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Archive for the ‘Cardiology – Electrophysiology -Pacemaker’ Category

SA node is  the ultimate   power  center  of heart located in the junction of SVC and right atrium .In normal physiology  it fires  at a rate of  60 -90 /minute   that  dictates  the  ventricular rate  .

SA node is a linear  spindle shaped structure with a length of  1.5cm . The P cells with unique mitochodria  are  responsible for pace making activity  . The ion responsible for pacemaker current is mainly  calcium  with the initial 25 % push given  by  sodium current as well .  These cells are predominately under vagal control.Even though  pace making activity  is normally restricted to the SA node  , the vagal innervation is such that  the pacemaker  has a  potential to shifts it’s activity  both functionally  geographically.

In fact , there is constant flux of pacemaker activity  with  the entire length of SA node.The  cranial   aspect  SA node has more fire  power than its caudal tip . It is possible Sinus tachycardia  and sinus  bradycardia could represent  minor changes in the firing focus in its cranio-caudal axis.Further the P cells of  sinus node can spill all over the atria and even up to AV node.

What is wandering  atrial pacemaker ?

This entity is poorly defined  in literature.  With pace making cells scattered all around  there is no surprise to note dynamic pacemaker  shifts  even in healthy people. This is  especially common in young athletes.

Wandering can occur

  • Within SA node ( Shift of focus of p cell firing .No visible changes in ECG )
  • Within SA node and atria
  • Between SA node and AV node. (Sino-Junctional rhythm )

Effect on ECG

  • Baseline bradycardia.
  • Changing P wave morphology
  • Change in PR intervals
  • Intermittent absent (Rather concealed  )  P wave if  is also possible
  • RR interval can also show minor variation.

Image Modifed from http://www.eheart.org

Clinical significance of  Wandering pacemaker(WAP )

  • A Benign condition generally has no clinical significance.
  • It is often an expression of  high vagal tone.
  • Usually transient.
  • Can be unmasked by beta or calcium blockers.
  • Severe forms of wandering  pace maker can be a marker of sinus node dysfunction  and  would need  further evaluation
  • In  the coronary care units it is  associated  with infero-posterior MI when the vagal fibers are  insulted.

Differential diagnosis .

  • Some times it  need to  be differentiated form ectopic atrial rhythm /Low atrial/Coronary sinus rhythm etc .
  • Sinus  slowing  followed by a  functional escape and  reemergence of sinus beat   can be a termed as a form of wandering  pacemaker

Final message

WAP : This attractive and  descriptive ECG entity  is   largely insignificant in clinical cardiology .

It should not be confused with more dangerous cardiac arrhythmia  like sinus pauses and arrest .

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Read with caution . This  may either injure or cure your patient !

Click on the ECG to view what happend !

 

How does  verapamil  terminate a  VT  ?

Physicians  often  debate  vigorously before   labeling  a cardiac arrhythmia as ventricular , atrial junctional  , abberant or not etc etc .  But  for  an arrhythmia   it matters little  from what  chamber it is going to to originate . After all ,  any cell in the heart if excited can generate an arrhythmia .  The ion channel abnormality and the influx and efflux of ions  that determines how a drug is going to terminate an arrhythmia.

In fact , way back  in 1989 the Sicilian Gambit stressed this concept when classifying anti-arrhythmic drugs .This classification taught us  , even though there is a  huge list of  clinical cardiac arrhythmias  , from the therapeutic point of view there are only a handful of receptors  (scattered  all around ) to target  !

When we look at this angle , we realise  , many of  ventricular action potentials  have  important slow  calcium currents  similarly  junctional action  potentials do have some  sodium currents.  Calcium current  is present in every  myocardial cell  more so in the vicinity of AV junction.  Further , at times of ischemic or hemodyanmic stress these ion channels  may  take a different avatar altogether.Slow sodium channels and fast calcium channels etc !  (A wild imagination or is it a fact ?) Other important targets are potassium channels

Heart is a complex structure both macro and microscopically  .  In the three dimensional  histopathologic   interface between atrium  and ventricle (Especially in the  basal areas , outflow tracts  , around the AV grooves ) there  are  lot of sharing  and overlap of  different morphology  of cells . A high septal VT can behave  exactly like an SVT  which  includes the  tendency to get terminated by calcium channel blockers.

Amiodarone is a most popular  drug for VT termination ? Are we clear about the mechanism of it’s  action in terminating VT ?

