Digoxin Explained Clearly – Exam Practice Question

By Adem Lewis / in , , , , , , , , , , , , , , , , , , , , , , , , , , , /

well welcome to another MedCram lecture
with bored vitals question this question comes from the NA ple X question Bank
and the question is about digoxin so let’s get into it here a seventy year
old male with a history of diabetes GERD and COPD develops atrial fibrillation
with a rapid rate after cardioversion he begins treatment with digoxin which
of the following is true of treatment with digoxin select all that applied
there could be more than one or maybe just one so it’s basically true/false so
let’s just review briefly what it is that the johnson does so if you can
imagine a myocardial cell and as you recall in just about every cell of the
body there’s something called a sodium potassium ATPase and this is a enzyme
that is in the cell surface and basically what it does is it maintains
the fact that there’s a lot of potassium inside the cell and a lot of sodium
outside the cell so the way it does that is by pumping in potassium and pumping
out sodium so that’s what maintains this now interestingly what digoxin does is
it actually blocks that pump it slows it down so as a result of that sodium
starts to build up inside the cell relative to what it would be of course
there’s still a lot more outside the cell but sodium starts to build up
inside the cell and as it turns out there’s another way of sodium to get out
of that cell and that’s something called the sodium calcium exchanger so here
sodium can leave the cell in this direction and as a result of that what
comes in is calcium of course it’s two positive charges and
that increase in calcium because of this blockage of the sodium potassium ATP
leads to increase in inotrope e that just means the strength of contraction
so let’s go over this one more time so normally the ATPase this is an enzyme
that uses ATP pumps in potassium pumps out sodium however digoxin blocks this
or slows it down and as a result of that the amount of sodium leaving is slowed
down therefore the sodium concentration in
the cell increases and as a result of that goes down this concentration
gradient and at the same time brings in calcium increasing the calcium
concentration inside which leads to increased in a trophy so that’s how the
jocks in actually makes your heart beat stronger the other thing that digoxin
does is if you recall we’ve got the SA node here and we’ve got the AV node here
and those of course are connected and then you’ve got the hiss Purkinje system
this is the electrical conduction system of the heart these two areas here are
susceptible and are innervated by the vagus nerve and the digoxin levels or
digoxin actually stimulate the vagus nerve and up regulates it so as a result
of that you’ve got up regulation here of vagal stimulation using acetylcholine
and as a result of that it should slow down the SA node and also slow down the
AV node conduction especially apropos when you’ve got a situation here where
you have atrial fibrillation and all of these electrical conduction coming down
the AV node will slow down the conduction so you don’t have RvR or
rapid ventricular response so digoxin not only increases intracellular calcium
but it also improves vagal nerve stimulation which in fact slows the
heart rate down now as it turns out digoxin has a pretty
narrow therapeutic window what does that mean that means if we were to look at a
dose range of digoxin there would be a very small area where we would actually
get the good benefit of digoxin and if we went too high we would get
deleterious effects of the digoxin and if we went too low we would get not
enough concentration to do the things that we would want it to do so in other
words what we try to do is we try to get the concentration of the jocks in high
enough for it to work but not too high that it actually causes cardiac
arrhythmias that’s what we’ve referred to when we say that it has a very narrow
therapeutic window and exactly what is that therapeutic window well several
different publications and guidelines have said that that narrow therapeutic
window for congestive heart failure is 0.5 to
0.9 and this is of course in units of nanograms per milliliter so 0.5 0.9 is
that narrow therapeutic window that we’re looking at and this goes along
with the guidelines that are seen in up-to-date and also the American College
of Cardiology typically this can be achieved via intravenous loading or it
can be done by oral loading the key though that you’ve got to remember is
it’s typically about seven days until you get to steady states can be longer
in some cases but at least seven days is the key now as we mentioned this upper
limit of therapeutic window of 0.9 which is what we see right about here if we go
above that we can see things like arrhythmias
and the interesting thing about that is that having a low potassium can actually
increase that risk so what you have to do is if you have a low potassium is
you’ve got to watch this level very very carefully it doesn’t mean that you can’t
use the jock sin’ if you have hypokalemia it just means you have to
make sure that you’re not super therapeutic because the risk of
arrhythmias goes up in that sort of a situation the other thing that’s
interesting about digoxin itself is that when it’s ingested there are some
medications that can interact with it now there are of course like things like
amiodarone and verapamil which can increase the risk of arrhythmias but in
terms of medications for gastroesophageal reflux disease which
our patient has there can be interaction with digoxin now the one of the things
that I want you to be aware of is the difference between antacids
and actually medications like proton pump inhibitors now antacids neutralize
the stomach pH and that has the effect of increasing the pH in the stomach
proton pump inhibitors shut down the ability of your stomach to make acid by
blocking this proton pump and that also increases the pH the thing that’s
interesting though is that there’s actually differences in how this
interacts with digoxin and obviously it’s not through the pH a proton pump
inhibitor will actually increase the levels of digoxin because of drug
interaction however antacids because of what they contain and these are
over-the-counter antacids they can actually decrease the bioavailability of
the Jackson and so as a result of that you would have to take more digoxin to
compensate for the decreased bioavailability when taking antacids so
let’s go back to our question and as you can see we’ve got them correct here and
correct here let’s go through them though with a an oral
with the jocks and results in steady-state concentration in three to
four days actually that’s incorrect it’s more like seven to ten days be patients
who take antacids may require an increase in dosage that is correct we
actually just talked about that where there are actually things in the
antacids themselves that will reduce the bioavailability of digoxin the Jackson
has a broad therapeutic window that’s not the case it actually has a narrow
therapeutic window and specifically that narrow therapeutic window is 0.5 to 0.9
nanograms per ml and so that’s the second correct answer and we skip D and
let’s read D patients with hypokalemia should not take the jocks until the
serum potassium is normal well we know that hypokalemia can increase the
arrhythmia s’ti of digoxin it’s not a reason to not take the jock sin’ until
the level is normal we just need to watch and make sure that
the patient doesn’t become too high on the ditch levels so the answers here are
B and E well thanks for joining us

