Atrial Fibrillation | Etiology, Pathophysiology, Diagnosis, Clinical Features, Treatment

what's up ninja nerds in this video we're going to be talking about atrial fibrillation this is an extremely important topic that every clinician should know so before we get started i completely urge you guys down in the description box we have links to our website on our website we have comprehensive notes that cover everything we're going to talk about in this lecture and additional topics that will help you along with references and citations we'll also have drawings illustrations of the the board before everything's drawn out as a template to follow along and then the end product so go check that out if you like this video if you benefit from it please hit that like button comment down the comment section and please subscribe let's get into it all right engineers let's get to talking about the potential causes of atrial fibrillation atrial fibrillation is basically it's an arrhythmia it's a supraventricular attack urine meaning that the arrhythmia originates from some irritability or re-entrant circuit above the ventricles and it causes this classic irregularly irregular rhythm now with atrial fibrillation we actually if we're being very very picky there actually is no complete identifiable cause there's what's called risk factors we're going to use the term causes but do remember if we're being very very picky or technical they're actually risk factors and there's two different types there's cardiac risk factors and causes and there's non-cardiac causes or risk factors let's first focus on what are some of the actual intrinsic cardiac issues that can lead to this supraventricular tachyarrhythmia that causes an irregularly irregular rhythm and tons of complications the first thing that you want to think about is really atrial fibrillation is due to anything that stretches the myocardium causing it to kind of dilate or hypertrophy anything that causes ischemia decrease oxygen to the myocardium of the atria anything that causes inflammation of the atria or near the proximity of the atria right and anything that causes an increased kind of sympathetic nervous system kind of stimulation onto the atria because that causes a lot of calcium loading and agitation to the atria so what are those things well cardiac issue wise someone think about what causes stretching of the myocardium what if somebody has congestive heart failure their muscles are really floppy and flabby and they're causing stretching and distension of the myocardium not just of the ventricles but also of the atria that could be a potential cause so think about congestive heart failure and again this is by increasing the stretch of the myocardium that may lead to atrial dilation that may lead to atrial hypertrophy but either way it's changing the morphology of the atria that's a potential trigger what else what else is something that can increase the stretch of the myocardium what if somebody has a disease called dilated cardiomyopathy you ever heard of that one so cardiomyopathy they get really thin very floppy very ballooned kind of ventricles and it can even involve the atria a little bit so we can say a cardiomyopathy particularly dilated cardiomyopathy will abbreviate cmp right and so again this is through that mechanism of an increased stretch all right this one is again increasing the stretch causing the dilation of the ventricles and potentially the atria okay what else what if i have something that actually causes some irritation of the mitral valve or problems with the mitral valve or maybe the mitral valve isn't working very well and maybe it's stenotic unless blood flow is going from the atrium to the ventricles and then more more volume is in the atria than you desire and so the atria starts ballooning up what's that called mitral stenosis so sometimes if you have certain types of valvular diseases or disorders and the most particular one is mitral stenosis think with me here for a second imagine i have stenosis of this mitral valve the atria is trying to be able to contract and push blood from the atria down to the ventricles but you have this stenotic valve not letting as much volume go from the atria to the ventricles you know the atria doesn't really push too much of the blood down during the cardiac cycle what maybe 20 30 from the atrial kick but still that's volume so 20 to 30 percent of the blood can kind of stay within the atria and that can cause the atria to kind of stretch a little bit and as it stretches and dilates a little bit what can that do that's enough to potentially trigger what an atrial fibrillation issue so mitral stenosis may lead to some dilation of the atria or stretch of the atria makes sense to a less common degree you may get some of the same issues with regurgitation it's just less common okay let's write that down less common in that sense but it's a potential but i really really want you guys to remember mitral stenosis okay so we got chf dilated cardiomyopathy and valvular heart diseases particularly mitral stenosis all of them kind of working through the same kind of process where they're really stretching the atria stretching the ventricles causing remodeling of the actual myocardium right what else what if i actually just jack up parts of the atria or the ventricles because i have less oxygen being delivered to them i have them undergoing ischemia what could that be do too you know if someone has very severe coronary artery disease or maybe they have a past history of an mi or they had an mi if you have some type of ischemia let's say that that area is ischemic or infarcts now tissue in the atria is going to have to undergo remodeling near that area and that ischemia could trigger those atria to start developing ectopic foci or re-entrant circuits nearby causing an atrial arrhythmia okay so but this is by the mechanism of ischemia right so less oxygen maybe even to some degree infarction what else what else could we think about well what if i actually again kind of cause like some inflammation of the myocardium i really inflame it i agitate it maybe i have some antibodies that are attacking it maybe i have some immune system cells that are attacking it for some reason right and i cause a lot of inflammation of like the valves or i cause inflammation of the atria or i cause inflammation of the endocardium or maybe even i involve the myocardium itself but i'm causing massive inflammation you know there's a condition called rheumatic fever that can then lead to rheumatic heart disease so rheumatic heart disease could be a potential trigger of someone developing atrial fibrillation due to the massive inflammation of valves sometimes what rheumatic heart disease will do is it can actually lead to mitral stenosis and the mitral stenosis can lead to atrial fibrillation or you can have rheumatic heart disease that causes enough inflammation it's enough to agitate the atria and again potentially trigger atrial fibrillation but again inflammation sometimes may be related to mitral stenosis which then leads to that but either way we got chf died of cardiomyopathy valvular disorders particularly mitral stenosis coronary artery disease or mi and then we got rheumatic heart disease what's the last one big one that i want you guys to remember sometimes if you have high blood pressure right so let's say here you have high blood pressure right and so your left ventricle is having to work harder it's having to contract more and contract more and contract more and by some unknown kind of mechanism maybe it's just via the hypertrophy so you have something like hypertension that hypertension leads to left ventricular hypertrophy and maybe that hypertrophy over time is enough to be able to cause some type of hypertrophy of the atria by some way or it just causes some remodeling of the atria by some way that may be enough to cause the atria to become irritable enough and generate these abnormal electrical activities okay so again big kind of intrinsic cardiac disorders that i really want you to remember to take away here chf dilated cardiomyopathy mitral stenosis all of these kind of really causing dilation stretching of the actual myocardium of the heart cadmi potentially causing ischemia to the heart rheumatic heart disease leading to inflammation and hypertension kind of leading to some hypertrophy and other associated kind of itch issues where you might cause the atrium to go remodeling or hypertrophy itself these are the cardiac causes now let's talk about the non-cardiac causes all right so we talked about the cardiac causes now let's talk about the non-cardiac causes in the same way you have to remember the potential triggers or causes of someone developing atrial fibrillation those atria abnormally firing is by mechanisms of some type of increased stretch whether it causes dilation whether that causes hypertrophy of the atria and the ventricles whether it be due to inflammation whether it be due to some type of ischemia or whether it be due to