Afib with RVR: admit or r/o in ED

[Boondahgle]

62 yo WF with PMH HTN, no other known cardiac risk factors who presents with 1.5 hour history of palpitations, chest pain, fluttering sensation. Pt's BP is stable, HR found to be 170 and EKG shows Afib with RVR. Pt has ST depressions throughtout that resolve after 20-30 minutes with rate control and conversion to sinus rhythm (received Dilt gtt first and then IV Metoprolol). 1st set of cardiac markers is negative. Is this something you would automatically admit to cardiology? Would it be inappropriate to have serial cardiac enzymes checked in ED? If enzymes remained negative, should the patient still be admitted?

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[Instatewaiter]

New afib probably should be worked up a bit more than just some cardiac markers. I say admit to general medicine; this shouldn't be a cardiology admission

 

[indiamacbean]

I think this should be admitted. as to whether it goes to medicine or cardiology I guess is program/hospital dependent. guideline recommended evaluation for afib includes: A chest radiograph to detect intrinsic pulmonary pathology, thyroid, renal, and hepatic functions, serum electrolytes, and cbc be measured at least once in the course of evaluation. All patients with AF should also have 2-dimensional, Doppler echocardiography to assess LA and LV dimensions, LV wall thickness, and function and to exclude occult valvular or pericardial disease and HCM.

I think it would also be reasonable depending on age to make sure there is not an infection driving this if the patient has anything pointing towards that. I think the majority of this could be performed on an outpatient basis but in order to discharge from the ER you would have to demonstrate hemodynamic stability with suitable rate control which is certainly not the case in someone who is going 170 and in whom you just used IV metop. I think the issue here is that very often the ER does not make an adequate attempt at using good doses of a longer acting rate control medication and these people get admitted. also if the patient is in Afib chronically and you just chemically converted them to NSR without anticoagulation they will be at higher risk of thrombus formation from myocardial stunning.

 

[dragonfly99]

New/never before seen a fib with HR of 170 is a pretty legit admission.
Whether it goes to cards or IM I guess is hospital dependent...I've never worked at a hospital where the hospitalists/IM docs would admit this kind of thing. They generally whine about evening admitting old/recurrent CHF or a fib at all...ever.

If someone comes in with a fib to clinic that is rate controlled, or with a fib to the ER that is recurrent and rate control isn't too bad (like 120-140 and comes down w/meds) they can go on home, but an over 60 patient with completely new a fib and HR of 170's that is requiring IV meds is going to be a little hard for ER to just send out. They don't have time to fool with a patient for 8 hrs getting the rate controlled, checking the thyroid, etc.

 

[tkim]

I think the issue here is that very often the ER does not make an adequate attempt at using good doses of a longer acting rate control medication and these people get admitted.

Nope.

They don't have time to fool with a patient for 8 hrs getting the rate controlled, checking the thyroid, etc.

This.

If I have half a day to fool around with meds to rate control someone, I'm not doing emergency medicine - I'm doing floor medicine, or maybe even cards. I'm neither an internist or cardiologist.

 

[langtaogdmc]

I think this patient should be admited to cardiology. You don’t that whether this patient suffer an recurrent afib again or no. maybe his heart rate will be more than 200 bpm and even develop into ventricular fribrilation without promptly therapy. It is hard to convert to NSR next time. I think it is better check out the cardiac markers several hours later, and repeat the ecg. Do you think that it is a good idea to give an angiography for that patient to rule out some coronary artery disease?

 

[NDESTRUKT]

Admit to medicine with cardiology consult.

 

[pseudoknot]

Why are you checking cardiac enzymes in someone with a-fib RVR?

 

[taurus70]

Can you imagine an ER physician actually keeping this guy in the ER that long. He would be admitted to medicine faster than the word GO!. I mean, even ortho dumps hip fractures in 20 year guys to medicine at my hospital.

 

[taurus70]

Why are you checking cardiac enzymes in someone with a-fib RVR?

ER checklist:

U/A: check
CT chest with contrast to R/O PE: check
BNP: Check
Cardiac markers: Check
Examine Patient:--------
Call MAR to admit patient: Check!

