qq1 - 2confused2bdoctor

[ArchivalUser]

guys distal to occlusion tissue is dead . i dont think the answer so far posted is right

[ArchivalUser]

Increased interstitial K+ conc from infarcted area sure can have impact on adjacent non-infarcted areas. That's a contribution to infarction-induced arrhythmias.

[ArchivalUser]

but he is asking abt flow deprived region

[ArchivalUser]

The hyperK is from the flow-deprived region, bt the q didn't ask wht that does to the flow-deprived region, it's just asking what the hyperK does.

[ArchivalUser]

The answer is C. With an accumulation of extracellular potassium, the transmembrane
potential will become less negative. Interstitial potassium is elevated because of Na+/K+-
ATPase pump hypoxic failure. Choice A is incorrect because elevation of extracellular
potassium (via the Nernst equation) will partially depolarize the resting membrane potential,
thereby decreasing phase 0 amplitude and decreasing the conduction velocity.
Choice B is incorrect because repolarization of myocardial cells requires potassium extrusion
from the interior of the cell. This is more difficult with elevated extracellular
potassium. Choice D is incorrect because automaticity (firing frequency) is related to
the time to reach threshold potential, which is decreased in the less negative cells closer
to their threshold potential. Choice E is incorrect because a decrease in ventricular
muscle conduction velocity will increase the likelihood of reentry dysrhythmias.