Atrial Fibrillation is a Pain in the Butt
Your patient is pale and diaphoretic. Blood pressure is 70/50. Heart rate is 178. EKG shows atrial fibrillation… What are you going to do???
Yeah, yeah the Pavlovian ACLS response–You cardiovert. Wonderful, except it didn't change a thing. Now what?
In this episode, I discuss the crashing atrial fibrillation patient.
Shock
If the patient is chronically in atrial fib, the shock rarely works. Your patient is unstable, so you decide to give it a shot. You might as well give yourself the best chance of success, so go right for 360 J on monophasic, or equivalently high on your biphasic. This will not cause more injury than lower joules (Heart 1998, 80:3 and Resuscitation 1998;36:193). PA is probably better than AA if you have pads. Make sure the synch is on.
You need to give your patient something to disguise the fact that you are electrocuting them. Yet you don't want to drop their pressure. Ketamine is ok in disassociative dosing, but then your patient is loopy and you lose your mental status exam. Consider 5-7 mg of etomidate along with a pain dose of ketamine, 10-15 mg.
Screen for WPW
If you have a. fib with a wide QRS and a rate > 250-300, be scared, very scared. This is WPW and these patients just love to ruin your day by going into v. fib. Shock early, shock often, light them up.
Get the BP Up
So you made sure it's not WPW and the cardioversion has failed, as it so often does in chronic a. fib. Now you need to raise the BP before anything else. Use push-dose phenylephrine. 50-200 mcg every minute or so until you get the blood pressure above a diastolic of 60; this will temporize the situation and make the patient's heart more likely to slow down.
Though things look better, you have not really fixed the problem, you have just temporized.
Slow them them down
Give either amiodarone 150 mg bolus and then the drip (may repeat the bolus x 1)
Or
Use diltiazem, but not as a push. Drip it in at 2.5 mg/minute until HR < 100 or you get to 50 mg. (Resuscitation 52:167, 2002) See here for more.
Still not working?
- Consider magnesium
- Consider reshocking
- Consider cardiology consult
- Consider something else is going on
- Consider signing out to one of your colleagues and running away
- Consider Ibutilide (See this amazing Steve Smith Post)
Now on to the Podcast…
Additional New Information
Update:
- This study would indicate that perhaps we are doing more harm than good when we aggressively try to control rate or rhythm in stable (non-crashing) patients (Ann Emerg Med 2015;65(5):511)
- LOw dose MAGnesium sulfate versus HIgh dose in the early management of rapid atrial fibrillation: randomised controlled double blind study. Acad Emerg Med. 2018 Jul 19. doi: 10.1111/acem.13522.
- Wait and See rather than rhythm restoration seems non-inferior1
- Esmolol compared to Amiodarone for recent-onset afib showed superiority of esmolol. They used 500 mcg/kg q 3-5 min with stepwise increase of infusion of 50-100-150-200 mcg/kg/min (4 boluses max)
- Afib in the ICU
- IBCC Chapter on Afib with Critical Illness
- New AHA Afib Guidelines [10.1161/CIR.0000000000001193]
- Symptoms now rec. <12 hrs and Cha2DS2Vasc Score 0-1 without ruling out thrombus
- Use 200J biphasic for initial shock
- For pharm cardioversion: normal LV function: IV amiodarone or ibutilide, with procainamide being a second-tier recommendation. In patients with heart failure with reduced ejection fraction (HFrEF, EF <40%): IV amiodarone.
- Anticoagulate if CHA2DS2-VASc shows risk >=2% per year
More on EMCrit
- The Case of the Irregular Irregularity(Opens in a new browser tab)
- PulmCrit – Magnesium infusions for atrial fibrillation & torsade(Opens in a new browser tab)
- Cardiogenic shock following cardioversion of atrial flutter(Opens in a new browser tab)
Additional Resources
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Professor
Nassau University Medical Center
No conflicts of interest (coi).
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I’m sure the cardiology consult will make everything better…
C
hee hee
Dear Scott,
Why don’t you use beta blokkers to slow them down?
No reason you can’t. I just have not found them to be as effective as dilt or amio.
