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Archive for the ‘cardiology -ECG’ Category

This 70 year old man in routine check up showed up this ECG.

What is it ? a  quick debate ensued !

Is this

  1. RVH
  2. RBBB
  3. Or Both ?
  4. Neither RBBB nor RVH
  5. Wrong lead placement
  6. Is it a normal ECG after all ?

Incidentally the ECG shows a Wenkebach AV block in the bottom strip lead 2.

I thought it was RVH. (do considered RBBB) but since lead V 2 showed tall R , I was more than sure RVH was likely . Many voted for RBBB. .Some others said RBBB can never occur in monophasic form.I said it’s possible.

Some body challenged me without Echo Imaging a  monophasic RBBB can never be differentiated from RVH. After a mini argument I reluctantly agreed.Yes, it seemed there is no way to differentiate the two.

What do you think ?

Curious to know the Echo finding in the above patient  ? Yes , your guess was right /wrong. There was no RVH.He had normal Echocardiogram.

How to diagnose RVH in RBBB ?

  1. Look at the r’ wave if its taller than initial r by more than 5mm suggest RVH (Not absolute evidence though)
  2. Look for other evidence like Right axis , RV strain etc.

How to diagnose RBBB in RVH ?

Sorry.I don’t know the exact answer.It could be masked within Qrs complex of RVH.RVH could convert biphasic  RBBB into monophasic RBBB.

Some more about this RVH/RBBB duo

  • The term incomplete RBBB is liberally used with minor rsr’ pattern.It is not advisable to do so.
  • RBBB is classically multiphasic (To be precise RBBB can be complete to incomplete  rsr’ with various combinations of small r and big s big R or big S).
  • But more than the morphology of Qrs in V1 the S wave in lead V 6 or Lead 1 could be Important.It should be delayed slurred.
  • QRS width has no great use to diagnose RBBB as it can be narrow or wide.

Final message 

To diagnose monophasic RBBB( in V1 ) by itself requires some guts.However ,the entity do exist.

Finally , please recall there is a traditional list for  tall R in V1 other than RVH.

  • Wrong lead placement
  • RBBB
  • Some cardiomyopathy(RV myopathy)
  • Systemic Duchenne’s muscular dystrophy
  • Pre-excitation
  • Posterior MI
  • Normal variant*

*Why should normal guys grow a tall R in V1 , it mystifies ! but true.

What is the rarest cause of tall R in V1 ?

Localised cardaic tumors over RVOT. Cagli K , Tok D, Basar FN   .An unusual cause of tall R wave in lead V1: cardiac lipoma.Heart Asia. 2013 Mar 7;5(1):33. 

 

Annexure : Further questions in RBBB

 

1.How does AV bundle penetrate to become bundle of HIS and branches ?
Note AV node is fully Intra atrial structure , while part of His bundle is atrial , after crossing the membranous septum second part lies within the ventricle at the crest of muscular septum .Then the bundle of His goes for the famous division. Left fans out  tow streams, while right descends on right side of IVS. Note : Applied anatomy 1.Its this small portion of HIS we are trying to physiologically pace the ventricle 2.In proximal LAD lesions both RBBB and LBBB is common still LBBB can’t be used to localise but RBBB can be.Guess why ? Read the next question and find the answer..

 

2.What is the blood supply of bundle branches ?

 

3.What is the mechanism of RBBB in ASD ?

Is it true RBBB or Right bundle delay ? Students should know there need not be conduction system pathology to cause RBBB. Simple delayed conduction in RVOT can cause a RBBB. (The concept of central RBBB vs Peripheral RBBB) This is what happens in ASD.

In fact , true pathological damage due to right bundle branch due to necrosis, Ischemia, Infiltration is much rarer than pathological LBBB.

4. What are the  structural , histological  difference between right and left bundle branches that has electrophysiological Importance ?

