Fixed splitting in ASD but not VSD

[okokok]

FA p 277 (2015): ASD -> L to R shunt -> inc RA & RV vol -> inc flow thru pulm valve so regardless of breath, pulm closure greatly delayed.

Could anyone explain to me why this would occur in ASD but not VSD?

UW qid 187 offers some explanation: fixed splitting exists in ASD but not VSD bc ASD "allows equalization of left and right atrial pressures, thus minimizing the respiratory variation in left and right ventricular flow."

However, it's still not totally clicking for me. Could anyone help?

Thank you.


Edited - I accidentally wrote that UW said fixed splitting exists in VSD not ASD. They said it exists in ASD not VSD.

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[okokok]

Not sure how to edit previous post on my phone but in case I wasn't clear - I understand why increased RA and RV volumes (as in ASD) lead to fixed splitting due to delayed pulmonic valve closure, but I don't understand why an increased RV volume alone (as in VSD) wouldn't do that.

 

[okokok]

For that matter - why does ASD allow equalization of RA and LA pressures while VSD (I believe) does not allow equalization of RV and LV pressures?

 

[zhopv10]

I haven't looked this up but this would be my intuition on the matter: in VSD you have higher pressure in the left (stronger) so of course you get the left to right shunt and then you get increased right ventricular volume and fixed splitting as you said. Now with ASD you have two lower pressure chambers that are connected by a hole basically. Neither is really (that I know of) stronger. Thus when they are filling/pumping the pressure differences should equalize out and then you shouldn't see as much of a asymmetric volume in the ventricles leading to splitting. Basically one side is not stronger and able to force volume to the other side so the fluid goes to whichever side is lower volume (just gradient stuff) so things equal out. Hopefully that made sense. Feel free anyone to correct me if that's totally off.


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[zhopv10]

Also, just as a heads up your question in the original post says the opposite of the uworld explanation and your clarification as does the title of the post (why does ASD cause splitting and not VSD instead of the other way around).


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[okokok]

I haven't looked this up but this would be my intuition on the matter: in VSD you have higher pressure in the left (stronger) so of course you get the left to right shunt and then you get increased right ventricular volume and fixed splitting as you said. Now with ASD you have two lower pressure chambers that are connected by a hole basically. Neither is really (that I know of) stronger. Thus when they are filling/pumping the pressure differences should equalize out and then you shouldn't see as much of a asymmetric volume in the ventricles leading to splitting. Basically one side is not stronger and able to force volume to the other side so the fluid goes to whichever side is lower volume (just gradient stuff) so things equal out. Hopefully that made sense. Feel free anyone to correct me if that's totally off.

Hey, thanks so much for your input. That's exactly my intuition too, but it's incorrect. Both First Aid and UWorld say that fixed splitting occurs in ASD but not VSD.

Also, just as a heads up your question in the original post says the opposite of the uworld explanation and your clarification as does the title of the post (why does ASD cause splitting and not VSD instead of the other way around).

You're totally right, sorry about that--when I quoted UWorld, I switched ASD and VSD (fixed it now) but the title and the clarification are correct. The exact wording of the UWorld explanation is: "Fixed, wide splitting of S2 occurs in patients with atrial septal defects. ... Fixed splitting is more indicative of an intraatrial communication than a VSD, as the former allows equalization of left and right atrial pressures, thus minimizing the respiratory variation in left and right ventricular blood flow."

Ok, I can understand how equalized atrial pressures would minimize respiratory variation in left and right ventricular blood flow. Normal physiological splitting is due to the increase in blood flow to the right atrium during inspiration -> increased volume in right ventricle -> delayed closure of pulmonic valve due to extra blood flowing across and increased pulmonary capacitance to accept that blood -> pulmonic valve closes later than the aortic valve, which receives the same amount of blood regardless of respiration. So if both atria have the same amount of blood, even during inhalation, due to the hole between them, I understand that there would be minimized respiratory variation in the aortic valve and pulmonic valve. However--doesn't that mean the time interval between A2 and P2 closures would actually be decreased, and not increased as in seen in fixed splitting?

Also, First Aid doesn't say that pressure equalizes between the atria; it says that the right side has an increased volume due to L to R shunting, thus there is an even wider delay in P2 closing. This explanation makes more sense to me than the UWorld one.

So then with the question of a ventricular septal defect. I don't understand why fixed splitting wouldn't occur with a VSD according to either explanation (UW or FA). Couldn't you say that pressure would equalize between the ventricles (the reason UW gives for fixed splitting) or that the LV ventricle would have more volume than the RV due to shunting (the reasons FA gives for fixed closure)?

Edited for typos & clarity

 

[zhopv10]

Ah ok, gotcha, dang that is odd. And now that you say that I do remember talking about this in our cv block and coming to a good explanation...one that I no longer can remember! Haha but ya I agree that is odd. I'll see if I can't find it here in my class notes and share if I do (P.s. I don't know if in my hurry I read the physiologic splitting part you wrote wrong but it is increased/becomes apparent with a deep breath due to increase volume return to the right atrium and thus right ventricle which leads to the pulmonic valve closing second/later.).


