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Posts Tagged ‘ICD’

We live in curious times .As we  advance in our intellect and wisdom ,bullet firings (either cross or straight !) have become an important cause  for sudden cardiac death.Sometimes a life is saved by unexpected way in extraordinary circumstances. Here is a man  from Florida , whose life was saved by  an ICD not by shocking a VF . . . but by blocking a bullet

ICD acts like a bullet proof jacket

 

A case report from Heart Rhythm

 

Bullet proof ICD jacket saves life

Complete Heart  Bullet Block : The Aftermath

ICD_Shot_Bullet

It seems ICD is strong enough to stop a bullet !

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This post , is  probably not meant for cardiology professionals.

Few technologies are clear winners in modern medicine. ICDs play  games  that would rival the God !

What is an ICD ?

Here is a man , who  drops almost dead by a fatal cardiac arrhythmia . In few seconds  ICD  machine recognises this arrhythmia ,charges itself and  fires a shock  of about 30 joules direct current .The arrhythmia is reverted and the fellow gets up as if  nothing has happened !

Watch this video

This revolutionary devices are  to be used judiciously in individuals with high risk  for dangerous cardiac arrhythmia.

The current  indications  as on 2012

Post MI  ( Only after  4O days*)
LV dysfunction EF ≤ 35%   NYHA  II or III  ( Please note , If  ≤ 30%, even Class I  NYHA can be implanted an ICD) *Why 40 days ?  Residual ischemic, Irritable  focus  should settle down
Myocardial disease
  • Nonischemic DCM  EF ≤ 35% with documented VT
  • Rarely other structural heart disease with recurrent risk for VT ( Few HCMs)
Primary electrical disease
  • Survivors of cardiac arrest due to VF without any completely reversible causes (Includes Brugada )
  • Malignant forms of syncope  with   idiopathic recurrent VT /VF
  • Congenital Long QT syndromes not amenable to beta blockers

Reference

Guidelines ICD pacemaker 2012 ACC AHA

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Implantable cardiovertor defibrillator(ICD)  is one of the major revolution in cardiology practice  that happened last century. We know , the number one killer of mankind is the ventricular fibrillation induced by acute or chronic CAD.

In the  later half of 20th century we  learnt  that , the only way to prevent a sudden cardiac death is the defibrillating   the  heart as soon as the deadly killer arrhythmia strikes !

Whenever cardiac arrest happens  in  a susceptible population , following  things are possible.

  • Call 911 /108  start CPR .
  • Have  Automatic external defibrillator AED at home
  • ICD implantation -Percutaneous trans-venous approach

And now new mode of defibrillation

Transvenous implantation  becomes  technically complex in many  .Abandoning the procedure  or using subcutaneous pads are necessary in few . Then , this question was asked

Why not the entire ICD implantation be in  subcutaneous plane ?

Yes , it is possible . After all , current can reach the  place where  it is needed ,  irrespective of the site it is delivered. The aim of this technique is to  simplify the ICD implantation  , so that it can be practiced in a wider clinical set up Preliminary  results  of subcutaneous ICD are available and was published  recently in NEJM.

The issues that need to be tackled are

  • Amount of energy required
  • Battery life

http://www.cameronhealth.com/product-info.htm

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Acute coronary syndrome is the commonest cardiac emergency. STEMI and NSTEMI are the two clinical limbs of ACS. Generally they have distinct clinical, ECG, angiographic features.(Ofcourse,  with some degree of overlap) . It is  a  mystery , both clinical presentations differ so much inspite of the common denominator  , namely ,  an injured plaque with add on thrombus  within the coronary artery.

The mystery is since  decoded , the primary difference between these two entities is STEMI the occlusion occurs sudden and complete and in NSTEMI it occurs slow and incomplete

In STEMI ,  most of the clinical features and , need for emergent treatment , response to thrombolysis /PCI are dictated by the time dependent risk to myocardial loss .

Cardiac arrhythmias in ACS

It is a  much published  factoid   for  many decades  only one third of STEMI patients  reach the hospital alive ! The reason being , STEMI  is very much prone for primary VF.

