I'm hosting this FAQ because I believe it's so good it should be available to
anyone with an interest in the ecg.
The author, Mark Hammerschmidt describes himself as "an RN with 'too much ICU experience' from Massachusetts". Any comments should be addressed to Mark Hammerschmidt email@example.com
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Hi all here's another one this one took a while, but it was a lot of fun to hunt around the web for strips and images.
1- What is an arrythmia?
The nodes: SA and AV
The normal complex:
1-1: What is a P-wave? What is the P-R interval?
1-2: What if there's no P-wave?
1-3: What is the QRS complex?
1-4: What if there's no QRS complex?
1-5: What is the T-wave? What is the QT interval?
1-6: What if there's no T-wave?
1-7: What is the isoelectric line?
2- Why do people have arrhythmias?
3- What is the difference between a bad arrhythmia and a not-so-bad arrhythmia?
4- What is "ectopy"?
5- What does "supraventricular" mean?
6- What are the supraventricular arrhythmias that I'm likely to see in the MICU, which ones do I need to worry about, and how are they treated?
6-1: Sinus arrhythmia
6-2: Sinus bradycardia
6-3: Sinus tachycardia
6-4: Paroxysmal Atrial Tachycardia (PAT)
6-6: Atrial bigeminy
6-9: Wandering Atrial Pacemaker & Multifocal Atrial Tachycardia (MAT)
6-10: Nodal beats
6-11: Junctional "escape" beats
6-12: Escape capture bigeminy
6-13: Junctional rhythms
6-14: Accelerated junctional rhythms
6-15: What if the atria and the ventricles aren't talking to each other? How can I tell?
6-15-1: What is A-V dissociation?
6-15-2: What does "marching out" mean?
6-15-3: Different rates for A and V is the clue to dissociation.
Even Further On South How this FAQ is organized.
7- What ventricular arrhythmias am I likely to see in the MICU, when should I worry about them, and how are they treated?
7-1-1: What are couplets? Triplets?
7-2: Ventricular bigeminy, trigeminy, quadrigeminy?
7-3: What is a "run"? What is a "salvo"? What is "Non-sustained ventricular tachycardia"?
7-6: What is the difference between "narrow complex" and "wide complex" tachycardia?
7-7: What do I do if I see VT on the monitor?
7-8: What if the patient is still awake?
7-9: What if the patient rolls up her eyes and becomes unresponsive?
7-10:What is a precordial thump? Does it work?
7-11: What if I see VF on the monitor?
7-12: Torsades de Pointes
A copyright apology: I would like to give sincere thanks to all the website developers whose EKG strips I've "lifted". You'll notice that this is a not-for-profit site, and there is no intent to use any of these materials for anything other than staff education in the ICU environment. If using these strips violates copyright anywhere or at any time, please let me know, and I'll remove the material right away. Thanks!
By the time they get to the MICU, most people have a good basic idea of what arrhythmias are all about, but enough new people are coming in that we thought it might be helpful to put together a quick review.
The idea that helped me the most in actually understanding what arrhythmias do to people was correlating, or maybe I should say learning to visualize in my head, what the heart was actually doing during one arrhythmia or the other. Each part of the normal cardiac cycle has a specific mechanical event associated with it, and if you can get a mental image in your head of what is, or isn't happening, then the effects of the arrhythmias become much clearer.
Take a look at the diagram that follows.
Remember these? These are the "intrinsic pacemakers". Not too hard there's only two of them. First is the sino-atrial node which lives in the right atrium, in something called the coronary sinus, which I have no idea what that exactly is. There it is in the picture, in yellow up at the top. This is the one that generates P-waves. P-waves travel from the SA to the AV, or atrioventricular node, which lives at the place where the atria and the ventricles join. As the signal travels through the RA, both atria contract.
This is the key thing: as the signal goes through it's part of the heart, that same part of the heart responds mechanically, with movement. That movement, of one set of chambers or the other atria or ventricles - is what you want to try to visualize mentally as you think your way through arrythmias. So:P-wave atrial contraction.
Next comes the AV node, which is also called the "junction", and sometimes confusingly called "the node" even though it's sibling up above is also called a node. (I have no idea where this second name came from anybody know?) The signal that came from the SA node gets to the junction, and is passed along to travel through the ventricles, producing the QRS complex on the EKG. In response to this part of the signal, the ventricles contract. So this time: QRS ventricular contraction.
Let's take a second to look at how lead II works. I couldn't find a decent diagram anywhere, so let's get creative here and use the node diagram:
The point here is that the normal pathway that the signal takes is going from the negative electrode,towards the positive one. See that? Going towards the positive electrode, the signal makes anupward blip on the cardiac monitor.
This is actually really important, and I'll probably make this point too many times, but the direction that the signal is moving tells you where the beat is coming from. If it makes an upward blip on a lead II, then it has to be moving in the normal direction, towards the positive electrode. So it must be coming from somewhere in the normal pathway: SA or AV node. If the signal goes downwards meaning, the signal is going the other way, towards the negative electrode where's it coming from?
See why Lead II is used as the standard monitoring lead? It reflects the normal conduction path.
A word about depolarization - my son wanted to explain this, because he's figured out what it means. "Depolarization is when you take one of those white bears, and take it away from the arctic it gets depolarized!" Just so everybody's clear on that one
Now let's take a quick look at the normal cardiac cycle on the EKG:
This is a pretty good diagram looks like lead II from a 12-lead EKG. Lead II is used as your basic reference lead for looking at cardiac rhythms, because it reflects the normal path of the signal moving through the heart. In lead II, the positive electrode is near the apex of the heart - the bottom of the cone formed by the ventricles, pointing southeast; (that's "down and towards the right" for you non-map people ow! Violent daughter.) The negative electrode is up on the right chest near the clavicle, northwest. Now imagine a line drawn connecting the two electrodes. Got that? The normal signal follows that path, moving through the chambers, always towards that positive electrode, making an upward blip on the ekg trace as it does. See those upward blips?
