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Archive for the ‘Cardiology-Arrhythmias’ Category

Sino-Junctional rhythm : When a restless pacemaker goes for a walk down the lane !

Posted in cardiac drugs, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology-Arrhythmias, tagged , , , , , , , , , , on April 3, 2011| Leave a Comment »

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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V for . . . ventricular tachycardia

Posted in cardiac drugs, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Arrhythmias, tagged , , on March 31, 2011| 1 Comment »

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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Propably this is the most important paper on Brugada syndrome* !

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology-Anatomy, Cardiology-Arrhythmias, tagged , , on March 29, 2011| Leave a Comment »

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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What are the “Nine” vulnerable points in the atria for focal atrial tachycardias ?

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology-Arrhythmias, tagged , , , , on March 4, 2011| Leave a Comment »

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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Outflow tract ventricular tachycardias : Best review articles.

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -Therapeutics, Cardiology-Arrhythmias, Cardiology-Land mark studies, tagged , , , , on February 24, 2011| Leave a Comment »

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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Prevent SCD with SCD ! (Subcutaneous defibrillation ) : Simplifying the concept of ICD !

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Cardiology-Arrhythmias, Uncategorized, tagged , , , , , on September 14, 2010| Leave a Comment »

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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How common it is , for an “Acute STEMI” to present with stable ventricular tachycardia ?

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Arrhythmias, Uncategorized, tagged , , , , , , , , on August 31, 2010| 2 Comments »

Acute MI and ventricular tachycardia are closely related entities.In fact ,  the earliest response to ischemia could be a VT .But what  is peculiar about this VT is,  it  almost always degenerates into VF  within a minute or so.(Unlike idiopathic VTs /RVOT/LVOT VTs)

This arrhythmia in  every sense  can be called as  “primary VT“ which is the cause for “primary VF”

It is strongly  believed VF cannot occur without  a  brief episode of VT preceding it .Logic would also suggest  the ischemic myocardium  can not suddenly  become chaotic  “with the first  beat  “. There is little documentation available to unprove this presumption.

In spite of  this intimate relationship between VT and STEMI ,  it is very rare for a STEMI patient   to enter  ER with a sustained stable  ventricular tachycardia .  While  many VTs are known for it is hemodyanmic stability and immunity against degeneration   into  VF  , it is extremely rare  for  VT to remain as VT  in acute STEMI.

*Note : NSVT can be common   in  hospitalised patient in the coronary care unit . In our experience a sustained  VT in STEMI  will enter the VF mode within 60 seconds .If not , it is a highly  unusual phenomenon .

“But surprise is the other name of medicine ”

Here is  case report, a patient walked into coronary care unit with sustained( relatively stable) VT with LBBB morphology .We thought  it was   a  non- ischemic VT  (cardiomyopathy  , RVOT etc) .As we were examining him,  he became  unstable  and  was shocked 50 J biphasic .To our surprise a classical STEMI was unmasked and he was immediately  thrombolysed.

* It is possible ,  the patient had  suffered a  old MI  which got infarcted again and the VT  was scar mediated .

But it is still uncommon  for  it  not to degenerate into VF  with fresh  STEMI

Final message

Nearly all episodes of  ventricular tachycardia , that occur in the early minutes/ hours of  STEMI would degenerate into VF.This includes  VTs  that  occur within the CCU . Most  of the times , the CCU physicians and staffs  revert this VT  promptly and deny the  ventricles  from performing the dance of death !

It is extremely rare for an acute ischemic VT associated with STEMI to walk in to the hospital,  which our patient did !

Further reading and unanswered questions

  • What determines a VT to degenerate into VF ?
  • Why macro-reentrant , scar dependent VTs  often  are well tolerated ? ( In spite of LV dysfunction !)

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Does Digoxin know, which ventricle it is supposed to act in patients with cor- pulmonale ?

