Treatment of Acute Afib with RVR

[DrMetal]

so, we all know in the treatment of AF with RVR, we want to be cautious about giving ionitropes (dilt especially). If the patient has NYC 3/4 HF, we want to avoid them.

So then, why does the ER throw dilt at everyone that walks in the door? I know I know, it's the ER, but I want to understand their mentality. If you don't know the patient, if you don't know whether or not they have HF (and to what extent, don't have a recent EF), wouldn't it be safer to avoid dilt at first, do amio instead? Or do nothing at all (if the patient is stable), wait for Cardiology, a formal TTE?

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[IMGASMD]

so, we all know in the treatment of AF with RVR, we want to be cautious about giving ionitropes (dilt especially). If the patient has NYC 3/4 HF, we want to avoid them.

So then, why does the ER throw dilt at everyone that walks in the door? I know I know, it's the ER, but I want to understand their mentality. If you don't know the patient, if you don't know whether or not they have HF (and to what extent, don't have a recent EF), wouldn't it be safer to avoid dilt at first, do amio instead? Or do nothing at all (if the patient is stable), wait for Cardiology, a formal TTE?

Because it’s ER.
It’s relatively fast on and fast off, whether as amiodarone/dig takes a long time to load.
And also common things receive common treatment. Just like you have a first line treatment for PNA, the first line treatment for most AF is.....
Lastly, it’s ER. I literally had an airway with EMS doing chest compressions for 15 mins. What did the ED attending asked for? I hope you guessed it. Etomidate and succinylcholine, for a dead patient? That’s all they’ve trained to do.

 

[aafisahar]

90-99% of the time, afib is a symptom, not the primary process. Unless it's going >140-150, treat the underlying processes and the afib will get better. If EF nl, I typically do metop 25mg q6 and titrate as needed. Amio drip is usually reserved for HfrEF and if they aren't tolerating the HR (eg can't diurese, hypotensive, etc) and everyone is comfortable with the theoretical stroke risk from conversion. If they still aren't controlled on amio, I'll throw in dig, but that'll take a couple days to actually kick in.

Once the acute stuff is over, then you can talk about cardioversion. I get consults for afib all the time and I've never seen emergent (debatable if that's what it was) cardioversion stick. Their drivers are too much (hypotension, sepsis, bleed, etc etc). Stabilize them and we can try cardioversion right before they leave.

 

[mszzeta]

I am not a cardiologist nor a ED physician, but IM trained

From what I understand from my training and the above messages, if pt with hemodynamically stable a-fib w RVR and suspecting 2/2 a secondary process, what the ED should do is to find and treat the primary process, and just leave the "supportive care" of Afib to the medicine team. If pt is hemodynamically unstable, they should do electrical cardioversion. If Afib with very high HR (150+), HD stable and suspecting a primary process, they could do either pharmacological cardioversion, or a delayed approach with attempting rate control first as this paper ( https://www.nejm.org/doi/full/10.1056/NEJMoa1900353) shows?

 

[DrMetal]

Ok. So I'm not talking about the unstable patient. We would all agree they need to be immediately cardioverted.

If EF nl, I typically do metop 25mg q6 and titrate as needed. Amio drip is usually reserved for HfrEF and if they aren't tolerating the HR (eg can't diurese, hypotensive, etc)

So in the acute setting, in the ER, how do you know their EF is normal? How do you know if they have HFrEF? Sure if you have records to look this stuff up, you can get it . . .but if the patient is completely new to you---say an 81-yo with HR 150s---what do you do? Wouldn't it make sense to do maybe a bedside limited echo, to get at least a qualitative EF, before giving something ionotropic? I've never seen this done. If they could shoot dilt out of a nerf gun, they would! I'm just wondering why they throw caution to the wind like this.

Again, I know it's the ER. Does their literature show something else? Is the fast on/of properties of dilt relevant here, making it 'safe' to give, even if reduced EF? Are we being too cautious as internists?

