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Posts Tagged ‘hear rate in various tachycardia’

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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