It is  more of a perception and belief  that  class 3 action   may be   responsible for termination of VT by Amiodarone . In reality it is very difficult   to prove this point.  As Amiodarone  has all the  4 classes  action that includes beta and calcium blocking properties.. In fact ,  now  there is evidence  to  suggest   beta or calcium blocking action  may be more important in terminating  VT when  it is administered  IV  . (While  the class 3 action predominates in long term oral therapy )

A verapamil sensitive   VT may  successfully  be terminated by  Amiodarone  not by its  unique  action  instead it   may simply represent  its  calcium blocking  property.

Final message

Many  of the  VTs terminated by Amiodarone   could  also be verapamil sensitive . Since verapamil is never tried first we will never ever know the incidence of such phenomenon that gives pseudo credit  to Amiodarone

It may not be big crime to try injection verapamil in some of  the  stable ventricular tachycardias( As my fellow did ) especially  when we we know there is an entity called verapamil sensitive VT !


Q for the readers :

How many deaths are reported in cardiology  literature  regarding    fatality  following   verapamil  in   VT ?

I am trying to find  the answer the  data is very hard to come by !

Critical comments welcome.

 

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Ever since Brugada found the unique pattern of ECG on right pre- cardial leads and its  association with  premature electrical death ,cardiac electro-physiology got a new impetus. Hundreds of articles(May be thousands !) on Brugada are  available . Many criterias  were proposed.  Brugada  and his colleagues should be credited for bringing  in such an interest in the  field of inherited ventricular arrhythmias.

On the down side ,  as we have a habit of  prematurely formulating criterias  ,  it brings  an artificial academic  barrier  Funnily , in medical  science  deviating   from a criteria (However hastily it  was  proposed  )   is a considered  big  offense Further . the hype surrounding  any new scientific  entity makes it difficult  for others  to overwrite  it .

Brugada recognized a ECG pattern with  a genetic predisposition for VT and VF  . Now , we know there are many etiologies  with a similar pattern  of ECG . What Brugada did was ,  he  exposed the tip of Iceberg called inherited ventricular arrhythmia . But the essential criteria –  Absence of structural heart disease ,  to diagnose Brugada   was  always questionable.

(Please realize , presence  or  absence of structural  heart disease depends , more  on  how advanced  our  imaging modalities are . If you can map a virtual histology of RV epicardium one may detect some  microscopic abnormality in every case of Brugada. In human biological system , God  usually bonds  structure and function too  closely  and hence  functional  abnormality rarely occur  in isolation )

Brugada is  not  a new disease ,   it is  a  recognition  of a  pattern of ECG  related  to sudden deaths . Subsequently , we  realized any dispersion in repolarisation in RV epicardial surface  , the   risk of sudden death  is increased. From the days of  Brugada  we  have  come  a long way.

What is new in Brugada syndrome  ?

(Not exactly new . . .  it is  known  for many years )

Brugada is no more an exclusive  functional disorder of  sodium channels of RV  epicardium .It can have structural defect (known & unknown ) .It may  have infective , degenerative etiology as well .

How does these structural changes appear ?

Chronic sodium channel malfunction  can result in cell membrane defects which can augment   Idio-osmole   inside  the cell and result in  apoptosis   etc .

Which comes first ,  electrical or structural abnormality ?

It is an  another  chicken- egg tale  waiting to be decoded   within the RV epicardial cells

Can wall motion defect occur in Brugada ?

Early observations done in out hospital (MMC Chennai ) has found anterior  RV free wall motion defects. Tissue Doppler studies are  being undertaken.

Final Message

The  following paper  wonderfully documents  the structural and histo-pathological  changes in RV epicardium .  This  implies ,  our belief   about this  unique electrical  disorder  is  bound to take a beating  and  we  expect a major perception makeover regarding Brugada  in the years to come .

Probably the most important paper on Brugada syndrome was published in circulation in 2005

*http://circ.ahajournals.org/cgi/content/full/112/24/3680

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Human atria is a rough terrain infested with peaks and  troughs like the  Himalayan range . The two atria together has a minimum of ten entry or exit points . Cardiac arrhythmias are   something similar to the  uneven  earth plates  triggering an  earth quake.  Like the earth surface there are  areas in the atria  with high seismic activity !

It is now discovered there are nine vulnerable points in human atria that can initiate focal electrical activity at times of hemodynamic/ischemic/metabolic stress .