 

[Radetzky]

People with compensated mild to moderate heart failure tolerate dilt just fine. The ones who won’t come in looking decompensated or with cardiogenic shock. Whether your ED is thinking about these things or not is of course unclear, but diltiazem is not as bad as it’s made out to be

Safety of Intravenous Diltiazem in Reduced Ejection Fraction Heart Failure with Rapid Atrial Fibrillation - Clinical Drug Investigation

Background and Objective Diltiazem is a nondihydropyridine calcium channel blocker that is used to control rapid ventricular response in patients who have atrial fibrillation or flutter. Diltiazem has a negative inotropic effect and may cause hemodynamic decompensation in patients with reduced...

link.springer.com

 

[DrMetal]

People with compensated mild to moderate heart failure tolerate dilt just fine. The ones who won’t come in looking decompensated or with cardiogenic shock. Whether your ED is thinking about these things or not is of course unclear, but diltiazem is not as bad as it’s made out to be

Safety of Intravenous Diltiazem in Reduced Ejection Fraction Heart Failure with Rapid Atrial Fibrillation - Clinical Drug Investigation

Background and Objective Diltiazem is a nondihydropyridine calcium channel blocker that is used to control rapid ventricular response in patients who have atrial fibrillation or flutter. Diltiazem has a negative inotropic effect and may cause hemodynamic decompensation in patients with reduced...

link.springer.com

Ok, that's interesting. So maybe the take away is, chronic HFrEF (but not an acute decomp), perhaps ok to use dilt? Acute Decomp HF, obviously not.

 

[Radetzky]

Ok, that's interesting. So maybe the take away is, chronic HFrEF (but not an acute decomp), perhaps ok to use dilt? Acute Decomp HF, obviously not.

Personally I would still avoid if EF 35% or less. This is purely an anecdotal take. But I would think if you have no known history of heart failure and you come in not looking decompensated the chances of having significant undiagnosed HFrEF thats going to be worsened by dilt is pretty small.

Agree though, in that many times I see beta blockers and dilt being used as a reflex in people who have cardiogenic shock

 

[chessknt]

Well locally it is a quick ticket to stepdown/ICU which results in near instant dispo so I understand from that perspective.

What annoys me is when I call EP/cards for afib with RVR in ICU that refuses to be controlled by anything on pressors and they ask me to shock the patient because thats what ACLS says. Oh yea Im sure they studied ACLS on 74 year old with sepsis and the trigger for afib will be magically gone after I hit the reset button why didnt I think of that? I love watching them glide in, order sedatives on a sick patient who then starts agonal breathing, shock, afib comes back in 30 seconds, shock again, same result, then tell me they need an ep study.

 

[Chemist0157]

Probably the technically right answer is giving beta blocker frequently.

It seems like anecdotally diltiazem is fine as long as someone is not decompensated HF.

Not sure how helpful a bedside echo will be if someone is tach’ing away at 150.

When I’ve called cardiology, the sick people get cardioverted or started on amiodarone.

 

[mszzeta]

with attem

Personally I would still avoid if EF 35% or less. This is purely an anecdotal take. But I would think if you have no known history of heart failure and you come in not looking decompensated the chances of having significant undiagnosed HFrEF thats going to be worsened by dilt is pretty small.

Agree though, in that many times I see beta blockers and dilt being used as a reflex in people who have cardiogenic shock

I would agree

Decompensated HF is a clinical diagnosis that the ED should notice. HF and HF meds should be a part of history taking that all ED physicians should be doing. And if a secondary cause of A-fib with RVR is suspected, an appropriate work up should be initiated before giving any rate control medications (controversial whether suppressing RVR would be detrimental to the HD status if it is secondary to something else, such as sepsis or PE? I have seen some physicians being "permissive" with high HR in such conditions), which would unravel the occult CHF.

Again, I am not practicing in this area and please take it as a grain of salt

 

[Radetzky]

Well locally it is a quick ticket to stepdown/ICU which results in near instant dispo so I understand from that perspective.

What annoys me is when I call EP/cards for afib with RVR in ICU that refuses to be controlled by anything on pressors and they ask me to shock the patient because thats what ACLS says. Oh yea Im sure they studied ACLS on 74 year old with sepsis and the trigger for afib will be magically gone after I hit the reset button why didnt I think of that? I love watching them glide in, order sedatives on a sick patient who then starts agonal breathing, shock, afib comes back in 30 seconds, shock again, same result, then tell me they need an ep study.

