Posts Tagged ‘avnrt’

Adenosine is a  purine analogue. Acts by stimulating outward K+ channel  of AV nodal tissue, more specifically  in the posteriorly   located  slow pathway in the vicinity of  coronary sinus.

Another action of adenosine is inhibition of cAMP , which is similar to beta blocking action may also help in terminating the tachycardia.

Adenosine : A 10 second cardiac miracle

  • 12mg bolus is administered , preferably in a central vein (Not mandatory  though)
  • Termination is usually abrupt . Transient VPDs are observed during termination.
  • Transient flushing may occur.
  • If the patient is taking Aminophylline group of drugs (Which are adenosine antagonists) the AV nodal blocking action may be neutralised .

(It may be apt to recall  at this juncture ,  Aminophylline is used in sinus node dysfunction or AV block to increase heart rate )


A good one from Medscape http://www.medscape.com/viewarticle/585287_2

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AV node is the  “Go slow” region in the cardiac highway .Every impulse is delayed  for about 120ms and then pursue its  onward journey to depolarize the ventricle.

Since  AV node  has inherently slow conduction properties , it is not  surprising  this zone  is vulnerable  for developing  AV block .We know AV junction and the adjacent his bundle  is the site  for many types of AV block. In  classical  Mobitz type  2 AV block ,  for every two or three supra ventricular impulse only one is  conducted and we call this as   2:1  or 3: 1 AV block ( More appropriately AV conduction  )

Can we have reverse of the above situation ?  That is , for each supra ventricular  impulse  can ventricles  fire twice or thrice   ?

Yes it can  ,  what looks like a funny situation ,  could be more common   .We are not recognising it often.

How is  this possible ?

This can happen only if there are two different  tracts of conduction from atrium to ventricle and  both of them conducting  fully to  reach ventricle and complete the depolarisation.

This situation can  occur in

  • Dual AV nodal pathway*
  • Triple nodal pathway**
  • Multiple AV accessory pathways (All contributing  AV conduction )

* Exact incidence in general population is not known ,but it could be higher than what  we believe !

** Very rare

 Some what  related  phenomenon , never the less , it   mimics 1:2 or 1 : 3 AV  conduction

  • AV nodal echo beats
  • Non sustained AVNRTs

How is simultaneous conduction possible in dual AV nodal  physiology  ?  Will ( it not  ! ) the first impulse make the ventricle refractory to the following impulse ?

Under normal physiological conditions simultaneous conduction*  is not possible .It happen if  . . .

  • The first impulse goes relatively fast  and activate the ventricles .
  •  The second component of the first impulse, ie  through  the slow path conduction   is sufficiently  slow ,  it  reaches the ventricle and  able to depolarize it , well after  the  first beat’s  refractory period .
  • A Further requirement is , the initial  fast response fails to block the incoming slow  response  by a retrograde   slow path block .

* It need to be further clarified , even in physiology ,  simultaneous conduction is possible , but it is  often incomplete . At best it can result in ventricular fusion beat as in pre -excitation beat or it can be a concealed one travelling halfway through the AV node or the bundle.

Why recognising this 1:2 conduction  is important ?

  • It is traditional  to  think  , an unexpected beat  occurring prematurely  in a given strip of ECG is always thought to be an ectopic beat .This is not the case. An  unexpected premature narrow QRS  complex  with out a  p wave , should  make us suspect   dual AV nodal conduction .
  • If  this  dual AV nodal  pathway  is intermittently  conducting or conducting with  varying velocities ,  it becomes  an     irregular narrow QRS  rhythm  .This  can ,  very well  be confused with  atrial fibrillation.
  • If  one of the paths in the dual AV pathway  is conducted aberrantly   it  mimics a  VPD.

Final message

1:2  AV conduction may not be rare . Cardiac physicians are encouraged to look  for this phenomenon whenever they encounter an abnormal  early  narrow  QRS  beat without preceding P waves. Apart from academic curiosity , it can  solve many mysteries in CCUs and EP labs .

