TEXAS TECH UNIVERSITY HEALTH SCIENCE CENTER HEALTH.EDU 12-LEAD EKG: PART Presenter Jamie Roney, RN, BSN, CCRN

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1 TEXAS TECH UNIVERSITY HEALTH SCIENCE CENTER HEALTH.EDU 12-LEAD EKG: PART Presenter Jamie Roney, RN, BSN, CCRN Hi. My name is Jamie Roney and I am a Registered Nurse who works at Covenant Medical System in Lubbock, Texas, and my background is primarily cardiac nursing and we are going to talk about EKGs today. We are going to look at some of the dysrhythmias that we see that come from the atria, the AV node, and/or the ventricle. Atrial fibrillation comprises 90+% of all dysrhythmias that are seen in healthcare. This will be the rhythm that we see and so as I start talking about atrial rhythms, because it is associated with congestion or pump failure in the heart, we think of water back-up. Now, an atrial rhythm originates within the atria. So as we look at the heart s electrical system, all sinus rhythms originate here in the sinoatrial node. A junctional rhythm will originate here in the atrioventricular node. But there are rhythms that originate in the atria themselves. Here is your right atrium and your left atrium, and so any rhythm that originates in the atria we call it an atrial rhythm. Now, the skinny on atrial rhythms. The first thing you need to know is the atrium is the pacemaker next in line to the throne behind the sinoatrial node. That impulse will then travel through the four intranodal tracks, the four intranodal atrial tracks, and those four tracks meet up at the atrioventricular node. He slows down rhythm, stops rhythm, he kind of has a sign and he decides who gets to go through, who gets stopped, who gets refused or slowed down. And so theoretically it positions itself in a place that it can act to escape in an escape way if the sinus node gets sick or dies, it really doesn t do that very much. The inherent rate of the atrium again is beats per minute and atrial escape beats are very uncommon. The atria likes to fire rapidly and is very likely to become hyper or usurp control from the SA node than to fire slowly in the escape node when the SA node fails. Since atrial rhythms often result in very rapid heart rates, the patients that come to us with atrial rhythms are usually presenting because of the symptoms associated with those fast heart rates. The faster the heart rate goes, if it affects their cardiac output, they are now tired, they are dizzy, they are lethargic, they have problems that we would associate with anybody that had a low cardiac output whether it was because of a slow rate or a fast rate. Some of them feel like their heart is racing and so we see these people that are coming to us, you know, weak, unable to catch their breath, feeling like they have a fast heart rate. Treatment of atrial rhythms is always going to be aimed at giving control back to the SA node. With anything that any rhythm where the heart rate is controlled by somebody other than the SA node, that is going to be our primary goal. We want things to work the way they were meant to work. There are a lot of drugs that we give with atrial rhythms and what we need to

2 know is that these drugs don t really act as cardioverters. They don t actually convert that rhythm back to what it should be and give that control back to the SA node. Most of those drugs are only there to help us control rate so we ve got things like our beta blockers, our calcium channel blockers, you know you think of metoprolol, Cardizem, those kind of drugs, to slow down the heart rate. There is a chemical drug or a chemical cardioversion that can be done using the drug Adenosine. Adenosine will completely stop all electrical activity so you see asystole on your monitor and when that rhythm comes back we hope that the SA node will take over and take control of that rhythm, so there is a potential for a physician to order a chemical cardioversion. The other drugs that we give like digoxin, beta blockers, calcium channel blockers, those drugs only help with control rate but the only one that can truly cardiovert is Adenosine. The other way that we can cardiovert the heart and give control back to the SA node is through electrical cardioversion. Electricity, as we shock the heart, that shock is delivered and all the electrical activity stops at that one point in the heart. What we hope is once the heart regains its consciousness per se, that the SA node takes over its place as controlling factor in the heart rhythm and the heart rate. So both ways that we treat things like atrial fibrillation, atrial flutter, things that we can shock or cardiovert, is really aimed at giving control back to that SA node. How we know which one to do is based on symptoms. Are they stable? If they are stable we can try drugs, we have all the time in the world. If they are unstable with a fast atrial rhythm, and it is covered in American Heart Association s Advanced Cardiac Life Support, we then go to electrical cardioversion as the treatment of choice, and nurses can do that covered under ACLS without a physician as long as you are ACLS certified. How do we see instability? We look at blood pressure would be a good one. We look at, in fact blood pressure and your vital signs are probably your key determining factors of whether you are going to say they are stable or unstable with that rhythm. Sometimes if you have an atrial rhythm like atrial fib with a low blood pressure, converting them out of atrial fibrillation and putting them back into sinus rhythm alone brings up their blood pressure so it is the atrial fibrillation rhythm itself that has decreased their cardiac output to the point where they lose their blood pressure so it takes no drugs, nothing more than just getting them out of that rhythm. Now as we look at atrial rhythms, they are very variable in their presentation. Some rhythms have no P-waves, some have no obvious P-waves. Those that don t have P-waves have fibrillatory or flutter waves instead between the QRS complexes. Some atrial rhythms are regular and others are completely irregular, even what we would call chaotic. We think of a chaotic rhythm when we talk about atrial fibrillation. Though most atrial rhythms are rapid, there are a few that are slow. So, let s look at the criteria for atrial rhythm qualification. Unlike the sinus rhythm, when we look at criteria if you have any of the criteria, if you fall into any of those categories, you then can be called in atrial rhythm. So instead of having a common set of criteria, atrial rhythms have multiple and variable possible criteria. If the rhythm