Are they allowed to order sedatives in your ICU without your approval?

 

[DrMetal]

. Amio drip is usually reserved for HfrEF and if they

Why don't we use amiodarone more often in acute Afib wRVR? If we don't know the patient, if we don't know whether they have HFref or not, if your clinically hunch tells us they may have HFrEF just by lookin at 'em, wouldn't it be the safe thing to do, to give amio instead of ionotropes?

I understand everybody worries about the side effects of amio . . . but we're not necessarily intending to send the patient home on it. We'd just be using it in the acute setting to safely get control. After a thorough eval, if you deem no HFrEF (or just chronic stable), you can send home on rate control.

And I understand amio is slower than dilt/IV BB, but in a stable patient, you have some time, and you do bolus it, it's not that slow, right?

 

[WheezyBaby]

Well locally it is a quick ticket to stepdown/ICU which results in near instant dispo so I understand from that perspective.

What annoys me is when I call EP/cards for afib with RVR in ICU that refuses to be controlled by anything on pressors and they ask me to shock the patient because thats what ACLS says. Oh yea Im sure they studied ACLS on 74 year old with sepsis and the trigger for afib will be magically gone after I hit the reset button why didnt I think of that? I love watching them glide in, order sedatives on a sick patient who then starts agonal breathing, shock, afib comes back in 30 seconds, shock again, same result, then tell me they need an ep study.

Thankful my cardiologists arent ****ing stupid.

Agree with dilt generally being well tolerated in compensated HFrEF with a not ridiculously depressed EF - our cards will frequently recommend it. Somewhat tangential, but I've had cards get somewhat in a tizzy interestingly about cardene in HFrEF but the only data I've been able to find are that the afterload reducing effects more than outweigh any negative inotropic effect

 

[aafisahar]

Ok. So I'm not talking about the unstable patient. We would all agree they need to be immediately cardioverted.



So in the acute setting, in the ER, how do you know their EF is normal? How do you know if they have HFrEF? Sure if you have records to look this stuff up, you can get it . . .but if the patient is completely new to you---say an 81-yo with HR 150s---what do you do? Wouldn't it make sense to do maybe a bedside limited echo, to get at least a qualitative EF, before giving something ionotropic? I've never seen this done. If they could shoot dilt out of a nerf gun, they would! I'm just wondering why they throw caution to the wind like this.

Again, I know it's the ER. Does their literature show something else? Is the fast on/of properties of dilt relevant here, making it 'safe' to give, even if reduced EF? Are we being too cautious as internists?

You typically don't especially if it's new onset. Clinically, you should have some pointers (eg pulm edema, peripheral edema, cardiomegaly on CXR). If there's no clear driver (eg infection, bleeding, etoh withdrawal, CHF) then should be safe to start rate control meds.

Why don't we use amiodarone more often in acute Afib wRVR? If we don't know the patient, if we don't know whether they have HFref or not, if your clinically hunch tells us they may have HFrEF just by lookin at 'em, wouldn't it be the safe thing to do, to give amio instead of ionotropes?

I understand everybody worries about the side effects of amio . . . but we're not necessarily intending to send the patient home on it. We'd just be using it in the acute setting to safely get control. After a thorough eval, if you deem no HFrEF (or just chronic stable), you can send home on rate control.

And I understand amio is slower than dilt/IV BB, but in a stable patient, you have some time, and you do bolus it, it's not that slow, right?

It really depends on how fast they are good and what the clinical picture looks like. For CHF, if they are 110s-130s and in CHF, just let it ride; afterload reduce them if necessary to get to diurese, or use milrinone. It's usually less tachycardic/arrhythmogenic than dobutamine. If it's like 150s-170s, then it's time to bust out the amio/dig especially if they aren't diuresing well. Amiodarone takes 24 hrs to really kick in based on my experience, but so does dilt in most patients.

 

[JustPass]

This topic has been in my head for a bit now so I'll ask on here.

