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Archive for the ‘Cardiology – Electrophysiology -Pacemaker’ Category

Have you felt like this query any time in your office ?

If “Yes” is your answer, then you are not alone .There was a unique  conference  that  took place  in 2010 to answer the same query in Rome , Italy on behalf of Italian cardiology society  , where this entity is researched more than any other place.Its worth going through this.

Reference

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We have been taught right from first year cardiology residency  how to trouble shoot a pacemaker .It has been a real complex thing for us. Now looking  back ,all the troubles we took to understand seems to be redundant.Here is a summary of my thought process on the issue. It can be approached  with reference  to time, symptoms and ECG features.  With due respects to all those brainy hardworking   EP experts  , I have taken few academic liberties!

pacemaker trouble shooting

Timing

  • Within 24 hours -100% technical or procedural Issues , like lead dislodgement/Screws and nuts.
  • Within 1-2 week – Again technical , Pocket issues , Infections.
  • Within 6 months – Benign pacemaker syndrome ,Threshold settings, Scars
  • After  first year – Generally Issues are rare , Lead issues , Associate disease progression.
  • Beyond 8-10  years /Near end of life – 95% Energy depletion leads issues .( Please note , pacemakers do not stop all of a sudden it has a intrinsic end of life indicators .We have to look for it. May be ,we can expect a  warning siren in the future ? )

Symptoms

  • Vague dizziness – Pacemaker syndrome ? Anxiety ?
  • Near syncope – Show some concern (For many , Impending true syncope is a non existent entity )
  • True syncope  – Real emergency*

* Syncope can be unrelated to pacemaker but always consider  them electrical  unless proved otherwise . Few patients  may continue to have significant symptoms  in-spite of   normal pacemaker parameters. This would  mean , the original symptom for which  pacemaker was put is not related to the Brady-arrhythmia .It could   suggest alternative hemodynamic explanation  like vaso-depressive component of vagal syncope ,autonomic dysfunction , orthostatic intolerance or  a coexisting neurological /systemic condition.

**Never forget syncope is not an exclusive symptom of bradycardia .A new onset  tachycardia  , which is either a part of  brady- tachy syndrome or separate arrhythmia can continue to provoke the symptom.

Gross ECG findings

Bradycardia /Often implies back to original rhythm –  Indicates real trouble . Since ,in a paced patient HR cannot be less than programmed rate of 70.

Tachycardia -No spike.( Not to worry ?) A common  situation if the original indication was  sinus node dysfunction . Many of them are  in own sinus rhythm or AF . Just ensure spikes reappear when the rate falls below 70 . If the rate never goes down , what to do ? Try a carotid massage or observe a nocturnal ECG  or call analyst and increase the rate to document pacing . (In DDD mode we have a rare PM mediated re-entrant tachycardia , which is mainly used to grill cardiology fellows in their board exams with all those PVARP stuff !)

Simple pauses – Any pause more than the pacing interval is a definite concern .

Spikes more than QRS  – Indicate capture failure.

No spikes (Can be so benign  to ultimate danger )

  • No spikes , but  excellent own rhythm – Good  functional  SA node
  • Regular  spikes ,but intermittent own rhythm or only random spikes with good own rhythm – Needs bedside hairsplitting and  EP assistance !
  • “No spikes -No Own rhythm” -Most dangerous .Sudden lead issues or hyper sensing .(Emergency  switch off  by magnet  application before inserting temporary pacing advised )

* Anatomical issues like lead dislodgement , fracture , compression ,  perforation are to be ruled out in every pateitn with intermittent capture or failure .This is done by combinations of imaging as well physiological assessment.Dislodgement must be visualized .The term micro dislodgement may not exist.

Other Investigations

  • X ray
  • Echo for any new structural lesion (RA,RV dilatation , TR RV clots or vegetation )
  • Holter
  • Event monitors ,Loop recorders.

Pacemaker analysis

  • Battery life ( Very important parameter .Usually around 10 -12 years.Unexpected early drain can occur.)
  • Threshold (Most failure to capture associated with high threshold Note :Threshold will be normal in battery depletion Acute threshold can increase marginally .Should be reasonable other wise battery will drain.New protocols like auto capture and managed pacing will help optimal threshold
  • Impedance – Normal in battery depletion , dislodgement and exit block,  Increased in lead fracture and loose screws.Decreased or lost in insulation failure.

Management

The principle of management are simple. Few logical questions ,

  • Is the pacemaker generator is alive and has has enough energy ?
  • Are the  leads okay ?
  • The problem is in the settings ? can it be rectifies by the programmer
  • Or should we replace the pacemaker ?

Technical jargon like  under sensing , over sensing or no sensing  , fusion beats , micro dis-lodgement  etc are important for  academic reasons . We may talk any thing , realistically , what  the ventricle want  is a non stop heart beat  every second or so !

Emergency

Bradycardia – Insert a temporary pacemaker /Call the analyst  /Inform the  electrophysiologist /Senior cardiologists /(Please realise ,  some fellows  can be better than the personnel mentioned above in tackling emergencies !)

Tachycardia : Native or machine induced ?

