p53
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Facts from 'Kaplan Lecture Notes: Physiology':
Fact #1. In hyperkalemia increased extracellular potassium ions will reduce the efflux of the potassium ions from the cell or even create an influx of potassium ions, the net result of which will be depollarisation.
Fact #2. In acidosis H+ will enter the cell and K+ will leave it to maintain equilibrium inside the cell, creating hyperkalemia.
My first question: hyperkalemia due to acidosis will also cause depollarisation and hyperexcitability according to fact #1, or hyperkalemia due to acidosis is different in this respect from hyperkalemias due to other causes? in acidosis K+ already left the cell and this was the cause of hyperkalemia, why it will go back to cause depollarisation?
Now, fact from Katzung's 'Basic and Cilical Pharmacology': The effects of changes in serum potassium on cardiac action potential duration, pacemaker rate, and arrhythmias can appear somewhat paradoxical if changes are predicted based solely on a consideration of changes in the potassium electrochemical gradient. In the heart, however, changes in serum potassium concentration have an additional effect to alter potassium conductance (increased extracellular potassium increases potassium conductance) independent of simple changes in electrochemical driving force, and this effect often predominates. As a result, the actual observed effects of hyperkalemia include reduced action potential duration, slowed conduction, decreased pacemaker rate, and decreased pacemaker arrhythmogenesis. and vice versa.
My Second question: to recapitulate my first question, what would be the effect of hyperkalemia due to acidosis on cardiac cell excitability, i.e. arrhythmogenesis?
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| ssrpk
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well, i think you are mixing two concepts here, despite the fact that individually they are perfect!
First of all realize, whenever acidosis occurs, it's true that K+ will be shifted to ECF in order to maintain electrical neutrality however, that would'nt necessarily lead to hyperkalemia, as K+ is tightly controlled by RAA therefore if kidney's are working fine then no matter what type of acidosis it is, there should'ne be enough accumulatrion of K+ ions in the ECF so as to constitute hyperkalemia and it's subsequent effect on RMP. [Developement of hyperkalemia depends upon renal handling of K+, primarily]
Second, in case of acidosis, if however somehow hyperkalemia develops (due to some other contributory factors), then it would have arrythmogenic effects on the heart (again not due to acidosis but due to high K+) which could be quite varied (bradyarrythmias, heart block etc.)
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| mildus
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thanks ssrpk, it's a nice explanation
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| p53
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Thank you, ssrpk, for your explanation, but I still have some doubts.
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| waqastariq
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good explanation...I was goin to write the same..
just a simple point here...
shifting of ions from one compartment to other in case of acidosis not that LARGE so it can be easily compensated by kidneys...only a small amount of H ions move inside to move K out  tc
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