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Posts Tagged ‘narrow qrs vt’

Why VTs have wide QRS complex?

Brief answer: VT  usually presents with wide QRS tachycardia because it originates in ventricular myocardium, travels muscle to muscle instead of the normal conduction system. However, VTs need not be wide always, if it captures the conduction system early and more proximally it can be as narrow as SVT.

Further reading: Only for cardiology fellows 

Two empirical statements are made here. (The scientific chances of both being reasonably correct are fair)

  1. 80 % of wide QRS tachycardia by default is VT. That means 20 % of wide QRS is not VT. We all accept that.
  2. 80 % of narrow QRS tachycardia is SVT. It may also mean, up to 20 % of VT can be narrow QRS.

It’s obvious, not all VTs are dramatically wide. When it is not wide, they test our knowledge and patience. Let us be clear about the factors that determine the QRS width during VT. Once we know this we can have our own inference.

What determines the width of QRS  in VT?

1.Origin of VT 

The focus of origin is extremely important. Pure myocardial focus distal to the conduction system is invariably very wide. We know VTs originating right over the fascicles are narrow.

2.His Purkinje breakthrough

The time taken to capture the normal septal conduction system is a critical determinant of QRS width during VT.This makes the VT from septal origin narrower.VT arising from the free walls obviously takes a longer time to engage the HIS Purkinje system. Imagine , If VT originates from the lateral mitral annulus,  how much time it may take to reach RV free wall and lastly RVOT. Here the VT will become bizarrely wide.

3.The structural integrity of His Purkinje

It is important to emphasize a fact , even if the VT captures HIS Purkinje early, if they are diseased , still the VT will be wider.(Example bundle branch reentry in DCM in which VT keeps going around the conduction system still, it’s wider)

4.Course 

Length of the re-entrant circuit. Macro reentry is expected to be wider. Focal or micro reentry will often be narrow, provided the distal circuit is not diseased.

5. Scars as barriers and boulders 

If the VT circuit is interrupted by random scars en-route (from origin to exit) the  VT width prolongs. (Evidence for scars is often visible in sinus rhythm ECG as notches /slurs or fragmentations in QRS )

6.Exit point of VT

This is a poorly understood term (at least for me) It is believed,  VT can exit only epicardially. The line joining the focus of origin and the exit point is expected to decide the QRS axis. The problem comes when VT breaks out multiple paths and possibly sub-endocardial as well.

7.LV dysfunction 

A severely dysfunctional ventricle can stretch the QRS irrespective of conduction system integrity.

8.The Ionic milieu of cells Interstitial resistance

We know,  biological current is nothing but Ions in motion. So, no surprise it can alter the QRS morphology. The classical example is hyperkalemia , that can make ECG a wide and blunt sine wave. Local acidosis, hypoxia also influence the QRS duration.

9.Drugs 

Any drug which has class 1C or 3 properties can slow the VT circuit velocity. Typically flecainide is well known to make QRS wider. Amiodarone may  reduce the ventricular rate. in VT instead of reverting it. Apart from this these drugs depress the ventricular myocardium severely and prolong the QRS width independent to its action on the conduction system.

10.Mechanism  of changing width 

VTs can have varying QRS width as reentrant circuits change or experience slow conduction due to autonomic influences. VT with downstream aberrancy is also possible as the VT rate by itself influences the conduction property distally.(Just lie SVT with aberrancy)

A paradox about the width of QRS in VT

A curious phenomenon is often seen, when VT occurs in patients with baseline ECG which is already wide (As in an ischemic dilated cardiomyopathy with LBBB/RBBB). Here, the VT  prematurely stimulates viable muscles distal to the diseased HIS  Purkinje system (Which they are deprived of early activation of till then) .They seem to relish the early arrival of electrical impulse by brisk activation that converts wide QRS complex to narrow one. (This  behavior is one of the principles of cardiac resynchronization therapy where we attempt to rewire the heart with multiple leads and shrink the QRS.)