Wait . . . I am trying to collect info for this .Meanwhile ,Why don’t one of the energetic young  fellows in cardiology find the answer and post here !

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These are the common ECG terminologies with which clinical cardiology is being practiced over the years .In this era of instant interventions the exact meaning for these terms  may not matter much for many of us.Still , Ischemia could denote a more benign connotation , while injury suggests an emergency (like an accident) .Of course , this is a dangerous way of defining them. Still, there may not be an entity called  “chronic injury”. while chronic ischemia is all too common.

Logistically , both could  mean the same (except the perception) and related to the intensity of the index reduction in blood supply to the varying thickness of myocardium.While injury is diagnosed by ST segment elevation , ischemia is diagnosed by ST depression  or T inversion.

No, its wrong , come again please ,

Shall we say . . . most injures are ST elevating  while most ischemia are ST depressing , but  still injuries can be ST depressing  as well.  We know Ischemia can be sub-endocardial , transmural or  rarely sub-epicardial ,while injury can either be sub-endocardial or subepicardial (Rarely transmural ?)

Can you refine it ?

Only  subepicardial ischemia(Injury)  elevates  ST  segment while sub endocardial ischemia depress it.The leads facing the affected subendocardial and epicardial surface will determine whether its going to be ST elevation or depression .

Go further,

Does the opposing sub-endocardial and sub-epicardial forces negate or  cancel out  ? If so what is the status  of reciprocal ST depression in STEMI if remote ischemia occurs in sub-endocardial  or  sub-epicardial zones ?  Can there be reciprocal ST elevation for primary ST depressive forces ?

If ischemia and Injury are to be defined only with reference to ST segment , which area of myocardium is linked to  critical T wave ischemia (Both Tall T and dynamic Wellens type T )

Still more , If Injury is  represented by ST elevation,  then what represents  infarct ?

ST elevation in acute MI-STEMI is actually due to  transmural* injury while infarct is represented by Q waves in strict sense.In that case not all acute STEMIs are not true Infarcts.Thats why many STEMI can get totally aborted with zero LV dysfunction and negligible enzyme release.  (Should we call these as Non Infarct STEMIs ?)

*Though STEMI results in  transmural ischemia , it is the sub-epicardial zone of injury that elevates the ST segment. This  implies any degree of subepicardial injury is suffice to elevate ST segment (eg pericarditis) and transmurality of ischemia is not mandatory.

What is reversible vs irreversible Injury ?

If irreversible injury is equivalent to infarct , reversible injury is same as ischemia ? (Whats the histopathological  correlates , Cell swelling, mitochondrial / nuclear death .(We know , enzyme release are  linked to cell death even in  chronic stable angina )

Where is the epicardium  for the IVS ?

Most ACS involve interventricular septum .In this case does septum has  any defined sub-epicardium or endocardium? How does septal STEMI forces behave with reference to partial or full thickness septal  infarct ?

Final message

Acute Ischemia and injury can mean “one and the same thing” or  “totally different” entities  depending upon  the totality of obstruction within the coronaries and  sparing of  sub epicardial zones of  myocardium. In my view , any acute ischemia can be labeled as injury.Bifurcating ACS into STEMI and NSTEMI has largely removed the embarrassment of these entities .

Be grounded

Forget the basic science , electro-physiological concepts can wait.Lets live in a realistic world. Get to know the underlying lesion . What can be done for it ? Go ahead , wheel your patient to cath lab . Alert the staff .Be pragmatic ,make sure your patient has sufficient insurance coverage to open up  all his blocks ! That’s it !

Postamble

The intention is not to confuse the readers.Only to make us realise ,the gap in  basic science is “huge and wide” which I hope is  filled up by the generation next !

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J point is a critical point in the  ECG  when the ventricles hand over the baton in  the  electrical relay race from depolarization to repolarization .This the time the sodium  channels extinguish itself  and the potassium current begins its activity  from Phase 0 to 1 .

