fixed S2 splitting in ASD but not VSD

[bbaggins]

Fixed splitting occurs in ASD because of the increased blood flow across the pulmonary valve. So why doesn't a VSD cause fixed splitting also, since there is increased flow across the pulmonary valve also?

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[Phloston]

I had actually encountered a practice question (it may have been in Kaplan QBank; I can't entirely recall), where fixed splitting was mentioned in the vignette, as well as a holosystolic murmur, and I remember that confused me. I took the risk and put VSD based on the latter, but it was still ASD.

In terms of the USMLE, if fixed splitting is mentioned, invariably go with ASD.

 

[bbaggins]

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."

 

[Phloston]

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

That's really good. Thanks for posting that.

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."

ASDs can easily present with RVH and pulmonary HTN.

 

[Sharkanatomist]

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."

the fact that it is not affected by venous return means that it is FIXED so how does all of this make sense?

 

[Flintwire]

the fact that it is not affected by venous return means that it is FIXED so how does all of this make sense?

Not affected by venous return in this case just means not stopped or decreased by venous return. Meaning, in VSD the pressure for the L->R shunt is VERY high (ventricular pressure), so on inhalation we get extra venous return (like normal) PLUS shunt blood, and on exhalation we get ONLY shunt blood, leading to NON fixed splitting.

But in ASD: Inhalation increases venous return (like normal), and the increased pressure in the RA from the increased venous return can “stop” the L->R shunting, because pressure in the LA isn’t high enough to overcome the increased RA pressure from the extra venous return. On exhalation we don't get that extra venous return, so the shunt can fill the RA with extra blood. Thus, no matter what, there is ~ the same amount of extra blood in the RA that goes to the RV to increase RV emptying time by the same amount, leading to fixed splitting.

Hope that helps make sense of it 🙂.