The Jocksin is, you know, it's one of those drugs that a lot of people have difficulty understanding.

And the main reason why students have a difficult time understanding the Jocksin is because of the potassium. It's very complicated where people trip themselves up and wonder

does hibokhelemia occur, does hyperkheliumia occur, which predisposes to the joxin toxicity.

So we're going to get into that right now and we're going to put up a couple of graphs to

show you exactly how the joxin works, but very simply the joxin is going to inhibit the sodium potassium atepase pump right so the

sodium atep a aptease pump inside the myocardial cells we're going to inhibit this and we're going to block this pump,

we're going to stop it from working. And what does this do? Well, we stop allowing the intracellular sodium,

meaning the sodium that's in the cell, we are not the

in the cellular sodium, meaning the sodium that's in the cell, we are not allowing it to leave the

cell, right? We're stopping this pump. This pump is an exchange between

potassium and sodium, it's stopping it from working, and we're not allowing

sodium to leave the cell, we're not allowing potassium to enter the cell.

So what does this do?

If the sodium cannot leave, it continues to build up, and we have high sodium within the cell.

We have high levels of potassium outside of the

out of the cell, right? So we have rising intracellular sodium,

and when we have this rise in intracellular sodium,

this eventually leads to a rise in intracellular calcium.

Remember, calcium is going to be responsible for

contractions of the heart, right? So if we have intracellular calcium that's rising,

we have increased contractions of the heart.

Remember, contractions of the heart, positive inotropic effect.

...