What about in case when BP is low? Not in shock per say but low.
Amio is chemical cardioversion so there is risk of emboli. But I've seen amio used by some without anticoagulation and in some with. I've asked this to fellows and attending but never got a clear answer.
Sure if someone is critical, DC CV or amio outweighs the benefits. But what if their BP is low and you are concerned BB will drop them?
When someone orders (not me... at least not anymore) metoprolol for BP control, people say "is BB a good BP medication?", but then when it comes to controlling RVR in hypotensive pts, people at my hospital always refrain from using BB.

 

[thehundredthone]

This topic has been in my head for a bit now so I'll ask on here.

What about in case when BP is low? Not in shock per say but low.
Amio is chemical cardioversion so there is risk of emboli. But I've seen amio used by some without anticoagulation and in some with. I've asked this to fellows and attending but never got a clear answer.
Sure if someone is critical, DC CV or amio outweighs the benefits. But what if their BP is low and you are concerned BB will drop them?
When someone orders (not me... at least not anymore) metoprolol for BP control, people say "is BB a good BP medication?", but then when it comes to controlling RVR in hypotensive pts, people at my hospital always refrain from using BB.

Is the BP low because of the RVR and insufficient ventricular filling? Then a BB may actually help fix the problem (again, as long as not in decompensated HF). It's sort of like using an ACEi in cardiogenic shock, the afterload reduction actually helps improve CO and BP despite fact that it's an "anti-hypertensive". And it's the CO that really needs fixing in both cases, BP is simply a surrogate marker.

Esmolol has a quick onset of action and is extremely short acting, and will last ~45 min after the infusion is stopped (although it is a fair amount of volume as an infusion). Amiodarone requires loading given its high volume of distribution, will take longer to control the rate as an infusion (vs. a bolus, which can also cause hypotension), will potentially result in cardioversion (which as mentioned, may not be desirable in the absence of anticoagulation), and has a longer half life.

 

[Chemist0157]

This topic has been in my head for a bit now so I'll ask on here.

What about in case when BP is low? Not in shock per say but low.
Amio is chemical cardioversion so there is risk of emboli. But I've seen amio used by some without anticoagulation and in some with. I've asked this to fellows and attending but never got a clear answer.
Sure if someone is critical, DC CV or amio outweighs the benefits. But what if their BP is low and you are concerned BB will drop them?
When someone orders (not me... at least not anymore) metoprolol for BP control, people say "is BB a good BP medication?", but then when it comes to controlling RVR in hypotensive pts, people at my hospital always refrain from using BB.

I guess define "low." SBP 90-100? I'm fairly comfortable giving BB to AFib RVR if I am suspicious that is the cause of the hypotension. BP should improve. If they are hypotensive for some other reason like sepsis, well, maybe they need to be on some pressor support anyway if you think it is shock. Can always start that kind of thing quickly if necessary.

 

[sss2g2]

This topic has been in my head for a bit now so I'll ask on here.

What about in case when BP is low? Not in shock per say but low.
Amio is chemical cardioversion so there is risk of emboli. But I've seen amio used by some without anticoagulation and in some with. I've asked this to fellows and attending but never got a clear answer.
Sure if someone is critical, DC CV or amio outweighs the benefits. But what if their BP is low and you are concerned BB will drop them?
When someone orders (not me... at least not anymore) metoprolol for BP control, people say "is BB a good BP medication?", but then when it comes to controlling RVR in hypotensive pts, people at my hospital always refrain from using BB.

Dig does not get enough support around here. You can start Dig if the BP is low. Dig is especially great in HF. Jut make sure kidneys are fine.

 

[Shams al Deen]

90-99% of the time, afib is a symptom, not the primary process. Unless it's going >140-150, treat the underlying processes and the afib will get better. If EF nl, I typically do metop 25mg q6 and titrate as needed. Amio drip is usually reserved for HfrEF and if they aren't tolerating the HR (eg can't diurese, hypotensive, etc) and everyone is comfortable with the theoretical stroke risk from conversion. If they still aren't controlled on amio, I'll throw in dig, but that'll take a couple days to actually kick in.