Now everybody knows where the electrodes go, right?
(Wait this was the one for the vet school, right? What do you mean, "No!"?)
So. In lead II, as the signal goes through the small muscle mass of the atria, it generates a small upward wave you guessed it, the P-wave. Atrial depolarization ends, sort of obviously, at the AV node at the beginning of the QRS. Actually we ignore the Q-part of the complex in measuring the PR interval. A normal PR interval is supposed to be equal to, or less than .20 seconds (5 little boxes, or one big box what kind of problem does the patient in the diagram have, almost?)
No p-wave means that the SA node hasn't generated a signal. No signal, no atrial motion. Can you live without atrial motion? probably, although you lose your atrial kick which they say accounts for something like 25% of your total cardiac output.
As the contraction signal gets passed along through the large muscle mass of the ventricles, it generates a large waveform. The QRS is not supposed to be longer than .12 seconds three little boxes. Longer means the signal is taking longer-than-normal to get through maybe there's a bundle branch block?
No QRS complex means that no signal has gone through the ventricles. No signal, no ventricular motion. Can you live without ventricular motion?
Now that both sets of chambers have contracted, the electrical system resets itself producing the T-wave. The significant thing we worry about as regards the T-wave is the length of the waveform from the beginning of the QRS, to the end of the T-wave, called the QT interval. A QT interval that lasts too long can mean that bad things may be happening usually one kind of drug toxicity or another which may show up as nasty tachyarrhythmias like VT.
Well if there's no QRS, there won't be a T-wave. Otherwise, the ventricles are definitely going to have to reset themselves producing a T-wave of one kind or another. It's very important to remember that T-waves, or more correctly the ST segment of the complex, can change if the patient goes through an MI, or is having an ischemic, or anginal episode. If the T-waves on your patient look different at the end of your shift get suspicious. There's lots more on ST segments and what they're trying to tell you in the "Localizing Infarcts" FAQ.
Let's look at a normal sinus rhythm strip.
Do you see the area where the line is flat between the beats? After the T-waves and before the next p-waves? That's the "isoelectric line". When ST segments go up, as in an MI, or down, as in ischemia, what you're hoping is that they will come back to their original position with treatment, and that position is: where they started out on the isoelectric line.
Lots of reasons, but if you think about things that are going to make the heart unhappy, then those are the things that will produce arrhythmias acutely cardiac ischemia, hypoxia, MI, changes in electrolytesobviously in a situation like this you are going to be treating the underlying problem either with anti-ischemic treatments in situations like anginal CHF (remember "LMNOP"- Lasix, Morphine, Nitrates, Oxygen and Position); or clot-busting an acute MI and hopefully this will minimize the conditions that are producing the arrhythmias in the first place.
Chronic changes that produce arrhythmias have to do with processes that make cardiac chambers do things over long periods of time that they don't want to do, producing an abnormal change in their size. Anything that makes a chamber "stretch" chronically, will produce chronic arrhythmias the classic example is cor pulmonale ("lung-heart" that is, heart problems caused by the lungs.) The lungs, remember, are supposed to be nice and soft, and the relatively thin-walled right ventricle doesn't have any trouble sending blood through them. Any process- whether acute or chronic- that makes the lungs stiffen up, will increase the pressure needed to send blood through them. Now the RV has to work harder since it's not built too powerfully to start with, if it has to work harder for a long time, it begins to grow like your biceps during weight training (mine never did).
This chamber growth is actually not a happy thing the heart wants to stay small it works better that way, small and tight and the bigger it gets, the more stretched and boggy it gets, and this stretching and bogginess characteristically produces arrythmias. I was taught that a stretched-out RV and RA produces atrial fibrillation the classic arrhythmia of smokers and COPDers. Make sense?
Likewise, anything that makes the left side of the heart grow and stretch will produce arrhythmias usually the more unpleasant ventricular ones. These will be your CHF patients with low EF they will often have a certain amount of ventricular ectopy at baseline, and you'll hear people say "Is Mr. Yakowitz allowed to have triplets, or should we wake up the team to look at him?", and someone will answer "Oh yes, he has them all the time, and we're not supposed to call the team unless he starts having long runs."
The basic point here is: is the patient able to make a blood pressure? I mean, clearly there are lots of other things to consider for example, a patient may go into VT and maintain a blood pressure nicely, talking to you, maybe complaining of chest pain would you shock that patient? You would need to know that in VT, a patient may sometimes maintain a pressure for a while, and then lose it abruptly does this happen with other arrhythmias? It takes time, study and experience to learn your way around these situations don't feel bad if you find that it takes you quite a while. (It takes years to get really comfortable in the ICU. I'm still waiting)
Let's try the visualization thing to see if it helps to analyze the threat that is produced by one arrhythmia or the other. Let's take atrial fibrillation for example you've probably seen people with this.
Right here we are in A-fib. Are there P-waves? MM. maybe? What are those fluttery looking waves along the isoelectric line? Nope no P-waves. So no P-waves means no kind of normal atrial contraction. Are there Qr.'s? Definitely. So there are ventricular contractions and how many in a minute? This looks like a six-second strip -count the QRS's and multiply by 10 to get the ventricular contractions in one minute. Everybody get 70? (Don't count that last QRS at the end it's beyond the 6-second measurement). Should this patient be able to maintain a nice blood pressure with a rate of 70? Probably the ventricles need time to fill up, and at this rate they are probably filling very nicely. Depends on the strength of the ventricle the "ejection fraction". There's all sorts of good stuff about EF, and filling pressures and the like in the PA-line FAQ.
