Atrial Fibrillation | Clinical Medicine

What's up, ninja nerds? In this video today, we're going to be talking about atrial fibrillation. This is a part of our clinical medicine section. If you guys like this video, it benefits you, it helps you, please support us, hit that like button, comment down in the comment section, and please subscribe. Those are the best ways you can do it. Also, we have a link down in the description box below takes you to our website. There we have a lot of great notes, great illustrations that I think will be helpful to follow along with during this lecture. On top of that, we're developing courses on those preparing for your step one, step two, your pants, etc. And we got some great merchandise that I suggest you guys go check out. All right, talking about atrial fibrillation. So, atrial fibrillation is a type of arrhythmia. We will discuss this in the actual arrhythmias lecture, but atrial fibrillation is a very specific type of arhythmia that we have to discuss because it's so common and it has a lot of different problems associated with it. So it's a super ventricular tacoc cardia meaning it originates in the atria that's the name atrial fibrillation. What I want you guys to think about when you think about atrial fibrillation is two particular eeological uh problems here. So one is it's due to a cardiac problem or it's a non-cardiac problem. Let me explain what I mean and I think this helps us to remember it and oriented in our brain a little bit easier. So cardiac causes one is there is something something that is causing high left atrial pressures. All right. So the left atrial pressures are super high. And one of the reasons why that the left atrial pressures can be through the stinking roof is because there is something wrong with the mitro valve. Now when the left atrial pressures are high, what it will do is is it will actually trigger atrial dilation. So now the atria will have to dilate because of that just high pressure. It's going to have to find a way to accommodate. When you cause atrial dilation, what you do is you cause what's at least in this term called atrial remodeling. Basically, it jacks up the circuitry. There's supposed to be normal circuitry here within the atria with the way electrical activity is conducted via the meioytes. But when you alter that, it leads to a lot of problems. And this is how aphib develops. So aphib will actually develop as a result where you'll develop these like weird types of problems here like these reentrant circuits due to this remodeling process. And this is going to be the problem here. these little areas develop these little like circular patterns of electricity that shoot off and they get sent down to the ventricles and that's the problem. You develop this irregular heart rate. It doesn't follow the normal conduction pathway. That's one particular problem, right? Is high left atrial pressure causing dilation causing remodeling which can lead to aphib. The question then arises is what is causing this left atrial pressure to be high? We already mentioned one of them. One of these is going to be mitro stenosis. And it's important to remember this because mitro stenosis is a disease of the mitro valve where blood can't get from the left atrium into the left ventricle. This part's being inhibited. And so that's one way that we can stimulate an increase in left atrial pressure is mitro stenosis. An important terminology here is when the mitro valve is diseased particularly during like roheatic fever which is a big common cause. This is a specific term, a specific type of aphib. We call this valvular AIB. We mentioned this briefly in our valvular heart disease lecture. That's one reason. So, it's blood not getting from the left atrium to the left ventricle. So, the pressure here is a lot higher. What's another thing that would cause blood not to be able to go from the left atrium into the left ventricle? Heart failure. Diastolic heart failure would be a big one here. So, another one would be CHF. Particularly diastolic heart failure, but also systolic heart failure is another problem because it's filled with so much blood, it's hard for it to accept any more blood because it's so congested. So CHF will also cause the left atrial pressures to be super high, cause it to dilate, lead to electrical remodeling, and then associated aphib. These are really, really big ones to remember. The next one, believe it or not, people usually think that this is a very, very common cause of aphib. It's really truly not. But one other reason that you can develop electrical remodeling is you have an area of the atria that is eskeemic or fibrodic. And now this creates these weird if you will reentrance circuits around that eskeemic or fibrodic tissue which then shoots off and creates these abnormal electrical activities in irregular rhythm that doesn't follow the normal conduction pathway. What would be this thing? Cardiac eskeeia. So again, one other reason that you can develop Aphib is you can develop this cardiac eskeeia which can lead to cardiac maybe fibrosis during the healing process lead to atrial remodeling and then you jack up the atrial circuitry. When you jack up the circuitry you potentially increase the risk of atrial fibrillation. So cardiac eskeeia, cardiac fibrosis, atrial modeling and aphib. This is the problem. But we have to ask ourselves the question what is precipitating the cardiac eskeeia. This is usually coronary artery