In response to your latest blog, Would you prefer metoprolol for rapid afib if the pt is already on it? For years, I’ve been encouraged to avoid using more than one class of AV blocking agents at a time if avoidable. Most chronic Afib pts come in on metoprolol, sometimes in addition to another agent (e.g. Digoxin). I have the most experience with diltiazem for treating rapid afib, but would it make sense to start with metoprolol for this patient, as we may avoid combining agents to increase the chance of causing complete heart block? It seems like the ED… Read more »
Great talk about a scary topic. In Australia, instead of phenylephrine, Metaraminol (Aramine) is a more popular drug, It is a fast acting peripheral vasocontrictor, loved by most anesthetist. In common practice, most doctors would mix one ampoule (2 mg) with Normal Saline to make up 20 ml and give one to two ml at a time. The bolus dose of Amiodaro0ne recommended is 3oomg followed by an infusion. I came across a similar case of crashing AF > 170 and hypotension 70/50 not long ago. To make the situation worse, he had infective COPD /type 2 respiratory failure with… Read more »
Paul,
Thanks for the info and the comment. It sounds like metaraminol is very similar to phenylephrine. So you folks start with the higher dose of amio right off the bat? Do you see a lot of hypotension from it?
scott
Dear Scott,
I ve read about the use of calcium as a pre treatment agent prior the use of calcium channel blockers ie ditialzem. They advocated us to give 5-10cc of calcium gluconate as to offset the hypotensive effect of the drug.
What do you think?
Calcium showed good effect as a pretreatment for verapamil. The data have not supported Ca pretreatment for dilt (J Emerg Med. 2004 May;26(4):395-400). However even though this study was an RCT, it was fairly useless b/c almost none of the patients got hypotensive in either group. However, calcium is an excellent inopressor in any patient, so I heartily agree that it would be a great thing to give in the patient above. Thanks for the comment.
Scott
Thanks for this podcast.
Can you do one on all remaining tachyarrythmias!
Regarding shock is it defibrillation or cardioversion in atrial fib with lo BP!.
I believe its cardioversion; the machine should still be able to sync on the R wave. I’ll add tachy rhythms to the future show list. thanks for listening.
Scott
nice lecture, pharmacist guy is learning alot, amio and diltiazem is very good for rate control, question why Phenyleph of all the pressors, u just want pure alpha effect and nothing to accelerate an already 250-300 HR?
exactly right. Phenyl will not make the heart rate higher and may actually lower it through vagal tone.
Hi Dr. Weingart,
In light of your push dose pressers update- are you still using push dose phenylephrine for these patients, or are you now using push dose epi? Do you have any concern about the B agonist activity of epi worsening the A fib (Or is it already as bad as it gets?)
Thanks!
Hey Scott,
Great podcast. I heard the “gray hairs” in my dept talk about Dig, but it takes forever to kick in, right? Any role for it acutely, EVER?
Another obscure but cool-sounding strategy I have actually done a few times is to pretreat with CaGluconate then give small (5mg) Diltiazem boluses. Taught to me by said gray-hairs, this has little evidence. There was a small RCT in JEM 2004 that showed no difference in hypotension with Calcium vs. Placebo in RVR patients (J Emerg Med. 2004 May;26(4):395-400).
Have you done this?
Yup, CaGluc study is mentioned further up in this comment stream as well. Calcium pretreatment clearly works for verapamil, not as clear with dilt.
Dig takes hours as you mention so it generally won’t help in this scenario.
Thanks so much for commenting and listening!
Hi Scott. NICE talk on the Crashing AFib patient – which I’m only getting to in 2012 … (you first recorded this in 2010 … ). As per above few comments – Calcium pre-treatment seems an option (realizing as you mention the data is with Verapamil) – but I believe YOUR emphasis in your podcast of using lower doses of IV Dilt given slower is the REAL key. Doing so has got to minimize the hypotensive effect. Clearly there is a balance one is seeking – which is to slow the rate of AFib (so as to increase diastolic filling… Read more »
Ken,
We have been having the same conversation about Dig on our tachy septic patients. What dose are you giving?
Absolutely agree. I love digoxin for the “nearly crashing” patient, and even if the peak effect may take hours, you get 80-90% effect in most patients in 15-30minutes, which, depending on the scenario, may be perfectly fine. And of course, no hypotension…
I agree with the use of digoxin in these situations. I presume it is inexpensive, and it does seem to kick in within fifteen minutes or so. I start with 0.25 mg and never had to go beyond a total of 0.5 mg. Digoxin is an example of “an oldie, but goodie.”