Sorry, couldn't help it. I just came off a 24 hour call.

 

[Instatewaiter]

Why are you checking cardiac enzymes in someone with a-fib RVR?

2 reasons. Ischemia can cause Afib. Also RVR is basically a poor man's stress test- when you're going 160 and you have a fixed lesion you leak troponins from demand. It's good to know.

 

[jdh71]

I've never worked at a hospital where the hospitalists/IM docs would admit this kind of thing.

And I've never worked at a hospital where cardiology would have admitted this patient. It is pretty hospital dependent.

Maybe it's regional, but bad hearts come to the MICU if they are sick enough, and medicine floor if they are not - cardiology consults. The University has a bad HF/Transplant unit, but otherwise the in-patient cardiology service seems to be going the way of dinosaur in my neck of the woods.

 

[IMDoc607]

Admit to telemetry....r/o any ischemic etiology, maybe 2D echo, and bridge with heparin to coumadin if appropriate.

Thats what we do

 

[EPADHA]

New afib probably should be worked up a bit more than just some cardiac markers. I say admit to general medicine; this shouldn't be a cardiology admission

completely agree. I would take this one step forward..is this the first episode of a fib? if so, everyone deserves at least one chance at sinus rhythm esp if they are symptomatic- wd consider rhythm control here vs ablation if he has had some more paroxysms ( and anatomy if favorable-LA id not dilated, MR is not severe etc). Also with ischemic EKG changes, you know that you have had a good stress test which is positive ( or there is tight stenosis some where) ...so that needs further work up. ST depressions throughout sounds very concerning.

The discussion about rhythm control and anticoagulation can be done in the outpatient setting. If this is truly the first episode, I might do metoprolol and pradaxa, and follow him periodically. If more paroxysms occur, wd offer him either drugs or ablation.

 

[IMDoc607]

ER checklist:

U/A: check
CT chest with contrast to R/O PE: check
BNP: Check
Cardiac markers: Check
Examine Patient:--------
Call MAR to admit patient: Check!

Sorry, couldn't help it. I just came off a 24 hour call.

My bad

 

[IMDoc607]

completely agree. I would take this one step forward..is this the first episode of a fib? if so, everyone deserves at least one chance at sinus rhythm esp if they are symptomatic- wd consider rhythm control here vs ablation if he has had some more paroxysms ( and anatomy if favorable-LA id not dilated, MR is not severe etc). Also with ischemic EKG changes, you know that you have had a good stress test which is positive ( or there is tight stenosis some where) ...so that needs further work up. ST depressions throughout sounds very concerning.

The discussion about rhythm control and anticoagulation can be done in the outpatient setting. If this is truly the first episode, I might do metoprolol and pradaxa, and follow him periodically. If more paroxysms occur, wd offer him either drugs or ablation.

We also bridge to coumadin unless there is a specific concern/consideration.

 

[Instatewaiter]

BNP really makes no sense unless you think the patient is in CHF. CT PE is also questionable if the scenario is not suspicious for a PE. Why put someone thru a unnecessary CT with contrast. Maybe LE dopplers

Why do you think a BNP would be helpful? I am assuming that you are thinking the person is in CHF?

I think you missed the fact that he was poking fun at the ED.

In the ED at my hospital, if the patient has lungs, they will get a CT scan- usually with contrast.

 

[Instatewaiter]

We also bridge to coumadin unless there is a specific concern/consideration.

You don't really need to bridge to coumadin for A-fib

 

[IMDoc607]

I think you missed the fact that he was poking fun at the ED.

In the ED at my hospital, if the patient has lungs, they will get a CT scan- usually with contrast.

My bad....lol

The attendings where I am like to bridge to coumadin to an INR close to 2 then follow up as outpatient.

I asked that question to many attendings and got different answers....some like to others don't feel its necessary

 

[supp-2]

1) New-onset AF w/ RVR that converts in ED will admit (to Cards service at my institution)
2) Known AF w/ RVR that settles down in the ED I can usually get them to send out
3) I usually only push to bridge if history of previous stroke/TIA or super high CHADS2

 

[jdh71]

You don't really need to bridge to coumadin for A-fib

heresy!!

