Atrial Fibrillation | Clinical Medicine

0:06What's up, ninja nerds? In this video

0:08today, we're going to be talking about

0:09atrial fibrillation. This is a part of

0:10our clinical medicine section. If you

0:13guys like this video, it benefits you,

0:14it helps you, please support us, hit

0:16that like button, comment down in the

0:17comment section, and please subscribe.

0:18Those are the best ways you can do it.

0:19Also, we have a link down in the

0:21description box below takes you to our

0:23website. There we have a lot of great

0:25notes, great illustrations that I think

0:26will be helpful to follow along with

0:28during this lecture. On top of that,

0:29we're developing courses on those

0:30preparing for your step one, step two,

0:32your pants, etc. And we got some great

0:34merchandise that I suggest you guys go

0:36check out. All right, talking about

0:37atrial fibrillation. So, atrial

0:39fibrillation is a type of arrhythmia. We

0:42will discuss this in the actual

0:43arrhythmias lecture, but atrial

0:46fibrillation is a very specific type of

0:48arhythmia that we have to discuss

0:50because it's so common and it has a lot

0:52of different problems associated with

0:53it. So it's a super ventricular tacoc

0:55cardia meaning it originates in the

0:57atria that's the name atrial

0:58fibrillation. What I want you guys to

1:00think about when you think about atrial

1:01fibrillation is two particular

1:04eeological uh problems here. So one is

1:08it's due to a cardiac problem or it's a

1:10non-cardiac problem. Let me explain what

1:12I mean and I think this helps us to

1:14remember it and oriented in our brain a

1:16little bit easier. So cardiac causes one

1:18is there is something something that is

1:21causing high left atrial pressures. All

1:25right. So the left atrial pressures are

1:27super high. And one of the reasons why

1:30that the left atrial pressures can be

1:33through the stinking roof is because

1:36there is something wrong with the mitro

1:38valve. Now when the left atrial

1:40pressures are high, what it will do is

1:42is it will actually trigger atrial

1:45dilation.

1:47So now the atria will have to dilate

1:50because of that just high pressure. It's

1:52going to have to find a way to

1:53accommodate.

1:54When you cause atrial dilation, what you

1:56do is you cause what's at least in this

1:58term called atrial remodeling.

2:02Basically, it jacks up the circuitry.

2:06There's supposed to be normal circuitry

2:08here within the atria with the way

2:09electrical activity is conducted via the

2:11meioytes. But when you alter that, it

2:15leads to a lot of problems. And this is

2:18how aphib develops. So aphib will

2:21actually develop as a result where

2:23you'll develop these like weird types of

2:25problems here like these reentrant

2:27circuits due to this remodeling process.

2:31And this is going to be the problem

2:33here. these little areas develop these

2:35little like circular patterns of

2:36electricity that shoot off and they get

2:39sent down to the ventricles and that's

2:40the problem. You develop this irregular

2:42heart rate. It doesn't follow the normal

2:43conduction pathway.

2:45That's one particular problem, right? Is

2:47high left atrial pressure causing

2:48dilation causing remodeling which can

2:50lead to aphib. The question then arises

2:53is what is causing this left atrial

2:55pressure to be high? We already

2:56mentioned one of them. One of these is

2:59going to be mitro stenosis. And it's

3:03important to remember this because mitro

3:05stenosis is a disease of the mitro valve

3:07where blood can't get from the left

3:09atrium into the left ventricle. This

3:12part's being inhibited. And so that's

3:15one way that we can stimulate an

3:17increase in left atrial pressure is

3:18mitro stenosis. An important terminology

3:21here is when the mitro valve is diseased

3:23particularly during like roheatic fever

3:25which is a big common cause. This is a

3:28specific term, a specific type of aphib.

3:31We call this valvular AIB. We mentioned

3:34this briefly in our valvular heart

3:36disease lecture.

3:38That's one reason. So, it's blood not

3:39getting from the left atrium to the left

3:41ventricle. So, the pressure here is a

3:42lot higher. What's another thing that

3:44would cause blood not to be able to go

3:45from the left atrium into the left

3:46ventricle? Heart failure. Diastolic

3:48heart failure would be a big one here.

3:50So, another one would be CHF.

3:54Particularly diastolic heart failure,

3:55but also systolic heart failure is

3:57another problem because it's filled with

3:58so much blood, it's hard for it to

4:00accept any more blood because it's so

4:02congested. So CHF will also cause the

4:06left atrial pressures to be super high,

4:08cause it to dilate, lead to electrical

4:10remodeling, and then associated aphib.

4:12These are really, really big ones to

4:14remember. The next one, believe it or

4:16not, people usually think that this is a

4:18very, very common cause of aphib. It's

4:21really truly not. But one other reason

4:23that you can develop electrical

4:24remodeling is you have an area of the

4:27atria that is eskeemic or fibrodic. And

4:31now this creates these weird if you will

4:35reentrance circuits around that eskeemic

4:39or fibrodic tissue which then shoots off

4:41and creates these abnormal electrical

4:43activities in irregular rhythm that

4:45doesn't follow the normal conduction

4:46pathway. What would be this thing?

