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Posts Tagged ‘amiodarone’

As I expected ,  my earlier algorithm “An Idiot’s approach to tachy-arrhythmias” has  elicited  mixed reactions  .Some  EPs calling it a dud while few  physicians termed it awesome . Here is  a follow up .

Heart rate of a tachycardia is the most neglected parameter by physicians .  They are often seen spending  hours together for decoding  arrhythmia , splitting the brains   for P wave  location , VA conduction, Fusion beats etc .Finally they end up  either administering  Amiodarone a broad spectrum anti arrhythmic agent or DC shock.

Here is an unusual algorithm  for arriving at a diagnosis in all tachy-arrhythmias  based only on heart rate and the width of he qrs complex.

(Click over the table for high resolution image )

approach to cardiac arrhythmias narrow qrs vs wide qrs brugada wellens criteria

General principles in diagnosis of tachycardia

Narrow  qrs tachycardias.

90 % rule : If regular It is sinus tachy if irregular it is A-FIB . Take some efforts to r/o sinus  tachycardia . (In children and young adult it can be extremely difficult at times )* Please note : Sinus tachycardia can show some irregularity due to sinus arrhythmia and  frequent  APDs and JPDS . Further at  fast rates P may fuse with T it should not be confused with  A-fib .

Wide qrs tachycardia

Common things  are common , if  you sight a large animal with a huge trunk  in a Kenyan safari ,  it is most likely to be an  elephant and not a Dinosaur !  Please diagnose VT  when you encounter wide qrs tachycardia by default especially when the BP drops  !

  Management issues

It  would be  foolish to split our heads for decoding an arrhythmia when a patient is unstable .Any hemo-dyanmic unstable tachycardia needs DC shock . (Synchronized will be better unless it is dire emergency )There are very few arrhythmia where DC shock is contraindicated   ( MAT/Dig toxicity/Underlying sinus node dysfunction )

Only if the patient is hemo-dynamically  very much stable   the  physicians  have enough time to  confuse themselves  and the real  ordeal begins .Please remember  the 5 arrhythmias  constitute 98  % of all known tachy-arrhytmia . So where ever  you practice ,  whether  in remote Nigerian village  or  sophisticated  Cleveland  university hospital , when you are  confronted with a tachycardia  the diagnosis  should be one among the  following  five  !)

  1. Sinus tachycardia .
  2. AF/A-fib
  3. Atrial tachycardia  with  or without blocks
  4. ventricular tachycardia /VF
  5. AVNR/AVRT with or without aberrancy

All  other tachy-arrhythmiaa  are  largely  academic !

Regarding  drugs

Knowing the mechanism of  arrhythmia genesis  is less important  at bed side . They are  triggered , sustained, and maintained by either functional or structural component .Ionic basis operates in every arrhythmia  , but it is the anatomical  substrate that maintains it .This happens in only diseased heart.The only point worth remembering regarding mechanism of arrhythmia  genesis  is ,  automatic and focal tachycardias  will not respond to DC shock . All other can be termed some form of re-entry . Micro reentry  for all practical purposes behave like  triggered  activity. Ischemic and electrolytic VTs are primarily ionic based and often polymorphic.Structural VT are commonly mono-morphic. Any VT just prior to degeneration to VF become polymorphic

Every patient with cardiac arrhythmia should be checked for hypoxia,acidois , electrolyte defect or exposure to any  pro arrhythmic drugs. (The commonest  cause of tachycardia in any  IMCU , is inotropic induced (dopamine /doubtamine ) tachycardia .

