mitral stenosis and fixed S2 split

[Ramoray]

I was reading some stuff on mitral stenosis following RHD and one of the key wasy clinically to differentiate it from VSD, as far as heart sounds goes, was that MS had a fixed S2 whereas VSD has a very wide S2 increasing further on insp( as usually happens) but its even more. I understand the VSD split since the RV is getting more blood, making it longer to empty, so it closes later. But for MS and its increased pulm hypertension which to me should make the RV empyting slower and also prolong closure and also further split S2. I dont see where the fixed S2 comes in. FOr that matter why is S2 fixed in general? thanks

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[Long Dong]

I always thought that a fixed split is ASD?

 

[idq1i]

I always thought that a fixed split is ASD?

Sure is! Higher RV blood volume due to ASD = fixed S2

 

[Ramoray]

Yes ASD does also and that is teh 'classic" example given but asd fixed split makes sense since with an asd the RA recieves two blood sources, which vary on inspiration and exp. Ie inspir return is higher from IVC and SVC and on expiration return is higher via the asd and lower in IVC and SVC due to thorax pressure effects so in the end there is no change of blood flow to RV during insp or exp therefore its fixed but in something like MS.. oh i guess i just answered my own question during insp blood return fron svc and ivc as usual increase flow to RV and therefore prolong closure but an MS would force blood back around pulm system and increase blood volume in RV on expiration so in the end insp and exp have equal amounts of blood in RV and a fixed split. ahhh good to talk things out! thanks!

 

[mellow yellow]

Here's the reason for the fixed split S2 seen in ASD... It actually has nothing directly to do with the ASD!!!

Why do murmurs occur? Because there is rapid and significant FLOW. Particularly, turbulent flow. In an ASD, there is NO murmur resulting from the septal defect! Why? Because there's no FLOW! Think about it. The difference in interatrial pressures is pretty minimal.. around 6-7 mm Hg. There is no real significant flow occuring between the ASD but rather MIXING is more prominent. In addition, the atria don't contract robustly in healthy adults and normally contribute <10% to diastolic filling. In the case of an ASD, more blood is sent/shunted to the RT side of the heart and what ultimately happens is a relative 'pulmonic stenosis' develops due to the overloading of fluid in the right side of the heart. Remember, that S2 normally varies with inspiration. When there is significant fluid overload to the RT side of the heart which can occur in the setting of an ASD, pulmonary HTN, or end-stage mitral stenosis, a fixed split S2 develops.

 

[Ramoray]

WIth that reasoning then, which makes sense, why does a VSD, which also basically does the same thing as an ASD or more severe, which is give more blood to right side of heart. , why would a VSD not be fixed if an ASD is fixed. I know VSD Is not as i just spent time tryign to reason out why not after looking it up in uptodate. i would lvoe to know why its really pissing me off!

 

[HiddenTruth]

Yes ASD does also and that is teh 'classic" example given but asd fixed split makes sense since with an asd the RA recieves two blood sources, which vary on inspiration and exp. Ie inspir return is higher from IVC and SVC and on expiration return is higher via the asd and lower in IVC and SVC due to thorax pressure effects so in the end there is no change of blood flow to RV during insp or exp therefore its fixed but in something like MS.. oh i guess i just answered my own question during insp blood return fron svc and ivc as usual increase flow to RV and therefore prolong closure but an MS would force blood back around pulm system and increase blood volume in RV on expiration so in the end insp and exp have equal amounts of blood in RV and a fixed split. ahhh good to talk things out! thanks!

but you could use that same reasoning for VSD then, couldn't you? I tried looking it up, but no luck on the exact mechanism. I don't have uptodate at home--maybe i'll read it at school tomr. Man, I wasted like an hr!! I'm not too far from the 'Lou--i'll definately come and find you if it doesn't show up on my test (which I don't think it actually will). 😉

 

[Ramoray]

ha god if you ever just want a few good laughs spend an hour reading uptodate or harrisons valvular abonormality sections. Like literally by the time i briefly read through, there was like 200 diff heart sounds and variations in timing, how to amke them louder, softer. Its insane. I mean i have a totally new respect for a cariologist if they can actually hear all that **** in a noisy hosp room and diagnose.. man the old school docs must have been alot more savy, i bet half the docs couldnt do that anymore. All that to say is that **** is super confusing. The good news is the depth of that wont show up on the boards i hope but is good to understand the cardiac cycle but hell its tough ****. let me know if you find any solid explanations id lvoe to understand it!

 

[bonovox]

For both, you have delayed closure of the pulmonic valve. This is normal in inspiration when you have increased VR to the RV, resulting in more blood being pumped out into the PA, resulting in delayed closure of the pulmonic valve.

In ASD, you have a situation of volume overload of the right heart resulting in delayed closure of the pulmonic valve. However, this does not vary with inspiration for the following reason. Increased return to the RA during inspiration is countered with decreased blood flow through the left to right atrial shunt. This occurs at the same time, and this is independent of the right ventricle and the pumonary artery.

In VSD, again you have volume overload and delayed closure. With inspiration, you have more blood coming to the right ventricle. You can argue that the blood should be counterbalancd like it did with ASD, but the thing is... pulmonary artery capacitance is also increased (and resistance decreased) during inspiration. This means simply that the right ventricle can continue and continue to pump blood into the pulmonary artery during systole when this splitting occurs, including the additional VR. The back pressure needed by the PA to close the pulmonic valve is delayed. The end result is WIDE but NOT FIXED splitting in VSD.