4:48Cardiac eskeeia.

4:50So again, one other reason that you can

4:53develop Aphib is you can develop this

4:55cardiac

4:57eskeeia

5:00which can lead to cardiac

5:02maybe fibrosis during the healing

5:04process lead to atrial

5:08remodeling and then you jack up the

5:11atrial circuitry. When you jack up the

5:13circuitry you potentially increase the

5:15risk of atrial fibrillation. So cardiac

5:18eskeeia, cardiac fibrosis, atrial

5:20modeling and aphib. This is the problem.

5:22But we have to ask ourselves the

5:24question what is precipitating the

5:26cardiac eskeeia. This is usually

5:29coronary artery disease.

5:32All right. So this is usually a patient

5:33who has underlying coronary artery

5:35disease or they suffered a myioardial

5:37infarction. All right. So we have the

5:40cardiac causes. One, it's my it's both

5:42of these particular scenarios. Left

5:44atrial pressure is high. you can't get

5:46blood from left atrium, left ventricle.

5:47One is because the valve is damaged or

5:49one because the left ventricular

5:50pressure is so high and you can't get

5:52blood in there because of heart failure

5:54or you have eskeeia. Both of these

5:56things create atrial remodeling and

5:58aphib. All right,

6:01next one is non-cardiac causes. This

6:03one's actually pretty cool. And what

6:05happens with this one is there's three

6:07particular things that I want you to

6:08associate this with. One is it's due to

6:10the lungs, some type of pulmonary

6:12disease. And usually the most prominent

6:14trigger here is going to be some type of

6:17hypoxia. So we're going to put here

6:21um hypoxia is the profound stimulus here

6:25that causes these patients to go into

6:28aphib. So hypoxia now when we talk about

6:31this let's actually put this here in

6:32black. So hypoxia is the primary

6:34stimulus.

6:36What are things that can cause hypoxia?

6:40Well one is you have to have some type

6:41of lung disease. Maybe you have a

6:43patient who has something like

6:44pneumonia. So they have an infection

6:46here of one of their actual lungs and

6:48it's causing VQ mismatch. Another one is

6:51patients who have COPD particularly

6:53chronic bronchitis because that causes a

6:55lot of like hypoventilation.

6:57And the last one is like a pulmonary

6:59embolism. All of these things can cause

7:01profound hypoxia. You know what that

7:03does is that ticks off you know near the

7:05atria you have these things called the

7:07pulmonary veins. Blood is supposed to

7:10come back from the lungs via these into

7:11the left atrium. The cells right around

7:14this area are super sensitive to hypoxia

7:18and they become ticked off. And when

7:21they get ticked off, they start firing.

7:24You know what we call that? We call that

7:26ectopy. So they develop this ectopy.

7:28This ectopic firing of these atrial

7:31cells here. And when this ectopy occurs,

7:34it doesn't follow the normal electrical

7:36pathway which then leads to atrial

7:40fibrillation. So these are the things

7:42that we start seeing in these patients

7:43is they get a ton of ectopy and this can

7:46then precipitate something like atrial

7:48fibrillation.

7:50Another thing here is that they may

7:51let's come to this one. Another one here

7:54is they have lots of catacolamines.

7:57This is a big one. So tons of

7:59catacolamines.

8:01You're like, "What in the stank is

8:03that?" That's norepinephrine and

8:05epinephrine. These are the primary ones.

8:08These puppies are stimulating the heck

8:12out of these atrial cells right here

8:14near the pulmonary veins and just

8:16agitating them. You know, there's

8:18receptors on the atrial cells. You guys

8:19know what kind of receptors? What are

8:20they stimulating? You guys know this

8:22would be really particularly stimulating

8:24what's called the beta one receptors.

8:27They're stimulating the heck out of them

8:28and they're really getting agitated. And

8:30that will cause increased ectopy and

8:32potentially aphib. The question then

8:34arises what's causing this catakolamine

8:36release? Why is our sympathetic nervous

8:39system on hyperdrive, right? And the

8:43things that I want you guys to remember

8:44is usually sepsis. So some type of

8:48infection if you will. I'm going to use

8:49sepsis as the example. Another one is it

8:53could be postoperative.

8:56So sometimes after a patient has just

8:58gotten a surgery, their body is trying

8:59to heal. And this can create an

9:00opportunity for this. Another one is fo

9:05chromoso

9:08cyto. This is a adrenal medularary tumor

9:11that's pumping out epinephrine and

9:13norepinephrine stimulating these beta 1

9:14receptors in the atrial cells. And the

9:16last one is thyrotoxyosis.

9:19So whenever you're pumping out way too

9:21much thyroid hormone, so you got to stop

9:24being thyroid. You guys know that kind

9:25of reference, right? So hyperthyroidism,

9:28they really increase the sensitivity of

9:30beta 1 receptors. So if you're really

9:33hitting these, particularly this one I'm

9:35going to put here. These are really

9:37hitting those beta 1 receptors. They are

9:39really stimulating them. This is going

9:41to cause these atrial cells to become

9:42ectopic. All right? And then generate a

9:44rhythm that's not normal sinus rhythm.