We  have  5  pharmacological options

  1. Blocking  adrenergic  receptors(IV Esmolol, Metoprolol)
  2. Blocking calcium channel (Dilitazem,Verapamil)
  3. Blocking potassium channel  (Amiodarone  ,Sotolol Adenosine  to a cetian extent )
  4. Blocking sodium channel . ( Procainamide , Lignocaine (Wonder drug almost forgotten now ! ) Flecanide Mexilitene etc)
  5. Digoxin ,Adenosine  magnesium are special  anti-arrhythmic  agent which  has very useful role in certain specific situations (Magnesium -Torsades/Polymorphic VT / Adenosine in LVOT/RVOT VT etc)

General principle is ventricular arrhythmias  are blocked successfully  by sodium or potassium blockade  Atrial and functional tachycardia are blocked by calcium or adrenegic blockade  .Of course,  there would be  some degree of overlap  when the arrhythmia  origin  hovers  around the junction  on either side of the AV  ring . This is basis of verapamil sensitive VT .Clusters of  calcium  channels are scattered  in the junctional  region

Refractory tachycardia

  1. Consider ablation  in AVNRT/AVRT
  2. ICD +Drugs  in VT
  3. Ablate and  Pace(Some A-fibs)
  4. Ablate and ICD (Some  incessant VTs)
  5. Surgery in minority

In AVNRT/AVRT 90 % success can be achieved  in most EP centers .VT ablation  is still a complex process  with  success rate around 60 % ICDs  are indicated in all recurrent VTs except incessant forms .(Where the battery will deplete within a month !) Surgical cure (Maze etc  ) is possible in selected few while undergoing mitral valve surgery.Contrary  to the modern scientific  mood ,  I can ay with conviction most A-fibs can be managed medically except a fraction will require pulmonary vein ablation / isolation .

Final message

Mastering the field of of  cardiac  arrhythmias ,  though  appear a daunting task ,  it does not  require   immense  sense  to understand real world problems are  only a  few and can be tackled in a simplistic manner !

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Amiodarone acts  by

  1. Correcting the  rhythm  to sinus .
  2. Controls  ventricular rate  alone
  3. Does both ?

Answer is 3

How can it correct the rhythm alone ?  If  the rhythm is corrected ,  rate will automatically be controlled,  unless Amiodarone converts AF into Sinus tachycardia  which is very unlikely !

Of course  Amidarone  is not a  magic drug .The success rate of  Amiodarone  restoring  sinus rhythm is far . . . far less . . . than our expectations ! . It fails to  convert to sinus rhythm in a significant chunk *. Interestingly ,   it may still  control the  ventricular response  by its beta blocking action .

*Our estimate is , the failure rate Amiodarone  is  between  30-40%  or even higher ,  as   bulk of AF we witness   is due to Rheumatic heart disease.

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Dronedarone is a drug which was developed to replace the very effective  , (but side effect prone ) antiarrhythmic drug Amiodarone.

After years of study ,  Dronedarone has been  approved for use in some* of  our  patients with atrial  fibrillation

* Who are they ?

That is the only thing  , we are  unclear about Dronedarone  ! ! !

The recent studies on Dronedarone DIONYSOS have  clearly  proven it , to be  a  less effective  agent in controlling  AF  , but has a  advantage of fewer adverse effects.

Hence ,  for preventing the potential  side effects  of Amiodarone , let our patients  take an inefficient drug ! This is  how we are inclined  to think ! But the medical industry can not be blamed altogether  , after years of research they develop  a molecule and they would like to  have at least a small pie in the atrial fibrillation market place !

It again proves the centuries old adage,  that all drugs are poisons .If a drug lacks side effects it ceases to have the desired effect also . If you want a drug with zero side effect  a sugar coated placebo  is the best choice !

Is there  really a  role for Dronedarone ?

  • Yes , may be in patients  who have recurrent AF in spite  of stabilising  the underlying conditions that perpetuate AF( Hypertension, CAD, COPD etc)
  • When Amiodarone is contraindicated or withdrawn due to side effects
  • Remember ,  Digoxin, Beta blockers, or even calcium blockers  , can have an  important role in the  chronic management  of AF. But they are unpopular  for many reasons other than academics!

Final message

Dronedarone is power-less antiarrhythmic  drug  ( “Less- powerful ” could be a more  polite  and decent  word !) that has a specific role in the management of AF when  efficient rate or rhythm  control is  deemed unnecessary !

