#15: Arrhythmia Basics for Nursing Students

[Music] Hi, I'm Cassidy, and I'm April, and together we are fashion historians, friends, and co-hosts of Dress, the history of fashion. A podcast about why the clothes we wear matter throughout history and around the world. From the cultural and societal to the personal and often political, with each episode we explore the multitude of meanings quite literally sewn into the clothes we wear. Please join us in unraveling the hidden histories residing in your closet. New episodes are available on Wednesdays and are dressed classic episodes re-air each Friday on Apple Podcasts, Spotify, or wherever else you listen to your favorite shows. [Music] Hey everybody, welcome back to the Straight A Nursing Podcast. As I mentioned in the last episode today we will be talking about dis-rhythmia's and a little bit about the common features of each one and what you're going to do about it. So note that what you're going to do about a part is based on general knowledge and is in no way intended to replace your hospital or school or clinical locations, policies and procedures. So with that said, let's just do a quick, quick review of the main elements of the electrocardiogram and that is your P-Wave, your QRS in your T-Wave. So the P-Wave represents your atrial de-polarization which is basically your atrial contracting. The QRS represents the ventricular de-polarization. So ventricular contraction, that's the QRS and the T-Wave is your ventricular repolarization and that's as the ventricle begins to relax. So again, that's P, QRS and T. So let's talk a little bit about the dis-rhythmia's that occur in the atria and we'll start very simple with premature atrial contractions. These are basically extra little beats that occur within a normal rhythm. So P-A-C's are not a rhythm in and of themselves. So what you will have is sinus rhythm with P-A-C's or sinus-tackocardia with P-A-C's or even sinus-braidocardia with P-A-C's. So the rate can vary wildly from slow to fast. And basically it's just a little interruption in the rhythm. You will see a little bit of irregularity where these P-A-C's occur. When you look at the P-A-C's on these, the wave that corresponds to the atria contracting, it's probably going to look a little bit different than your other P-A-C's. It, look at, we call it the morphology, how it shapes. Look at the morphology of the P-A-C and it's probably going to look different from all the other beats. Because it's occurring from a slightly different location in the atria. Note that sometimes, especially if you're looking more at a faster rate rhythm, the P-A-V for that premature contraction could even be hidden in the T-Wave. So look for a T-Wave that looks a little funky and maybe has an extra little bump to it. And that will give you a clue that you're looking at a P-A-C. Your QRS complexes are going to be the same because again, this occurs. The beat originates in the atria. So there's no issues with it once it gets to the ventricle. It's going to conduct through just fine. And let's talk a little bit about what causes a P-A-C. Caffeine is a huge one. Caffeine anxiety stress. Okay. Also heart failure, pulmonary disease, nicotine. I forgot to mention when I mentioned caffeine, I kind of usually group nicotine in there as well. You can have P-A-C's within MI. So they're not always totally benign. You can have them with hypoxia, ischemic, myocardium. So even though sometimes they're usually something that we just take note of and move on. You do want to keep an eye out, obviously. But they can be associated with some things that aren't so great for your patient. But in a nutshell, usually not a big deal. You have P-A-C's all the time. I have P-A-C's when I drink way too much coffee. You're going to make note of them when you do your monitor strips, make note of how often they're occurring. Keep an eye on them and you're going to move on with your day. So that is the nuts and bolts, the down and dirty on P-A-C's. So how about something a little bit more interesting? How about atrial flutter? So atrial flutter, don't see it that often. I see atrial fibrillation probably, you know, 10 times more than atrial flutter, maybe even more. But what this is, is this is that one that has that sawtooth pattern. Very easy to recognize, very, very distinctive. So typically your atrial rate in atrial flutter is going to be really, really fast. We're talking 250 to 350 beats per minute. Note that not all of these atrial beats conduct on through to the ventricle. So your ventricular rate is going to be usually like one for every three atrials or one for every four. So your ventricular rate can can be normal while your atrial rate is really fast. But typically what we'll see in atrial flutter, especially when it first occurs, is that both will be a little fast. And that's what we call uncontrolled or R-V-R rapid ventricular response. And we say it has R-V-R or is uncontrolled when the rate is above 100. The ventricular rate is above 100. So you're going to look at the rhythm. It's going to be fairly consistent. You're going to have probably four or so atrial flutter waves and then a ventricular beat and then four atrial flutter waves and then a ventricular beat. And it'll be pretty regular. You will not be able to see the P waves. They're called flutter waves in the