Amiodarone for Atrial Arrhythmia

cannonball88

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Can anyone out there give some insight as to what kind of luck you have had in using Amiodarone to treat atrial arrhythmia such as A-Fib with RVR?

How does it compare to Cardizem or Verapamil?

Yes, I realize that we're talking apples vs. oranges when comparing potassium channel blockers and calcium channel blockers, but the concept of amiodarone being used in that fashion is somewhat new to me.
 
Why would you want to use it for AF + RVR? Are you talking about an unstable patient? If the patient is unstable, cardiovert. If they are fully stable, but you are worried about a very fast rate, then try a calcium-channel blocker. Amiodarone is going to convert the rhythm, so it is not something to use for a stable patient since you may be worried about causing an embolic stroke.

I'm probably telling you something you already know, but Cardizem and Verapamil block impulses going through the AV node, so they are used for rate control. Verapamil is not much in favor because it causes more vasodilation than Cardizem, and the only reason you have it on the ambulance is because Cardizem requires refrigeration. Amiodarone is not used primarily for rate control.

Amiodarone will convert the rhythm (if it works), so you shouldn't be doing that prehospital. Consider also that amiodarone is likely to drop the BP, which is a concern especially if the patient is borderline stable.

There is one scenario where amiodarone is used for unstable patients, but it really doesn't apply to the ambulance. In the ER, if an unstable patient is shocked but does not convert, amiodarone could be used, but then you also need a vasopressor due to the likely hypotension that will result from infusing amiodarone. From my understanding, amiodarone is not every docs first choice in this scenario anyhow. Some people seem to like procainamide instead, but I don't know the evidence base for this.
 
Our cardizem is powder that we mix so no refrigeration is required .

I have used amio for Afib with RVR and it works but I feel that it's kinda of over doing it especially with the effects that it has on the kidneys. Cardizem is nice because you can titrate it.
True Afib with RVR is only a matter of time before it becomes a problem so i think its kind of caregiver discretion when to use.
I also feel that when you cardiovert due to them being unstable its nice to hang a drip to prevent reentry
 
I would estimate 25-35% of the patients I see will experience at least one episode of a-fib with RVR while under my care. It can be an absolute nightmare to treat after cardiac or thoracic surgery.

There is a lot of intuition involved when choosing treatment. And while some of the professional societies have put out position papers on anti arrhythmic choice, the evidence grades are pretty poor. Thus, clinicians rely a lot on their own past experiences to determine their practice styles.

In general, folks with normal ejection fraction and normotensive with an initial episode get beta blockers first line. Those refractory to beta blockade may get Dilt or amio depending on my gut feeling. For lack of a better term, a patient with "soft" a-fib, meaning one which is likely temporary, usually due to myocardial irritation or inflammation, I like Dilt.

For those with "tough" a fib, folks with concomitant critical illness, history of recurrent a-fib, low ejection fraction, I tend to lean toward amio.

Again, these are generalizations.

I have seen hypotension with amio, though honestly I have experienced far more hypotension with dilt (especially when bolusing).

I try my best to avoid amio in pneumonectomy patients or those with severe COPD. I also tend to avoid it in patients with thyroid disease, though I have no evidence to account for either of these practices.

No matter which treatments I chose, I have found it best to "optimize" the physiologic conditions prior to any attempt at conversion or rate control. Typically this involves driving up the magnesium and calcium levels, high oxygen concentration prior to attempted conversion, increasing the coronary perfusion pressure and correcting any acid base abnormalities.

Overall, I think amio has great utility, even though it is not usually my first-line choice in hemodynamically stable patients.
 
Personally, I can't say I have ever used Amio for AFib. If they are tachy, I will either use cardizem or a beta-blocker, if they are already on one. We also use a lot of flecainide, but that is not something that you would give in the field.
 
For rate control of any etiology, I think it's hard to beat beta blockers. Esmolol especially - if you have it - is very predictable and very short acting. Diltiazem is a good drug too, but I think a little less forgiving than esmolol.

Personally I would not attempt to convert the rhythm with amio (or any other antidysrythmic) without the involvement of a cardiologist or intensivist.
 