disease. All right. So this is usually a patient who has underlying coronary artery disease or they suffered a myioardial infarction. All right. So we have the cardiac causes. One, it's my it's both of these particular scenarios. Left atrial pressure is high. you can't get blood from left atrium, left ventricle. One is because the valve is damaged or one because the left ventricular pressure is so high and you can't get blood in there because of heart failure or you have eskeeia. Both of these things create atrial remodeling and aphib. All right, next one is non-cardiac causes. This one's actually pretty cool. And what happens with this one is there's three particular things that I want you to associate this with. One is it's due to the lungs, some type of pulmonary disease. And usually the most prominent trigger here is going to be some type of hypoxia. So we're going to put here um hypoxia is the profound stimulus here that causes these patients to go into aphib. So hypoxia now when we talk about this let's actually put this here in black. So hypoxia is the primary stimulus. What are things that can cause hypoxia? Well one is you have to have some type of lung disease. Maybe you have a patient who has something like pneumonia. So they have an infection here of one of their actual lungs and it's causing VQ mismatch. Another one is patients who have COPD particularly chronic bronchitis because that causes a lot of like hypoventilation. And the last one is like a pulmonary embolism. All of these things can cause profound hypoxia. You know what that does is that ticks off you know near the atria you have these things called the pulmonary veins. Blood is supposed to come back from the lungs via these into the left atrium. The cells right around this area are super sensitive to hypoxia and they become ticked off. And when they get ticked off, they start firing. You know what we call that? We call that ectopy. So they develop this ectopy. This ectopic firing of these atrial cells here. And when this ectopy occurs, it doesn't follow the normal electrical pathway which then leads to atrial fibrillation. So these are the things that we start seeing in these patients is they get a ton of ectopy and this can then precipitate something like atrial fibrillation. Another thing here is that they may let's come to this one. Another one here is they have lots of catacolamines. This is a big one. So tons of catacolamines. You're like, "What in the stank is that?" That's norepinephrine and epinephrine. These are the primary ones. These puppies are stimulating the heck out of these atrial cells right here near the pulmonary veins and just agitating them. You know, there's receptors on the atrial cells. You guys know what kind of receptors? What are they stimulating? You guys know this would be really particularly stimulating what's called the beta one receptors. They're stimulating the heck out of them and they're really getting agitated. And that will cause increased ectopy and potentially aphib. The question then arises what's causing this catakolamine release? Why is our sympathetic nervous system on hyperdrive, right? And the things that I want you guys to remember is usually sepsis. So some type of infection if you will. I'm going to use sepsis as the example. Another one is it could be postoperative. So sometimes after a patient has just gotten a surgery, their body is trying to heal. And this can create an opportunity for this. Another one is fo chromoso cyto. This is a adrenal medularary tumor that's pumping out epinephrine and norepinephrine stimulating these beta 1 receptors in the atrial cells. And the last one is thyrotoxyosis. So whenever you're pumping out way too much thyroid hormone, so you got to stop being thyroid. You guys know that kind of reference, right? So hyperthyroidism, they really increase the sensitivity of beta 1 receptors. So if you're really hitting these, particularly this one I'm going to put here. These are really hitting those beta 1 receptors. They are really stimulating them. This is going to cause these atrial cells to become ectopic. All right? And then generate a rhythm that's not normal sinus rhythm. And here, let's actually make sure that this is an up arrow with the red there. All right? This is the concept I want you to understand here. So too much catakolamines, hypoxia. The last one here that I want you to remember is electrolyte disturbances. All right, so this is usually going to be the most common particular thing here would be things like where your potassium is really really low or your magnesium is really low. When these are low, they really alter they alter a lot of the electrical activity here and really trigger ectopy. There is one more. It's not crazy common, but they love to ask it on your exam. When patients go and they just binge and binge tons of alcohol and like this one time setting, there is a high risk of something called holiday heart syndrome. And you can have enough alcohol that it causes both hypoalemia, hypomagnesmia, and sympathetic activation. So, it's a weird one. Last thing real quick just because I'm remembering this here is for the sympathetic effects. One other thing that I would also consider in patients who just went into new onset AIB is sympathomimedics. So sympathtics. We talked about this um in the hypertension lecture. This is things like cocaine, uh methamphetamines, uh PCP. These are all drugs that have the capability to act like