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Looks very much a infarct of  infero posterior territory is it not ?

Have a look at her 2D echo still picture . . .

Are you convinced ?

This women had normal LV systolic and diastolic function with no evidence of constriction.

The explanation for the asymptomatic pericardial thickening is due to a healed  chronic pericarditis .This sort of localised thickening in the posterior aspect is all the more likely following a loculated pericardial effusion.Tuberculosis is a very likely etiology.But this women do not have any markers for tuberculosis.Since she is symptomatic no treatment was offered.She is being followed up.

Discussion .

Q waves are not ” sacred waves” to diagnose myocardial infarction.It simply indicates the  direction of current flow is away from the  recording lead of the ECG .Any thing  electrically inert , that come in the interface between the heart and the recording electrode   can record a q waveWhat are the pathological entities that can produce q waves other than infarct ?

  • Fibrotic myocardium(DCM-Cardiomyopathy)
  • Myocardial Scars
  • Myocyte dis array(LVH, HCM)
  • Air,fluid in pericardium /pleural space
  • Pericardial thickening (As in this patient)
  • Electrical shortcircuits (WPW syndrome)
  • Rarely pure ischemia without necrosis can produce q waves (Electrically stuned myocardium)

Final message

Localised pericardial thickening is  a rare  (?unrecognised) cause for pathological q waves , that may mimic a MI.

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Ventricular tachycardia is the most common wide qrs tachycardia.It is generally taught VT is a  regular wide qrs tachycardia.It indeed appears regular most of the time but in reality it is not.

There are few  situations it shows irregularity . Of course , this irregularity may be due to the associated phenomenon ,  even as the VT focus  fire regularly. But for a physician what is manifested in the given ECG matters.

Frequent capture beats and fusion beats.

We know   AV dissociation is sine qua non of VT. Not withstanding this fact , the sinus impulses always try to enter into the ventricle and looking for the door at AV node to open.Even a fraction of a second is enough for the sinus impulse to sneak through it , the only question is the timing .It should be noted that an  intact VA conduction precludes antegrade AV conduction and fusion and capture beats are rare. So whenever the VA conduction lags behind or sluggish , more capture  beats occur.This obviously make  a VT irregular. This sort of irregular VT can occur in up to 20% .So it is indeed wrong to assume that the  presence of  irregularity one should make a diagnosis of VT.

VT induction phase cycle length fluctuations.

The other reason for VT may be irregular  during the early minutes after the onset of VT. Here the electrical circuit fluctuates till it attains a steady state.

The  VT often takes off  with a turbulent course (Bumpy myocardial boulders due to electrical reactionaries and mechanical scars ) Then the circuit optimises .This happens more so in post MI scar induced VT where the tract can be long and circuitous with considerable delay in conduction. But, once the VT reaches the cruising speed it becomes fairly regular. In ischemia mediated micro reentry or automatic focal VT cycle length variations are less common and they maintain the classic property of the VT namely the regularity.

Drugged VT: The Amiodarone effect.

The effect of class 1 a or 3 drugs on VT is a complex one.Either they revert to SR or it may reduce the VT rate, widen the qrs complex, and make it little irregular.This is especailly common after the cumulative amiodarone effect.

Polymorphic VT

The VT that has polymorphism obviously will be irregular.Torsades is the typical example.

Multifocal ventricular tachycardia(MVT)

Every one is aware of multi focal atrial tachycardia.It is surprising the MVT as an entity is rarely described in literature.Are the ventricles protected against such arrhythmia ? When multifocal VPDs occur very often why it is not transforming into MVT ? It is  possible , once a VT is  initiated it suppresses the other focus like a overdrive pacer  and extinguishes all surrounding electrical activity. But as in parasytolic tachycardia MVT can occur occasionally when  each focus is protected against the other by an entry block.

A VT may switch over from one focus to other.During the time of transition or competition between the two focus if you happen to record a ECG it can be really irregular  and chaotic !