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[okokok]

I couldn't search the forum when I was using my phone earlier (I don't know why but that feature never works on my phone), but on my computer I saw a thread from five years ago asking the exact same question and this was what someone said -

So I got an answer from one of my professors, a cardiologist. At the end of the day, for test purposes, fixed splitting is an ASD, as noted above. But for the curious who like to know the why...

"An ASD produces wide, fixed splitting, whereas a VSD produces wide splitting that may also become fixed. Why the difference?

Let's take the case of the ASD first: During inspiration, there is increased venous return to the right atrium, causing P2 to delay its closure even a little longer than with physiologic splitting. Why? Because the right heart also has to handle the blood coming from L to R through the ASD due to the higher pressure on the left atrial side. So P2 is delayed by the venous return plus some left-to right shunting. On expiration, the wide splitting stays "fixed" because though there is not venous return, there is now MORE shunting of blood from left-to-right since the pressure differential between the LA and RA is greater. The increased shunting makes up for the volume of absent venous return, so the pulmonic valve closure is delayed on expiration just as much as when there was venous return on inspiration: hence, wide, fixed splitting.

In the case of the VSD, there is also always going to be wide splitting of S2, for the reason discussed above. However, splitting will not become fixed until the RV pressure rises and thus diminishes (or reverses) the L to R shunt. In the early stages of a VSD, there is a significant shunt of blood from L to R during both inspiration and expiration, and that amount is not appreciably altered during inspiration since the pressure in the RV (even filled with venous return) is still much lower than that of the LV. As the RV pressures rise over time due to chronic volume overload, the RV hypertrophies. When it does, the L to R shunt then diminishes during inspiration (due to elevated RV pressure plus venous return) causing the split to become fixed. In other words, once the shunt diminishes, then RV pressure plus the venous return during inspiration approximates RV pressure occurring during expiration from the shunt, making P2 fixed.

An even easier way to think of it is this: atrial pressures are low, and therefore the shunt in an ASD is greatly influenced by the pressure generated by venous return. In a VSD, the much higher ventricular pressures maintain the shunting throughout the cycle and early on are not appreciably altered by venous return.

Step 1 pearls about FIXED splitting: the case is likely about an ASD, unless the patient has RVH, pulmonary HTN, etc. Then it is likely a VSD, with reversal of shunt. Uncomplicated VSDs have only wide splitting; All ASDs have wide, fixed splitting."

 

[zhopv10]

Ok, i actually found this, I think the problem was I was forgetting some of what was involved in the terminology of "fixed splitting" vs "splitting"

"An ASD produces wide, fixed splitting, whereas a VSD produces wide splitting that may also become fixed. Why the difference?

Let's take the case of the ASD first: During inspiration, there is increased venous return to the right atrium, causing P2 to delay its closure even a little longer than with physiologic splitting. Why? Because the right heart also has to handle the blood coming from L to R through the ASD due to the higher pressure on the left atrial side. So P2 is delayed by the venous return plus some left-to right shunting. On expiration, the wide splitting stays "fixed" because though there is not venous return, there is now MORE shunting of blood from left-to-right since the pressure differential between the LA and RA is greater. The increased shunting makes up for the volume of absent venous return, so the pulmonic valve closure is delayed on expiration just as much as when there was venous return on inspiration: hence, wide, fixed splitting.

In the case of the VSD, there is also always going to be wide splitting of S2, for the reason discussed above. However, splitting will not become fixed until the RV pressure rises and thus diminishes (or reverses) the L to R shunt. In the early stages of a VSD, there is a significant shunt of blood from L to R during both inspiration and expiration, and that amount is not appreciably altered during inspiration since the pressure in the RV (even filled with venous return) is still much lower than that of the LV. As the RV pressures rise over time due to chronic volume overload, the RV hypertrophies. When it does, the L to R shunt then diminishes during inspiration (due to elevated RV pressure plus venous return) causing the split to become fixed. In other words, once the shunt diminishes, then RV pressure plus the venous return during inspiration approximates RV pressure occurring during expiration from the shunt, making P2 fixed.

An even easier way to think of it is this: atrial pressures are low, and therefore the shunt in an ASD is greatly influenced by the pressure generated by venous return. In a VSD, the much higher ventricular pressures maintain the shunting throughout the cycle and early on are not appreciably altered by venous return.

Step 1 pearls about FIXED splitting: the case is likely about an ASD, unless the patient has RVH, pulmonary HTN, etc. Then it is likely a VSD, with reversal of shunt. Uncomplicated VSDs have only wide splitting; All ASDs have wide, fixed splitting."

 

[zhopv10]

Also something I had forgotten that makes sense now: the pressure is higher in the left atrium so you do get more shunt in the L --> R manner, it is not two equal pressure chambers with a hole like I was thinking.