norepinephrine and epinephrine and increase your blood pressure and increase your heart rate or increase ectopy that can cause aphib. So these are the things that I want you to remember. Now if you're like Zach, how am I supposed to remember all this? I want you to remember maybe the pirates pneummonic. We're gonna have that pop up here on the board and that's going to stand for all of the things that you guys need to know to remember the causes of atrial fibrillation. Okay. Now with that being said, let's come to the last component here of atrial fibrillation which is when a patient develops aphib, we know why. It's either due to ectopy or reentrant kind of like circuits or remodeling if you will. One other thing that I really need you to know is when a patient develops Aphib, you can also really define them based upon the time that they have been in aphib. So what do I mean? Let's say you're here you have a patient and they are in Aphib but their AIB has lasted let's say less than 7 days. All right. In this particular situation this is called peroxismal aphib. So we're going to put peroxismal All right. So this means that these patients usually they have remodeling that's that has not yet occurred and so they may be able to snap right out of proxisal aphib and go back into normal sinus rhythm. So that's a potential for these patients is they're in aphib but they're usually in it for less than seven days and they snap back out into their native rhythm if it goes greater than seven days. So now if the patient has then branched into greater than seven days that they have been in Aphib, their heart's really starting to remodel and it's going to make it really hard for these patients to snap back into Aphib, but they definitely can. When they have been in AIB for more than 7 days, we call this persistent persistent AIB. The last particular scenario is let's say that this patient does snap into a out of a their native rhythm. Okay, good. But if they continue for more than seven days up to at least one year, this is usually what we call permanent AIB. The reason why this is important is really differentiating these two proxismal and permanent. Proxismal is these patients may have a little bit more of an ability to convert them from aphib into a normal sinus rhythm. Whereas patients who are in permanent AIB, they're already locked into this new remodeling and altered kind of like circuitry that it's literally impossible to snap them into a native rhythm. So that's really important terminology and we'll come up with a lot of other terminologies as we go throughout this lecture. Let's move into the complications of Aphib. All right, my friends. Aphib, what kind of problems can it cause? It can do a lot to be honest with you. Probably the most terrifying one and the one that you have to remember is going to be thrombboic complications, right? So the concept behind this is actually kind of interesting where if a patient has atrial fibrillation regardless of what the cause is cardiac non-cardiac causes atrial modeling ectopy doesn't really matter if they have this from aphib there is in effective atrial contractions. So all that electrical activity is causing like the atria just imagine it to like beat here beat here beat here it's just not good contractions. So, we're going to write here that it causes ineffective contractions. Because of that, it doesn't get the good kick that you'd want it to do and push enough blood in the from the atria to the ventricle. So, a lot of blood stays in the atria, unfortunately. What's that called? Stasis. And from the stasis of blood flow, what do we know about that? According to Veros triad, it increases the risk of a thrombus. So then you can get a thrombus that forms like a clot and usually it forms on the inner side here of the atria near like this little like appendage. It's called the left atrial appendage. That's usually the most common area for that thrombus to form. What's terrible is if that little piece of that clot breaks off a tiny little piece. So now you have a tiny little piece that it flicks off and these little guys go flying everywhere throughout the systemic circulation. Now you get an emblei. And that is really what is terrifying about this disease is if you have all these ineffective atrial contractions, whether it's due to ectopy or remodeling, whenever they're in aphib, they're going to have stasis of blood flow. They're going to have a thrombus and then they can break that off and cause an emblei. If these little pieces break off and they get into the systemic circulation, they can go and get blocked up into the vessels of various peripheral systemic vessels, right? So imagine in the central nervous system that little clot flicks off into like one of the corateeds or into the vertebral artery goes and gets stuck in one of those vessels blocks off the blood flow to the actual brain tissue and now you end up with a stroke. So some of these times they can present with a TIA like a transit eskeemic attack or it can prevent with a full-on infarction of the tissue called a CVA. And this is usually one of the most terrifying effects of this because again the neurological deficits. The other one is you could flick a little piece off that gets stuck in what's called the superior mesenteric artery or the inferior mesenteric artery. And either way you can lead to something called acute messenteric eskeeia. Sometimes it could lead to es schemic colitis but either way