Posted in Cardiology - Clinical, Cardiology-Arrhythmias, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , on June 6, 2010| Leave a Comment »

Digoxin is a wonder cardiology drug used for more than a century.We know the pioneering efforts  of  William withering  in detecting the potential  of the unknown  herb  Foxglove.

Mechanism of action

The beneficial effects of Digoxin is attributable  to

  • Positive inotropic  action
  • Vagal action

Digoxin blocks the sodium potassium ATPase in the  myocyte cell membrane .

This cause accumulation of NA + ions within the cells. The excess  Na , then   facilitates  the Na -Ca exchange port .

This pumps in more calcium   into the myocyte.

Increased  calcium means more forceful contraction and that is positive inotropism* .

* This is a  highly simplified version of   Digoxin’s action . It should  be remembered  simple availability of excess calcium can not guarantee  contractility,   as it requires adequate number  of receptors.

Digoxin  is used in which type of cardiac failure  ?

Digoxin is used for both for LV and  biventricular  failure .

Digoxins is still  often  in isolated RV failure  of any cause (Cor pumonale, PPH, Eisenmenger etc)


Digoxin and RV dysfunction

Digoxin  has a tendency  to  hit the atrial muscles  at random causing  multiple short circuiting (Micro reentry )   forming  a perfect nidus  for complex atrial arrhythmias  including MAT .The coexisting    hypoxia  (which is all the more common here )  aggravates the problem .

Inotropism of RV : Does it really exist ?

It is often quoted , RV is a passive pump. It does not mean inotrpism is an exclusive property of LV.

RV has to generate about 30mmhg to pump the blood into  the lungs.

In cor-pulmonale the RV works against an afterload of around 50-70 mmhg  , making  RV inotropism  much more important  concept.

Rate control in atrial fibrillation Digoxin lowers the heart rate by vago mimetic action ,  primarily in  AV node  and to a  certain  extent in SA node .Ventricular rate reduction  is the prime requirement  in the management  atrial fibrillation and this property  is still the crowing  glory of  Digoxin.

Though beta blockers and  verapamil  can be used as rate controlling agent ,  lack of negative  inotropism makes  digoxin    prevail   over , especially in severely dysfunctional  ventricle .

But , one disadvantage of Digoxin is , since it requires  a vagal traffic to mediate it ‘ s rate controlling effect , it  is less effective ,  when there is  high sympathetic activity as during exercise.

What is the action of digoxin on interventricular  septal contraction ?

Digoxin , simply does not know where it acts when administered in cor pulmonale  ! We believe in cor-pulmonale the maximum action would be the area of maximum dysfunction .This is purely  an assumption. In cor -pulmonale septum shifts it’s loyalty from LV to RV as the later is the distressed chamber.So , logic would be there  is a theoretical  compromise of LV function in  patients with cor -pulmonale. These factors make  the   inter ventricular  interaction and dependence a complex one.

Some believe  the improvement of sub clinical LV dysfunction in cor pulmonale may be more important factor in giving relief  to  the patient’s  symptom.

What are the other RV inotropes ?

Doubtamine has some RV inotropy  .This again may be due to a spill over effect from LV rather than a primary RV inotropism .

As such , there is no great breakthrough  in creating a powerful isolated RV  isolated RV inotropic dug.

Probably  the best way to  give relief to RV is to reduce the pulmonary artery pressure as invariably sever PAH  is the predominate  accompaniment

(Nitric oxide ,  Epo prostenol etc)

Final message

  • Digoxin , indeed has  some useful  role in cor- pulmonale .
  • But ,the benefits are more pronounced in late stages of RV failure.
  • Since the dose required to get an optimal RV inotropy is high the safety margin  is reduced.
  • Since there is a propensity   for complex atrial  arrhythmias  ,  it has to be used very cautiously in management  of   atrial fibrillation due to cor pulmonale .(Than in other forms of AF)

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Tough hearts never die ! Surviving with a heart rate of 6 / mt

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology-Arrhythmias, tagged , , , , , on May 30, 2010| Leave a Comment »

Bradycardia is a common cardiac arhythmia. Sinus bradycardia  is  often considered an arrhythmia from a disciplined heart. It denotes high vagal tone .  A  heart rate  of  40 , some times even 35 is well tolerated . But bradycardia due to heart blocks are dangerous.