case of atrial flutter. So don't try to measure a P or an Aval because it doesn't really work because you don't have a Q-R-S for every flutter wave. Your Q-R-S again is going to be completely normal because again the conduction deficit or conduction dysrhythmia is up top. Once it gets through to the ventricle, all is good, it's going to conduct normally. So what can we say are the common causes with atrial flutter? Heart failure is a big one. Ischemia NMI. Again, you could also have it with rheumatic heart disease and thyrotoxychosis. Things like that can cause some atrial flutter pulmonary embolism. You could have valve disease can cause atrial flutter. So a little bit more pathology associated with atrial flutter than say just the one we just talked about, the premature atrial contractions. So what are you going to do about atrial flutter? You want to find out right away, is this new for the patient or not? If your patient just got there, you hook them up to the monitor and they're in a flutter, find out if it's new if you can. And if it is, you have a little bit more options with treatment than if it's chronic. So if it's a new onset, typically less than 48 hours, you can typically get someone out of atrial flutter using synchronized cardioversion. And that's where we put the pads on them, sedate them so they're comfortable and give them a little and kick start that sinus node into doing what is supposed to do. Works a lot of the time and not all the time. Some people have resistent atrial flutter and they need different treatments. But if your patient's been in a flutter for a while, you're probably not going to synchronize cardiovert them, especially if they have not been getting anti-coagulation treatment. So as the heart is in atrial flutter and the atrial is beating 250 to 350 times a minute, it's very turbulent in the atrial. So clots can form, blood clots can form. And when you kick the heart into a regular rhythm, quickly like in synchronized cardioversion, that clot can be ejected out and huge risk for stroke. So you're not going to cardiovert someone who's been in atrial flutter for an unknown and out of time, but they're in the hospital and they've been working. monitored and voila you look on the monitor they're in a flutter and you know maybe you try some medication treatments first and they don't work you can go to synchronize cardioversion so what would be some of those medication treatments if your ventricular rate is really fast basically the ideas that you want to slow things down so basically we're not going to worry so much about the h-roll flutter part as we are worried about the ventricular rate part so beta blockers calcium channel blockers, deltaisum the common one are going to be used for that also amiodarone I see a lot for controlling that ventricular rate and amiodarone will often put someone back into sinus rhythm which is super cool so the down under on h-roll flutter you want to control the ventricular rate cardiovert if you can and the patient will need to be anti-coagulated if they're going to stay in a true flutter and that's just going to be their chronic heart rhythm they need to be anti-coagulated huge risk for stroke so the cousin to atrial flutter is atrial fibrillation this is the one that we see more often of the two way more often of the two so with atrial fibrillation actually pretty easy to recognize it is the hallmark of this is irregularly irregular which is very hard to say and what that means is your atrial rhythm is all over the place you'll maybe when you first glance you'll think it's P.A.C. but when you look at it more closely you'll see that the atrial rhythm is just wacky it's just all over the place there's no rhyme or reason to it you will also not be able to see P waves so those would be the two core things with atrial fibrillation no discernible P waves they're just it just looks kind of bumpy but you can't pick out a P wave and all that mess and it will be irregularly irregular and all those little bumpies are atrial contractions they are basically kind of like P waves but we're not going to count them as P waves because they're not corresponding each and every one to a discernible present Q or S so that atrial rate when you look at those little bumpy bumps is going to be high super high like 300-ish high so the basically the atrial just kind of quivering more less they're not really they're not doing a lot the ventricular rate again just like with a flutter is what we really want to pay attention to so if it's controlled we say it's controlled if the rates below 100 we say it's uncontrolled or again R.V.R. rapid ventricular response when it's above 100 so the way you would chart that would you say you'd say atrial fibrillation with R.V.R. or A.C.B. with R.V.R. or A.C.B. uncontrolled again you're not going to see P waves the P.R.I. not measuring it so one less thing to do right the Q.R.S. is typically going to be less than 0.12 but note that you can have atrial fibrillation in the presence of a bundle branch block and this one is actually kind of hard to see and recognize because when you have a wide Q.R.S. because of a bundle branch block and it's all irregular it's going to look like at first glance it might look like polymorphic V-tac and that would be very bad so you would need to take a close look at something with a