Treatment of Acute Afib with RVR

[Redpancreas]

very variable, only like a 30% chance to convert with a good load of amiodarone. it depends on a lot of things including how remodeled their atria are, the underlying substrate (DMII, HTN, COPD, OSA, etc), EF/LV dilation, cause of AF (eg primary vs secondary), etc etc. Generally, the more normal the heart and the more acute the drivers, the more likely someone will go back into sinus.

IV amiodarone isn't there to cardiovert them, it's to rate control.

I've seen people spontaneously convert the moment cardiology arrives at the bedside before we discuss Amio. It seems like a very hit or miss thing.

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[wjs010]

what would you do in this case? I have a colleague who had a patient present as such: new onset flutter/fib, rates 150s, hypotensive but normotensive after going back into sinus. Etiology of afib unclear,but primary has no major reversible cause. But BP fluctuating overnight, soft 90s/50s. Flutter is presumed new. Cardiology is considering TEE vs amio , but they at least want heparin, which is start by primary team. unfortunately, patient rips out all IV's overnight and has zero access. 1 wrist IV is obtained in the morning, through which heparin is run. Primary team delays amio because they don't have access (also an ESRD patient you can't put a picc in ), so they just keep running heparin but can't really control the flutter because patient gets hypotensive with rate control. So, at this point, would you cardiovert, given the patient is getting heparinized? obviously you could make the case for "instability" and opt for DCCV already, but other than slight hypotension which was corrected when patient went back into sinus, he was relatively stable. OR: would you do everything you can, including putting in whatever IV possible, so that you could run amio in attempt for chemical CV/rate control. I know this is very esoteric and that's why I ask.

 

[Chemist0157]

what would you do in this case? I have a colleague who had a patient present as such: new onset flutter/fib, rates 150s, hypotensive but normotensive after going back into sinus. Etiology of afib unclear,but primary has no major reversible cause. But BP fluctuating overnight, soft 90s/50s. Flutter is presumed new. Cardiology is considering TEE vs amio , but they at least want heparin, which is start by primary team. unfortunately, patient rips out all IV's overnight and has zero access. 1 wrist IV is obtained in the morning, through which heparin is run. Primary team delays amio because they don't have access (also an ESRD patient you can't put a picc in ), so they just keep running heparin but can't really control the flutter because patient gets hypotensive with rate control. So, at this point, would you cardiovert, given the patient is getting heparinized? obviously you could make the case for "instability" and opt for DCCV already, but other than slight hypotension which was corrected when patient went back into sinus, he was relatively stable. OR: would you do everything you can, including putting in whatever IV possible, so that you could run amio in attempt for chemical CV/rate control. I know this is very esoteric and that's why I ask.

You could have IR put in a Hickman line if that is available. Little easier on the central veins than the other options. Just seems like atrial flutter not infrequently comes right back after cardioversion.

 

[Splenda88]

Is the BP low because of the RVR and insufficient ventricular filling? Then a BB may actually help fix the problem (again, as long as not in decompensated HF). It's sort of like using an ACEi in cardiogenic shock, the afterload reduction actually helps improve CO and BP despite fact that it's an "anti-hypertensive". And it's the CO that really needs fixing in both cases, BP is simply a surrogate marker.

Esmolol has a quick onset of action and is extremely short acting, and will last ~45 min after the infusion is stopped (although it is a fair amount of volume as an infusion). Amiodarone requires loading given its high volume of distribution, will take longer to control the rate as an infusion (vs. a bolus, which can also cause hypotension), will potentially result in cardioversion (which as mentioned, may not be desirable in the absence of anticoagulation), and has a longer half life.

I have yet to see anyone (even cardio) doing that.

 

[aafisahar]

I have yet to see anyone (even cardio) doing that.

We often do hydral/isordil for afterload even on borderline patients or can do nipride but that needs the unit since it needs to be titrated frequently. I prefer afterload reduction as a first go instead of inotropes because you have a sense of how much entresto or arb they can tolerate despite a pressure of 100/80. Not unusual to crank the hydral/isordil up to 50/20 or 75/20 in these patients even with a BP like that.