 Reference :


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AV nodal reentrant tachycadia(AVNRT) is the commonest mechanism of SVT. It is divided into slow-fast, fast-slow, slow-slow , representing the two limbs of he circuit.

Slow -Slow circuit is  the rarest  type of AVNRT.  It should be appreciated  ,  the scientific validity of  slow-slow circuit is  applicable  only in relative terms . A virtually  similar antegrade and retrograde limbs with identical conduction velocity and refractory  properties  , can neither  initiate  nor  sustain an AVNRT.

Caveat in the definition of slow -slow AVNRT.

Even though ,  we call it   a  slow-slow  tachycardia , one of the limbs need to be faster than the other.  So , every slow -Slow AVNRT in reality will have  two types

  • Slow- Slow ( Still , faster than antegrade slow) mimic a slow-fast physiology
  • Slow( Faster than retograde slow )  -Slow closely mimic typical  fast slow .

Implication for electrophysiologists  and   points of contention for the ablationist !

  • In Slow -Slow AVNRT ablation we do not know exactly ,  which of the slow pathway is being ablated , unless we specifically  analyse  the post ablative  data.
  • Very often it is not done.Every one in the lab is happy , for breaking the tachycardia circuit. Only after the procedure is over , we may realise the tachycardia is not really killed as it finds an alternate highway to complete  the short circuiting of heart.
  • We need to  suspect this type of AVNRT   prior to the  procedure .Electrophysiologist  shall  spend little   more time and a wide area ablation done , in the vicinity  of coronary sinus ostium can be attempted. .

It is not a smart practice to advocate  wide area ablation as a routine protocol in all AVNRT

as it directly  increase the rate of complication >

Final message

A   hurriedly  done slow pathway ablation  which  may  temporarily terminate the AVNRT ,only to recur later as  the retrograde  slow pathway may again form  a substrate  .The area of slow conduction  acts as a turnaround gateway and capture  the  retrograde fast  pathway which  could be  available in plenty in the anterior aspects of AV node  .   (Note : The unablated  slow pathway  now  form the antegrade  circuit )

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Ectopic beats , other wise called premature depolarisaton are one of the common ECG abnormalities  diagnosed by physicians.

  • Atrial premature beats (APDs)
  • Ventricular premature beats(VPDs) 

APDs and VPDs  form  the bulk of all clinically important ectopic beats.

Heart has a specialised electrical conducting system , every cell in this system is capable of firing on it’s own. But why then only the atrium and ventricle produce ectopic beats .Other structures like AV node, His bundle , purkinje are relatively rare to produce ectopic beats .

Is the AV junction relatively immune to develop JPDs?

The answer to this question would be  “May be yes” . Yet, we need to recognise they may not be as rare as we think , many times we fail to  diagnose  it or rather recognise it !

Certain observation about Junctional premature depolarisation are made .AV junction has unique properties than any other parts of the heart.The basic purpose of AV junction ( AV node is not a preferred word as it has no anatomically distinct demarcation)  is to apply a electrical break on the incoming electrical signal .Nature does this with a purpose .   It is essential for the ventricles to fill adequately . We call it as PR interval.

So, when the basic purpose of AV junction is slow down the conduction it is logical to expect it won’t get irritated that  easily  and  result in ectopic beats. So JPDs are less common than other forms of ectopic beats.

What is invisible JPD and HIS ectopics ?

We should realise many of the JPDs  & his bundle ectopics are not conducted ,  the impulses simply dissipate down hill .  Unlike the atrium and ventricle the junctional and his tissue has no associated chambers to depolarise , hence they are not  often visible in the surface ECG.The only evidence in the surface ECG may be an unexpected pause which represents concealed conduction. A EP  study  of the bundle  ECG often unmask these silent JPDs and His VPDs.

