Explanation of ECG in MI using an electrostatic model
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. 



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.