Atrial Fibrillation | Clinical Medicine

foreign 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 the comment section 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 arrhythmia 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 tachycardia meaning it originates in the Atria that's the atrial fibrillation what I want you guys to think about when you think about atrial fibrillation is two particular etiological 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 I think this helps us to remember it and Orient it 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's something wrong with the mitral 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 atrial the way electrical activity is conducted via the myocytes but when you alter that it leads to a lot of problems and this is how afib develops so afib will actually develop as a result where you'll develop these like weird types of problems here like these re-entrant 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 AFib 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 mitral stenosis and it's important to remember this because mitral stenosis is a disease of the mitral 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 mitral stenosis an important terminology here is when the mitral valve is diseased particularly during like rheumatic fever which is a big common cause this is a specific term a specific type of afib we call this valvular afib 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 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 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 AFib 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 afib 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 ischemic or fibrotic and now this creates these weird if you will re-entrant circuits around that ischemic or fibrotic tissue which then shoots off and creates these abnormal electrical activities an irregular Rhythm that doesn't follow the normal conduction pathway what would be this thing cardiac ischemia so again one other reason that you can develop afib is you can develop this cardiac ischemia 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 ischemia cardiac fibrosis atrial modeling and afib this is the problem but we have to ask ourselves the question what is precipitating the cardiac ischemia this is usually coronary artery disease all right so this is usually a patient who has underlying coronary artery disease or they suffered a myocardial infarction all right so we have the cardiac causes one it's my it's both these particular scenarios left atrial pressure is high you can't get blood from left age from left ventricle one is because the valves damage 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 ischemia both of these things create atrial remodeling in AFib 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 afib 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 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 into this one another one here is they have lots of catecholamines and this is a big one so tons of catecholamines you're like what in the stink is that that's neuroepinephrine and epinephrine these are the primary ones these poppies 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 atrial cells you guys know what kind of receptors what do they stimulate do you guys know this would be really particularly stimulating what's called The beta-1 receptors they're stimulating the heck out of them and they're really getting agitated and that'll cause increased ectopy and potentially afib the question that arises what's causing this catecholamine 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 post operative 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 Theo Chromo cytoma this is a adrenal medullary tumor that's pumping out epinephrine and norepinephrine stimulating these beta 1 receptors in the atrial cells and the last one is thyrotoxicosis so whenever you're pumping out way too much thyroid hormone so you've got to stop being thyroid you guys know that kind of reference right so hyperthyroidism they really increase the sensitivity of The 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 catecholamines 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 I 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 higher risk of something called holiday heart syndrome and you can have enough alcohol that it causes both hypokalemia hypomagnesemia 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 AFib is sympathomimetics so sympatho my Medics we talked about this um in the hypertension lecture this is things like cocaine methamphetamines PCP these are all drugs that have the capability to act like norepinephrine epinephrine and increase your blood pressure and increase your heart rate or increase ectopy that can cause Afib so these are the things that I want you to remember now and if you're like Zach how am I supposed to remember all this I want you to remember our matey the Pirates mnemonic we're going to 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 aphid we know why it's either due to ectopy or re-entrant kind of like circuits or remodeling if you will one other thing that I really need you to know is when a patient develops AFib you can also really Define them based upon the time that they have been in afib so what do I mean let's say you're here you have a patient and they are an afib but their afib has lasted let's say less than seven days all right in this particular situation this is called paroxysmal afib so we're going to put proximal 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 proximal afib and go back into normal sinus rhythm so that's the potential for these patients is they're in afib 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 an afib their heart's really starting to remodel and it's going to make it really hard for these patients to snap back into afib but they definitely can when they have been an afib for more than seven days we call this persistent persistent AFib the last particular scenario is let's say that this patient does SNAP into a out of afib in 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 AFib the reason why this is important is really differentiating these two proximal and permanent proxism was these patients may have a little bit more of an ability to convert them from afib into a normal sinus rhythm whereas patients who are in permanent afib 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 afib all right my friends afib what kind of problems can it cause it can do a lot to be honest with you probably the most tear buying one and the one that you have to remember is going to be thromboembolic 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 it doesn't really matter if they have this from afib there is in effective atrial contractions so all that electrical activity is causing like the hatred 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 