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Why ECG evidence for AV dissociation does not occur in majority of patients with ventricular tachycardia ?

Posted Sep 10 2009 10:25pm

AV dissociation is the specific marker for diagnosing VT. Evidence for AV dissociation manifest in many ways in ECG. *Random p waves unrelated to qrs complexes , fusion beats , capture beats are  the common features that help us diagnose AV dissociation. Unfortunately these  occur only in about  40 % of patients  with VT.(Fusion beats in VT are also  called as Dressler’s beat)

For clinical features of AV dissociation follow this link

What is the normal AV association ?

In  normal physiology ,  even though atria are passive , powerless chambers  in terms of mechanical activity  ,  it reigns  supreme control over ventricle and   dominates   electrically  . In fact , the atrium  and the AV node together ,    dictates when the ventricle has to contract and at what rate  .  So,  in normal human  beings in  sinus rhythm ,  there is a complete AV  association   where both chambers live in a perfect harmony.

What is VA association ?

The atrium and ventricles are  not only related   antegradelyy it  also  has a concealed  retrograde  relationship , (which is often pure electrical ! ) called VA conduction .The conduction velocity and the refractory period of VA  junction is  variable .The AV junctional refractory period is determined by the penetrating power of both atrial and ventricular impulses .

What is complete AV dissociation ?

For complete AV dissociation to occur there should be no physiologically or electrically  linked relationship between the atria and ventricle.For it  to occur the atrial impulse has to get  blocked  in AV junction .

This block can   either be functional  or organic,   partial or total , persistent  or intermittent

This occurs in   primarily in   AV junctional pathology like CHB  etc, that result  in complete AV dissociation . The next major cause for AV dissociation , is   by an  interference from  an accelerated lower pacemaker as in ventricular tachycardia or accelerated idioventricular rhythm .

What does the atria do when the ventricle  starts  contracting rapidly and  independently as in ventricular tachycardia ?

When the ventricle , starts firing independently at a rate of > 200 each of the impulse and  tries to  traverse  the AV junction retrograde . At the same time , the sinus impulse which does it’s normal routine job  by beating around 70/beat ,   faces an  unusual interference on its normal downward journey by  the pathological bombardment  from  the upcoming  ventricular impulse . What happens when both these wave fronts  meet head on . (The hither to perfect harmonical  relationship becomes  a rivalry for the electrical control of heart.)

Sadly , the ventricle mostly succeeds  in the race and  most of the   ventricular impulses    retrogradely  enter  the AV  junction and colludes with  the incoming atrial impulses. When this happens , the AV dissociation is said  to occur. The important point here is,  many times if the retrograde VA conduction is fast and optimally timed , it can cross the AV node without difficulty  and reach the atria  and  subsequently  even    depolarise  the SA node   and  reset  it  . If the VT is persistently conducting  retrograde  it can suppress the SA node as long as the VT is there. This makes a P wave becoming totally absent.  (Note of caution : If you say VT as one of the causes of absent P wave you may be failed in your cardiology board , but this remains a fact !)

So the atrial  depolarisation  and contraction During VT is a complex one. It depends  mainly on the  intensity of the  upcoming    electrical wave front   from the ventricle  . The distance traveled by this wave front  determines  the location of  p waves .It may be in one of the following ways .

  • P waves can be totally absent
  • P wave may occur antegrade
  • On the QRS
  • Over the T wave

In effect the P wave can  literally be any where   in the given strip of  VT

When does a fusion  beat occur ?  When does a capture occur ?

This again is determined by the AV  junctional refractory period. If it permits ,  an   occasional atrial impulse may sneak through the AV junction and capture the ventricle . This is capture beat. Capture beats   are usually narrow qrs  . So in a wide qrs tachycardia  if we note  an occasional narrow or relatively narrow  qrs complex it could denote a VT.

If the atrial impulse after crossing the AV junction   collides with the   upcoming ventricular  impulse  the surface ECG inscribes  a fusion beat. An incomplete capture beat is a fusion beat. It is a combination of two qrs complex one activated from above , one from below .The width of the fusion beat may be wide , narrow or intermediate.

So the evidence for AV dissociation  in surface ECG  is rarely  manifested  if the VT is successfully  traverse  the AV junction and   reset  the SA node  or keep it in a semi depolarised state  .This could be clinically important  some times , the SA node takes time to recover following  A DC shock especially in elderly

An episode of VT can unmask  a hidden sinus node dysfunction , as VT is technically similar to an atrial override pacing   of course  from  below .

Final message

During VT , electrophysiologically  there must be a dissociation between  the atrial  and ventricular contraction.But the evidence  for which is not manifested in surface ECG in the majorty.The primary reason for this,  due to  the  intact  VA  conduction  that    result in  retrograde VA  association.This  makes the  classical findings of   AV dissociation a redundant or invisible  one .

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