The common causes for Focal /Ectopic atrial tachycardia are

  • Hypoxic AT -COPD ( Probably the most common cause .If persistent it will degenerate to MAT- AF )
  • Structural atrial disease
  • Hypertensive heart
  • CAD
  • Valvular heart disease
  • Drug induced

Note ,  all these  vulnerable points are located either in the  junction of  an anastomosis  with a venous structure or valve or septum.

Further, these sites are often the  embryological fusion points making it still more vulnerable due to tissue defects.

Why free wall of atrium  is  a less common  focus ?

They are relatively smooth, lack ridges and joints. Unless the walls of atria are diseased  focal tachycardias are less common from these sites .

Other forms of Focal atrial tachycardias

Indian perspective  and Rheumatic atrial tachycardia.

In developing  countries  focal atrial tachycardia in rheumatic heart  differ very much from the tachycardia described above. In fact many of the rheumatic atria present straight away  to atrial flutter or fibrillation.

Pulmonary vein focus should rarely be considered in atrial tachycardia that occur in RHD.

Post operative tachycardias

Surgical scars can result in what  is called  Incisional tachycardia.(Especially after complex atrial  surgeries like Sennings, Glean/TCPC  etc )

Multi focal atrial tachycardia .

This is nothing but a focal tachycardia which tend to fire from different angles towards different targets  often lead to a chaotic atrial rhythm .  Digoxin and DC shock paradoxically aggravate this arrhytmia.

Atrial epicardium/pericardium interface as a focus

When pericarditis is the predisposing  event  then it can emanate from anywhere from  epicardial surface .

Since left atrium is only  partially covered by pericardium it is not logical to assume pericarditis related AT arise from RA epicardium.

Atrial tachycardias in congenital heart disease.

Complex atrial anomalies, SVC type ASDs, PAPVCs can  give raise to abnormal  electrical focus

Reference

An excellent original work from  Royal Melbourne Hospital, Melbourne  Australia.

A must read  . . . http://content.onlinejacc.org/cgi/reprint/48/5/1010.pdf

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A well researched article on a difficult topic. By Kim et all from Cornell university , New york.

A must read by all cardiologists . The link is placed with the courtesy of Jacconline

http://content.onlinejacc.org/cgi/reprint/49/20/2035.pdf

After reading this article   one  should be able to answer the following questions.

  1. What is Gallavardin VT ?
  2. Classification of RVOT VT
  3. How a non sustained VT becomes a sustained one ?
  4. Why some VTs cause syncope ?
  5. What is the association  between idiopathic VT and Idiopathic VF ?
  6. How does exercise  trigger a  VT ?
  7. What do we mean by structurally normal heart ?

Readers are encouraged to post link to good articles on this topic.

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God has created  and arranged every organ in an order  with a purpose .  The unique  relationship  of the food tube and  the heart which run silently , posterior  to the heart has evoked much interest for the cardiologists.

Whenever LA is enlarged it pushes the Esophagus back .We also know  the vintage clinical entities   of cardiac  dysphagia that occurred with rheumatic mitral stenosis.

Since the  lower end of  esophagus just hugs  the left atrium , this anatomical concept was successfully exploited   for imaging heart in TEE.Now cardiac  anesthetists routinely use the esophagus as an imaging port during complex mitral valve surgeries.

How  esophagus can be utilized to resuscitate the heart at times of emergency ?

Note , the esophagus does a friendly hug as it crosses the heart posteriorly .It is a perfect anatomical sense , to Image and pace the heart from within the esophagus !

 

In a  cardiac  arrest  situation , when we need to   rapidly   access to heart  , we have  multiple  options  .Each has some  advantage and few draw backs.

  • Trans-venous pacing   is the standard method,   but even for experts  it needs   few minutes to reach the heart for pacing
  • Trans cutaneous pacing (Zoll)  is  a viable option , but  not widely  popular for some  unknown  reason (Patient discomfort ? High threshold ?)
  • Emergency trans-thoracic  needle pacing option is  a primitive method still can save a life or two on it’s day !

It was in 1980 ,  a dramatic  concept was conceived  . Why not    use the  esophagus as an access   for pacing  the  heart

after all ,  it  reaches as close as possible to the heart !

How to convert  a  Ryles tube into a  a  trans – esophageal  pacing lead ?

There was a certain article on this topic , which I read , when I was cardiology resident. It answers the following. Distance form mouth ,  Discomfort of  the lead ,   Pacing threshold ,  Esophageal burns .

I am unable locate that article. Will  post  it  once I get it.

