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.
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.