3 or beat in question meets any of these criteria, again, we are going to call it atrial. Matching upright Ps and an atrial rate grater than 160 by textbook definition is an atrial rhythm. So even if you have your upright P-waves, which we usually think of coming from the SA node, if that heart rate is greater than 160 we now call it atrial tachycardia; it s an atrial rhythm. If there are no Ps at all, and you have a wavy or a sawtooth baseline between QRSs present instead, it is an atrial rhythm. Or, if you have P-waves of more than three different shapes, it is an atrial rhythm. Now your P-waves should all look alike. The QRS complexes that follow them should all look alike, and our T-waves should all look alike. It the T-wave looks different then we know it is hiding a P-wave in it. But if the P-waves all look the same we go, oh yeah, they are coming from the sinoatrial node. If you have two different shaped P-waves, we go oh one is coming from the sinoatrial node and one is coming from somewhere else within the atrium. But anytime you get three or more different shaped P-waves, we now way that they are all coming from within the atrium from different foci; they have different focuses so different cells are creating them. And because of that we now call it an atrial rhythm and we will look at some of those and tell you what those names are, but that would be your multifocal atrial tachycardia and your atrial wandering pacemaker are the two rhythms that meet that criteria. Premature abnormal P-waves with or without a QRS complex, so if you have a P-wave that comes early that is an atrial rhythm or an atrial beat whether or not it conducts through to the ventricles is here to none, I mean it is just there so we know it is premature and it s atrial if we see a P-wave that comes early. Any heart rate greater than 130, rhythm regular, and P-waves are not discernible, they may be present but you really can t be sure, we call that atrial. The key there would be do you see the P-wave. If you don t see the P-wave at 130 to 160 we are now going to call that atrial. That is kind of that gray zone, of okay we know the set zone the set number we have is 160 but 130 to 160 if you don t see the P-wave then we are going to call it an atrial rhythm. Now, the first rhythm we are going to look at is the wandering atrial pacemaker. As we look at this strip, one of the first things we look at are there P-waves. First question we ask ourselves are there P-waves. And here we see a P-wave here, we see P-wave here, a P-wave here, a P-wave here, a P-wave here, yeah, there is P-waves here. The next question we need to ask ourself is what is their relationship to the QRS complex. Are they all married to their partner, this one has a complex, this one has a complex, this one has a complex, this one has a complex, and so forth and so on. Then we go does their shape look the same or does their shape vary. Here you see this P-wave has a clear shape. When we look at the next P-wave here it has a completely different shape. Then you go down here to this P-wave and it has another different shape, so if you have three or more different shaped P-waves, we are going to call it atrial, remember? So the definition of an atrial wandering pacemaker is you have an irregular rhythm with three or more different shaped P-waves and your heart rate is less than 100. So if we calculate our heart rate on this, and you know there are several ways to calculate heart rate, this

4 looks like a six second strip so we could take how many beats do we see in a six second strip and multiply that times ten. One, two, three, four, five, six, seven, eight, nine would give us a heart rate of 90. One of the other ways we could calculate out that rate would be to count the squares in between two complexes so we would have five, ten, fifteen, sixteen, seventeen, eighteen, nineteen squares. We could divide that into 1500 or use a quick heart rate calculator which I am going to look down at real quick, gives us a heart rate of 79. However you calculate that heart rate, you will see your three second markers on your paper, but if that heart rate is less than 100 then we call that a wandering atrial pacemaker. A PAC, what we refer to as a PAC is a premature atrial contraction. Remember anytime you see a P-wave that comes early we are saying that is atrial and its abnormality shaped P-wave followed by a QRS complex and they interrupt a rhythm that is regular. So here we have a sinus rhythm going along and we have a beat that comes early; this beat right here. And then we go along again and have our rhythm kick back in. This is a PAC. You ve got a premature atrial contraction. Now the next thing we are going to look at is a non-conducted PAC. All that means is yes you had a premature atrial contraction but that premature atrial contraction did not follow the normal conduction down through the ventricle. So here we see we have a normal rhythm of sorts, sinus, sinus, sinus, beat, and here, see that little hump right there on this rhythm, that is a P- wave and it is coming early so it is premature, but there is not a QRS complex following that P- wave so we are going to call that a premature atrial conduction that is non-conducted, so nonconducted premature atrial conduction. Now, PAT or paroxysmal atrial tachycardia. First I want to break down the name. The term paroxysmal means a sudden onset; sudden onset, sudden stop. So that term alone we use with other rhythms, if you see it start suddenly and then you see it stop suddenly, that is what that word itself means is paroxysmal so we are going to call it paroxysmal because we see a sudden burst of atrial activity. Now the atrial tachycardia by definition is a burst of atrial tachycardia that interrupts another rhythm, that gives it the word paroxysmal, interrupting another rhythm, and when we look at that heart rate, to be called atrial tachycardia, the rate is between 160 and 250 beats per minute. Remember anything greater than 160 we call atrial so an atrial tachycardia or a PAT is between 160 to 250 beats per minute with a narrow complex. So if we calculate the rate of this burst we ve got one, it falls on a big square so we can take that five, six, seven, we have seven little squares, so we have a heart rate of 214 on that burst of activity. So you can see how important it is to know how to calculate rate because I am going to tell you all of our definitions of what we call something is based on what rate we calculate. So that is a good example of a run of paroxysmal atrial tachycardia. We don t see a P-wave anywhere in that, but even if we saw a P-wave remember because it is faster than 160 even with a P-wave we are going to call that PAT.