Now the mental part. (My wife laughs at this point) In my mind, when I see Afib, I think of the atria, well, fibrillating. Remember the "bag of worms", which is how they describe what a fibrillating ventricle looks like? Same thing, but up on top. The ventricles, I can see, are pumping properly, because there is a normal QRS this means that the path of conduction is travelling normally through the ventricular muscle mass, just the way it normally should so they're at least conducting okay.
The important part in this situation is:
I recognize this as A-fib, which is a fairly "stable" arrhythmia it may be cheating in a FAQ for new RNs to say that I, the old guy, already recognize the rhythm, but we learn by example, right?
The ventricular rate is not too fast. This is a very important concept in grasping the significance of arrhythmias: speed matters -usually we're talking about ventricular speed here. Ventricles beating at a rate of 200 bpm have no time to physically fill up with blood therefore they don't have much blood in them to pump out therefore cardiac output and blood pressure fall, and other bad things like death may ensue. Too slow a rate may have the same result sure, the ventricles have all the time they need to fill, but at such a slow rate, the cardiac output is still too low to maintain a blood pressure. What's the ventricular rate in the strip above 70, we said. Sounds good to me. If the ventricular rate is kept around this range, the patient will probably do fine.
A helpful basic concept: the ventricles do most of the pumping in generating a blood pressure. The rule is, no matter what else is happening, if the ventricular rate is somewhere near the normal range of sinus rhythm say 60 to 100 bpm, then the resulting blood pressure will probably be all right.
"Ectopy" means: "something occurring where it isn't supposed to." Pregnancy anywhere in the body but the uterus is "ectopic pregnancy". Seizures result from ectopic electrical activity in the brain. If the signal that starts a heartbeat originates from someplace other than it's supposed to, it's also called ectopic.
Two points to make here: first, you'll remember learning years ago that cardiac tissue has the property of "automaticity" which means it is able, all of it in one way or another, of acting as a pacemaker, not connected in any way to the normal, built-in pacemaker/conduction system.
Second, the heart responds to the fastest signal it receives. This means, for example, that if the AV node should wake up and start feeling frisky and quick, it could capture and pace the heart if it were generating a rate faster than the SA node. (Smart guys in the audience what arrhythmia would this be? Right accelerated junctional rhythm. Smart guys)
The result is that electrical pacemakers can pop up just about anywhere in the atria or in the ventricles, and if they produce a beat sooner than the current pacemaker (I'm talking about built-in, natural pacemakers here) does, that ectopic beat will capture the heart. For example, a single PAC. Or a single PVC. The key is that these signals are premature , they're arriving sooner, at a faster rate than whatever else is normally pacing the heart. As a result, they capture.
Or, if it's a sequence of rapid signals, it will capture the heart for as long as that sequence lasts any examples from the audience? VT for sure. SVT also for sure rapid Afib as well. The normal, slower rhythm will not recapture the heart until the faster rhythm is controlled and if the rapid rhythm doesn't allow the ventricles enough time to fill, there you have your lethal arrythmia situation. More on these later.
You'd think that this meant "atrial" in reference to arrythmias, but I believe we're supposed to add AV-node (sometimes called "junctional", or just "nodal") rhythms to this group.
Let's begin by looking at normal sinus rhythm the normal supraventricular rhythm:
Look familiar? Normal intervals, rate in the 70's nice! Everybody see the p-waves the little ones in front of the big ones? Then the QRS's, which are the big ones. Then the t-waves, coming after the QRS's
Here are some of the common supraventricular arrythmias some aren't really so common, but you should have a basic grip on them anyhow.
This is not one to worry about, as far as I know. Sinus arrhythmia is when the normal sinus rate speeds up and slows down slightly, as the person breathes in and out. In 22-odd years I've never seen any physician show the slightest concern about this one. (Yes, this is a strip from a French website)
Here's a nice sinus bradycardia, rate in the 50's. Everyone remember what the intrinsic rate is for the SA node: 60 to 100bpm, right? Is this rhythm coming from the SA node? Sure see the p-waves? But it's slow, isn't it "bradycardia", of sinus origin. Sinus bradycardia is often a good thing it means your patient has finally fallen asleep, or that her metoprolol is finally starting to work. Areally slow bradycardia is not such a good thing clearly, you don't make much of a blood pressure with a rate of 20.
Scenarios causing sinus bradycardia:
- Inferior MIs "IMI"s are famous for classically producing brady episodes, where the patient's rate drops to the twenties, and you run into the room and give a milligram of atropine, and start looking around for the external pacing pads. If I'm getting a patient with an acute IMI, I put a vial of atropine in the room just for good voodoo.
- Sedation: being sedate will drop most people's heart rate.
- Ischemia: definitely. If you think about it, you'll remember that there are three main coronary arteries these perfuse the SA and AV nodes, and if the nodes become unhappy, then arrhythmias certainly result. In the case of ischemia in inferior territory, as above, the RCA is usually the problemthere's lots more on the coronary arteries, where they go, and how they show up on EKG's in the "Localizing Infarcts" FAQ.
Sinus tachycardia pretty easy. P-waves? Yes. So the rhythm is coming from the sinus node. What's the rate somewhere near 130? So, faster than the normal range of 60-100. Tachycardia. Let's do the mental thing just quickly: P-waves mean that the atria are contracting, QRS's mean that the ventricles are too, and in the right order, atria first, ventricles second. Which is of course better than if they're doing it backwards or even simultaneously, which does happen sometimes.
Reasons for sinus tachycardia:
- Agitation, pain or distress pretty easy.
- Fever also pretty easy.
