Posts Tagged ‘ventricular tachycardia’

A young man with   VT  (LBBB morphology ) and  apparently normal heart by   echocardiogram  is  a  real  diagnostic challenge .
Here is a comparison  of  the two  closely mimicking  entities. RVOT VT and ARVD .
Please note -Micro reentry and triggered activity  are very closely related cellular evens. For all clinical reasons there is generally no purpose in differentiating the two.

*Please note -Micro reentry and triggered activity  mimic each other at the cellular level . For all clinical reasons there is generally no purpose in differentiating the two.

*RVOT- Right ventricular outflow tract. ARVD/ARVC -Arrhythmogenic  right ventricular dysplasia /cardiomyopathy

(Caution : RVOT vs ARVD  -In  the traditional medical teaching system , we are often taught to differentiate  two closely related  entities.Our brain also loves to look things in either black or white . Realise , medical science always brings  surprises . There can be significant overlaps between the very entities we want to differentiate.Bear that in mind)


1. Hoffmayer KS, Machado ON, Marcus GM, Electrocardiographic comparison of ventricular arrhythmias in patients with arrhythmogenic right ventricular cardiomyopathy and right ventricular outflow tract tachycardia. J Am Coll Cardiol. 2011 Aug 16;58(8):831-8.

2 .Ainsworth CD, Skanes AC, Klein GJ Differentiating arrhythmogenic right ventricular cardiomyopathy from right ventricular outflow tract ventricular tachycardia using multilead QRS duration and axis. Heart Rhythm. 2006 Apr;3(4):416-23.

T wave inversion in V1 TO V3 for diagnosing  RVOT VT .

3.Daniel P. Morin,  Andreas C. Mauer, Kathleen Gear, Usefulness of Precordial T-Wave Inversion to Distinguish Arrhythmogenic Right Ventricular Cardiomyopathy from Idiopathic Ventricular Tachycardia Arising from the Right Ventricular Outflow Tract .Am J Cardiol. 2010 June 15; 105(12): 1821–1824

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Ironically  , in medicine we need to peep into the  past for updating and scrutinizing current knowledge .   Here is free ticket for   a  retro journey   to  the  the Electro-physiology Laboratory of  the  University of Wisconsin-Milwaukee  .  This article  , which was published in 1990 ,    still  can explain many  intriguing   concepts  of VT succinctly .

Thanks to   circulation  for sharing this article free !

Akhtar M . Clinical spectrum of ventricular tachycardia. Circulation 1990;82:1561-73.

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Ventricular tachycardia is  a major cardiac electrical disorder. Even though it  connotes a deadly meaning the prognosis and outcome vastly vary.It can be a benign arrhythmia in  structurally normal heart that present as occasional fasicular VT  or Exercise  induced RVOT , to dangerous ischemic polymorphic VT which rapidly degenerate to VF and SCD if not reverted . It is ironical we are  trained  to put all VTs in a single basket and  propagate fear psychosis among   physicians and patients .

Management of VT has certain broad principles.

  • Identify the cause
  • Whether  specific structural heart diseases present or not
  • Identify the mechanism if possible
  • Rule out transient metabolic cause as a trigger

Therapeutic targets

  • Stabilising the cell of origin
  • Passifying the scars
  • Interrupting bundle branches in  BBR  mediated tachycardia
  • Ischemia related  Focus – Re-perfusion
  • Reversing LV dysfunction



  • Correct Cell hypoxia /Acidois
  • Pharmacological ( Class 1A/1B /1C , class 3 and Beta blockers , Magnesium  )
  • Role of  beta blockers for VT management is largely under recognised.It has an important role to play in both acute and chronic  VTs)

Electrical (DC shock ,Ablation and ICD)

  • DC shock is treatment of choice  all emergency VTs
  • Ablation  aims  at preventing episodes of VT .Ablation needs EP study and  expertise of  an electro physiologist.
  • ICDs  revert it only after the VT emanates from the focus . ICD can be implanted without knowing the focus .May not require a EP consult.


