Digoxin

I don't know, but the first one is possible and the second one isn't. If a cation like k+ is entering, some other cation(s) is/are leaving to maintain electrical balance (equal out the charges).

The main thing I now about digoxin is to withhold it if the apical pulse is under 60.

As you know, digoxin slows down the heart rate. The drug books will tell you that hypokalemia can lead to digoxin toxicity...digoxin slows down the release of potassium into your muscles - which somehow interacts with calcium, which goes on to produce a muscle contraction - in this case heart beat. I'm fuzzy on all the specific sodium/potassium pump/sarcoplasm(sp)/cross bridges thing...but in general, my explanation is a fair 'high level' version:)

Dig inhibits the enzyme (sodium-potassium ATPase) that regulates entry of K, Na and Ca into the heart's muscles..This will increase the amount of Ca inside the heart's cells, but then reduces the level of K inside the cells

I saw your post and remembered I had trouble visualizing how this works when I took pharmacology for my masters program. So I found the notes I made and hopefully it will help you better understand this too.

The inihibition of the Na+/K+ ATPase induces a rise in intracellular cardiac Na+, causing an increase in intercellular Ca++, via the sodium-calcium exhanger. The sodium-calcium exchanger is particularly active in myocardial smooth vascular muscle. The increase in Ca++ increases the force of contraction of the heart and contraction of smooth vascular muscles.

So basically, you inhibit the sodium/potassium pump with digoxin, and have all this sodium inside the cell, which then causes another pump (the sodium/calcium exchanger) to pump sodium out and bring in calcium. There is now more calcium available inside the cell, which increases the force of heart contractions and improves cardiac output.

As far a potassium, if I remember correctly, potassium and digoxin bind to the same ATPase (enzyme), and will compete with each other. So if you have a low serum potassium, digoxin will be more active and could produce toxicity. Therefore, keeping potassium levels normal or slightly high will prevent this. Also, digoxin toxicity can be alleviated by giving potassium to prevent digoxin from binding to the ATPase.

Hope this helps.

Thanks everyone! :heartbeat

All the info was very helpful.

I saw your post and remembered I had trouble visualizing how this works when I took pharmacology for my masters program. So I found the notes I made and hopefully it will help you better understand this too.

The inihibition of the Na+/K+ ATPase induces a rise in intracellular cardiac Na+, causing an increase in intercellular Ca++, via the sodium-calcium exhanger. The sodium-calcium exchanger is particularly active in myocardial smooth vascular muscle. The increase in Ca++ increases the force of contraction of the heart and contraction of smooth vascular muscles.

So basically, you inhibit the sodium/potassium pump with digoxin, and have all this sodium inside the cell, which then causes another pump (the sodium/calcium exchanger) to pump sodium out and bring in calcium. There is now more calcium available inside the cell, which increases the force of heart contractions and improves cardiac output.

As far a potassium, if I remember correctly, potassium and digoxin bind to the same ATPase (enzyme), and will compete with each other. So if you have a low serum potassium, digoxin will be more active and could produce toxicity. Therefore, keeping potassium levels normal or slightly high will prevent this. Also, digoxin toxicity can be alleviated by giving potassium to prevent digoxin from binding to the ATPase.

Hope this helps.

This is exactly how it was explained to us and also if you have hyperkalemia you can not get a therapeutic level of Digoxin for the same reason.