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Archive for the ‘Cardiology-Arrhythmias’ Category

Why Localising IRA with ECG is essentially a guess work ?

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged , , , , , , , , , on June 24, 2012| Leave a Comment »

IRA localization for both LAD and RCA , LCX  is a fascinating  exercise for cardiologists.I suspect  our understanding  about this crucial issue is  far from complete .While  localizing  level of lesion within LCA  or RCA requires more precise data and erring is acceptable  , it is not uncommon to  call  even the  IRA wrong  especially in multi -vessel disease.

Why current   criteria of IRA localisation goes awry many times  ?

The  factors  that operate are not few   . . .  it  runs into a dozen  at least  !

  1. Dominance  is never considered during IRA localization  (A right dominate system can vastly influence the LAD localization  algorithm PLV branches  can protect LV postero- lateral segments in spite of proximal LAD lesions )
  2. The length of  mid LAD   IS  controversial entity ( Traditionally  it refers  to  the  segment  between first major diagonal to second  major diagonal or septal  leads to faulty   coronary mensuration .It is not uncommon to have a  mid LAD measuring few  mm  when  full the full  length of  LAD  is about 15-19cm
  3. Diagonal vs OM  trade off occurs  in every alternate patient which is ignored  !
  4. Ramus  is never considered worthy enough  to be included in the IRA  localization scheme (In spite its presence  in 20 % )
  5. Type of LAD is not given allowance.
  6. Finally &  most importantly these rules of IRA localization will not apply in  the setting of  multivessel  CAD
  7. In the presence of Pre existing CTO
  8. STEMI following chronic stable angina
  9. Extensive collaterals
  10. Re Infarctions
  11. Post CABG etc

Final message

Decide for yourself  . . .  how good is the value of IRA localization  after  considering all the above variable. . It is not a great thing to predict  correctly RCA from LCX in an  inferoposterior MI  with a  70 % accuracy  . (It actually means  20 % accuracy  )    statistically when there are only two options  . . .  we are blindly  right 50% of times   !

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Break through in Brugada syndrome ! . . . always carry this vital data in FINGER tips !

Posted in cardaic physiology, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged , , , , , , , , , , , on June 10, 2012| 2 Comments »

Brugada syndrome continues to fascinate  us for two reasons.

One , it deals with mysterious sudden  deaths of young  men and women

Two , it is one of the  fine  examples  of how  advances in molecular biology , links  physical defects in ionic channels to  sudden electrical  death (Most of them  are due to inherited defects  sodium channels  of myocyte cell membrane )

While high risk subsets of Brugada are easily managed , it is  the asymptomatic  ones  that bother us.

The following are some of the  difficult  questions ,   a  cardiologist faces when dealing with   patients , who exhibit  only Brugada pattern in ECG .

  1. Should I go for an EP study Doctor  ?
  2. Will  I  require an ICD  Doc ?
  3. Do I carry a significant risk of  dying  suddenly  ?
  4. Do  I need a genetic test for sodium channel mutation ?

Fortunately,  we can answer  all these questions with much  courage than before.

(Thanks  to the European Finger registry published in 2010  !)

“No” is the  clear  answer for all of them !

Summary from the FINGER registry. 

(France  , Italy, Netherlands, GERmany)

The registry included 1029 consecutive individuals

(1) Aborted SCD (6%);

(2) Syncope otherwise unexplained (30%);

(3) Asymptomatic patients (64%).

In the  follow-up of 31.9 (14 to 54.4) months . A total of  7 death occurred .

The cardiac event rates per  year was 

  • 7.7% in patients with Aborted SCD,

  • 1.9% in patients with syncope

  • 0.5% in Asymptomatic patients.

Predictors of cardiac  event

  1. Previous syncope
  2. Spontaneous type 1 ECG

Non predictors ( Surprisingly there were more non predictors ! )

  1. Gender has no predictive role
  2. Familial history of SCD,
  3. Inducibility of ventricular  tachy-arrhythmias during  EP study,
  4. Presence of an SCN5A mutation

 

Follow up

PRELUDE study  almost reaffirms  Finger data

(PRogrammed ELectrical stimUlation preDictive valuE)

Just publicized in JACC 2012 from the pioneer of   Brugada Silvia  Priori of   university of Pavia  Italy

Reference

http://circ.ahajournals.org/content/121/5/635.full.pdf+html

http://content.onlinejacc.org/cgi/content/abstract/59/1/37

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How relevant is oral magnesium for recurrent ventricular tachycardia ?

Posted in cardiac drugs, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, Cardiology-Coronary artery disese, tagged , , on May 29, 2012| 1 Comment »

Magnesium   is a powerful anti-arrhythmic drug . It has a well  established role in controlling VT when administered  Intravenously   especially in polymorphic VT .