increased sympathetic nervous system activity some of the ones above where inflammation were ischemia and were stretched what about these ones down here non-cardiac causes that can cause atrial fibrillation could be something wrong with the lung you know and patients who have like copd or who have pneumonia or who maybe have an acute onset pulmonary embolism what can all of these things potentially have in common if the lungs aren't working well they're supposed to take oxygen bring it into the alveoli push that into the blood and get rid of co2 right that's that's the job of the lungs to be able to do that if there's some pathological process of the lung parenchyma such as in copd and pneumonia the ability to get oxygen to the blood is going to be decreased but the other aspect is that you need blood to be able to flow to that area to pick up the oxygen so if by some reason there is a clot in the vessel that's supposed to be able to pick up oxygen and take it to the tissues if you have something like a pulmonary embolism you may be able to ventilate appropriately but the oxygen might not be able to get into the blood and pass past that distal past that occlusion right but either way through any of these mechanisms whether it be a problem with the lung or problem with perfusing the actual area to pick up oxygen this is going to lead to low amounts of oxygen now this isn't causing like ischemia of like the myocardium it's causing hypoxemia that could potentially cause ischemia but there's low oxygen leading to this hypoxemia effect and that might be enough to be able to trigger the atria to become irritable and then start causing that abnormal ectopic foci or re-entrant circuits okay so we got these particular causes we got lung causes we got the cardiac causes what are some other non-cardiac causes all right this one's interesting and someone who has what's called thyrotoxicosis you're like what the heck we call them thyrotoxicosis or hyperthyroidism one of the other what's the issue they're just popping out tons of t3 popping out tons of t4 so they have hyperthyroidism or thyrotoxicosis what's the issue with thyrotoxicosis and atrial fibrillation believe it or not the hyperthyroidism t3 and t4 increases the beta adrenergic receptor stimulation if you make the beta beta 1 adrenergic receptors more sensitive to epinephrine and norepinephrine what's going to happen you're going to get an increased sympathetic nervous system type of effect what was one of the potential triggers for atrial fibrillation increased sympathetic effect boom we good all right what else this one they'd love to throw this on your exams okay it's just an important one that you have to remember if someone decides to go out and have an all-night bender okay and just drink tons and tons of alcohol so they drink tons and tons and tons of alcohol and they have an all-night bender there's something called holiday heart syndrome that can develop now the mechanism by which it does this isn't completely known there's ideas but whenever someone goes out and they just have an acute binge kind of alcohol kind of drinking event the increase in the alcohol within the body can do a couple things one is it can increase like the reactive oxygen species and that can lead to inflammation that inflammation may be something that can cause irritation and agitation to the atria the other thing it does is is it kind of increases the sympathetic nervous system effects on the heart so then you get kind of an increased sympathetic effect on the heart and if you get this increased sympathetic effect on the heart that also is a potential trigger so there's these kinds of thoughts that maybe alcohol itself may also just have some type of you know cytotoxic or in it hurting kind of effect on the heart but it may be through reactive oxygen species leading to inflammation or increased sympathetic nervous system activity another thing is if you drink tons and tons of alcohol it can alter your electrolytes so there may be electrolyte abnormalities and this may be in potassium and this may be in magnesium which are two particular cations that are important for electrical activity of the heart okay and this may be because of vomiting associated with it or because of the alcohol not having lots of you know particular like nutrients micronutrients that we need there okay so big things lungs like copd pneumonia acute ppe thyrotoxicosis holiday heart syndrome please don't forget son of a gun please don't forget holiday heart syndrome that's probably going to show up on your exam okay what's the next one the next one is actually very interesting you know there's a condition where you can have like a tumor of your adrenal medulla it's called pheochromocytoma chromocytoma so it's a tumor on the adrenal medulla and it just spits out epinephrine and spits out norepinephrine that's tons of what catecholamines what do these things do bind onto beta-1 adrenergic receptors what does that do to the heart it causes lots of calcium influx and cation loading that's enough to agitate the atrium potentially cause it to go into a atrial fibrillation type of rhythm so this is going to really increase the sympathetic nervous system activity man all right you decide to go and do some booger sugar right some cocaine or methamphetamines of some kind and not good why because guess what these drugs do coke and methamphetamines they act as sympathomimetics so they bind on to the different receptors that epinephrine and norepinephrine would do and they increase your sympathetic nervous system activity causing more cation loading more irritation of the atria boom good what else you know this is another one but this is like a good thing for an acute onset so this can be an acute onset this other one could be an acute onset you know if someone has like a really bad infection like a sepsis they have a really bad sepsis okay in that septic kind of response whenever there's vasodilation capillary permeability infection causing fever your sympathetic nervous system gets hyper activated because it's a protective response when you're septic your blood pressure drops you start to become kind of fibril you start to have a ton of issues so your body tries to go into this fight or flight mode in response to that stressful event and so sepsis can increase your sympathetic nervous system activity particularly if someone's going into a hypotensive state it'll try to increase your heart rate increase your blood pressure so that you can kind of counteract the negative effects from sepsis the next thing that i want you guys to think about here is if someone actually goes and gets surgical procedures so sometimes if there is some kind of surgery post-op this can cause just generalized stress on the body and that post-op stress may be something to trigger a catecholamine response it's just a natural thing that can happen if it was a significant surgery and there's just a significant amount of post-op stress from a very invasive kind of procedure that may be something that caused your sympathetic nervous system to become super hyperactive and just push you into a new onset afib or atrial fibrillation in general the last thing that i want you guys to remember is electrolyte abnormalities let's actually squeeze this one in here so sometimes if someone has any electrolyte abnormalities for example if they have two particular cations in the blood that are low these really alter the electrical activity of the heart and this is one of the other causes so there's a couple other causes we said inflammation low oxygen some type of stretch dilation hypertrophy increased sympathetic activity the last one that i want you to remember is electrolyte abnormalities so if there is low potassium and low magnesium this can alter the electrical activity of the heart in a way that it could potentially push someone into an atrial fibrillation or push them into some kind of supraventricular tachyarrhythmia so that's again a big thing to think about this covers all of our cardiac and non-cardiac causes or risk factors let's talk about how these actual things lead to the pathophysiological and clinical features and complications associated with afib all right engineers let's talk about the path of fizz so again we talked about all the causes and what those causes can do let's test your memory as well as adding in how these things actually do this right so go back what were some of the triggers we said there was a bunch of them right the first one that i wanted you guys to remember is if there was some kind of increase stretch on the heart right so increased stretch on the heart could have been from chf could have been from dilated cardiomyopathy could have been from mitral stenosis right causing that actual uh valvular narrowing and leading to the dilu the ballooning and dilation of the atria could have been things like that what else there could be something that's causing some kind of inflammation of the actual myocardium so what if there's inflammation maybe that's