wider Q.R.S. so what can cause atrial fibrillation well you know what let's back up just to touch I want to kick hit on something pretty important with atrial fibrillation notice that the atrium is just kind of quivering and it's not really doing anything remember the concept of atrial kick where the atria contract and they push out you know that little bit of extra blood into the ventricle we're going to lose atrial kick in a fib so you're going to lose I want to say it's about 25% of your atrial kick in a cardiac output win an a fib so if your patient goes into a fib just right in front of you keep a close out of their blood pressure it is likely to drop a bit when they lose that atrial kick if they've been in a for a while they've compensated they're kind of used to it but definitely keep an eye if this is new onset for your patient watch their blood pressure okay so what can cause some atrial fib relation how about acute MI you could have coronary artery disease some CHF some cardiomyopathy hyperthyroidism ischemia I've even heard of it being brought on by an alcohol binge any kind of heart disease pulmonary disease can cause a fib so you will see this quite a fair amount in the hospital clinical setting so then of course the next question is what are we going to do about a fib again name of the game is controlled of a tricular rate you will do that with mostly what I see happen is we give an amiodarome we give that as a there's like a loading dose and then a continuous drip for like I want to say 18 hours maybe so you start with a higher dose for about six hours and then you drop it down to 0.5 milligrams and that goes for the next 18 hours so you can usually not always but usually get them to convert back into sinus rhythm with an amiodarome drip and then you transition them over into PO amiodarome and that often does the trick but there's a few other things that you can give or do beta blockers sometimes calcium channel blockers again you can cardiovert them again if it is new onset and you know that they don't have big clocks developed yet and if it's going to be chronic and this is just what they do and if people live in atrial fibrillation all the time is they need to be anti-coeulated very important okay let's go into super super goodness gracious super ventricular tachycardia I have had my coffee today I promise SVT so this is you know you have your sinus tachycardia which we didn't really talk about but this is different from sinus tachycardia in that the rate is faster and because it is so fast you cannot see the P waves the QRSs are so close together the P waves are getting lost in prior you know EKG tracings like maybe they're lost in the T wave you just can't see them everything's just so close together but you can tell it's sinus because the QRS is narrow so you know it's originating up top once the message gets to the ventricles everything runs fine so your QRS is normal because you can't see a P wave you don't know where in the atria the rhythm is originating so all you know is it's above the ventricle super ventricular means above the ventricle so this is just a tachycardia that occurs above the ventricle it is going to again be very fast 150 180 220 really fast so why are we concerned about this people you know you're working out your heart rate might get up to 180 you're not in any danger but someone in the hospital who's chugging along at 180 for a while that's really dangerous why well first of all filling times and the ventricle are going to be vastly reduced so again their cardiac output will be decreased the blood pressure will drop you're also going to have way increase myocardial oxygen demands and when the heart gets the schematic it gets unhappy and bad things happen so you definitely want to control your SVT and how you do that depends on if the patients stable or if they're unstable and how do you tell if they're stable their blood pressure is okay they don't feel dizzy they don't feel short of breath they don't feel out of the ordinary and anyway if they are unstable maybe their mentation is decreased their blood pressure drops they have chest pain if they're unstable you're going to treat more aggressively so the first thing I would do if I had someone go into SVT is I'd put a little oxygen on them give their heart a little extra help as it works so hard with this really fast rhythm you can synchronize cardiovert SVT happens all the time you would If you do this, if someone is unstable because you want to get the heart back into a normal rhythm as quickly as possible, you could also give them adenosine. You might try adenosine first. It just depends on how unstable they are. Adenosine is that medication that's going to reset the sinus node. It will show acistually on the monitor for about seven seconds, really, really long seven seconds. When it kicks back in, it will be hopefully normal sinus rhythm. You can give amiodarone twice. I think I've only personally given it once in six years. I had floated a telly that day. Floating out of the unit is always disorienting. Suddenly, you're taking care of four patients who are only on telemonitoring and not every monitoring device known to man, which for an ICU nurse, it's really weird to take care of patients that are not on pulse, ox, blood pressure, telemonaduring, everything all at once. I had a patient