05-17-2008, 11:28 AM
guys distal to occlusion tissue is dead . i dont think the answer so far posted is right
qq1 - 2confused2bdoctor
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05-17-2008, 11:28 AM
guys distal to occlusion tissue is dead . i dont think the answer so far posted is right
05-17-2008, 11:33 AM
Increased interstitial K+ conc from infarcted area sure can have impact on adjacent non-infarcted areas. That's a contribution to infarction-induced arrhythmias.
05-17-2008, 11:34 AM
but he is asking abt flow deprived region
05-17-2008, 11:37 AM
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.
05-17-2008, 11:49 AM
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. |
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