CABG + Surgical scar excision , Aneurysectomy  might help in certain refractory VT.

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Clinical cardiac  problems can be very demanding at  times. Here  is a  situation even the toughest will struggle.

A 52 year old man comes with a wide qrs tachycardia  with a blood pressure of 90 /70 with class 4 dyspnea .He was restless , trying to sit up because of  orthopnea. The ECG showed  a definitive ventricular tachycardia  with LBBB morphology.The patient was   connected  the   oxygen line ,  cardiac monitor, oximetery, etc

The consultant  on call instructed   immediate DC shock   and  he  warned  about  impending ventricular fibrillation .He  casually told the fellow to  do a echocardiogram also and rule out any structural heart disease. Even as  the staff was  arranging the defibrillator , the fellow did   a  rapid bed side echocardiogram . He was  shocked to find a  large mobile LV clot   with a  dilated ,  severely dysfunctional left ventricle  having an  EF  of  25 % .

Now comes  the critical time . Should we shock this man with VT and LV clot?

What will be your option now ?

  1. I will not mind the LV clot  ,  will go ahead with DC  Shock . Let him dislodge his LV clot . If It is his fate  let it be !
  2. Defer the   DC shock . Fall back on medical cardioversion like  Bretyllium, Amiodarone or magnesium  . After all . . .  it is not a pulse less VT. He is not in cardiac arrest . He can afford to wait .We can’t risk a stroke .
  3. Give a low energy  shock  25 joules  with paddles  avoiding the LV apex.  .It may not dislodge the apical clot , still  VT may be terminated.
  4. Try overdrive  pacing instead of DC shock
  5. Refer the patient for emergency surgical removal of LV clot
  6.  Suck out the LV clot with a   LV suction catheter and plan elective DC version*
  7. Insert a temporary Aortic filter and shock the patient **

*  Such catheters are in preliminary stage of development . Is  that true ?  ( If  no I  should get the royalty for the idea  ! )

(Read the related article in my blog )

** A loud imagination . Such filters do not exist.( If  IVC  can be filtered   why not  Aorta ? )

What was finally done ?

After analysing each  of the above  , we decided   option one “Prey the  God  and shock the heart” ) After all if it is  a VF ,  this  issue becomes null and void !  . Luckily God was with us.  The  patient  was  reverted to sinus  rhythm with 50joules   and  had  no  untoward events . He was subsequently anti-coagulated .  He is being planned for CRT/ICD therapy

Final message

Critical care  medicine is all about risk taking .Many times , therapeutic maneuvers  confer a  significant   risk  to life  comparable  to the   index problem.  But that  should not be a deterrent .  A careful learned decision  is warranted.

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AV dissociation is  the most specific diagnostic clue in VT.But this is not a constant finding. In fact one  would be  lucky to spot a fusion beat  which denotes AV dissociation . It occurs in less than 30% of patients with VT .

Technically ,  for AV dissociation to occur atria and ventricle should  not be related in either direction .

If there is  a retrograde VA association ante grade AV conduction   is not possible  and hence one can not get a  fusion beat or so.

What happens to p waves during VT ? How does atria depolarise during VT ?

Atrial chambers can not sit idle during  VT .It has to somehow get depolarized  and contract   but  the  timing    may not be appropriate .

P waves  during VT can either be antegrade or retrograde .

Theoretically both can be present   but most times  it is   the  retrograde  p waves we see.

The occurrence and timing of p waves  is related  to the VA conduction .

If there is  1 :1  VA conduction during VT there can not be AV dissociation  for the simple reason  we have VA association.In fact there is constant vigil to depolarise the ventricle  through the normal AV node and his purkinje  in spite of the VT .SA  node is aware of this fact ,  how difficult it is going to be  confront the upcoming  rapid ventricular impulse . Usually the ventricular impulse   prevails  over the atrial impulse and much part atria is controlled by the VT . In fact  the VT reaches  all the way to SA node and simply  overdrive it . At these fast heart rates  retrograde p waves are not visible. ( But surprisingly one may see a regular  cannon wave in the neck with 1: 1   VA conduction.