who was in SVT and symptomatic, not feeling good, having chest pain, etc. We did adenosine. I called my friend who was a rapid response nurse that day from the ICU to come do it with me because you need extra hands on deck if something should go wrong or whatnot. We got the crash cart in the room, not because we thought the patient would crash, but because we needed to have him hooked up to the monitor on the crash cart because it prints a continuous strip. We wanted to be able to document and record that acistually on the adenosine. So, Porcay, he was so scared and so nervous. I learned that the name of the game with giving adenosine, if your patient is awake and conscious, is to just stay really calm. Their heart is racing. They're already super anxious because they can feel that pounding in their chest and then suddenly they're going to have their heart stopped for seven seconds. What? So just staying super calm really is contagious for your patient. Turn the monitor so that the patient can't see it. There's a little tip for you so that you can see it because if they see that flat line, they are going to freak out. So anyway, little tip for giving adenosine. And I believe it worked the second dose we gave. I believe it did work and he was fine. So anyway, you're going to give adenosine for SVT or synchronized cardiovert, which is where you sink the electricity to the exact right place so that you don't cause what's called R on T phenomenon. And I'm not going to go into all of that, but just know if you hear R on T and me, it can induce V-Fib, ventricular fibrillation and that would be very bad. So you synchronize cardiovert when you have a rhythm that you're shocking. Okay. So what can cause SVT? Big one is stimulants. You know, again, anything that stimulates cocaine, caffeine, probably also nicotine. I'm going to throw that in there as well. Big ones, hyperthyroid. Someone in hyperthyroid storm could be an SVT. High fevers, very dehydrated. You could have hypoxia, ischemia, causing SVT and conduction deficits. So if you go into the room and your patients in SVT and they feel okay, you could try a vagal maneuver. It might work. I've never seen it work, but it might work. I've also, for those stable patients that are having it and then not really compromised and you're not going to give a dent in a cardiovert, you can give a calcium channel blocker, like heart exam or a beta blocker. And again, put some of those on everybody. Just give their heart a little extra help. Okay. So those are the main atrial dysrhythmias. And now let's move on to talking about some ventricular dysrhythmias. So the first one to talk about would just be PVC's. Super simple, premature ventricular contractions. So these are going to look a little bit more obvious than your PAC's because they're, you know, they're just bigger, they're wider. So the QRS is a bigger wave when it just looks bigger when it's wider. So you'll see a PVC on the monitor. And basically what you want to do is just look at how often are they happening and are they perfusing. You can palpate a pulse and watch the monitor and see what the monitor rate is. You know, if the monitor rate says 82, but as you physically count the pulse, it's 62. And then you know, the monitor is picking up those beats just because the monitor reads electricity. But as you palpate, you're only getting 62. You know that those PVC's are not perfusing. They're not creating blood pressure. So that would definitely be an issue if say your monitor read 62, but they weren't perfusing beats and they were happening frequently and you go and take a pulse and it's, you know, 40, then we have an issue. And for the most part, they do perfuse. They do create blood pressure and we're just going to keep an eye on them until they become very frequent until they are multifocal meaning you've got PVC's that look different from one another meaning that they're coming from different places in the ventricle, which means you've got, you know, more conduction deficits. And if your patient is symptomatic again, chest pain, decrease in L.O.C. dropping O2 sets, dropping blood pressure, anything like that is going to be an issue. So let's just look at one of the main things that can cause PVC's is going to be your electrolyte deficiencies. So if they're having frequent PVC's, they're very frustrating that you're going to do to try to figure out why is probably check a K level on a mag level. You know, run a 12 leads, you can really get a look at them, see if they have varied morphology, meaning are they shaped differently and get a really good look at how often are they happening. If they are occurring in a row, that's worse than if they're occurring every few beats. Okay, so the treatment for PVC's, you know, correct electrolyte deficiencies, you might give a meodaron if they're really frequent and, you know, keep an eye on them definitely. For the most part, what I've seen is as we correct potassium, magnesium, and balances, the PVC's generally resolved themselves. Okay, so that's PVC's. Let's talk a little bit about, well, there's a few other things that can cause PVC's besides K-MEG. So I didn't mean to just gloss over that. You know, hypoxia can cause it any kind of stress on the heart. You'll notice a stress on the heart is a common cause for many of these, you know, mi ischemia, heart