Posts Tagged ‘ebstein anomaly’

Right ventricle is a passive venous component of the heart .It simply acts a  transit pump for blood to reach the lungs.

It  is true  , RV is dispensable in many complex congenital heart disease as we  can connect the great veins directly into the pulmonary artery  by  Fontan , Glean and it’s clones  bye passing this chamber . Still , by no means the importance of this chamber is to be underestimated.  RV dysfunction and failure  is the key to survival  many  disorders.RV shock is is cause of sudden cardiac death in acute pulmonary embolism and RV infarction .

RV is an unique muscular chamber .It is more of a triangular shape. It has  three different parts connected by three different angle .There is no true  apex  for RV , it is   connected  to Inflow and outflow in peculiar fashion .

In the  following table I have  tired to  describe  of how different parts of RV  behave in various disorders.

what is the morphology of  RV enlargement RV inflow outflow body sinus portion of RV

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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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An excellent article from H.Watson in british heart journal

HERNANDEZ FA  The intracavitary electrocardiogram in the diagnosis
of Ebstein’s anomaly. Amer J Cardiol 1: 181,  1958

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