How digoxin cause hypokalemia ?

[DrXmIsH0]

digoxin will inhibit K Na pump --> more K outside the cell --> the kidney will excreat the increase of k --> long use of digoxin will cause hypokalemia -->depletion in potassium will cause high toxic levels of digoxin effect

thats what I think ,is it right or not ? 😛
whats the complication of long use of digoxin ?

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[Perrotfish]

Does it cause hypokalemia? I thought that hypokalemia causes digoxin toxicity, not the other way around.

 

[DrXmIsH0]

Does it cause hypokalemia? I thought that hypokalemia causes digoxin toxicity, not the other way around.

I Know 😀 but may be it couse hypkalemia as what I mention above

 

[phospho]

not that this has anything to do with this thread, but I think there was a serial killer nurse who used digoxin to kill his patients...

 

[Tygacil]

My understanding is that digoxin inhibits Na/K+ pumps, causing a buildup of sodium that can be used at a higher rate of exchange for Na/Ca pumps - extra influx of calcium means higher contractility (this leads to the ionotropic effect).

Hypokalemia means less potassium available for those na/k pumps along with the inhibition of dig leads to a greater effect. AFAIK digoxin itself does not cause hypokalemia.

hypercalcemia can do the same, but obviously from a different angle.

 

[Ableton]

My understanding is that digoxin inhibits Na/K+ pumps, causing a buildup of sodium that can be used at a higher rate of exchange for Na/Ca pumps - extra influx of calcium means higher contractility (this leads to the ionotropic effect).

Hypokalemia means less potassium available for those na/k pumps along with the inhibition of dig leads to a greater effect. AFAIK digoxin itself does not cause hypokalemia.

hypercalcemia can do the same, but obviously from a different angle.

You've got the direction of your pumps mixed up. Digoxin inhibits Na/K-ATPase (normally moves 3 Na out, 2 K in), which results in high intracellular Na that indirectly inhibits the Na/Ca exchanger (normally moves Na in, Ca out). The end result is a buildup of intracellular Ca which can be used in the next contraction cycle to increase contractility. The Na/Ca exchanger is indirectly inhibited, not stimulated.

As for digoxin causing hypokalemia, I don't think that's the case. I think hypokalemia just predisposes to digoxin toxicity, since it competes with potassium for the same binding site.

 

[RySerr21]

digoxin will inhibit K Na pump --> more K outside the cell --> the kidney will excreat the increase of k --> long use of digoxin will cause hypokalemia -->depletion in potassium will cause high toxic levels of digoxin effect

thats what I think ,is it right or not ? 😛
whats the complication of long use of digoxin ?

it seems that hypokalemia is a complication when taking digoxin in that it lowers the levels that the drug will become toxic.

" Several factors (such as hypokalemia) can predispose to toxicity at levels below 2 ng/mL (2.6 nmol/L), which is usually considered the upper limit of normal. "

The reason is that hypokalemia will decrease Na/K pump activity on its own, but then you are giving them digoxin which will potentiate that effect so it takes less for the drug to do some serious damage.

 

[DrXmIsH0]

not that this has anything to do with this thread, but I think there was a serial killer nurse who used digoxin to kill his patients...

I wanna kill this nurse 😡

You've got the direction of your pumps mixed up. Digoxin inhibits Na/K-ATPase (normally moves 3 Na out, 2 K in), which results in high intracellular Na that indirectly inhibits the Na/Ca exchanger (normally moves Na in, Ca out). The end result is a buildup of intracellular Ca which can be used in the next contraction cycle to increase contractility. The Na/Ca exchanger is indirectly inhibited, not stimulated.

As for digoxin causing hypokalemia, I don't think that's the case. I think hypokalemia just predisposes to digoxin toxicity, since it competes with potassium for the same binding site.

it seems that hypokalemia is a complication when taking digoxin in that it lowers the levels that the drug will become toxic.

" Several factors (such as hypokalemia) can predispose to toxicity at levels below 2 ng/mL (2.6 nmol/L), which is usually considered the upper limit of normal. "

The reason is that hypokalemia will decrease Na/K pump activity on its own, but then you are giving them digoxin which will potentiate that effect so it takes less for the drug to do some serious damage.

Thanks Alot I mixed up 😛

 

[engineeredout]

I wanna kill this nurse 😡

You're gonna use digoxin?

 

[dienekes88]

You've got the direction of your pumps mixed up. Digoxin inhibits Na/K-ATPase (normally moves 3 Na out, 2 K in), which results in high intracellular Na that indirectly inhibits the Na/Ca exchanger (normally moves Na in, Ca out). The end result is a buildup of intracellular Ca which can be used in the next contraction cycle to increase contractility. The Na/Ca exchanger is indirectly inhibited, not stimulated.

As for digoxin causing hypokalemia, I don't think that's the case. I think hypokalemia just predisposes to digoxin toxicity, since it competes with potassium for the same binding site.

That is also my understanding.

Digoxin actually causes hyperkalemia.

Potential treatments... charcoal if recent, insulin/glucose/beta-agonist/HCO3- to drive K+ intracellularly, diuretics, Dig-Fab fragments.