in something like somebody has some rheumatic heart disease of some kind so if they have rheumatic heart disease that's causing a massive amount of inflammation or what if they had like that holiday heart syndrome and they had the cytotoxic effects from the ethanol or there was a lot of reactive oxygen species that were being produced and that was also causing a lot of inflammation okay what else well not only could it be inflammation but what if it's due to some type of like low oxygen what if there's low oxygens being delivered to the myocardium for some reason maybe it's because there's a clot within the coronary vessel maybe it's because there's actually some type of decreased oxygen coming from the lungs it could be things like that right so if there's a decreased oxygen delivery that is going to the lungs and again coronary artery disease mi copd pneumonia acute pulmonary embolism these could be potential causes what else what if it's not just due to increased stretch what if it's not just due to increased inflammation what if it's not just due to some type of decrease in oxygen delivery by some mechanism what if it's due to an increased sympathetic nervous system activity effect so there's increased sympathetic activity so if there's increased sympathetic activity in situations such as what if someone has thyrotoxicosis if they're drinking tons and tons of alcohol if they have a feochromocytoma cocaine methamphetamine septic reaction postop all of those things are potential triggers as well and what's the last one that i mentioned kind of squeezing that in at the last minute electrolyte abnormalities what is the two particular types of electrolyte abnormalities that i really want you guys to remember hypokalemia and hypomagnesemia all of these things can just cause a significant agitation to the myocardium and if this myocardium becomes agitated enough and starts having some reason that it needs to remodel it becomes agitated enough that it starts to want to fire it can start generating some abnormal electrical activity and it may generate this abnormal electrical activity in two ways you may form these areas multiple areas in the myocardium of the atria that you have these things called ectopic foci and they start firing off electrical activity and this creates a arrhythmia or it could be due to what else what if you have some type of remodeling in a way where you have an alpha pathway and a beta pathway that's kind of generating that we talked about in our arrhythmia lecture the overview one you could develop these things called re entrance circuits and these re-entrance circuits can actually start to form and whenever they form they can fire off electrical activity off of that and again that can also lead to an arrhythmia the same concept can exist so again thinking about how all of these triggers whether it be cardiac or non-cardiac causes this may produce what some type of irritable foci causing these ectopic foci to fire or they could be something from outside outside of the heart that's influencing the atria to develop ectopic foci or re-entrant circuits and then causing these abnormal electrical activity coming from the atria a supraventricular tachycardia which again we call atrial fibrillation in this case that is the big concept so again without going into all the things because we actually don't know exactly how these mechanisms produce this process within her we just know it causes them to become irritable triggerable maybe undergo remodeling process and then by that process they develop ectopic foci or re-entrance circuits all right ninja so now we have to understand basically how does atrial fibrillation lead to the particular clinical manifestations and stuff like that right so so the first thing i want you guys to understand is let's pretend right we have one of the the causes and the triggers and we have these areas of ectopic foci that are generating these abnormal electrical activities and they're starting to just fire right but you have to remember who is the pacemaker of the heart who's the one that says hey i generate the sinus rhythm and i send electrical activities down to the av node telling the av node to say oh here's the firing from the atria send this down to the ventricles via the bundle of his the bundle branches in the purkinje system that's our sa node he is the one that generates our sinus rhythm if you have areas other than the sa node that are actively firing because of all the triggers we talked about they're going to start firing whether it be ectopic foci whether it be re-entrant circuits and they're going to start interfering with the normal sinus pathway in such a way let's pretend here that you have this one ectopic foci it's close it fires it gets to the av node before the sa node and all these other ones and so it's able to trigger you know a qrs complex because it goes down to the ventricles then after that you have the next one it comes right after and then but it comes just a little bit later so you get a little bit of a delay boom you get your qrs complex because it sends it down to the ventricles then you get the other one but that one comes right behind it and then you get the other one and that one comes right behind it you start getting this variation in the rhythm but it's not coming from the sa node it's coming from these other ectopic foci re-entrant circuits in the atria this causes there to be no visible p waves so therefore it's not a normal sinus rhythm you also cause an irregular rhythm because now i have variations in my r to r interval because of different ectopic foci hitting the av node and then telling the av node hey send this down into the ventricles the problem with this is that you can get variations in heart rate sometimes you can have heart rates that are really fast greater than 100 or sometimes you can have lower heart rates that are less than 60 beats per minute and we'll talk about the different classifications of a-fib the thing is is that sometimes you may be completely asymptomatic you may have no symptoms and not even know that you have atrial fibrillation or an irregular rhythm but sometimes if it's fast enough if it goes just a little bit fast and your these abnormal electrical activity causes palpitations sometimes that could be something that we can experience so palpitations may be an experience maybe there's shortness of breath maybe there's fatigue so there is sometimes common symptoms and these tend to be some of the most common symptoms that you can see with atrial fibrillation that being palpitation shortness of breath or fatigue sometimes you may even get a single pull episode as well so what if the heart rate's going really fast though and i mean fast like what if the heart rate's starting to tack away you're getting greater than 150s you know on your heart rates now you guys remember our equation that it says cardiac output is equal to heart rate multiplied by stroke volume right so correlationally you would say oh if there's an increase in heart rate it should increase their cardiac output you'd be correct but if the heart rate is so fast that you're not giving the ventricles an adequate amount of time to fill so that way it has a good end diastolic volume and then when it contracts it contracts out a good amount of volume you could potentially lower your cardiac output because you're lowering their filling time so effectively very very high heart rates greater than 150 generally can lower your end diastolic volume if you lower your end diastolic volume you can lower your stroke volume and if you lower your stroke volume you can lower your cardiac output why is that a problem there's another equation it is that your mean arterial pressure is equal to your cardiac output times your systemic vascular resistance right so if you start actually doing what if you start increasing your credit output you should increase your map if you lower your cardiac output you could potentially lower your mean arterial pressure and so as a result of that this may produce hypotension and since it's coming from the heart this can lead to a cardiogenic shock so this is one of the complications that could potentially present it's usually when the heart rate gets really really fast that it's a possibility but again sometimes it can be completely asymptomatic with just some minor palpitations fatigue maybe some shortness of breath maybe some sinkable episode if it gets really really fast to the point where it alters your cardiac output it could lower your blood pressure and cause cardiogenic shock okay now here is the part where you got to be on your on point because this is going to be the big thing sometimes patients will never have this issue of cardiogenic shock of really fast heart rates they might not even have any symptoms and you know what happens all right ready if the atria is having these ectopic foci re-enter its circuits and it's causing these weird depolarizations and contractions here's the big thing these you know abnormal electrical activity