Native – Mostly safe ,  Ignore  or treat with drugs.

Machine induced :(very rare) Switch of the pacemaker . No off switch available as in a mobile phone ? *What to do ? if unclear about the  whereabouts  tachycardia origin . If hemodynamically unstable no harm in shocking .Nothing will happen .Call the EP  guys on hot line and decide.

Elective symptom guided.

  • Asymptomatic -Normal ECG : Reassure and send home.
  • Vague symptoms   -Do Holter and Observe
  • Syncope -Normal ECG needs extensive all system investigation.
  • Syncope -With pauses /Bradycardia /Asystole  – Ironically ,decision  making is easier. Temporary pacing is the  ultimate savior. Later , check the lead,  generator .One may need to change  either one or both of of them.

** While the above principles apply  for both single  and dual chamber pacemakers , the later doubles our thinking burden . While atrial tracking is a great technological advancement , what to  do with those sensed event can be really  tricky .The response of  ventricles and the AV intervals  can be tentative at times. Cross talks from unexpected atrial and ventricular arrhythmia can occur.  Further , mechanical atrial lead  issues are far  more common . When confronted with recurrent atrial lead related  problems , one  simple solution is  silently convert the mode to  single chamber VVI mode.

Final message

Pacemaker trouble shooting appears complex at the first look .It’s all common sense.Thinking with simple state of mind and  being clear about the intended  goal is vital. Electrical intricacies are tough to understand  but most situations do not require them. However ,If the initial indication was for complete heart block one has  to be very alert.

Principles of medicine argue us to make an exact diagnosis before treating . But,realise  this is rarely  possible or even desirable in emergency .Curiously , most pacemaker troubles can be solved successfully without making a proper trouble shoot !

If  we can summarize in one line  , a prompt emergency  back up temporary pacemaker insertion  is key to  management most of the serious  pacemaker related problems.It ,not only tackles the emergency ,  buys time till we decode the real problem . . .  if we wish to !

Related article.

Role of magnet application in pacemaker trouble shoot

 

 

 

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We know , any wide QRS tachycardia  would argue us to make a default diagnosis of VT.But,  one has to be extremely cautious to apply this rule if  wide QRS  tachycardia shows  significant irregularity in RR interval .

All classical VTs are fairly regular tachycardia (Note the  key words , fair and regular) . Small cycle length variations are observed in VT,  but they are usually not discernible in surface ECG.

There are no practical rules .A well  appreciable  irregularity in RR interval will seriously  question the diagnosis of classical VT. To make an another statement, most of the  irregular wide QRS tachycardias infact turns out to be  atrial fibrillation with some form distal widening mechanism .(Preexisting blocks, or rate dependent  or antidromic conduction through accessory  pathways)

However , irregularity  is still possible during VT .(May be less than 10% of times)

When can VT can be irregular ?

  1. Irregularity is observed  immediately at the onset of VT as the re- entrant circuit warms up and tries tosettle down
  2. AV dissociation  can make the VT irregular but it is subtle .(This AV dissociation is absent if retrograde VA conduction is intact)
  3. Multiple reentry circuits with two morphological VTs dissociating themselves
  4. VT with multiple exit points and epicardial breakthroughs
  5. A drugged VT.Amiodarone modified VT can be irregular as it can variably lengthens  the re-entrant  circuits and inducing VA block and precipitating AV dissociation.
  6. Multi- focal VT  (We have MAT in atria do we really have MVT ? (Why not , are we missing it ?)

Final message

Statistically , as well as realistically  , the commonest cause for  any highly irregular tachycardia turns out to be AF , whether  QRS is wide or narrow !

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ICDs are primarily life saving devices.Whether single or dual chamber  it does this function  effectively.They will also  take care of  bradycardia by  default  back up pacing .For most indications single chamber ICDs are good enough.

My professor used to tell us , dual lead  means ,  dual expertise , dual cost , dual caution and  dual set of complication . One should avoid it whenever possible. Make things as simple as  it could be , without compromising the main goal (Here prevention of SCD) . The incidence of inappropriate shocks being lesser with dual chamber ICD  has not been truly  realised in real world scenario.

Recent studies  tend to give  credence to this  perception .(Peterson JAMA 2013)

Dual  Chamber ICDs  may have an edge only in few situations .

  • When there are both indication for pacing as well as ICD like heart block and LV dysfunction.
  • In extreme LV dysfunction were benefits of dual chamber pacing may have advantage.(If CRT is not an option )

Reference.

1 .Peterson PN, Varosy PD, Heidenreich PA, et al. Association of single- vs dual-chamber ICDs with mortality, readmissions, and complications among patients receiving an ICD for primary prevention. JAMA 2013; 309:2025-2034.

2.Medscape review

 

single vs dual chamber pacing indication

 

 

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In the last few decades  we have  understood a major concept in the genesis of cardiac arrhythmia.Slowing in the propagation of cardiac impulse is a key  trigger to precipitate a reentry circuit and initiate a tachy- arrhythmia.Still , many conditions like first degree AV block, chronic RBBB or even LBBB are  benign entities  as along as the heart is structurally normal .They seem never increase the incidence or life time risk of  cardiac arrhythmia . Longevity is unaffected.( Or do we assume many things ?)