 

[IMDoc607]

heresy!!

Agree.....new onset we start heparin gtt then begin coumadin dosing if appropriate.

 

[Top Gun]

62 yo WF with PMH HTN, no other known cardiac risk factors who presents with 1.5 hour history of palpitations, chest pain, fluttering sensation. Pt's BP is stable, HR found to be 170 and EKG shows Afib with RVR. Pt has ST depressions throughtout that resolve after 20-30 minutes with rate control and conversion to sinus rhythm (received Dilt gtt first and then IV Metoprolol). 1st set of cardiac markers is negative. Is this something you would automatically admit to cardiology? Would it be inappropriate to have serial cardiac enzymes checked in ED? If enzymes remained negative, should the patient still be admitted?

If new onset, admit to telemetry, get free T4, TSH, do at least 2 more sets of cardiac markers to rule out ischemic etiology, check electrolytes, control rate with beta-blockers or calcium-channel blockers. Start anticoagulation depending on CHADS2 criteria. Keep in mind that HTN alone is a risk factor for development of atrial fib.

 

[jdh71]

Agree.....new onset we start heparin gtt then begin coumadin dosing if appropriate.

actually I was agreeing with Instatewaiter

Fib is different from PE or DVT, situations where you have KNOWN clot. If the fib is new onset, it'll take awhile to form a clot, and you don't really need a bridge. Fib of unknown length? Starting on new anti-coag? Maybe. Patient with known fib on (generally) therapeutic anticoag, no reason to drip them if they come in low or you have to reverse for some reason, restart the coumadin when it's time.

 

[IMDoc607]

actually I was agreeing with Instatewaiter

Fib is different from PE or DVT, situations where you have KNOWN clot. If the fib is new onset, it'll take awhile to form a clot, and you don't really need a bridge. Fib of unknown length? Starting on new anti-coag? Maybe. Patient with known fib on (generally) therapeutic anticoag, no reason to drip them if they come in low or you have to reverse for some reason, restart the coumadin when it's time.

Oh ok....quick question then. If you are going to anticoagulate them wouldn't you want to start heparin gtt then go to coumadin. I have heard differently from many attendings. They are worried about warfarin induced skin necrosis.

Let me know....thanks

 

[turkeyjerky]

Oh ok....quick question then. If you are going to anticoagulate them wouldn't you want to start heparin gtt then go to coumadin. I have heard differently from many attendings. They are worried about warfarin induced skin necrosis.

Let me know....thanks

Just an aside--you guys seriously use a heparin drip? Even if you're gonna bridge, why not just use lovenox.

 

[jdh71]

Oh ok....quick question then. If you are going to anticoagulate them wouldn't you want to start heparin gtt then go to coumadin. I have heard differently from many attendings. They are worried about warfarin induced skin necrosis.

It's a concern for sure, but what do they do in the out-patient setting when a patient's INR drops to say 1.2-1.4? Bring them in for a heparin gtts to restart the coumadin? No they simply up the coumadin dose. You think protein C and S stayed low despite the normalish INR? I've not seen a plague of skin necrosis cases with these patients coming in, have you? Look, everyone gets nervous, especially the cardiologists who seem to think every patient is going to MI in the parking lot on the way to their cars, but what medication does come with it's own side effect profile? I simply don't see why coumadin should be any different.

If you're really nervous about it, just give a slug of therapeutic lovenox (or similar LMWH) and start the coumadin.

 

[IMDoc607]

Just an aside--you guys seriously use a heparin drip? Even if you're gonna bridge, why not just use lovenox.

One or the other but most go to heparin gtt.

 

[Top Gun]

One or the other but most go to heparin gtt.

.

 

[Top Gun]

One or the other but most go to heparin gtt.

It would depend on the renal function. If the renal function is good, I might just go with Lovenox. At least with Lovenox, the PTT doesn't have to be checked every 6 hours and the dose adjusted each time.

 

[IMDoc607]

6

It would depend on the renal function. If the renal function is good, I might just go with Lovenox. At least with Lovenox, the PTT doesn't have to be checked every 6 hours and the dose adjusted each time.