Final message

VT is a regular wide qrs tachycardia  in majority.But this rule is applied only in monomorphic unifocal VTs. Even in monomorphic VTs there are  occasions it may show irregularity due the associated phenomenon.A grossly irregular wide qrs tachycardia always indicate a antidromic AF with accessory pathway.

* Title talks : With due respect to the  experts  ,there is no reason for getting confused .For the  practical working formula VT can be considered as regular tachycardia.

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Every one knows VT  presents as a wide qrs tachycardia  .Few of us ,   know VT can be narrow or even a normal qrs complex . But .none of us know what is the exact reason , why the width of  qrs complex  in VT swings from narrow  to wide.

Factors determining qrs width in VT.

  • Origin of VT :Septal, freewall , apex etc
  • Epicardial exit points make it wider
  • Rate dependent Intraventricular conduction (VT with aberrancy a possibility ?)
  • Drugged VT(Cumulative dose of amiodarone widens the  VT  )
  • Associated LV dysfunction/Myopathy
  • Electrolytic milieu (K + etc )
  • Preexisting bundle branch blocks (Surprisingly common and still more a surprise some BBB  may convert  a VT from wide qrs to narrow qrs ) 

* Another unique , but common observation is  variation in qrs width between different leads.This again points to different exit points and tachycardia circuits traversing and looping around the epicardium to endocardium at different depths  from the chest wall leads.

The commonest explanation of VT being narrow is it’s origin near the septum and travel down the fairly physiological his purkinje tracts and resultant uniform depolarisation.While myocardial,free wall apical VT are bizarre and wide. We now know , many factors come into play in determining the  qrs width.In fact , we are only beginning to understand the complex conduction pattern of VT.

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It is the classical description of wenkebach AV block type 1 there is progressive prolongation of PR interval followed by a blocked p wave and hence a dropped qrs complex. The usual conduction ratio for wenkebach AV block is 3:2 or 4:3 .

It is well known wenkebach AV block is usually a benign form of AV conduction defect and it recovers spontaneously without any pacemaker support.The block is at the level of AV node and since the his purkinje conduction is intact and the prognosis is good. In type 2 AV block the disease is often(Not exclusively ) located in the infra hisian area .This makes this type of block very unstable and these patients have a high risk for going in for complete heart block and often require pacemaker implantation. The reason for the poor outcome in type 2 AV block is now more attributable to the more extensive myocardial damage these patients suffer than the location of the block itself .

So it is important for the physician to differentiate the two entities .

It is a simple task in most situations , but when the condition ratio is 2:1 one can imagine the difficulties as none of the classical criteria of wenkebach’s AV block are applicable .When alternate qrs complex is missing there is no question of progressive PR prolongation .

How common is 2:1 AV wenkebach ?

It is considered rare , but may not be recognised in surface ECG so real prevalence is under reported.

What are points to differentiate the two ?

  • The qrs width : A normal qrs width suggests wenkebach .A widened qrs indicate the block is infra hisian.
  • The conducted basic PR interval is usually normal in ttype 2 AV block. In wenkebach the PR interval is usually prolonged.(Not always though! )
  • Response to atropine *:Wenkebach tend to accelerate while type 2 AVblock tend to worsen.
  • Response to excercise :Wenkebach conduction ratio improves , type 2 does  not, some times worsens
  • Response to carotid massage: Wenkebach AV block worsens ,Non Wenkebach improves

*The principle behind the varying response is due to the fact that AV node is under the influence of vagal fibres than the his purkinje system.

**It should be noted the atropine effect on AV conduction  is a complex one .Atropine by it’s direct vagolytic action improves AV conduction , while it’s effect on sinus node accelerates the heart rate and make the AV node more prone for physiological AV delay (Decremental conduction: Increased refractionary period at fast hear rates) .This effect is in exact opposite of it,s direct action on AV node.So the net effect will be the balance between these two.Hence atropine effect on heart can be quite variable in both physiological pathological situations.

