Feeds:
Posts
Comments

Posts Tagged ‘bbr’

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

Management

General

  • 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.

Surgical

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

Read Full Post »

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

Note:

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

Read Full Post »