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The functions of the atria are to contract blood into the ventricles. The AV node is another slow conducting system, small cells. It allows a certain physiologic delay between A and V. If we did not have that, the atrium and the ventricles would be contracting nearly simultaneously. That’s not good. If the ventricles contract when the mitral and tricuspid valves are open, blood tends to go backwards instead of forwards.
Also, if you think about it, the mitral and tricuspid valve, remember the aorta sits right on top of the mitral valve. If we are going to design a pump, we have to figure out how we get blood from the base
How does that happen? Well, you have the specialized His-Purkinje fibers. These are like the Autobahn. If the sinus node and AV node have a conduction velocity of about 25 mph, if you will, and
Now let’s go on to talking about cardiac antiarrhythmic medications. As I tell my patients, they are a poison with desirable side effects. As we go in here, if we understand their mechanisms we understand generally both their effects and their side effects. And again the five tissues, I don’t want to get you too far away from thinking about basic physiology, I was thinking about bringing some formaldehyde to give you that real sophomore medical school feel but I held off. Sinus node, working atrium, AV node, His-Purkinje and ventricular muscle. For us electrophysiologists, this produces an A, a His-Purkinje
Now, in 1970, Vaughn Williams came up with a classification system and the thing that I don’t like about classification systems and I like about them are the same thing – they are easy. If I say this is a Class I antiarrhythmic, most of you would nod your head and say okay. If I’m a marketing person, I now tell you everything is a Class III antiarrhythmic. The difficulty with classification schemes is the simpler they are the more likely they are to be inaccurate. So in 1970, Vaughn Williams came out and they said, Well Class I antiarrhythmic drugs are those which effect Vmax which was that upstroke, that sodium activation that we talked about, that phase 0. When you block those sodium channels, you are a Class I. Class II drugs were antisympathetics. Now the sympathetic system has alpha and beta but we kind of lump those together. So if you are a beta blocker or alpha blocker, you are an antisympathetic. Class III prolonged action potential duration. Class IV was a calcium channel blocking drug and we said oh that’s great and that’s fine and life was good.
1974 came and unfortunately we said, "You know, some of these antiarrhythmic drugs don’t behave the same. Some seem better for this and others seem better for that. I-A agents are those drugs which effect Vmax and lengthen action potential duration. Now, I have to apologize. You need to put an up arrow here. I-Bs are drugs like lidocaine that effect Vmax but shorten action potential duration. So that
What happens is you have a classification scheme that is trying to say here are the specific channels that are available for block. You now realize if you say, "Well, we want drugs that affect sodium channels, then we’re going to block this current, but we also want ones that prolong action potential
Digoxin. It’s an antiarrhythmic drug that works through the sodium potassium ATPase and I love asking the students on rounds, "Well, how does this make it an antiarrhythmic?" We now understand how it helps contractility. It’s kind of confusing. You block sodium potassium ATPase, sodium accumulates inside the cell, the sodium calcium exchange pushes sodium out of the cell and brings more calcium in. That explains why it’s a better inotropic agent. It has nothing to do with how it works as an antiarrhythmic. It turns out that its entire effect as an antiarrhythmic is through the vagal mechanisms, through enhanced vagotonia.