Mean while ,  the SA  is always under look out for a opportunity to sneak into the ventricles thorough AV node. This happens  when the VT focus slightly slows down or shifts to a new site . this sis the time  we are able to  witness the AV dissociation . When the atrial impulse capture fully or partially the ventricle fusion beats occur confirming  AV dissociation .

Final message

AV dissociation is present in  less than 30% of VT because in  70%  there is a VA  association.(Retrograde  VA conduction ) . When V is associated with A there can not be AV dissociation.

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Mark E Jospehson  is the man who single-handedly carried  the burden of teaching  generations  of electro-physiologists  from  Harvard  Thorndike electro physiology services , Boston USA. Today , whatever  we know  about the mechanisms of VT , it is because of such great men who  spent thousands of hours  in the  first generation EP labs in early 1970s and 80s  , meticulously analysing   the data emanating  from  over  600   scar mediated VT with complex circuitry .

He along with  Miller published this seminal paper  in circulation 1988 , which gave us  the  algorithm  that localises  Post MI VTs.

Following table summarises their finding.

VT localisation in Infero-posterior MI

The general principles  of localisation of VT  

  • Localising VT following myocardial infarction  is difficult but distinctly  possible with  about 60 % accuracy.
  • Whenever we locate a focus we generally refer to epicardial site of exit not the focus of  origin.
  • Ischemic VTs with complex scars are difficult to locate .
  • The rule  that RBBB VT arise from  LV and LBBB VT from RV is too simplistic  in scar mediated VT.
  • The fact  that IVS is common to both RV and LV confounds the issue .Further, in a given  clinical VT  the origin  , course   and exit points of VT can considerably vary .For example  septal VT can exit  on  either side and  result in  either RBBB or LBBB morphology (Epicardial break thorough )
  • Multiple exit points are also possible.
  • VT induced in EP lab may not be reproducing the same clinical VT. So we have to be careful in what  we ablate and claim success !
  • VT with  structurally normal heart  has   more predictable behavior  , for  example RVOT VT  almost always have LBBB morphology.

Other important rules of thumb are

  • LBBB VT has more localising value .
  • Superior  axis is the most common  axis.
  • Bulk of the ischemic VT are located within the septum either in the apical or basal region .(75%)
  • Infero posterior MI has more complex scars , hence VT morphology is heterogeneous.

The purpose of localising VT is important  only with reference to  ablation.(Of course for academic reasons  as well )   With advent of electro anatomic imaging (Carto ) it is becoming   easier  to locate and track them . Still only a minority of VTs are amenable for RF ablation .

Please note ,  the most common modalities we use  in the management of VT  ,   Amiodarone  and ICDs   simply do not   bother  about   focus of origin  for it’s action !  That makes our job easy !



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Read with caution . This  may either injure or cure your patient !

Click on the ECG to view what happend !


How does  verapamil  terminate a  VT  ?

Physicians  often  debate  vigorously before   labeling  a cardiac arrhythmia as ventricular , atrial junctional  , abberant or not etc etc .  But  for  an arrhythmia   it matters little  from what  chamber it is going to to originate . After all ,  any cell in the heart if excited can generate an arrhythmia .  The ion channel abnormality and the influx and efflux of ions  that determines how a drug is going to terminate an arrhythmia.

In fact , way back  in 1989 the Sicilian Gambit stressed this concept when classifying anti-arrhythmic drugs .This classification taught us  , even though there is a  huge list of  clinical cardiac arrhythmias  , from the therapeutic point of view there are only a handful of receptors  (scattered  all around ) to target  !