Why don’t  we have study  with  one to one comparison of Digoxin ,Beta blocker and Dronedarone  in the chronic management of   atrial fibrillation !

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It is one of the greatest innovation in medicine  . . . that is . . . electric current being  used as  a  drug to  treat disorders of heart . Of course ,  it is not a surprising finding  when we know heart is an  electro mechanical organ ,  and electricity can be used  to treat various disorders of heart by delivering it  in an optimal dosage and site.

Devices  that help administer  electric  current in cardiac disease.

  1. External  cardiovertor and defibrillator
  2. Implanted defibrillator
  3. Anti bradycardia  pacemaker
  4. Anti tachycardia pacing
  5. Cardiac  resynchronisation device

What  is  the  difference  between cardioversion and  pacing ?

Cardioversion  is reverting  a tachycardia with  a electric shock that is delivered diffusely throughout the heart This  electrical wavelets traverse the  focus of tachycardia  and the adjoining myocardium  which is called critical electrical mass (Usually reentrant) .This depolarises the cells responsible for tachycardia and extinguishes the abnormal electrical activity.

Defibrillation is same as cardiversion except that it is a high energy shock  and delivered without synchrony with qrs complex . In VF, we defibrillate in all others  we cardiovert .

What are the disadvantages of cardioversion ?

Eventhough it is a very successful modality for treating cardiac arrhythmias it also has some issues.

  • Cardioversion is not infallible. It rarely works in tachycardia due to enhanced automaticity (Multifocal atrial tacycardia , Automatic junctional tacycardia , Digoxin induced tacycardia it may even be dangerous !)
  • Many times multiple shocks are required and may result in myocardial damage, stunning , and elevated cardiac enzymes.
  • In susceptible patients, especially in elderly it may depress the natural pacemaker ie the sinus node and dangerous  bradycardia

over drive pacing paired pacing anti tachycardia

What is difference between cardioversion   applied externally on the chest wall and intracardiac cardiversion as in Implantable cardiovertor defibrillator(ICDS) ?

The underlying principle is same except that the energy required is a fraction of that applied in the chest wall . The average energy required is up to 20 joules . while it requires up to 300 joules

What is anti tachycardia pacing ?   Why this concept came into vogue ?

When it became clear , cardioversion may not work in all forms of tachycardia and risks of multiple shocks  on the myocardium  not be taken lightly , experts in those times (1970s)   thought  a pace maker lead in a optimal site can do the job of cardiovertor. .

Pacing rapidly  in the tachycardia zone  provide us an opportunity  to  enter  the  tachycardia circuit , interfering , interrupting  and blocking the reentrant circuit  (We call it entrainment)  . If it is an automatic tachycardia pacing in close vicinity of the tachycardia   focus result in a  electrical  line of  barrier  which acts as an  exit  block ( Like the lakshman  reka !  in Ramayana )

The term ATP is used as a  general term as anti tachycardia pacing .Over drive pacing  can be used synonymously.

What is the  main advantage of ATP ?

  • Less injury as it avoids recurrent shocks  .
  • Can be administered as many time as  required .
  • Some tachycardias specifically respond to ATP only (Read below)

How to perform overdrive pacing ?

  • Conventional  temporary  pacing lead can be used .
  • Special  leads  may be required for paired pacing .
  • The rate of pacing is generally between 50- 150 /mt
  • Technically we call it as  over drive pacing ,   in reality most  of the  time   pacing is domne at a lesser heart rate than the tachycardia itself .This should be recognised because, the term overdrive pacing connotes a meaning of pacing at more than the tachycardia rate.
  • The duration of pacing  may be 30 seconds to 2 mts as necessary .

Can we use the external transcutaneous pacemaker paddles for overdrive  pacing ?

Yes we can, it may be termed a  non invasive external overdrive pacing .This  mode is not popular among cardiologists  not because it is ineffective  , rather we have not fully realised it’s  potential .

Different types of  overdrive pacing

What is coupled pacing ?