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Is aberrancy  same as functional bundle branch block ? Some electrophysiological entities are used too liberally  without much meaning . The terms  functional bundle branch block or rate dependant bundle branch block  is actually used  interchangably with aberrant conduction .It should be noted aberrant conduction can occur at extremes of heart rate .Even though tachycardia is expected to produce aberrant conduction extreme bradycardia as it can also  make the  cardiac  conduction turbulent  . Why aberrant conduction happens ? The his purkinje system expects some discipline and order from the SA node. Abnormal  fluctuations in sinus  heart rate  keeps  the downstream  cardiac conduction system guessing and confused. The antegrade  impulse penetrate to various levels and get struck with different refractory periods. In this scenario  , if  suddenly the basal heart rate swings further  to different rates ,   the new  incoming impulse  finds , the preceding impulse has produced a functional block /barrier at the his purkinje level  . (Note it should be called functional delay in conduction  rather than a block as every impulse gets conducted ultimately with a widened qrs complex ).

  • This type of  conduction velocity mismatch between atrium and ventricle occurs in many of the SVTs and also in AF.
  • It is found , aberrancy occur more commonly in the right bundle.
  • It is usual for the aberrancy to disappear after the rate correction . Some times there could be a temporal delay . The conduction system might have gone for prolonged stunning . Some times this is referred to as ” memory blocks”
  • Underlying heart disease, ischemia , degenerative heart disease  may amplify this aberrancy or  convert this transient aberrancy into a permanent block .
  • It is also possible  even a ventricular tacycardia might conduct with aberrancy ,  widening the already wide qrs tachycardia .(Refer this blog 🙂

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It is one of the greatest innovation in medicine  . . . that is . . . electric current being  used as  a  drug to  treat disorders of heart . Of course ,  it is not a surprising finding  when we know heart is an  electro mechanical organ ,  and electricity can be used  to treat various disorders of heart by delivering it  in an optimal dosage and site.

Devices  that help administer  electric  current in cardiac disease.

  1. External  cardiovertor and defibrillator
  2. Implanted defibrillator
  3. Anti bradycardia  pacemaker
  4. Anti tachycardia pacing
  5. Cardiac  resynchronisation device

What  is  the  difference  between cardioversion and  pacing ?

Cardioversion  is reverting  a tachycardia with  a electric shock that is delivered diffusely throughout the heart This  electrical wavelets traverse the  focus of tachycardia  and the adjoining myocardium  which is called critical electrical mass (Usually reentrant) .This depolarises the cells responsible for tachycardia and extinguishes the abnormal electrical activity.

Defibrillation is same as cardiversion except that it is a high energy shock  and delivered without synchrony with qrs complex . In VF, we defibrillate in all others  we cardiovert .

What are the disadvantages of cardioversion ?

Eventhough it is a very successful modality for treating cardiac arrhythmias it also has some issues.

  • Cardioversion is not infallible. It rarely works in tachycardia due to enhanced automaticity (Multifocal atrial tacycardia , Automatic junctional tacycardia , Digoxin induced tacycardia it may even be dangerous !)
  • Many times multiple shocks are required and may result in myocardial damage, stunning , and elevated cardiac enzymes.
  • In susceptible patients, especially in elderly it may depress the natural pacemaker ie the sinus node and dangerous  bradycardia

over drive pacing paired pacing anti tachycardia

What is difference between cardioversion   applied externally on the chest wall and intracardiac cardiversion as in Implantable cardiovertor defibrillator(ICDS) ?

The underlying principle is same except that the energy required is a fraction of that applied in the chest wall . The average energy required is up to 20 joules . while it requires up to 300 joules

What is anti tachycardia pacing ?   Why this concept came into vogue ?

When it became clear , cardioversion may not work in all forms of tachycardia and risks of multiple shocks  on the myocardium  not be taken lightly , experts in those times (1970s)   thought  a pace maker lead in a optimal site can do the job of cardiovertor. .

Pacing rapidly  in the tachycardia zone  provide us an opportunity  to  enter  the  tachycardia circuit , interfering , interrupting  and blocking the reentrant circuit  (We call it entrainment)  . If it is an automatic tachycardia pacing in close vicinity of the tachycardia   focus result in a  electrical  line of  barrier  which acts as an  exit  block ( Like the lakshman  reka !  in Ramayana )

The term ATP is used as a  general term as anti tachycardia pacing .Over drive pacing  can be used synonymously.

