I have read in many sources that ischemia-induced depolarization is due to the opening of ATP-sensitive potassium channels and inactivation of Na/K exchangers [1,2]. However, K-atp channels are inward-rectifiers and their extensive opening should cause extracellular hypokalemia besides the fact that in low [ATP]i during ischemia, Mg++ ions are free (not complexed with ATP), and magnesium ions are outward potassium current blockers (i,e, they increase the rectifying power of k-atp, Kir, K-Ach channels)[3,4]. this would cause extracellular hypokalemic depolarization. What is the source of hyperkalemia then?
Inward-rectifying means positive current passes more easily in the inward direction, however it won't flow differently than the membrane voltage and reversal potential dictate. See for example https://en.m.wikipedia.org/wiki/Inward-rectifier_potassium_channel
The only time you'll have potassium flowing in to a cell, rather than out, is if the cell is very hyperpolarized, beyond the reversal potential for potassium, which is more negative than the resting potential.
Open potassium channels will almost always reduce intracellular potassium concentration as potassium flows out of the cell. Without ATP to fuel the sodium-potassium pump, there's no way to restore the lost potassium.
The existence of a negative resting membrane potential is due to relative concentrations of potassium (high inside cells) and the existence of primarily potassium conductance in the membrane, which means a few positive ions leak out to make the inside negative. If you don't maintain that concentration gradient, the cell is going to depolarize.