failure, being in a esodotic state can cause PVC's, even digoxent toxicity can cause it. Pay attention if your patient has a central line and maybe if they turn on their side, you see PVC's in the monitor and then when they roll back onto their back, they go away. Check that x-ray and see if the central line is maybe a little deep. If it's a little deep and it's, you know, way not just right above the atria, but actually in the ventricle, it can make the ventricle irritable and you will get PVC's. So there you go. Also, I mean calcium is another electrolyte, but for the most part K and mag are the big ones. Okay, how about V-tack, ventricular tachycardia? So somewhat common to have runs of V-tack. These are, you know, maybe 4, 6, 8, 10 ventricular beats in a row. And then the heart goes back to doing, it's a regular sinus rhythm. If your patient's in sustained V-tack, that's a code situation. Okay, you're going to follow your ACLS protocol on that. But if you're just having runs of V-tack, you are again going to check K and mag levels. Make sure that they are having a blood pressure. while they have these runs of e-tack notice it their blood pressure drops. to check when you're on a cuff pressure because about a time you take the cuff pressure, the V-tack is probably ended. But if they have an art line and you can watch blood pressure in real time, you can see if they're dropping their blood pressure with those. So correcting electrolytes is big with V-tack, you know, get them some oxygen. If it's sustained amiodarone, is probably the way that they're going to go. And then if it's a code situation where it's, the patient is unstable, then they are going to get cardioverted. And you know, I want to take something back from before I said you could give a denazine twice. You can give it three times. I apologize for that. I just noticed that I said that so you can give a denazine the first dose of six twice. So six milligrams, six milligrams. And if that doesn't work then you give a 12 milligram dose. So sorry for the backtrack on that. So V-tack again, you're going to see if it's runs a V-tack and how many beats. And are they perfusing correct electrolytes and possibly have to give amiodarone or cardiovert? Okay, so that was V-tack. How about. let's look at Torsaud's de poins. This is a really interesting rhythm and I've only seen it maybe once. And I don't even think I saw while it was happening. I just saw someone had printed out a strip to say, "Hey, cool. Look at this." Because it is kind of, well, it's not cool for the patient, but it is a really interesting looking ventricular rhythm. And so what this is, it's a very particular type of polymorphic V-tack that occurs when your QT is prolonged. That's why if you haven't read my post, I think it's titled "Why the QT interval matters." You want to read that. So you can go back and look over that if you're interested. So basically, your curious impulses in Torsaud's de poins revolve around the isoelectric line creating this distinctive EKG tracing that looks very distinctive. It looks like wider and more narrow and then wider and more narrow. And when I say wider and more narrow, I mean, vertically, like taller, shorter, taller, shorter, taller, shorter, V-tack, polymorphic V-tack. So they're all different shapes. And basically Torsaud's de poins translates to turning on the point. It's that turning around the isoelectric line that gives its name. And it's more or less got a pretty simple treatment. Usually it's magnesium deficiency that causes, well, not that causes it, but that treats it. You want to stop any drugs that prolong the QT interval. Correct. All electrolytes, not just mag, but mag is definitely going to be the first one that you're going to correct or treat. Mag inhibits calcium, which inhibits that early depolarization that precipitates Torsaud's if you want to get into the path of physiology of that. So GIF mag, correct any electrolyte imbalances, they may need to be defibrillated and note that Torsaud's can very easily deteriorate into a V-fit. So you want to definitely jump on that if you see it. And then there are the idioventricular rhythms. So what are these? These are, you know, you have those pacemaker sites in the heart, right? If they fail, then you're going to get what's called an idioventricular rhythm. And that rate is like 20 to 40 beats per minute, which is not good. Okay, cardiac output is going to be really low with a heart rate of 20 to 40. Usually idioventricular is the sign of the heart dying. When we have patients on comfort care and we're allowing natural death, you'll see oftentimes rather than them just going straight into ecistually. A lot of times you'll see the QRS widening, widening, widening, and they'll end up in an idioventricular rhythm before it just widens progressively until it gets to ecistually. But if you have a patient and you don't want them, you know, to be an idioventricular rhythm or it's unexpected for them, then you need to do something about it. And basically, you're going to give CPR. You're going to increase profusion by getting on that chest. They might get a pacemaker placed. You can give drugs to bump up the heart rate like a penethran, atropine, and maybe dopamine. So again, following your hospital, your facilities, policies, if there's a physician there, you'd follow