Sinus bradycardia can not get lower than 30/mt or so , as invariably either the  junction or the  ventricle , escapes with its own rhythm. Near syncope, dizziness , giddiness followed by  syncope  occur as the  heart rate  slows progressively below this level .It is often taught humans can not survive  when the heart  rate  goes below 10/mt .

Case report :

Here is middle-aged man who  presented  with a history of  recurrent syncope over a period of  3 days . He has no  history of CAD.

As he entered  the ER, this ECG was recorded.

At this pint of time  , when the ECG was recorded,  he was  conscious and talking ,  only to complain  of  little dizziness. After seeing this ECG , he was immediately put on a  temporary pacemaker.

Note : The ECG shows a single qrs complex per tracing of 10  sec duration .Ie HR of 6 /mt.One qrs complex for 50 large squares !  .Divide  300/50 and HR is 6 . Note also the p waves fire at 150/mt due to atropine effect .

The procedure  took 15 minutes to perform  , he was comfortable  and was administered atropine , and isoprenaline *, which increased his heart rate  from  6/mt to 10/mt .

Later he went on to receive a permanent pacemaker a week later.

* Temporary trans-cutaneous pacing using paddle stickers  is  an another  modality available in such situations where trans-venous pacing is  likely to be delayed  .

Message from this case

Cardiology’s  ultimate  moment of glory and truth  is experienced  when a  life  is saved with  a pacemaker.

Extreme bardycardias are  often  fatal , but here is a patient with  dangerously  low heart rate , still not resulting in asystole  or brady induced VT/VF . We had adequate  time to plan a strategy . Severe bradycardias  need not result in cardiac  arrest always.  Some hearts  have amazing capacity   and their  fighting spirit   amazes  us !  .It should be noted that , the above example may be  an exception than a rule .

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Making sense out of non sense : Three cheers to “care free” rate control in atrial fibrillation !

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Cardiology -unresolved questions, Cardiology-Arrhythmias, Cardiology-Land mark studies, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged , , , , , , on March 15, 2010| Leave a Comment »

Management of  atrial fibrillation has been a  big puzzle for cardiologists  for many  decades  till  it became a corporate game , and  now in the era of recession it has become  medicare’s  night mare !

So , we  were  made to dance to the tunes of the so called evidence based cardiology . . .

  • From only rhythm control to . . . in 1990s
  • Either rhythm or rate control  . . .       in early  late 1990s
  • Then cost control  was found  more important than rate control  . . .
  • . . . So rate control became superior to rhythm control in early 2000s

In 2010 , even the  rate control  became  a luxury ,  here comes the  real ace !   ” Casual rate control may be  suffice in most cases of AF “

Read this article  from  NEJM , which tries to  make  sense out of nonsense  and judge for yourself

Probably the most influential  article  in electrophysiology over  the  next decade

Click  below to reach Nejm article

http://content.nejm.org/cgi/content/full/NEJMoa1001337?query=TOC

http://content.nejm.org/cgi/content/full/NEJMe1002301?query=TOC

Gist of the trial

Technically and literally it  means a  “Take it easy attitude” as long as patient is comfortable , even a rate  of  more than 100 is allowed . Few years back the above concept could be termed a “non sense”

Final message

In this  perennial  management issue  of AF  ,  Whether ,   we were successful in  restoring   sinus rhythm or not , we have restored  the common sense*  Thanks to RACE 2 investigators.

* Do not unnecessarily trouble a  asymptomatic  patient with those powerful  and costly  antiarrhythmic drugs .

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