The most common cause we see to give digoxin acutely is for atrial fibrillation and as we get into treating people with atrial fibrillation when I talk about that, we’ll talk about where it doesn’t work. Half-life, 36 to 48 hours. Remember it has renal elimination so you need to decrease the dosage frequency in renal failure. Isorhythmic AV dissociation is the classic. Digitalis toxicity, we rarely see it
Verapamil. This works by blocking the slow calcium channels, probably the T channels. It has a half life of 4 to 10 hours. It has hepatic metabolism. The caveat. Where do you have to watch out for the
Similarly diltiazem. Same mechanism. A little shorter half-life, still hepatic conversion. Danger in
Beta blockers. There’s both selective Beta-1 and nonselective. There’s Beta-1, Beta-2 blockers, antiadrenergic half-life depends on the medication. Variable hepatic and renal. One of the things I like
Lidocaine. It is a fast sodium channel blocking drug and when I say that I mean it binds and releases in a matter of 200 milliseconds. This is "the 1B". Because it doesn’t have any potassium channel blocking effects, it tends to shorten action potential duration, not lengthen it. Cousins to lidocaine include Dilantin and mexiletine among our antiarrhythmic drugs. Half life is short. Remember it is predominantly
Quinidine. Great drug, been around for over 400 years. The tale goes that there was a sea captain, the
Disopyramide. I always remember when this drug first came out. It was the first of the wonder antiarrhythmic drugs. It was the drug that ended all other drugs because it didn’t have the side effects of quinidine and procainamide. Sodium channel blocking drug, potassium channel blocking drug, fairly weak. Very potent vagolytic effects. One of the strongest. So strong in fact we use it to treat neural
Moricizine you don’t hear much about. Sodium channel blocking drug, moderate persistent. 3 to 5
Propafenone, Rythmol. It is a sodium channel blocking that is moderate to persistent. I should point out that both with Moricizine and propafenone, they were 1C drugs when it was good to be a 1C
Flecainide, very potent sodium channel blocking drug. Good long half-life. Hepatic and renal metabolism and as we talk about the CAST trial in the future, we’ll get into flecainide and its cousin encainide. But this sodium channel blocking effect, I guess one of the difficulties, if you think about the
Sotalol, Betapace is another very potent drug. It has weak sodium channel blocking drugs, very potent potassium channel blocking drugs and also is a potent beta blocker. It has a half life of 7 to 15 hours.
Amiodarone. Very potent antiarrhythmic drug. The best and the worst of antiarrhythmic drugs. Mechanism. Sodium channel blocking effects, moderate. Again, they will try to tell you in the
Ibutilide is a newer drug. Ibutilide is marketed for acute conversion of atrial fibrillation. It is an effective drug for acute conversion of atrial fibrillation and generally that’s defined as people who have been in
Now, just out of curiosity, what is the mechanism of arrhythmia for atrial fibrillation? Reentry. That’s right. If you have a 95% chance of being right with that, I just wanted to see how we went from one
When we look at tachycardia, here is a tachycardic rhythm. It is going at about 160 beats per minute. Here we see an upright P wave in one, upright in 2, upright in AVF. The PR interval is relatively
Now, here is an example of Wolfe-Parkinson-White. You see this pre-excitation here. Short PR delta wave. Let me just take one second to go through this. This delta wave with Wolfe-Parkinson-White is
Treatment options. One treatment option for SVT is no treatment. AV nodal slowing agents, drugs that work on the atrium, DC cardioversion and then we will go through some atrial fib. Again, as a review, AV nodal agents slow ventricular response so as we give a drug, if we want to slow the response, digoxin, as I said, enhanced vagotonia. Works at rest, not so well during exercise. Beta blockers. The most common thing I see with this is concern that heart rates get too slow. This typical is a saturatable phenomena and they tend not to get a whole lot slower. Diltiazem, verapamil. Who knows, we may see Posicore up here after they figure out about T channels. Adenosine, again, very effective. If you have someone in atrial flutter, it’s a wonderful drug to look at SVTs that are about 150 beats per minute because if you give it to flutter, it effects the AV node. It does not cure their rhythm. The flutter continues but you get to see the flutter waves. Amiodarone, propafenone and sotalol all slow conduction through the AV node because of their beta blocker effects. Atrial muscle tissues, procainamide, quinidine, disopyramide, propafenone, flecainide, sotalol, amiodarone and I should add efmazine there.
Differential diagnosis. Inappropriate sinus tachycardia, sinus node reentry. AV node reentry, accelerated junctional rhythm. Intraatrial reentry, ectopic atrial tachycardia. If you notice, this is
What should we take home from this? Atrial fibrillation and flutter is due to reentry and should be treated as such. 90% of the remaining SVTs are due to AV node reentry tachycardia or AV reentry tachycardia due to Wolfe-Parkinson-White syndromes. Most SVTs can be controlled with medications or cured with catheter therapy. So anymore when you have patients with PSVT, it’s a