5 Now here is an atrial tachycardia with a 2:1 block. This is a very interesting rhythm. Atrial tachycardia with a 2:1 block, when we calculate heart rate most people will calculate heart rate on the R-wave. But remember the first thing we could do is we look at a strip and say do we have a P-wave; yeah we have P-wave. Are there any P-waves not married to a QRS complex? The answer in this example is yes, we definitely have P-waves that aren t followed by QRS complexes. Is the relationship to the QRS complex there in the ones that have a complex, and if we calculate that PR interval it is regular. So if we calculate out this PR interval and we calculate out this PR interval and we calculate that PR interval, those are going to be regular but what we see is we see these P-waves and they look like if we march them out with calipers or a piece of paper where we make tic marks, we would see that the same distance is between these P-waves; they march out exactly so they are at a set rate and regular. Here is a good example of a T-wave hiding a P-wave. Here is another example of a T-wave hiding a P-wave by the way, you see how irregular shaped they are. So as we march through that, then we have the question, okay, we have to calculate out a ventricular rate and an atrial rate so as we calculate out our ventricular rate, let s choose this complex right here. Five, ten, fifteen, sixteen, we have a heart rate of 94. We need to calculate our atrial heart rate because our atrial heart rate is obviously different than our ventricular rate. So when we go to find out what that is, we calculate out, let s use this P-wave here, five, six, seven, eight, so we look on that remember the distance between the other one was 16 blocks we are exactly half of that which is 8 which gives us an atrial rate of 187. So, a heart rate of 187 is atrial tachycardia; it is between 160 and 250. So we ve got an atrial tachycardia but looking at the ventricular rate it is half of that, exactly, so that s what atrial tachycardia with a 2:1 block is. Every other atrial beat is not getting through and every other beat is getting through so we have this variance and how I would document that is I have an atrial rate of 187 and I have a ventricular response of a rate of 94 and we call that atrial tachycardia with a 2:1 block. Now multifocal atrial tachycardia is your wandering atrial pacemaker; same thing, same definition with the exception that now your heart rate is greater than 100. So it s the same criteria. You see three or more different shaped P-waves followed by a QRS complex but now the heart rate is greater than 100. The next rhythm we are going to talk about is atrial flutter. Now we refer to atrial flutter as having the sawtooth appearance, it looks like the teeth on a saw. It also looses the P-waves. Any wave that you see in atrial flutter we now call a flutter wave and not a P-wave. It s that zigzag or sawtooth shaped wave between QRS complexes, there are no P-waves at all, and flutter waves are all the same distance from each other. So as we look at this strip, this is a flutter wave here, another flutter wave, and you see they are the exact same distances from themselves in between complexes. So there is our flutter wave. How you document a flutter wave, and in this

6 complex you have more than one flutter wave between complexes, is just that. If it is 1:1 I say I have atrial flutter 1:1. If I have atrial flutter with two flutter waves between complexes I say I have atrial flutter 2:1, atrial flutter 3:1. If it is irregular by definition we call it uncontrolled atrial flutter, so if it is an irregular rate and so with atrial flutter you can either see an irregular rhythm where the RR interval is not constant or you may see a regular rhythm where the RR interval is constant but you see that sawtooth baseline in between. So on the monitor here you see an ongoing atrial flutter. You see narrow complex QRSs with that flutter or that sawtooth appearance in between, of course our heart rate is at 149 which is another good indication that it is atrial remember the atria likes to fire faster and not slower and we call that atrial flutter 1:1 or you ve got a controlled atrial flutter there. The next rhythm we are going to talk about is atrial fibrillation. Atrial fibrillation again accounts for 90% of all rhythms that you will see that are dysrhythmias. Atrial fibrillation we associate with diagnoses such as congestive heart failure, chronic obstructive pulmonary disease, we see it a lot in our cardiac patients post coronary artery bypass surgeries, valve replacements, those kinds of things. Atrial fibrillation is known for being very irregular. If you look on your monitor and see an irregular rhythm, think of it being atrial fibrillation unless you can prove otherwise. So you are going to assume it s a-fib. Now sometimes in a-fib you think you are seeing a P-wave, you are not sure if you are seeing a P-wave, if you have to focus that hard then you are probably not seeing a P-wave. It s very, like, almost like water ripples, it s chaotic baseline between your complexes. If you calculate out your RR interval or the distance between your R-waves, it is very irregular. Here on the monitor you see atrial fibrillation as it goes across a monitor. At first glance you notice that you ve got a narrow complex and so you realize that it originates above the AV node. When you look for your P-wave, because remember, what s our first question always is there a P-wave? You look for that P-wave and you don t see one. Now, the AV node decides how many beats get through to the ventricles from the atria. The atria can fire as many as 320 beats per minute. The atria is going crazy. It s like a bowl of Jell-O sitting there just jiggling, and what the AV node is doing is saying okay I m going to let you through, I m not going to let you through, so you can actually have a-fib or atrial fibrillation with a rate of 40 beats per minute or you can have atrial fibrillation with a heart rate of over 200 beats per minute and really it s the AV node s job to try to slow down and let through different people, or different impulses. What we call that is if we have atrial fibrillation with a very fast heart rate we call that atrial fibrillation with a rapid ventricular response, or a-fib with RVR and a lot of times those are the patients who present with symptoms of the fast heart rate and those are the guys that we need to do cardioversion on to get them out of that rhythm as quickly as possible. The other thing that we worry about with atrial fibrillation of course is claudication. Your blood gets from the atrium to the ventricle through gravity % of our blood is going to plop down from the atrium into the right ventricle by gravity alone. It s that additional 20% of

