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