- Dehydration anything that decreases the circulating volume for any reason will produce a rise in heart rate as the body tries to keep blood pressure up. Dehydration would mean a relative loss of water in the circulation, but certainly blood loss will do the same thing. There's lots more on how blood pressures work in the "Pressors and Vasoactives" FAQ.
- There can certainly be combinations it wouldn't be unusual at all to see all three of these conditions at once in a septic patient. Remember sinus tachycardia is usually something the body is doing on purpose, for a reason, such as trying to maintain a blood pressure. Don't be too anxious to start giving drugs like beta-blockers in tachycardic situations until you have some idea of why the patient is doing what they're doing. (The exception would be during an acute MI. Hearts get tachycardic during MIs, usually because their owners are in pain, or terrified, or both. Bad.)
PAT is a very rapid supraventricular rhythm that comes from the atria usually it runs at a very rapid rate, about 250-300bpm. You sometimes see young people have short bursts of this rhythm, which in my experience doesn't last more than a couple of seconds. This strip shows the PAT breaking spontaneously to NSR. It may set your alarms off unless it persists, most physicians don't get too involved with this. Document it. If it persists could be very bad, in the sense that the blood pressure may suffer what drugs would you think about having on hand for this?
Here are some nice premature atrial contractions. That is, we assume that the heart is contracting in response to these signals. Anyhow, if you look at the early beat 5 th complex, right? you'll see that it has a different P-wave shape (the impressive word for shape is "morphology"), meaning that it comes from someplace other than the normal sinus node. (My son loves to find little words that mean the same as big ones.) Ectopic. The other thing you'll notice is that it comes too soon premature. Coming sooner than the normal SA node impulse, the PAC captures the heart, just for that one beat then that ectopic source (an ectopic pacemaker is often called a "focus") shuts off again, and the regular sinus rhythm comes back. To speak impressively, remember to say that the different p-wave "has a different morphology, arising from an ectopic focus".
PACs don't get physicians worried, as a rule. The thing to worry about is: if they start getting too frequent, it may mean that a-fib is coming.
this means that every other beat is a PAC. Again afib may be coming.
Right here we are in atrial flutter. Remember a normal, upward QRS means that the conduction from the AV node on down is in a normal direction assuming this is a lead II - that means that conduction through the ventricles is happening the way it's supposed to.
So what are the atria doing here? Who said "fluttering"? You in the back, very good. You get to buy us lunch. Right the atria, if you looked at them, would be contracting at about what rate you guys know how to count boxes to determine rates, right? We'll get to that later in a-flutter, the atria contract at a rate around 300 bpm. Are the signals from the atria all being conducted to the ventricles? No? Good thing! Would the ventricles have time to fill if every atrial signal made the ventricles contract at a rate of 300 bpm? No! What is the ventricular rate? Six-second strip, count the complexes, multiply by 10 about 100 close enough to a normal sinus rate to tell us that the patient is probably going to generate a decent pressure with this rhythm.
What's the ratio of atrial to ventricular contractions here? 300 atrial bpm, 100 ventricular bpm I would call this "3-to-one a-flutter", and I would document the rhythm carefully strip-wise, but I wouldn't feel pressed to get the team to treat this. A-flutter usually is transient people don't stay in it too long, because they're usually on the way towards developing a-fib.
Another point worth mentioning the ventricles are responding to roughly one out of three signals here, right? This is called the "ventricular response rate". Duh. But obviously, it matters a lot, because if the response rate gets too high, then the chambers don't fill, and the pressure drops, and etc. What if the ratio were 2-to-1? What would the ventricular response rate be? Around 150 not too too fast, but pretty darn fast, faster than I'd like to see my patient go, especially some older MICU patient who gets ischemic very easily what in this case would be called "rate-related ischemia". I would definitely wake up the team for an episode of 2:1 flutter, for that very reason in the old days physicians would compress one of the carotids to try to provoke the "carotid body response" namely, bradycardia, specifically by slowing AV node conduction partly a diagnostic, and partly a therapeutic maneuver. (We used to call this "doing the neck thing", as in "Are they going to do the neck thing?") You would look for the ratio to change fewer QRS's.
I got lucky searching the web here's a really neat strip of someone "doing the neck thing".
Nowadays they don't do the neck thing much any more people with carotid disease don't usually enjoy it too well threatens the brain, and all although some physicians will do it if they don't hear any carotid bruits on exam. Instead you may see maneuvers with verapamil, sometimes metoprolol, sometimes adenosine I've seen all of them work, but my experience leans toward verapamil in this situation. I hate adenosine ten seconds of terror.
Okay, here's the nice picture of a-fib that we looked at earlier. A-fib is a pretty similar scenario to a-flutter the atria are going too fast, and only the occasional signal gets conducted through the AV node to the ventricles, which is a good thing! Remember, you want the ventricular rate to be something like what the normal sinus rate would be 60's to 100's. Let's do the mental thing what are the atria doing? Is there a nice stable p-wave? No. Can you visualize the motion of the atria? Bzzzzz fibrillating, and not contracting in any organized way. Signals are not coming from organized sources, or "foci", but from all over the atrial tissue, simultaneously. Some signals are getting through the AV node and being delivered to the ventricles again, they speak of ventricular response rate you'll hear people describe an episode of "rapid afib with RVR" rapid ventricular response which often requires a quick cardioversion back into sinus rhythm to restore a failing pressure. Or the patient might need IV blocking agents of one kind or another betas, calciums, digoxin maybe, to bring the RVR down to a rate that produces a better pressure.