ROB – I’ll qualify my response by advising that I retired from my faculty slot in July, 2010 (after 30 years). I’m now “Emeritus” (which means I’m no longer practicing) – but the dosing I used for many years when practicing (and attending) regarding use of Digoxin is as follows: – IF the patient has not previously been on the drug – consider IV loading (with 0.25-0.5 mg as the initial dose). – May follow this with smaller IV increments (of 0.125-0.25 mg) every 2-6 hours, until a total loading dose (0f ~0.75-1.5mg) has been given over the first 24… Read more »
Ooops – I meant to say Scott (Rob does the other great podcast show = ERCast)!
Hi Scott! I’m revisiting this post (as I revisit many of your “classics”) for a refresher and for the first time noticed the recommendation for ketamine during cardioversion. I’ve switched to ketamine or ketamine/propofol for most of my ED sedation needs at this point, but given its propensity for causing tachycardia in otherwise healthy people I wonder if there is any theoretical or practical concern about exacerbating a tachydysrhythmia with it. On an unrelated but amusing note I used ketamine/propofol for a semi-elective cardioversion recently and had the closest thing to an emergence reaction I’ve ever seen where the poor… Read more »
Julie, the rec here is for pain dose ketamine. No tachycardia, no hypertension. Just nice pain relief. Feel free to sub fentanyl if the patient is hemodynamically stable.
I had a similar concern about ketamine during a recent case: I had recent case of a late 40s, relatively healthy man who presented with shortness of breath. He was in a rapid SVT (probably a fib) with a rate of 190 and systolic BP in the 60s in the field and was cardioverted without sedation to sinus rhythm. SBP improved to 80s. When I saw him he was in sinus tach in the 110s, SBP 70s-80s. CXR showed dense right middle and lower lobe infiltrates. He was aggressively fluid resuscitated and BP temporarily improved, but then he went back… Read more »
Ben, I’m not seeing any actual problem with the ketamine in your case description
In a similar situation i.e. hypotensive, septic, unstable tachycardia would it have been your choice? Or something different? Thanks.
as above etomidate if I have it b/c it disappears quicker, otherwise ketamine is a fine choice
Julie’s comment led me to relisten to this podcast – which gave me 2 additional thoughts I wanted to comment on re the ‘Crashing AFib Patient’: The rate of AFib doesn’t have to be 300/minute for me to begin thinking about WPW. Rapid AFib with a wide QRS over 220/minute is enough to start one thinking. An interesting accompaniment of very rapid AFib with WPW is that there will often be marked variation in the length of the R-R interval (some relatively long R-R interval intermixed with much shorter ones). For a nice illustrative case – GO TO: http://ecg-interpretation.blogspot.com/2012/02/ecg-interpretation-review-37-irregular.html /… Read more »
great points as always, Ken
Hi Scott,
While using amiodarone for a crashing a-fib patient, is there any concern that although the patient does not have the typical HR associated with WPW, that there is an accessory pathway? Amiodarone does have BB and calcium channel effects that can block AV nodal conduction and therefore leave the heart susceptible to v-fib by allowing conduction to travel freely through the accessory channel. Is there any harm in using procainamide as the first line antiarrythmic in this scenario?
Thank
It only matters if the patient is demonstrating antidromic conduction. Known WPW, sure don’t use amio. But in a patient with unknown WPW, but with a narrow QRS and a rate <200, I would not worry about it. Wide, fast, and A-Fib--give procainamide or shock them.
How long would you typically observe a elderly patient after administering a 150 mg bolus of amiodrone with the drip to follow. We recently had a patient 5 days post CABG who went into a-fib with long pauses of 7 to 8 seconds.
???? Not sure what you mean. We would admit a patient that required an amio bolus and drip generally.
For us prehospital folks without access to lots of pressors…any consideration for starting a dopamine drip at alpha-dominant doses? Or is there enough beta-blocking activity, even at 15-20 mikes, to speed the rate up further and defeat the purpose?
To get to the alpha, you have already maxed out the beta, so prob. not the best agent.
Thanks for the great podcast . What about norepinephrine which has mainly alpha stimulant effect so little change in heart rate can it be used instead of norepinephrine? What do you think?
