Question about A fib

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nope80

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Hopefully this isn't an obvious answer question but i've been randomly reading articles on uptodate in areas that I feel like I need review...So I was wondering about when we actually make the decision to treat paroxysmal afib.

Since the definition of paroxysmal afib is afib spontaneously terminating in less than seven days, how long does one allow afib to go untreated before initiating therapy? I know if someone is unstable and depending on how long they have had it as well as risk factors, you consider cardioversion. But lets say they are not unstable and you get called about new onset afib. Do we immediately initiate rate control?
 
Hopefully this isn't an obvious answer question but i've been randomly reading articles on uptodate in areas that I feel like I need review...So I was wondering about when we actually make the decision to treat paroxysmal afib.

Since the definition of paroxysmal afib is afib spontaneously terminating in less than seven days, how long does one allow afib to go untreated before initiating therapy? I know if someone is unstable and depending on how long they have had it as well as risk factors, you consider cardioversion. But lets say they are not unstable and you get called about new onset afib. Do we immediately initiate rate control?

Keep in mind that because of the electrophysiologic and structural remodeling caused by AF, many patients with paroxysmal AF will progress to persistent and permanent AF so paroxysmal or not, I'd treat it as soon as I have a diagnosis.

You can achieve rate control with BBs or CCBs. Reasonable rate control is defined as a ventricular rate of 60-80/min with an increase with excersise to 90-115/min.

If your patient with Paroxysmal A-Fib is young, you might consider rythm control. In older patients it is not that important (most will not remain in sinus rythm and are more likely to experience serious side effects).

If that fails, catheter ablation is recommended as an alternative to pharmacologic therapy to prevent recurrent paroxysmal AF in significantly symptomatic patients with little or no structural heart disease or severe pulmonary disease.

Well, that's what I know but I'm not a cardiologist 🙂.
 
Hopefully this isn't an obvious answer question but i've been randomly reading articles on uptodate in areas that I feel like I need review...So I was wondering about when we actually make the decision to treat paroxysmal afib.

Since the definition of paroxysmal afib is afib spontaneously terminating in less than seven days, how long does one allow afib to go untreated before initiating therapy? I know if someone is unstable and depending on how long they have had it as well as risk factors, you consider cardioversion. But lets say they are not unstable and you get called about new onset afib. Do we immediately initiate rate control?

Afib is going to get out of hand rate wise, so if you recognize A-fib and you don't have a reason for it (such as lone a-fib in PE or COPD), then you need to treat it with beta-blockers, and have a discussion about anticoagulation. I need to track down the guidelines, but I'm almost certain you do antuicoagulation based on the CHADS-2.
 
Lets see if there is anyone smart that knows the answer. Cardizem is easy you titrate between 5-15 mg/hr with a drip after a 20 mg bolus.

What Beta blocker do you use and how much IV for acute afib for someone that cant take a calcium channel blocker.
 
Lets see if there is anyone smart that knows the answer. Cardizem is easy you titrate between 5-15 mg/hr with a drip after a 20 mg bolus.

What Beta blocker do you use and how much IV for acute afib for someone that cant take a calcium channel blocker.

You don't always need a drip after a bolus (but most of the time you do).

Use labetalol or esmolol. Though you can't use esmolol unless you've got a central line. I prefer esmolol if I can use it.

What do you use if your patient is hypotensive but not unstable?
 
Though you can't use esmolol unless you've got a central line.

What's this based on? I routinely use esmolol intraoperatively, including for a fib. It goes in the peripheral without any issues. It's not caustic and the osmolarity of the infusion is 312 (almost same as saline). Also, the prescribing information doesn't even mention central administration.
 
I submitted a precordial thump vs punch in the face for acute arrhythmia . . . the IRB had issues

Stupid IRB. They ruin everything.

Perhaps "precordial thump compared with kick in the jimmies for treatment of stable, acute cardiac arrhythmias" will be better received.
 
What's this based on? I routinely use esmolol intraoperatively, including for a fib. It goes in the peripheral without any issues. It's not caustic and the osmolarity of the infusion is 312 (almost same as saline). Also, the prescribing information doesn't even mention central administration.

"Can't" was a little hyperbolic here, but central line is the prefered method of giving esmolol because it's a pretty nasty extravasation, probably because of a low pH. I can't really speak about how it may need to be used within the context of the OR, but in a situation where you're starting a drip for rate on control of Afib on the floor, there's simply no need to use esmolol if you only have peripheral access, given the rare but serious complication related to extravasation - bolus doses of metoprolol or a labetalol drip work well enough for just about any Afib.
 