you're causing damage to the actual small bowel and large bowel and this is going to become es schemic and it's going to cause crazy abdominal pain. So if a patient has a known history they develop neurological deficits think about that complication. develop crazy abdominal pain, think about these complications. The other one is if they develop intense leg pain, uh maybe even like decreased pulses, then you really want to start thinking about did they throw a little clot that got stuck in one of the actual peripheral vessels and now it's causing a patient to experience acute limb eskeeia. These are all medical emergencies and the most terrifying effect because you could potentially lose a leg, cause massive eskeemia to the bowel and need a callectomy or some type of like bowel surgery and have permanent neurological deficits. So this is something that you have to know as a potential complication of atrial fibrillation. The next one here is acute heart failure. So this one's kind of interesting. I wouldn't say it's crazy common unless the patient is in what's called aphib with RVR, which we'll talk about a little bit when we get into this tacic cardio component. But let's say that a patient has Aphib. We're going to say Aphib and we're going to use this term with rapid ventricular rate. That usually has to be at least at least greater than 150 beats per minute. If you're not pumping up greater than that, it's really hard to cause this problem that we're going to talk about. When a patient is in aphhib and they are really having lots of ectopine remodeling and the the ventricles are firing at a rate of 150 beats per minute, that's really fast. What happens is is it literally gives the ventricles almost no time to fill. Imagine if they're beating 150 times per minute. That is literally giving them very little time to fill with blood and then contract a normal volume of blood. So their filling process is decreased. So now because of them having such a fast rate, they end up with what's called a decreased filling time. So their filling time is going to drop. And if their filling time drops, they're not going to fill their ventricles adequately. So now they're in diastolic volume drops. That causes their stroke volume to drop. That causes their cardiac output to drop. If they have a decreased filling time and then they drop their cardiac output, now they're not profusing tissues and this could potentially lead to a low blood pressure and worst case scenario, it may lead to shock. So you want to be thinking about this. If a patient has AIB, they snap into AIB and they're going greater than 150 beats per minute and their blood pressure is low, this could be potentially driving their hypotension. It's always tough. Usually in these patients if they have an underlying disorder like mitro stenosis that definitely supports that or if they have heart failure it they're already having reduced diastolic filling. You have them go at rates of greater than 150 their diastolic filling drops even more. But this is one particular problem that I want you to think about. The other concept here is if your heart's beating so fast it doesn't allow the ventricles to adequately fill. So then a lot of blood stays in the atria. And if a lot of blood stays in the atria, it's going to start backflowing right into the pulmonary veins. And that's going to cause the pulmonary capillary wedge pressure to kind of go up a little bit. And if that goes up a little bit, then the fluid starts leaking out into the interstitial spaces and then you start getting edema here. You start getting fluid here. And what is this called? You guys better know this. This is called pulmonary edema. And the problem with this is is depending upon the severity, this may just cause generalized disna or it may cause this fluid to kind of like segregate out into different parts of the lung when they're laying flat. You guys remember this? This is going to be when they're laying flat or they're sleeping. They can have proxismal nocturnal disnia or thopia or maybe they just exhibit dysnia. And this could be at rest. This could be with exertion. But these are the classic findings of patients with pulmonary edema. In worst case scenario where they have mitro stenosis or heart failure and they start beating at a rate of 150 or more, they can really fill up their alvoli and I mean a lot of them and then you start causing massive alvolar filling with fluid that leads to something called VQ mismatch and this can present as hypoxmia. And if they become hypoxmic, this can cause increased work of breathing. Their respiratory rate may go up and these are definitely concerning signs. And you don't want to miss this in a patient who is definitely an AIB with RVR. All right, so these are the things that I want you to watch out for. If a patient has a known history of Aphib and they are beating at greater than 150 beats per minute, they're not presenting with low blood pressure or features of pulmonary edema, you really want to think about this. The reason why is that this type of AIB, an AIB where they're exhibiting uh low blood pressure, they're exhibiting features of dysnia or pulmonary edema. This can sometimes be referred to as I'm going to write it right here. Um what's called a unstable AIB. And I think that's important to remember this terminology. If a patient's heart rate is super fast, they're hypotensive, having dysnia, um this is definitely a sign that they're not perfusing