9:47And here, let's actually make sure that

9:48this is an up arrow with the red there.

9:50All right?

9:52This is the concept I want you to

9:53understand here. So too much

9:54catakolamines, hypoxia. The last one

9:56here that I want you to remember is

9:59electrolyte disturbances. All right, so

10:02this is usually going to be the most

10:04common particular thing here would be

10:06things like where your potassium is

10:08really really low or your magnesium is

10:13really low. When these are low, they

10:15really alter they alter a lot of the

10:18electrical activity here and really

10:20trigger ectopy. There is one more. It's

10:24not crazy common, but they love to ask

10:27it on your exam. When patients go and

10:30they just binge and binge tons of

10:32alcohol and like this one time setting,

10:36there is a high risk of something called

10:38holiday heart syndrome. And you can have

10:40enough alcohol that it causes both

10:43hypoalemia, hypomagnesmia, and

10:45sympathetic activation. So, it's a weird

10:47one. Last thing real quick just because

10:49I'm remembering this here is for the

10:52sympathetic effects. One other thing

10:54that I would also consider in patients

10:56who just went into new onset AIB is

10:59sympathomimedics.

11:01So sympathtics.

11:05We talked about this um in the

11:09hypertension lecture. This is things

11:11like cocaine, uh methamphetamines, uh

11:14PCP. These are all drugs that have the

11:17capability to act like norepinephrine

11:19and epinephrine and increase your blood

11:21pressure and increase your heart rate or

11:23increase ectopy that can cause aphib. So

11:25these are the things that I want you to

11:26remember. Now if you're like Zach, how

11:30am I supposed to remember all this? I

11:32want you to remember maybe the pirates

11:36pneummonic. We're gonna have that pop up

11:38here on the board

11:44and that's going to stand for all of the

11:45things that you guys need to know to

11:47remember the causes of atrial

11:50fibrillation. Okay. Now with that being

11:54said, let's come to the last component

11:55here of atrial fibrillation which is

11:57when a patient develops aphib, we know

11:59why. It's either due to ectopy or

12:02reentrant kind of like circuits or

12:03remodeling if you will. One other thing

12:06that I really need you to know is when a

12:08patient develops Aphib,

12:11you can also really define them based

12:13upon the time that they have been in

12:15aphib. So what do I mean? Let's say

12:18you're here you have a patient and they

12:19are in Aphib but their AIB has lasted

12:22let's say less than 7 days. All right.

12:27In this particular situation this is

12:29called peroxismal aphib. So we're going

12:32to put peroxismal

12:37All right. So this means that these

12:39patients usually they have remodeling

12:41that's that has not yet occurred and so

12:44they may be able to snap right out of

12:47proxisal aphib and go back into normal

12:48sinus rhythm. So that's a potential for

12:50these patients is they're in aphib but

12:52they're usually in it for less than

12:53seven days and they snap back out into

12:55their native rhythm

12:57if it goes greater than seven days. So

13:00now if the patient has then branched

13:01into greater than seven days that they

13:03have been in Aphib, their heart's really

13:05starting to remodel and it's going to

13:07make it really hard for these patients

13:09to snap back into Aphib, but they

13:11definitely can. When they have been in

13:13AIB for more than 7 days, we call this

13:16persistent

13:19persistent AIB.

13:21The last particular scenario is let's

13:23say that this patient does snap into a

13:25out of a their native rhythm. Okay,

13:27good. But if they continue

13:31for more than seven days up to at least

13:33one year, this is usually what we call

13:36permanent AIB. The reason why this is

13:39important is really differentiating

13:41these two proxismal and permanent.

13:43Proxismal is these patients may have a

13:46little bit more of an ability to convert

13:48them from aphib into a normal sinus

13:51rhythm. Whereas patients who are in

13:53permanent AIB, they're already locked

13:55into this new remodeling and altered

13:57kind of like circuitry that it's

13:59literally impossible to snap them into a

14:02native rhythm. So that's really

14:03important terminology and we'll come up

14:04with a lot of other terminologies as we

14:06go throughout this lecture. Let's move

14:08into the complications of Aphib. All

14:09right, my friends. Aphib, what kind of

14:11problems can it cause? It can do a lot

14:13to be honest with you. Probably the most

14:15terrifying one and the one that you have

14:16to remember is going to be thrombboic

14:18complications, right? So the concept

14:21behind this is actually kind of

14:22interesting where if a patient has

14:23atrial fibrillation regardless of what

14:25the cause is cardiac non-cardiac causes

14:27atrial modeling ectopy doesn't really

14:29matter if they have this from aphib

14:32there is in effective atrial

14:35contractions. So all that electrical

14:37activity is causing like the atria just

14:39imagine it to like beat here beat here

14:40beat here it's just not good

14:42contractions. So, we're going to write

14:44here that it causes ineffective

14:48contractions.