If the  potassium channels  activate little early and snatch the baton prematurely from sodium , we get early repolarization pattern .When this happens , the J point of ECG show a conspicuous wave  called J wave , originally  denoting  Junctional wave between QRS/ST segment  (Now  perceived as  Jitter waves ?) The other implication of premature K+ activity is , lifting up of  ST segment , making it the most common cause of non ischemic ST elevation.

* J wave in hypothermia is referred to as Osborne wave and  may not be  not related to ERS(Ref.4)

J wave and J point early repolarisation syndrome

Image source.www.cardiology.org

The Ito current is responsible for the phase  1 of action potential (AP), where a rapid outward k + ion flux take place and draws the dome of AP . The dynamics of Ito is complex .It depends  upon the density of epicardial K + channels , which are  clustered in a heterogeneous manner .There seems to be a concentration gradient   along the epicardium and endocardium , making the wave appear prominent in some. This is especially true in healthy, athletic  male population  where we have some evidence for androgen  to  play a role on how  these channels will behave.Here comes the overlap between Brugada  syndrome and ERS as well.

The subset of patients with J wave pattern were recently shown to have increased risk of primary VF due to phase 2 reentry ,  when they develop ACS. (Rather J wave pattern was more common in patients who had primary VF following STEMI(Ref 1).This resulted in a spate of worrying articles .Now we know , the  fear is  largely unfounded ,the risk is far less.

Current thinking is,  persons who have asymptomatic ERS pattern with prominent J waves should not be investigated electro-physiologically . (Please remember , every human  heart can be induced  to VF in EP lab  if appropriately  stimulated ! )

In fact , I used to tell the  young men  who  harbor  prominent J wave , as a marker of healthy heart  rather. Let us not  fear them with a remote risk  that could be as  negligible as risk of  intercontinental flight crashing into the ocean  !

References

1.Haissaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med. 2008;358:2016–2023.

2.Idiopathic Ventricular Fibrillation “Le Syndrome d’Haïssaguerre” and the Fear of J Waves , Sami Viskin, J Am Coll Cardiol. 2009;53(7):620-622. 11

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

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

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

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

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

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

Final message

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

Reference

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Many  readers  of this site might have wondered  , about a  series of biased articles  pulling down the  superiority of pPCI in STEMI.

This  French  study (FAST-MI) throws stunning data  from the real world. Initial Fibrinolysis* defeated pPCI in all aspects of coronary reperfusion !

FAST MI primary PCI  trialFAST MI primary PCI  trial 2

*When we say fibrinolysis arm it means Pharmaco -Invasive approach .Today our  brain  is irreversibly conditioned to believe standalone fibrinolysis is  forbidden in STEMI . (Which I strongly disagree!) I am sure, very soon another stunning study will unmask the truth about standalone fibrinolysis  as well !

Final message

  • The truth  is ,  pPCI is really a superior  modality in some of the complicated  subsets of STEMI that too if performed fast.
  • In all other situations Initial fibrinolysis will rule supreme !
  • pPCI is not an Innovation for mass consumption!
  • Hence, “the roof top call” for  pPCI for every STEMI is nether desirable nor feasible.

Now, we have this evidence from France (Which was well known to us a decade ago) As always , truth takes time to arrive , while falsehood can come instantly !

 

In 2014 , after two decades of celebration of pPCI  the flagship Circulation journal  throws this Editorial !

primary pci vs thromolysis debate fast study

 

 

 

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CHB with CAD is a  common combination especially in the elderly.

Which will you Intervene first ?  Is the AV block related to CAD  ?

How to differentiate Ischemic from degenerative AV block ?

Differentiating is often difficult.Even coronary angiogram may not answer the query unless it is totally normal . For AV block to occur usually  LCX / RCA lesion is required.  LAD lesion in isolation are rare to cause CHB .

How often re-vascularisation  reverses  ischemic CHB ?

Logically  you expect more reversals.In real world it rarely happens.