Once the acute stuff is over, then you can talk about cardioversion. I get consults for afib all the time and I've never seen emergent (debatable if that's what it was) cardioversion stick. Their drivers are too much (hypotension, sepsis, bleed, etc etc). Stabilize them and we can try cardioversion right before they leave.

Dig just takes a couple hrs to work if you load

 

[Radetzky]

Amiodarone kicks in pretty quickly, as long as you load.

 

[Drrrrrr. Celty]

A fib comes in 2 flavors in my head. You're stable and you can tolerate a cardizem drip or you're not. People like it because you can honestly convert the hourly dosing to a 24 once a day dilt cd as well. This as opposed to mucking around and trying to figure out how much toporol xl you need to give after you're off the esmolol drip.

 

[rokshana]

so, we all know in the treatment of AF with RVR, we want to be cautious about giving ionitropes (dilt especially). If the patient has NYC 3/4 HF, we want to avoid them.

So then, why does the ER throw dilt at everyone that walks in the door? I know I know, it's the ER, but I want to understand their mentality. If you don't know the patient, if you don't know whether or not they have HF (and to what extent, don't have a recent EF), wouldn't it be safer to avoid dilt at first, do amio instead? Or do nothing at all (if the patient is stable), wait for Cardiology, a formal TTE?

hate hate amiodarone...but then I'm an endocrinologist...how about just use some metoprolol?

 

[DrMetal]

hate hate amiodarone...but then I'm an endocrinologist...how about just use some metoprolol?

I'm not advocating (necessarily) for it's long term use, I just wonder why we don't use it more often in the acute setting, especially when we're unsure (or may even clinically suspect) heart failure (that could be made worse with ionotropic agents). Use the amio to convert, get a formal TTE when in NSR (say next day, same admission), if EF is good to go, then certainly start on rate control.

I guess the take home here is that chronic HFrEF (NOT in an acute decomp), it's still ok to do dilt/BB to convert.

 

[DrPcv]

I think the old adage of treat the patient not the number is extremely important with rvr.
why is the patienr tachycardic?
-where you run into problems with dilt, cardizem and even beta blockers is when you have someone with adhf specially a very low ef and you try to rate control them. If their stroke volume is 20 cc/beat then their heart rate of 150 is what’s keeping them alive, so if you drop their heart rate to 100 you are going from a Cardiac output of 3 lts to 2.0 lt. Just let them ride, diurese and support them with initropes if needed. Then afterwards restore NSR w electricity and antiarrthmic

I'm not advocating (necessarily) for it's long term use, I just wonder why we don't use it more often in the acute setting, especially when we're unsure (or may even clinically suspect) heart failure (that could be made worse with ionotropic agents). Use the amio to convert, get a formal TTE when in NSR (say next day, same admission), if EF is good to go, then certainly start on rate control.

I guess the take home here is that chronic HFrEF (NOT in an acute decomp), it's still ok to do dilt/BB to convert.

The problem with amio is that is a nasty drug and yes it’s ok in the short term but then what? Unless you are 80+/heading end off life you probably shouldn’t be on long term amio.
What usually happens is patient gets placed on amio and they never get followed up and the med stays on their list forever and people just renew it.
There are better/safer medications for maintenance of sinus rhythm or (and specially if there’s ventricular dysfunction) ablation.

On a separate note please do NOT cardiovert atrial flutters. Call your cardiologist first. Ablation is easy and curative (if typical flutter) and the patietnt can be taken of AC a month after ablation.

 

[wjs010]

But inevitably a ton of them will need to be on a BB for HFrEF to some degree and or CAD, so they still need the toprol. The 25 q6 and titrate is great. It is more convenient to go from dilt drip to PÓ though, if they don’t have indications for BB. The argument that you shouldn’t block a compensated rate in the 150s if there’s an EF of 20% makes sense in the acute sense if there’s very good evidence that the CHF is the underlying issue. I don’t know of the data behind this logic .

A fib comes in 2 flavors in my head. You're stable and you can tolerate a cardizem drip or you're not. People like it because you can honestly convert the hourly dosing to a 24 once a day dilt cd as well. This as opposed to mucking around and trying to figure out how much toporol xl you need to give after you're off the esmolol drip.

