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Hey what’s going on guys and in today’s video we’re going to be answering a reader’s question regarding digoxin and the mechanism of action in atrial fibrillation now before we get into the question i want to get gout for just one second so if you bear with me for 30 seconds i just want to say how excited i am how happy i am i was able to get the new macbook pro i
Thought that because i’m gonna be doing these videos more frequently especially in the month of february i needed something with a little bit more power and i’m i’m a huge apple i’m a huge apple product kind of guy so very excited to be playing around with this so much more powerful my last macbook was i don’t know six seven years old so there’s definitely time for
An upgrade especially when working on these videos so that’s my twenty-second geek out moment now today we’re gonna be answering a question regarding digoxin and this is gonna be from james he’s one of the one of our readers and his question is specifically regarding its mechanism of action with atrial fibrillation so this is his question he asks hi andrew thanks
For your continued efforts in educating the medical practitioners you reach in this forum one question relating here digoxin presentation this is an email that i sent out maybe a week or two ago discussing the mechanism of action but i focused more on its chf effects on its positive inotropic effect and he said you describe the jaques enzyme entropic activity
But how does it work in atrial fibrillation when this is used so a couple of things that i first want to talk about before getting into the mechanism of action with digoxin digoxin is by no means used first-line the dachshund is used as an adjunctive medication when the first-line therapies don’t work so first-line therapies calcium channel blockers beta blockers
This is gonna be first-line now when we’re discussing calcium channel blockers we’re talking about that non dihydropyridine verapamil diltiazem verapamil diltiazem beta blockers these are going to be first-line medications these these are the medications we’re gonna be for rate control when we’re a control patients with atrial fibrillation we’re separating them
Into two types of or two two subsets i should say those that are asymptomatic and those that are symptomatic the asymptomatic patients right the patients who don’t have chest pain who don’t have shortness of breath the patients who feel just fine but have atrial fibrillation we can ray control those patients to less than 110 less than 110 beats per minute the
Patients that are symptomatic they do have symptoms we want to ray control these patients to less than 85 beats per minutes so very quickly first-line atrial fibrillation rate control beta blockers calcium channel blockers specifically verapamil diltiazem second we separate by symptomatic versus asymptomatic these symptomatic patients we are ray controlling to
Less than 85 the asymptomatic i feel just great but i have atrial fibrillation we’re going less than 110 beats per minute now if these medications fail to rate control or we have a comorbidity and we’re going to be using the docs in any way for congestive heart failure then we can consider the jock suit for a control for atrial fibrillation rate control right now
Very quickly how does the jocks in work remember the jocks and acts on the sodium-potassium atpase pump right when it acts on this pump we have a rise in intracellular sodium and then we have the sodium calcium exchanger the sodium calcium exchanger when we have a rise in sodium we then have a rise in calcium right what happens when we have a rise in calcium we
Have depolarization of the myocytes of the pacemaker in the av node we have prolongation of this action potential that occurs in the myocardial cells so what are we doing we’re increasing the length of the action potential and slowing down depolarization of these pacemaker cells of these pacemaker cells down the av node and reducing ventricular rate the johnson
Also works in the setting by inhibiting av node conduction via vagal tone this means that when we have more sympathetic tone for example when we’re exercising we’re running lifting weights digoxin is not going to be as effective so it’s affecting or it’s it’s affecting the av node via vagal tone it’s also increasing the action potential it’s increasing or it’s
Prolonging the depolarization of the pacemaker cells in the av node so it’s slowing down conduction via the av node very important to note though the jaques and only works for rate control it slows the heart down but it cannot convert to sinus rhythm it will do nothing for the actual rhythm right it’s not getting rid of atrial fibrillation we’re simply using it
To rate control with that said the majority of patients are still going to need a calcium channel blocker or a beta blocker the majority patients will not be adequately rate controlled with the jocks and alone right so very quickly we have the sodium potassium atpase we have an intra we have a rise in intracellular sodium this then causes an arising intracellular
Calcium this is intracellular calcium causes contractions this is how it’s beneficial in chf because we have increased contractions we have a positive inotropic effect it allows the heart to pump more and buy more i simply mean it doesn’t mean it pumps faster it increases the force of the contractions this is beneficial and symptoms only does not decrease mortality
And actually there have been some studies when we are using the g oxen for atrial fibrillation that shows that we can have increased mortality in patients now this is controversial some studies say yes there might be an increased increased incidence of mortality when used for atrial fibrillation some studies say no the studies that do indicate that there’s a
Possible increase in mortality the mechanism is completely unclear so this is controversial it might be related i was doing some reading it might be related to the increased serum levels of the jock sin’ but it’s unclear speaking of serum levels of the jock sin’ the digoxin level does not correlate to the ventricular rate so we don’t want to use serve the toxin
Levels as a way to measure titration for atrial fibrillation right we don’t want to do that the only reason or the only benefit for measuring serum digoxin levels is to avoid toxicity so if we have very very low serum digoxin levels and we’re not adequately rate controlled then we can consider increasing the rate because we know we’re not at increased risk for
Added toxicity now what can be a sign of the jaques and toxicity when we have a junctional rhythm so we have these periodic junctional rhythms this can be an indication that we have the jaques and toxicity one little caveat though before i let you go is a junctional escape beat alright so if we have an escape beat a junctional escape beat this is normal and this
Is often seen patients with digoxin this does not mean we have toxicity it’s when we have more than an escape beat now we have eight junctional rhythm this is an indication that we might have digitoxin ii so i hope this makes it clear it does the same increases sodium increases calcium and this is going to prolong the action potential depolarization which is going
To slow the heart down it also acts via vagal tone so this also means that if the patient is exercising the jock sense probably not going to be all that useful so i hope this was beneficial like i said starting in february we’re gonna be doing these videos monday through friday if you have any questions for me if you like clarification advice you know i get emails
Regarding finding jobs things of that nature anything at all send an email to andrew a physician assistant boards comm more than happy to answer any questions i’m here to help however i can you can also check out the website physician assistant boards calm where i try and post different articles different videos podcasts though anyway this concludes today’s episode
This will be live tomorrow which will be january 20th i hope everyone had a great new year until next time have a great day
Transcribed from video
Digoxin's mechanism of action when used for AFIB By Medgeeks