Therapeutic options in combined CAD and CHB

  1. PCI and pace maker in the same sitting .
  2. PCI first followed by pace-maker at a later date.
  3. Pace maker first followed by PCI at a later date if required.
  4. CABG  and epicardial pacemaker ( best option In all critical TVD and CHB)
  5. Pace maker followed by CABG later
  6. Pacemaker followed by medical management (CHB with Insignificant CAD)

Can worsening of ischemia  occur after pacemaker  ?

Very much possible . Since the patient  has been benefited by low heart rate in terms of MVO2 consumption .(Inserting a pacemaker  is  like sudden withdrawal of beta blocker !)

Rate adoptive pacing can confer chronotropic competence which  may bring back the angina.So,what was a insignificant lesion  can become hemodynamicaly relevant  and  may require  angioplasty  later.

*The above clinical issue is applicable  for sinus node dysfunction and CAD as well.

Final message

There is no  fixed rule in the management strategy in combined  CHB and CAD .

Generally , electrical  therapy  should be given preference .Symptom guided approach  may be practical.

In this scientific era , one may argue to deal both issues  together by simultaneous  PCI and pacemaker ,  still  option 3 and 6  remain clear  favorites !

If angina  occurs  even in  baseline bradycardia  it is obvious the obstructive CAD  is  significant and needs immediate fixing .

Finally , though it looks an attractive  concept , It is very rare for CHB  to get reverted by PCI or CABG.

 

 

 

 

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Any new ST depression occurring during  EST is sine qua non for inducible ischemia.But,this rule does not uni-formally apply  in all 12 leads .ST depression occurring is certain leads is more important. While severe global ischemia can depress  ST segment  in most leads ,factually  only the leads V 5 and V6  predict true Ischemia.This because , bulk of LV muscle mass faces these two leads.

Isolated ST depression in inferior leads  during exercise

  • Is a frequent issue occurring at the peak exercise.
  • Is least predictive of significant CAD.
  • The exact mechanism is not clear.
  • Some continue to  believe it is indeed significant .
  • We have  observed  isolated  ST  depression > 2mm in inferior leads with significant CAD.
  • What really matters is the quantum of ST depression , symptoms, and exercise time and preexisting CAD .

Probable mechanism

  • Apart from true ischemia ,ST depression may indicate relative sub endocardial strain rather than ischemia.(By the way can simple stretch can cause ST depression ?)
  • The Infero posterior surface of heart represent  right ventricle .RV volume overlooked peaks exercise.Some think it represents acute raise in RV load during peak exercise.

How to report such EST ?

You can report it as such,  what you have observed.

  • ST depression noted in Inferior leads at peak exercise.
  • Mention whether it was angina free,
  • At what METS,
  • Total exercise time .

If you are statistically inclined  you can also mention the likely hood of CAD by positive predictive value (PPV) of the test (Low with isolated Inferior ST depression )

If you are really confused , and do not want to scratch your brain we have the most convenient terminology  invented by cardiac physicians ie Borderline EST, or Mildly positive EST “

Should we do Angiogram for such patients ?

In this era of catching normal people  who attend master health check ups  for a day care CAG  . . . it is not all  a crime to do angiogram in a  patient who shows suspicious  ST depression in three of his leads (2,3,AVF) especially if he also complains of vague chest pain.

Alternate investigation

Of course , we  always have the luxury of using  MDCT  that can stunningly  photograph the coronary arteries.

It is a mystery investigation, if it comes entirely normal every one is happy.Even slightest  defects in the photography  has a potential to confuse both physician and the patient .

What I do ?

I hesitate to  do routine CAG  if ST depression occur exclusively at  peak exercise beyond 10-12  METS , which disappear fast.(Many times we can apply this rule  to classical ischemic ST depression of lead V4 as well !)

ST  depression  in any leads (with any degree) following an episode of  ACS seems to be important.

Related topic

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