Mechanism of action

  • It acts at the cell membrane.
  • It has a unique action of blocking calcium channels  that reduces the number of oscillations of  both  early and late  after potentials

Link for more  on mechanism  of action

https://drsvenkatesan.wordpress.com/2010/01/13/how-does-magnesium-acts-as-an-antiarrhythmic-drug/

How often cardiologists administer oral magnesium for long-term control of VT ?

As for as I know ,  no one uses it ! but dietary  supplements are used for general well  being .

Why ? Is it because

  1. Magnesium does not get absorbed in the gut
  2. Magnesium levels are un- predictable in plasma if administered orally

Answer : No one has really tried  it as a  chronic therapy in VT  yet  !

Final Message

Tablet Magnesium can give a tough fight to Amiodarone and Flecanaide in refractory VT at a fraction of the cost !

Who has the audacity  to  compare Magnesium  with Amiodarone head on ?

Reference

Magnesium as health supplement . 

Magnesium is available  in tablet form as  Malate , Stearate, Taurate and Aspartate  along with calcium and Zinc etc .

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Atrial fibrillation with wide qrs tachycardia : Don’t get obsessed with WPW syndrome

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged , , , , , on May 26, 2012| Leave a Comment »

Irregular  wide qrs tachycardia is a fairly common clinical entity in any cardiac emergency room. The moment you ask about  such tachycardia ,  9/10  fellows will  come out with a  prompt answer   ” AF with WPW syndrome” even before you complete the question !  It is not that common  as we perceive .The problem is with  our traditional teaching methods and the attraction of human brains to  rare and exotic disorders.

traditionally   SVT with aberrancy  is   diagnosed  mainly  in the setting of regular tachycardia .

We often  forget  “AF with aberrancy”  is equally common  , and  it presents   with a  irregular  wide qrs tachycardia . 

I  wonder whether  this phenomenon  can be termed as  orthodromic aberrancy .This can directly compete  in the differential diagnosis  of  antidromic AF  with  WPW !

It should also be mentioned antidromic  AF can run into very high rates  as accessory pathways do not check the incoming signals while orthodromic aberrancy the ventricular rates can not exceed 220 or so at least theoretically . (This simple clue can clinch the issue in favor of  WPW )

There is no proper  published data available for the true  incidence of AF with orthodromic aberrancy in general population

In fact , there are  many  electrical  environments for AF  to  become a  wide qrs AF

1. AF  with  Antidromic conduction through accessory WPW pathway.

2. AF with Orthodromic aberrancy ( Non WPW – Similar to  any SVT with aberrancy )

3. AF with pre existing LBBB

4. AF  with Amiodarone effect. (Especially with DCM and cumulative load of Amiodarone )

5. AF with electrolytic /  especially excess  intra-cellualr  potassium

6. Finally , even  Atrial based pacing (DDD)  can cause wide qrs irregular tachycardia when  mode switching  fails .Here the  ventricles  may track the  atrial irregularity  and respond with a  wide qrs  bizarre tachycardia .

Final message

There are many causes for  wide qrs tachycardias  in  Atrial fibrillation . WPW with anti-dromic conduction is just  one of them .We need to approach the issue with an open mind .Please  be reminded , once contemplated  WPW syndrome  can be a powerful thought blocker  !

Note : *We are not including   polymorphic ventricular tachycardia here .It is an  important subset of  wide qrs irregular  tachycardia.

** VT can co-exist with AF .This is not   surprising  as  many of the diffuse cardiomyopathies  involve  both atria and ventricle  with extensive scarring and fibrosis  a perfect trigger for  both atrial and ventricular arrhythmias .

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How to diagnose complete heart block without ECG ?

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology-Arrhythmias, tagged , , , on May 18, 2012| Leave a Comment »

You are asked to see a patient with a pulse rate of 45 /mt .  Is it sinus bradycardia  or  complete heart block  ? 

Only one condition , . . .  you must conclude in the bed side !

  • Heart rate  may give a clue ( HR of  30-40 is common in CHB . Less common in sinus bradycardia.)
  • Pulse volume is large in both (More so in CHB )
  • JVP  shows occasional cannon waves hitting the neck  in CHB. Cannon wave can never occur in sinus rhythm
  • S 1 intensity may vary in CHB (As  Marching through  of  P waves  occur in CHB  ,  when it falls close to QRS  , it results in a  short PR interval  and a  loud S1   . Since marching through is a intermittent phenomenon S 1 intensity also varies.)
  • A short systolic murmur may be  heard intermittently due to   trivial MR/TR in CHB  ( Competitive AV valve movement )
  • A  simple bed side test  . Ask the patient  to exert for a minute -Sinus bradycardia raises  the HR with a fair regularity  to 80-90/mt  or so. CHB doesn’t  (Note :  CHB with  junctional rhythm can  sometimes increase the HR  significantly )
  • Finally response to Atropine   is prompt with sinus bradycardia.