Once brought under control rate-wise, afib in and of itself is a stable arrhythmia, but it does have a couple of significant bad things that go with it:
First, fibrillating atria don't empty themselves very well. The result is that clots can form in them, and if the a-fib suddenly converts back to sinus rhythm, those clots will get shot out into the circulation arterial or venous, or both off to the lungs if on the right side, producing a PE, or if on the left, then off to all sorts of interesting places down the arterial tree, such as brain, or foot, or mesenteric artery (producing bowel infarct), or elsewhere. "Paroxysmal a-fib" as a result is seen, rightly, as very dangerous. What could you do to prevent this from happening not the a-fib, I mean, but the clots? Audience? Right anticoagulation. Acutely, with heparin, long-term with coumadin.
Working our way south from the SA node, the next source of arrythmias is the AV node, otherwise called the "junction" or just "the node", as in producing "nodal rhythms". No idea why, probably some historical reason.
Here's a rhythm you see once in a while see how the p-waves have a number of different morphologies? (79 cents for the word, please) The idea here is that the atrial focus shifts from the SA node to the atrial tissue, in various places, each of which generates it's own signal, which goes on to capture. If the rate is less than 100, they call it WAP if it's over 100, the name changes to Multifocal Atrial Tachycardia.
Everybody see something strange in beats 5 and 7? Are they early? Sure. Are they PACs? There's no p-wave, is there? But look the direction of the QRS is normal this means the signal is moving in the normal direction through the ventricles.
These are premature nodal, or junctional beats. No p-wave means they're not coming from the atria. What's happening here is that sometimes the junction, for reasons of it's own will accelerate somewhat and send out premature beats, which very nicely depolarize the ventricles in the normal southward direction. My experience is that these are considered benign that doesn't mean that they are benign, but I've never seen anything done acutely about them.
This one's a little different. Here's a nodal beat no p-wave, and normal QRS conduction, just like in a sinus beat. But is it early? No actually it's a little late. This is a rescue situation, not unlike demand pacing. The SA node, for some reason, probably ischemia, is slowing and the AV node, like a demand pacemaker, senses the time difference, and jumps in with a beat to replace the one from the SA that never came. They call this an "escape beat" I think if it more as a "rescue beat" the AV node loyally sits there passing along beats from above, all it's life, and then one day, the SA node gets hit by some bad cheeseburger byproduct, and the AV node wakes up and starts delivering a rhythm on it's own. If you're lucky. If not you know how to work the external pacemaker, right?
As you work your way through all these rhythms, try to get a sense of which beats are coming early, which are coming late, and why. The early, or premature beats are the ectopic ones, coming from someplace that they're not supposed to. The late beats, at least these nodal ones, aren't ectopic really, because they do come from an "intrinsic pacemaker", right? the AV node. I think of the premature beats as "abnormal" more than I do the nodal ones, except the nodal beats wouldn't be appearing if the SA node weren't in trouble.
This is a complicated name for the rhythm in which sinus beats alternate with nodal escape beats. This is probably happening for an unhappy reason, like MI or ischemia affecting the SA node the AV node is having to rescue the rhythm with every other beat I'd worry if I saw this one, because heart block might be coming. Any disease process that affects the rhythm that much has probably done some real damage to the SA node. There's lots more (why do I keep hearing this phrase?) about heart blocks and pacemakers in the FAQ files with those titles.
Everybody see what's different about this one what's going on here? Let's be systematic about it: are there p-waves? I don't see any. But do the QRS's look normal? Yup, normal. So what have we got - let's visualize this please Shirley, you can channel if you want to. Are the atria doing anything? Not that I can tell, they aren't. Ventricles? Yes they are. And since the QRS's appear normal, this means that the rhythm has to be coming from the junction, and going southwards. Everybody see that? What about the rate? About 40. Perfect! Junctional! Dude!
This ought to be pretty much the last of the supraventricular rhythms that we're going to look at. I'm sure there are more, but these cover pretty much the ones you run into in the MICU setting. As usual, please let me know what I've left out!
This is a junctional rhythm too, but obviously it's faster than the normal 40-60 rate that you'd expect. Anybody know why this happens? I have no idea. It's generally considered benign one thing that does matter when the atria aren't pumping however is that you lose whatever output they add this can be as much as 25% of the total cardiac output.
I'll explain this as I understand it (which is what everybody does, right?) this can happen in a couple of different ways, for a couple of different reasons. Here's the first one:
You all know complete heart block when you see it? Look at all those p-waves floating around on an empty isoelectric sea with no QRS's to talk to. Here's how to tell if your patient's atria and ventricles aren't communicating: it has to do with the relative rates. What's the atrial rate here? Let's count boxes going to the right from the p-wave just above the "?" in the first line of this paragraph: 300-150-100-70 somewhere in the sixties. How about the ventricular rate? Yow! wicked slow, as we say up here in Mass. somewhere around 20. Well, the SA and AV nodes, aren't communicating very often, if at all. Is there "a": any kind of visible relationship between the p's and the qrs's that you can see? Or "b": are the p's just sort of appearing in amongst the QRS's at random? I'd say "b". And is there any kind of predictable ratio between the p's and the qrs's? Such as 2:1, or even 8:1, or some varying number? Not really. Take a look at the "Heart Block" FAQ for more on this subject.
By the way why is this happening? What would you do in this situation?
Here's the second scenario:
The folks who recorded this strip have helpfully put little arrows showing that the p-waves are actually popping up all over the place. Even though the last complex looks normal, that's actually just a lucky hit the atria are doing their thing, and the ventricles are doing theirs, but they're not on speaking terms. Ready for another question? Where are the QRS's originating?
This is almost the same thing as complete heart block actually, it probably is complete heart block, but difference is in the ventricular rate. Complete heart block usually describes the first situation, in which the junction isn't generating much of a rate at all.