14:49Because of that,

14:52it doesn't get the good kick that you'd

14:53want it to do and push enough blood in

14:56the from the atria to the ventricle. So,

14:58a lot of blood stays in the atria,

15:00unfortunately. What's that called?

15:02Stasis. And from the stasis of blood

15:06flow, what do we know about that?

15:08According to Veros triad, it increases

15:10the risk of a thrombus. So then you can

15:12get a thrombus that forms like a clot

15:15and usually it forms on the inner side

15:18here of the atria near like this little

15:20like appendage. It's called the left

15:21atrial appendage. That's usually the

15:23most common area for that thrombus to

15:24form. What's terrible is if that little

15:27piece of that clot breaks off a tiny

15:30little piece. So now you have a tiny

15:31little piece that it flicks off and

15:34these little guys go flying everywhere

15:36throughout the systemic circulation. Now

15:38you get an emblei.

15:40And that is really what is terrifying

15:42about this disease is if you have all

15:45these ineffective atrial contractions,

15:47whether it's due to ectopy or

15:48remodeling, whenever they're in aphib,

15:50they're going to have stasis of blood

15:52flow. They're going to have a thrombus

15:54and then they can break that off and

15:55cause an emblei. If these little pieces

15:59break off and they get into the systemic

16:02circulation, they can go and get blocked

16:06up into the vessels

16:09of various peripheral systemic vessels,

16:11right? So imagine in the central nervous

16:14system that little clot flicks off into

16:16like one of the corateeds or into the

16:19vertebral artery goes and gets stuck in

16:20one of those vessels blocks off the

16:22blood flow to the actual brain tissue

16:24and now you end up with a stroke. So

16:27some of these times they can present

16:28with a TIA like a transit eskeemic

16:30attack or it can prevent with a full-on

16:32infarction of the tissue called a CVA.

16:35And this is usually one of the most

16:36terrifying effects of this because again

16:38the neurological deficits. The other one

16:41is you could flick a little piece off

16:42that gets stuck in what's called the

16:43superior mesenteric artery or the

16:45inferior mesenteric artery. And either

16:47way you can lead to something called

16:49acute messenteric eskeeia. Sometimes it

16:52could lead to es schemic colitis but

16:54either way you're causing damage to the

16:56actual small bowel and large bowel and

17:00this is going to become es schemic and

17:01it's going to cause crazy abdominal

17:02pain. So if a patient has a known

17:04history they develop neurological

17:06deficits think about that complication.

17:07develop crazy abdominal pain, think

17:10about these complications. The other one

17:11is if they develop intense leg pain, uh

17:14maybe even like decreased pulses,

17:17then you really want to start thinking

17:19about did they throw a little clot that

17:21got stuck in one of the actual

17:22peripheral vessels and now it's causing

17:24a patient to experience acute limb

17:27eskeeia. These are all medical

17:29emergencies and the most terrifying

17:32effect because you could potentially

17:33lose a leg, cause massive eskeemia to

17:35the bowel and need a callectomy or some

17:37type of like bowel surgery and have

17:39permanent neurological deficits. So this

17:42is something that you have to know as a

17:43potential complication of atrial

17:44fibrillation.

17:46The next one here is acute heart

17:47failure. So this one's kind of

17:49interesting. I wouldn't say it's crazy

17:51common unless the patient is in what's

17:53called aphib with RVR, which we'll talk

17:54about a little bit when we get into this

17:55tacic cardio component. But let's say

17:57that a patient has Aphib. We're going to

18:00say Aphib and we're going to use this

18:02term with rapid ventricular rate. That

18:06usually has to be at least at least

18:10greater than 150 beats per minute. If

18:14you're not pumping up greater than that,

18:16it's really hard to cause this problem

18:19that we're going to talk about. When a

18:20patient is in aphhib and they are really

18:22having lots of ectopine remodeling and

18:24the the ventricles are firing at a rate

18:26of 150 beats per minute, that's really

18:28fast.

18:30What happens is is it literally gives

18:32the ventricles almost no time to fill.

18:35Imagine if they're beating 150 times per

18:37minute. That is literally giving them

18:39very little time to fill with blood and

18:41then contract a normal volume of blood.

18:44So their filling process

18:47is decreased. So now because of them

18:49having such a fast rate, they end up

18:52with what's called a decreased filling

18:55time. So their filling time is going to

18:59drop. And if their filling time drops,

19:03they're not going to fill their

19:04ventricles adequately. So now they're in

19:07diastolic volume drops. That causes

19:09their stroke volume to drop. That causes

19:11their cardiac output to drop. If they

19:15have a decreased filling time and then

19:17they drop their cardiac output, now

19:19they're not profusing tissues and this

19:21could potentially lead to a low blood

19:23pressure and worst case scenario, it may

19:25lead to shock. So you want to be

19:29thinking about this. If a patient has

19:31AIB, they snap into AIB and they're

19:35going greater than 150 beats per minute

19:38and their blood pressure is low, this

19:40could be potentially driving their

19:42hypotension. It's always tough. Usually

19:45in these patients if they have an

19:46underlying disorder like mitro stenosis

19:49that definitely supports that or if they

19:50have heart failure it they're already

19:52having reduced diastolic filling. You

19:54have them go at rates of greater than

19:55150 their diastolic filling drops even

19:57more. But this is one particular problem

19:59that I want you to think about. The

20:01other concept here is if your heart's

20:03beating so fast it doesn't allow the

20:05ventricles to adequately fill. So then a

20:08lot of blood stays in the atria. And if

20:10a lot of blood stays in the atria, it's

20:13going to start backflowing right into

20:16the pulmonary veins. And that's going to

20:18cause the pulmonary capillary wedge

20:20pressure to kind of go up a little bit.