 JPDs are  less common  , while  junctional escape beats are the  hall mark of any  severe supraventrcualr bradycardia . How  does  that occur ?

AV junctional cells have  an unique behavior in that , it comes to the rescue of the heart whenever the native SA node becomes too slow  . This happens as a passive response .We call this as junctional escape beat.The major difference between a JPD and Junctional escape beat (JEP or JED )  is in the initial timing of the beat . Escape beat comes late .The coupling interval of escape beat (We generally use coupling interval for ectopic beats only , but  it helps to understand )  will be longer than the previous sinus cycle. So escape beat is never premature (Rather a  post mature beat !) .Ectopic beats are always premature ,( except Interpolated ) and occurs earlier than the next anticipated beat.

The other difference is escape beats are tolerated well as the primary purpose is to rescue back up.Their rate is generally equal to the  intrinsic rate  of AV junction ie around 40-50.

General characters  of  Junctional  premature beats and tachycardia

  • Fortunately rare,  fires at a  higher rate.(Unlike junctional escape beats )
  • Enhanced automaticity is a common mechanism
  • Reentrant JPD is rare , unless the patient has AVNRT or it’s variant  physiology.
  • Manifest as narrow qrs complex . JPD with aberrancy is distinctly possible .In that case differentiation from VPD may be difficult.Retograde  P wave morphology may help.But it is non specific as VPDs also have varied atrial capture depending upon the VA conduction .
  • Causes include Hypoxia,  (Rarely ischemic junctional tachycardia. ) common causes include  digoxin induced , post operative states, incessant JT
  • JTs are Difficult to control.Overdrive pacing may be needed. May lead onto tachycardic cardiomyopathy.
  • A benign form of junctional ectopic tachycardia is also reported .

Importance of Junctional escape rhythm

The role of AV junctional escape is vital in extreme bradycardia , as if the junction fails to escape the dangerous ventricular cells take  over  electrical control  and that’s  bad news for the heart  with  sinister consequence.The situation can rapidly degenerate to VT  , what we call  as phase  dependent or brady dependent VT. The treatment for which is increasing the proximal heart rate. By isoprenaline or pacing. So the AV junction does  a delicate balancing act .At times of tachycardia it blocks unnecessary impulses.At times of extreme  bradycardia it assists the heart as escape rhythm . The problem here is many of the disorders that affect SA node , affect the AV node as well .So ,  AV node may not be able to help the SA node always.That is the reason many extreme myocardial end up with VT straightaway.

Final message

JPDs are not very uncommon as one would believe.It has some unique properties. There are vital difference between JPDs and junctional escape beats.JPDs can trnasform into JTs in local pathological milleu and as a rule they are difficult to control.

AVNRT is also a type of  junctional  tachycardia  but,  it  is delinked from  the ( unofficial  ! ) classification of JT  , not  with  any  academic purpose  but by tradition.

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Ischemic ventricular tachycardia is a  too well recognised clinical  entity  . But , ischemia triggered atrial arrhythmias are less often encountered .

Does that mean , atria are relatively protected from the effects of ischemia ?

Not really  . . .  It  is possible  it may not be  that rare ,  as we think .

And then ,  the semantics play  a major  role !

Atrial fibrillation  is the commonest supra ventricular  arrhythmia  in human ,  we also know CAD is the leading cause of the AF apart from HT & Cardiomyopathy . So technically , ischemic SVT  is  more common than Ischemic VT ,but we do not call it so !

If we analyse the triggers for AF it is more often hypoxia  (than ischemia )  . . .yes there is huge difference between the two .In the ventricles it is more often ischemia that  trigger a VT.

Atrium is very sensitive to systemic  oxygen saturations especially in elderly and COPD patients. This is the reason we get many of the complex atrial arrhythmias in hypoxic situations ( Ectopic atrial, Multi focal atrial , etc) .These arrhythmias are difficult to control unless oxygen saturation is corrected. While  many of AF episodes are transient and disappear after correction of hypoxia.