Final message

Bed side skills in recognising cardiac arrhythmias are still relevant even in the current  era of carto and 3d electro anatomic mapping .

After all ,  the 19th century clinical wizard Wenke back recognised the second degree  AV  block at the bed side  well before  the ECG machine  was invented. He meticulously observed progressive prolongation of a-c interval and subsequent drop of c wave in the jugular  vein !

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What does Amiodarone do to the ventricular rate in AF ?

Posted in cardiac drugs, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -Therapeutics, Cardiology-Arrhythmias, Clinical cardiology, tagged , , , , on April 23, 2012| 2 Comments »

Amiodarone acts  by

  1. Correcting the  rhythm  to sinus .
  2. Controls  ventricular rate  alone
  3. Does both ?

Answer is 3

How can it correct the rhythm alone ?  If  the rhythm is corrected ,  rate will automatically be controlled,  unless Amiodarone converts AF into Sinus tachycardia  which is very unlikely !

Of course  Amidarone  is not a  magic drug .The success rate of  Amiodarone  restoring  sinus rhythm is far . . . far less . . . than our expectations ! . It fails to  convert to sinus rhythm in a significant chunk *. Interestingly ,   it may still  control the  ventricular response  by its beta blocking action .

*Our estimate is , the failure rate Amiodarone  is  between  30-40%  or even higher ,  as   bulk of AF we witness   is due to Rheumatic heart disease.

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What are the therapeutic targets in Ventricular tachycardia

Posted in cardaic physiology, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology-Arrhythmias, tagged , , , , , on April 22, 2012| Leave a Comment »

Ventricular tachycardia is  a major cardiac electrical disorder. Even though it  connotes a deadly meaning the prognosis and outcome vastly vary.It can be a benign arrhythmia in  structurally normal heart that present as occasional fasicular VT  or Exercise  induced RVOT , to dangerous ischemic polymorphic VT which rapidly degenerate to VF and SCD if not reverted . It is ironical we are  trained  to put all VTs in a single basket and  propagate fear psychosis among   physicians and patients .

Management of VT has certain broad principles.

  • Identify the cause
  • Whether  specific structural heart diseases present or not
  • Identify the mechanism if possible
  • Rule out transient metabolic cause as a trigger

Therapeutic targets

  • Stabilising the cell of origin
  • Passifying the scars
  • Interrupting bundle branches in  BBR  mediated tachycardia
  • Ischemia related  Focus – Re-perfusion
  • Reversing LV dysfunction

Management

General

  • Correct Cell hypoxia /Acidois
  • Pharmacological ( Class 1A/1B /1C , class 3 and Beta blockers , Magnesium  )
  • Role of  beta blockers for VT management is largely under recognised.It has an important role to play in both acute and chronic  VTs)

Electrical (DC shock ,Ablation and ICD)

  • DC shock is treatment of choice  all emergency VTs
  • Ablation  aims  at preventing episodes of VT .Ablation needs EP study and  expertise of  an electro physiologist.
  • ICDs  revert it only after the VT emanates from the focus . ICD can be implanted without knowing the focus .May not require a EP consult.

Surgical

CABG + Surgical scar excision , Aneurysectomy  might help in certain refractory VT.

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Why RR interval is irregular in Atrial fibrillation ?

Posted in cardiac physiology, cardiology -ECG, Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged , , , , on April 5, 2012| Leave a Comment »

RR interval in Atrial fibrillation is irregular because . . .

  1. The Atria  fires irregularly
  2. AV node conducts irregularly
  3. Atria confuses the AV node  with  its random firing  and varying penetration *
  4. The ventricle just reflects  irregular  response of atria .

The answer is all of the above. Response 3  explains  best.

*Please note , the AV nodal property is predominantly  responsible for the irregular RR interval in AF  . Atria confuses the AV node  with its random firing .The varying penetration into different depths of AV nodal structure and  the resultant concealed conduction make the   the AV nodal refractory period into continuous oscillation .This  random delays in AV node  is reflected in RR interval as irregularity   )

The response we get in ventricles  in AF  can be summed up as  “A filtered atrial rhythm”

Paradoxically,  amidst the chaos in atria  the rate  is fairly constant within the atria (Fibrillatory   wave firing  at up-to 600/mt )  Of course  , the FF interval in the atria will also be varying  .  At a rate of 450-600 this is difficult to quantitate  especially in fine AF.

When does RR interval becomes regular in AF ?

  • When the patient develops complete heart  block.
  • Digoxin toxicity
  • Associated Sinus node dysfunction

For advanced readers in EP : A mystery explanation for irregular  rhythm in AF  in the offing ?

AV node is a physiological and electrical sink .

When atria fires at 600/mt it absorbs about 60-70  % of the atrial response .Whether it releases the original impulse or initiate a new rhythm in the junction  is not clear.