 

[Laryngophed]

That is also my understanding.

Digoxin actually causes hyperkalemia.

Potential treatments... charcoal if recent, insulin/glucose/beta-agonist/HCO3- to drive K+ intracellularly, diuretics, Dig-Fab fragments.

Dialysis too? 😕

 

[Speculatrix]

Dialysis too? 😕

Yes, but obviously depends on the severity of the electrolyte disturbances. Why would you dialyze someone who responded to more conservative measures and digifab/digibind?

 

[Laryngophed]

Yes, but obviously depends on the severity of the electrolyte disturbances. Why would you dialyze someone who responded to more conservative measures and digifab/digibind?

Wouldn't that depend on the degree of responsiveness and just how far away from the desired end-point they were? I wouldn't just dialyze someone who responded but I would think it'd be on my short list of stuff-to-do if the hyperkalemia didn't come back down to Earth in a reasonable time-frame.

 

[dienekes88]

Wouldn't that depend on the degree of responsiveness and just how far away from the desired end-point they were? I wouldn't just dialyze someone who responded but I would think it'd be on my short list of stuff-to-do if the hyperkalemia didn't come back down to Earth in a reasonable time-frame.

As I understand it, dialysis would only be added on in a patient with concurrent kidney failure.

Regarding dialysis for treatment of hyperkalemia in a patient with adequate kidney function... well, dialysis ain't exactly a party. There are potential complications of the access technique (obviously it'd be too late to get an A-V fistula going with the hope of arterializing the vein) including stenosis. Also, if it's a graft, I think you need a vascular surgeon and an OR. It'd probably only happen if conservative management failed.

It'd be on "the short list of stuff-to-do if the hyperkalemia didn't come back down to Earth in a reasonable time frame." So it'd be on the short list assuming conservative management failed. Why assume that conservative management will fail?

Side note: this is just what I remember from a conversation after a discussion section in the renal section (months ago). Can't for the life of me remember why Digoxin came up. There was something about Calcium being contraindicated in Dig toxicity too.

ETA: Uptodate says concurrent renal failure, and hemodialysis doesn't help with the dig part.

 

[Speculatrix]

Wouldn't that depend on the degree of responsiveness and just how far away from the desired end-point they were? I wouldn't just dialyze someone who responded but I would think it'd be on my short list of stuff-to-do if the hyperkalemia didn't come back down to Earth in a reasonable time-frame.

Dig toxicity tends to respond to conservative measures from what I have seen. Anyway, you can also obtain EKG's to assess severity. Also it is a completely different situation if someone has been living with a K of 5.5+ than a more acute onset.

Also, the dialysis would be for the electrolyte disturbances and not to clear the dig. Obtaining access can be a nightmare. Think of your AEIOU mnemonic for dialysis, but this is vague enough to keep nephrologists gainfully employed to consult 🙂

 

[obiwan]

as far as dialysis for something like electrolytes issues, you will put in basically a large central line like quintin catheter so you're not messing around with fistulas and stuff for chronic HD

 

[cpants]

That is also my understanding.

Digoxin actually causes hyperkalemia.

Potential treatments... charcoal if recent, insulin/glucose/beta-agonist/HCO3- to drive K+ intracellularly, diuretics, Dig-Fab fragments.

Don't forget STAT EKG and Ca-gluconate before those other things you mentioned. Also make sure you check to see if the specimen was hemolyzed before you start messing with the guy's lytes.

as far as dialysis for something like electrolytes issues, you will put in basically a large central line like quintin catheter so you're not messing around with fistulas and stuff for chronic HD

Yeah, in a good hospital, you can have dialysis running within an hour or two.

 

[richse]

You've got the direction of your pumps mixed up. Digoxin inhibits Na/K-ATPase (normally moves 3 Na out, 2 K in), which results in high intracellular Na that indirectly inhibits the Na/Ca exchanger (normally moves Na in, Ca out). The end result is a buildup of intracellular Ca which can be used in the next contraction cycle to increase contractility. The Na/Ca exchanger is indirectly inhibited, not stimulated.

As for digoxin causing hypokalemia, I don't think that's the case. I think hypokalemia just predisposes to digoxin toxicity, since it competes with potassium for the same binding site.

Wouldn't the constant increase in [Ca] cause a reduction in the contractility because there would be less of a gradient for Ca influx during the action potential? This is what we seem to be learning at the moment anyway (similar to the way Beta1 agonists cause increased Ca influx but also faster Ca clearance from the cytosol).

 

[Scottish Chap]

That is also my understanding.

Digoxin actually causes hyperkalemia.

Potential treatments... charcoal if recent, insulin/glucose/beta-agonist/HCO3- to drive K+ intracellularly, diuretics, Dig-Fab fragments.

This is what you generally worry about - hyperkalemia, not hypokalemia. You can explain anything by esoteric physiology, but you have to keep it simple and that usually means understanding the common things you'll see on the wards. Digoxin binds to the K+ site of the K+/Na+-ATPase, which normally shuttles K+ into cells and Na+ out. Too much digoxin, and you end up with hyperkalemia as less K+ is shuttled into cells. This is one reason why we need to monitor dig levels.....