produces inadequate atrial contractions now go back to what you guys remember from the cardiac cycle in the cardiac cycle blood from the atria naturally flows down to the ventricle passively anywhere from 70 to 80 percent is passive where's the remaining 20 to 30 percent coming from the atrial kick right so the atria at the end of that kind of period where it's filling it contracts and squeezes down the remaining 20 to 30 percent when you get this in you get this atrial quivering from the atrial fibrillation inadequate electrical activity it causes inadequate atrial contractions you decrease the atrial kick and so what happens here is you increase you cause more blood to kind of stay within the atria it doesn't move down at the ventricles what does that call when blood stays in one area longer than it should be stasis so then you get this increased stasis what's the what's a virtuous triad there's a stasis of blood flow endothelial injury or hypercoagulability it increases the risk of a clot i have a potential factor here and that is going to lead to a blood clot if i form a clot in the atria or i form it on the valve guess what could happen for whatever reason maybe you get you convert sometimes people with atrial fibrillation they just naturally convert and then their heart starts beating on its own regularly and you get good contractions now the atrium might be strong enough to pop that clot off or for some other reason you potentially have an increased stressful event and your heart starts contracting more and you pop that clot off if i pop this clot off it can then flow through the systemic circulation up to the brain down through the descending aorta and just go and embolize into multiple different organs and the problem with this is that you can get emboli that can hit multiple different organs what are the organs that we should be very very much so thinking about the brain sometimes one of the first signs is a cerebral vascular action so developing an ischemic stroke another one is the spleen you can develop a splenic infarct sometimes it's the kidney and so you can develop a renal infarct and sometimes it's the actual gut particularly like the small bowel large bowel and you can develop what's called acute mesenteric ischemia and so thinking about these some patient may come in with abdominal pain someone make him come in with an increased bun creatinine some patient might come in with some pain in their left upper quadrant and maybe some other issues with their actual cbc some patients may come in with neurodeficits and then you have to go back and say why did that happen oh they had atrial fibrillation and they weren't anticoagulated for some reason or we never knew it that is the big thing to think about so now we have an understanding of the causes how those causes can lead to the pathophysiological mechanisms that lead to the clinical manifestations or complications now let's talk about some classifications and diagnostic tools all right engineers let's talk about diagnosis now before we actually start going through all the diagnostic tools of imaging and labs and so on and so forth it's important that we actually develop this classification of atrial fibrillation this is something that you'll definitely have to know not just for your exams but also in your actual clinical practice it's important to understand when this terminology is getting thrown around what the heck it means the first one is sometimes we can describe atrial fibrillation with respect to how it's affecting our hemodynamics so it's important to understand that terminology and so when we say they have a hemodynamically unstable atrial fibrillation what does that mean because not only is it important to know what it means but it determines our treatment plan for it so hemodynamically unstable refers to particular things such as maybe them having low blood pressure so being hypotensive maybe them having something like pulmonary edema which this can happen especially if they go into that cardiogenic shock state where their ef is not actually adequate enough and blood starts kind of backing up to the pulmonary circulation and that cardiogenic shock state or they have an altered mental status or lastly they have severe chest pain so these are things to think about so if a person has any of these particular types of things such as hypotension pulmonary edema altered mental side of their chest pain we call that hemodynamically unstable atrial fibrillation and usually those patients get fit into a category of like electrical cardioversion of some type hemodynamically stable means that they have none of the above issues none of above issues pretty simple right we don't have to be too crazy on that one they have they have normal blood pressure they have no pulmonary edema they have normal mentation and no obvious significant refractory chest pain boom done the next thing that you have to be able to talk about because we talked about this a little bit back there is that atrial fibrillation right if somebody has atrial fibrillation they have all those ectopic foci that are firing and it's firing really really fast and a lot of it's hitting the av node and a lot of it's actually going down to the ventricles and the ventricular rate is going faster and faster and faster we're starting to get greater than 150 beats per minute greater than 100 beats per minute they can start having rapid ventricular conduction and so we say rapid ventricular radar rvr can be a type of afib so sometimes patients can have what's called afib with rvr and that just means that their heart rate is getting really fast particularly their ventricular rate is what we're talking about not the atrial rate the ventricular rate is getting fast greater than 100 beats per minute but sometimes you can have these re-entrant circuits or not many ectopic foci and they're not firing as fast or as frequent that it's causing the av node to send tons of conduction down into the actual ventricles and so they're not having a very fast ventricular rate and so we call that a-fib with a slow ventricular rate or conduction and so that's whenever the heart rate is usually less than like 60 beats per minute okay so that's important to remember you can have a-fib with a normal rate you can have a-fib with rvr where it's greater than 100 beats per minute or a-fib with a slow ventricular rate where it's less than 60 beats per minute so now we have hemodynamic an instability type of afib hemodynamically stable afib we have a-fib with rvr afib with svr all right so the other way that we can classify afib is based upon onset did it happen did it just start have they had afib for a long period of time is this a type of afib that even though we've tried to convert them it's there's no need to even convert them at all anymore because they have this consistent like permanent afib so that's an important thing to differentiate so we have what's called new onset atrial fibrillation meaning that the atrial fibrillation developed less than 48 sometimes we even say 72 hours ago paroxysmal meaning that it developed within less than seven days persistent meaning that it's been actually they've had atrial fibrillation for greater than seven days long-standing atrial fibrillation is they've had known afib for greater than one year and lastly permanent afib is when someone has persistent aphid which is usually again greater than seven days somewhere between seven days and a year so it's greater than seven days without any attempt to cardiovert the patient to normal sinus rhythm that is how we define permanent afib okay so again quick recap new onset less than 48 to 72 hours proxismal less than seven days persistent greater than seven days long standing greater than a year permanent is they're greater than seven days but there's no attempt to be able to convert them to normal sinus rhythm okay that is how we define and classified in that category the last classification of afib is does it have valvular involvement and this goes back to that mitral stenosis so valvular afib meaning that is there evidence of mitral stenosis or is there a do they have some type of valve do they have like an actual mechanical valve so that could be another potential thing because again this determines what kind of anticoagulant they need and then non-valvular is obviously there is no mitral valve involvement or mechanical valve okay so that is how we define these so we got how we define them again and what particular categories we got hemodynamic stability we got ventricular rate we got onset and duration and mitral valve involvement now let's talk about some of the tests that we utilize to diagnose and aid in determining the risk factors or causes for this condition all right so now we have to start trying to diagnose atrial fibrillation the best test that you could potentially use that's the cheapest it's the most non-invasive it's a quick test is to see what their ekg tells you do they have evidence of atrial fibrillation on their ekg so looking at