Archive for the ‘Basic science -Physiology’ Category

How many times you have treated cardiac arrhythmia in both emergency & non-emergency situations?

Infinite times.

How many times did you really bother to know the mechanism of a given arrhythmia before ordering medication or shocking?

Hmm,.. let me think. (Except for AVNRT/ AVRT, and few VTs, very rarely I have worried about the mechanism  !)

Why is it so? because treatment takes priority and we are able to tame the arrhythmia even without knowing the real mechanism.

The following slide is a gross summary of the cardiac arrhythmia mechanism

Understanding cardiac arrhythmia is vitally important for a few reasons in a few settings.

  • In acute settings, we need to know automatic tachycardias will not respond to shocks. Reentry tachycardias will respond more promptly. (Of course, we may not know it till we shock ) Calcium blockers like verapamil might block triggered activity in MAT. Overdrive pacing is the answer for many automatic tachycardias and some refractory reentrant tachycardias (ATP protocols in ICD has taught us this ) 
  • In the chronic setting when you contemplate mapping, locating, and ablating arrhythmias, mechanisms are important. The task here is locating slow conduction paths and decoding the diastolic circuit around the scar  (If you plan ICD, knowledge about mechanism  becomes redundant again)

  • Finally, knowing the mechanism of arrhythmia is a fascination by itself to help understand the great subject called cardiac electrophysiology, where 100s of ion channels work nonstop drawing the action potential on a moment to moment basis sustaining our life.

A challenge

Can you localize a VT and find the mechanism in a patient who is Ischemic /hypoxic and acidotic? You can never do it. Please note, most polymorphic VTs can’t be localized. The mechanism is either automaticity, trigger activity, or even micro-reentry. You need to shock and look for the causes.(Link to How does the treatment of monomorphic VT differ from Polymorphic VT? )

Final message

Should we need to know about the mechanism of arrhythmia we treat?  Definitely yes, if you have that passion to know the truth, or else just order Amiodarone or shock and check out of CCU. (Of course, we have a very good option of calling EP consult the next day.)

 A review article on mechannism of cardiac arrhymias

Rev Esp Cardiol. 2012;65(2):174–185

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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 !


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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