Hi all – here’s another one – this one took a while, but it was a lot of fun to hunt around for strips and images. As usual, please remember that this file is not meant to be a final medical reference of any kind, but is meant to represent knowledge passed on by a preceptor to a new orientee. Please let me know when you find mistakes, which I’m sure you will!
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?
Why do people have arrhythmias?
What is the difference between a bad arrhythmia and a not-so-bad arrhythmia?
What is “ectopy”?
What does “supraventricular” mean?
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?
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.
The Nodes: 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 exactly is, exactly. Jayne knows – she works in the EP lab… anyhow, 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 its part of the heart, that same part of the heart responds mechanically, with movement.
Well – it’s supposed to! (grin! – what if it doesn’t? What’s that called? What would you do?)
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 its 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:
Negative electrode goes here
(here) (Ground electrode goes here…)
Positive electrode here
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 an upward blip on the cardiac monitor.
This is actually really important, and I’ll probably make this point too many times, but the direction in which 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: either the SA or the AV node. If the signal goes downwards – meaning, the signal is going the other way, backwards towards the negative electrode – where’s it coming from?
Like these guys. They go downwards, mostly, right?
So – they’re going the wrong way. Hm. So that means they must be coming from where? Well… they’re PVC’s, right?
Premature… aha! - ventricular contractions! They’re going backwards because they’re coming from the other end of the heart, down in the ventricles, and heading backwards towards the negative electrode in lead II… so the signal goes downwards… bing! Lightbulb go on? Which way are the normal ones headed?
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…
The Normal Complex: 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. Let’s say it again: Lead II is used as the 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. Who exactly do you think paid for drivers’ ed, anyhow?) 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?
(What do you mean, “Nice picture of your first girlfriend!”?)
1-1: What is a p-wave? What is the PR interval?
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 on the EKG paper.)
1-2: What if there’s no P-wave? No p-wave means that the SA node hasn’t generated a signal. No signal, no atrialmotion. 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.
1-3: What is the QRS complex? 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 it should to get through – maybe there’s a bundle branch block?
1-4: What if there’s no QRS complex? No QRS complex means that no signal has gone through the ventricles. No signal, no ventricular motion. Can you live without ventricular motion?
1-5: What is the T-wave? What is the QT interval? 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 an otherwise normal 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 “corrected” QT interval that lasts too long can mean that bad things may be developing – usually one kind of drug toxicity or another – which may show up as nasty tachyarrhythmias like VT. Haldol is infamous for this.
1-6: What if there’s no T-wave?
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 FAQ on “Reading 12-lead EKGs”.
1-7: What is the isoelectric line? 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 positions with treatment, and that position is: where they started out, on the isoelectric line.
Why do people have arrhythmias?
Lots of reasons, but if you think about things that are going to make a heart unhappy, then those are the things that will produce arrhythmias acutely: cardiac ischemia, hypoxia, MI, changes in electrolytes…obviously 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 or even reverse 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, usually 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” – meaning, 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 that makes the lungs stiffen up - whether acute or chronic - will increase the pressure needed to send blood through them. Now the RV has to work harder, and since it’s not built too powerfully to start with, if it’s made to work harder over time, it’s going to grow – like your biceps do during weight training (mine never did…).
This chamber growth is actually not a happy thing, because 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. And liver patients. Make sense?
We had another neat example of chronic chamber stretch recently: patient came in with a primary liver tumor that had been treated for a while. He was in a-flutter, probably because the impaired perfusion through the liver had kept his right sided pressures high for a long time. (His CVP was 20, and he was not wet – wasn’t making much urine.) Right-sided stretch.
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 yeah, he has them all the time whenever his K gets below 4, and we’re not supposed to call the team unless he starts having long runs.”
What is the difference between a bad arrhythmia and a not-so-bad arrhythmia?
The key concept: 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 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. Here’s an example – you’ve probably seen people with this.
Right – here we are in A-fib. Are there P-waves? Hmm – maybe? What are those fluttery looking waves along the isoelectric line? Not really p’s. So - no P-waves means: no kind of normal atrial contraction. Are there QRS’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’re probably filling very nicely. A lot 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 a-fib, I think of the atria, uh… 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, should be pumping properly, because there is a normally upright QRS – this means that the path of conduction is travelling in the right direction through the ventricular muscle mass, just the way it normally should – so they’re at least conducting okay.
The important points in this situation:
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 the old guy already recognizes 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. Probably. (grin!)
What is “ectopy”?
“Ectopic” 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. (CCU nurses in the audience – what arrhythmia would this be?)
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 idea is that these signals are premature, 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. (Pardon me – supposed to say: “A-fib with RVR” – rapid ventricular response…) 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.
What is “supraventricular”?
You’d think that this meant “atrial” in reference to arrythmias, but I believe we’re supposed to add AV-nodal (sometimes called “junctional”, or just “nodal”) rhythms to this group.
What are the supraventricular arrhythmias that I’m likely to see in the MICU, which ones do Ineed to worry about, and how are they treated?
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.
6-1: Sinus arrhythmia
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, varying with respiration. In 26-odd years I’ve never seen any physician show the slightest concern about this one. (French website…)
6-2: Sinus Bradycardia
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 sometimes a good thing – it means your patient has finally fallen asleep, or that her metoprolol is finally starting to work. A really 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 classically famous for 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. Mojo. Whatever.
Sedation: being sedate will drop most people’s heart rates.
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. As with an IMI, in the case of ischemia in inferior territory, the RCA is usually the problem… there’s lots more on the coronary arteries, where they go, and how they show up electrocardiographically in “Reading 12-lead EKGs”.
6-3: Sinus Tachycardia
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 “Pressors and Vasoactives”, and “PA – Lines”.
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.)
6-4: Paroxysmal Atrial Tachycardia (PAT)
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. How much caffeine did they drink today? 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 – as what you would then probably call SVT - things could get ugly, in the sense that the blood pressure might suffer – what drugs would you think about having on hand for this? Might need a machine, too.
6-5: PAC’s: (Premature Atrial Contractions)
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 – 5th 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. “Yo Ralphie! Your face has a weird morphology!”) Ectopic. The other thing you’ll notice is that it comes too soon – it’s 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”. Wooo….
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.
6-6: Atrial bigeminy – this means that every other beat is a PAC. Again – afib may be coming.