Posts Tagged ‘Mechanis m of tall T in hyperacute MI stemi’

Most of my students were  struggling to answer this  seemingly simple question . I  realised  later it is indeed a difficult one !

tall t waves

Some thoughts

Tall T waves are observed in very early phase of STEMI .(Within 30 minutes ?)  What is the mechanism ? Since ST shifts occur little later than T elevation ( considerable overlap may occur)  it may not be related to current of Injury.It is an  inherent alteration in the T wave genesis .T wave is inscribed when rapid phase 3 K+ efflux happen (Mainly by Iks and also  IKr )

What is the effect of ischemia on K + channels ?

No uniform answer.(Blocks, stimulates, irritates, Bi-phasic, variable ?)

There are 6 important K  channels in every cardiac myocyte adding to the complexity.

Does  the  Ischemic cells leaks potassium or accumulates it ? 

Though It does both ,  predominantly it should leak .If it’s leaking there is local extracellular hyperkalemia . Is that the explanation for tall T waves ?

What is the influence of QT interval on T wave morphology ?

Long QT as occurs in hypokalemia  pulls the  T down  and it may even  invert it.  .Short QT tends to push it up as in ERS .The effect of ischemia on QT interval is again unpredictable.Further regional and remote ischemia in a given patient can alter this.

Once the ST begins to elevate  the T  waves  losses it power to grow tall .It only can regress. I think this is the time the QT is sort of prolongs .

Effect of reperfusion on T waves

The tall T tend to regress as some form perfusion takes place as  K+ Is pushed back into the cells or  flushed away  from the vicinity.

The dynamic nature of reperfusion  makes the behavior of T wave amplitude further complex. But one thing is certain , a well perfused IRA  is associated with inverted  T wave  which we call it as completion of the process of evolution of MI .

Finally and most importantly this hyper acute T phase is not a constant  phenomenon. In fact it is uncommon in  persons who  have baseline T inversion .After analysing many things we are back to the original state of ignorance .


Researchers with intra-myocardial micro electrodes try to decode the mysteries in electrophysiology . Still there is a huge disconnect  between  clinicians and physiologists.

In simple terms  I would  believe the mechanism of   ischemic tall  T waves are almost similar to renal  hyperkalemia. (A local , transient  extracellular k + excess ) The base of the T waves are not narrow and tented as in CKD because  some degree of ST elevation (that always is expected )  widens the base of T wave. Further  ,the  prolonged QT interval in  renal hyperkalemia  stretches the QT and encroach   the base of the T wave to the left making it  appear narrow.

A simplest  version for  students

Tall T waves  are due to  transient  local extra cellular hyperkalemia , when K + leaks due to cellular  Ischemia.

Caution: This is  a superficial scientific attempt .I need inputs from more scientific  brains and electrophysiologists.


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