7 blood that depends on atrial contraction to squeeze it into the right ventricle, and if you don t have atrial contraction, or you don t have atrial kick, because the atrium is not contracting with atrial fibrillation, that 10-20% of the blood is just hanging out in the atrium and can form blood clots. If you were to get one good atrial kick it could force that blood clot through the body and cause pulmonary embolus or cause cerebrovascular accidents or strokes, and so we really do worry about claudication with atrial fibrillation. These patients a lot of times if they live in atrial fibrillation they are on anticoagulant Coumadin to keep blood clots from forming because they are at risk for it. Before you cardiovert atrial fibrillation you have to know a few things. You have to know A are they stable or unstable. If they are unstable we need to get them out of it. But, if they have been in this rhythm more than 72 hours, you cannot cardiovert them or you could send a blood clot throughout the body. So the other thing we need to know is do you know or are you able to identify when they went into this rhythm and if the answer is no, you do not cardiovert. You want to know how long they have been in it. If it is fast enough it needs to be cardioverted, you can t do that unless the physician does a TEE or a transesophageal echocardiogram to confirm there is no claudication in that atrium, and if they confirm it then of course after that you could do the cardioversion but at that point you are going to need a physician involved. If they do have claudication, I have seen patients that have right atrial clots, you would give the drugs to help control the rate; again, your beta blockers, your calcium channel blockers, your digoxin, those kinds of drugs to help control the rate know that you can t make the attempt to cardiovert them out of that and then the physician, once enough time has evolved for that clot dissolve will then take them back and cardiovert them at a later date. Now, this is supraventricular tachycardia, the next rhythm we are going to talk about. Now the term supraventricular is kind of an all inclusive. If it happens above the ventricles we can use the term supraventricular. Supraventricular can happen at the AV node, it could happen in the atrium, it can happen in the sinoatrial node. Anytime you hear somebody use the term supraventricular you just know it originated above the ventricles. Now it s a regular rhythm with a narrow QRS complex and indistinguishable P-waves. The key here is that gray heart rate zone. So, we have a heart rate greater than 130 but less than 160 and the origin of the rhythm is unclear but we know it is above the ventricles because we see the narrow QRS. So, theoretically, a paroxysmal atrial tachycardia is a SVT. Technically, a sinus tachycardia is a SVT, so if you are really not sure where it s coming from and you are not sure of the origin, you are never wrong to call it supraventricular tachycardia. Just realize greater than 160 we definitely call it atrial tachycardia, even if you see a P-wave. If it s , and you are not sure if you see a P-wave, you re just not sure so you don t know whether to call it sinus or atrial so that is your SVT or your supraventricular tachycardia. Here is an atrial tachycardia. We call it atrial tachycardia because the heart rate is greater than 160, it s , it s automatically atrial tachycardia whether or not you see that P-wave or not.