what they have to say. But idioventricular, one is too slow to produce a perfusing heart rate with a good cardiac output and blood pressure you need to get on there and pump the chest for them. Note that idioventriculars can be accelerated. They can be faster than that 20 to 40. And in this case, the rate would be 40 to 100. And when the rate is faster like this, the patient's tolerated better. You can see it after an MI as the heart is repurposed. They can go into this accelerated idioventricular rhythm. And in that case, you're just going to kind of keep an eye on it. It can also be caused by drug toxicity, ischemia, always ischemia, right? And just structural problems with the heart. So, you may need to give atropine to get the rate up and give them some O2, let the doc know what's going on, of course, and see if there are further steps that need to be taken. Okay, so we've done idioventricular, we did V-tack, we did dors-torsods. Okay, so let's go into some of the, the pulseless rhythms. So, you can have a great looking EKG on the monitor that is not producing a pulse. And that would be PEA, pulseless electrical activity. And this is of all the rhythms, I think this is the one that scares me the most because it can look completely normal. So, your heart, if you got your patient on a heart monitor, the heart monitor isn't going to alarm at you because it sees a normal rhythm. What you will see, and this is why I love working I see where people are on multiple types of monitoring devices, you will see a drop in their oxygen saturation and their blood pressure. So, PEA looks normal, but it's not, it's not producing any kind of mechanical pumping action. Okay, so if you're at the nurse station and you've got a patient, let's just say you've got everything, you've got an SPO2 pulse ox, and you've got an art line. And you look up and your art line pressure is 50 or 40, and your O2 sat is 50 or 40, but your heart rate and EKG, like fabulous, you need to be highly suspicious that your patient just went into PEA and you're going to run into the room and do a coat. So, basically the ACLS algorithm for PEA is the same as for ASISTALE, first thing you want to do, um, call it for help as you're running and start compressions. Okay, get the crash card in there so that you can give all your ACLS drugs and get them on the monitor and all of that. So, PEA to me, one of the scariest rhythms out there because it can look so benign and you might not catch it as fast as you would say ASISTALE or V-Fib or V-TAC. Okay, so that was PEA. Speaking of V-Fib and V-TAC, they are also pulseless rhythms. So, let's talk about pulseless V-TAC first. This is a V-TAC that looks just like regular old V-TAC on the monitor, but like PEA, it is not perfusing. So, your patient's in V-TAC, you're going to high-tail it into the room. Check for pulse. Look at the patient. Don't look at the monitor. The monitor is going to tell you that they're in V-TAC. You already know that. You can, you know, assess their O2 SAT if they've got that on artline blood pressure. If they've got that on, obviously, but look at your patient. Check for pulse. You're not going to find it if they're in pulseless V-TAC. Hit the code button, call it for help, start CPR. And again, you're just going to follow your ACLS algorithm for that. If they're on a ventilator and you are doing CPR on a patient, you will take them off the vent and manually bag the patient. That is because as you were doing chest compressions, you are drastically increasing pressure in the thoracic cavity. Your vent is set with pressure limits. What's going to happen is as you're doing chest compressions, the vent is going to think that inter thoracic pressures are really high, long pressures are too high and it's not going to deliver a breath. You need to take them off the vent and bag them manually. V-Fib, another postless state, very bad. V-Fib is really easy to spot. It's usually a sign of a very bad thing. I've only had one patient of mine go into V-Fib as I was taking care of them. Thank goodness. I was not alone in the room. For some reason, there were two other nurses in the room helping me with something. I think I was having trouble with his pick line. I can't remember, but there was an issue. I remember his arms were really swollen and we might have just been trying to get the swelling down by propping his arms up on these big wedges. It was something like that. I remember being kind of at the foot of the bed and there were two nurses up at the top of the bed messing with this pick line or getting his arms elevated or something. In hindsight, looking back, I think they were hovering and helping me because I was a pretty new nurse at the time and I had a really sick patient. I have great co-workers and they're never going to leave anybody stranded and they probably just knew that I needed a little extra love, which was great because at that moment, the patient kind of woke up a little bit. He was in a sedated, just had come from a big, big big big big big big surgery. I woke up a little bit, dropped his O2 sat. Everything kind of happened all at once. I wouldn't say woke up, moved around a little bit and then V-Fib on the monitor instantly. So instantly started pulling stuff off the bed. Somebody hit the code button. It wasn't me and they started compressions immediately, which