 

[shouldigomd]

This topic has been in my head for a bit now so I'll ask on here.

What about in case when BP is low? Not in shock per say but low.
Amio is chemical cardioversion so there is risk of emboli. But I've seen amio used by some without anticoagulation and in some with. I've asked this to fellows and attending but never got a clear answer.
Sure if someone is critical, DC CV or amio outweighs the benefits. But what if their BP is low and you are concerned BB will drop them?
When someone orders (not me... at least not anymore) metoprolol for BP control, people say "is BB a good BP medication?", but then when it comes to controlling RVR in hypotensive pts, people at my hospital always refrain from using BB.

You are talking afib so they will be on AC per their CHDS regardless of "chemical cardioversion." If they are sick in the ICU and can't tolerate AC then the risk of emboli probably isn't the biggest concern anyway as this is cumulative risk over the long term.

Generally speaking you shouldn't give a hypotensive (<90/60) patient beta blockers unless you feel the afib w/ RVR is driving the hypotension. For hypotensive patients your options are limited (amio vs dig vs dccv) but IV amio also has a significant b-blockade effect as well. Dig by itself is a pretty lousy rate control agent (works best with bbl or ca bl).

 

[jdh71]

Pushing two grams of Mag is often really effective in dealing with the RVR. Patients HATE if but, sorry, I didn’t give you afib, the rvr, and the critical illness.

 

[DrMetal]

Pushing two grams of Mag is often really effective in dealing with the RVR. Patients HATE if but, sorry, I didn’t give you afib, the rvr, and the critical illness.

You don't mean just Mg by itself, do you?

 

[jdh71]

You don't mean just Mg by itself, do you?

I do. Mag. Nee. See. Um.

2grams. Push it.

 

[IMGASMD]

I do. Mag. Nee. See. Um.

2grams. Push it.

Mag Née See Um, by itself?!

 

[gutonc]

I do. Mag. Nee. See. Um.

2grams. Push it.

 

[jdh71]

Mag Née See Um, by itself?!

Yes

 

[WheezyBaby]

Yes

I've heard good things about mag bolus for afib recently, have never tried it. Do you see a fair amount of people converting or mostly just rate control?

 

[jdh71]

I've heard good things about mag bolus for afib recently, have never tried it. Do you see a fair amount of people converting or mostly just rate control?

Rate control. Patients hate it though. It's not the first thing I reach for. Usually the last.

 

[turkeyjerky]

Rate control. Patients hate it though. It's not the first thing I reach for. Usually the last.

Man, I've never seen or heard of pushing a mag bolus (outside of a code setting). Over the past year I've been using a 4 g bolus (given over 30 min) in combo w/ other rate control agents and anecdotally I think it helps. Sometimes get pushback from pharmacy, but then I point out that in the recent trial, this was the low dose of magnesium. Much better than 2 g (over 15-20 min) ime.

Are your nurses comfortable actually pushing the mag?

 

[jdh71]

Man, I've never seen or heard of pushing a mag bolus (outside of a code setting). Over the past year I've been using a 4 g bolus (given over 30 min) in combo w/ other rate control agents and anecdotally I think it helps. Sometimes get pushback from pharmacy, but then I point out that in the recent trial, this was the low dose of magnesium. Much better than 2 g (over 15-20 min) ime.

Are your nurses comfortable actually pushing the mag?

I don’t remember them balking.

 

[IMGASMD]

I don’t remember them balking.

Presumably they’re also in a monitored bed while you’re doing this.

Why don’t they like it? Does it burn, does it make them feel funny? If that the last drug you use, what do you start with?

 

[dadaddadaBATMAN]

Responding from the ed perspective.

I’m generally thinking about it from a couple lines when I first see it

1. Stable/unstable.
2. Primary cause of symptoms or secondary
3. If primary, new or old, and rate or rhythm controlled as outpt if old, and clear onset time or not
4. If secondary, what is cause: usually pursue infectious, pe or electrolyte abnormality, if obviously not these requires more thought and tailored process.