Can we use midazolam for sedation in the shocked patient and would it be enough for cardioverting the shocked patient?…thank alot for your kindness
norepi is currently infusion, so too slow. A tiny dose of midazolam may offer amnesia but not sedation
What about Afib with slow v.response like 40/min & bp 80/50 ? Recent onset in healthy man? Will cardioversion improve BP?
would not cardiovert, screen for dig and a/v blocking meds
Hi Scott
In the crashing Afib pt with an ‘unhappy’ myocardium-ie runs of VT but awake, no CP, but poor LV function (get the picture) after Amio and MgSO4 would you consider Ca?
I’d want to see a low iCAL first. Calcium can sig. increase myocardial workload.
do you mean you can’t give CaGluconate blindly . what about if not responding to inotropes ?
I had trouble deciding what to do recently on a patient who presented with decompensated CHF and rapid a fib. The cardioversion worked, but his pressure remained in the 70’s in NSR afterwards, with signs of poor perfusion. I thought about push dose phenyl, but second guessed myself because I didn’t want to worsen the afterload on an LVEF that was previously documented around 30%, maybe making perfusion worse. Thought about + inotropes, but didn’t want to worsen ischemia or revert back to rapid a fib. I ended up calling cardiology and they scratched their heads for about 30 minutes… Read more »
if the pt is hypotensive, you can’t make LVEF worse unless you think the pt is profoundly hypovolemic. Pressors will increase coronary perfusion and therefore bolster CO.
Scott,
Wondering about your thoughts on this piece:
http://www.theheart.org/columns/trials-and-fibrillations-with-dr-john-mandrola/untangling-knots-how-a-feeforservice-model-complicates-the-work-of-an-af-doctor.do
My thoughts about which part? The dilt drips? I don’t use dilt drips for all of the reasons they mention. Makes no sense and forces the pt to a higher level of care. Would only use on pts who are NPO.
That link isn’t working here is the correct link: http://www.medscape.com/viewarticle/810008
Hi Scott,
Minor question but why do you mix the Diltiazem into 50ml? Wouldn’t it be better to draw off 10ml before you put the Dilt in so you get 1mg/ml? Seems more confusing than it needs to be.
Thanks for all this info
Paul
Paul,
the ? is easier for whom? It is sharply frowned upon to withdraw fluid from the bag before adding medications b/c it adds to complexity of mixing, leads to more likelihood of breaks in sterility, and more potential for mishaps. Even if you made a nice 1mg/ml drip, managing the infusion rates and dosing without a drip sheet is just setting yourself up for error. With a drip sheet, it doesn’t matter what the concentration is, because you are just following the sheet.
Got it. Thanks.
Just heard this podcast. I am an intensive care paramedic in australia and we see a few of these cases every year.
In our ambulance service we do not carry an alpha agonist but adrenaline which we can set up as an infusion usually starting at 5mcg/min.
What are your thoughts on using an adrenaline infusion to improve the BP before infusing amiodarone? (which is a 300mg dose over 20 minutes for us).
Cheers
Anthony
IC Paramedic
I think it is fine, the beta may increase automaticity and therefore make the a-fib harder to break but this is purely theoretical.
What are your thoughts on the use of procainamide for the acute, non-crashing AFib patient? US and European guidelines cite a lack of evidence for their non-promotion of it. There was a recent study out of Canada promoting it, and we have a couple doctors here that seem to go after it as their first choice, and it makes me, as a pharmacist, a little uneasy.
Canadians in Ottawa demonstrated safety and efficacy quite nicely. Search for articles by Ian Stiell
Scott,
Had a few crashing A-Fib pts of late. I used Esmolol in both cases. Revisited this cast. Surprised Esmolol specifically not mentioned here. What is your gen experience and take on Esmolol for the crashing A-Fib pt?
At the time of the podcast, it was still brand name only–which I never recommend. Now that it is generic, it is definitely an option.
Scott, I’d like to thank you for the great work you’re doing, I have learnt really a lot from your podcasts and some times when I’m in doubt what to do I ask myself WWWD (what would Weingart do) and it always helps. A while ago I had a 60 yr old patient with a history of MI 6 month ago with monomorphic VT 220 bpm, his SBP was around 60, he was still conscious, we cardioverted him … would you chose the same sedation/analgesia (ethomidate + ketamine) agents as you have mentioned in this podcast? In one book of… Read more »
Excelente Podcast. Me gustaría que hablaras más acerca del uso de betabloqueadores. En mi hospital ( Cartagena, Colombia), no disponemos de algunos medicamentos que mencionas. Por ejemplo: Si no hay Etomidato o Ketamina? Con qué otra droga se pudiese realizar la sedoanalgesia?