Limitations of trans-esophageal pacing*

  • The most important limitation is it can pace only the atria with high degree of success.
  • Ventricular pacing is not that successful for the simple reason esophagus is anatomically insulated by the atrial chambers.
  • Tran gastric positioning  may reach  the basal aspects of Left ventricle , but the threshold needed  is too high that will invariably cause  discomfort.This can be used in a dying patient  when there is no  other option .

* Primarily  useful in acute SA nodal defects, sinus arrest or any other atrial electrical failure. Infra- nodal complete heart block trans esophageal pacing may not be effective .

Other potential uses  of trans-esophageal  leads

Over drive pacing

Overdrive entrainment of tachycardias ,  including resistant ventricular tachycardia is possible.

Trans esophageal ECG recording .

This can magnify p waves during supra ventricular tachycardias and aid in decoding narrow qrs tachycardias

Safety  Issues and Caution

Good earthing is necessary .Burns can occur.

Final message

Every cardiac physician is  expected to possess  the expertise to rapidly pace a heart  by trans jugular /subclavian access at times of  emergency .

Further , any modern CCU will have a defibrillator equipped with trans-cutaneous pacer as well. (The  disposable pads are too costly and is a deterrent in many hospitals  !).

This article  explores other possible way to pace the heart in dire emergency situations.

It has one more purpose !  It rekindles   the acumen , motivation  and hard work   of  our  cardiac  ancestors  (Which many of us are pathetically lacking !)

http://circ.ahajournals.org/cgi/reprint/65/2/336

Role of trans-esophageal lead during EP study  atrial fibrillation

http://cardiovascres.oxfordjournals.org/content/38/1/69.full

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In pacemaker science ,  any pacemaker that maintains AV synchrony is often referred to as physiological pacemaker. This is  of course , a  wrong reasoning .None of the pacemakers available today can be claimed to  be completely physiological .All  pacemakers  which paces the right ventricle  induces IVS dysynchrony (Including  the modern DDD)

Single chamber physiological pacing

AAI

Paradoxically ,  the most primitive of pacemakers AAI can be the near perfect physiological  pacemaker . The simple explanation  is ,  In AAI mode , expect for the origin of pacemaker impulse the entire depolarisation and repolarisation  is through the normally existing physiological conducting system .(AV node, HIS, Purkinje etc)

(It not only has atrio ventricular synchrony but also  has ventriculo ventricular and intra ventricular synchrony )

So, technically AAIR  is most physiological pacemaker possible .But  the practical utility of such a pacemaker is limited.It can be used  only in  isolated sinus node dysfunction with intact AV conduction . (The problem is the AV nodal conduction can develop later )  To over come this DDDR pacemaker can be programmed to AAIR as a default mode.

VVIR

This rate adaptive pacemaker  ,  to a  certain extent  can be termed physiological as the heart rate can improve with exercise . (Still it is unphysiological as it  paces the RV )

VVD

This is based on the concept ,  for pacing to be physiological , it  requires  atria  to be  at least sensed not necessarily paced.This mode which has a floating sensor attached to the lead as it crosses the atria.This facilitates atrial sensed ventricular pacing .But many believe  the atrial sensing is not consistent in VDD mode.Currently this mode is not popular.There is scope for improving the atrial sensor technology .

Dual chamber physiological pacing

DDD, DDRR

Both  these are the prototype dual chamber physiological pacing modes.

Bi-Ventricular or triple chamber pacing  ( one atria two ventricle)   are our  elusive answers for attaining perfect physiological pacing . it need to be realized, we simply ,  can not mimic the natural cardiac  conduction system.It is  estimated to be more than 10 miles long specialized fibers .

Final message

In our quest for physiological pacemaker we often forget the fact  , AAI is the most physiological pacemaker mode  available .(It even has  VV synchrony !  )

We should use it liberally whenever possible .Of course ,we cannot use it in complete heart block .Still 50 % the  permanent pacemaker  we implant is for sinus node dysfunction. Many of them could be candidates for AAI mode .If current generation cardiac physicians feel out dated to insert a AAI pacemaker, at the least they should program the DDDR into AAI mode with a mode switching to ventricular pacing modes whenever required.

In spite of all  advantages ,  why atrial based pacemakers are not gaining popularity ?

  • Ignorance
  • Lack of expertise
  • Technical difficulty of fixing atrial  lead
  • Perceived fear of lead dis-lodgement.
  • The fact remains  the  ventricular based pacing  is always safe  in case of sudden AV block due to any reason .