It is a type of overdrive pacing where   pateint’s own sponataneous  rhythm   is used trigger a  pacemaker stimulus    and  hence only alternate beats or pacing beats which is coupled with the pateint,s own rhythm it is called coupled pacing . This  is different from from paired pacing  in that only single pacemaker stimulus per cycle .

What is paired pacing ?

Two pacing stimulus are given .The first impulse is maintained constant and the second impulse is done with varying coupling  interval to scan the entire cardiac cycle .It is expected at some point of paired pacing the second impulse would  block the reentrant circuit.

What is random paired pacing ?

The atrium is   delivered a   pair of random stimulus ( . . Like a bite of snake !) is  delivered into the atria .This can revert many of the reentrant atrial and ventricular  re entrant tachycardia.

What is the  unique value of  sinus paired  pacing ?

In patients  with persistent sinus tachycardia,  especially  in patients with  high MVo2 situations or dysfunctional ventricle we have no option to control the heart rate without depressing myocardial contraictility . Most of the negative chronotropic drugs have negative inotropic action also.  In these situations pairing a pacemaker stimulus with a sinus impulse can produce a compenstatry pause  and result  in reduction in net heart rate as well  as increased  contractility due to post extrasystolic potentiation.

How does a  catheter whip inside the atria   terminate many of the procedure related  tachycardias in cath lab ?

It is a common maneuver  in cath lab ,  to  forcibly whip the   catheter for   terminating  many of the transient procedure related  SVTs and outflow tract VTs . The arrhythmias get terminated  either due to catheter hit induced mechano  electrical  cardioversion   (5 joules ?) or  the atrial subendocardial stretch due to the  whip lash .

What are the tachycardias that may  respond to overdrive pacing ?

It is logical to expect any of the reentrant tachycardia  might respond to ATP. The  exact success rate can  not be established  since this modality  is not applied  in vast majority of  patients . Only if a patient  is not responding to drugs or multiple DC shocks ATP is thought off . Of course ATP can not  considered  a first option   unless othe  patient is  on a temporary pacer.

What is the caution for using ATP ? Why  atrial overdrive pacing   is preferred over  ventricular  overdrive pacing ?

Pacing a ventricle rapidly carries a risk of inducing ventricular fibrillation . So whenever  possible ATP  should be administered  through  an  atrial lead. This may not be possible always as in the presence of AV block a VT  can not be captured  by atrial pacing  .

It is also  a fact  many times   when the    ventricular overdrive pacing  fails to revert a VT , an  atrial overdrive pacing has been successful . This is due to the  more uniform    depolarization  wave fronts , that reach the ventricle and reset the VT .

Currently ATP is useful in

  • Recurrent atrial tachycardia
  • Refractory ventricular tachycardia especially with enhanced automaticity (Early ischemic VT )
  • Digoxin induced tachycardias
  • Some cases of Tachy brady syndrome

In some of the modern pacemakers and  in all ICDs ATP is a an important programmable parameter .In fact using this mode liberally would conserve battery life .Many times a simple hemodynamically stable VTs are shocked by ICDs  instead an ATP will  do the job . It is a well recognised fact that   ATP is underutilsed in ICDs .This issue needs to be addressed.

Final message

Pacemakers are not only meant to treat bradycardias but also tachycardia . Even though it is a well known fact for over 3 decades , for some reason this simple and effective concept is not getting  the  attention of  the current generation cardiologists  which it definitely deserves!

Reference

  1. Overdrive Pacing for Ventricular Tachyarrhythmias: A Reassessment    P. R. KOWEY andT. R. ENGEL
    ANN INTERN MED November 1, 1983 99:651-656
  2. Pacing Techniques in the Treatment of Tachycardias  I. WIENER  ANN INTERN MED August 1, 1980 93:326-329
  3. Treatment of Recurrent Symptomatic Ventricular Tachycardia R. A. WINKLE, E. L. ALDERMAN, J. W. FITZGERALD, and D. C. HARRISON ANN INTERN MED July 1, 1976 85:1-7
  4. Treatment of Tachyarrhythmias by Pacing J. E. Batchelder andD. P. Zipes

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                                         Ventricular  tachycardia is considered as a dangerous electrical rhythm abnormality .It can immediately degenrate into ventricular fibrillation and result in SCD in many.Ironically, it is also a fact , a patient with VT can  present silently  without any symptom  .Some VTs are slow and recurrent without much affecting The hemodyanmics.