What is the  main advantage of ATP ?

  • Less injury as it avoids recurrent shocks  .
  • Can be administered as many time as  required .
  • Some tachycardias specifically respond to ATP only (Read below)

How to perform overdrive pacing ?

Can we use the external transcutaneous pacemaker paddles for overdrive  pacing ?

Yes we can, it may be termed a  non invasive external overdrive pacing .This  mode is not popular among cardiologists  not because it is ineffective  , rather we have not fully realised it’s  potential .

Different types of  overdrive pacing

What is coupled pacing ?

It is a type of overdrive pacing where   patient’s own spontaneous  rhythm   is used trigger a  pacemaker stimulus    and  hence only alternate beats or pacing beats which is coupled with the pateint,s own rhythm it is called coupled pacing . This  is different from from paired pacing  in that only single pacemaker stimulus per cycle .

What is paired pacing ?

Two pacing stimulus are given.The first impulse is maintained constant and the second impulse is done with varying coupling interval to scan the entire cardiac cycle .It is expected at some point of paired pacing the second impulse would  block the reentrant circuit.

What is random paired pacing ?

The atrium is   delivered a   pair of random stimulus ( . . Like a bite of snake !) is  delivered into the atria .This can revert many of the reentrant atrial and ventricular  re entrant tachycardia.

What is the  unique value of  sinus paired  pacing ?

In patients  with persistent sinus tachycardia,  especially  in patients with  high MVo2 situations or dysfunctional ventricle we have no option to control the heart rate without depressing myocardial contraictility . Most of the negative chronotropic drugs have negative inotropic action also.  In these situations pairing a pacemaker stimulus with a sinus impulse can produce a compenstatry pause  and result  in reduction in net heart rate as well  as increased  contractility due to post extrasystolic potentiation.

How does a  catheter whip inside the atria   terminate many of the procedure related  tachycardias in cath lab ?

It is a common maneuver  in cath lab ,  to  forcibly whip the   catheter for   terminating  many of the transient procedure related  SVTs and outflow tract VTs . The arrhythmias get terminated  either due to catheter hit induced mechano  electrical  cardioversion   (5 joules ?) or  the atrial subendocardial stretch due to the  whip lash .

What are the tachycardias that may  respond to overdrive pacing ?

It is logical to expect any of the reentrant tachycardia  might respond to ATP. The  exact success rate can  not be established  since this modality  is not applied  in vast majority of  patients . Only if a patient  is not responding to drugs or multiple DC shocks ATP is thought off . Of course ATP can not  considered  a first option   unless othe  patient is  on a temporary pacer.

What is the caution for using ATP ? Why  atrial overdrive pacing   is preferred over  ventricular  overdrive pacing ?

Pacing a ventricle rapidly carries a risk of inducing ventricular fibrillation . So whenever  possible ATP  should be administered  through  an  atrial lead. This may not be possible always as in the presence of AV block a VT  can not be captured  by atrial pacing  .

It is also  a fact  many times   when the    ventricular overdrive pacing  fails to revert a VT , an  atrial overdrive pacing has been successful . This is due to the  more uniform    depolarization  wave fronts , that reach the ventricle and reset the VT .

Currently ATP is useful in

  • Recurrent atrial tachycardia
  • Refractory ventricular tachycardia especially with enhanced automaticity (Early ischemic VT )
  • Digoxin induced tachycardias
  • Some cases of Tachy brady syndrome

 

 

In some of the modern pacemakers and  in all ICDs ATP is a an important programmable parameter .In fact, using this mode liberally would conserve battery life .Many times a simple hemodynamically stable VTs are shocked by ICDs  instead an ATP will  do the job . It is a well recognised fact that   ATP is underutilsed in ICDs .This issue needs to be addressed.

