Keeping PDA open vs. keeping it closed? uworld Q id 315

[as90]

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Hi,
I saw this question and normally I thought we would want to keep it open with prostaglandins if it is not causing cyanosis? Did they want to close it b/c of the systolic murmur at the infraclavicular region?

I thought in general it is vital to keep it open so long as it is not becoming left to right? Doesn't to keeping it open result in more pulmonary blood flow?

on a tangent, does anyone have any good videos on this? I totally suck at the physiology of this and DIT did not do a good job at explaining it either.

thanks so much

 

[thawunandonly]

Hi,
I saw this question and normally I thought we would want to keep it open with prostaglandins if it is not causing cyanosis? Did they want to close it b/c of the systolic murmur at the infraclavicular region?

I thought in general it is vital to keep it open so long as it is not becoming left to right? Doesn't to keeping it open result in more pulmonary blood flow?

on a tangent, does anyone have any good videos on this? I totally suck at the physiology of this and DIT did not do a good job at explaining it either.

thanks so much

It's not supposed to be open, so we close it. If you're thinking - hey, it's not cyanotic, so it's no problem - it will lead to shunt reversal later in life and then become cyanotic [Eisenmenger's syndrome]. (BTW, it is a LTR shunt...)

LtR shunt -> increase blood flow to the pulmonary circuit -> increase pulmonary hypertension -> now the pulmonary circuit has higher pressure than the systemic circuit -> becomes a RtL shunt -> cyanosis

But why wait for the reversal of the shunt? Let's just fix it now. If PGE keeps it open, then we use indomethacin (NSAID) to decrease PG synthesis and close it.

[One of] the only times we want it open is if there is transposition of the great vessels, which makes two closed loops, so we need a path between the two circuits.

 

[as90]

It's not supposed to be open, so we close it. If you're thinking - hey, it's not cyanotic, so it's no problem - it will lead to shunt reversal later in life and then become cyanotic [Eisenmenger's syndrome]. (BTW, it is a LTR shunt...)

LtR shunt -> increase blood flow to the pulmonary circuit -> increase pulmonary hypertension -> now the pulmonary circuit has higher pressure than the systemic circuit -> becomes a RtL shunt -> cyanosis

But why wait for the reversal of the shunt? Let's just fix it now. If PGE keeps it open, then we use indomethacin (NSAID) to decrease PG synthesis and close it.

[One of] the only times we want it open is if there is transposition of the great vessels, which makes two closed loops, so we need a path between the two circuits.

Thanks, i see PDA being a right to left shunt....then as you said as time progresses it will become Eisgenmenger's due to the increased RVH

is the cyanosis due to the blood not getting into the lungs? does this mean you have increased (purely deoxygenated blood going in through the hole between pulmonary artery and aorta). Eventually the blood will back flow and you get the cyanosis?

so essentially what you are fearing is that the PDA which should be R to L (right ventricle puts blood into the pulmonary artery--->goes through hole in PDA to the systemic through aorta)....then u get the L to R, with the increase pressure in the pulmonary circuit and not enough oxygenation?

I understand what you are saying with the transpositon of vessels though.

sorry for overthinking it maybe I have the flow wrong.

 

[Anastomoses]

Thanks, i see PDA being a right to left shunt....then as you said as time progresses it will become Eisgenmenger's due to the increased RVH

is the cyanosis due to the blood not getting into the lungs? does this mean you have increased (purely deoxygenated blood going in through the hole between pulmonary artery and aorta). Eventually the blood will back flow and you get the cyanosis?

so essentially what you are fearing is that the PDA which should be R to L (right ventricle puts blood into the pulmonary artery--->goes through hole in PDA to the systemic through aorta)....then u get the L to R, with the increase pressure in the pulmonary circuit and not enough oxygenation?

I understand what you are saying with the transpositon of vessels though.

sorry for overthinking it maybe I have the flow wrong.

whoa, are you serious?

the fetal ductus arteriosus is right to left. PDA is obviously Left to right due to the lung + placental changes at birth. And how did you not learn that treatment is ligating it right away...? The shunt can get bigger with age. And even if it is getting more oxygen, what about cardiac reserve?

