Quick question about right sided heart failure

[caxoo]

So as I understand, usual right HF presents w/ systemic backup [periph edema, JVP, etc] and possibly low pulm perfusion

So for example, tricuspid regurgitation -> RV dilation -> eventual R HF and systemic backup

But ASD/VSD and its resulting RV dilation and right HF presents as pulmonary HTN? How to explain the discrepancy in presentation?

Googling around isn't helping - my intuition says the difference is because in ASD/VSD, the RV still has less contractility due to dilation/remodeling, but since there's still a constant infusion of volume from the left side, it still results in net increase in volume in pulmonary circulation



Actually typing that out raises another question - in Eisenmenger syndrome, the pathogenesis is L-R shunt -> pathologic remodeling -> pulmonary HTN. Wouldn't the pulmonary HTN be DESPITE the remodeling, not because of it?

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[TheOther]

So for example, tricuspid regurgitation -> RV dilation -> eventual R HF and systemic backup

You got these mixed up. RV dilation leads to TR due to the increased volume pulling apart the valves.

But ASD/VSD and its resulting RV dilation and right HF presents as pulmonary HTN? How to explain the discrepancy in presentation?

Actually typing that out raises another question - in Eisenmenger syndrome, the pathogenesis is L-R shunt -> pathologic remodeling -> pulmonary HTN. Wouldn't the pulmonary HTN be DESPITE the remodeling, not because of it?

You answered your own question. Your first statement of ASD/VSD presenting as pulmonary HTN is Eisenmenger.

 

[baclofen]

So as I understand, usual right HF presents w/ systemic backup [periph edema, JVP, etc] and possibly low pulm perfusion

So for example, tricuspid regurgitation -> RV dilation -> eventual R HF and systemic backup

But ASD/VSD and its resulting RV dilation and right HF presents as pulmonary HTN? How to explain the discrepancy in presentation?

Googling around isn't helping - my intuition says the difference is because in ASD/VSD, the RV still has less contractility due to dilation/remodeling, but since there's still a constant infusion of volume from the left side, it still results in net increase in volume in pulmonary circulation


Actually typing that out raises another question - in Eisenmenger syndrome, the pathogenesis is L-R shunt -> pathologic remodeling -> pulmonary HTN. Wouldn't the pulmonary HTN be DESPITE the remodeling, not because of it?

In general, with right sided heart failure, there is no increase in blood being pumped from the right side of the heart. For example if a patient has a right sided MI, the lack of proper muscle contraction on the right side decreases the amount of blood that goes to the lung (as you said- "low pulm perfusion"). This causes backup of the blood that should be emptying into this part of the heart ("systemic backup").
In an ASD/VSD, there is an increase in the volume of blood in the right side of the heart (due to L->R shunt). This increases the amount of blood that goes to the lung. The increase in blood flow to the lung can be severe enough to cause pulmonary HTN, since pressure is correlated with flow (Q=P/R). Over time, this volume overload can cause a dilated cardiomyopathy of the right side, which can cause systemic backup and a RELATIVE decreased flow to the lungs, but the volume overload may still allow for an increased pulmonary flow relative to the healthy individual. All of this increased pressure in the lung may result in remodeling of the pulmonary vasculature, which is characterized with thickening of the vessel walls among some other things. This increases the resistance of the pulmonary vasculature, and since P=QR, it will have an additive effect on the already existent pulmonary HTN, which may lead to reversal of the shunt.

 

[Surgeria]

In general, with right sided heart failure, there is no increase in blood being pumped from the right side of the heart. For example if a patient has a right sided MI, the lack of proper muscle contraction on the right side decreases the amount of blood that goes to the lung (as you said- "low pulm perfusion"). This causes backup of the blood that should be emptying into this part of the heart ("systemic backup").
In an ASD/VSD, there is an increase in the volume of blood in the right side of the heart (due to L->R shunt). This increases the amount of blood that goes to the lung. The increase in blood flow to the lung can be severe enough to cause pulmonary HTN, since pressure is correlated with flow (Q=P/R). Over time, this volume overload can cause a dilated cardiomyopathy of the right side, which can cause systemic backup and a RELATIVE decreased flow to the lungs, but the volume overload may still allow for an increased pulmonary flow relative to the healthy individual. All of this increased pressure in the lung may result in remodeling of the pulmonary vasculature, which is characterized with thickening of the vessel walls among some other things. This increases the resistance of the pulmonary vasculature, and since P=QR, it will have an additive effect on the already existent pulmonary HTN, which may lead to reversal of the shunt.

You explained well but you didn't mentioned about the remodeling of the right ventricle. When after left-->right shift person develops pulmonary hyperstension (caused by pulmonary arteiolosclerosis) this will cause right ventricle to become hyperthrophic aand hypertrhophy + pulm hypertension this both together will cause reversal of shunt hence eisemenger syndrome. I think pulm hypertension + right ventricle hypetrohphy is the point that drives reversal. And what I also want to mention is that dilated cardiomyopathy develops only in cases when you are volume overloaded, but when you develop "pressure overload" in other words conditions when your heart must work against high pressure (pulmonary hypertension caused by pulmonary vessel arteriolosclerosis) this will cause hypertrophy of the muscle, not dilation. So called Concentric hypertrophy, not eccentric (that causes dilation) just to add. Good luck with the studies.

 

[caxoo]

Thanks all for responses, it makes bit more sense now

You got these mixed up. RV dilation leads to TR due to the increased volume pulling apart the valves.
You answered your own question. Your first statement of ASD/VSD presenting as pulmonary HTN is Eisenmenger.

I know that RV dilation -> TR, but wouldn't TR -> [RA dilation -> increased filling P on next systole] -> RV dilation? That was how I understood why TR eventually progresses to R HF. If TR doesn't RV dilation, I don't get how it progresses to R HF

You explained well but you didn't mentioned about the remodeling of the right ventricle. When after left-->right shift person develops pulmonary hyperstension (caused by pulmonary arteiolosclerosis) this will cause right ventricle to become hyperthrophic aand hypertrhophy + pulm hypertension this both together will cause reversal of shunt hence eisemenger syndrome. I think pulm hypertension + right ventricle hypetrohphy is the point that drives reversal. And what I also want to mention is that dilated cardiomyopathy develops only in cases when you are volume overloaded, but when you develop "pressure overload" in other words conditions when your heart must work against high pressure (pulmonary hypertension caused by pulmonary vessel arteriolosclerosis) this will cause hypertrophy of the muscle, not dilation. So called Concentric hypertrophy, not eccentric (that causes dilation) just to add. Good luck with the studies.

But wouldn't there be volume overload since there's a constant increased volume coming from the left side? I guess the increased pulm HTN causing hypertrophy is more important/outweighs?

 

[Surgeria]

Thanks all for responses, it makes bit more sense now



I know that RV dilation -> TR, but wouldn't TR -> [RA dilation -> increased filling P on next systole] -> RV dilation? That was how I understood why TR eventually progresses to R HF. If TR doesn't RV dilation, I don't get how it progresses to R HF




But wouldn't there be volume overload since there's a constant increased volume coming from the left side? I guess the increased pulm HTN causing hypertrophy is more important/outweighs?

Yes as I remember pulmonary hypertension is the driving force for the reverces , at least in TOF (pulm stenosis was driving pressure for flow in tof, so I think same will be here)