 

In chronic recurrent, beningn VT (Some may consider it , ” height of  absurdity ” to call a VT beningn ! but it  is a reality , the term beningn denotes –  very remote chance of converting into VF) ” Is there any other therapeutic option other than convertng into sinus rhythm. “(  Read related topics)

 

The following paper was presented in the Annual scientific sessions of  Cardiological society of India,  Kochi , seven years ago in  2002

 

VENTRICULAR RATE CONTROL  IN  VENTRICULAR TACHYCARDIA 

S.Venkatesan,,. Madras Medical College. Chennai

 

                           Mangement of  hemodynamically  stable  recurrent   ventricular tachycardia  remains a  delicate clinical problem. Reverting to  sinus rhythm  is  considered as  the only aim  of  treating  VT.While rate control is accepted as a therapeutic  option  in atrial fibrillation,  it is not  so,  for  ventricular tachycardia.In this  context  we attempted to analyse  the effect of  Amiodarone on   ventricular  rate  in stable ventricular tachycardia  which fail to convert  to sinus rhythm.

 

                            The  study cohort consisted of 49 patients with stable VT  who were admitted in the coronary care unit  of  Govt. General Hospital  between 1998 to 2002.The criteria for inclusion   were systolic BP>100mmHg and absence of  hypoperfusion of vital organs  The mean age was 52 years (range 26-68)  with a male female ratio  of 4:1.   Of the study group 36 patients  were either reverted with  IV lignocaine , Amiodarone ( 150-300mg   bolus )  or  DC  cardioversion . 13  patients  who did not respond to   either of these   were  followed up  with  Amiodaroneinfusion(1000mg)  for 24 hours.  The baseline  diagnosis were old MI (6)) DCM (3)  Arrhythmogenic RV displasia(2). Idiopathic VT was diagnosed in  2 patients.All these patients had  VT  during  most part of  the   24 hour  follow up.

                     

                         The pre Amiodarone mean  ventricular rate was  152  (124 –196).  Post amiadaorne (at 24hrs) mean ventricular rate was 128(88-142). The time taken for   50% heart  rate reduction was  6.6h (4-24h).  The average  systolic blood pressure  improved from  100   to  112mmhg . These patients were  discharged  in stable clinical status with oral Amiodarone and  were  referred for  EP study.

 

                          It is concluded that Amiodarone, apart from it’s cardioverting ability , has a distinct ventricular  rate controlling  effect  which  can be of therapeutic value in  at least certain subset of chronic recurrent VT.

Final message

 

Some of  the patients  with VT carry a very low risk of VF  and SCD .In these  patients , the only  other major  aim is to prevent tachycardiac cardiomyopathy  that can be done with drugs which  controls  the ventricular rate whenever  VT occurs !

Corrrecting the primary cause like cardiac failire , revascularisation ,detailed EP study  ,tachycardia mapping , followed by RF ablation and ICD implantation is  the state of the art approch in the management of VTs.But this small clinical observation was made to  impress rate control could also be an option  in patients  in whom these procedures are  contraindicated  or not  available . 

 

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Lignocaine , probably has saved more lifes  world over  than any other cardiac drug .

It was the only choice for ventricular tachycardia  till 1990s, both in pre and post  thrombolytic era.Every coornary care unit has reverted tens of thousands of  unstable VTs with this simple and cheap intravenous drug.the utility value of lignocaine is not limited to ischemic VT alone it is effective in in almost all forms of VT.It was classically administered in two or more boluses followed by an infusion.

What happened to this wonder drug  with great performance record ?

The  power of   statistics , and inappropriate interpretation by the scientific community  has left a serious blow to this wonder drug .Now the drug has been made redundant, and mainstream cardiac literature has made everyone feel  guilty , if  anybody  uses this drug for VT .