Can anyone out there give some insight as to what kind of luck you have had in using Amiodarone to treat atrial arrhythmia such as A-Fib with RVR?

How does it compare to Cardizem or Verapamil?

Yes, I realize that we're talking apples vs. oranges when comparing potassium channel blockers and calcium channel blockers, but the concept of amiodarone being used in that fashion is somewhat new to me.
Question from the ignorant: prehospitally, what is your goal? Cardizem is used to reduce the rate of symptomatic A-fib; as such, if they are in A-Fib with a rate of 80, you aren't using it right?

So if you throw in the RVR, the rate jumps above 150, they are often are symptomatic, give the cardizem, as it will reduce the rate (and have the symptoms subside), and let a cardiologist work on fixing the underlying cause of the a fib. sound right?

why use amiodarone?
 
Not everyone can carry cardizem on there ambulance, so amioderone is a fall back option if you use it appropriately and understand the risks
 
Maybe another dumb question: Why is everyone moving away from verapamil. Given the choice between verapamil and amio for rvr, which is preferable.
 
For those using Amio, are you going for rate control or rhythm control?
 
How do you ensure that it has not been going on more than 48 hours? Why is there a huge push to convert?
 
For those using Amio, are you going for rate control or rhythm control?
How do you ensure that it has not been going on more than 48 hours? Why is there a huge push to convert?

I think that is where it gets a little tough in the prehospital world. I have the luxury of lots of info regarding PMHx, early notification when patients convert to a-fib, and a TEE probe when I really need a definitive answer.

Clearly, these things are not usually available out in the street.

I think in the field the best option would be to aim for rate control and allow more definitive therapy once at the hospital. If they happen to convert with just a little beta blocker, chances are they were probably not in it that long.
 
Maybe another dumb question: Why is everyone moving away from verapamil. Given the choice between verapamil and amio for rvr, which is preferable.
Compared to diltiazem, verapamil is known to cause more hypotension. That is why it has fallen out of favor.
It is not a quesiton of diltiazem vs amiodarone because the two medications have different applications.
 
Thank you all for your replies. Just for a little insight that I probably should have thought to include:

We don't carry ANY CCB, including Cardizem or Verapamil.
We don't carry ANY beta blockers.

I'm not specifically trying to convert the rhythm, but it would be nice to get the rate under control BEFORE they become unstable and require cardioversion, hence why I asked about the amiodarone.
 
But really, how often do people in Afib become unstable? People live in Afib for years with no problems. Personally, if you don't have something for rate control, I'd prefer you did nothing and just transport instead of doing something and causing a stroke.
 
But really, how often do people in Afib become unstable? People live in Afib for years with no problems. Personally, if you don't have something for rate control, I'd prefer you did nothing and just transport instead of doing something and causing a stroke.

By slowing A-fib, thus giving the blood more time to coagulate in the left atrium?
Or am I missing something here?
 
My understanding is that if you have been in A-fib for greater than 48 hours, the blood has been effectively pooling in "eddys" in the atria and runs a greater risk of developing emboli but is relatively stable as long as the rhythm is consistent. If you convert A-fib at this point, you run a greater risk of setting these emboli free.

Bottom line: convert in less than 48 hours of onset or leave it for the hospital.
 
By slowing A-fib, thus giving the blood more time to coagulate in the left atrium?
Or am I missing something here?
The risk of converting afib is that a clot could form in the atrium while the patient is in afib and if you convert it the heart will then throw the clot and cause a stroke.
 
Just a quick point for learning. And many of you may already know this-

Those clots do not exclusively travel to the brain. That is only the case of they happen to fly up into a carotid.

They can also bypass the cerebral circulation and travel onward to cause more insidious problems. These are the things you may not see in the prehospital setting because they take longer to manifest.

An embolus to the renal vasculature can cause acute renal failure, but again you may not see that for days. The same holds true for emboli which lodge in the vasculature of the mesentery. It can take anywhere from hours to days before the gut ischemia shows up on lab data or physical exam. Dead bowel can be just as devastating, and frequently moreso, than a stroke. Mortality in these folks is very high.
 
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