Mostly I care that the person is safe and unlikely to die if/when neglected for four hours on the floor if I am putting them there. If they’re going to the icu or they are floorable with a secondary cause I usually discuss appropriate agent (or deferral of therapy) with the doc who is taking over for me on floor or icu. I think it makes life easier if you get to pick your poison.

A lot of people use dilt in the ed preferentially because the limited rcts performed in the ed (only two I know of that are about 80 pts each) show improved time to rate control and better % responding with dilt. The time is 30-40 minutes and the %is around 10 if I remember right. It also allows quick icu dispo in many hospitals as noted above, which I’m sure is part of people’s decision.

That is not meaningful to pts necessarily: but it is meaningful to our waiting room and our corporate overlords.

I tend to choose between them (or defer therapy) based on multiple things from factors 1-4 above, and also the ef which is typically two epic clicks away in these pts. <30 or decomp chf I usually favor metop if I’m treating.

Anecdotally I have never seen a meaningful adverse outcome from dilt use (mine or colleagues) but maybe that’s because I am selective.

I usually avoid amio due to possibility chemical cardioversion unless they are already on it or I talk with someone (cards) to cma if they were to stroke. I also think id be irritated if I were an internist and someone gave my pt a medication that would be in their system the entire admission without any input from me, but maybe that’s a flawed view. If I give it I document shared decision making when possible.

One thing I have not seen discussed above or in many treatment algorithms is what to do when an agent fails at maximal dosing. My usual response is to discuss with cards or admitting team, then give second agent of choice. do any of you folks have a more nuanced or evidence based approach? I’m a fresher attending so im always looking to learn

 

[jdh71]

Presumably they’re also in a monitored bed while you’re doing this.

Why don’t they like it? Does it burn, does it make them feel funny? If that the last drug you use, what do you start with?

I usually push drugs when patients are sitting on a folding chair in the hallway

They flush

 

[Radetzky]

Amiodarone is slated as having beta blocking effects but I doubt this is clinically relevant. Hypotension with amiodarone is caused by the alcoholic solvent and is a vasodilatory effect, rather than depressing your cardiac output like bb or Ccb. Amiodarone formulated in a different solvent is free of a hypotensive effect. Plus you can manage the hypotension by slowing the infusion rate.

 

[chessknt]

One thing I have not seen discussed above or in many treatment algorithms is what to do when an agent fails at maximal dosing. My usual response is to discuss with cards or admitting team, then give second agent of choice. do any of you folks have a more nuanced or evidence based approach? I’m a fresher attending so im always looking to learn

The secret is they dont know how to fix it either hence the recommendation to shock.

For hypotensive sepsis afib my general approach is
1. amio bolus x1, wait a few hours, then bolus again
2. Dig load (depending on kidneys) and wait a few hours, repeat if kidneys ok
3. Call EP

 

[aafisahar]

The secret is they dont know how to fix it either hence the recommendation to shock.

For hypotensive sepsis afib my general approach is
1. amio bolus x1, wait a few hours, then bolus again
2. Dig load (depending on kidneys) and wait a few hours, repeat if kidneys ok
3. Call EP

What is EP going to do? Ad hoc ablate them?

The treatment of afib in sepsis is straightforward. Treat the infection, correct hemodynamics, and maybe some rate/rhythm control. You don't need cardiology for this and certainly not EP.

 

[IMGASMD]

What is EP going to do? Ad hoc ablate them?

The treatment of afib in sepsis is straightforward. Treat the infection, correct hemodynamics, and maybe some rate/rhythm control. You don't need cardiology for this and certainly not EP.

Share the wealth, of course.

If I tried, presumably, four agents, cardizem, BB, Amio, and Dig. Still unable to control afib with RVR? You bet I am calling expert.

Maybe I am missing something, that I don’t see every day. Can’t have it both ways. Can’t say Afib is complicated, and faulting people calling experts for a consultation.

 

[chessknt]

What is EP going to do? Ad hoc ablate them?

The treatment of afib in sepsis is straightforward. Treat the infection, correct hemodynamics, and maybe some rate/rhythm control. You don't need cardiology for this and certainly not EP.