their ekg i want us to kind of not focus particularly on what the ekg would look like we'll talk we'll look at some examples in a little bit but i want you to notice to take a look at v1 v1 is going to be one of the leads that i really want you to focus on because that tells you about what their atrial activity looks like if you don't see anything in v1 then you can go ahead and take a look at 2 3 and avf because that also will give you some activity of what their atria looks like as well so that's one thing i want you to look at but what can an ekg tell us well the first thing you can tell us is do they have atrial fibrillation right because that that might be one thing right away the other thing i think is really important is sometimes there's a very dangerous condition we talked about this in arrhythmia video if someone has afib with heart wolf parkinson's white syndrome look for very fast rates so you look for wide complex tachycardia generally you look for this irregular kind of rhythm and you look for rates that are close to 200 beats per minute that might make you think about that so look is there any wolf parkinson's white syndrome that could be present the other thing think about what were some of the potential causes of somebody having atrial fibrillation could it have been that they had a recent myocardial infarction they have coronary artery disease so look to say can i rule out that they don't have any st segment elevation or st segment depression the other thing is do they have any left ventricular hypertrophy because what was another potential trigger hypertension and hypertension can cause lvh okay so you utilize your ekg here's the thing though here's what you really want to realize sometimes you can get an ekg on somebody and they may not be an afib right now they may be in normal sinus rhythm or have no obvious afib what can i do outpatient that'll track their uh their electrical activity over maybe a certain amount of time i can do something called a halter monitor so the other thing that i want you guys to remember is that if you do outpatient continuous studies you may need to do something like a halter monitor that's kind of like your gold standard they can also do loop recorders but what if you're impatient what if the person's really really sick they have something else that's making them have to go to the hospital and you have to do inpatient continuous you know investigation of their electrical activity the heart you do telemetry so you hook them up and you have them connected to the actual interface the computer and they'll kind of give you an electrical activity of their heart over their entire state when they're at the hospital so sometimes you may have to do what's called telemetry but these are big big things that are going to be really important for your exam continuing just because you do a one-time ekg and it's not there doesn't mean that they have afib it just might not be that they're an afib at that moment all right so what's the next thing we can get we get a chest x-ray why would we get a chest x-ray chest x-ray could tell us a little bit about things generally when someone comes in with like palpitations or shortness of breath or they have fatigue it's not a bad idea to get chest x-ray there could be other reasons of why they have that fatigue that shortness of breath those palpitations anything like that so it's not a bad idea plus it also may key us into as to what what's the trigger for this afib if they have a new onset afib what if it's because i get a chest x-ray and i notice that they have pneumonia right so maybe you want to rule out pneumonia maybe you want to see if they have pneumonia and that's the trigger what if they have copd they have lungs that are hyperinflated they have hyperlucid lungs you can see that they have a flattened diaphragm that's not diagnostic of copd but if they have tobacco abuse and maybe a chest x-ray that suggests of it you have kind of an idea what else well the other thing that you could look for is what if they have a big old heart they got cardiomegaly cardiomegaly make kias in to say oh they got some cardiomegaly what if they have chf what if they have dilated cardiomyopathy that could be a potential trigger as well that could be something related to their atrial fibrillation so it's not a bad idea to get a chest x-ray so start off with an ekg maybe diagnose it continue it outpatient as a halter continue with impatient heli tell us if there's any kind of other things associated with it chest x-ray kind of ruling out other kinds of things that may be related to it or just ruling out uh these conditions that you're trying to you know make sure it's actually a-fib what else next thing is we're going to get an echo all right so what else can we do we got the ekg we either diagnose it off the ekg that one time 12 lead or we follow them on telly we follow them as a halter maybe we diagnose afib we also find out maybe some other reasons on their ekg that was suggested or something we get a chest egg sugar really like pneumonia rule out copd to rule out any kind of other kind of things that may be there also look to see if there's any obvious cardiomegaly then we can get an ultrasound an ultrasound particularly an echo now i put t-e-e here it's kind of like our kind of gold standard if you really wanted to get kind of an echo there a te is actually going to kind of be best but you could get a t e or you could actually get a t t e so a transthoracic echocardiogram it doesn't really matter they're both pretty good sometimes the tee is a little bit better at picking up something within the atria but either way you can get a tte as well all right what are we looking for in this well the big things that you're looking for within this particular study is this can tell you a couple different things first thing is it can tell you is there any atrial thrombus that's the first thing i can tell you if you have an atrial thrombus that is a big big deal because that tells you hey there's a cloth there you got to be careful if you try to convert them or if they go out into normal sinus rhythm or something happens you can pop that clot off may have to start anticoagulating them right now or it can tell you if there's any mitral valve issues so is there any mitral valve disorder of some kind maybe they have a mitral valve stenosis maybe they have a mitral regurgitation maybe they have a mechanical valve and they didn't know it you didn't know it and it wasn't in their history who knows or it also can tell us if there is any it tells us the left ventricular ejection fraction which is important because we want to know what if their ejection fraction is really low what if they have an ef of like 30 to 35 percent and i didn't know that they have heart failure with a reduced ejection fraction oh that might be why that you know this is also related to it so that's something that it can also tell us and also can tell us if they have any left ventricular hypertrophy which again was something that we also associated with atrial fibrillation associated with hypertension so again getting a whole overall look at the heart is a great thing but one of the big things to take a look at is their atrial thrombus is the mitral valve disorders is their left ventricular ejection fraction like abnormality what is it and what do they have any left ventricular hypertrophy okay and the last thing here one more thing is what's the size of the atria so atrial size the big thing is is there any atrial dilation is the atria really big if the atria are dilated that is a big thing and that might help to cool you in oh they never knew that they had atrial fibrillation but they got a dilated atria that could be diagnostic of atrial fibrillation even though their ekg hasn't shown it even though their whole term monitor at this point in time hasn't shown it even though their inpatient telemetry hasn't shown it that's another thing too so do they have an atrial thrombus is a big one do they have any mitral valve disorders and is there any atrial dilation okay so once we've done that we have a pretty good idea if we need ekg holter telemetry and tte these are the most important studies that i want you to remember you can order labs you can order a chest x-ray they just may help you in other particular ways so for example think about some of the particular causes go back to some of those is there any labs that may help me may help me it might not be diagnostic enough but you know with someone who has heart failure you can get a bmp and sometimes if somebody's bmp is elevated it may help you to think of is there any chf how can i tell that correlate it with their echo does their echo show that they have obvious signs of left ventricular ejection fracture abnormalities dilated ventricles hypertro hypertrophic ventricles anything like that the other thing is what were some other causes do they have any myocardial ischemia well do their ekg show any sd segment changes and what does their tropes tell us do they have