8 The next thing we are going to talk about is junctional rhythms. Now a junctional rhythm is a rhythm that originates at the atrioventricular nodal level. As we look at our first criteria when we talk about junctional rhythm, junctional rhythms are less common than sinus rhythms or atrial rhythms. It is very uncommon to see a true junctional rhythm. The inherent rate of the atrioventricular node is beats per minute and the heart rate may be faster or may be slower and can result in symptoms of either. Treatment is always going to be aimed at alleviating the junctional rhythm and giving control back to the SA node. Just like atrial rhythms, we really want the SA node to be in control of what is going on so our treatment goal is always going to give control back where it needs to be. Now junctional rhythms are easy to identify. The criteria for junctional rhythms are this you have a regular rhythm or premature beat, narrow QRS complex which tells us it is coming from above the ventricle which the AV node counts as that, and it has one of the following. You may not have a P-wave at all because what is the P-wave really telling us? The P-wave is telling us that that signal came from the atria. The P-wave represents atrial contraction so if you don t have a P-wave at all does that make sense? Because if that originates at the AV nodal level, it s going to depolarize the atria and the ventricles at the exact same time therefore you don t see a P-wave. So it either has no P-wave or a junctional rhythm can have an inverted P-wave with a PR interval of less than.12 seconds. And the reason for that is sometimes the atria does depolarize slightly before the ventricles so you do have the P- wave but it is inverted because remember the electricity is flowing towards a positive lead or electrode; you see a positive or upright complex. If it is moving away from a positive electrode that s reflected as a negative complex. Well now instead of moving from the SA node down towards the AV node which would give us a positive P-wave, as it is depolarizing it is depolarizing from the atrium up towards the SA node, that is what gives you that inverted P- wave. Now, a PJC. We have already looked at a PAC which was a premature atrial contraction. PJC is a premature junctional contraction. It s a premature beat that meets all the criteria we just talked about with either an inverted P-wave and a PR interval less than.12 seconds, an inverted P-wave behind it, or no P-wave at all. And a narrow QRS complex interrupting a sinus rhythm of sort. So here as we look at this PJC we see a sinus beat here, we ve got a P-wave followed by a complex followed by a T-wave, P-wave followed by a complex followed by a T-wave, P-wave followed by a complex followed by a T-wave, and here prematurely we have this beat. If it had a P-wave in front of it we would call it a PAC but as you see here there is no P-wave before or after it so this is a PJC or premature junctional contraction. The next thing we are going to talk about is junctional bradycardia. You ve got a regular rhythm and a narrow QRS complex, an inverted or absent P-wave, the heart rate is now less than 40. Now I am telling you we are relearning everything we have already learned. All of our careers we were told a heart rate greater than 100 is tachycardia, a heart rate less than 60 is bradycardia. But what we need to realize is we change that definition based on what is normal

9 for that part of the heart. So now since we know that at the AV nodal level or at the junctional level, a junctional rhythm is beats per minute, if it is junctional brady it is going to be less than that 40. And in this example, if we calculate out this rate, beautiful example of junctional, A when you go to look for a P-wave it s just nice and pretty and straight before all of these. In fact, as you see here, you see the inverted P-wave right here following the complex so it s a great example of a junctional rhythm. But we have a heart rate of 37 which is less than 40, that makes it junctional bradycardia. Now the next one we are going to look at is junctional rhythm. Junctional rhythm is the same as junctional bradycardia but now it falls within that heart rate; the normal intrinsic rate for the AV node which is beats per minute. In this example here, again, you look before the complex and you see nothing. You don t see a P-wave at all and when we look after the complex we don t see a P-wave at all, so this is a junctional rhythm. What determines what we call it is really based on the rate. So we have already made the definition of junctional looking for that P-wave and not seeing it. To call it junctional rhythm we ve got to look at rate so we are going to calculate rate again and if it s beats per minute we are going to call that junctional rhythm. The next rhythm we are going to look at is accelerated junctional rhythm. And again, the same criteria are there that make up the definition of whether we are going to call it junctional or not, same P-wave criteria; either none, short PR interval, inverted, or inverted following the complex. But now what makes the determination of what we call it is, so that tells us it s junctional, it will be rate again. It s always going to boil back down to what is the rate of what we are looking at. As we look at this strip, we see no P-wave at all, beautiful textbook again junctional; it s just straight all the way up to the complex and straight after. You see in the pattern here every name we give it is based on rate and origin. So, the next thing we are going to look at is junctional tachycardia. Yea, we go back to the fact that if it is greater than 100 we are going to call it tachycardia. So, we see the same criteria again. As we look at this strip we see no P-wave, we see an inverted P-wave, we see no P-wave, no P-wave, no P-wave, and that s provably the first time we have seen an inverted P- wave before the complex in any of our examples. So that meets the criteria of junctional. We would calculate our heart rate, if our heart rate is greater than 100 we call it junctional tachycardia. Now next, we are going to talk about ventricular rhythms. They are rhythms that originate somewhere down here in those ventricles at the Purkinje fiber level. Now the ventricles are your very last back-up generator. The normal rate of the ventricles is beats per minute and there are not many people outside of Olympians or our NFL players that can