properly and they should be shocked. All right. All right. Anyway, let's come down to the next component here. Tacocardia. So, whenever you have a patient who you go into the room or they come in and they say maybe maybe the only symptom they experience is like palpitations. Tacardia sometimes can be completely asymptomatic. But what I want you to understand is whenever these patients have tacoc cardia right and it's because they're either having these re-entranted circuits or they're having these areas of ectopy which is causing crazy firing. These patients can present in a couple different ways. They can present in aphib with what's called rapid ventricular rate. All right. And so this is generally whenever their heart rate is greater than 100 beats per minute. Right? If it gets greater than 150, then they're definitely affecting their filling and they can cause heart failure, acute heart failure. And I think this is really really important. Sometimes you can have atrial fibrillation that's not even causing tacoc cardia. Some a lot of people live in a live with aphib and they're not having these fast heart rates. They could have a normal rate or sometimes they can even have a slow ventricular rate. So we call it aphib with a normal heart rate, aphib with a slow ventricular rate. So these exist. What I think is really important though is when patients are exhibiting this type of AIB and I want to use this term very very important um chronically. So they live in Aphib where their heart is beating greater than 100 beats per minute chronically. This can definitely lead to what's called cardio myopathy and it's specifically dilated. So this can lead to dilated cardiomyopathy and this is usually if there is chronic tacocardium and the reason why is you're literally just telling the heart hey you have to beat super fast you're going to have very little filling times the heart will then have to compensate for that and it'll start dilating. So if a patient develops dilated cardiammyopathy which is a type of heart failure with a reduced ejection fraction which is not due to eskeeia you really want to think has it be been because they've been chronically tacocartic. All right. So the three things that I really want you to watch out for in a patient who has atrial fibrillation is what? Do they have risk of throboili? Watch out for those features. Do they have features of acute heart failure that makes them unstable? And if they are chronically tacocartic over time, they have a high risk of dilated cardiammyopathy. All right, my friends. Now let's go into how we diagnose atrial fibrillation. All right, how do we approach atrial fibrillation? Well, I have a patient. I think that they have AIB. What do I do? First thing is you got to get that 12 lead. All right, the 12 lead ECG will be the breadandbut test because if I do this, what I'll be able to see is what's the rate? Are they going fast? Are they going a normal rate or are they going slow? Aphib can exhibit in a slow ventricular rate, a normal ventricular rate, or a rapid ventricular rate. The most common I'd say is like the rapid ventricular rate. So if they're going really fast, I'd be able to determine that. And then I'd have to look to see a irregular rhythm. So a variable RTOR interval. So if I see a variable R to R interval and a fast rate, I want to think about atrial fibrillation. Also, sometimes V1 is usually a helpful lead too, but we'll talk about that more in ECG interpretation. But I get the 12 lead, this should help me to see if they have AIB. Now, if you get the A if you get the ECG, you see Aphib, boom, there's the diagnosis. It's done. But sometimes patients can be in proxismal AIB, they can flip out of Aphib into normal sinus rhythm. So in those situations, you may miss it. Either way, if a patient has an ECG that shows aphib, I would also consider getting an echo cardiogram. The reason why is this can show you is there any big dilation of the left atrium, but even more important, is there any thrombus that's present in the left atrium because now those patients are at super high risk of breaking that off and embilizing. So really want to look is there any left atrial thrombus that is actually present. Look at this huge goombach that's terrifying. Or do they have any valvular problems? In other words, did they have mitro stenosis, a prosthetic valve, anything like that, or any cardiac issues that could explain their recent like new onset AIB? Now, if a patient gets their ECG, their echo, doesn't really show much, but you still think that the patient could have AIB for whatever reason, and you think that you missed it, you should monitor those patients. And so, generally outpatient, we do something called a halter monitor for 24 hours or a loop recorder. And so it basically continues to monitor their actual electrical activity of the heart for about 24 hours or more. Then they can come and they can actually be reviewed to see if they have any bouts of atrial fibrillation. And so that'd be good for missing, you know, if you have you're looking for a cult atrial fibrillation. If it is positive, all right, then they got an atrial fibrillation. The last thing I would say is really look on your exam. Sometimes the causes that we mentioned, not all of them are reversible, but the things that are reversible, you want to send off labs for. Potassium and magnesium abnormalities are super quick and you can fix those and also thyrotoxicosis. So you