Why did lignocaine lose the battle ?  The reason is three fold

  1. The advent of  much fancied Amiodarone
  2. One negative study  for antiarrhythmic drugs in post MI period (CAST) 
  3. And two so called  positive studies  for Amiodarone (ALIVE & ARREST) has sounded the death bell for this drug  which has resuscitated millions of life !

CAST study http://content.nejm.org/cgi/content/abstract/321/6/406 

All , CAST  said was routine suppression of  asymptomatic ventricular arrhythmias  in the post MI period is unwarranted. But you know , how this  world interpreted it  “Lignocaine  has no role in ventricular arrhythmias in post MI setting ”  The most funny thing  was  lignocine was never used in CAST study .

The  studies involving one to one comparison  of Lignocaine and Amiodarone (ALIVE and ARREST study) was also not interpreted  properly.These studied only shock resistant VTs. What about the role of lignocaine where defibrillator was not available ?

Link to ALIVE and ARREST  read and make your own conclusion.

http://content.nejm.org/cgi/content/abstract/346/12/884

http://content.nejm.org/cgi/content/full/341/12/871?ijkey=8fa241f3cebb86a177632ec6ccadfb5a3ded7bc2

 Final message

  • Lignocaine is not  only a topical anesthetic  , it is powerful and gentle myocardial anesthetic when administered in post MI period.
  • With this property it  successfully cardioverts and prevents dangerous ventricular arrhythmias.
  • Time tested and worthiness proven.
  • While , we are made to believe  the success rate of  Amiodarone in VT is far superior than ligncaine .It is a falsehood.
  • Any experienced cardiologists will recognise ,  many times even  Amiodarone resistant VTs often respond to Lignocaine .
  • The fact of the matter is , without a good quality  one to one study  , lignocaine was ditched. One reason for this could be  Lignocaine ,  is a generic drug and has no market value.

Let us take home , the message (scientific or unscientific ! ) Lignocaine still has a great role to play in the management of dangerous ventricular arrhythmias .The only caution is ,  it should not be used routinely and indiscriminately in all asymptomatic patients with  VPDs or nonsustained VT . (Acknowledging CAST conclusion.)

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The cell of origin of ventricular tachycardia is rarely discussed at bedside. It is still in research labs !

                                    Ventricles are not made up off entirely myocytes. Apart from myocytes it contains specialised  purkinje cells , fibrocytes, interstitial cells and  some times primitive mesenchymal cells. Ventricular tachycardia can arise either in purkinje cells, the myocytes  or even the fibrocytes. The myocyte  VT  classically occur during ACS or post infarct VTs.They are  more often hemodynamically unstable and quickly degenerate into ventricular fibrillation. Myocardial VT is likely to be pulseless and require DC cardiversion frequently. Purkinje VTs are relatively less unstable. If VT arise proximally in the septum near the distal his, or in bundle branches (BBR) the VT is more stable.They  are likely to respond to be medical management.

What is the therapeutic implication of knowing  myocardial VT ?

                               In fact  ,simply knowing the cell of origin of VT is not suffice .The ionic currents inside the cell that trigger and sustain the VT is more important. There are few ionic circuits responsible for VT. Sodium , Intra cellular calcium, potassium , beta receptor mediated calcium current.If we know the individual ionic culpirit we can block that specifically  . Now we have multi purpose ion blockers  like amiodarone which acts like a broad spectrum antibiotic and terminates a VT.

                              So as of now there is no real purpose of breaking our head  in locating the cell  of origin  and the ions responsible for VT  at  the bed side ,( Researchers will do that for us !).  We have only few  antiarrhythmic drugs available in our crash cart  .Our job is to choose the optimal  drug  which will fit in for our patient. In electro physiology labs, radio frequency ablation is done .This is  nothing but shooting down the abnormal electrical  focus (Cluster of cells or a samll segment of myocardium).  In future,  a single abnormal  cell could be selectively neutralised with cell based therapy assisted by  nanopore robots !

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