GRacias
Regarding hypotensive patients with Atrial fibrillation in RVR, Ive had some success with a combination of digoxin 0.5mg IV and a Dobutamine drip. I tend to shy away from dopamine since it too can increase the heart rate.
Hi Scott
Had this today and just wanted to thank you for this post. Came in very handy.
Used Bedside ECHO in this setting to help out – in my head to ensure I wasn’t missing a tamponade as cause; and to check the heart wasn’t just a massive dilated bag of scar tissue long term
Intubated and this did seem to settle a lot of issues – rate came down with sedative / fentanyl ect
Thoughts ?
Thanks again
Casey
Scott, I’m a medic – what if I’m in the field – and cardioversion fails, and I do not have push-dose phenylephrine? This was nearly the case recently (transfer of very unstable a-fib RVR patient, hypotensive, but the patient crashed just before we got there, and thus the transfer was cancelled). My service carries Epi and Dopamine.
1/2 ml (50 mcg) of cardiac epi will usually do the trick if you can’t mix up formal push dose epi
hi Scott, excellent as always, and thank you. did you hear Laura Bontempo’s cool talk also on this topic (the 2016 the crashing patient conference. its on emedhome.com. she talks about the crashing rapid fib, hypotensive new onset a-fib patient who happened to be the Vice President for ED operations of her hospital. and he was refractory to synchronized biphasic shocking. neosynephrine , very ginger slowing with amiodurone , or esmolol, or dilt, , then Ibutilide 1 mg over 10 minutes, wait ten minutes , and re-shock. what she called “pharmacologic enhancement”, to increase the chances that the cardioversion would… Read more »
Hi everyone. I am one of these patients. But im 32 ive had afib since i was 20. Im running at 180s now. I dont like going to the hospital because ive been told to go home and deal with it. Im on digoxen and its not helping. I.honestly dont know what to do. I have a pacemaker had my heart shocked and ive had a cryo-ablation and nothing has helped. I live in tempe az anyone know a really good cardiologist in my area that can maybe figure out whats wrong with me!?
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Hi Scott, I have used Diltiazem for unstable AF patients in the ED setting multiple times, with great effect. I am now on the training program for Anaesthestics (Anaesthesiology) and whenever we have this scenario in the OT and I suggest IV Diltiazem the Anaesthetists (Anaesthesiologists) always look at me like I’m crazy and tell me I would cause a cardiac stand still and kill the patient (usually the patient is already on a Beta-blocker long term or they have already tried carefully titrate in some Esmolol with little effect). I’ve tried to look at the literature myself but am… Read more »
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Hi Scott, listening to this old podcast, and now that I know how you feel about push dose epi, I was wondering if you would now use push dose epi instead of phenyl in this case. Also, in the Canadian CV Guidelines 2020 ( I work in Quebec), they avoid CCB when patients have an EF < 40%. Do you check the EF before deciding to chose low-dose diltiazem? Thank you for your time and great podcasts! I would pay even more for a subscription you know… just saying…
hey if you have both, phenyl is more elegant, but i advocate most shops just stock one push-dose and that should be epi. in an ideal world norepi would be the one for everything, but would like to see more data. Amio is preferred if you actually know the pt’s baseline EF and it is low. You can’t do POC echo and make a judgment b/c their EF is impaired by rapid rate.
Thank you so much for your answer, so helpful. We are lucky to have both phenyl and epi push at my shop, so I’ll try to be more elegant then ;).
Hello, I work in Switzerland, I had to face same situations but with elderly patients who have an “NTBR” guidelines and were refused to ICU. I had to do my best and put them in internal medicine unities. So septic/cardiogenic shock with atrial fibrillation. The way I deal with those patients is some iv fluids, iv digoxine, amiodarone, orale midodrine, (and antibiotics if needed) I keep the betablockers if they already had in their everyday treatment without increasing the dosage drastically… and I hope… do you have any other advices about that type of patients? Of course, I avoid therapeutic… Read more »
Cedric, My interpretation of a NTBR is that I only should treat things that may lead to discomfort, so I probably wouldn’t go with the midodrine, the dig. I probably would just give fluids if dehydrated, antibiotics; but that is just me–your practice pattern is your own and don’t disagree with any of it.