The second strip describes the situation that people call "AV dissociation" which involves the same kind of non-communication, but for a different reason. This can occur if the junction suddenly wakes up, and begins to generate a rate that is a little faster than the one from the SA node (junctional tachycardia). Remember: the fastest signal captures. So the ventricles are driven by the rapid junctional rate. The SA signal captures the atria so they run at one rate, while the ventricles run at another. Different relative rates that's the clue that the nodes aren't communicating. Usually the atria are inhibited in a junctional tachycardia sometimes a signal coming from the AV node will actually depolarize the atria backwards upwards! This can show up in a couple of ways: the p-wave may be abnormally short, maybe upside down, maybe on top of the QRS. All in all something isn't right, because the signal transmission isn't happening the right way. Watch these folks carefully. Remember, the AV node is not a reliable pacemaker it can poop out at unpredictable times, and there you are, high and dry without an escape rhythm to bail you out.
Even Further On South
Everybody's starting to realize how this file is organized, right? The first part is about arrhythmias coming from the upper part of the heart, and we're moving downwards in sequence. Just making sure everyone was awake
Premature Ventricular Contractions
These are pretty easy to recognize. A couple of points to make:
Premature ventricular contractions they're early, as in the strip above- which is to say they come sooner, or faster, than the sinus beat would. Since they're faster, they capture.
Ventricular: They're ectopic- coming from a focus somewhere in, uh, the ventricles!
Why do they look so strange? Let's put this one to the audience. Why do PVCs look the way they do? The clue is: which way is the signal travelling?
Context is everything. If your patient has been in perfect sinus rhythm, and suddenly develops PVCs, your task is to figure out if something has changed. Or the other way have the PVCs suddenly gone away? On the other hand, some people have chronic ventricular ectopy they may even have short bursts of VT these will usually be patients with stretched, boggy hearts: people who have had a couple of MIs, people with cardiomyopathy, CHF patients you get the idea. We say: "Oh, he's allowed to have short runs, he has lots of ectopy all the time."
Things that cause PVCs: by now this should be clear enough anything that interferes with the delivery of blood; things that make the heart unhappy: ischemia, obviously MI, hypoxia.
PVCs may or may not make a blood pressure. You can observe this really well if your patient has an A-line just look at the arterial waveform following the PVC is the wave lower than one following a sinus beat? Probably. If your patient has a run of PVCs are they all lower than the sinus pressure? Did your patient lose pressure completely with the run? You'll see people respond to a VT alarm by going over to the central monitor, looking at the printer strip, and saying "Wow, he doesn't perfuse those beats very well! Sure looks like VT to me - the team has been having a hard time figuring out exactly what the rhythm is. Whatever it is, he doesn't like it very much."
This is an essential point of "surviving" the arrythmias that you will run into in the MICU. Your patient may make a fast rhythm of one kind or another, the cardiologists may have a great time debating whether it's "type-2-accelerated-idioventricular- rhythm", or "rapid-A-fib-with re-entrant-something", or "nonsustained-supraventricular-tachycardia with pre-excitation syndrome of the Lown-Ganong something else" your immediate problem is what? All together now: Is the patient making a blood pressure? If they are, this does not mean (obviously) that you can now go downstairs for lunch! Get the patient seen by the team, don't leave the room - the rhythm may deteriorate into something you will recognize as bad!
Couplets are easy two PVCs in a row. Again, context is everything. Has your patient had couplets before? Or never before? Is she doing something clinically having chest pain, getting hypoxic, sweating, getting restless? Is her K+ low, or magnesium? Is she acidotic?
Or is this an improvement? Has she been having long runs of VT, which are now going away because you started lidocaine?
Are you sure that's actually your patient? (Actually not a stupid question when you're using remote central monitoring.)
So, couplets: easy to recognize, but don't forget to try to figure out what they're telling you.
Triplets: same as couplets, except three PVCs in a row.
Bigeminy means that every other beat is ectopic. Trigeminy means the same, for every third beat. Quadrigeminy for every fourth. This strip goes from bi- to tri-. Once again put this into context: is this acute or chronic? Does his ectopy go away if his K, or his Mg is low? How would you treat the low K? Would you take KCl on an empty stomach? What do BUN and creatinine have to do with giving K replacement?
These are all pretty much interchangeable terms for a series of PVCs that's "longer than a triplet". Some runs are short maybe 6 beats long, some are lots longer, but the main idea is that the run stops by itself, and the rhythm goes back to whatever (hopefully stable) it was before. This strip doesn't show that change, but that's pretty much what a run looks like. You'll see the alarm go off, and the board will say "VT alarm" your job is to go down to the printer and look at the strip printout.
Things to think about in this situation include the usual suspects: are the runs coming when the patient is doing something else that might indicate trouble? Angina, diaphoresis, changes in electrolytes, hypoxia, fluid overload, evolving an MI? What is this run of VT trying to tell you? Or is the patient "allowed to have runs of VT"? Maybe they shouldn't!
A lot of the VT alarms are artifact alarms caused by people moving, or scratching. Water in corrugated O2 tubing can collect in the bend where the tube hangs down, and vibrate as the air is pushed through I've seen this produce artifact that looks just like VT. Chest PT will do it.
The thing to do though, is to darn well go down to that printer and check the alarm printout every single time. No exceptions. You might think: "Well, Mr. Gerbilowitz has had artifact 32 times already this shift", but you'd hate to be wrong! Often artifact problems can be fixed by changing chest electrodes I usually take them all off, and replace the whole set. Another useful trick is to move the electrodes inwards on the chest towards the borders of the heart people who have lost cardiac muscle mass often have very small ekg complexes, and you can see them much better this way.
Now things are starting to get a little scary. Now is when you need to remember your ACLS class, and/or your defib class. We'll go over that stuff a little later in the file.