How is this possible ? or is the theory of slow conduction triggering reentry is flawed ?

Think again . . . if these patients who later on develop a structural heart disease , with an episode of ACS , myocardial or valvular disease,  the original slow conduction substrates these people were harboring ,  will it become important ?

Surprisingly , we have no answers in literature.When Haissaguerre et al found preexisting ERS pattern could be a trigger for primary  VF in case they develop ACS  , he opened up a huge debate as it involved converting  a vast number of normal population electrically anxious.

Now ,is it possible the so called  benign  blocks of heart like first degree AV blocks , RBBB , LAHBa , would be important  at times of ACS  and possibly make them prone for for primary ischemic arrhythmia .

Is bundle branch re-entry possible in structurally normal heart ?

We need answers. Some one , (Any EP fellow) somewhere  could take up the issue and enlighten us !

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ICDs are one of revolutionary devices , invented last century  that can defy “death & fate”  in high risk cardiac patients who are threatened with ventricular tachycardia or fibrillation .A decade long hard work by  Mirowski  and team from John Hopkins culminated in the dramatic  the first AICD implant in 198o. ( In my opinion, this medical invention can be compared to an event of such  significance as moon landing by Armstrong and team ! ) Ironically , in the last decade such a revolutionary device was sort of misused and thousands of devices were explanted for inappropriate indications.

Fortunately , better sense prevailed recently .The indications are getting  refined. I am sure ICD will go a long way in prevention of  both expected and unexpected sudden  electrical deaths .We are into  the 4th decade of its evolution.While the electrical circuitry has been mastered , power supply remains an issue as they require continuous power supply like a mobile phone. Current technology allows about 6-8 years of battery life.

EL-ICD boston scientific longest life icd smallest profiale dynagen inogen madit indication for icd

Now , Boston scientific  has come out with new technology which make its  battery life extend  by 100%  to 12 years.  It is a major break through , expected to evolve  further  until probably we have rechargeable  batteries or biological power sources .Stretching a wild thought , the days couldn’t be far off  when the smart phones which are omnipresent in every human-being  , could not only power the ICD  remotely and control it too !

 

Indications (ESC/AHA 2012)

CAD

  •  Post MI* /LV dysfunction  ≤ 35% /NYHA   class II or III  (*  > 40 days)
  •  Post MI* /LV dysfunction ≤ 30% /NYHA Class I (* > 40 days )
  •  With non-sustained VT due to prior MI, LVEF < 40%, and inducible VF or sustained VT at  EP study

Non ischemic structural disease ( Idiopathic DCM, ARVD etc)

  • With structural heart disease and spontaneous sustained VT, whether hemodynamically stable or unstable.

Primary electrical disease

  • With syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at electrophysiological study

 

Reference

Link to Product manual form Boston scientific.

Boston scientific

 

 

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Brugada syndrome is due to a genetically  impaired  sodium channel activity  ( SCN5A)  in phase o, of action potential .This results in phase 1 (Ito channel) failing to inscribe the transition between phase 0 and  1 that result in loss of  dome .This loss of dome is dominant in epicardial cells compared to endocardial cells.This result in  electrical heterogeneity and a hence a voltage gradient in repolarisation phase  that can trigger a Phase 2  reentry mediated  VT /VF.The above said defects are either dormant, manifest, self extinguishing , dynamic  subjected to autonomic tone , ambient myocardial temperature (Febrile VTs) making this a complex entity.

There are three distinct types according to surface ECG.It can be either spontaneous or induced. The arrhythmic events and prognosis and hence management differs according to the types.

mechanism of brugada syndrome three types of ecg 2All types carry  a minimal risk of SCD , variable though . Of course  syncope  has to be  much more  common. Curiously every episode of syncope is seen as naturally aborted SCD by physicians ! (No one  to be blamed for this .The definition of syncope is like that !If the patient doesn’t wake from syncope it becomes death !).

When a patient with Brugada  has a  syncope , it  doesn’t  imply  he  experienced a dreaded VT or VF.While SCD is invariably due to ventricular fibrillation , a spontaneously terminating VF  as a cause for syncope is rare in Brugada . (Ref 2 : ILRs have documented though in few)

So what exactly is the cause for syncope in Brugada ? The issue is  real  and critical in clinical decision-making. We are beginning to document variety of mechanisms. Following are the possible causes

  1. Sustained  VT or NSVT with
  2. Non sustained self terminating  VF
  3. Extreme bradycardias (Vaso vagal )
  4. AV blocks
  5. Unrelated neurogenic

Final message

It is to be strongly emphasised a significant subset of Brugada patients especially in Type 1   Brugada (spontaneous or drug induced )  the mechanism of syncope is often not related to the dreaded VT/VF. It can simply represent high vagal tone and unexplained dynamism of autonomic activity .ICD is not a default indication for all those with syncope in Brugada syndrome.Think , pause and decide when you deal with such patients. ICDs are true revolutionary devices  . . . no two thoughts about it,but it can make a hell out of heaven if used in an inappropriate situation !

Reference

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