When we look at this angle , we realise  , many of  ventricular action potentials  have  important slow  calcium currents  similarly  junctional action  potentials do have some  sodium currents.  Calcium current  is present in every  myocardial cell  more so in the vicinity of AV junction.  Further , at times of ischemic or hemodyanmic stress these ion channels  may  take a different avatar altogether.Slow sodium channels and fast calcium channels etc !  (A wild imagination or is it a fact ?) Other important targets are potassium channels

Heart is a complex structure both macro and microscopically  .  In the three dimensional  histopathologic   interface between atrium  and ventricle (Especially in the  basal areas , outflow tracts  , around the AV grooves ) there  are  lot of sharing  and overlap of  different morphology  of cells . A high septal VT can behave  exactly like an SVT  which  includes the  tendency to get terminated by calcium channel blockers.

Amiodarone is a most popular  drug for VT termination ? Are we clear about the mechanism of it’s  action in terminating VT ?

It is  more of a perception and belief  that  class 3 action   may be   responsible for termination of VT by Amiodarone . In reality it is very difficult   to prove this point.  As Amiodarone  has all the  4 classes  action that includes beta and calcium blocking properties.. In fact ,  now  there is evidence  to  suggest   beta or calcium blocking action  may be more important in terminating  VT when  it is administered  IV  . (While  the class 3 action predominates in long term oral therapy )

A verapamil sensitive   VT may  successfully  be terminated by  Amiodarone  not by its  unique  action  instead it   may simply represent  its  calcium blocking  property.

Final message

Many  of the  VTs terminated by Amiodarone   could  also be verapamil sensitive . Since verapamil is never tried first we will never ever know the incidence of such phenomenon that gives pseudo credit  to Amiodarone

It may not be big crime to try injection verapamil in some of  the  stable ventricular tachycardias( As my fellow did ) especially  when we we know there is an entity called verapamil sensitive VT !

Q for the readers :

How many deaths are reported in cardiology  literature  regarding    fatality  following   verapamil  in   VT ?

I am trying to find  the answer the  data is very hard to come by !

Critical comments welcome.


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Wide qrs tachycardia has a unique place in clinical electrocardiography .It is  a much fancied and glamorous entity for the simple reason , it continues to be the  cardiologist ever solved puzzle .For over three decades of research, clinical debates , symposiums , seminars have effectively failed to take away the uncertainties in decoding the wide  QRS  tachycardia . (Specifically ,  VT vs SVT with aberrancy)

Some wondered , should we really waste our efforts in differentiating the two . In emergencies it never matters , in fact one need  not attempt to do this often futile exercise !

Few dedicated criterias like Brugada etc have helped us .

While the difficulties in differentiating between VT and SVT with aberrancy remain over the decades .A less reported  , but more common issue is  confronting  us .

It is  the big question of  differentiating a  wide  QRS tachycardia from a narrow QRS  tachycardia

wide qrs tachycardia vt svt aberrancy

This  occurs  more often than we realise  ,because we define wide  QRS  tachycardia in a vague manner

  • Normal qrs width between Up to 80 / up to 100 ms acceptable  ?*
  • Narrow qrs tachycardia 80 ms?
  • Wide qrs tachycardia i> 120ms  ?
  • Definitely wide qrs >140msec

* The confusion is mainly because 20ms difference between limb leads and chest leads .

In reality one may not be able to all  tachycardia into narrow or wide .

There is big  overlap zone that need to be labeled a intermediate qrs tachycardia

If we can  triage the tachycardias into three instead of two it may help us arrive  fast  ,  to the  correct diagnosis

Narrow QRS tachycardia ( qrs 80ms)

  • Sinus
  • All svtS (avnrt etc)

Intermediate QRS tachycardia 90-120

  • Most of the SVT with  aberrancy  ( Except antidromic SVTs which are really to wide !)
  • Septal VTs*
  • Fascicular VTs*
  • VT in PPM and ICD /CRT patients **

*  Any VT that arise near the major conducting system of ventricle conduct  fast and hence qrs are relatively narrow.