Contrary  to this ,  almost all patients with NSTEMI reach the hospital alive ! How ?

Both are ACS, if ischemia is a powerful trigger for dangerous ventricular  arrhythmia’s ,  NSTEMI should also behave  similarly .

So what protects against arrhythmias in NSTEMI ?

  • We realise ,  by observational experience (Not EBM !)  It is the suddenness and totality of ischemia that trigger dangerous form of arrhythmia  .
  • Further, a balanced  ischemia in two contralateral segments (or global  ischemia) some how protects against development of ventricular  fibrillation .This may be due to preservation  of  electrical homogeneity  , and the spherical VT spiral waves are not sustainable.
  • In contrast , STEMI has a sudden  focal , ischemic  zone that initiates the VT and    ischemia free  contralateral segment  welcoming  and sustaining the  reentrant wavelet.
  • The observation of primarily single vessel disese in STEMI and multivessel disease in NSTEMI also give credence to this concept.
  • Further , ischemic preconditioning can exert an important anti arrhythmic  effect in NSTEMI as  patients with unstable angina have   slow, repetitive episodes of ischemia prior to the index event .
  • Post MI scar mediated VT/VF is independent of degree of overall ischemia
  • It is also established ,  a sub group of  STEMI pateints  who  had  preinfarction angina(  ie . a brief  period of UA/NSTEMI) have very low risk of SCD  supporting the concept of sensitising the myocardium against ventricular arrhythmias.

Final message

Even though , there is a convincing concept  of   ischemia induced  cardiac arrhythmia in literature , in real patients it is very difficult to link the two.

UA/NSTEMI is the most common  acute ischemic event but the incidence of VT/VF here,  is far less than one would expect.

In ACS , focal , total  ischemia is more likely to precipitate a VT/VF than multifocal and global ischemia.

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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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                                          CRT , cardiac resynchronisation therapy  is being  projected  as a revolutionary treatment for cardiac failure , where a failing heart is rewired electrically through multiple leads and make it contract  more effectively.The success rate of CRT was highly variable.The basic question here  is,  there should be a  significant  documentation of desynchronisation  prior to CRT , for resynchronisation to be effective. Further , the sites of  myocardial  stimulation ( Coronary sinus/LV epicardial) , dose of electricity and the sequence of stimulation and the  electrical delay  are very  critical. Achieving this into perfection  is not a simple job and is  real rocket science ! ( If we can achieve 5 % of what  the normal purkinje network do within the LV we can term it a huge success.) Let us hope we catch up with nature . Finally , it is ironical  the sites of LV pacing ,  electrophysiologists  select currently  is infact not selected by them but pre selected by the patients coronary venous anatomy ! .So as on date ,  one can imagine how scientific this treatment could be !

                                         Initially it was adviced for patients with only wide qrs later for even normal qrs patients.When people started using it indiscriminately  insurance companies started to rethink and thus came the   RETHINQ study in NEJM  and brought a full stop to CRT in normal qrs CHF.

How to identify who will benefit from  the costly CRT  ?

It is a million dollar question. So millions of dollars were spent to identify the correct tool to identify the true responders to CRT.Echo cardiography with sophisticated methods tissue doppler, tissue tracking and , 3 D echo ,velocity vector imaging were done .These methods are not only costly but also time consuming and  hugely expertise driven.

Does all this  efforts with  advanced echo techniques worthwhile ?

This simple question was addressed in PROSPECT study in circulation

Click to read the article

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Patients  with permanent pacemaker  can have disastrous consequences  if inappropriate sensing of external  electrical events during surgery. Electro cautery or diathermy should be used judiciously .

1. Aviod diathermy if possible.

2. If neccessary use only bi- polar diathermy .

3. If bipolar diathermy not available use the indifferent electrode pad away from pacing  zone , behind  the thigh.

Other options.

A .Use a magnet to remove the sensing function of PPM. Application of magnet converts VVI into VOO mode so that external current will not be sensed by the pacemaker and diathermy can be safely used.

B.The other option is use the magnet only if interference problem occur .Magnet should be availableas safety measure.

 

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