A-fib protocol

The first choice where I work for Rapid A-fib is a diltiazem gtt. We'll sometimes try a 5mg IV metoprolol first, but if that hasn't been effective after 10-15 minutes (2-3 doses) we move on to the dilt gtt. I don't know of any of our Docs that would tolerate 170's all night without trying something else. At a rate like you mentioned of 190-200 we just go by the ACLS algorithm, start the drugs, and then inform the Doc, we don't necessarily wait for orders since all ACLS algorithms are standing protocols at my facility. The Docs might simultaneously Dig load the patient and/or start an Amio gtt, but the Dig will take a while to do anything and the Amio is an anti-arrhythmic and not indicated for rate control, and even then we're hesitant to Dig load in a patient who is in an intermittent A-fib, particularly if their SR rate is not particularly fast.

You might point out to them that there is an ACLS algorithm for this which calls for beta blockers or calcium channel blockers, not Dig or amiodarone alone.

Very informative. Thank you. I work on Med/Surg and have had a few go into RAFib. I call the doc and try to get them on the cardiac floor since we don't do cardiac drips on my floor. They have had me push a couple of caridac meds, sorry I don't remember what they were, but they were ineffective hence the move to the next floor.

How quickly do you see a change with the metropolol? I am assuming that it is iv and not po, but just checking. We have at least half of our pts on tele on my Med/Surg floor, so we do get quite a bit of cardiac on my unit, just no cardiac drips.

Just curious, because I am still a newish nurse: what happens when a pt stays in RAFib? I am assuming clots, since there is not a full emptying of the chambers, but what else. Can the heart just give up since it has been running a marathon since the start of the rapid Afib? What are you looking for as a nurse other than what is on the tele screeen? (cool, clammy, slow cap refil, stroke symptoms, pulmonary emboli, and MI?)

Good topic, thanks.

Tonya

Very informative. Thank you. I work on Med/Surg and have had a few go into RAFib. I call the doc and try to get them on the cardiac floor since we don't do cardiac drips on my floor. They have had me push a couple of caridac meds, sorry I don't remember what they were, but they were ineffective hence the move to the next floor.

How quickly do you see a change with the metropolol? I am assuming that it is iv and not po, but just checking. We have at least half of our pts on tele on my Med/Surg floor, so we do get quite a bit of cardiac on my unit, just no cardiac drips.

Just curious, because I am still a newish nurse: what happens when a pt stays in RAFib? I am assuming clots, since there is not a full emptying of the chambers, but what else. Can the heart just give up since it has been running a marathon since the start of the rapid Afib? What are you looking for as a nurse other than what is on the tele screeen? (cool, clammy, slow cap refil, stroke symptoms, pulmonary emboli, and MI?)

Good topic, thanks.

Tonya

IV metoprolol is fast acting, you should see some effect within 5-10 minutes after it's infused if it's going to do anything. Personally I much prefer a diltizem gtt, IV metoprolol seems to be effective less often, and you don't get the consistency of HR control you get with the dilt gtt.

The immediate concern with rapid a-fib is poor perfusion, due to a couple of factors. First is the rate; a rate of 170 doesn't allow for adequate filling time, resulting in a lower stroke volume and therefore a lower cardiac output that isn't adequately compensated for by the rate. The second issue, which is true for all a-fib regardless of the rate, is atrial kick. The coordinated timing of the filling and ejection between the atria and ventricles provides atrial kick, which accounts for about 1/4-1/3 of the heart's pumping effectiveness, in atrial fib that coordination is lost, contributing to poorer perfusion.

Mainly you'd be looking for signs of poor perfusion and heart failure (BP, lung sounds, sats, distal pulses, LOC, etc). A patient who has significant symptoms should be considered for elective cardioversion. Clots forming are also a concern due to the erradic flow through the heart, but that typically takes a few days to become a significant concern, at which point the patient would have an echo prior to any attempts to convert to rule out a clot. It's not unusual for cardiac enzymes to be elevated as a result of rapid A-fib due to demand ischemia. Not only is the heart working much harder with a rapid rate, the decreased length of diastole can also starve the heart of oxygen, since the coronary arteries perfuse during diastole. On an EKG, demand ischemia would show as a non-focal ischemia - a bit worse in the LV leads, but otherwise not particularly focused in any particular lead.

Don't do anything out of protocol without an MD's order. If they patient is decompensating call the emergency team, code team or whatever your hospital has. Otherwise bother the on-call until the patient gets better.

This is actually a bit of a complex issue to deal with. Another poster discussed the physiology so I won't go into it here. About the protocol issues, many hospitals use many different ones.

