Atrial Fibrillation with RVR and Diltiazem

[Almostmedic]

What if the patient had been in atrial fibrillation for an unknown duration and wasn't currently anticoagulated?

I would be wary to cardiovert without knowing for a fact it was a new onset of Afib with fear of moving that coagulated blood around.

[Bieber]

I would be wary to cardiovert without knowing for a fact it was a new onset of Afib with fear of moving that coagulated blood around.

So would I. So what would be the tipping point for you? True hemodynamic instability? Or is evidence of cardiac ischemia enough to cardiovert?

Anybody got any numbers to the incidence of thromboembolic events with cardioversion in non-anticoagulated patients who receive cardioversion?

[ERDoc]

So would you guys not push calcium channel blockers or beta blockers either? They both have the potential to put people back into sinus rhythm.

[Bieber]

Doc, what's the best way to achieve rate control WITHOUT conversion to a sinus rhythm? I've been trying to find that out to no avail.

[ERDoc]

Anything that changes the rate has the potential to change the rhythm, it is just the risk you run.

[Almostmedic]

So would I. So what would be the tipping point for you? True hemodynamic instability? Or is evidence of cardiac ischemia enough to cardiovert?

Good question, I guess I'm stuck after my straight out of medic school answer I gave .

I know this is a bad answer but the hospitals are so close to where I am I probably wouldn't cardiovert the cardiac ischemia I would work on the bp with fluids and obviously O2 therapy.

I guess the tipping point would be the pt being hemodynamicaly unstable.

I just don't know if the risks of a clot out way the benefits of stopping the ischemia.

[systemet]

I think there's a few things that have to factor into the decision here:

(1) Duration: Obviously this is difficult to pinpoint, as the patient may have had an asymptomatic period prior to the rate increasing and becoming symptomatic, but if you have a clear history of paroxysmal onset of symptoms, it might be easier. The longer the symptoms have been ongoing, and the less certain you are that you can pinpoint the time of onset, the greater the risk of rhythm conversion.

(2) Primary versus secondary a.fib: Is the rate really our problem, or do we have someone who has a separate problem, in which a fast rate might be expected or compensatory e.g. fever, pain, dehydration, sepsis, acute MI, etc.

(3) Transport time, and the center you're transporting to: are you 10 minutes from a center with board certified EM docs and cardiology? Or is it a rural hospital an hour away with the FM guy who's seeing patients at the local clinic, who might not be at the ER until some time after you arrive, even if you call first, and might not be particularly comfortable with this patient?

(4) Risk of underlying WPW? Because we don't want AV nodal blocking agents here, at least not the ones we commonly carry.

Honestly, I think most of the time, this is a situation where it's better to tread very lightly, especially if they're somewhat stable. Most of the time it's not the a.fib that's the problem.

So would you guys not push calcium channel blockers or beta blockers either? They both have the potential to put people back into sinus rhythm.

Regarding this, I have this potentially flawed idea that when you cardiovert you get a very fast and perhaps supraphysiologic contraction of the myocardium that could cause embolisation, that you'd lack with a chemical conversion. I was under the impression that the risk with electrical cardioversion was greater? Do you know if anyone's looked at this? Am I just hilariously poorly informed here?

[Bieber]

Thanks for the great and well thought out response, Systemet! I'll throw in my two cents on your final point, and hopefully one of our docs can correct me if I am mistaken.

Regarding this, I have this potentially flawed idea that when you cardiovert you get a very fast and perhaps supraphysiologic contraction of the myocardium that could cause embolisation, that you'd lack with a chemical conversion. I was under the impression that the risk with electrical cardioversion was greater? Do you know if anyone's looked at this? Am I just hilariously poorly informed here?

According to the AHA, the risk is about the same for electrical cardioversion as chemical cardioversion in non-anticoagulated patients IF there is a conversion from atrial fibrillation to a sinus rhythm.

http://circ.ahajourn...04/17/2118.full']

The risk of thromboembolism or stroke does not differ between pharmacological and electrical cardioversion. Thus, recommendations for anticoagulation are the same for both methods.

The primary issue (to my understanding) is when you get the atria effectively pumping again, in which case if there is a thrombus that has formed in the left atrial appendage, it may become dislodged as opposed to simple rate control where the patient remains in atrial fibrillation without rapid ventricular rate. However all forms of rate control carry the risk of converting atrial fibrillation into a sinus rhythm, as ERDoc pointed out.

Also from the AHA, another little useful tidbit:

http://circ.ahajourn...04/17/2118.full']

Thromboembolic events have been reported in 1% to 7% of patients who did not receive anticoagulation before cardioversion (^101,102 ).

Edited June 12, 2012 by Bieber

[systemet]

Thanks Bieber!

[Bieber]

So, I dug through some of the old memos by our medical director about the issue of diltiazem. Her rationale for it was that the physicians in the area felt that "there were enough patients that had been turned from stable to unstable by treatment with diltiazem" that it didn't meet the risk-benefit criteria. I haven't ever heard of diltiazem causing stable atrial fibrillation to become unstable, and as quoted above the risk of thromboembolism is the same as electrical cardioversion (which is still in our protocols).

Anyone have any idea what this might be about? Anybody ever heard of diltiazem causing stable patients to go unstable?