20:22And if that goes up a little bit, then

20:24the fluid starts leaking out into the

20:27interstitial spaces and then you start

20:29getting edema here. You start getting

20:31fluid here. And what is this called? You

20:34guys better know this. This is called

20:36pulmonary edema.

20:39And the problem with this is is

20:41depending upon the severity, this may

20:43just cause generalized disna or it may

20:45cause this fluid to kind of like

20:47segregate out into different parts of

20:49the lung when they're laying flat. You

20:51guys remember this? This is going to be

20:53when they're laying flat or they're

20:54sleeping. They can have proxismal

20:56nocturnal disnia or thopia or maybe they

21:00just exhibit dysnia. And this could be

21:03at rest. This could be with exertion.

21:05But these are the classic findings of

21:08patients with pulmonary edema. In worst

21:10case scenario where they have mitro

21:13stenosis or heart failure and they start

21:14beating at a rate of 150 or more, they

21:17can really fill up their alvoli and I

21:20mean a lot of them and then you start

21:22causing massive alvolar filling with

21:23fluid that leads to something called VQ

21:26mismatch and this can present as

21:29hypoxmia.

21:31And if they become hypoxmic,

21:34this can cause increased work of

21:36breathing. Their respiratory rate may go

21:38up and these are definitely concerning

21:40signs. And you don't want to miss this

21:42in a patient who is definitely an AIB

21:44with RVR. All right, so these are the

21:47things that I want you to watch out for.

21:48If a patient has a known history of

21:49Aphib and they are beating at greater

21:50than 150 beats per minute, they're not

21:52presenting with low blood pressure or

21:54features of pulmonary edema, you really

21:56want to think about this. The reason why

22:00is that this type of AIB, an AIB where

22:04they're exhibiting

22:06uh low blood pressure, they're

22:07exhibiting features of dysnia or

22:10pulmonary edema. This can sometimes be

22:13referred to as I'm going to write it

22:14right here. Um what's called a unstable

22:20AIB.

22:22And I think that's important to remember

22:24this terminology. If a patient's heart

22:26rate is super fast, they're hypotensive,

22:29having dysnia, um this is definitely a

22:32sign that they're not perfusing properly

22:34and they should be shocked. All right.

22:37All right. Anyway, let's come down to

22:39the next component here. Tacocardia. So,

22:41whenever you have a patient who you go

22:43into the room or they come in and they

22:45say maybe maybe the only symptom they

22:46experience is like palpitations.

22:48Tacardia sometimes can be completely

22:49asymptomatic.

22:51But what I want you to understand is

22:53whenever these patients have tacoc

22:55cardia right and it's because they're

22:56either having these re-entranted

22:57circuits or they're having these areas

22:59of ectopy which is causing crazy firing.

23:03These patients can present in a couple

23:05different ways.

23:07They can present in aphib with what's

23:10called rapid ventricular rate. All

23:14right. And so this is generally whenever

23:15their heart rate is greater than 100

23:19beats per minute. Right? If it gets

23:21greater than 150, then they're

23:23definitely affecting their filling and

23:24they can cause heart failure, acute

23:26heart failure. And I think this is

23:28really really important. Sometimes you

23:30can have atrial fibrillation that's not

23:32even causing tacoc cardia. Some a lot of

23:34people live in a live with aphib and

23:36they're not having these fast heart

23:37rates. They could have a normal rate or

23:39sometimes they can even have a slow

23:41ventricular rate. So we call it aphib

23:42with a normal heart rate, aphib with a

23:45slow ventricular rate. So these exist.

23:48What I think is really important though

23:50is when patients are exhibiting this

23:52type of AIB and I want to use this term

23:54very very important um chronically. So

23:57they live in Aphib where their heart is

23:59beating greater than 100 beats per

24:00minute chronically.

24:03This can definitely lead to what's

24:05called cardio

24:07myopathy

24:09and it's specifically dilated. So this

24:12can lead to dilated cardiomyopathy

24:15and this is usually if there is chronic

24:18tacocardium and the reason why is you're

24:20literally just telling the heart hey you

24:22have to beat super fast you're going to

24:24have very little filling times the heart

24:26will then have to compensate for that

24:28and it'll start dilating. So if a

24:30patient develops dilated cardiammyopathy

24:32which is a type of heart failure with a

24:35reduced ejection fraction which is not

24:36due to eskeeia you really want to think

24:39has it be been because they've been

24:41chronically tacocartic. All right. So

24:43the three things that I really want you

24:45to watch out for in a patient who has

24:46atrial fibrillation is what? Do they

24:49have risk of throboili? Watch out for

24:52those features. Do they have features of

24:54acute heart failure that makes them

24:55unstable? And if they are chronically

24:57tacocartic over time, they have a high

24:59risk of dilated cardiammyopathy. All

25:02right, my friends. Now let's go into how

25:03we diagnose atrial fibrillation. All

25:05right, how do we approach atrial

25:06fibrillation? Well, I have a patient. I

25:08think that they have AIB. What do I do?

