USMLE Forums banner
1 - 14 of 14 Posts

·
Registered
Joined
·
137 Posts
Discussion Starter · #1 ·
Why is there fixed splitting of S2 in ASD but not in VSD?

On page 254 of FA it says that ASD leads to a left to right shunt and therefore increased flow through the PV so pulmonic closure is greatly delayed. Doesn't the same thing happen in VSD? It's just a shunt between the LV and RV, so wouldn't there would be increased flow through the pulmonic valve in that condition too?

Note: I'm studying one of my weakest subjects (cardiology) today so I will probably end up asking a lot of questions that may seem dumb. Thanks for being patient. :)
 

·
Registered
Joined
·
137 Posts
Discussion Starter · #2 ·
I don't understand the explanation. The tricuspid valve is between the RA and RV. The pulmonary valve is between the RV and the pulmonary artery. In ASD blood goes from LA -> RA. In VSD blood goes from LV -> RV. So technically wouldn't a VSD produce more flow or at least just as much flow through the pulmonic valve as ASD?
 

·
Registered
Joined
·
2 Posts
fixed splitting of S2 in ASD and not in VSD

fixed splitting means when there is no variation of S2 splitting with inhalation which normally occurs.
normally; s1 is produced by closure of mitral and tricuspid valves and s2 by closure of pulmonic and aortic valves..producing 2 components of s2 i.e a2 and p2..normally a2 precedes p2,but on inspiration p2 precedes a2,means pulmonic valve is taking longer to shut,n that is because on inspiration the blood flow to the right heart(RA and RV) increases, making the pulmonic valve to take longer to close.

In ASD: on inspiration the increased blood flow towards RA which occurs normally, is there, but every time the amount of blood equalizes between RA and LA due to the septal defect.now the blood entering the RV equals to the blood entering LV regardless inspiration or expiration..hence producing fixed splitting.

Now VSD: it is a defect between the two ventricles..normally the pressure of LV is more than the Pressure in RV, so initially the direction of the shunt will be left to right. the blood entering the RA wud be more than LA on inspiration which happens normally and this mechanism is not disturbed in VSD ,as the defect is between ventricles not atria.. so more blood coming in RA during inspiration, goes to RV.. but what happens there, it is a left to right shunt ! so even more blood wud be entering RV. so the closure of pulmonic valve would be even more delayed.
so there wont be any fixed splitting... but when the disease get worsen with RV hypertrophy and the shunt get reversed, then there might be some fixed splitting ,but by that tym u get murmurs of regurgitation of pulmonic and aortic valve. So we don't hear 1.
 

·
Registered
Joined
·
2 Posts
thanks guys!:)
hm yup i made a lil mistake thea.. aortic valve n pulmonic valve close almost simultaneously with a difference of say few milli or microseconds but this gap becom more obvious or the gap increases on inspiration...
the info is not from a single book its kinof random..but the concepts will get very clear if u read RR Pathology by Goljan..best notes on CVS..also listen to the golgan audios..i recommend to listen to the audios before u do the chapterz from book..ull retain maximum..
best of luck
 

·
Registered
Joined
·
2 Posts
fixed splitting is in VSD

Dazzles logic makes sense. I'm here because i had the same but got a UW question wrong because of it. but according to *cough* wikipedia and Physical diagnosis secrets By Salvatore Mangione (http://books.google.com/books?id=-BmjqujomUMC&pg=PA215#v=onepage&q&f=false) a VSD can also cause fixed splitting due to increase RV preload (longer ejection time) and also due to decrease LV preload (shorter ejection time) giving a wide S2 split.
 

·
Registered
Joined
·
36 Posts
amazing question.dont think this is because u r new to cardio,thats a very deep Q actually.

first of all,all about splitting from harrison and cecil:
1. wide inc. of nl split in these scenarios,
a. PS,VSD,PHtn,PE--->B/C of inc RV work
b.MR(dec in LV work so A closes early NOT a delay in P)
c.RBBB (delayed RV work)
d.Idiopathic dilation of the PA(delayed P complete closure,there is
more space between the lats)

2.pradox split,
AS LBBB LVMI HCM (delayed left work)

3.fixed split
ASD,sever R-sided failure

and now,
in ins,return to RA inc while in ins again,L to R shunt in ASD decreases(y?less blood returns to left.in SEver R failure the reason is inc afterload agains left,the outcome is the same) and finally these two opposite forces equal each other and the split remains FIXED.in VSD these forces dont equal so the splitting remains under the influence of ins/exp.

Good Luck
 

·
Registered
Joined
·
2 Posts
it depends

Did a little more research. and It looks like it depends on the severity of the VSD. If a VSD is relatively mild, with a L to R shunt and no pulmonary hypertension then there is a wide relatively fixed split according to this British Heart Journal article:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC487191/?page=1

But if the VSD is large the two ventricles act like one chamber, and if there is pulmonary hypertension the R ventricle will shut off sooner. A R to L shunt would make the L ventricle shut off later. All of these contribute to making the S2 sound more narrow.
 

·
Registered
Joined
·
36 Posts
the core concept is that when inspiration is gonna widening it,you need an opposed force trying to narrowing it,resulting in fixation n this happens in these two situations,

ASD
sever R failure(pre eizen-menger stage in case of a severed VSD).after eizen-menger it`ll actually disappear BC the left side comes delayed this time.BTW the fixed splitting is not a finding to look 4 in VSD.
 

·
Registered
Joined
·
7 Posts
I disagree with Mashremn's explanation

Dear Mashremn,

As per you, in ASD the volume of blood in the RA and LA equalize and so there would be a fixed split in ASD. If the volume of blood in LA and RA equalize, there wouldn't be any difference in the blood flow through the pulmonic and aortic valves and so there wouldn't be any difference in the timing of closure of those valves. You WOULD NOT HAVE ANY SPLIT in that scenario which is described as a PARADOXICAL SPLIT or NO SPLIT. Fixed split is different. In fixed split, you would hear a split regardless of the part of respiration you are in (you would hear split both during expiration and during inspiration)

I believe that the split you see in VSD depends on the size of the VSD and the age of presentation after the onset of disease. Correct me if I am wrong. Thanks.
 

·
Registered
Joined
·
1 Posts
Dear Mashremn,

As per you, in ASD the volume of blood in the RA and LA equalize and so there would be a fixed split in ASD. If the volume of blood in LA and RA equalize, there wouldn't be any difference in the blood flow through the pulmonic and aortic valves and so there wouldn't be any difference in the timing of closure of those valves. You WOULD NOT HAVE ANY SPLIT in that scenario which is described as a PARADOXICAL SPLIT or NO SPLIT. Fixed split is different. In fixed split, you would hear a split regardless of the part of respiration you are in (you would hear split both during expiration and during inspiration)

I believe that the split you see in VSD depends on the size of the VSD and the age of presentation after the onset of disease. Correct me if I am wrong. Thanks.
I agree with docchitra.

The main reason behind fixed splitting of S2 is, overloading of right ventricle to it's limit so that no further blood (as a result of inspiratory increased venous return) could be accommodated by it. So increased inspiratory venous return doesn't make any difference to right ventricular volume which is already loaded due to presence of ASD. This also infers that additional inspiratory volume would be reflected as increased JVP.
 
1 - 14 of 14 Posts
Top