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?
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?
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.
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 :)