was awesome. They were right there. Then the doc came in immediately because he had been close and when he heard that code called overhead, he knew it was his patient. So got in the room and I worked my tail off all night long on that guy. I stayed until like 10 a.m. the next morning just catching up on paperwork. But anyway, so V-Fib, very bad. That's the moral of this story. So in V-Fib, the ventricles are quivering and not contracting, not producing a blood pressure or pulse. So getting right on the CPR, getting your crash cart in the room, getting your ACLS drugs on board, and hopefully getting back into sinus rhythm with the pulse and neurologically intact. Okay, so those are the main ones. Assistually, obviously, the classic flatline. If you're watching a show, like one of those medical TV shows, they always shock the patient. That's so wrong. And I wish people would stop doing that because then the public, when the family's in the room and they're in a Sicily and you're not shocking the patient, they're probably wondering, "Why aren't they? Where's the pads?" But that's not how you treat Sicily because there's nothing to shock. There's no rhythm. So basically, this is compressions, compressions, compressions, and epinephrine. And if you're listening to this and ACLS has changed by the time you listen to this, obviously, you're going to follow current guidelines. So, assistively, flatline, super easy to see, hit the code button, get on the chest. Your team will be there soon, I promise. So let's talk a little bit about heart blocks. I have a whole post about heart blocks. I think it's called heart blocks, a relationship and trouble. And you can check that out, but I'll just go over the down and dirty of them real quick. So, so that you can at least get a little bit of a refresher or maybe you've already listened to that one. And this is just review for you. But for heart blocks, there's a few different kinds. First degree heart block is the one that you're going to see the most often. And in this one, your PR interval is just longer than normal. You'll have a regular rhythm. You know, it can be fast, it can be slow, it can be normal. But the PR eye is a little bit longer than normal. So, you want to make sure that all the impulses are getting through. If they're not, then you are, you're getting to a higher degree of block. Okay, higher degree, like second degree, third degree. So, first degree heart block, you want to monitor the PR eye, see if it starts to get longer. Take a note of what drugs the patient is on. First degree heart block is often caused by drugs that affect the AV node. So, like beta blockers, something like that. They could be having an inferior MI. So, if it's a brand new, like, oh, look, Joseph first degree, all of a sudden, then you're probably going to be grabbing a 12-litre and taking a closer look at what's going on with his heart. It can also occur in patients with, you know, coronary artery disease or rheumatic heart disease. So, basically with first degree, keep an eye on the PR eye, see if it gets longer and longer and longer. If it does, you want to obviously, you're going to let somebody know, especially if this is new. But take a look at the drugs that the patient is getting and what could be causing that first degree is this new for them, things like that. For the most part, if they are really symptomatic, they could be getting a pacemaker if they're at high risk for progressing to a more dangerous heart block. So, then you have the next highest degree of block is second degree heart block type 1. And I really wish that whoever named these had named them first degree, second degree, third degree, fourth degree, that would be so much easier to remember because this is where I always and still after all these years, I still get confused about second degree type 1, second degree type 2. And I have to stop pause think about it. The second degree type 1 also goes by winkybock or mobets 1. So, there's three names for one type of heart block, second degree type 1, winkybock, mobets 1. I know it's just whatever it is what it is. We just have to do with it. Caused basically by the same things that cause a first degree block. It could also be caused by mitral valve prolapse. And what you will see in second degree heart block type 1, aka winkybock, aka mobets 1 is this gradual lengthening of the PR interval. It'll be, you know, maybe normal, slightly longer, slightly longer, slightly longer, and then a dropped QRS. And then the cycle will repeat like clockwork. So you'll see the PR I get progressively longer with each beat and then drops a beat. So your ventricular rate and your H2O rate will be different. And you just want to make sure that that dropped beat doesn't cause a hemodynamic compromise. So if their rate is too low and they're symptomatic, you can give atropine for the most part, second degree type 1 is kind of a transient rhythm. And they'll come out of it. You want to obviously take a look at any any medications that would slow conduction through the AV node. You know, if they're maybe calcium channel blockers and digs can make this a little bit worse. So just keeping an eye if the braided cardia makes them symptomatic or if they are in a braided cardia because of it, you want to treat that, you know, give them a little oxygen if they're