want to check and see is there any hypoalemia, hypomagnesmia or thyrotoxyosis if a patient went into nuance at aphib. All right, how do we treat atrial fibrillation? I want you to remember these three goals. One is rate control and we'll talk about the the actual goal that we have is to get their heart rate according to some of the trials is less than 110. Rhythm control. The whole purpose of this is is the patient have a need to restore them to a normal sinus rhythm and get them out of atrial fibrillation. And last one is anti-coagulation. I don't want them to embolize to the brain. All right, so let's talk about each one. Ray control. What I'm trying to do is shut the AV node down. I don't want this thing to actually send signals and so I have to do that by giving them drugs like a beta blocker. Usually this would be things like mtopriol, carvdalol. Those are the big ones. And oftentimes what will happen with these is they will actually help to block the beta 1 receptor. That'll decrease the intracellular calcium and decrease the actual firing of these cells. I would say avoid this in acute decompensated heart failure and avoid it in brada cardia and maybe even COPD patients. The calcium channel blockers this would be things like verapim deltyazam. These are also beneficial and these are generally going to shut down the a node and block calcium entry as well. But again avoid these in decompensated heart failure and avoid these in brada cardia. The last one is your cardiac glycosides. This is usually dejoxin and this is a pretty beneficial drug but I would say the primary benefit of this one is to be helpful in patients who are underlying uh who have heart failure. So if they have heart failure, I would say especially if there's a reduced ejection fraction, this is the patient population that could benefit from adding on to Jojoin is if they have atrial fibrillation and a heart failure with a reduced ejection fraction at least less than 35% you may find a benefit to adding these on. All right, the other one is you can consider amiodarone, but we're going to talk about that one a little bit later. All right, rhythm control. With rhythm control, the purpose is to try to restore them back to their normal sinus rhythm. All right, we can do what's called direct current cardio version. Old sparky. You can get out the pads and start, you know, zapping people. When you do this, you have to remember why you would do this because rate control is usually always the primary mode that which we kind of like try to treat AIB. The reason you would opt for rhythm control over rate control is if the patient is hemodynamically unstable, low BP, anga, pulmonary edema, acute left heart failure, and an altered mental status, right? or if they've been in AIB for less than 48 hours. Let me kind of like think make you guys think about that. If a patient has been in AIB for less than 48 hours and it's at least nuance and we know that they've only been in AIB for less than 48 hours, that's not enough time for them to form throi in their atria. And it's less likely that if we zap them and give them the normal contraction back to their atria that they won't break a piece of that off. So a less than 40 hours, less chance of a thrombus. Another one is add to the fact have they been anti-coagulated for at least three to four weeks if they did have a thrombus prior or do they have a TE that shows no left atrial thrombus because in this scenario this would probably be the biggest one is hemodynamically instability shock them if you know that they haven't been in aphib long enough for them to get a thrombus shock them and if you've anti-coagulated and showed no thrombus shock them you can do this because it is going to be the best type of treatment possible and I would always go with direct that current cardioversion over pharmacological therapy which we're going to talk about next because there's some complications with that. All right, the ones that we use to cardiovert patients are going to be things like amiodarone, fleconide, lidocaine. There's a bunch of other medications, but the primary like issue with these is that these have a very high risk of torsads to points. Um, and the reason why is they can increase and prolong the QT interval which can increase the risk of these problems leading to things like torsad. So I would say if you ever have to convert a patient via rhythm control, the primary way that you should do that is going to be direct current cardioversion. And if you're not going to do that, the pharmacological agent of choice is usually amiodarone. But the reason you would actually convert somebody is these indications here. Otherwise, continue rate control. All right, that's the big concepts here. The other one that I want to talk about that doesn't involve immediately zapping them or putting them on an amiioderone infusion is you can do something called a radio frequency ablation um or a maze procedure. And basically this kind of like tries to get rid of the damaged kind of like electrically remodeled pathways in atrial fibrillation. Um and generally this would be if a patient is in complete refractory aphib. You've tried things like rate control. You've considered things like rhythm control and they're not being properly controlled. You could do that. All right. It's a coagulation. This is to prevent the risk of throbo emblei. So how do I know when to do this? I rate control the patient to keep their heart rate less