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Myocardial scars remain forever ! It forms the focus for many chronic  ventricular tachycardias following MI. A healed scar is not often benign . It blocks the electrical wavelets and deflects into multiple directions some of them may reenter and form re-entrant VT .

This scar fascinated  one man from Holland -De Bakker . . . his quest for myocardial  scars produced this excellent paper .

No one  can do  such a meticulous work  today !

He did a extraordinary  study with the scarred  papillary muscle of infarcted myocardium . It included stunning histo-pathological analysis .He found for the first time , how the scar  even though mechanically idle conducts in multiple directions that precipitate the arrhythmias

 

We need to classify myocardial scar for understanding better the VT circuits. The newer imaging like Carto system can help us in imaging the ventricular scars.

 

A rough approach for myocardial scar classification could be .

Location

  • Epicardial
  • Endocardial
  • Transmural

Combined

  • Predominantly endocardial
  • Predominately epicardial

Septal scars

Anterior

Apical

Posterior scars

*With or with out Pap Muscle

Based on thickness and volume**

Small< 2CC  >5CC

Intermediate up to 10cc

Large >20cc

**Scar volume

Based on electro-physiological properties

  • Inert
  • Inducible
  • Spontaneous with clinical VT

Based on Metabolic activity

PET matched

Mismatched

Scars with reference to vascularity

  • Vascularised scars
  • Avascular scars
  • Revascularised scars

Further modification of the scheme by the readers are welcome

 

Clinical implication of scars apart from arrhythmias ?

CRT lead positioning

 

 

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No one would have believed a century ago when electricity was first dosvovered  for the mankind by Benjamin Franklin  with glorious  purpose , would now  be used as a drug for treating  life threatening heart ailments  !

Yes , electricity is a drug by definition.

It is administered percutaneously  by focusing  a beam  of current into the heart.

  • There is a dose , shape , energy  and direction for this drug.
  • Paddle size determine the energy.
  • Paddle location determine the direction of  current vector.
  • Dose is selected by the  physician.

Mechanism of DC shock / Defibrillation *

When  heart suddenly behaves abnormally  and start generating its own electricity and sends it through abnormal channels other than its natural paths ,  it becomes a dangerous arrhythmia .This propagation of wave front can occur in multiple directions  in a chaotic manner , resulting in VT/VF and imminent death.

Like an air to air missile ,this  abnormal wave front  can  be tackled only by an another electrical  wave front . Nothing else will work.

* The difference between DC shock  and defibrillation is only technical. If one gives a  synchronised shock  ( with qrs complex ) it becomes  DC shock .If not ,  it is defibrillation

The success of defibrillation depends on many factors .

The following are most important.

  • The critical myocardial mass must be depolarized by the current delivered.Sufficient  amount  of sodium channels /less  of calcium  currents  need be activated for this to happen .(JACC 2008)
  • The direction  and the angle  of current entry with reference to  advancing  end of abnormal wave front. is also  important .
  • Distance between the paddles.(Antero posterior paddles more effective than Apex /Sternal pads )
  • Energy level (seems to be less important ! )

Two shock forms are used

  • Monophasic shocks
  • Biphasic shocks

A biphasic DC shock has  replaced the traditional mono phasic  sine wave  shocks in most machines.

What is  the  fundamental difference between the two  ?

  • In bi phasic  shocks , the current traverses the myocardium twice .
  • So, it has a second chance to interrupt the critical tachycardia  circuit , if the first one fails. In other words, biphasic shocks are  technically equivalent  to  “two  sequential low energy shocks”  delivered in opposite polarity . This change in direction happens in micro seconds .
  • The shape of biphasic DC current  wave form can be a truncated  sine wave or square wave .The maximum  energy of DC shock in biphasic mode  is  200 joules (In Monophasic it is  360joules) . All AEDs, ICDs, now use bi phasic shocks to conserve energy .

Final message

A biphasic shock waveform has a proven advantage . It has  greater efficacy ( because it traverses the heart twice ) , requires fewer shocks  with low  delivered energy and hence  less myocardial  and  dermal injury.

References

Even though there is general  acceptance of superiority of bi phasic  shocks ,  it is still considered by some ,  that there is no great difference in the  overall outcome .

http://content.onlinejacc.org/cgi/reprint/52/10/828.pdf?ijkey=5a8f50ff2542182c857d4f3fe553aef8df6e3fd3

http://circ.ahajournals.org/cgi/content/full/94/10/2507

Bi phasic shocks in atrial fibrillation

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768486/

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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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