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Hello everyone,
I finally got my head around the concept of coductance and read that hyperkalemia induces an increase in potassium conductance so you end up with a faster repolarization and hence the peaked T waves. At the same time, hypokalemia induces a decrease in potassium conductance and traps potassium in the cardiac cells making them depolarized and increasing the action potential duration and hence the prolonged QT interval.
Now I'm back to my kaplan pharm lect note and I read this in the antiarrhythmic chapter:
Hyperkalemia inhances the effects of Quinidine
As far as I know, Quinidine blocks the sodium channels of phase 0 and also blocks potassium channels of phase 3 so it increases the action potential duration and you endup with a prolonged QT interval much like hypokalemia
Could some one please clarify this for me I have put so much time and effort to understand this for kaplan to throw it in my face like that.
I finally got my head around the concept of coductance and read that hyperkalemia induces an increase in potassium conductance so you end up with a faster repolarization and hence the peaked T waves. At the same time, hypokalemia induces a decrease in potassium conductance and traps potassium in the cardiac cells making them depolarized and increasing the action potential duration and hence the prolonged QT interval.
Now I'm back to my kaplan pharm lect note and I read this in the antiarrhythmic chapter:
Hyperkalemia inhances the effects of Quinidine
As far as I know, Quinidine blocks the sodium channels of phase 0 and also blocks potassium channels of phase 3 so it increases the action potential duration and you endup with a prolonged QT interval much like hypokalemia
Could some one please clarify this for me I have put so much time and effort to understand this for kaplan to throw it in my face like that.