25:11First thing is you got to get that 12

25:12lead. All right, the 12 lead ECG will be

25:14the breadandbut test because if I do

25:16this, what I'll be able to see is what's

25:19the rate? Are they going fast? Are they

25:21going a normal rate or are they going

25:23slow? Aphib can exhibit in a slow

25:25ventricular rate, a normal ventricular

25:27rate, or a rapid ventricular rate. The

25:30most common I'd say is like the rapid

25:31ventricular rate. So if they're going

25:33really fast, I'd be able to determine

25:34that. And then I'd have to look to see a

25:36irregular rhythm. So a variable RTOR

25:39interval. So if I see a variable R to R

25:41interval and a fast rate, I want to

25:44think about atrial fibrillation. Also,

25:46sometimes V1 is usually a helpful lead

25:48too, but we'll talk about that more in

25:49ECG interpretation. But I get the 12

25:51lead, this should help me to see if they

25:52have AIB. Now, if you get the A if you

25:55get the ECG, you see Aphib, boom,

25:58there's the diagnosis. It's done. But

26:00sometimes patients can be in proxismal

26:02AIB, they can flip out of Aphib into

26:05normal sinus rhythm. So in those

26:07situations, you may miss it. Either way,

26:10if a patient has an ECG that shows

26:12aphib, I would also consider getting an

26:15echo cardiogram. The reason why is this

26:17can show you is there any big dilation

26:20of the left atrium, but even more

26:22important, is there any thrombus that's

26:24present in the left atrium because now

26:26those patients are at super high risk of

26:27breaking that off and embilizing. So

26:29really want to look is there any left

26:31atrial thrombus that is actually

26:32present. Look at this huge goombach

26:34that's terrifying. Or do they have any

26:36valvular problems? In other words, did

26:37they have mitro stenosis, a prosthetic

26:39valve, anything like that, or any

26:41cardiac issues that could explain their

26:42recent like new onset AIB? Now, if a

26:46patient gets their ECG, their echo,

26:49doesn't really show much, but you still

26:51think that the patient could have AIB

26:53for whatever reason, and you think that

26:56you missed it, you should monitor those

26:57patients. And so, generally outpatient,

26:59we do something called a halter monitor

27:02for 24 hours or a loop recorder. And so

27:04it basically continues to monitor their

27:06actual electrical activity of the heart

27:08for about 24 hours or more. Then they

27:10can come and they can actually be

27:12reviewed to see if they have any bouts

27:13of atrial fibrillation. And so that'd be

27:15good for missing, you know, if you have

27:16you're looking for a cult atrial

27:18fibrillation. If it is positive, all

27:20right, then they got an atrial

27:21fibrillation.

27:22The last thing I would say is really

27:24look on your exam. Sometimes the causes

27:27that we mentioned, not all of them are

27:29reversible, but the things that are

27:30reversible, you want to send off labs

27:32for. Potassium and magnesium

27:34abnormalities are super quick and you

27:36can fix those and also thyrotoxicosis.

27:39So you want to check and see is there

27:40any hypoalemia, hypomagnesmia or

27:42thyrotoxyosis if a patient went into

27:44nuance at aphib. All right, how do we

27:47treat atrial fibrillation? I want you to

27:48remember these three goals. One is rate

27:51control and we'll talk about the the

27:54actual goal that we have is to get their

27:56heart rate according to some of the

27:57trials is less than 110. Rhythm control.

28:00The whole purpose of this is is the

28:02patient have a need to restore them to a

28:05normal sinus rhythm and get them out of

28:07atrial fibrillation. And last one is

28:09anti-coagulation. I don't want them to

28:11embolize to the brain. All right, so

28:14let's talk about each one. Ray control.

28:15What I'm trying to do is shut the AV

28:17node down. I don't want this thing to

28:19actually send signals and so I have to

28:21do that by giving them drugs like a beta

28:22blocker. Usually this would be things

28:24like mtopriol, carvdalol. Those are the

28:27big ones. And oftentimes what will

28:30happen with these is they will actually

28:31help to block the beta 1 receptor.