any elevated tropes well if their tropes are elevated maybe they're having like some type of mi that could be leading you into something what else think about um particularly some of the non-cardiac causes we did our chest x-ray right what else could we do potentially thinking if there's like some type of pneumonia i could do a cbc i could do a cbc to look to see if there's any elevated white count maybe that'll clue me off that there could be potentially a pneumonia related to this you can even get things like procalcitonin not great stuff but you can correlate things with your chest x-ray what else could i get what if oh thyroid that's a big one right i can get a tsh with reflex so i'm checking the tsh to see what that looks like if the tsh is really low that means that the thyroid hormone's potentially high and you check that t3 t4 so this may tell me about hyperthyroidism which could be a potential thing that could be going on back there right what else what if they uh what if they're drinking a little bit go go coco you know they had a all night bender they were drinking and tons of alcohol what else can i check i could check a blood alcohol lever i could check their blood etoh to see if that's positive right what if they've been uh they got a feochromocytoma so if they've got a fetal chromocytoma you can do what's called a meta we can do it check what's called their urine metanephrines and look to see if those are positive you can also get an adrenal ct to see if there's an obvious mass within the adrenal gland what else could i do well if they're doing the booger sugar or they're doing something like that you gotta check that talk screen so maybe doing like a urine tox screen also wouldn't be a bad idea to look to see if that's positive for any kind of cocaine methamphetamine or even like any metabolites of urinary alcohol so there's a bunch of labs that you could utilize is it going to be helpful in diagnosing afib not really it might just help me to figure out what's the thing that could have been triggering the afib okay but the most important test and i can't stress this enough is the ekg and the echo those are the big things that we need to know all right ninja nerds let's talk about the treatment of atrial fibrillation so we've established the diagnosis of afib now the next question is okay how do we go about treating this and first things first most important is what is their hemodynamic status so it goes back to that classification are they hemodynamically unstable what does that mean to be hemodynamically unstable do they have hypotension do they have pulmonary edema do they have refractory chest pain do they have an altered mental status because if they do it's a quick easy decision they're unstable i'm not going to mess with all this other stuff that we're going to go through i'm going to shock them and then we'll deal with all of the other stuff a little bit later so in an unstable state i'm going to do what's called direct current cardioversion so i'm going to hit them with some electricity baby shock the crap out of them hope that sets them back into a normal sinus rhythm and allows for me to be able to you know have a better control of their hemodynamic status now that's that pathway the other pathway is if they're hemodynamically stable so they have normal blood pressure they don't have any pulmonary edema they do not have any altered mental status or refractory chest pain that leads me to the first decision which is to rate control these patients and usually the two preferred agents of rate control that are quick is beta blockers and calcium channel blockers but we'll go over those a little bit later now after i rate control them to target a heart rate a little bit lower maybe like desirably less than like 110 100 beats per minute the next thing i have to determine is this is primarily going to kind of control their rapid afib but the next decision i have to make is are these patients at risk for developing an imbalancation of a clot that i don't know if they have in their atria or potentially of developing a clot within their atria and then embolizing that i need to determine their need for anticoagulation we'll talk about that process in a little bit more detail but that has to be the second step for two reasons we want to reduce the risk of embolization and second it's going to play a role within the next decision which is am i going to stick with ray control and anticoagulation or am i going to go to the third step which is cardioverting the patient so it's kind of like a nice bridge thing here right so the second decision is do i anti coagulate the patient okay and usually if they're getting admitted you start with something like unfractionated heparin or low molecular weight heparin and if they're going out patient you do like or if generally you could do something like oral anticoagulants you can even do that in patient as well so we rate control them first second we determine their need for anticoagulation now here's the interesting thing sometimes actually not sometimes like 50 to 70 percent of the time it's like that fifty to seventy percent of the time within you know usually within 24 hours these patients may do what's called spontaneous cardioversion meaning that they convert themselves back to normal sinus rhythm without any kind of electricity or chemical induction process so that is important thing to remember so sometimes they can spontaneously convert like 50 to 70 of the time within the first 24 hours of their onset and so that's another thing especially if it's an acute onset afib now after we again have rate controlled them anti-coagulated them and let's say that they have not spontaneously converted back into normal sinus rhythm let's say that they're still in their abnormal rhythm right now we then have to make the decision is it necessary do i need to cardiovert this patient back into their normal sinus rhythm if i do i have to start taking into consideration cardioversion and again there's two types of cardioversion we will talk about this in a little bit more detail but there's electricity and then there's chemicals so now i go to the third step which is do i consider cardioversion after i have determine their hemodynamic status and intervene in that way ray controlled them first anticoagulated them along with the ray control if they did not spontaneously cardiovert into normal sinus rhythm and they're still in that afib i need to make the decision do i need to cardiovert them okay how do we make that decision well it kind of depends upon how long this person's been in afib and what's their risk of a stroke so two factors determines kind of your need for cardioversion at that moment usually if someone has been in afib for less than 48 hours and they have a low risk of a ischemic stroke you can just cardiovert them it's unlikely if it's been less than 48 hours and you definitively know that and their chadvas score kind of shows a low risk of stroke you can say okay i'll cardiovert them and then from there you can cardiovert them and again there's two options you can do this chemically you can do it electrically and then you can decide based upon their chad vas score based upon other associated risk factors if i need to put them on oral anticoagulants for four weeks after i cardiovert them so then you're going to cardiovert and then decide based upon their chad vasque their risk factors if they need to be anticoagulated for four weeks after they've been cardioverted so that would be that pathway all right so you've rate controlled them you've anticoagulated them potentially okay to in case but if they spontaneously cardiovert you have to consider cardioversion if they've been in afib for less than 48 hours you cardiovert them and then you have the decision of oral anticoagulation for four weeks continuously okay now if they have been an afib for greater than 48 hours or you don't know maybe it's not even known how long they've been in afib oh and they have a high risk of a cerebrovascular accident or an ischemic stroke you have two options here you can either see if they have a clot within their atria at that moment how do i do that well i can get a tee right so i can get a trans esophageal like a cardiogram a tte but either way i get a t e let's say that it's positive so it's positive for a left atrial thrombus worst case scenario right it's positive for a left atrial thrombus then what i have to do is i have to do what's called i'm going to do oral anticoagulation for three weeks empirically okay then after i orderly anticoagulate them i have two options here let's say that i want to be a little extra okay i have a person who's been in afib for more than 48 hours or an unknown time period they have a high risk of a cee i mean a cva i get an echo i see a left atrial thrombus i orally anticoagulate them for three weeks what i can do is i can recheck their tee after those three weeks and see is there still left atrial thrombus because there is then i might have to anticoagulate them