The facility I'm currently at (a university teaching hospital to give you an idea of where I practice), our cardiac surgeons use Amiodarone as a first line drug. 150 mg bolus, may repeat x 1 then start a drip if need be. The important issue is to consider WHY the patient may be going into A fib. (Valve replacement? Prior history? Irritated pericardium? Electrolyte imbalance? Are they POD #2?- seems it always happens around POD#2, like clockwork.

So, if I"m calling a doc (which I don't need to do due to our protocol), I'm drawing stat lytes to make sure they are optimized, giving an Amio load. If they are still tachy, yes, we use betablockers to try to rate control them (and sometimes it will cardiovert them as well). The issue becomes if they are tolerating the Afib. I've had some "fibbers", few that they were, that were refractory to both Amio and Beta blockers who became hemodynamically unstable who then needed transfer to the ICU for immediate cardioversion and pressor support. It can definitely be an issue if your pressure isn't giving you much room to use meds.

Couple of things to keep in mind: half life of Amiodarone is pretty long, so once you start to load them, they're going to hang on to it for a while. Also need to take into account any liver issues this patient may have, it will take even longer to clear the liver for a basic load. Electrolytes: we like to keep our K levels at least at 4.5 and Mag level 2.5-3.0. We've found in our patients, this can really head off a lot of issues. Frequently we will give prophy 1 gram Mag IV without even waiting for a lab return.

Something you mentioned is important: the pause the patients had after receiving treatment is caused a compensatory pause. Basically, the patients heart is resetting itself..similar to an electrical cardioversion if you will. Unless your patient is unstable, the pause itself isn't a reason to pace someone...it's the expected result of treatment. Granted, when you're the staff nurse that pause can seem to take a looonnnnggg time to kick the heart back in but it's a very rare patient that I've had to pace after that. If I have had to pace, they've usually been having block issues prior to their fib and their nodes appear pretty irritated. We will usually have those patients at a VVI of around 50, just in case.

So, calling the doc: I personally wouldn't ask for Dig, I'd ask for stat lytes, try the beta blocker then maybe the Amiodarone. It's also good to know the reason for surgery: valve, CABG, etc. By the way, all our straight CABG patients get an Amio load prophy, to try to prevent Afib post-op.

Hope this helps

Don't do anything out of protocol without an MD's order. If they patient is decompensating call the emergency team, code team or whatever your hospital has. Otherwise bother the on-call until the patient gets better.

I don't think the OP was stating they were going to do something out of a doctor's order but they were looking for recommendations of what to ask for when they called the "baby docs".

^ exactly, plus I wanted to know if there are other hospitals with more clear protocols with more positive effect. The intern who was on was a decent one (not our worst, not our best). She did consult with the ICU PA who said that "they do dig load sometimes," and since that is what our protocol said, that is what she did. I personally don't think that is best practice since it is going to take too long for it to work, and the patient's heart rate was unstable. I am a little disappointed in my hospital for having a seemingly outdated protocol still in place.

Otherwise he was hemodynamically stable. The SBP was initially 113 and went to 103 after the digoxin. He maintained that pressure all night, and tended to run a little low. He was completely asymptomatic, and I drew labs when this happened. From the resident's perspective, his pressure was 113, he had had IV metoprolol before and it had dropped his pressure about 20 points. From my perspective, if we control his rate he will have better cardiac output and therefore a better blood pressure. But it is a judgement call and not one that I am qualified to make. I have been a nurse for a year and most of the a-fibbers I have had have been responsive to metoprolol, or were going to get a PPM placed anyways for tachy-brady syndrome.

BTW this patient had a CABGx2 but was POD#6. When I left this morning it sounded like they were going to do an EP consult. I was really not comfortable with the way last night's shift went. The charge nurse and I were the "senior" nurses on staff...we had the same start date in July of last year. One nurse was fresh off orientation, the other has been here since February-ish. In retrospect I don't think that a call to the CRN would have been out of line at all. In my head I was thinking "he is still stable," and I don't think that it fully hit me how quickly he could become unstable and how screwed we would have been if he did. I'm going to do some reading on cardizem drips and mention it to our NP's. I do know that we don't take titratable cardiac drips simply because we don't have the staffing to safely monitor them. I have seen them on our floor a couple times, but usually only on medicine patients who get transferred to our floor because they need tele, and always with a set dose and strict Call HO parameters. I don't think I have ever seen one of my cardiac surgery patients on cardizem.

Thank you everyone for your replies! I appreciate it :)

Edit: Someone mentioned prophylactic amiodarone. We do this as well, but I think that I mentioned that for this specific patient, he had had this issue a couple days ago and was put on an amiodarone drip. He then had a long pause (the progress note I found didn't say how long..isn't that lovely). That is when they stopped all amiodarone and beta blockers...again I didn't hear this in report and am not really sure of the whole history behind it. I don't know if the resident on call knew about this because she didn't mention it to me. I found out when I was reading his notes trying to find a history of a-fib at baseline.