Same strip as above, except "sustained", which is what that strip is, anyhow. VT is really one of the scariest things that comes up in the MICU, along with it's nasty cousin VF. I'll go into cardioversion and countershock a little later in this file, but this might be a good place to talk about lethal emergencies.
- Rule number one: try do your best to keep from getting panicky. Always remember: the MICU is a group process. You are never, ever alone. Senior staff nurses are always around.
- Subrule to rule number one: the only way to get over being afraid of these situations is to spend a lot of time in the unit doing them. Everyone has trouble with this at first.
- Rule number two:remember the basics, and keep it simple.
Let's take a minute at this point, and walk through a scenario briefly. The VT alarm goes off you turn your head to look at the central monitor, and there it is the real thing. You immediately go into VT yourself, but because you are probably about a third of your patient's age, you still make a blood pressure, so you can still stay upright. You bolt for the patient's room.
First move is? Call for help as you run.
Second move? Always the same let us stress this: look at the patient. Is she smiling at you? Comatose? Seizing? This is what the CPR course means by "establishing unresponsiveness". You need to know that some patients can make an adequate blood pressure with VT, maybe for a short time, maybe for quite a while. They may be awake, may be having chest pain, may not be feeling anything at all. You donot want to start running a code on a patient who is awake! This is what ACLS is all about learning what to do in different situations.
Let's take the unresponsive scenario. Very important, you must say the following words very loudly: "Annie, Annie, are you all right?". This usually works in class, anyhow. She never says much though unresponsive. You've run down the hall, called for help, you arrive in the room, you determine that the patient is not responsive. Is the rhythm still VT? Old guy that I am, I would thump this patient I've done it enough through the years to know that it works sometimes. This has become a debatable move nowadays, and it's been a while since I took ACLS can anybody clear this up from the group?
I actually remember one episode: I was standing by the bed in the patient's room, and the crisis alarm went off I heard it coming from her bedside monitor, about a foot above my head as well has from the hallway. I looked up VT! Low, or no blood pressure on her A-line trace. I looked down her eyes had closed, she was shivering maybe seizing? I thumped her this all happened in about the space of seven seconds. She broke immediately into sinus rhythm. The team came bolting into the room at the call of the nurses at the station, who'd seen the rhythm on the central monitor and came to a screeching halt, burning rubber. They looked at the monitor, looked at the patient, looked at me. I looked at the monitor, looked at the patient, looked at them. Yikes!
Where were we oh yes. Keep it simple. Remember that stuff in Basic Life Support CPR about A, B and C Airway, Breathing, and Circulation? Same deal applies. Lethal arrhythmia?- sure you want to shock them, but get the backboard under them, start compressions, establish an airway here, let's scenario-ize this one too.
Alarm goes off. Mr. Hamsterowitz is in VT not artifact this time. You run down the hall from the central monitor, you're calling for help, you try not to plow into the other nurse coming from the opposite direction. There's Mr. Hamsterowitz not looking too good. Bedside monitor clearly shows VT. No BP well, maybe a little BP on the A-line trace. Not enough to perfuse his head, clearly, since he is really not responsive. First move? I'd thump him. I understand that this has to do nowadays with "witnessed" vs. "unwitnessed" events as far as I'm concerned, in the MICU they're all witnessed, so I'd thump him. Do not let thumping get in the way of defib maneuvers, however. (Duh!)
Second move did he break from VT with the thump? No? Get him lying down, get the board under him one poor nurse I know, in her first code, swung the backboard over the bed and clocked the nurse on the other side, right on the head. Start compressions. Is the airway open? No? Is he in VT because he aspirated a piece of steak? Did you have to push his dinner tray out of the way when you got into the room? How are you going to clear his airway in this position?
Or: airway's open? Got an oral rubber airway in place? Good motion of the chest with the ambu-bag? Holding his chin the right way? Remember how to hold his chin?
Here's an important point that I try to emphasize. Take your time. Doesn't sound right, does it? But look, you're in a very controlled environment. You have all the personnel and equipment around you that you need. You have what 3 to 6 minutes before the patient sustains anoxic brain damage, and that's if you're not doing anything! So you really do have all the time you need. Take a deep breath, and take a few seconds, and just think of the ABCs then get on with the fancy stuff.
Okay, so now here comes the defibrillator. What's the rule nowadays? it's been a while since I did ACLS. For VT, I learned that the maneuver to make was to do a synchonized cardioversion. Let me lean over and ask my wife, who is an ACLS instructor. Okay here's the word. For pulseless VT shock the patient as if they were in ventricular fibrillation; that's to say, unsynchronized DC countershock, starting with 200 joules. Didn't work? 300 joules. Still didn't work? 360 joules. For VT with a pulse, if they're unresponsive but very hypotensive, she says you can try doing a synchonized cardioversion at 200 joules, but it may not be worth it. Make sure they're not awake! Don't forget the paddle gel!
We'll go more into defibrillators, how they work, and what joules and things are a little later on, but there's one more point that I'd like to make. There really is no reason to yell and scream and shout in a code. A well-run code is quiet. There may indeed be lots of activity, but the basics, the basics, the basics are being done A, B, C are established, IV access is established, drugs are coming in, equipment is being used you have a great deal to contribute by staying calm, and communicating your sense of calm to the others. You'd be amazed how much this can help. Don't yell. Speak clearly. Make sure someone is in command it may have to be you at first! Give the process time I always say that the first, oh, 125 codes are the toughest(grin!)
Here's the other big scary one. For this one, you want to shock them as soon as possible, no cardioversion, no synchronization, no nothing but electricity, 200 joules, as quickly as possible, followed if necessary by 300, then 360 joules. Establish ABC, get ACLS going.