Yea....if renal function is ok it would depend on the attending. I agree that its so much easier so you do not need to check the PTT Q6H.

 

[Instatewaiter]

Agree.....new onset we start heparin gtt then begin coumadin dosing if appropriate.

New onset (<48h) should be anticoagulated with heparin to prevent atrial thrombus so that you can give them a change at cardioversion. You start the heparin immediately b/c it will limit the risk the fibrillating atrium and thus the crappy blood flow in the atrium will clot. That way, when they go for TEE cardioversion there isn't a clot and they can be shocked out of fib.

If you cannot succesfully cardiovert and your EP won't do an ablation, there really isnt a need to bridge to coumadin.

If they get cardioverted and go back into sinus, they need to be bridged b/c the risk of atrial clot after cardioversion is higher than being in a-fib for ~4 weeks after the procedure.

Now with dabigitran, no need to bridge.

actually I was agreeing with Instatewaiter

Most people do.

Yea....if renal function is ok it would depend on the attending. I agree that its so much easier so you do not need to check the PTT Q6H.

I HATE lovenox in the hospital and I encourage everyone on this board to hate it too.

As an outpatient it is a good drug but in the hospital, I don't use it. I can't tell you how many times I have been burned with a patient on lovenox. You can't easily reverse it and the effects last much longer than heparin. Just for convenience, heparin is the way to go in the hospital.

The hospitals around us seem to love it. It's great when they send us a MICU disaster bleeding out of every orifiace who is getting lovenox...

 

[EPADHA]

New onset (<48h) should be anticoagulated with heparin to prevent atrial thrombus so that you can give them a change at cardioversion. You start the heparin immediately b/c it will limit the risk the fibrillating atrium and thus the crappy blood flow in the atrium will clot. That way, when they go for TEE cardioversion there isn't a clot and they can be shocked out of fib.

If you cannot succesfully cardiovert and your EP won't do an ablation, there really isnt a need to bridge to coumadin.

If they get cardioverted and go back into sinus, they need to be bridged b/c the risk of atrial clot after cardioversion is higher than being in a-fib for ~4 weeks after the procedure.

Now with dabigitran, no need to bridge.



Most people do.





I HATE lovenox in the hospital and I encourage everyone on this board to hate it too.

As an outpatient it is a good drug but in the hospital, I don't use it. I can't tell you how many times I have been burned with a patient on lovenox. You can't easily reverse it and the effects last much longer than heparin. Just for convenience, heparin is the way to go in the hospital.
.

spot on.. perfect! I think you have made a great teaching point that most internists dont focus on.

 

[turkeyjerky]

So do you keep someone in house on a heparin drip for 5 days til they're therapeutic on warfarin, or are you guys discharging them after a day or two on lovenox to bridge them?

Sorry for the thread hijack, I'm just curious.

 

[Instatewaiter]

Kick 'em out. I'm not running a hotel here.

 

[IMDoc607]

Kick 'em out. I'm not running a hotel here.

 

[IMDoc607]

So do you keep someone in house on a heparin drip for 5 days til they're therapeutic on warfarin, or are you guys discharging them after a day or two on lovenox to bridge them?

Sorry for the thread hijack, I'm just curious.

If its ~1.8 we'll discharge them and follow up with their primary in about 5 days

 

[Top Gun]

If its ~1.8 we'll discharge them and follow up with their primary in about 5 days

Completely agree

 

[gutonc]

So do you keep someone in house on a heparin drip for 5 days til they're therapeutic on warfarin, or are you guys discharging them after a day or two on lovenox to bridge them?

Sorry for the thread hijack, I'm just curious.

Lovenox for a week or (better yet) rivaroxaban or dabigatran for a week...(or forever if they have insurance) while getting therapeutic on coumadin. Coumadin clinic visits weekly for 2-4 weeks until stable.

A week of therapeutic lovenox is 3-10x more expensive than either of the oral Xa inhibitors. And since the data for their FDA approval was all done in A Fib, there's no excuse to not use them in patients with average bleeding risk (they're not really reversible).