28:33That'll decrease the intracellular

28:34calcium and decrease the actual firing

28:36of these cells. I would say avoid this

28:38in acute decompensated heart failure and

28:40avoid it in brada cardia and maybe even

28:41COPD patients. The calcium channel

28:44blockers this would be things like

28:46verapim deltyazam. These are also

28:49beneficial and these are generally going

28:51to shut down the a node and block

28:52calcium entry as well. But again avoid

28:55these in decompensated heart failure and

28:57avoid these in brada cardia. The last

28:59one is your cardiac glycosides. This is

29:01usually dejoxin and this is a pretty

29:04beneficial drug but I would say the

29:05primary benefit of this one is to be

29:08helpful in patients who are underlying

29:10uh who have heart failure. So if they

29:13have heart failure, I would say

29:14especially if there's a reduced ejection

29:16fraction, this is the patient population

29:18that could benefit from adding on to

29:19Jojoin is if they have atrial

29:21fibrillation and a heart failure with a

29:23reduced ejection fraction at least less

29:24than 35% you may find a benefit to

29:26adding these on. All right, the other

29:29one is you can consider amiodarone, but

29:31we're going to talk about that one a

29:32little bit later. All right, rhythm

29:33control. With rhythm control, the

29:35purpose is to try to restore them back

29:37to their normal sinus rhythm. All right,

29:39we can do what's called direct current

29:40cardio version. Old sparky. You can get

29:42out the pads and start, you know,

29:44zapping people. When you do this, you

29:46have to remember why you would do this

29:48because rate control is usually always

29:49the primary mode that which we kind of

29:51like try to treat AIB. The reason you

29:54would opt for rhythm control over rate

29:57control is if the patient is

29:59hemodynamically unstable, low BP, anga,

30:02pulmonary edema, acute left heart

30:03failure, and an altered mental status,

30:05right? or if they've been in AIB for

30:07less than 48 hours. Let me kind of like

30:09think make you guys think about that. If

30:11a patient has been in AIB for less than

30:1248 hours and it's at least nuance and we

30:15know that they've only been in AIB for

30:16less than 48 hours, that's not enough

30:18time for them to form throi in their

30:19atria. And it's less likely that if we

30:22zap them and give them the normal

30:23contraction back to their atria that

30:25they won't break a piece of that off. So

30:27a less than 40 hours, less chance of a

30:28thrombus. Another one is add to the fact

30:31have they been anti-coagulated for at

30:33least three to four weeks if they did

30:34have a thrombus prior or do they have a

30:36TE that shows no left atrial thrombus

30:38because in this scenario this would

30:40probably be the biggest one is

30:41hemodynamically instability shock them

30:44if you know that they haven't been in

30:45aphib long enough for them to get a

30:47thrombus shock them and if you've

30:49anti-coagulated and showed no thrombus

30:51shock them you can do this because it is

30:55going to be the best type of treatment

30:57possible and I would always go with

30:59direct that current cardioversion over

31:02pharmacological therapy which we're

31:04going to talk about next because there's

31:05some complications with that. All right,

31:08the ones that we use to cardiovert

31:09patients are going to be things like

31:10amiodarone, fleconide, lidocaine.

31:13There's a bunch of other medications,

31:15but the primary like issue with these is

31:18that these have a very high risk of

31:20torsads to points. Um, and the reason

31:22why is they can increase and prolong the

31:24QT interval which can increase the risk

31:27of these problems leading to things like

31:29torsad. So I would say if you ever have

31:31to convert a patient via rhythm control,

31:34the primary way that you should do that

31:36is going to be direct current

31:37cardioversion. And if you're not going

31:39to do that, the pharmacological agent of

31:41choice is usually amiodarone. But the

31:43reason you would actually convert

31:45somebody is these indications here.

31:48Otherwise, continue rate control.

31:52All right, that's the big concepts here.

31:55The other one that I want to talk about

31:56that doesn't involve immediately zapping

31:58them or putting them on an amiioderone

32:00infusion is you can do something called

32:02a radio frequency ablation um or a maze

32:04procedure. And basically this kind of

32:06like tries to get rid of the damaged

32:09kind of like electrically remodeled

32:11pathways in atrial fibrillation. Um and

32:14generally this would be if a patient is

32:15in complete refractory aphib. You've

32:18tried things like rate control. You've

32:20considered things like rhythm control

32:21and they're not being properly

32:23controlled. You could do that. All

32:25right. It's a coagulation. This is to

32:28prevent the risk of throbo emblei. So

32:31how do I know when to do this? I rate

32:33control the patient to keep their heart

32:34rate less than 110. I try to convert

32:36them to sinus rhythm if they're

32:37hemodynamically unstable. They have no

32:39thrombus on uh EEG and echo sorry. and

32:43they also have been anti-coagulated or

32:45they've been in a less than 48 hours and

32:46I want to zap them out of it. Rhythm

32:48control. Anti-coagulation is going to be

32:50for preventing them from having strokes.

32:53You calculate the Chad's vast score.

32:55This is guaranteed at some point in time

32:57going to be on your exam. Memorize this.

32:59So, CHF, hypertension, age greater than

33:03equal to 75, diabetes, stroke or TIA,

33:07vascular disease like P A and age 64 to

33:1175, sex female. You're going to

33:13calculate all of these out. The one that

33:15have two points is age and stroke/TIA.