**These are rare entities where  base line wide QRS getting narrower with the onset of VT . (Ref : http://europace.oxfordjournals.org/cgi/content/full/eun254v1)

Wide qrs tachycardia >120ms

  • Most of the genuine VT (Ischemic , myocardial origin)
  • Post MI VTs
  • SVT aberrancy especially AVRT
  • Any SVT with preexisting BBB
  • Marked electrolytic disorders

Unresolved questions

  • Which lead we should look for measuring the width of qrs ?
  • Should we take the narrowest qrs or widest qrs or should we take the average ?
  • Should we calculate how much the tachycardia has widened the qrs from the baseline  width of a given patient ?  Is it not possible , what is wide for some may be normal for another !
  • If  there is no isoelectric line  and ST segment  blends with qrs complex  how to mark end of qrs ?
  • If  limb leads show a narrow qrs and chest leads shows  wide qrs what is the significance  ?
  • In precardial leads  if one lead alone shows a narrow qrs , what is the significance ?
  • Can a narrow qrs VT conduct  with aberrancy and making it  really  wide ?

Final message

When we are  able to solve   complex electrophysiological  problems  , we must also realise  even   simple  tasks can be demanding in medicne ! It is proposed to create a  new  group “Intermediate QRS tachycardia “that can help solve the issue where we have difficulty in labeling these  tachycardias which fall  in the  greyzone .We can try &  apply the modern EP based VT criterias  to this group and find out the hidden truths !

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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


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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Acute coronary syndrome is the commonest cardiac emergency. STEMI and NSTEMI are the two clinical limbs of ACS. Generally they have distinct clinical, ECG, angiographic features.(Ofcourse, with some degree of overlap) . It is  a  mystery , both clinical presentations differ so much inspite of the common denominator  , namely ,  an injured plaque with add on thrombus  within the coronary artery. The primary difference between these two entities is, in  STEMI the occlusion occurs sudden and complete and in NSTEMI it occurs slow and incomplete

Cardiac arrhythmias in ACS

It is a  much published factoid  for  many decades, that  only one third of STEMI patients  reach the hospital alive ! The reason being , STEMI  is very much prone for primary VF.  Contrary  to this ,  most pateints with NSTEMI reach the hospital alive ! How ?

Both are ACS, if ischemia is a powerful trigger for dangerous ventricular  arrhythmia’s , NSTEMI should also behave  similarly .So what protects against arrhythmias in NSTEMI ?

  • We realise ,  by observational experience (Not EBM !)  It is the suddenness and totality of ischemia that trigger dangerous form of arrhythmia  .
  • Further, a balanced  ischemia in two contralateral segments (or global  ischemia) some how protects against development of ventricular  fibrillation .This may be due to preservation  of  electrical homogeneity  , and the spherical VT spiral waves are not sustainable.
  • In contrast , STEMI has a sudden  focal , ischemic  zone that initiates the VT and    ischemia free  contralateral segment  welcoming  and sustaining the  reentrant wavelet.
  • The observation of primarily single vessel disese in STEMI and multivessel disease in NSTEMI also give credence to this concept.
  • Further , ischemic preconditioning can exert an important anti arrhythmic  effect in NSTEMI as  patients with unstable angina have   slow, repetitive episodes of ischemia prior to the index event .
  • Post MI scar mediated VT/VF is independent of degree of overall ischemia
  • It is also established ,  a sub group of  STEMI pateints  who  had  preinfarction angina(  ie . a brief  period of UA/NSTEMI) have very low risk of SCD  supporting the concept of sensitising the myocardium against ventricular arrhythmias.

Final message

Even though , there is a convincing concept  of  Ischemia induced  cardiac arrhythmia in literature ,in real patients it is very difficult to link the two in many situations..UA/NSTEMI is the most common  acute ischemic event but the incidence of VT/VF here,  is far less than one would expect.In ACS , focal , total  ischemia is more likely to precipitate a VT/VF than multifocal and global ischemia.

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