Posts Tagged ‘electrophysiology’

In the last few decades  we have  understood a major concept in the genesis of cardiac arrhythmia.Slowing in the propagation of cardiac impulse is a key  trigger to precipitate a reentry circuit and initiate a tachy- arrhythmia.Still , many conditions like first degree AV block, chronic RBBB or even LBBB are  benign entities  as along as the heart is structurally normal .They seem never increase the incidence or life time risk of  cardiac arrhythmia . Longevity is unaffected.( Or do we assume many things ?)

How is this possible ? or is the theory of slow conduction triggering reentry is flawed ?

Think again . . . if these patients who later on develop a structural heart disease , with an episode of ACS , myocardial or valvular disease,  the original slow conduction substrates these people were harboring ,  will it become important ?

Surprisingly , we have no answers in literature.When Haissaguerre et al found preexisting ERS pattern could be a trigger for primary  VF in case they develop ACS  , he opened up a huge debate as it involved converting  a vast number of normal population electrically anxious.

Now ,is it possible the so called  benign  blocks of heart like first degree AV blocks , RBBB , LAHBa , would be important  at times of ACS  and possibly make them prone for for primary ischemic arrhythmia .

Is bundle branch re-entry possible in structurally normal heart ?

We need answers. Some one , (Any EP fellow) somewhere  could take up the issue and enlighten us !

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LBBB is probably the most important  conduction defect of the heart .When we say LBBB , we visualize a  strikingly  wide bizarre qrs complex .

Left bundle even though is considered  a discrete structure , the fascicles  make it a diffusely spread structure. Many varieties of LBBB with various degrees of involvement occur.

Talking about the basics of  LBBB  electrophysiology  is out of place for the current generation cardiologists,  who  have little spare time as  they sweat it out inside the cathlabs.

In early 1960s and 70s great articles came from pioneers regarding these defects. If we want get a good insight  read  this  articles from  Sodi palleres .Who  says LBBB is a dynamic process, where it can occur from mild functional  delay to a total block .

The conduction  properties of left bundle is very much influenced by heart rate.

Law of statistics would  suggest  for every complete LBBB  at least three to 4 times incidence of incomplete  LBBB

Then . . .

Why we are not diagnosing ILBBB often ?

  • We miss it
  • Mistake it with LVH
  • We know it  is there , but we do not  want  to diagnose it .

How to diagnose ILBBB?

See  Sodi palleres criteria*

What is the relationship between qrs width and completeness of LBBB ?

Surprisingly and contrary to the belief , the width of the qrs has no linear correlation between severity of LBBB. In fact incomplete  LBBB can occur with even 150ms qrs !

Then ,  what  exactly determine the completeness of LBBB ?

What  matters is , whether the down coming impulse gets blocked  and split in the  left side of the IVS or not ? This causes the  the septal vector to  change  it’s direction ( ie  right to left instead of the normal left to right) It  removes the initial small r wave in v1  and q in v6  in complete LBBB. In  incomplete LBBB these  r and q are  often retained .

What is the differential diagnosis of ILBBB ?

Type B WPW may mimic LBBB and vice versa.

LV hypertrophy .

Differences : See table in  the Barold’s article  linked above .

Unanswered questions

  1. How common is ILBBB in STEMI ?
  2. How often ILBBB progress to LBBB ?
  3. ILBBB in dilated cardiomyopathy : Is desynchrony an issue ? (Normal QRS CHF !)
  4. Is functional  rate dependent  LBBB in cornary care units  same as transient  ischemic LBBB ?
  5. Intermittent LBBB and Incomplete LBBB  aren’t they  synonymous ?

Final message

ILBBB is not that uncommon as one would  tend to perceive.


My humble tributes to  Barold, Sodi -palleres , and Leo  Schamroth . Probably  one of the best  article on ILBBB is linked below. Reviewed    in 1963 !  Not much data has been added  in the next 47 years as on 2010

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  • It is only rarely a journal of International caliber is published from India . IJEP is one such journal.
  • Cutting edge articles on Electrophysiological science  break here !
  • This is an online journal . No print issues . Enjoy, it is free !

Here is the  Link

Just sample an article  : A great review about cardiac arrhythmias in congenital heart diseases , Must read by  all cardiologists    http://www.ipej.org/0906/khairy.htm

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Ventricular tachycardia as a group , constitute a major  group of cardiac arrhythmias. Most of the VTs are managed  by cardioversion  followed by medical management.  Few require , implantable defibrillator when there is severe LV dysfucntion .(ICD) Localising the origin of  VT and subsequent , ablation is the treatment of choice in some of the  patients  with VT.

Traditionally VT was thought to arise fro the endocardial aspects of myocardium. Now  we realise many times VT originate from the epicardial aspects of  ventricle.