Final message

Pacemakers are not only meant to treat bradycardias but also tachycardia. Even though it is a well-known fact for over 3 decades, for some reason this simple and effective concept is not getting the  attention of the current generation cardiologists which it definitely deserves!

Reference

  1. Overdrive Pacing for Ventricular Tachyarrhythmias: A Reassessment    P. R. KOWEY andT. R. ENGEL
    ANN INTERN MED November 1, 1983 99:651-656
  2. Pacing Techniques in the Treatment of Tachycardias  I. WIENER  ANN INTERN MED August 1, 1980 93:326-329
  3. Treatment of Recurrent Symptomatic Ventricular Tachycardia R. A. WINKLE, E. L. ALDERMAN, J. W. FITZGERALD, and D. C. HARRISON ANN INTERN MED July 1, 1976 85:1-7
  4. Treatment of Tachyarrhythmias by Pacing J. E. Batchelder andD. P. Zipes

 

Over-drive pacing : A practical approach

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This was written originally in 2009 early days of this blog. Now, re-posting it in 2021  , wonder any one has new data on this! 

We know diabetes, smoking, hyperlidemia, hypertension are major risk factors for progressive vascular disease. They damage the vascular endothelium either directly or indirectly , by aggravating the atheroscelortic process .  Diabetes apart from affecting the medium sized arteries , also affect the microvasculature.  Smoking  has a direct effect on endothelial function .It depletes vascular nitric oxide. High levels of circulating lipids injures the sub endothelial structures and invades the media by entering macrophages .So , all these 4 risk factors either operate independently or interact with each other and result in progressive vascular    disease.

While we  believe , these risk factors do not have any bias in attacking the human vascular  tree, in the real world it is observed they have their own  behavior pattern and  have unique predilection and a deadly alliance .

For example , in  chronic smokers TAO is the commonest manifestation , thrombo angitis is far too less common to occur in the coronary arteries.

Similarly  hypertension  per se  rarely results in an acute coronary syndrome while it is  the  single  important  cause for cerebro vascular  disease. Diabetes especially in women has very strong predilection for CAD , while diabetic per se is a lesser risk for stroke. Hyperlipedimia may be the one which has fairly even risk throughout the vasculature. Similarly there is  a difference in renal and   carotid arterial involvement with reference to  the conventional  risk factors .

SHT diabetes dyslipidemia coroanry risk factor

Why this apparent difference ?

We are unlikely  to get an answer to this question in the near future .  Left to the youngsters  . . . of tomorrow !

* Note of  clarification

The source for the above chart is collected from various studies and also a huge observational data from our hospital. There could be some geographical variation , a given individual may respond differently to these risk factor depending upon his genetic predisposition and susceptibility . So the above data can be applied to general population and not to a individual.

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Ischemic ventricular tachycardia is a  too well recognised clinical  entity  . But , ischemia triggered atrial arrhythmias are less often encountered .

Does that mean , atria are relatively protected from the effects of ischemia ?

Not really  . . .  It  is possible  it may not be  that rare ,  as we think .

And then ,  the semantics play  a major  role !

Atrial fibrillation  is the commonest supra ventricular  arrhythmia  in human ,  we also know CAD is the leading cause of the AF apart from HT & Cardiomyopathy . So technically , ischemic SVT  is  more common than Ischemic VT ,but we do not call it so !

If we analyse the triggers for AF it is more often hypoxia  (than ischemia )  . . .yes there is huge difference between the two .In the ventricles it is more often ischemia that  trigger a VT.

Atrium is very sensitive to systemic  oxygen saturations especially in elderly and COPD patients. This is the reason we get many of the complex atrial arrhythmias in hypoxic situations ( Ectopic atrial, Multi focal atrial , etc) .These arrhythmias are difficult to control unless oxygen saturation is corrected. While  many of AF episodes are transient and disappear after correction of hypoxia.

If the ventricle also  responds with fibrillation  at times of systemic  hypoxia ,  one can  imagine the disastrous consequence ! God is kind enough , systemic hypoxia per se  rarely trigger a VF ,  though  it can maintain a VT which was initiated by some other mechanism.