maybe a little bit longer or move to this next step but let's say that you do it let's say that you go this way they have high risk you get an echo they have atrial thrombus you anticoagulate them for three weeks you recheck their tee and then they have no left atrial thrombus anymore then what do you do then you can cardiovert this patient and you can put them on oral anticoagulants for about four plus weeks and maybe you have to continue it long term because of them having high risk of further embolization but either way look look what you can do here ready you can get if they have afib for more than 48 hours an unknown time period high risk of stroke you get a tee positive left atrial thrombus you orly anticoagulate them recheck the te after that and then if they have a negative thrombus you can cardiovert them and then anticoagulate them after that for four weeks or if they have afib for more than 48 hours or an unknown time period high risk of cea you can orally anticoagulate them empirically then after you do that three weeks cardiovert them and then anticoagulate them for four weeks or more that is how we go about kind of the algorithmic approach of treating atrial fibrillation now let's take a little bit of time talking about the depths of rate control the depths of anticoagulation and the depth of cardioversion all right so now let's talk about rate control rate control what are we doing with rate control and why is it actually helping us the whole concept is take here you have your conduction system right your sa node your av node your bundle of hiss your bundle branches per kg system all that stuff and we kind of zoom in on it we want to focus on this av node right when we give drugs like rig control agents what they're trying to do is they're trying to block the actual electrical activity that's coming from those ectopic foci or from those particular re-entrant circuits from moving through the av node and then down into the actual bundle of his purkinje system all that stuff that's causing the rapid ventricular rates we want to block that if we block that we basically kind of sift through all of the excess electrical activity and only allow for certain things to go down to the ventricles which should slow down the ventricular rate a little bit right that's the goal so what are drugs that can block this av node well the first one is we can use things called beta blockers and if you want an example of that think of something like metoprolol this is a very commonly utilized drug metopr law the next one now real quick because they might ask this on your exam it'll be a contraindication to give him a topology they it's not it shouldn't always be like this but it's sometimes us person who has a reactive airway disease they have underlying copd because it is a beta blocker there's beta2 receptors in the lungs so if it interacts with that it may cause bronchoconstriction and potentially exacerbate their condition so that's something to think about on your exam the next one in pink here calcium channel blockers so calcium channel blockers they ba they block the calcium channels in those av cells blocking calcium entry that slows down the electrical activity that's being transmitted through the av node what is a common drug there's two types but the more commonly utilized one is what's called diltiazem so diltiazam is going to be another type of calcium channel blocker there's also verapamil what is a potential contraindication to giving deltaizen that they may ask you on the exam if they have decompensated heart failure you should try to stay away from calcium channel blockers these are your two preferable agents the third line one that you can use it just takes a little bit longer to kick in is digoxin digoxin actually is a very weird drug and it actually targets what's called sodium potassium atp aces which alters some calcium sodium exchangers but either way this is a drug that is good if they have hypotension or heart failure it's kind of a preferable drug because you also get increased contractility from this drug so that's another thing to think about for your exams the last one which is your third line agent is amiodarone so amiodarone is a very interesting drug because this one has both rate control effect and rhythm control effect but it's actually kind of one of the ones that are a little bit more hemodynamically stable kind of drugs so to give you a quick concept here here in purple this would be your beta blockers they're blocking the epinephrine norepinephrine from binding on here and the whole effect is you're kind of trying to decrease like the calcium entry right the particularly the calcium channel blockers they're blocking the calcium entry into the actual muscle cell this amiodarone it actually does a couple things it blocks sodium entry and it blocks calcium entry and it actually has a little bit of beta-blocker effect so you can actually get three effects from amiodarone a beta blocker effect a calcium channel blocker effect and a sodium channel blocker effect the digoxin is the one that's really weird man it loves to stimulate the vagus nerve which is cranial nerve 10. that's your parasympathetic nervous system if it stimulates your parasympathetic nervous system that causes an increase in acetylcholine if you increase your acetylcholine right what would that do what would that do that would slow down your heart rate right that would slow down your heart rate so if that slows down your heart rate what would digoxin want to do to that stimulate that increase the acetylcholine release cause more potassium to leave the cell and then again lower down your heart rate so that's its effect on the av node its effect on the contractility effect is the sodium potassium atpases in the sodium calcium exchanger so make sure that i want to make sure i separate that so the effect on how it works on the av node is stimulating the vagus nerve via the parasympathetic nervous system effect okay all right these are the drugs that we utilize for rig control it's the first step there above okay rhythm control okay where since we're here it is the third step but we're going to talk about it since it's ease of access in this part of the board rhythm control that's kind of that third step which we're determining cardioversion there's three ways that we can kind of control someone's rhythm the first one is we can utilize drugs so we can utilize particular types of drugs or you know chemicals we can use what's called chemical cardioversion and my gosh is there so many different types of chemicals that we can use we are not going to list them all we'll have a separate lecture that focuses on all of these antiarrhythmic agents but you have different drugs like type 1a like procainamide you have drugs like type 1c like fleconite and propafenone you have drugs like type 3 okay and this gets into things like a butylide and amiodarone and all these different types of other drugs but these are ways that we can kind of alter the activity of different types of channels like sodium channels and potassium channels altering their activity which in a way helps to regulate some of the electrical activity within the myocardial cells of the atria and then again helping to regulate that rhythm so there's chemical drugs the only thing that you want to remember about this that they may ask on the exam is that these can potentially some of them can potentially affect the qt interval and therefore increase your risk of what's called torsades de points this may come up on your exam that you should know about the other option is we can just shock the crap out of the heart right we can apply electricity so the other option is we do what's called electrical cardioversion so electrical cardioversion and the whole idea with this is that you're trying to basically shock the heart reset all the electrical activity of the entire myocardium so that you can get them back into a normal sinus rhythm okay the last one here that you want to be thinking about though is radio frequency ablation so this is kind of like getting into the last aspect where maybe you've tried some chemical cardioversion you tried some electrical cardioversion you can utilize radio frequency waves so radio frequency ablation to kind of destroy some of these agitated irritable ectopic atrial foci you know where they most commonly love to sit around the entrances of the pulmonary veins in the atria so in the entrances of the pulmonary veins you'll try to take this like little thing here this catheter and shoot radio waves and burn those ectopic areas so that they're not existing anymore so they can't generate those abnormal rhythms so that's something that you can do something called radio frequency ablation and the big thing to remember is that this is usually near the pulmonary vein entrances another option that kind of goes along with this one so you could have radio frequency ablation the second one that it can come up on your exam to think about it's a surgical procedure where you do what's