Tachycardia: Atrial Fibrillation: Treatment

by Carlo Raj, MD

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    00:00 Atrial fibrillation, you want to control that rate. You want to control that rhythm and decreased risk of embolic stroke. That is your objective for management. Is that clear? When you do these, then for the most part, you should be able to manage your patient effectively. How do you control the rate? Slow down the cardiac rate by maybe digoxin.

    00:22 Hold on. Now what you know conventionally for digoxin is a positive inotrophic agent.

    00:31 Think about what I just said here. A positive inotrophic agent in this step of setting would make no sense. Because if there was an atrial fibrillation with increased heart rate, what does that mean to give a positive inotrophic agent? Is that why you have given dig? Obviously not. So even if have nothing about digoxin and its secondary effect and why is it so important to give it here? Then by common sense you know that there has been another mechanism that comes in handy. It is the fact it slows down AV. It slows down the AV conduction.

    01:05 Is that important? Yeah. That atrial rate, that P wave is ridicously high. So if you are able to slow down the conduction a little bit with dig, then it works. Is that clear? Now digoxin of course in the setting of, let us say a congestive heart failure patient, then you start thinking about inhibition of sodium-potassium pump increasing, intercellular sodium, increasing intercellular calcium thus bringing about positive inotrophy right there.

    01:32 That makes sense for congestive heart failure. It wouldn't make sense here. That's using it because it's slowing down the rate. Beta-blockers? Obviously not, that was easy. You slow down your beta 1 and by doing so you should be able to control that rate.

    01:45 Rhythm control. How do you do this? You re-establish your sinus rhythm. What does sinus mean to you? Sinoatrial and that sinus rhythm was completely irregular. Anti-arrhythmic medication such as? Well it depends, right. It really depends. Now at this point what I would like for you to do from pathology? Because at some point when you bring in the management issues or the management administration, you want to understand the concept first and then maybe chose a drug that makes more sense for that particular arrhythmia, okay. So at this point, while you are thinking about the SA node, you are thinking about things like the action potential 403 with SA node. What are they? 4, 0, 3. So what is the deep polarization phase here for an SA node? Phase 0. Is that sodium channel? Not for an SA node. It is the calcium channel. Is that clear? So where is the sodium here? In 403, phase IV because it is funny.

    02:52 What does that mean? Remember it is called the funny channel. In other words, it's the sodium channel. So we will talk about this as we move forward. Well let me ask you this because at some point when you do take a look at pharmacology, I want to make sure that we will reinforce it.

    03:07 It is the fact that how is it that you are able to control the sodium channel with phase IV? Is it a class I drug? Good, it is not. That phase IV granted its sodium channel.

    03:23 It is not of a voltage-gated. "Really? Dr. Raj, I don't think you know what you are talking about." Yes, I do. That phase is 0 and let me talk to you about another action potential? If it is phase 01234, that is mechanical activity, isn't it? Mechanical activities 01234.

    03:43 Tell me about that phase 0, that's the voltage-gated sodium channel. That is the mechanical activity let us say of the ventricle. So that phase 0 in 01234. Are you picture that action potential? Close your eyes. Here it is. That phase 0 is a voltage-gated sodium channel. That is class I. Let it be Ia or Ib. What have you, okay? But here in SA node, in its action potential 403 and the sodium is in phase IV, funny, then it is controlled by ligand-gated.

    04:15 Really? Because that phase IV you control by giving a beta-blocker. A class II type anti-arrhythmic.

    04:24 All I am doing here is lying down the foundation or should I say reinforcing the foundation.

    04:30 So then we understand the pathology and how you manage this. If at this point, if you are confused, if you are a little frustrated or if you have lost what I have just said, repeat what I am telling you and take a look at your normal physiology of two action potentials in the heart and then take a look at anti-arrhythmic drugs and you put all this together, alright.

    04:53 Then you do electrical cardioversion. At some point, you have to cardiovert. You have to.

    04:58 Because when you talk about atrial fibrillation, because you want to get that rhythm under control.

    05:04 Decreased risk of embolic stroke. Now this one we have mentioned a few times. You want to use anticoagulation. You are worried about CVA, which stands for cerebrovascular accident, a.k.a. stroke and you could prevent this from happening by giving a warfarin. In other words, you are thinking about the mnemonic, well I do. Use whatever you want. WEPT. W, warfarin, E, extrinsic. What test are you going to use to measure warfarin? PT/INR of course. Now, decrease risk of embolic stroke with CVA. CHF, well aspirin alone. Hypertension.

    05:46 Age of greater than 75, diabetes mellitus and stroke. So ultimately it is a score that you are going to give. Now depending on the score that you are going to give meaning to say each one of these conditions that you are seeing here is given a certain point.

    06:02 And so therefore, wherever point that you are going to get now in this column, then it is going to prevent a stroke from occurring. 0 to 1, aspirin. More than 2, there is coumadin.

    06:14 What is coumadin? That is your warfarin. High risk of CVA, enlarged left atrium, left ventricular dysfunction. So these are the individuals that we have talked about already in which let us say that you have atrial fibrillation that took place for mitral stenosis. Think about that for one second. I don't know what you are doing. What just happened? Well that was a patient with mitral stenosis. Why was he talking like that? Because while the left atrium got enlarged due to mitral stenosis. There is an opening snap, a diastolic rumble, the left atrium is huge. I am having hard time eating. Sound like Marlon Brando perhaps, but left atrium becomes enlarged. It is compressing upon the esophagus, dysphagia and also left recurrent laryngeal nerve, hoarseness. So what you are worried about with that enlarged left atrium? Development of a thrombus. Sure you are. Left ventricular dysfunction, myocardial infarction and if it is not working properly, once again high risk for stroke, cerebrovascular accident. That is the objective of this entire slide and those are the points that you want to keep, it's called the CHAD's point.

    About the Lecture

    The lecture Tachycardia: Atrial Fibrillation: Treatment by Carlo Raj, MD is from the course Arrhythmias.

    Included Quiz Questions

    1. Improve inotropic effect
    2. Rate control
    3. All are goals
    4. Thromboembolism prophylaxis
    5. Rhythm control
    1. Lidocaine (Class Ib antiarrhythmic)
    2. Warfarin
    3. Digoxin
    4. Beta blockers
    1. Decreased dromotropy
    2. Increased inotropy
    3. Increased dromotropy
    4. Increased chronotropy
    5. Decreased inotropy
    1. CHADS2 score = 2; treat with warfarin
    2. CHADS2 score = 3; treat with aspirin
    3. CHADS2 score = 1; treat with aspirin or warfarin
    4. CHADS2 score = 2; treat with aspirin
    5. CHADS2 score = 0; treat with warfarin

    Author of lecture Tachycardia: Atrial Fibrillation: Treatment

     Carlo Raj, MD

    Carlo Raj, MD

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    Buena correlación entre fisiología, clínica y farmacología
    By José V. on 09. December 2020 for Tachycardia: Atrial Fibrillation: Treatment

    Muy completa la explicación y clara, además de correlacionar muy bien la fisiología con la clínica y semiología. Muy buenos tips semiológicos.