10 tolerate a heart rate of because we just don t have good efficient cardiac output with a rate that low. So almost 100% of the population minus athletes will be very symptomatic with a rate that low. When you talk about ventricular rhythms they are potentially the most lethal of all rhythms. A lot of ventricular rhythms take us into advanced cardiac life support and don t have pulses associated with them. They can result from escape or usurpation so you can have either the SA node fail, get sick and die, and so somebody has to take over so the ventricles play that role, or they get very rowdy and they take over control. So escape is what we call it if the SA node should fail so you can have a rate or a ventricular rhythm of a rate anywhere from 20 to 250 beats per minute and at either end of that spectrum we are not going to get good cardiac output and are life threatening situations. Now the inherent rate of the ventricle is, again, beats per minute and though some of the rhythms can be well tolerated in this situation, most of them will not be and will result in death; frank cardiac standstill. I wanted to talk about medications we use to treat ventricular rhythms. Bretylium was a drug that we used to use when I first started nursing 20 years ago to treat v-tach and v-fib in a code. You know, it was epi, then lidocaine, then Bretylium was our, you know, our list of drugs we used in the order we used them in. Well Bretylium is known for causing long QT syndrome and so we have taken it out of the equation now because the longer it takes the ventricles to repolarize the more likely it is that we are going to end back up in v-fib or v-tach, or torsades really with long QT syndrome it is usually v-tach or torsades. But Bretylium, the same drug we used to treat a ventricular rhythm, hey look, it caused our QT interval to prolong out and look, we are causing a ventricular dysrhythmia. Same thing is true with lidocaine. Lidocaine is weight based and lidocaine is still used to treat cardiac arrest patients today but remember we only give 1-3 mg/kg to any patient. Why do we have a weight limit? Because anything over 3 mg/kg can cause cardiac dysrhythmias or ventricular dysrhythmias. Same is true with Cordarone. Cordarone is a drug that we now use for v-fib and v-tach if somebody goes into cardiopulmonary arrest we use amiodarone if it is ventricular fibrillation or pulseless ventricular tachycardia, but we start at a dose of 300 mg followed by a dose of 150 mg and we give no more bolus doses after that. If you have a physician ordering Cordarone or if you have somebody continuously coding on you and you give the same drug, just remember that Cordarone toxicity can also lead to those ventricular dysrhythmias. So we when talk about medications, I think a lot of times we talk about hepatotoxicity and renal toxicity, and we give little thought to the cardiotoxic effects of many of our drugs. But I want you to know that many of the drugs that we give to treat these things can actually cause what we are talking about. Some ventricular rhythms can only be treated by electrical shock of the heart and despite aggressive treatment we are just not going to be able to save them. Ventricular beats have wide bizarre QRS complexes. Because they originate below the AV node, they ve got to take this weird route. If it originates on the right side of the heart, it s got to

11 depolarize the right side of the heart first as it moves over to the left. Remember if it comes from the sinus node, it goes down the Bundle of His to the right and left side at the exact same time. So why you see that wide complex, why it gets wider is because of the fact it has to take a longer pathway, it takes a longer time to depolarize both sides of the ventricles. Some ventricular rhythms have no QRS complexes at all; ventricular standstill is a good example of that that we will look at. They do have very wide QRS complexes and this is just my hint to you, if you have a QRS complex that is.12 to.14,.16 seconds, it s usually bundle branch related. When you talk about the QRS complex associated with a PVC or a ventricular beat, you can have as wide a beat as.26 seconds, so the wider and the more bizarre looking it is, it s ventricular and you won t have a P-wave preceding it. You may have no QRS complexes at all, you may have a wide bizarre QRS complex interrupting a rhythm of sorts. Now the first thing we are going to look at since we have already looked at premature atrial contractions and premature junctional contractions is a premature ventricular contraction. It s a premature wide QRS complex without a preceding P-wave interrupting another rhythm, usually sinus. So in this example we have a sinus beat here, we have this wide bizarre complex here, and we go back into a sinus rhythm that we see here. That is a premature ventricular contraction as compared to the PJC and the PAC. The next thing we are going to look at is a rhythm that we refer to as the dying heart, the agonal rhythm. This is when the heart is kind of getting really tired and wearing out, and it s associated with a heart rate less than 20. You see it is a ventricular beat, it s wide and bizarre, but when we calculate the heart rate of this strip we have two beats in a six second strip which would give us a heart rate of 20, so any heart rate less than 20 is what we call agonal rhythm or the dying heart. Could you do something with this? One of the treatment things we could do is maybe transcutaneous pace this. We can put the pads from the crash cart on the chest, on the upper right of the chest and in the lower left mid axillary line and along there, and then we can turn the machine on to pace and we are actually doing what we call transcutaneous pacing. We are sending an electrical impulse at 60 beats per minute, at least on the monitor we have is where it will start, through the heart and what that will do is it will give them a heart beat and hopefully we can transcutaneous pace them until something else can be done. Or, this rhythm will probably lead into asystole and then death. Idioventricular rhythms, this is what it looks like; this is it. It is because the ventricles beat at an inherent rate of beats per minute, this is the back-up generator rhythm that you would see. If no other electrical signal is received by the ventricles, God made them to beat at this rate to keep us alive until hopefully something can be done. And as we look at that idioventricular rhythm, I see a lot of times in codes people see a wide QRS complex so they want to treat it. We treat ventricular rhythms with stuff that suppress the ventricles right? We treat v-tach and v-fib with amiodarone, with lidocaine, with those kinds of drugs. If you see this rhythm and you give them lidocaine or amiodarone you will kill your