 

[turkeyjerky]

Kick 'em out. I'm not running a hotel here.

So if you don't have any problem w/ lovenox at home, why the vitriol against in in-house? I doubt the risk of serious bleeding is really any higher in the hospital--is it just cause it's your problem if they do bleed? Not trying to start an argument, but it seems to me like the extra nursing care and PITA factor of being on a drip vs the ease of lmw tip the scale in favor of the latter. Is there any actual data to suggest heparin is safer?

Lovenox for a week or (better yet) rivaroxaban or dabigatran for a week...(or forever if they have insurance) while getting therapeutic on coumadin. Coumadin clinic visits weekly for 2-4 weeks until stable.

A week of therapeutic lovenox is 3-10x more expensive than either of the oral Xa inhibitors. And since the data for their FDA approval was all done in A Fib, there's no excuse to not use them in patients with average bleeding risk (they're not really reversible).

Interesting--good to know.

 

[gutonc]

So if you don't have any problem w/ lovenox at home, why the vitriol against in in-house? I doubt the risk of serious bleeding is really any higher in the hospital--is it just cause it's your problem if they do bleed? Not trying to start an argument, but it seems to me like the extra nursing care and PITA factor of being on a drip vs the ease of lmw tip the scale in favor of the latter. Is there any actual data to suggest heparin is safer?

I was kind of wondering the same thing. Lovenox is reversible enough that it's not really a significant clinical issue (in my experience at least) for anybody who's not already at a high risk of bleeding.

I can understand not using LMWH in-house being a cost issue since the bean counters will only consider the cost of the drug (UFH borders on free), not the cost of administration/monitoring (nursing and phlebotomy time and hourly PTTs are very not free). But, for clinically stable, average bleeding risk folks, there's no real need for a 5 day hospital stay (just) for a heparin gtt.

 

[turkeyjerky]

Getting back to the original topic, came across this article regarding troponins in SVT:

http://www.ncbi.nlm.nih.gov/pubmed/21329868

which showed a pretty low (1/24) rate of significant CAD in the setting of SVT and +troponin. In an accompanying editorial, they recommend only selective use of enzyme measurement in SVT.

 

[sacrament]

Getting back to the original topic, came across this article regarding troponins in SVT:

http://www.ncbi.nlm.nih.gov/pubmed/21329868

which showed a pretty low (1/24) rate of significant CAD in the setting of SVT and +troponin. In an accompanying editorial, they recommend only selective use of enzyme measurement in SVT.

This has never made an ounce of sense to any clinician who has ever consulted me for a troponin elevation (which was invariably checked "just in case").

 

[gutonc]

Getting back to the original topic, came across this article regarding troponins in SVT:

http://www.ncbi.nlm.nih.gov/pubmed/21329868

which showed a pretty low (1/24) rate of significant CAD in the setting of SVT and +troponin. In an accompanying editorial, they recommend only selective use of enzyme measurement in SVT.

Actually, it's almost completely unrelated to the original topic. The question was about how to to deal with a fib/RVR, not a positive Tn in the setting of SVT (or any tachycardia frankly). The reason for admission in these cases is not necessarily to send them to the cath lab to see what their corns look like (unless they've got good insurance, in which case, by all means, let's shoot some dye and see what's up), but to figure out why they're in a fib and deal with it if an underlying cause can be determined, get them rate controlled and anti-coagulated (if appropriate) and then ship them out.

That's not to say that we don't trend the trops, or pay close attention to EKGs after the rate is controlled, or closely monitor them. But the findings in that study are pretty obvious to any IM intern come February.

Digging on the EM guys for ordering the trop is just bad sport. A lot of these people present with CP and palpitations...most cardiologists would order the trop too in this case.

 

[P Diddy]

Digging on the EM guys for ordering the trop is just bad sport. A lot of these people present with CP and palpitations...most cardiologists would order the trop too in this case.