There is some evidence to suggest the rhythm that control the ventricle in AF may not be  filtered original rhythm from the atria .Instead it could be a fast junctional  escape rhythm (Is that a junctional fibrillation ?)

 

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A funny Arrhythmia called Acclerated Idioventricular rhythm

Posted in cardiology -ECG, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Arrhythmias, Uncategorized, tagged , , , on March 31, 2012| 1 Comment »

Cardiac arrhythmias by nature connote a serious implication ,especially  so  with ventricular ones. Here is an  arrhythmia which arise from the ventricle by excessive automaticity  ,   fires independently  ,   still  very   benign compared  to others ventricular arrhythmias.

Why AIVR is a stable arrhytmia ?

Primarily due to its low rate.

Since  it is a  reperfusion arrhythmia the outcome is good.

Mechanism

It is not due to reentry , it is thought to be due to enhanced  automaticity  without pathological  intra-myocytic  calcium spikes  (Like true VT )

Absence in surface  ECG does not mean it is not existent.  In-fact there  is some  evidence to call this arrhythmia as a form of ventricular parasystole.

Focus of arrhythmia

Since it is a reperfusion arrhythmia it has to arise somewhere from  re-perfused myocardium.

The fact that  it  can occur in both RCA and LCA reperfusion  indicate the focus can be  in any of the ventricle .

Usually it follows the reciprocal rule of bundle branch block  pattern  (RBBB in LV focus LBBB in RV focus.)

Septal AIVR  can have either RBBB or LBB morphology.   Usually  left axis is noted .

How to differentiate it from  non sustained VT ?

  • Ventricular rate in AIVR should be between 60 -110 .(Note -The inherent ventricular rate is 35/mt .There is three fold acceleration )
  • Basic idoventricular rhythm is about 35.  Three times accelerated
  • Characteristically   AIVR  starts with an escape beat rather than an  ectopic beat .

AIVR  is common  in  RCA or   LCA reperfusion ?

It is supposed to be more common in infero-posterior MI  as sinus slowing is an important predisposing factor  for releasing   the idio ventricular rhythm.

AIVR after primary PCI

Is not reported much as  current interventional  cardiologists  do not bother much to watch about this arrhytmias

Other causes for AIVR

  • Myocarditis.
  • Digoxin toxicity

Management

(The commonest issue with AIVR  could be    . . . Nurses  /Fresh interns may mistake it as VT and  pressing the false alarm ! )

  • Rarely  requires treatment .
  • Atropine ,Isoprenaline to increase sinus rate.

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Arruda scheme for rapid localisation of WPW syndrome

Posted in cardaic physiology, cardiac physiology, Cardiology - Clinical, cardiology -ECG, Cardiology-Arrhythmias, tagged , , , on February 14, 2012| 1 Comment »

Localising  WPW syndrome is a favorite  time pass  for cardiologists in spite of  serious  limitations of surface ECG .Still , it is vital to generate a rough idea about the location of  these pathways ,  so that we can focus  our efforts  on  some sort of ablation procedure .

Arruda algorithm is probably a simple and fairly useful technique to remember. It asks us to climb 4 steps   and pause at each  step and look sideways   for the accessory  pathways !

Step 1 (Left free wall step )

Initially one need to look only two leads .

Look at lead 1  and  V1 for   delta wave and R/S ratio .After Identifying delta wave look for the polarity of delta wave (This can sometimes be really difficult ) .If there is iso-electric or negative delta it immediately  fixes the pathway  in left free wall . Similarly if V1 R >  S it also fixes in left free wall. To locate more precisely in left free wall  look  for  delta  wave polarity in  AVF  and proceed down*

If none of these finding are present then  Go to step 2 .

Step 2 (Coronary sinus step )

It is the most simple step . If negative delta  located in lead 2 (often mimic inferior MI)

Here the pathway is often located in coronary sinus /middle cardiac vein often as diverticulum.

After excluding left free wall and coronary sinus origin one has to look at possible septal  pathway  .

For this  go to step 3

Step 3  (Septal step ) And  again v1 lead  becomes important if v1 shows negative or iso-electric  go down  to septal  pathway decoding

After ruling out septal origin the scheme takes us to right free wall by default.

Step 4  (Right free wall step)  If the delta wave does not fit in  any   of the above three steps (Including  positive  delta in V 1 )  it  fixes  the right free wall  pathway

Arruda scheme summary

Arruda scheme  guides  us  to scan  systematically  for pathway from left free wall  to  septum and lastly  the right free  wall  (The key  to  locate  the APs is  to look at  delta waves in lead  1, 2  AVF and R/S ratio In V1 )

Here is a  simplified version for basic localization

Reference

  1. Arruda MS, McClelland JH and Wang X , et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. J Cardiovasc Electrophysiol 1998;9:2–12.

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