33:18When you calculate all of these out,

33:20you're going to get some different

33:22scores. What score you get determines

33:24the thing that you will do. If it is

33:27greater than equal to two, you need to

33:29anti-coagulate these patients because

33:31they have a high risk of stroke. All

33:33right, very high risk. The only thing is

33:36you have to weigh out the risk of

33:37bleeding too. If it's one, take into

33:40consideration clinical judgment. Do they

33:43have a GI bleed? Are they old? Are they

33:45at higher risk of bleeding? Do they have

33:47recently have a stroke and now they

33:48actually don't want to make them bleed

33:49into that stroke? Take those things into

33:51consideration. If it's zero, you

33:54shouldn't really anti-coagulate them.

33:55You can consider aspirin if they need it

33:57and they have risk factors that would

33:58actually be bene beneficial to use

34:00aspirin but otherwise don't

34:01anti-coagulate them. So let's say that

34:03they have a score of greater than equal

34:05to two or clinical judgment decides that

34:07these patients are still high risk for

34:08stroke and I need to anti-coagulate them

34:10you need to pick the proper

34:11anti-coagulant on the exam. If they have

34:14non valvular AF they have no mitroenosis

34:17no prostatic valve pick a doack

34:19riveroxaban a pixaban adoxaban deigatran

34:22are your choices. if they have valvular

34:26AIB or non-valvular AIB with chronic

34:29kidney disease. Let me repeat that

34:30again. If they have valvular AIB, mitro

34:32stenosis prosthetic valve or nonvular

34:34AIB with chronic kidney disease, use

34:38warfin. But the only big thing with this

34:39one is you have to monitor the INR to

34:41make sure that you're the super you're

34:42in the therapeutic level. So depending

34:44upon that, it's usually two to three for

34:47those with not having a prosthetic

34:48valve, 2.5 to 3.5 for those patients who

34:51do have a prosthetic valve.

34:54Lastly, sometimes if patients are in the

34:57hospital and you need to bridge them for

34:59some particular reason over to a DOAC or

35:02over to Warin, depending upon the choice

35:05that you're going to make, sometimes

35:06patients will actually be on Heperin for

35:08a little bit and then they'll be bridged

35:10over outpatient onto one of those two

35:12medications, the DOA or Warin. But that

35:15is the big thing I need you guys to

35:16remember for this. Again, when we talk

35:19about atrial fibrillation, we know know

35:21for long-term rate control, rhythm

35:23control, anti-coagulation. What about

35:26the patient who comes in with new onset

35:28Aphib or acute AIB and they just popped

35:30into it for some reason in front of you?

35:32You have to ask the question, are they

35:34stable or not? If they are stable, all

35:37right, then what would you do? All

35:38right, we'll talk about that. But if

35:39they are in unstable, hemodynamic

35:42instability, what do you do? Well, in

35:44this situation, I have to remember my

35:46indications for direct current

35:48cardioversion is going to be if they are

35:49hemodynamically unstable. All right? So,

35:51is there fast heart rate causing them to

35:53become hypotensive? If they are, shock

35:56them. If they are not unstable, you

35:58should go to rate control. So, do things

36:00like a beta blocker, a calcium channel

36:02blocker or dejoxin.

36:04If they remain in aib despite that, then

36:07you can consider rhythm control again.

36:09Do I need to shock them or do I need to

36:11use something like amiodarone or

36:13fleconide?

36:14The reasons you would consider doing

36:16that and the next steps here is going to

36:18be saying, okay, have they been in AIB

36:20for less than 48 hours? Oh, they have,

36:22there's less chance of them forming a

36:23thrombi there. I'll cardiovert them. If

36:26they've been in aphib for greater than

36:2848 hours, that's a different story. Now,

36:30there is a chance that they actually

36:31could be having a thrombus there. So I

36:34should anti-coagulate them for a couple

36:35weeks, get a TEE to make sure that

36:38there's no left atrial thrombus. And if

36:40there is not one, then I can consider

36:42cardioverting them. After these patients

36:45have been cardioverted, then I need to

36:47consider, okay, how long do I consider

36:49consider this anticoagulation going

36:51forward? After they're cardioverted, we

36:52should at least do it for four weeks.

36:53But determining how long we'll do after

36:56that is dependent upon their Chad's vast

36:58score. So again, hemodynamically

37:00unstable, yes, cardiovert, no rate

37:03control them. If they're not being

37:04controlled with rate control, consider

37:06rhythm control. So you'll do

37:08pharmacological or direct current.

37:09Direct current is usually always better.

37:11If it's less than 48 hours, you can

37:12cardiovert them. Use direct current.

37:15After you've done the antiquagulate them

37:16for four weeks, and then from that point

37:17on, depends upon their Chad vas score.

37:21If it's greater than 40 hours, there's a

37:22chance of the thrombus there.

37:23Anti-coagulate them for a couple weeks,

37:25get the TE to make sure that it's not

37:27there. And if it's not there, then you

37:28can cardiovert them, do anticoagulation

37:30for 4 weeks, and to determine how much

37:32longer you'll keep doing that based upon

37:34their Chadvas score. As always, until

37:36next time.

37:41[Music]