Feeds:
Posts
Comments

Posts Tagged ‘wellens’

                                         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 . 

 

Read Full Post »

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 !

Read Full Post »