"Can't" was a little hyperbolic here, but central line is the prefered method of giving esmolol because it's a pretty nasty extravasation, probably because of a low pH. I can't really speak about how it may need to be used within the context of the OR, but in a situation where you're starting a drip for rate on control of Afib on the floor, there's simply no need to use esmolol if you only have peripheral access, given the rare but serious complication related to extravasation - bolus doses of metoprolol or a labetalol drip work well enough for just about any Afib.

Fair enough. Central is likely preferred for any potent cardiac medication (though the MICU where I did residency loved peripheral norepi). I never considered esmolol to be a high risk extravasation drug. Esmolol's pH is 5, labetalol's pH is 3.

A lot of the a fib that happens intraoperatively terminates with a bolus of esmolol, amiodarone or cardioversion and is a different animal than the classic IM-type patient.
 
coumadin for all a fibbers!!!
Unless they are bleeding.
Just kidding...but at least for almost everyone.
I agree that postop a fib is a different animal...there isn't really a consensus regarding what to do with these people...we can't just commit everyone to a lifetime of coumadin because of one episode of postop or intraop atrial fibrillation.
 
coumadin for all a fibbers!!!
Unless they are bleeding.
Just kidding...but at least for almost everyone.
I agree that postop a fib is a different animal...there isn't really a consensus regarding what to do with these people...we can't just commit everyone to a lifetime of coumadin because of one episode of postop or intraop atrial fibrillation.

Oh. There's our resident cardio fellow. Thanks DF.
 
As an aside, the ACC pocket guideline app is free with registration with the ACC for iPhone/smartphone.
 
coumadin for all a fibbers!!!
Unless they are bleeding.
Just kidding...but at least for almost everyone.
I agree that postop a fib is a different animal...there isn't really a consensus regarding what to do with these people...we can't just commit everyone to a lifetime of coumadin because of one episode of postop or intraop atrial fibrillation.

I just want to add that heparin can be used concomitantly until the INR is 2-3 in patients with afib that has persisted for more than 48 hours.

And in patients at low risk of stroke (as determined by the CHADS2 score), aspirin is a better option.
 
I just want to add that heparin can be used concomitantly until the INR is 2-3 in patients with afib that has persisted for more than 48 hours.

And in patients at low risk of stroke (as determined by the CHADS2 score), aspirin is a better option.

you won't be bridging with heparin for most of your run of the mill new a-fib presentations. the only time that i've really considered heparin bridging is if you're thinking about intervention with cardioverting etc but otherwise your risk of CVA isn't that urgent (unless they've had previous CVA or sky high CHADS score) then you might think about heparin

and yeah... ASA for CHADS = 1 but otherwise coumadin unless your patient is resistant to the idea or is a 95 year old female who will fall if someone farts in her face.

just wanted to know what you guys thoughts were regarding CCBs in patients with CHF who have AFib. i've been told that is better to avoid them.
 
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just wanted to know what you guys thoughts were regarding CCBs in patients with CHF who have AFib. i've been told that is better to avoid them.

I avoid CCBs in general for chronic management of Afib - more side-effects, and like you pointed out so many of these patients will have failure anyway OR these patient with have CAD, so they'll need the BB anyway.
 
You should not use calcium blockers for a fib in CHF with significant systolic dysfunction, because calcium blockers depress myocardial contractility (i.e. can lead to worse CHF). However, the definition of "Significant systolic dysfunction" differs according to your cardiology attending. I generally avoid them if LVEF <40%, for sure, although I have seen experienced cardio attendings use them anyway even if LVEF is 30%. I usually start with beta blocker if there is any LV dysfunction at all. Some patients can't be rate controlled w/just beta blocker, though. Then I have to use either digoxin or calcium blocker. Calcium blockers for rate control are OK if no LV dysfunction, particularly if the patient has asthma or has COPD with wheezing (usually your COPD'er with really bad COPD, plus/minus component of underlying asthma/reactive airways).

The literature shows that even a lot of the patients with CHADS1 have significant stroke risk and benefit from warfarin. Most patients with a fib should probably get warfarin (unless truly idiopathic AF in maybe some 30 or 40-something guy with really CHADS 0). That's the way most arrhythmia docs manage anticoagulation in a fib. Of course, nothing exists in a vacuum and a lot of old people have GI bleeds, chronic anemia, etc. You have to balance the risk/benefit. Probably not enough people get warfarin because they are deemed "fall risk". Arrhythmia doc response to that is, "What will be the fall risk once patient has a big stroke?". CVA's with a fib tend to be without warning and can be big/hemispheric. Once you see a few it will raise you enthusiasm for trying warfarin in more patients.
 