in effective contractions because of that it doesn't get the good kick that you wanted to do and push enough blood in the age from The Atrium 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 Virgos 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 atrium you're 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 that that little piece of that clot breaks off a tiny little piece so now you have a tiny little piece that flicks off and these little guys go flying everywhere throughout the systemic circulation now you get an enveli 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 afib 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 emboli 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 on the central nervous system that little clot flicks off into like one of the carotids 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 ischemic 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 to get stuck in What's called the super mesenteric artery or the inferior mesenteric artery and either way you can lead to something called acute mesenteric ischemia sometimes it could lead to ischemic colitis but either way you're causing damage to the actual small bowel and large bowel and this is going to become ischemic and it's going to cause crazy abdominal pain so the patient has afib 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 maybe even like decreased pulses then you really want to start thinking about did they throw a little cloth that got stuck in one of the actual peripheral vessels and now it's causing a patient to experience acute limb ischemia these are all medical emergencies and the most terrifying effect because you could potentially lose a leg cause massive ischemia to the bowel and need a colectomy 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 afib with rvr which I'll talk about a little bit when we get into this tachycardia component let's say that a patient has afib we're going to say afib 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 an afib and they are really having lots of ectopine remodeling and 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 they're filling time is going to drop and if they're 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 perfusing 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 afib they snap into AFib 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 mitral stenosis that definitely supports that or if they have heart failure it are they're already having reduced isolic 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 that a lot of blood stays in the Atria and if a lot of blood stays in the Atria it's going to start back flowing 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 dyspnea 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 proximal nocturnal dyspnea orthopnia or maybe they just exhibit dyspnea 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 mitral stenosis or heart failure and they start beating at a rate of 150 or more they can really fill up their alveoli and I mean a lot of them and then you start causing massive alveolar filling with fluid that leads to something called VQ mismatch and this can present as hypoxemia and if they become hypoxemic this can cause increased work of breathing the 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 afib 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 aphid and they're 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 afib and afib where they're exhibiting low blood pressure they're exhibiting features of dyspnea or pulmonary edema this can sometimes be referred to as I'm going to write it right here what's called a unstable AFib and I think that's important to remember this terminology if a patient's heart area is super fast they're hypotensive having dyspnea 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 tachycardia so whenever you have a patient who you go into the room or they come and they say maybe maybe the only symptom the experience is like palpitations tachycardia Consignment is going to be completely asymptomatic but what I want you to understand is whenever these patients have tachycardia right and it's because they're either having these re-entered 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 afib with what's called rapid ventricular rate all right and so this is generally whenever their heart rate is greater than a hundred 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 tachycardia some a lot of people live in a live with afib 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 afib with a normal heart rate afib with a slow ventricular rate so these exist what I think is really important though is when patients are exhibiting this type of afib and I want to use this term very very important um chronically so they live in afib 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 tachycardia 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 cardiomyopathy which is a type of heart failure with a reduced ejection fraction which is not due to ischemia you really want to think has a been because they've been chronically tachycardic 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 thromboemboli watch out for those features do they have features of acute heart failure that makes them unstable and if they are chronically tachycardic over time they have a high risk of dilated cardiomyopathy all right my friends now it's going to how we diagnose atrial fibrillation all right how do we approach atrial fibrillation well I have a patient I think that they have afib what do I do first thing is you got to get that 12 lead all right the 12vcg will be the bread and butter 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 are they going slow afib 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 R to R interval so if I see a variable R to our interval and a fast rate I want to think about atrial fibrillation also sometimes V1 is usually helpful lead to 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 afib now if you get the if you get the ECG you see afib boom there's the diagnosis it's done but sometimes patients can be in proximal afib they can flip out of afib into normal sinus rhythm so in now situations you may miss it either way if a patient has an ECG that shows afib I would also consider getting an echocardiogram 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 embolizing so really want to look is there any left atrial thrombus that is actually present look at this huge Goomba that's terrifying or do they have any valvular problems in other words do they have mitral stenosis a prosthetic valve anything like that or any cardiac issues that could explain their recent like new onset AFib now if a patient gets their ECG their Echo it doesn't really show much but you still think that the patient could have afib for whatever reason and you think that you missed it you should monitor those patients and so generally