Epicardial VT : Defintion

Epicardial ventricular tachycardia (VT) is defined as VT in which the critical sites of the reentrant circuit (or the ‘sites of origin’) are located exclusively in the subepicardial tissue, as shown by entrainment manoeuvres or VT that is terminated within 10 s with standard radiofrequency (RF) pulses, or both.  E. SOSA,M. SCANAVACCA et  all  http://www.springerlink.com/content/w608142674154tp5/ 


 How to recognise epicardial origin of VT by surface ECG ?

  • Terminal S wave in V2 and q in lead 1 strongly suggest VT of sub epicardial origin.
  • Pseudodelta wave 
  • Intrinsicoid deflection time of  85 ms
  • RS complex duration of  >120msec

Suggest   epicardial origin of the VTs.

Important Links


Berruezo      criteria ,http://circ.ahajournals.org/cgi/content/full/109/15/1842  ( Must  read)



What is the clincal significance of epicardial VT ?

Endo cardial ablation  not likely to be successful

Trans pericardial approach may be needed.

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Ventricular  tachycardia (VT)  is one  of  the   dangerous form of  cardiac arrhythmias.

When it occurs , it may present  in  many ways

  • Cardiac arrest with immediate degeneration into ventricular fibrillation. 
  • Pulseless VT in a  conscious patient but in  in shock.
  • With pulse, relatively stable , not much fall in blood pressure.
  • Incidentally detected.*(Rare)

This , gives us  an idea  that VT  as an electrical abnormality has wide clinical presentations , life threatening  at one end and,  patient walking into the hospital with minimal palpitation on the other hand !

The management issues

  • In patients with hemodynamic instability , decision making is easy as there is only option of DC shock.
  • In patients with stable VT, it is natural for the physicians to get tentative or even confused.This is because , dangers of shocking a stable patient has to be weighed against the currently available excellent antiarrhytmic drugs( Amiodarone, Ibutilide etc) .


The major issue here is  in  ruling out underlying structural heart disease.

Never shock a stable VT, without knowing the myocardial and valvular function.There has been many occasions underlying  severe LV dysfunction is missed   and they may go for asystole.

VT in the setting of cardiomyopathy, Post MI(Scar mediated) are often refractory even to DC shocks.It is the drugs that will  ultimately control the arrhythmia.DC shock is just used to terminate the VT.

VT  structurally normal heart , especially arising the outflow tracts of LV or RV  behave very differently (Fortunately they are more benign)

  • Have less hemodynamic  impact as it involves the outflow tract and  not over the  the pumping  zone of LV as in conventional ischemic myocardial VT .
  • They  respond to calcium blockers  verapamil to be precise (As they share properties of SVTs)
  • Sensitivity to verapamil by no way convey a meaning of Amiodarone resistance.Out flow tract VTs will also respond to Amiodarone many times.
  • Degeneration into VF is rare.


Also  read  Therapeutic issues in stable ventricular tachycardia

Presented and published in Indian heart journal


Click  on link download PPT ventricular tachycardia


Related topics

Why some ventricular tachycardias are resistant , even to multiple DC shocks ?

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Sinus node  as the pacemaker , orchestrates the rhythm of life . It has  to fire for the entire life time of  a person.It  can not afford to take any rest ! But it can pause a little bit , of course that pause  could  be less  than 15% of it’s basic sinus length. This variation of sinus  cycle length is called sinus arrhythmia.This is physiological. When it exceeds 15 % of the previous sinus cycle it is referred to as sinus pause.

 Have a look at this ECG



What follows a long pause ?

By strict terms  of definition a sinus   pause should be followed by  a delayed , next sinus  beat only. A  sinus pause  , many times  is followed  by   JPD – Junctional escape beat.This situation should be ideally  referred to sinus arrest as the sinus node is taking too much of rest and it is not able to wake up from the slumber and it needs assistance form the junctional pace maker.

So even though sinus pause and sinus arrest is used many times interchangeably, it should be avoided. 

What are the electrophysiological mechanisms of sinus pause ?

  • Simple sinus bradycardia . The commonest  mechanism is  the  increased vagal tone. This occurs more often in young athletes. Eventhough increased vagal tone  conveys   a innocuous meaning , at times  this can also be symptomatic  and require intervention.
  • Sinus node exit block.
  • First degree, second degree, complete SA block can occur as in AV node.

First degree SA block can not be diagnosed by surface ECG. Third degree SA block is same as sinus arrest and subsidiary pacemaker will function in these patients.  Second degree SA block is usually diagnosed when the sinus pause is in the multiples of resting sinus cycles. If the pauses are not in exact multiples  sinus arrest is diagnosed. All these arrhythmia’s are collectively called sinus node dysfunction(SND)

How do you manage these patients?

Sinus node disorders can occur in number of systemic diseases*. It  needs to be  ruled out.

  • Infiltrating diseases like amyloidosis, hypothyroid states can result in SND.
  • Drug induced SND like beta blocker and calcium blockers are fairly common and should be excluded
  • Some congenital heart disease (SVC ASD) can involve sinus node.
  • Ischemic SA node disease is rare but can occur  following  infero posterior  myocardial infarction
  • Sinus node disorders are  very often related to degenerative atrial diseases associated with HT, cardiomyopathy etc

*The list is not exhaustive

A very important association is noted  with atrial fibrillation as  a part of tachy brady syndrome .The link between SND and AF  is obvious as   atrial pathology is the common denominator in both ! This will be discussed later.

