Arrythmias

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maninthemirror

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Two questions. If you can answer either or both, much appreciated.

1) What is the mechanism by which digoxin cases hypokalemia?

2) Why does hypokalemia and/or hypomagnesia put you at a risk for Torsades de Pointes?

Thanks.
 
1. inhibits NaKATPase
2. prolongs repolarization, phase 3 and 4 I think, bigger window for EAD to occur and induce a triggered arrhythmia. Torsades is actually a reentry arrhythmia after the EAD is triggered.
 
I'm only an M1 and don't have a pharm/pathophys background, but why would digoxin cause hypokalemia? My understanding is that, if anything, it would cause hyperkalemia by inhibiting the Na+/K+ ATPase and preventing re-uptake of K+ into the cell.
 
Hypokalemia can increase digoxin toxicity since potassium and digoxin compete for the same binding site on the sodium/potassium pump, but it does not cause hypokalemia as far as I know.
 
It can cause diarrhea. That could cause hypokalemia...
 
Hypokalemia can increase digoxin toxicity since potassium and digoxin compete for the same binding site on the sodium/potassium pump, but it does not cause hypokalemia as far as I know.

this..

Also, does anyone know the mechanism of increased digoxin toxicity in hypomagnesia?
 
this..

Also, does anyone know the mechanism of increased digoxin toxicity in hypomagnesia?
My guess would be that, since ATP must be bound to Mg2+ in order to be biologically active, hypomagnesemia would also inhibit the Na/K pump activity (by decreasing the stores of biologically active ATP). That, combined with digoxin's inhibition of the Na/K pump, would result in increased toxicity.
 
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