Ventricular tachycardia - why wide QRS?

[Lothric]

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Hey,

Why are the QRS-complexes wide in ventricular tachycardia?

In VT, for example torsades de pointes, you have the latent pacemakers Bundle of His/Purkinje fibers being faster than normal (which explains the increased heart rate of ventricles), but how does this connect to the wide QRS-complexes?

 

[Evolver]

If the cells the VT originates from is on the free wall of one of the ventricles, then the ventricles will be activated in series instead of at the same time as they would if the rhythm originated in the septum. This, along with disorganized propagation of the signal, can cause widening of the QRS interval.

 

[Lothric]

If the cells the VT originates from is on the free wall of one of the ventricles, then the ventricles will be activated in series instead of at the same time as they would if the rhythm originated in the septum. This, along with disorganized propagation of the signal, can cause widening of the QRS interval.

Thanks,

But I still don't understand why the signal transduction becomes disorganized or why activation occurs in series. I mean, the bundle of his/Purkinje fibers do get activated by the depolarization even in normal circumstances. It just happens to be that in VT the signal BEGINS from bundle of his/Purkinje, but everything from that point onward should be normal, no?

I guess I just should accept as it is and stop overthink/question why things are like they are.

 

[nlax30]

Thanks,

But I still don't understand why the signal transduction becomes disorganized or why activation occurs in series. I mean, the bundle of his/Purkinje fibers do get activated by the depolarization even in normal circumstances. It just happens to be that in VT the signal BEGINS from bundle of his/Purkinje, but everything from that point onward should be normal, no?

I guess I just should accept as it is and stop overthink/question why things are like they are.

That’s not really how it works.

You technically can have what we call fascicular VT which originates from one of the fascicles and since its utilizing the native conduction system (or at least part of it) it may not be all that wide. But that’s not common.

For the usual VT think of it as originating from any ventricular myocardial cell and then spreading via slower cell-to-cell connections. While a VT from the septum CAN engage part of the conduction system and appear narrower (not normal though) than VT from a free wall (further from the conduction system), it will not be as narrow as a native beat coming antegrade down the conduction system. These fibers conduct differently antegrade bs retrograde and sometimes may not conduct retrograde at all.

 

[Lothric]

That’s not really how it works.

You technically can have what we call fascicular VT which originates from one of the fascicles and since its utilizing the native conduction system (or at least part of it) it may not be all that wide. But that’s not common.

For the usual VT think of it as originating from any ventricular myocardial cell and then spreading via slower cell-to-cell connections. While a VT from the septum CAN engage part of the conduction system and appear narrower (not normal though) than VT from a free wall (further from the conduction system), it will not be as narrow as a native beat coming antegrade down the conduction system. These fibers conduct differently antegrade bs retrograde and sometimes may not conduct retrograde at all.

That's my problem though - nowhere in literature does it state that pacemaker rates can originate from myocardial cells. It's either from Purkinje fibers, bundle of His, SA or AV node. And since it is said that for VT the pacemaker rates originate from the ventricles, it can only be bundle of His or Purkinje fibers (SA and AV are further upstream in atria).

I've just assumed (for the sake of having some kind of background knowledge) that for VT the SA node is no longer solely dominating but instead Purkinje fibers/Bundle of His joins the pacemaker group and is responsible for the beats downstream (the impulses from SA node does not reach ventricles apparently and thus another pacemaker takes over this downstream region).

Is this reasoning wrong?

 

[nlax30]

That's my problem though - nowhere in literature does it state that pacemaker rates can originate from myocardial cells. It's either from Purkinje fibers, bundle of His, SA or AV node. And since it is said that for VT the pacemaker rates originate from the ventricles, it can only be bundle of His or Purkinje fibers (SA and AV are further upstream in atria).

I've just assumed (for the sake of having some kind of background knowledge) that for VT the SA node is no longer solely dominating but instead Purkinje fibers/Bundle of His joins the pacemaker group and is responsible for the beats downstream (the impulses from SA node does not reach ventricles apparently and thus another pacemaker takes over this downstream region).

Is this reasoning wrong?

Your reasoning is correct when talking about normal physiology. Yes, normally the SA node, AV node/AV junction, Purkinje fibers demonstrate automaticity at different rates with usually the SA node “winning out”.

For VT we’re now into arrhythmias and abnormal physiology. Under some pathological circumstances other atrial and ventricular myocardial can display automaticity.

So for arrhythmias there are only a few different mechanisms that cause them and can be separated into a problem with impulse formation by either abnormal automaticity or triggered activity, and then problems with impulse conduction such as reentry.

Think of triggered activity or automaticity as a small or single site that for whatever reason is depolarization and “firing” abnormally. You can have focal tachycardias (either atrial of ventricular) that arrive from a single focal site.

For VT clinically we are usually dealing with reentry as the mechanism which is where a conduction wavefront is circulating around an area of scar or through an area of slow conduction which then leads to an ongoing loop and continued tachycardia. This may be a small loop around a scar from a prior heart attack and each time the wavefront passes around the loop it then exists somewhere and activates the rest the myocardium (which is then what gives up the morphology on the 12lead ecg)

So definitely possible for the tachycardia to be originating from an atrial or ventricular myocyte outside the usual conduction system.