than 110. I try to convert them to sinus rhythm if they're hemodynamically unstable. They have no thrombus on uh EEG and echo sorry. and they also have been anti-coagulated or they've been in a less than 48 hours and I want to zap them out of it. Rhythm control. Anti-coagulation is going to be for preventing them from having strokes. You calculate the Chad's vast score. This is guaranteed at some point in time going to be on your exam. Memorize this. So, CHF, hypertension, age greater than equal to 75, diabetes, stroke or TIA, vascular disease like P A and age 64 to 75, sex female. You're going to calculate all of these out. The one that have two points is age and stroke/TIA. When you calculate all of these out, you're going to get some different scores. What score you get determines the thing that you will do. If it is greater than equal to two, you need to anti-coagulate these patients because they have a high risk of stroke. All right, very high risk. The only thing is you have to weigh out the risk of bleeding too. If it's one, take into consideration clinical judgment. Do they have a GI bleed? Are they old? Are they at higher risk of bleeding? Do they have recently have a stroke and now they actually don't want to make them bleed into that stroke? Take those things into consideration. If it's zero, you shouldn't really anti-coagulate them. You can consider aspirin if they need it and they have risk factors that would actually be bene beneficial to use aspirin but otherwise don't anti-coagulate them. So let's say that they have a score of greater than equal to two or clinical judgment decides that these patients are still high risk for stroke and I need to anti-coagulate them you need to pick the proper anti-coagulant on the exam. If they have non valvular AF they have no mitroenosis no prostatic valve pick a doack riveroxaban a pixaban adoxaban deigatran are your choices. if they have valvular AIB or non-valvular AIB with chronic kidney disease. Let me repeat that again. If they have valvular AIB, mitro stenosis prosthetic valve or nonvular AIB with chronic kidney disease, use warfin. But the only big thing with this one is you have to monitor the INR to make sure that you're the super you're in the therapeutic level. So depending upon that, it's usually two to three for those with not having a prosthetic valve, 2.5 to 3.5 for those patients who do have a prosthetic valve. Lastly, sometimes if patients are in the hospital and you need to bridge them for some particular reason over to a DOAC or over to Warin, depending upon the choice that you're going to make, sometimes patients will actually be on Heperin for a little bit and then they'll be bridged over outpatient onto one of those two medications, the DOA or Warin. But that is the big thing I need you guys to remember for this. Again, when we talk about atrial fibrillation, we know know for long-term rate control, rhythm control, anti-coagulation. What about the patient who comes in with new onset Aphib or acute AIB and they just popped into it for some reason in front of you? You have to ask the question, are they stable or not? If they are stable, all right, then what would you do? All right, we'll talk about that. But if they are in unstable, hemodynamic instability, what do you do? Well, in this situation, I have to remember my indications for direct current cardioversion is going to be if they are hemodynamically unstable. All right? So, is there fast heart rate causing them to become hypotensive? If they are, shock them. If they are not unstable, you should go to rate control. So, do things like a beta blocker, a calcium channel blocker or dejoxin. If they remain in aib despite that, then you can consider rhythm control again. Do I need to shock them or do I need to use something like amiodarone or fleconide? The reasons you would consider doing that and the next steps here is going to be saying, okay, have they been in AIB for less than 48 hours? Oh, they have, there's less chance of them forming a thrombi there. I'll cardiovert them. If they've been in aphib for greater than 48 hours, that's a different story. Now, there is a chance that they actually could be having a thrombus there. So I should anti-coagulate them for a couple weeks, get a TEE to make sure that there's no left atrial thrombus. And if there is not one, then I can consider cardioverting them. After these patients have been cardioverted, then I need to consider, okay, how long do I consider consider this anticoagulation going forward? After they're cardioverted, we should at least do it for four weeks. But determining how long we'll do after that is dependent upon their Chad's vast score. So again, hemodynamically unstable, yes, cardiovert, no rate control them. If they're not being controlled with rate control, consider rhythm control. So you'll do pharmacological or direct current. Direct current is usually always better. If it's less than 48 hours, you can cardiovert them. Use direct current. After you've done the antiquagulate them for four weeks, and then from that point on, depends upon their Chad vas score. If it's greater than 40 hours, there's a chance of the thrombus there. Anti-coagulate them for a couple weeks, get the TE to make sure that it's not there. And if it's not there, then you can cardiovert them, do anticoagulation for 4 weeks, and to determine how much longer you'll keep doing that based upon their Chadvas score. As always, until next time. [Music]