No. The minority of patients with AF and RVR present with chest pain, and even if there is 'chest pain' (which is usually anxiety), sending reflex troponins/BNP etc is never good medicine. A cardiologist would manage the AF and forget the ED ever sent troponins. Stick to gutonc.

p diddy

 

[gutonc]

No. The minority of patients with AF and RVR present with chest pain, and even if there is 'chest pain' (which is usually anxiety), sending reflex troponins/BNP etc is never good medicine. A cardiologist would manage the AF and forget the ED ever sent troponins. Stick to gutonc.

p diddy

I didn't say that it was good medicine, just that mocking them for shotgunning labs (including a trop) on somebody who walks in the door with CP, tachy and a funky EKG that some tech thrust in their face while they were busy intubating a trauma patient is weaksauce.

Once they hit the floor, I ignore the trop as well, as long as I have a good explanation for it.

Stick to being a douche P Diddy.

 

[turkeyjerky]

Actually, it's almost completely unrelated to the original topic. The question was about how to to deal with a fib/RVR, not a positive Tn in the setting of SVT (or any tachycardia frankly). The reason for admission in these cases is not necessarily to send them to the cath lab to see what their corns look like (unless they've got good insurance, in which case, by all means, let's shoot some dye and see what's up), but to figure out why they're in a fib and deal with it if an underlying cause can be determined, get them rate controlled and anti-coagulated (if appropriate) and then ship them out.

That's not to say that we don't trend the trops, or pay close attention to EKGs after the rate is controlled, or closely monitor them. But the findings in that study are pretty obvious to any IM intern come February.

Digging on the EM guys for ordering the trop is just bad sport. A lot of these people present with CP and palpitations...most cardiologists would order the trop too in this case.

Huh?

Title of this thread contains "r/o in the ED". I can't be totally sure, but I doubt the OP was referring to ruling out critical MS or thyroid storm. Also, there are numerous references in the thread to checking troponins and ruling out an ischemic etiology. Obviously, I don't know what the practice at your institution is, but here these patients are routinely "ruled out" and get a cards consult (by medicine) if greater than the reference level (this leads to a ton of cards consults for type II MI).

Now, I'm just a dumb med student (and soon to be a dumb EM resident), but I don't really see how a trop bump in the setting of SVT is really all that different than one in the setting of Afib w/ RVR. Setting aside the whole afib 2/2 ischemia thing (I really doubt that a fib as the sole or primary manifestation of ACS is common enough to inform our practice), I think the two have a lot in common and the applicability of requiring serial enzyme measurements in this case can and should be informed by the above study results. It appears that some people get trop leaks simply from rapid heart rates, not just as a 'poor man's stress test'. Obviously if i'm wrong I'd appreciate some education on this topic.

So I don't really get all the vitriol in your post. It seems like an odd response to mine. I think we agree on this topic (although me based on published (imperfect) evidence, you based on the experience of 'any IM intern'), but there are people who argue the opposite (including at least one osler marine above). I also don't get the insinuation that I'm digging on EPs--I ran across that article on an EM blog, and, in my experience, I've found shotgunning labs and over-testing to be a bigger problem w/ IM than EM (I mean, seriously, you guys start your morning report w/ the chem 10 results).

 

[Arcan57]

ER checklist:

U/A: check
CT chest with contrast to R/O PE: check
BNP: Check
Cardiac markers: Check
Examine Patient:--------
Call MAR to admit patient: Check!

Sorry, couldn't help it. I just came off a 24 hour call.

Sorry to back-track but I thought this was funny because one of the 4 cardiologists that take call at my hospital orders a CTA on every hypertensive chest pain and a d-dimer on anyone he doesn't order a CT on. These orders are entered into the computer from home.

FWIW, I do routinely get cardiac markers on new onset A. Fib w/ RVR because I'll get yelled at (or even worse have the in-patient doc refuse admission) for not having them. I have cardioverted (usually electrically, after sedation) recent new-onset a.fib if my cardiologist can provide timely oupatient follow-up and the baseline labs look good.

 

[wrx04silver]

This is a very good point.

 

[wrx04silver]

Without prior history of CVA/TIA or mitral stenosis, there is almost no reason to ever bridge someone with new onset arial fibrillation. If it has been >48 hours since onset, and one is considering TEE cardioversion, then starting heparin is a reasonable option.