outpatient we do something called a Holter 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 so that'd be good for missing you know if you have you're looking for occult 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 hypokalemia hypomagnesemia or thyrotoxicosis if a patient went into Nuance at AFib 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 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 anticoagulation I don't want them to embolize to the brain all right so let's talk about each one rate 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 metoprolol Carvedilol 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 a QD compensated heart failure and avoided in bradycardia and maybe even COPD patients the calcium channel blockers this would be things like Verapamil deltiazem these are also beneficial and these are generally going to shut down the AV node and block calcium entry as well but again avoid these in decomposated heart failure and avoid these in bradycardia and the last one is your cardiac glycosides this is usually digoxin 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 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 digoxin is if they have atrial fibrillation and a heart Fair where the reduced ejection fraction at least less than 35 percent 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 cardioversion old Sparky you can get the pads and start you know zapping people when you do this you have to remember why you would do this because Ray control is usually always the primary mode that which we kind of like try to treat AFib the reason you would opt for rhythm control over rate control is if the patient is hemodynamically unstable low BP angina pulmonary edemaq left heart failure and an altered mental status right or if they've been in afib for less than 40 hours let me kind of like think make you guys think about that if a patient has been an afib for less than 48 hours and it's at least nuanced and we know that they've only been an aphid for less than 48 hours that's not enough time for them to form thrombi in their Atria and it's less likely that if we zap them and give them the normal contraction back to their Atria they won't break a piece of that off so aphid less than 40 dollars less chance of a thrombus another one is add to the fact have they been anticoagulated 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 hemodynamical instability shock them if you know that they have men and afib long enough for them to get a thrombus shock them and if you've anticoagulated 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 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 flecanide lidocaine there's a bunch of other medications but the primary like issue with these is that these have a very high risk of torsos 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 amiod or an infusion is you can do something called a radio frequency ablation 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 and generally this would be if a patient is in complete refractory afib 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 thromboemboli 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 at their hemodynamically unstable they have no thrombus on uh EEG or an echo sorry and they also have been anticoagulated or they've been in afib less than 48 hours and I want to zap them out of it Rhythm control anticoagulation is going to be for preventing them from having Strokes you calculate the Chad's vas 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 pad 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 or equal to 2 you need to anticoagulate 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 need to coagulate them you can consider aspirin if they need it and they have risk factors that would actually be benefit beneficial to use aspirin but otherwise don't anticoagulate them so let's say that they have a score of greater than or equal to two or clinical judgment decides that these patients are still high risk for stroke and I need to anticoagulate them you need to pick the proper anticoagulant on the exam if they have non-valvular afib they have no mitral stenosis no prostatic valve pick a doact rivaroxaban apixaban a doxiban the bigotrano your choices if they have valvular afib or non-valvular afib with chronic kidney disease let me repeat that again if they have valvular afib mitral stenosis prosthetic valve or non-valular afib with chronic kidney disease use Warfarin but the only big thing with this one is you have to monitor the INR to make sure that you're the super durian the therapeutic level so depending upon that it's usually two to three for those with not having a prostatic 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 Doak or over to warfarin depending upon the choice that you're going to make sometimes patients will actually be on Heparin for a little bit and then they'll be bridged over outpatient onto one of those two medications the doact or Warfarin but that is the big thing I need you guys to remember for this again when we talk about atrial fibrillation we know no for long term rate control Rhythm control anticoagulation what about the patient who comes in with new onset afib or acute afib 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 I will 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 become hypotensive if they are shock them if they are not unstable you should go to raid control so do things like a beta blocker a calcium channel blocker or digoxin if they remain in afib 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 flecanide the reasons you would consider doing that in the next steps here is going to be saying okay have they been in afib for less than 40 hours oh they have there's less chance of them forming a thrombi there a cardiovert them if they've been in afib for greater than 40 dollars that's a different story now there is a chance that they actually could be having a thrombus there so I should anticoagulate them for a couple weeks get a te 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 their cardio order we should at least do it for four weeks but determining how long we'll do after that is dependent upon their Chad's vas score so again hemodynamically unstable yes cardiovert no rate control them if they're not being control of rate control consider Rhythm control so you'll do pharmacological or direct current direct current's usually always better if it's less than 40 hours you can cardiovert them use direct current after you've done the anticoagulating 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 anticoagulate 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 four weeks and to determine how much longer you'll keep doing that based upon their Chad vast score as always until next time [Music] thank you

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Length: 37min 57sec (2277 seconds)

Published: Mon Mar 11 2024