having any kind of issues. If they're really sick, you can pace them to get the rate up, give atropine, etc. Maybe they'll get a permanent pacemaker if this is something that they're in all the time. The next highest degree of block is second degree heart block 2. This is also known by an extra name, which is MOBITS 2. So as we go up in the degrees of heart block, they do get more serious. And this one, you do have drop ventricular beats, just like in second degree heart block type 1, also known as winky block or mopets 1. But in second degree heart block type 2, also known as mopets 2, you'll have ventricular beats that are dropped, but it's random. There's no rhyme or reason to it. And you know, second degree 1, it was every 4th or 5th beat maybe. And this one, it's random. It's here, there, harder to see because of that. Your p-waves are going to be jamming along just fine, so your h-wheel rate is regular. But some qrs is here and there, totally randomly, are going to be dropped. So your ventricular rate will be irregular. Second degree heart block type 2, also known as what? Mopets 2, very good. This one can be dangerous. This one can progress to third degree heart block pretty easily. It can also cause very symptomatic breathing cardiac. So your avi note and this rhythm, second degree heart block type 2, also known as mopets 2, is pretty sick. So you've got causes like ischemia, digitalis toxicity, could be beta blocking meds that are causing it, things like that. So you give atropine for the bradycardia, you can paste them. And if they're hypotensive, maybe some dopamine. So it's not a watch and wait kind of scenario. You want to let somebody know a sap, a sap, a sap, that your patient is in mopets 2, get them on some o's, make sure that I would put the pacing pads on the patient and have it ready to go just in case and be ready with things like atropine if you're going to need them. And then the most dangerous heart block is third degree heart block. This one's just called, well actually does go by another name, you might hear it called complete heart block, but that's a lot easier than the other ones. And this one's really bad, very bad. This can cause your patient to deteriorate very, very quickly. You're going to have it occur most likely in the cases of things like an mi, a conduction system disorder. It can happen after heart surgery, open heart surgery, again, dig toxicity and avianoblocking meds. So in this, in this third degree heart block, the atria is doing its thing, the ventricles are doing their thing and they're not communicating. They are atrous contracting over here, regular as all get out and the ventricles are contracting over here. Also, regular is all get out, but they're not talking to each other. And the ventricular rate could be very slow with this. So most likely in third degree heart block, your patient is going to have a bradycardia amy symptomatic. If they're not right now, they might get there, be highly suspicious that they would get there. I would put the pacing pads on them, right away, have them ready to go. They are at risk for sudden cardiac death and if that doesn't make you nervous, then nothing will. You want to definitely stop any avianoblocking meds, call the doc, make sure there's a cardiologist that is coming to see the patient and someone in third degree block probably going to need a permanent pacemaker. So for that patient, you will be super vigilant and ready for a code to be called. So have the crash card handy. It's going to be right there because you're going to have the pacing pads on them and you're going to be ready for anything. So I believe we've covered the main dysorhythmia. I hope that was super helpful for you guys. Again, if you want to read a little bit more about it, there's a post on the website, straightingrustingstudents.com, called Arithmias Don't Stand A Chance. The other one is titled Heartblocks, A Relationship and Trouble. And was there one more that I referenced? Well, if I did, I hope you wrote it down because now I can't remember what it was. But check those out and maybe we'll do a pod quiz on all the avianomias. I think that would be super helpful. I would have found it super helpful and I'm sure I probably made myself flashcards on all of this stuff and audio flashcards as well, back when I was a student. So anyway, if you have not visited the website and you're just found this podcast on iTunes, Stitcher or Google Play, then you can check out a ton more goodies for nursing students, new nurses, et cetera, at straightingrustingstudents.com. We are not just students when we are in school. We are students for all of our careers. You are a student though and you are having trouble or just starting and really nervous about school. You can check out my book Nursing School Thrive Guide available on Amazon as an audiobook, a Kindle book, and an actual holding your hands paperback book. And if you like this podcast, please rate and review on iTunes, Stitcher or Google Play. That really helps show up in the search results when other students are just randomly searching for things like nursing school or nursing that will help them in helping each other is what nurses do. So thank you all very much. I hope you have a great day and tune in next week for another episode of "The Straight Annersing Podcast." [BLANK_AUDIO]