We're speaking honestly here? Well honestly, I think there's a reason why God invented cardiologists. Narrow or wide complex, my concern is: are they making a blood pressure? If they are call for help and monitor closely. If they're not, call for help and start a code. This is not to say that narrow versus wide doesn't exist, or matter they do, and it does, and you will see this kind of thing. But the practical principle for you as the person at the bedside is always the same is the patient perfusing with this rhythm? Get all the help you need. I guess I should say that my own interpretation is that wider complexes tend to be coming from lower down, and therefore are probably VTs and that narrower complexes are probably coming from higher up, and may be things like SVTs supraventricular tachycardias. Compare the VF strip to the PAT strip, and you'll clearly see the difference.
Pretty much as described above. Try to remember which patients are DNR make sure you get the strip from the printer. If the run breaks on it's own, count the beats in the run, and document it that way: "Patient had two episodes of wide-complex tachycardia (ha!), one 22 beats, the other 30 beats. Potassium and magnesium repleted, am levels pending. Strip taped to flow sheet."
Don't shock her! Don't thump her either. Call for help, get the team to the bedside, monitor her closely because she may lose her pressure at any time at which point you can thump, or shock her. Patients in this situation are very tenuous - watch them very carefully. Usually the goal here is "chemical cardioversion" up until very recently all these maneuvers were made with lidocaine boluses and drips, followed sometimes by procainamide, but just recently I understand that amiodarone has come into the situation. Here's my wife, also a MICU old-timer, speaking from the couch on this subject: "People still use lidocaine in this situation because that's what they always did, so they just keep doing it, but it's of indeterminate value." Can you tell that she's in grad school? "There have been no studies that show that lidocaine is really effective it's all anecdotal. There's been one really good study out of Seattle called the ARREST study, that showed significant improvement in this kind of situation when people were treated with amiodarone." Whoa! You go, my girl!
This is why you were watching them.
My wife says that they don't teach this maneuver any more in ACLS, but that most experienced folks use it. The thump is a carefully delivered punch in the chest (my parents always taught me not to hit people, so this is hard for me). The idea is to strike downwards with your fist onto the middle of the sternum, right around where you'd do compressions, from a height of about 18 inches, full force, hitting with the fleshy part of your fist instead of the knuckles. I've seen this work myself, as I've mentioned above, and I'd always want people to know how useful it can be. You'll hear the old guys stand up when they see VT, and yell down the hall "Hit him!"
Make sure you look at the patient before you code him! Here's a relevant story from about a million years ago during the last Ice Age, it seems to me. I was working with a new nurse on one of the floors. She had a patient on a monitor, portable job outside in the corridor, and the nurse's task was to read the monitor every hour, and document the rhythm. A really frightened shout from the nurse down the hall I bolt down there the patient's wires had come loose, she'd seen something scary on the monitornext night, same nurse, same patient, another shout from down the hall the patient was in unresponsive VF. Full code. No go. Holy cow that was literally twenty years ago, the last time I did mouth-to-mouth.
This is a weird one, and pretty rare, but you should know about it. Torsades is an unusual kind of VT. In "normal" VT (ha!), you could think of the electrical signal going through the heart, back and forth, through the tissue, zipping along, but always along one axis, one direction of travel. In Torsades (they also call it "polymorphic VT" actually, whichever one you call it, they'll call it the other one), the axis actually rotates as the arrhythmia goes along it swings, rotating around the heart, as though around a pin stuck in the middle of the heart. There's a lot of scholarly debate about what to do for this arrhythmia my experience is that shocking them in the regular ACLS way does the job. The question then becomes: why did they get it? My understanding is that certain meds are usually the problem they cause the QT interval to get longer and longer, which in turn tends to set off this unpleasant problem. I've seen Haldol do this, and I've seen patients sedated with Haldol get taken off it, as their QT interval has been seen to get longer. Does this happen in quinidine loading? Procainamide loading? I forget anybody know? I need to look this one up again.
Here's how I understand it: the ventricles can generate their own escape rate, just as the AV node can, called the "idioventricular rhythm" it's very slow, around 20- 40bpm, and it looks like this:
See any p-waves? No p-waves. Wide and bizarre? Pretty bizarre, anyhow this and the rate tells you where the rhythm is coming from low down in the ventricles. Very slow not really fast enough to do what, group?: (All together now) "Generate a blood pressure!!" Right. Thank you.
The "A" in AIVR stands for "Accelerated". Meaning exactly that the strip shows an idioventricular rhythm: no p's, coming from the ventricles (remember how to tell if it's coming from the ventricles in lead II?) but faster than the "normal" ventricular rate of 20-40 bpm. Maybe 60, or faster even. Will this rhythm perfuse? Partly, anyhow. The ventricles will pump, if sort of slowly. Will this patient have, or not have, the benefit of atrial kick?
The mechanism here is like the escape, or "rescue" mechanism in the accelerated junctional rhythm. The AV node speeds up, for reasons of it's own which I certainly don't know about, (but which the cardiologists don't seem worried about), and so can the ventricular pacemakers speed up and, they capture assuming they're running faster than whatever the underlying rhythm is. Let's say you've aggressively beta-blocked your patient down to, say, a sinus rate of 50. That's slower than the intrinsic junctional rate, correct? A frisky ventricular pacemaker might wake up and capture at a similar rate "A" - IVR.
People don't get upset much about regular AIVR - the feeling seems to be: so the ventricle woke up and captured, so the patient is a little too beta-blocked, big deal hold the next lopressor dose, I'm going to bed. There's a rare second kind of AIVR, just in case you really wanted to know irregular AIVR. This one is dangerous I seem to recall being told that it's functionally the same as complete heart block. I don't think I've ever seen it, unless while watching that sad "rhythm of death" you see on the monitor just before your patient passes away.