I can say the same thing for a wide swath of conditions in medicine. This is Murica we need to drive costs up by getting more units generated and bring as much shared liability to the table as possible.

 

[Redpancreas]

so, we all know in the treatment of AF with RVR, we want to be cautious about giving ionitropes (dilt especially). If the patient has NYC 3/4 HF, we want to avoid them.

So then, why does the ER throw dilt at everyone that walks in the door? I know I know, it's the ER, but I want to understand their mentality. If you don't know the patient, if you don't know whether or not they have HF (and to what extent, don't have a recent EF), wouldn't it be safer to avoid dilt at first, do amio instead? Or do nothing at all (if the patient is stable), wait for Cardiology, a formal TTE?

More experienced ones have probably commented but I wanted to give my own take to learn before reading through them. To start, has the oral metop been restarted assuming this patient isn't in florid acute decompensated HF? If the patient is not hypotensive, why not scheduled IV metop (clinically causes HoTN) or an increase in the oral metop? If that didn't work, my next go to would probably be a cardiac calcium channel blocker. Not an exact science but my mentality is at least it's "clean" as opposed to most rhythm control agents (and btw also chemical cardioversion) like Amio, etc or the narrow-index Digoxin. Maybe my mentality's wrong but that could be why your ED is doing that?

Also, I know cardiac CCBs are not ideal for the same reason BB aren't for HF, but didn't think they would be contraindicated for NYHA 3 not admitted for an exacerbation. Now that I think about it, if Metop doesn't work, my second would be Dilt and would consult Cardiology before throwing Amio/Dig at something. Tell me where I'm wrong. Also, if the patient's hypotensive and in persistent afib, I'd worried about more worried about whether the patient's needs a shock as opposed to digoxin.

Obviously checking basic lytes, treating sepsis, ensuring patient is euvolemic is important.

 

[Redpancreas]

The secret is they dont know how to fix it either hence the recommendation to shock.

For hypotensive sepsis afib my general approach is
1. amio bolus x1, wait a few hours, then bolus again
2. Dig load (depending on kidneys) and wait a few hours, repeat if kidneys ok
3. Call EP

What is EP going to do? Ad hoc ablate them?

The treatment of afib in sepsis is straightforward. Treat the infection, correct hemodynamics, and maybe some rate/rhythm control. You don't need cardiology for this and certainly not EP.

This is the exact dispute between Cards/ICU where I trained. Cardiology represents @aafisahar and ICU is @chessknt

Cards consultant says something about treating the underlying cause (sepsis, etc.) and how less is more but then ICU is the primary and has to do something ultimately and opts for Amio.

Could someone explain the cons behind Amio further. From what I've gathered the cons are you're cardioverting (albeit chemically) and amiodarone hits organs hard (long term). If there's truly tenuous HF and you need to control a rate after you're doing your best and the patients on A/C, I think Amio is probably the best option at that point.

 

[Chemist0157]

I’ve read more about concern for chemical cardioversion here than I have ever seen in practice or from cardiology. Maybe it is related to the cardiology guys where I work inpatient? People aren’t shy to start amiodarone around my local hospital if the typical metoprolol or diltiazem rate control tactics are not the best play.

 

[wjs010]

follow up question with this: how long are you expecting to see NSR after starting an amio drip? I was under the impression that it took a few hours but I am now unsure. I have started a drip on a patient and stood in the room and watched them convert in 20 minutes. Coincidental maybe.

 

[aafisahar]

follow up question with this: how long are you expecting to see NSR after starting an amio drip? I was under the impression that it took a few hours but I am now unsure. I have started a drip on a patient and stood in the room and watched them convert in 20 minutes. Coincidental maybe.

very variable, only like a 30% chance to convert with a good load of amiodarone. it depends on a lot of things including how remodeled their atria are, the underlying substrate (DMII, HTN, COPD, OSA, etc), EF/LV dilation, cause of AF (eg primary vs secondary), etc etc. Generally, the more normal the heart and the more acute the drivers, the more likely someone will go back into sinus.

IV amiodarone isn't there to cardiovert them, it's to rate control.