So what are the causes of  narrow qrs tachycardia in the coronary setting

Apart from AF ,  Ischemic SVT  can occur in the following situations

  • STEMI -RVMI
  • Atrial infarction -Focal AT -Atrial flutter /AF
  • Post Pericarditis
  • Refractory , ischemic JT (Junctional tacycardia ) in elderly , perioperative , hypoxic patients

*Atrial arrhythmias are very rare during unstable angina for some unknown reasons . Atrial scar induced ischemic focal AT is underdiagnosed.

** Never  diagnose AVNRT /AVRT in a patient   who has an ACS. It is likely you will be 99.9% wrong.

*** Preexcited AVRTS are very rare in elderly CAD patients even in those with a history of SVT  .This is because as the age advances the accessory pathways undergo degeneration either by ischemia or  the wear and tear  and get self ablated .

Many times the associated , HT and diabetes may contribute to the arrhythmia.

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P waves represent atrial depolarisation. The p wave height  and width depends not only the size of the RA and LA but also the site of  origin of atrial  impulse .A normal SA nodal origin of P wave produce the normal shaped p waves.

We know  ectopic  p waves can have a wide variation of morphology.(Fully inverted, partially inverted, slurred, bi phasic, notched, rounded , deformed, etc. The morphology is dictated by the direction of p wave vector and thus it is quite variable in different leads. Further  it is also determined by the inter atrial and intra atrial conduction.So in summary , an ectopic p wave can have any morphology we can think off !

What is isoelctric P waves

It is rather a surprise we have not thought about so long,   like a low voltage QRS ,  a  p wave can also be very low amplitude and it may be entirely isoelectric , which could actually mean the p waves are as good as absent.This can happen in all leads or in few leads. .Atria gets electrically activated but fails to inscribe a p wave .This is termed as isoelectric p waves

The importance of isoelectric p waves

It  can  happen , both  in sinus rhythm  and in ectopic atrial rhythm . Absent p waves should be differentiated form isoelectric p waves. It is typically described in focal atrial rhythm arising from the right side  of  the  inter atrial septal near the   perinodal  tissue.The atrial tachycardias arising from this site are classically have isoelectric p waves in most of the leads especially  V1 .

Other causes of absent p waves

  • Atrial fibrillation

The classical example .in fact here p waves are replaced by fine or coarse fibillatory waves

  • Sinus arrest  plus Junctional rhythm with retrograde VA block

Not all junctional rhythm result in absent p waves .Many record inverted retrograde p if there is VA                            conduction.

  • Sino ventricular conduction .P waves appears  absent in surface ECG. It occurs in hyperkalemia /renal failure is due to high levels of pottassium   which suppress the atrial activity sort of atrial electrical paralysis but still impulse originates in SA node traverses  the inter atrial pathway and reach ventricles.typically P waves are absent or can be termed isolectric.
  • Atrial  stunning following cardioversion

Long standing atrial tacycardias may fail to resume it’s mechanical (or even electrical ) activity after  cardiversion  .If it is electrical stunning the p waves do not immediately appear  but occurs later .In fact this could be termed as failed cardioversion.

* Note  p waves are failed to identified in many of the VTs AVNRTs

Final message

Absent p waves ,  isoelectric p waves , hidden p waves, merged p waves , low voltage p waves , unrecorded p waves,  selective absence of p waves in some leads all can happen in clinical cardiology practice.

One should realise the importance  differentiating   absence of   p waves in the given strip of ECG from failure of p waves to  get recorded by the  ECG machine .This has diagnostic significance.

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Esophagus and the heart are closely related structures. Both can generate chest pain that can mimic each other. The squeezing substernal pain  is very characteristic of esophageal spasm  .The smooth muscle of esophagus can exactly mimic a vascular smooth  muscle  .The relief of chest pain following nitrates  though very classical of angina it can very well alleviate the pain of esophagal spasm also. This has important clinical implication

Also read

Cross talk between heart and esophagus

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