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 .
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 .