12 patient. Because what you are essentially doing is knocking out the back-up generator. You are suppressing ventricular activity that is all they got. If you see a wide rhythm, people tend to think lidocaine and amiodarone off the top of their head but know how important what is the rate of that rhythm. If you are acting in an escape pattern, remember those ventricular drugs or antiarrhythmics can actually kill your patient. Accelerated idioventricular is the exact same rhythm, it is a wide QRS complex without a P-wave so as we look at this example of accelerated ventricular, you see these wide bizarre complexes here. I have had monitor techs call me and say hey your patient had a run of v-tach. I go what s the rate on that. Why do I ask what s the rate on that because if the rate was 80 it s not v-tach it s accelerated idioventricular. The only difference in this rhythm and v-tach is that v-tach has a heart rate of greater than 100. Accelerated idioventricular is a heart rate of so this is accelerated idioventricular taking us right into ventricular tachycardia, probably one of the most easily identifiable rhythms that we do look at in healthcare. If you see this rhythm on your monitor this is what slow v-tach looks like going across a monitor. I am going to increase the rate of that to a fast v-tach, so that is a faster v-tach going across your monitor. So you can have ventricular tachycardia from anywhere from 100 beats per minute to 250 beats per minute. Remember the ventricles can beat very quickly. The other thing to say about ventricular tachycardia is this you may have a pulse with it, you may not have a pulse with it. So you can have pulseless v-tach or you can have v-tach that actually does have a pulse and usually the slower v-tachs are associated with a pulse, the faster ones, you lose that pulse. If they are awake and conscious in v-tach, what do we tell them to do? We tell them to cough, we tell them to bear down as if they are having a bowel movement. We are trying to use vagal nerve stimulation to cardiovert them out of this rhythm. Because remember, our goal is always to give control back to the sinoatrial node. If it doesn t work to do that kind of thing where we have them bear down or cough, and you know we tell them to cough several times, we can do a synchronized cardioversion on this rhythm just like you do with atrial fibrillation, you can sync your monitor and you can electrically cardiovert them out of this rhythm and hopefully back into a sinus rhythm. Now if you don t have a pulse with it and you witness it, you can do what we call a precordial thump. Take your fist, wad it up, and do a big ole thump right in the middle of their chest on their sternum. If you witness this without a pulse and they are unconscious, you start advance cardiac life support with a precordial thump. If you do not witness it you cannot do the precordial thump and at that point you need to, of course, call for help, give two breaths, look, listen, and feel, no pulse, start CPR at 100 a minute, and again you are going to have the you are going to proceed with advanced cardiac life support measures. Treatment for v-tach other than defibrillation which is the key is to shock or defibrillate, we are going to use drugs.

13 Without a pulse, epi will always be your first drug of choice in any rhythm without a pulse so we will definitely shock, then give epi, shock again, we can use lidocaine at 1-3 mg/kg, we can use amiodarone at 300 mg followed by 150, we can even hang a drip of either one of those but you would follow your ACLS algorithm for that rhythm. The next rhythm we are going to look at is torsades de pointes. On the monitor it looks like a rhythm that rotates like a ribbon that you are twisting or streamers are hanging at a party and twisting. It is a wide QRS complex without a preceding P-wave, the QRS complex rotates around an axis pointing up and down, the heart rate is greater than 200, and it is really recognized mostly because of that characteristic oscillating pattern than by any other criteria. When you see it, that twisting rhythm, we always think torsades. Torsades is really highly associated with a low serum magnesium level. So, when you have hypomagnesemia, it can lead to torsades. You always want to check the magnesium level if you see torsades. This is also the number one dysrhythmia that you will see following a dose of Adenosine so before you push Adenosine with a physician of course under his supervision, make sure you have a magnesium level on that patient because you really don t want to go into the scenario of torsades. We treat this with defibrillation. Again, we want to shock the patient out of this rhythm and get them back into a rhythm. The next one we are going to talk about is ventricular flutter. Ventricular flutter, much like atrial flutter is just the ventricles fluttering and you will usually see it for only mere microseconds before they go into ventricular fibrillation. It is one of those rhythms that if you really want to truly see it you are going to have to go back on your code history and catch whatever they were in right before they went into v-fib. Your heart rate with ventricular flutter is beats per minute and so ventricular flutter, the heart cannot tolerate that well. It can t even keep up with and beat with that because it can t relax enough to fill with blood before it is already beating again so even if you had a pulse with that, that pulse is not going to last for long and the heart is not going to tolerate that long before it goes into the next rhythm which is ventricular fibrillation. Ventricular fibrillation we see no QRS complexes at all. It is a wavy baseline looking just like static and on the monitor I am going to show you a coarse v-fib. This is the ventricular fibrillation I usually put people in when I do their ACLS mega code. And almost all of them go oh, that s torsades. So let me show you the difference in torsades and then go back to coarse v- fib. There s torsades, there s coarse v-fib. Coarse v-fib is good. You would rather have coarse v-fib than the next rhythm, which here it is, is fine v-fib because the coarser the v-fib the more electrical activity you have; that means there is more cells alive in the heart because as a muscle cell or a cell dies in the heart, that line will get finer and finer and finer until you get into asystole. So usually v-fib will start out coarse, get finer, finer, finer, and then we end up into what we call asystole which is our very next rhythm that we see here.

