Hey, hey, it's Medicosis Perfectionatus, where medicine makes perfect sense. We continue our medical mnemonics playlist. Today's topic is digoxin mnemonic. As you know, digoxin belongs to a class of medications known as cardiac glycosides, aka digitalis. This digitalis has three subtypes, three members in that group.
Member number one, digoxin. Member two, digitoxin. And number three is Wabain. Hi, Medico Sassa. Why do doctors give digoxin?
Two reasons. Number one, to boost your cardiac contractility, to make your heart contract harder. And this is important. Why?
Because some patients have congestive heart failure. When your heart fails to pump, it's time to boost the pump by giving digoxin. Reason number two, digoxin can increase the refractory period at the atrioventricular node.
What the flip does that mean? It means it delays the conduction in the AV node, which can lower your heart rate. Oh, so if the patient suffers from palpitations, arrhythmia, especially tachyarrhythmia, such as supraventricular tachycardia, we can give digoxin to slow the heart down.
So digoxin has two purposes. I can boost cardiac contractility, or I can delay. cardiac conductivity that was neat okay medicosis since the junction boosts cardiac conductivity we can use it in congestive heart failure right that's true but hey medicosis we have two types of heart failure there is failure during systole and there is failure of diastole which one should we use the junction in you should use the junction in systolic failure when the heart fails to contract, fails systole, because when the heart fails contraction, it's time to give a drug to boost contraction. Oh, that actually makes sense. Conversely, what kinds of supraventricular arrhythmias do we use in?
We have atrial fibrillation, we have atrial flutter, we have paroxysmal supraventricular tachycardia. Can we use the toxin in these arrhythmias? The answer is yes.
How about Wolff-Parkinson-White syndrome, which is an AVRT. No, never use the doxin in Wolff-Parkinson-White syndrome. Why not, medicosis?
Well, let's go back to square one and understand what Wolff-Parkinson-White syndrome is. In WPW, you have an accessory pathway, which is not normal, because normally the impulse should start here in the pacemaker, which is the SA node. The impulse should go to the AV node, and then the AV node will give it to both ventricles.
But... In Wolff-Parkinson-White syndrome, we will bypass the normal path, and the impulse will go from the SA node straight to the ventricles. This accessory pathway is faster than the natural path.
Oh, that's dangerous. That's why it's a tacky arrhythmia, because it's faster. All right, why can't I use digoxin then? Because digoxin delays the AV node, which makes it even slower.
then the faster accessory path and the accessory fibers are getting the impulse even faster from the SA node to the ventricle, you will worsen the tachyarrhythmia freaking doofus. So if the patient has Wolff-Parkinson-White syndrome, you are not allowed to give any drug that slows the AV node. Okay, Medicosus, tell me what are these drugs that slow the AV nodal conduction and therefore contraindicated in Wolff-Parkinson-White syndrome. Are you ready? A, B, C, D. A, adenosine is contraindicated.
B, beta blockers. The C, calcium channel blockers. And the D is the freaking digoxin.
Do not use any of these in Wolff-Parkinson-White syndrome. What should I use then? Slow down the ventricles.
Oh, whether you're coming on the normal path or the abnormal path, I can slow the ventricles either way. Yes, how do I slow the ventricles? Class 1A or class 3 antiarrhythmics. sodium channel blockers or potassium channel blockers.
See, medicine makes so much sense once you understand what the flip you're talking about. Let's talk about the action potential inside the ventricle muscles. All right, I did not say inside the SA node or AV node.
I said inside the ventricle muscles. All right, you have phase 0, phase 1, phase 2, phase 3, back to phase 4 on the floor. Who's responsible for phase zero?
Rapid sodium influx into the cardiac myocyte. What does digoxin do? Digoxin will slow this down. Decrease sodium entry? That's true.
Decrease the slope of the action potential? Yes. Slope of phase zero will go down, less deep. polarization, less activation of the ventricles.
However, when you decrease the conduction velocity too much, this can increase my risk of re-entrant arrhythmias, especially if digoxin works on some of the fibers, leaving others uninhibited. Now take a deep breath because we are switching topics. Now I'll tell you why digoxin boosts cardiac contractility. because the dioxin inhibits the sodium potassium primary 80 pace pump when you block this sodium will not leave and potassium will not enter okay when sodium cannot leave where do you think sodium accumulates it accumulates inside all right you have too much positive inside all right if there is too much sodium inside do you think the secondary active transporter will work no for two reasons number one secondary was dependent on the primary you inhibited the primary of course the secondary will suffer. Reason number two, you already have too much sodium in because you inhibited the primary.
When you have too much sodium in, I cannot pump more sodium in and therefore I cannot pump calcium out either because this exchanger is also toast. When calcium cannot leave, calcium will stay inside the cardiac myocyte. Hashtag calcium induced calcium release from the sarcoplasmic reticulum. calcium will make actin and myosin hug and kiss each other. Hashtag increased cardiac contractility.
And now to my digoxin mnemonic. Digoxin, digitalis, digitoxin, all of them have the D in them. So what's the mechanism of action? I destroy the sodium potassium ATPase. I destroy the primary pump.
And that's why the secondary exchanger is not going to work either. All right, what's going to happen? I am gonna deprive calcium from its ability to leave the cardiac myocyte.
Calcium will stay inside the myocyte, driving and boosting the cardiac contractility. Okay. I also delay the conduction of the AV node.
I slow the heart rate. I decrease the ventricular rate. But be very careful in Wolff-Parkinson-White syndrome, because I stopped and slowed down the normal path even more, leaving you only with the crazy fast.
Accessory pathway. I am a drug that requires loading dose. I have a large volume of distribution, and that's why I'm easily displaced by other drugs, because I bind hard to plasma proteins, and all of your tissue proteins for that matter. So other drugs can kick my butt. I have a delayed onset of action, therefore if the patient has acute heart failure, I'm gonna give deduction now, I'm gonna save his life.
It's not gonna happen. I am delayed slow to action. I'm good for chronic use, but not for the acute one. What should I do then?
Give dobutamine. Dobutamine is fast. Does digoxin lower mortality for CHF patients?
The answer is not. How about lowering mortality in patients with MI? The answer is also no.
It improves symptoms, but it does not lower mortality and it does not increase survival or longevity. Digoxin is a dangerous drug in general. Why?
Narrow therapeutic window with low safety margin. particularly if you have Wold Parkinson's-White syndrome. Side effects of digoxin, disorientation, visual disturbance, and you will see yellow-green halos, and as you know, green in French is verd, in German it's vert.
That's why we have Billy Verden. That's why we have very dense group of streptococci. See?
Medicine makes so much sense. I can also depress your ST segment and decrease the QT interval on EKG. all right menikosis my patient is suffering from the joxon toxicity how can i save the day give the antidote what's the antidote for the dixin digi bind which is going to bind the joxon these are antibodies against the joxon anti-dijoxin fragment antibodies oh and when you bind the joxon it will not be able to work and you will decrease its toxicity until your body eliminates the drug Okay, Metacosis, you told us that we should use it for CHF. Which type of CHF?
Only where there is decreased ejection fraction. This is the systolic failure. But you should not use digoxin if the ejection fraction is preserved.
Hi, Metacosis, there were so many Ds in your slide. Can you just summarize it? Tell us what's the most important.
All right, it destroys the sodium potassium ATPase and the secondary will not work. It drives the pump forwards, i.e. increases contractility. It delays the avian conduction, i.e. decreases conductivity and decreases heart rate, it does not lower mortality to treat its toxicity.
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