*One more mechanism of wide QRS sinus rhythm becoming narrow during VT is due to a concept called source -sink relationship. The VT delivers enough energy overcoming His Purkinje resistance downstream. (This property is used in HIS bundle pacing )

Postamble

*Forget about wide vs narrow QRS debate. A significant chunk of VTs falls within intermediate width QRS(100-120ms) . Whether to label these as wide or narrow QRS  squarely lies on whims of the reader. (Should we take the widest QRS in 12 lead ECG?  Pre-cardial  vs limb lead  etc are not clear) Unfortunately, we don’t have a separate algorithm for this category. This issue demands a separate discussion.

 

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How to name  a ventricular tachycardia ?

This  continues to be a  favorite past & present  time of  modern-day cardiologists. Especially ,  VTs associated with structurally normal heart  suffers with this  protracted problem .Widespread use of  EP study has not solved the issue as yet.

The   VTs that arise from the left ventricle in an apparently normal heart   has been referred  by  various terms.

  • VT with structurally  normal heart
  • Idiopathic left ventricular tachycardia
  • Verapamil sensitive  VT
  • Septal VT (It can be either myocardial /non myocardial origin)
  • Narrow qrs VT
  • Fasicular VT
  • LVOT tachycardia
  • Hemodynamically stable VT
  • Belhassen VT

Now we have still more exotic VTs like Cuspal , mitral annular , etc . All of the above can mean anything , or same thing   in different centers  ,  different cardiologists in different times .

* RVOT tachycardias also have  many synonyms.( Adenosine sensitive, Adrenergic,  Gallavardin, Parkinson Pop, etc )

VTs associated with CAD , valvular , myocardial diseases generally devoid of  nomenclature problems. Ischemic VT  is yet to be classified in a proper fashion.

The confusion in classifying VT is  not due to the complexity of heart disease. It is due to  the general  comprehension failure as  every VT can be described with reference to clinical , ECG morphology, hemodynamics and presence or absence of underlying heart disease. A simplified and clinically useful VT classification is being prepared in this forum .Will be published shortly .

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Traditionally we believed VT can originate only  from the ventricular myocardial cells . Then we realised many of the VTs shared the characteristics of SVT. When these were analysed , it was found VTs , after all ,   do not have   a big deal of   difference wth SVT s ! especially when it arises from the high septum .Contary to the conventional teaching  the AV node is not a anatomically distinct and discrete  structure  .Instead it is made up of  thousands of specialised cells located in AV junctional area .These cells ramify both superiorly and inferiorly like an octopus . Hence  , it does not require great academics to understand AV Nodal properties extend downward into the IVS for some distance . In some individuals   clusters of cells with  slow conducting  property (Which is a hall mark of AV nodal tissue )  may invade deep into the IVS .The interface of  these slow conducting tissue with that of  fast septal purkinje fibres , make it a  perfect platform for  the potential slow-fast reentry within IVS. This forms the basis of fascicular  VT.

Clinical features

  • Since it shares the  properties of SVT , the natural history is also relatively beningn
  • Occurs in young
  • Hemodynamically stable ( More physiological conduction : Superi inferior Like SVT)
  • Narrow qrs (Narrow because the VTdoes not travel by cell to cell instead  run through the normal conduting system for most part in the circuit)
  • Verapamil sensitive .(Mimic AV nodal Tach)
  • Degeneration into VF is  rare  and hence  SCD is not a big  issue
  • Tachycardic myopathy can occur.

fascicular vt ventricular tachycardia  ecg  svt avnrt avrt wpw

Note:

Fascicular tachycardia is also known in several names.

It forms the bulk of the causes for  idiopathic left ventricular VTs .Other being LVOT VT.

Described first by Cohen in 1974 , followed by Zipes , when they noticed  it was possible to reproduce atrial induction of VT.

Belhassen in 1984 found the verapamil sensitivity of this VT

Other synonyms some times used are

  • Septal VT
  • Narrrow qrs VT

Download high resolution table

Fascicular tachycardia

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