If the ventricle also  responds with fibrillation  at times of systemic  hypoxia ,  one can  imagine the disastrous consequence ! God is kind enough , systemic hypoxia per se  rarely trigger a VF ,  though  it can maintain a VT which was initiated by some other mechanism.

So what are the causes of  narrow qrs tachycardia in the coronary setting

Apart from AF ,  Ischemic SVT  can occur in the following situations

  • Atrial infarction -Focal AT -Atrial flutter /AF
  • Post Pericarditis
  • Refractory , ischemic JT (Junctional tacycardia ) in elderly , perioperative , hypoxic patients

*Atrial arrhythmias are very rare during unstable angina for some unknown reasons . Atrial scar induced ischemic focal AT is underdiagnosed.

** Never  diagnose AVNRT /AVRT in a patient   who has an ACS. It is likely you will be 99.9% wrong.

*** Preexcited AVRTS are very rare in elderly CAD patients even in those with a history of SVT  .This is because as the age advances the accessory pathways undergo degeneration either by ischemia or  the wear and tear  and get self ablated .

Many times the associated , HT and diabetes may contribute to the arrhythmia.

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P waves represent atrial depolarisation. The p wave height  and width depends not only the size of the RA and LA but also the site of  origin of atrial  impulse .A normal SA nodal origin of P wave produce the normal shaped p waves.

We know  ectopic  p waves can have a wide variation of morphology.(Fully inverted, partially inverted, slurred, bi phasic, notched, rounded , deformed, etc. The morphology is dictated by the direction of p wave vector and thus it is quite variable in different leads. Further  it is also determined by the inter atrial and intra atrial conduction.So in summary , an ectopic p wave can have any morphology we can think off !

What is isoelctric P waves

It is rather a surprise we have not thought about so long,   like a low voltage QRS ,  a  p wave can also be very low amplitude and it may be entirely isoelectric , which could actually mean the p waves are as good as absent.This can happen in all leads or in few leads. .Atria gets electrically activated but fails to inscribe a p wave .This is termed as isoelectric p waves

The importance of isoelectric p waves

It  can  happen , both  in sinus rhythm  and in ectopic atrial rhythm . Absent p waves should be differentiated form isoelectric p waves. It is typically described in focal atrial rhythm arising from the right side  of  the  inter atrial septal near the   perinodal  tissue.The atrial tachycardias arising from this site are classically have isoelectric p waves in most of the leads especially  V1 .

Other causes of absent p waves

  • Atrial fibrillation

The classical example .in fact here p waves are replaced by fine or coarse fibillatory waves

  • Sinus arrest  plus Junctional rhythm with retrograde VA block

Not all junctional rhythm result in absent p waves .Many record inverted retrograde p if there is VA                            conduction.

  • Sino ventricular conduction .P waves appears  absent in surface ECG. It occurs in hyperkalemia /renal failure is due to high levels of pottassium   which suppress the atrial activity sort of atrial electrical paralysis but still impulse originates in SA node traverses  the inter atrial pathway and reach ventricles.typically P waves are absent or can be termed isolectric.
  • Atrial  stunning following cardioversion

Long standing atrial tacycardias may fail to resume it’s mechanical (or even electrical ) activity after  cardiversion  .If it is electrical stunning the p waves do not immediately appear  but occurs later .In fact this could be termed as failed cardioversion.

* Note  p waves are failed to identified in many of the VTs AVNRTs

Final message

Absent p waves ,  isoelectric p waves , hidden p waves, merged p waves , low voltage p waves , unrecorded p waves,  selective absence of p waves in some leads all can happen in clinical cardiology practice.

One should realise the importance  differentiating   absence of   p waves in the given strip of ECG from failure of p waves to  get recorded by the  ECG machine .This has diagnostic significance.

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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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