 

[zhopv10]

I couldn't search the forum when I was using my phone earlier (I don't know why but that feature never works on my phone), but on my computer I saw a thread from five years ago asking the exact same question and this was what someone said -

haha i just finished posting the same thing, nice! hahah

 

[okokok]

haha i just finished posting the same thing, nice! hahah

I totally forgot about/unintentional ignored the whole concept of wide splitting even though it's right below the fixed splitting section on the FA page I was looking at! Ugh time for a break. Hopefully now that I've thought about it so much it'll stick Thanks for your help @zhopv10!

 

[zhopv10]

Same here, glad you had brought it up originally, cardio is one of my weaker topics and this was great review. I can't say I was much help but glad we both learned something from it haha


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[Phloston]

Inhalation = negative thoracic pressure = pulmonary vascular bed expands = decreased RV afterload = less resistance for blood entering the heart = more RA filling = more volume in RV = more preload in RV = more pressure in RV = more time required for RV pressure to fall below pulmonary artery pressure = pulmonic valve closes later = increased A2-P2 splitting. Vice-versa for exhalation.

An ASD will theoretically equalize RV end-diastolic volume in inspiration and expiration. The atria, as conduits, function as reservoirs, so their volume would be more greatly affected by the respiratory cycle. So deltaV would be greater in the atria vs the ventricles during the respiratory cycle. Since the atrioventricular valves are open during diastole, there is no reason, by the laws of physics, that there wouldn't be a transfer between the ventricles during diastole, but I suspect the transfer would be unnoticeable from an auscultation stance because it's so minor.

 

[Cytarabine]

Inhalation = negative thoracic pressure = pulmonary vascular bed expands = decreased RV afterload = less resistance for blood entering the heart = more RA filling = more volume in RV = more preload in RV = more pressure in RV = more time required for RV pressure to fall below pulmonary artery pressure = pulmonic valve closes later = increased A2-P2 splitting. Vice-versa for exhalation.

An ASD will theoretically equalize RV end-diastolic volume in inspiration and expiration. The atria, as conduits, function as reservoirs, so their volume would be more greatly affected by the respiratory cycle. So deltaV would be greater in the atria vs the ventricles during the respiratory cycle. Since the atrioventricular valves are open during diastole, there is no reason, by the laws of physics, that there wouldn't be a transfer between the ventricles during diastole, but I suspect the transfer would be unnoticeable from an auscultation stance because it's so minor.

Can you clarify the point you're trying to make in the bolded? Not sure I follow

 

[Phloston]

Can you clarify the point you're trying to make in the bolded? Not sure I follow

The atria have no valves behind them so inspiration/expiration will absolutely draw more or less blood into them. During systole when the AV valves are closed respiration couldn't affect ventricular volume. Only during diastole would they be susceptible to volume flux based on respiration. So if a VSD is present there would have to be even a minimal interventricular transfer during diastole due to being contiguous with the atria. My assumption is it's probably rare or just negligible. An ASD would allow interatrial transfer in both diastole and systole presumably.

 

[Cytarabine]

The atria have no valves behind them so inspiration/expiration will absolutely draw more or less blood into them. During systole when the AV valves are closed respiration couldn't affect ventricular volume. Only during diastole would they be susceptible to volume flux based on respiration. So if a VSD is present there would have to be even a minimal interventricular transfer during diastole due to being contiguous with the atria. My assumption is it's probably rare or just negligible. An ASD would allow interatrial transfer in both diastole and systole presumably.

Ah, gotcha, yes that makes sense.

Not specifically directed toward you, but just a side comment. In practice one VSD doesn't really equal another. Whether it's apical, muscular, fibrous, restrictive, or unrestrictive are all going to influence the physiology to some degree, along with how long the infant/child has been alive for

 

[Baraa Khalaf]

I totally forgot about/unintentional ignored the whole concept of wide splitting even though it's right below the fixed splitting section on the FA page I was looking at! Ugh time for a break. Hopefully now that I've thought about it so much it'll stick Thanks for your help @zhopv10!

I don't know if you meant the same thing that I want to talk about when you said " forgot" but anyway, I just want to adress it! and the reason is because this is a VERY important "caveat" most people having problem with this VSD vs ASD thing have and are unaware of, at least in my experience!

I used to discuss this point a lot with my colleagues and they always end-up forgetting or unintentionally skipping the concept of "wide splitting". VSDs do NOT produce normal S2 (of course the big ones) there's definitely a WIDE splitting but it's NOT a FIXED one... One mustn't take the "not fixed" and forget the "wide" part... It's definitely there!

Whenever I was discussing this with any of my colleagues who was confused about this; they always were solely fixated on "fixed" and forgot the "wide" part of the equation. I realized they hadn't had any problem understanding any of the effects of both ASD and VSD on the inter-chambers pressure and volume differences but they were too much concentrating on the "fixed' part and automatically assumed that this means : not fixed = normal S2 (ie. no splitting) which is wrong.

It's not a normal S2 it's just wide, "variably wide split"... which doesn't make it "not a clinical finding" but rather a not VERY distinct one!
It's not a distinguishing phenomenon of as much value as the ((unique)) "fixed split" of ASDs!