14 Asystole you see no P-waves, no QRS complexes, it s just a flat line. You have lost electrical activity in the cells. Now for v-fib of course we defibrillate, we shock that rhythm, we give epinephrine, we don t see a pulse with it even though we have checked for a pulse we won t see a pulse with it. With asystole the first thing you need to do if you see asystole is check your leads. Make sure that you really have asystole so have somebody make sure all the leads are in place. Two other things you need to do on your monitor, you need to check that in another lead and you need to turn up the gain on your monitor. So as I take my monitor back to, even let s go back to coarse v-fib, as you see coarse v-fib on the monitor, watch what happens when I turn the size of the complex down. And that is your coarse v-fib. Look at fine v-fib at one-half the size or one-quarter of the size. Fine v-fib can look like asystole so you ve got to, got to, got to, got to turn up your gain. So if I had this rhythm and I said okay what I need to do is increase the size to make sure I am really looking at asystole. I go up on my size then you take your paddles out and you shock it. How do we treat each of these rhythms is completely different. We want to initiate a heart rate or rhythm with asystole. With v-fib we ve got too much electrical activity so we look at them completely different. Look at asystole in a second lead so you always check it in two leads. This monitor I was in lead II, I go to lead III. Whatever you are looking at, check it in a second lead. Do not treat asystole until you do the three golden rules make sure they are not awake and alert and the pads just came off, that you ve turned up your gain, and that you have checked it in a second lead. That s American Heart Association ACLS and you know I am real fixy on that one, but what we do need to recognize now and what American Heart Association is really stressing now about asystole, is don t bring patients to the ER in this rhythm anymore. This is a rhythm that we should associate with end of life or death. We use to try to pace asystole. American Heart Association says don t pace this rhythm anymore. What are you really doing? Even if we can pace them with a heartbeat what are we really doing for them? So, they want us to recognize asystole as end of life. Yes, we could get a heartbeat back with this but are we really just beating a dead heart back to life? You can have ventricular asystole which we see here where you just have P-waves with no QRS complexes following them. We also see this pretty often with ventricular pacemaker spikes with nothing following them. That is ventricular asystole so the sinoatrial node is firing, it just is not getting anywhere therefore we don t see a response. This is a ventricular pacing example. Anytime you see this spike before a complex, that is what we call a pacemaker spike and this is just a pacemaker lead that sits outside the right ventricle that screws into the myocardium and we deliver the electricity through that wire to the heart and we stimulate the heartbeat that way and that is a ventricular pacer. This is an atrioventricular pacemaker example. Here we have the atrial pacemaker spike followed by a little P-wave and then right before this is actually a pretty long ventricular spike

15 but then we have it followed by this ventricular spike preceding all of your QRS complexes so that s AV pacing. PVCs defined just quickly, if you have two PVCs together we call it a couplet. If we have three PVCs together we call it a triplet. If we have four PVCs we call it a quadruplet. Anything more than four you caught a run so you got to name your run but anything less than five you have a name for that and that is either couplet, triplet, quadruplet. If your PVCs occur in a regular pattern, if every other beat is a PVC we call it bigeminy. Every third beat is a PVC we call it trigeminy. Every fourth beat is a PVC we call it quadrigeminy. Anything greater than five, every fifth beat is a PVC we call it frequent PVCs. We lose our name after four. Here is another example of quadrigeminy. Every fourth beat in this example is a PVC. R on T phenomenon, we worry about the R-wave hitting on the T-wave because the T- wave is ventricular repolarization and if we deliver an electrical impulse towards the end of that T-wave it can actually send that patient into v-tach or v-fib because it s already mostly repolarized. We can depolarize it again. In this example where you see R on T it did not send them into what we call supranormal activity or v-fib or v-tach but the potential is always there. If you have pacemaker spikes hitting close to your T-wave or if you have PVCs falling on your T-wave, any electrical activity occurring around your T-wave, I would call the physician. That concludes our talk on ventricular dysrhythmias, atrial dysrhythmias, junctional dysrhythmias. We were able to talk about a lot of things so I am glad you joined me for this part of the EKG courses that are being offered on Health.edu and invite you back for more learning. This program is intended for the private use of Health.edu subscribers. Any rebroadcast or redistribution of this program without the express written permission of Health.edu is prohibited. The clinical treatments described and recommended in this video are based on research and consultation with nursing, medical, and legal authorities. To the best of our knowledge, these procedures reflect currently accepted practice. Nevertheless, they can t be considered absolute and universal recommendations. For individual applications, all recommendations must be considered in light of the patient s clinical condition. Health.edu and its presenters disclaim any responsibility for any adverse effects resulting from the suggested procedures, from any undetected errors, or from the viewer s misunderstanding of the information presented. Health.edu recognizes that the use of this product/service does not imply or constitute endorsement of the product/service by the American Nurses Credentialing Center (ANCC) or of the Texas Nurses Association (TNA). Transcription typed verbatim as recorded on video and not responsible for content or context of document with occasional corrections for pauses, etc. (HHT).