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Posts Tagged ‘wide splitting of s2’

When I asked this seemingly simple  question to my cardiology fellows , I found they struggled  to come out with a proper  answer .I hope this will  make the  issue simpler .

Why the onset of PAH in VSD is early and late in ASD ?

Though number of factors are involved in the genesis of PAH , the single important reason  is  behavior of pulmonary circulation  especially the pulmonary arteriolar muscle .

Normal pulmonary vasculature losses it’s muscle rapidly after  birth and the pulmonary vascular resistance (PVR) falls to the adult level by 6 months .(Bulk of the fall occur in first 60 days) This is the same time the RV dominance is lost and RVH regresses . This also coincides with peaking of  left to right  shunting peaks and may result in cardiac failure .

Though  both ASD and VSD shunts are  highly dependent on PVR ,   VSD  shunting has more muscle power namely the LV contractility  , hence  VSD shunt is established  much earlier   than ASD . This can be ascertained in bedside as  VSD murmurs are heard even within 30 days while ASD is silent for many moths or even years . (Does not apply for Primum defects)

ASD  shunt rarely  meddles   lung  maturation process .(Maturation here means loss of  pulmonary arterioloar smooth  muscle -also  called as Involution  )  This vital  initial period lasts up to 6 months of life .VSD  interferes with this  involution of pulmonary arteriolar smooth muscle .( Please note near complete  involution still can occur in small VSDs with very little shunting )

In large VSD the PVR  will never ,  ever fall to normal levels  and   making it easier for  progressive vascular changes  that occur in  untreated large VSDs that  lead to Eisenmenger syndrome

*Please note  ASD can also reach that stage but it takes many years as the pulmonary vascular resistance has to raise from  very low levels which was made possible by complete involution of pulmonary vasculature .

It is obvious   AP window , PDA  express more  powerful left to right shunts which are associated with very high PVRs .

Final message

A simplified version of answer

Version 1

In VSD  the onset  of left to right  shunt occurs early even within 3 months of life  since VSD shunt is augmented by LV contraction . This is the crucial time of lung  vascular maturation   which gets interfered with  .ASD shunt is  established only after the pulmonary vasculature  involutes .This explains early onset of PAH in VSD  and late in ASD .

Version 2

ASD shunting is primarily depend on RV compliance which is high in early infancy so it takes time to establish the shunt .while VSD shunting does not  depend upon this RV regression.

* Please note  regression of  RV  dominance and compliance is directly dependent on maturation of lung.

** Note these  explanations are not absolute .Some of the complex forms of ASD and intrinsic vascular injury of pulmonary circulation (Various  fetal distress )  can progress into accelerated pulmonary arterial hypertension

Reference

  1. Excellent discusions are available in old edition of Moss and Adams
  2. Rabinovitch has done pioneering work on this topic .
  3. Robert Roberts text book of Adult congenital heart disease also explains it succinctly

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Like in neurological disease, one can locate the site of block in bundle branch blocks. Though it has never been thought ,  to be clinically important to localise a BBB . (Unlike coronary lesions)

Generally ,  RBBB can be proximal  or  distal peripheral type.The commonest site could be the distal  type.

It should be realised , for over 100 years in  electrocardiology , we have been using some inaccurate terminologies just because it is easy to understand or being traditional .It is difficult  to assimilate a fact , even today that   “An electrical delay in conduction and block are one and the same ”

In fact,  bulk  of  the RBBB is nothing but delayed conduction over this bundle. So whenever we say RBBB  , we imply an incomplete block  ie conduction still occurring   over the  so called blocked bundle.(This dogma applies for LBBB and AV blocks also to a lesser  extent)

Examples of delayed  RV /RVOT conduction

  • Any disease where  RVOT dilatation  occur can cause a RBBB
  • Atrial septal defect
  • Many cases of RVH
  • Pulmonary arterial hypertension

What is the benign rSr’ pattern in V1 ?

This is nothing but a relatively late depolarisation of  RV outflow or conus that produce a terminal RV activity .

Many of the ostium secundum ASD may show just this rSr’ pattern   confirming there is no organic damage to RBB in ASD .

Calling rSr’ pattern as incomplete RBBB is not advisable (As many ECG books may suggest ) .This is because , even full blown RBBB pattern may actually be an incomplete one .Further , the degree of terminal r’ in V1 or s in lead 1  does  not always   determine the completeness of RBBB.

Is there a totally blocked right bundle branch block ?

Yes , it is not common .

  • It can occur in extensive anterior MI .
  • Some cases of Ebstein anomaly.

It can be an working rule , complete RBBBs  locate the lesion proximally and incomplete  ones distally .

What is the other evidence for RBBB in ASD  is  only a simple   delay  in conduction ?

After ASD closure  in many of the patients the RBBB pattern may disappear.This indicate RVOT regression .

Can you clinically differentiate the proximal from  distal RBBB ?

Ironically ,what is difficult in ECG may some times be possible clinically.The classical description of wide splitting S2 occur often in peripheral RBBB.

It represents a delay in the closure of pulmonary valve due to delayed electrical activation or increased hangout interval as in ASD .Logically S1 should also be split in RBBB. But this is not often discussed.

This is because , the split in S1 is lesser in magnitude and is not influenced by the hangout interval .(Hang out interval is the time taken for the blood ejected from RV to fill the pulmonary circulation. Due to the low impedence of pulmonary circulation the the blood that is ejected into the MPA continue  to run off for about 100milli seconds even after the RV/PA pressure crossover .)

S1(T 1) occurs  immediately with the onset  of RV contraction . Similarly M1 occur with LV contraction.It should be recalled it requires hardly 5mmhg of RV pressure to close the tricuspid valve and about 10mmhg for LV to close the mitral valve.

If for some reason if  there is a delay  in RV contraction , as in very proximal RBBB the T1 is delayed and hence S 1 split.

Note in most of the peripheral or distal RBBB the bulk of the RV free wall contraction is not interfered with . So , in distal RBBB it is highly unlikely the S1 will be delayed or split while S2 will be delayed.

What happens to S2 in proximal RBBB ?

Logic would dictate both S1 and S2 should be wide split.

Final message

There is a simple way (Some would call this an futile  academic  excercise  !)to  differntiate proximal from distal RBBB.If the first heart sound is split wide , it fixes the lesion proximally. This may  indicate a more adverse outcome than a simple peripheral delay in conduction.

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