39 thoughts on “Digoxin Explained Clearly – Exam Practice Question

  1. Thank you so much for this video MedCram. There is just enough biochem so I understand Dig works along with why patient's have the side effects they do without confusing me. All of this had alluded me prior to viewing this video. Please continue the great work and any additional meds would be greatly appreciated!

  2. Just yesterday I was thinking why are there no new videos from your channel and that's when I found this. Your videos are the best I have come across. Please complete the series on antibiotics. And also if you can include the dosing in the treatment. Thanks a million!

  3. See more board questions like this one,
    and the complete library of MedCram videos at www.MedCram.com

  4. By the way you are the best!!! that is the best video/explanation on digoxin that I've ever seen/listened to

  5. I'm a pharmacy student and this video helped me a lot on understanding the mechanism of Dig .
    Thank you 😊

  6. There is an error in your explanation of the Ca/Na pump.
    The Calcium-Sodium exhanger pumps calcium OUT of the cell and sodium pumped IN to the cell. This pump is activated by low intracellular sodium. When Digoxin allosterically binds to the Na/K ATPase, it causes an increase in intracellular sodium levels (this part we agree on). This then would mean the Ca/Na exchanger would have to pump sodium against gradient from extracellular into the intracellular space that already has a high sodium content. This removes the driving force necessary for the Ca/Na pump to work and thus Calcium is not pumped out of the cell. This leaves more calcium available to increase contractility (useful in myocardium). Its nice to note also, Digitoxin while indicated for CHF really works for left ventricular failure and has minimal effect in the right.

  7. After watching several of your videos I have concluded it would be more efficient to just download from your knowledge; when completed the processes-there is your next million! How lucky students are to have this access – I can't thank you enough!!!

  8. Could you explain how you say Digoxin increases vagal activity? My understanding was digoxin increases phase 4 of the cardiac AP which shortens the AP. This decreases conduction velocity through the AV node and prolongs the AV nodal refractory period. This will help control the ventricular rate, especially useful in A-fib patients. I did not think that Digoxin had any direct effect on decreasing parasympathetic stimulation on the heart directly. Thanks.

  9. Na – K ATPase'ı inhibe ederek dolaylı yoldan hücre içine Ca girmesini sağlıyor canım Digoksin <3 Ca giren hücre de kasılıyor <3 Ca girince İNOTROPİ artıyor <3

  10. D should also be correct as digoxin binds to where K binds in the NaK ATPase protein, if you have hypokalemia it is VERY EASY to overdose on digoxin. .

  11. I feel like the A should be correct because they are usually given 1 to 2 loading dose or goal HR is achieved and E should not be correct due to Digoxin goal in AFib is 1.5 – 2.0 ng/mL and (0.5 -0.9 ng/mL is for Chronic Heart Failure patient). Could you please clarify? Thank you!

  12. Thanks again Dr. for video on Digoxin. Ur so SMART. You helped explain how it works, cause i take Digoxin(0.125mg) for my Heart Failure too. I'd learn alot.

  13. Love your videos!! I make my med videos on keynote… but I’m wondering what you use for your videos??

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