Atrial fibrillation is a specialty unto itself and there have been several relatively recent advancements made in the management of AF. If you're interested, I have included links below to the 2011 ACCF/AHA/HRS Update on the Management of Patients With Atrial Fibrillation which updates the previous 2006 guideline which was issued along with the ESC. They address most questions regarding the management of atrial fibrillation including indications for anticoagulation and appropriate AAD therapy based on presence and severity of pre-existing heart disease. It seems catheter ablation is still recommended as second-line therapy for those who've failed one or more AADs. The most recent guidelines (and updates) also address dronedaron, which is less effective than amiodarone but has far fewer side effects and is favored in patients at risk for stroke as it was shown (in a subanalysis of the ATHENA study) to significantly reduce by 34% the risk of stroke in patients receiving it on top of anticoagulation.

I know your question seemed to address rate- or rhythm-control but since later posts touched on anticoagulation and stroke-risk reduction I have also included a couple of other links including to the manufacturer of probably the best studied left atrial appendage closure device (the Watchman). The principal investigator of that study from Mayo is the president-elect of the ACC.

The last website I included because it was the only one I could easily find which had a table showing the rate of stroke by CHADS2 score without treatment and compared to both aspirin and warfarin. The current guidelines recommend ASA 325mg for CHADS2 of 0 and basically leave it to the clinician for a CHADS2 score of 1 as studies have been inconclusive regarding a net benefit with warfarin compared to ASA 325mg. However, as "dragonfly99" mentioned, you can find several (relatively large) studies in the literature which have concluded there is a benefit with warfarin therapy in this intermediate-risk group and the number of people with AF who should be on AC but are not is probably pretty scary. Also as "dragonfly99" mentioned, strokes due to AF tend to be much more devastating and disabling and roughly 25% of all ischemic strokes are due to AF. The clear indication currently is anticoagulation for CHADS2 above 2.

With the recent approval by the FDA of dabigatran (based on the RELY study which showed dabigatran was more effective than standard warfarin therapy) and the LAA closure device (based on the PROTECT AF study) there are now more options than ever. I guess it would important to mention the caveat that dabigatran was approved only for non-valvular AF and obviously the Watchman as well. But for those patients, its hard to imagine warfarin not quickly becoming a thing of the past especially given the evidence that these new therapies seem to be more effective and eliminate the need for monitoring or, in the case of the Watchman, lifelong anticoagulation altogether.

http://www.hrsonline.org/Education/...ment-of-Patients-With-Atrial-Fibrillation.pdf

http://www.hrsonline.org/Education/SelfStudy/Webcasts/2011-AF-Update-Webinar/index.cfm

http://www.atritech.net/protect-af-study/results.html

http://www.bcguidelines.ca/pdf/stroke_appendix_a.pdf

Sorry about the long post.

GO HEAT!!!
 
Thanks. Very informative.
 
whoops, didn't realize this was about the IM setting, please ignore post.
 
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DTIs crack me up. Super sweet, right? Yeah. Well. I can't get a single patient of mine on it. Might as well be talking about magic anticoagulation gnomes.

You just need to document it right and the insurance companies will follow. All it takes is one admission every 4-5 years for a complication related to over/under coumadin anticoagulation to cover the cost differential of the direct thrombin inhibitors vs. coumadin. We have an awesome benign hematologist here who can get even the stingiest insurance companies in the country (hey there Humana and Aetna) to cover dabigatran.
 
You just need to document it right and the insurance companies will follow. All it takes is one admission every 4-5 years for a complication related to over/under coumadin anticoagulation to cover the cost differential of the direct thrombin inhibitors vs. coumadin. We have an awesome benign hematologist here who can get even the stingiest insurance companies in the country (hey there Humana and Aetna) to cover dabigatran.

I work at the ghetto hospital in town plus the VA.

I'll keep that in mind for the increasingly rare patient with insurance.

Thanks.
 
In some ways, the best part of medicine is that there is no right answer.

Reasonable rate control is defined as a ventricular rate of 60-80/min with an increase with excersise to 90-115/min

Note that tight rate control (HR<80) was no better than lenient rate control (HR<110)

Lets see if there is anyone smart that knows the answer. Cardizem is easy you titrate between 5-15 mg/hr with a drip after a 20 mg bolus.

What Beta blocker do you use and how much IV for acute afib for someone that cant take a calcium channel blocker.

It is not uncommon to jump to IV rate control for acut afib. However, if the patient is stable, the best choice is often oral medications. They are simpler, cheaper, long lasting, etc. If your patient is taking oral meds, might as well give them an oral dose of metoprolol, diltiazem, or whatever drug of choice you have.

Calcium blockers for rate control are OK if no LV dysfunction, particularly if the patient has asthma or has COPD with wheezing (usually your COPD'er with really bad COPD, plus/minus component of underlying asthma/reactive airways)

Two meta analyses have shown no increase risk of using beta blockers in patients with COPD. A recent study in the Archives shows benefit from beta blocker use -- both cardiac and a decrease in COPD exacerbations. All of these studies are observational, although so were the concerns raised about non-cardio-specific beta blockers and COPD exacerbations.
 
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