 

[thawunandonly]

Thanks, i see PDA being a right to left shunt....then as you said as time progresses it will become Eisgenmenger's due to the increased RVH

is the cyanosis due to the blood not getting into the lungs? does this mean you have increased (purely deoxygenated blood going in through the hole between pulmonary artery and aorta). Eventually the blood will back flow and you get the cyanosis?

so essentially what you are fearing is that the PDA which should be R to L (right ventricle puts blood into the pulmonary artery--->goes through hole in PDA to the systemic through aorta)....then u get the L to R, with the increase pressure in the pulmonary circuit and not enough oxygenation?

I understand what you are saying with the transpositon of vessels though.

sorry for overthinking it maybe I have the flow wrong.

Well someone can clarify if I'm wrong. Otherwise I may be confusing myself too.

Rule of thumb: flow will go down a pressure gradient.

In utero, it is a RtL shunt. This is because the fetus has no use for lungs and with hypoxia the lung vasculature will vasoconstrict. Since there is such high pressure/hypertension, the flow will be RtL. At birth, oxygen makes the pulmonary hypertension drop to "normal" levels, and now the fetus uses its lungs and the shunt goes to what we know as LtR.

Now LtR shunt is normally not cyanotic. But if there is too much blood in the pulmonary vessels, over time it will again become a high pressure circuit (I believe via hyaline arteriolosclerosis), and flow will go back to being RtL. In the fetus this was okay because the blood was oxygenated by the placenta/mother. In the child/adult, now you have mixed venous blood going going to the body, when it should be freshly oxygenated blood only. The rest of the body becomes cyanotic.

Someone please save us and let us know if what I'm saying it clear/accurate.

 

[Jamiu22]

Well someone can clarify if I'm wrong. Otherwise I may be confusing myself too.

Rule of thumb: flow will go down a pressure gradient.

In utero, it is a RtL shunt. This is because the fetus has no use for lungs and with hypoxia the lung vasculature will vasoconstrict. Since there is such high pressure/hypertension, the flow will be RtL. At birth, oxygen makes the pulmonary hypertension drop to "normal" levels, and now the fetus uses its lungs and the shunt goes to what we know as LtR.

Now LtR shunt is normally not cyanotic. But if there is too much blood in the pulmonary vessels, over time it will again become a high pressure circuit (I believe via hyaline arteriolosclerosis), and flow will go back to being RtL. In the fetus this was okay because the blood was oxygenated by the placenta/mother. In the child/adult, now you have mixed venous blood going going to the body, when it should be freshly oxygenated blood only. The rest of the body becomes cyanotic.

Someone please save us and let us know if what I'm saying it clear/accurate.

Sounds about right. ...in addition the placenta makes PGE to keep the pda open... hence it makes sense why an nsaid would close a pde.

And lastly. ...I don't think it hyaline arteriosclerosis (HA) that you get with higher pressures in the pda but just your run of the mill medial hypertrophy due to the higher pressures on the vessel smooth muscle. You typically onky get HA with very small vessels. I may be wrong but it sounds right in my head lol.

 

[as90]

Well someone can clarify if I'm wrong. Otherwise I may be confusing myself too.

Rule of thumb: flow will go down a pressure gradient.

In utero, it is a RtL shunt. This is because the fetus has no use for lungs and with hypoxia the lung vasculature will vasoconstrict. Since there is such high pressure/hypertension, the flow will be RtL. At birth, oxygen makes the pulmonary hypertension drop to "normal" levels, and now the fetus uses its lungs and the shunt goes to what we know as LtR.

Now LtR shunt is normally not cyanotic. But if there is too much blood in the pulmonary vessels, over time it will again become a high pressure circuit (I believe via hyaline arteriolosclerosis), and flow will go back to being RtL. In the fetus this was okay because the blood was oxygenated by the placenta/mother. In the child/adult, now you have mixed venous blood going going to the body, when it should be freshly oxygenated blood only. The rest of the body becomes cyanotic.

Someone please save us and let us know if what I'm saying it clear/accurate.

Thank you all so much for the responses. I apologize for the late thank you, I have been trying to jam in as much studying. I understand it better now.

I have a very weak understanding of Cardiac Pathophysiology in general. But thank you for this.