called the maze procedure this is a actual surgical procedure usually if they're getting some type of cardiac surgery that's going to be done then you can do a maze procedure as an option but generally rfa would be the first line thing before you go to a maze okay so rhythm control we can do with drugs we can do it electricity or we can actually burn it or you can cut it okay the last but not least thing to talk about is anticoagulation so atrial fibrillation right we already kind of have an idea here that these patients are at high risk for forming clots and embolizing some of those those blood clots to different areas within the body so the way that we determine their need for anticoagulation is utilizing this score called the chad's vas score so the chad's vas score is a way that we can risk stratify so to use that it's a way that we can kind of risk stratify and determine the patient's need for anticoagulation okay big thing that i want you guys to remember is you should also correlate this test the chad vasco which is determining their need for anticoagulation compare it so it should go against you should compare this with the score called the has bled score and this determines their risk of bleeding so you should have both of those determining what's their need for anticoagulation and what's their risk if they're on anticoagulation that they bleed so it can kind of give you an idea of what you know risk versus benefit and stuff like that anyway knowing this how do we kind of calculate this well there's particular things that this is kind of an acronym it tells us what we know right what we need to know so chf is one okay hypertension is another one age is another one now this one at this point in the age there's two a's and they both mean age this is greater than 75 years of age d is for diabetes s so this part here is if they've had some type of recent stroke or maybe even a tia v if they have some type of vascular disease what does this mean do they have peripheral artery disease do they have some type of coronary artery disease of some kind do they have a valvular heart disease they have a vascular disease of some kind the next one you got another age this one is generally anywhere from uh from 65 to 74 years of age and then s is for sex okay and particularly this is obviously you have female and male now how do we score all of these things you can kind of utilize these numbers here to tell you what you need to know okay so first things first you have here the c there's no there's only there's no two in front of behind it or a subscript right so it's only one point so if you have chf you get one point hypertension there's no there's only no subscript of a two there so you only get one point if you have that age 75 greater than that so if you're greater than or equal to 75 that gets you two points diabetes there's no two there so that gets you one point if you've had a stroke or tia that gets you two points if you have vascular disease that gets you one point if you have an age of 65 to 74 years of age that gets you one point and if you have a sex particularly female that gets you one point male is zero okay so that will give you all that you need to know now let's say that you do this you calculate all of this once you've calculated a person's chad's vast score and you've compared it with their has blood score let's say that their score is zero do they need to be anticoagulated no not really they're kind of low risk so really there's no anticoagulation that's needed now obviously this is dependent upon provider to provider they may see other potential needs for them to have to get on anticoagulation but by definition no they don't really need anticoagulation score of one it's plus or minus again it kind of goes based upon their risk factors their medical condition thinking about other things that they may need so plus or minus anticoagulation for a score of one okay so as you can put it's possible but again you have to utilize your has bled score to see okay is the risk you know of them being on this going to be problematic or is the benefit of being on anticoagulation going to outweigh the risks the last one if they have a score of greater than or equal to two anticoagulation is needed okay so anticoagulation is needed now here's the thing you've got to be thinking about this if let's say let's say that they had a person who was who had a score of two or plus two plus right their has blood score was really high though frank what do i do i don't know what to do i don't know if i need to anticoagulate this person what if they have a bleed in their brain or something like that they need anticoagulation they have high risk of forming strokes what do i do what do i do in some kind of situation where you kind of run into this issue you lead into this next option which i really think it's important that you guys know there's something where they can do something what's called a watchman device and basically what they do is if someone can't be on an anticoagulant but you need to have some way of preventing them from forming clots they go in and they kind of occlude out the left atrial appendage where you commonly form clots and it's a way of kind of having some type of anticoagulant or you know anti-embolic kind of activity without actually being on a drug that puts them at risk of forming clots so something to think about now we've done the chad vasque we've risked stratified we know whether or not they need anticoagulation we compared with their has bled we said oh they need to be on anticoagulation but they have other features that would prevent them or contraindicating them from being on them that's where the watchman device comes in the last thing we have to talk about is which drugs do we utilize for anticoagulation and why are these drugs picked we're not going to make it hard warfarin this one is good for someone who has a valvular afib or if they have chronic kidney disease or they have liver disease so if they have liver disease they have chronic kidney disease or they have a valvular afib warfarin is kind of like your your go-to in this scenario the only thing that you have to remember is that when someone's on warfarin you have to monitor their inr and do your best to keep it within a two to three range if it's below there's still a risk of clots if it's above three they're at risk of bleeding so that is a thing to think about with warframe all right doax is a second option now dox is you know kind of a direct uh oral acting anticoagulant there's two categories you have your factor 10a inhibitors so this is things like rivaroxaban and apixaban a doxaband all of those and then you have your 2a inhibitors and this is things like debigatran these any of these are generally good for someone with a non-valvular afib okay they're good for someone with a non-valvular afib you can prescribe this one okay also you can do it if they're in the hospital as well these have a kind of a lower risk of bleeding in comparison to war from which you can't have higher risk of bleeding from the last option okay so we got warframe we got doax and we got heparin heparin is really a good drug especially in the hospital and this comes in you have what's called unfractionated heparin or you have what's called low molecular weight heparin either way the the nice thing about these drugs is they're good they're easily titratable very easily titratable which is good whenever you have someone in the hospital and you're really trying to control their actual anticoagulation status the way that we prefer to monitor very specifically unfractionated heparin is you utilize what's called its ptt there's also like anti-xa activity um but ptt's is a good way to kind of say are we within the range that i want happens because if it's too high i gotta lower the dose if it's too low i gotta increase the dose so it's easy to really really titrate okay so heparin is good in that situation and also it's also good as a bridge so whenever somebody is on warfarin they're hyper coagulable for a small period of time so they can get kind of like what's called clots and stuff like warfarin induced skin necrosis so generally you put them on heparin for a little bit of time to bridge them through that hypercoagulable state so that they can get into a state of where they can prevent clots for a little bit okay so i know it seems like paradoxical but yeah heparin is a good bridge while they're in the hospital and then af when you go outpatient you can bridge them into a doac or you can bridge them into warfarin long term so it's a good drug it's also very good in pregnancy as well so that covers our atrial fibrillation topic all right ninja nerds in this video we talk about atrial fibrillation i hope it made sense i hope that you guys enjoyed it as always ninja nerds until next time [Music] you

Channel: Ninja Nerd

Views: 197,795

Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science

Id: eGx98xA5ITg

Length: 72min 35sec (4355 seconds)

Published: Tue Oct 26 2021