When is a  pause  significant ?

Any pause that is producing significant symptoms is significant.This depends upon the overall  hemodynamic compensation of the patient.Young, and fit can even tolerate three second pause without symptoms.Underlying heart disease makes even a smaller pause symptomatic.But generally a 3  second or more  pause is almost always pathological .Pauses can be up to  5  seconds (  a 5 second pause actually means a  heart rate of 12/mt , obviously it can not go on for a minute, a patient will develop a syncope). A 3 second pause  corresponds to 20/minute.

How will you evaluate a patient with sinus pause ?

There are sophisticated electrophysiological studies (EP) available like sinus node ECG ,sinus node function studies like sinus node recovery time, activation time etc. But these are generally of  academic interest.

If a patient is symptomatic  (syncope) because of bradycardia  he requires a pacemaker and  EP study is redundant . Similarly , if  he is totally asymptomatic in spite of pauses , again  EP study is  not  indicated.

Only for patients  in the  grey zone,   further studies are indicated .This would include a extended holter, loop recorders, event monitors etc.

Another important issue to consider  is , before putting a pacemaker   patient”s   symptom  must be correlated  with their arrhythmia.

What is  the overlap  between sinus node dysfunction and neuro cardiogenic syncope ?

SND  can occur as an overlapping syndrome with neurocardiogenic syncope.(NCS ).NCS is also a very common cause of syncope .In NCS  there are two limbs .Cardio inhibitory and vasodepressive. The cardio inhibitory form can exactly mimic an SND. In a given patient  it is very difficult to pinpoint which of this limb is dominant.Head up tilt test(HUT)  might help in few.  If a patent’s symptoms are due to inappropriate vasodilatation pace maker may not reduce the symptom of dizziness or syncope.


  • There is no ideal  medical therapy* available as on date
  • Withholding all drugs which might aggravate bradycardia is of paramount importance.
  • Pace maker is the specific treatment in all symptomatic patients.

*Aminophyline tablet may be useful in some patients .It acts by antagonising adnosine receptors in SA node.Other drugs which can incrase the heart rate in the short term include  Orcipranaline(Beta 2 stimulant /Alupent ) Probantheline(M 1 blocker)

The key issue is to avoid unnecessary pacemaker implants in patients who have insignificant pause.

 Which pacemaker is ideal in SND ?


                                                              The need for dual or single chamber pacemker will be taken by the electrophysiologist .Atrial based pacemaker (AAI)  is preferred as it gives physiological pacing .But a simple ventricle based VVI pace maker is good enough in vast majority of patients. This takes care of   future risk of AV block also. DDD pace maker is the most physiological pacemaker and it is supposed to provide better quality of life. But it has an issue of insertion and  maintenance of  two leads, multi parameters to be programmed.It should switch to appropriate modes  at different times.(Like VVI mode during atrial fibrillation etc).Trouble shooting needs expertise , while  VVI is simple,  safe , and just effective as well .(In this turbulent world, quality of life is a  too trivial an issue  to be determined by a DDD  maker)

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                                          CRT , cardiac resynchronisation therapy  is being  projected  as a revolutionary treatment for cardiac failure , where a failing heart is rewired electrically through multiple leads and make it contract  more effectively.The success rate of CRT was highly variable.The basic question here  is,  there should be a  significant  documentation of desynchronisation  prior to CRT , for resynchronisation to be effective. Further , the sites of  myocardial  stimulation ( Coronary sinus/LV epicardial) , dose of electricity and the sequence of stimulation and the  electrical delay  are very  critical. Achieving this into perfection  is not a simple job and is  real rocket science ! ( If we can achieve 5 % of what  the normal purkinje network do within the LV we can term it a huge success.) Let us hope we catch up with nature . Finally , it is ironical  the sites of LV pacing ,  electrophysiologists  select currently  is infact not selected by them but pre selected by the patients coronary venous anatomy ! .So as on date ,  one can imagine how scientific this treatment could be !

                                         Initially it was adviced for patients with only wide qrs later for even normal qrs patients.When people started using it indiscriminately  insurance companies started to rethink and thus came the   RETHINQ study in NEJM  and brought a full stop to CRT in normal qrs CHF.

How to identify who will benefit from  the costly CRT  ?

It is a million dollar question. So millions of dollars were spent to identify the correct tool to identify the true responders to CRT.Echo cardiography with sophisticated methods tissue doppler, tissue tracking and , 3 D echo ,velocity vector imaging were done .These methods are not only costly but also time consuming and  hugely expertise driven.

Does all this  efforts with  advanced echo techniques worthwhile ?

This simple question was addressed in PROSPECT study in circulation

Click to read the article

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