only one or the other, never both, will be performed on the patient

the age of the patient will tell you what stage they are at

stage 1- Norwood- done in the first month of life, often the first week or two
stage 2- glenn or hemi-fontan- done at 5-7 months
stage 3- fontan- done at 35-50 pounds (around 3-5 years old)

good to know, I thought the bidirectional Glenn and hemi-fontan are synonyms
What are the differences between the two?

I know the ages for each stage, but part of the problem is I can't remember the age of the patient (it was a bit ago).
Says a lot of my memory...

 

[14022]

good to know, I thought the bidirectional Glenn and hemi-fontan are synonyms
What are the differences between the two?

Both procedures have the end result of shunting SVC return into the pulmonary arteries.

The Glenn shunt when first described was when they made an end to end anstamosis of the SVC to the right pulmonary artery. This obviously required the RPA to be divided from the main PA and essentially eliminating blood flow to the left lung. The bidirectional Glenn was a modification made by other surgeons (none of which were Dr. Glenn which is odd because his name is still on the procedure...but I digress)...the bidirectional Glenn uses anastamosis of the end of the divided SVC to the side of the right PA. Therefore the right PA is not divided and blood goes bidirectionally to both lungs. The main point here is that the SVC is divided from the heart and reanastamosed to the RPA.

The hemi-fontan also shunts blood from the SVC to the lungs. In this operation, the side of the right PA is connected to the atriacaval junction at the top of the right atrium. A patch is then put in the right atrium at the inflow site from the SVC to prevent SVC blood flow to the heart and shunting all of the flow to the lungs. Therefore, the SVC is not divided from the RA. Apparently, when you complete the Fontan at 3 years old, it is easier to do so after a hemi-fontan, than a Glenn, for reasons I am not too sure (I have not seen a hemi-fontan done during my elective), but I am sure this is surgeon dependent. The hemi-fontan also has shorter time on bypass than the Glenn.