what conclusion should the nurse draw when a clients digoxin level is reported to be 2.2 ng/ml? This is a topic that many people are looking for. bluevelvetrestaurant.com is a channel providing useful information about learning, life, digital marketing and online courses …. it will help you have an overview and solid multi-faceted knowledge . Today, bluevelvetrestaurant.com would like to introduce to you Digoxin Explained Clearly – Exam Practice Question. Following along are instructions in the video below:
Welcome to another medcram lecture with bored vitals question. This question comes from the na na ple x. Question.
Bank and the question is about digoxin. So lets get 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 its basically true false.
So lets 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.
Theres 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 theres 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 thats 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. Theres still a lot more outside the cell. But sodium starts to build up inside the cell and as it turns out theres another way of sodium to get out of that cell.
And thats 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.
Its 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 lets 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 thats how the jocks in actually makes your heart beat stronger. The other thing that digoxin does is if you recall weve got the sa node here and weve got the av node here and those of course are connected and then youve 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 youve 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 youve 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 dont 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. Thats what weve referred to when we say that it has a very narrow therapeutic window.
What is that therapeutic window well several different publications and. Guidelines have said that that narrow therapeutic window for. Congestive heart failure is.
05 to. 09 and this is of course in units of nanograms. Per milliliter so.
05. 09. Is that narrow therapeutic window that were 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 youve got to remember is its 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 09. 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 youve got to watch this level.
Very very carefully it doesnt mean that you cant use the jock sin. If you have hypokalemia. It just means you have to make sure that youre not super therapeutic because the risk of arrhythmias goes up in that sort of a situation.
The other thing. Thats interesting about digoxin itself is that when its 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 thats interesting though is that theres actually differences in how this interacts with digoxin and obviously.
Its 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 lets go back to our question. And as you can see weve got them correct.
Here and correct here. Lets go through them. Though with a an oral with the jocks and results in steady state concentration in three to four days actually thats incorrect.
Its 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.
Thats not the case. It actually has a narrow therapeutic window and specifically that narrow therapeutic window is. 05 to 09.
Nanograms per ml. And so thats the second correct. Answer.
And we skip d. And lets 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 sti of digoxin. Its 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 doesnt become too high on the ditch levels. So. The answers here are b.
And e well thanks for joining us. .
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