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I found a paper presenting an electrostatic model to explain the ECG recorded in various leads. This model essentially calls for considering the depolarization wavefront to be the major contributing factor to the potential difference measured at the leads, especially the limb leads, by means of an aggregation of momentary dipoles with dipole moments organised according to the direction of propagation. It is also used in this book here, under the ECG section under Measurements of cardiac function.

The paper does not explain the observed ECG deformities in case of MI in detail. ST elevation, is a common finding in most MI cases. How do we explain this in light of the aforementioned model?

My thoughts

In the normal case, ST segment is isoelectric, as there is no depolarisation/repolarisation wavefront propagating. How is this isoelectric nature compromised in MI? Assuming most infarcts include muscle death or damage due to focal insufficiency of coronary circulation, even if a region of heart was dead, during the ST segment, the graph should show an isoelectric line (no deflection) as the living tissue will either be depolarised or polarised, (but not switching states) and the dead tissue will have either a completely obliterated membrane polarity or an altered polarity throughout the cardiac cycle. In any case, no part of the heart will be switching its polarity then. Why is then, some resultant dipole (which indicates a propagating wavefront of altering polarities)obsereved during the ST segment?

alternative model
To explain the elevation, this book (pg 522) provides a two cell model, and explains that the anoxic damage somehow causes the basal depolarised state of the cell to have a lower membrane potential difference, which causes all the segments of the ECG except the ST segment to be lowered, making the ST segment appear raised. I don't understand three things regarding this explanation. How will anoxic damage cause such a specific alteration in the polarity and the subsequent action potential? How can this two cell model be extrapolated to the whole heart with a focal infarct? How does this explanation be reconciled with the model presented at the head of the question?

Let me know if the question appears too broad and needs to be split, or if my assumptions are wrong in any way.

MI-Myocardial Infarction

PS:- I seem to have lost the touch with the formatting on this site, and hence don't know which tags to use. Will take some time to get back :)

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    $\begingroup$ formatting and tag edits are fine! :) +1 $\endgroup$ – AliceD May 27 '15 at 13:34
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The concentration of K+ inside the cell is 30 time more than outside. Hypoxia causes loss of this intracellular Kalium and consequent/premature repolarization when measuring the potential of action.

As the all the ECG theory is Vector based, any abnormality in the electric pathways and myocytes will result in changes of ECG.

This picture depicts the ST changes due to different extension of injury. In addition, the explanation on this site will probably resolve the issue of understanding.

enter image description here

ADD

The article explains the ECG phenomena as a result of electric propagation of dipoles. If the dipoles propagate towards the lead we get upward wave etc.

As the electrostatic model takes the whole heart as one dipole (as a sum of multiple dipoles) the minor infarcts can be missed on ECG. It is an actual fact, this is why other tests are important (for example, the troponin test).

The confusion point in your understanding is a "dead" tissue. In a case of infarct there is an hypoxic damage which leads to elevated permeability of the cell membrane with resulting K leak (as I explained above there are 30 times more Kalium inside the cell than outside). This means that "dead" area will have abnormal depolarization/repolarization pattern just because there are multiple "non grouped" dipoles in that area (look at the picts). There are diastolic and systolic theories of ST elevation, but none of them has won the battle yet.

With time the scarring tissue replaces the infarcted myocardium and in that case the ST-segment will not be affected and will look nearly normal. This is the case you meant as "dead" tissue - scar tissue does not leak any electrolytes and consequently the ST segment is not affected in a chronic stage.

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  • $\begingroup$ Thanks for the answer. But I want to understand the genesis of the resting and the repolarised-state dipole which causes the said changes in the graph, considering the electrostatic model presented. $\endgroup$ – Satwik Pasani May 27 '15 at 14:06
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    $\begingroup$ @SatwikPasani I'll read the article and add the explanation if it could be reliable. $\endgroup$ – Ilan May 27 '15 at 14:17

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