Why the qrs complex becomes wide and tall in LBBB ?
The qrs complex is wide , due to delayed conduction over non specialized fibres .The qrs becomes are tall due to temporal dissociation of RV and LV forces , which leaves the LV forces unopposed , thus a tall qrs is inscribed , without the neutralizing effect of RV forces.
Is muscle to muscle conduction a hall mark of LBBB ?
No , it is not . Even though the left bundle is blocked , much of the conduction tend to occur in
specialized conduction system . It depends upon the level of block of LBBB.
What is the mechanism and clinical significance of left axis deviation in isolated LBBB?
The mean qrs axis is surprisingly not altered greatly , in LBBB . If there is a significant left ward shift it may imply associated organic LV pathology or involve ment of predominately left anterior fascicle
What is the impact of IVS contraction and timing in LBBB ?
In isolated LBBB, it is expected an abnormal septal motion due to altered sequence of septal activation. This results in an abnormal appearance of septal motion in Mode (Septal beak immediately following qrs complex) .In fact , this sharp downward movement indicate good LV function .Absence of which is a good clue for a pathological LBBB due to structural heart disease
Why does the abnormal septal motion in LBBB , do not desynchronize the normal LV ?
CRT is the much fancied treatment in patients with LBBB and cardiac failure. In normal ventricles LBBB do not destabilize LV function in spite of septal /free wall desynchronisation .This is still a mystery how IVS is cope up with the totally unexpected insult of asking to work in head over heal situation !In spite of this the ventricle gets used to the altered conduction pattern and the contractile pattern.(Nature’s at it’s best !)
What are the mechanical disadvantage of LBBB
- Septal contraction is ill-timed
- Mitral regurgitation
Most isolated chronic LBBBs do not confer any hemodynamic disadvantage to LV – why ?
LBBBs are dangerous looking ECG , but in most patients it is benign , in the absence 0f structural heart disease like valvular , myocardial or ischemic disease.
Can there be a small r wave in V1 and V2 in LBBB ?
Yes . Though we expect the reversal of septal depolarization extinguish the initial r in v1 to v3 .It is noted in many. Hence presence of small r in v1 to v3 does not rule out LBBB.
- The commonest explanation given is un-masking of RV free wall forces which is normally masked by early LV forces .
- Another possibility is the orientation of septum in pathological states.
- Third possibility is “r” may actually represent the septal q waves as in LVH or old AWMI .(Counterpart of small q in lateral leads )
How do we explain concordant pattern of QRS v1 to v6 in LBBB ?
We expect the qrs to transit from QS complex to RS , at-least by lead v5/v6 .Some times even V6 shows a RS complex.This is usually due to faulty lead position or a grossly enlarged LV, ie if we record V 7 or V8 we will be able to pick up the qs complex.
What will be the morphology of a VPD that is arising from LV in the presence of LBBB ?
A premature beat arising from a ventricle which is having a bundle block is sort of electrical blessing !The VPD often bye passes the block and makes the conduction near normal and a normal qrs may be recorded. So , when a patient with LBBB suddenly develops a normal qrs beat or normal qrs tachycardia one should consider a VT arising from the Left ventricle .
And a studious electro physiology fellow should be able to answer the following !
What will be the morphology of VPD if it arises from RV and septum in the presence of LBBB ?
Kindwall has tried answer this question
What is the effect of LBBB on S1 and S 2 ?
The classical description in LBBB is
- Paradoxical split of S2
- Wide split of S1
You are supposed to hear 4 components in complete LBBB ! In reality this does not happen . At best you can hear the reversed split of S2 with difficulty .
One more reason for the non manifestation of these splits is confounding factors like LV dysfunction , MR , PR interval etc .(Each one tend to pull or push S1 and S 2 in different directions )
Do patients with LBBB , are at increased risk for developing complete heart block when
beta blockers , calcium blockers etc are administered ?
Common sense would say yes. Scientific sense has no answer .
We know, ventricles are innervated by two bundles .When only one bundle is functional, it means the ventricles are experiencing 50 % power shutdown . In CAD , single vessel blood supply due to a CTO is considered dangerous but in electrical flow it is not so ! In spite of the fact that ventricle has numerous cell cell electromotive conduction it is always better to exercise caution when administering beta blockers, calcium blockers and digoxin in patients with LBBB . If it is a must periodic monitoring is advised .(HV interval in isolated LBBB is slightly prolonged ) Never administer beat blocker in a patient with recent onset LBBB and ACS
Also read the related article in this blog Incomplete LBBB