 

[thehundredthone]

I have yet to see anyone (even cardio) doing that.

Cardiology did it very frequently where I trained for residency. And it should usually only be cardiology doing that, like the quote below states, this is something to titrate in the unit.

We often do hydral/isordil for afterload even on borderline patients or can do nipride but that needs the unit since it needs to be titrated frequently. I prefer afterload reduction as a first go instead of inotropes because you have a sense of how much entresto or arb they can tolerate despite a pressure of 100/80. Not unusual to crank the hydral/isordil up to 50/20 or 75/20 in these patients even with a BP like that.

Have you ever used enalaprilat for IV titration? The rationale given to me was that it is more similar to the medication that will eventually be started, and possibly a bit less reflex tachycardia. Although our cardiac intensivists in residency did use both nitroprusside and enalaprilat in the CCU.

 

[Radetzky]

what would you do in this case? I have a colleague who had a patient present as such: new onset flutter/fib, rates 150s, hypotensive but normotensive after going back into sinus. Etiology of afib unclear,but primary has no major reversible cause. But BP fluctuating overnight, soft 90s/50s. Flutter is presumed new. Cardiology is considering TEE vs amio , but they at least want heparin, which is start by primary team. unfortunately, patient rips out all IV's overnight and has zero access. 1 wrist IV is obtained in the morning, through which heparin is run. Primary team delays amio because they don't have access (also an ESRD patient you can't put a picc in ), so they just keep running heparin but can't really control the flutter because patient gets hypotensive with rate control. So, at this point, would you cardiovert, given the patient is getting heparinized? obviously you could make the case for "instability" and opt for DCCV already, but other than slight hypotension which was corrected when patient went back into sinus, he was relatively stable. OR: would you do everything you can, including putting in whatever IV possible, so that you could run amio in attempt for chemical CV/rate control. I know this is very esoteric and that's why I ask.

You need more than one IV anyway to safely cardiovert this pt. Assuming it’s been more than 48 hours, get on with it and cardiovert.

 

[Redpancreas]

You could have IR put in a Hickman line if that is available. Little easier on the central veins than the other options. Just seems like atrial flutter not infrequently comes right back after cardioversion.

Agree with this. Have IR place a non-tunneled, small bore, central line (hickman). Double lumen if necessary. As an IM resident, listen to what Cardiology tells you. A lot of the quick titraters (nipride+lasix, captopril etc.) people mentioned come in CCU/HF territory with a swan which is not the case here. In my limited experience, RVR driven hypotension is really a very in-your-face diagnosis and is not something you make an argument by looking at the tele overnight and noting concurrent RVR/mild hypotension when the patient's sleeping. If unstable RVR occurs, the BP will drop with a clear change in MS and be sustained which then prompts discussion on urgent electrical cardioversion. AFlutter is likely to revert back after cardioversion anyways. You can medically manage with anticoagulation followed by amiodarone, and then call EP for definitive treatment.

 

[JustPass]

I have yet to see anyone (even cardio) doing that.

Our cardiology does it here all the time to reduce afterload.

 

[end stage fibro]

great thread.

1) i’ve gotten much more relaxed about treating afib rvr now that i’ve been out of residency for a bit. i used to have a hair trigger for the dilt.

2) is the litigation risk actually high for conversion to SR using amio resulting in a stroke? it’s not usually my go to but if other routine agents are contraindicated i’m gonna document my thought process and give some amio. hell, i’m sure we’ve all seen our share of conversion from a push of metoprolol

 

[Radetzky]

Our cardiology does it here all the time to reduce afterload.

I wouldn’t ever give a long acting vasodilator to someone in cardiogenic shock. Not all sick hearts can actually increase cardiac output in response to reduced afterload, and you just end up stinking up the coronary perfusion.

 

[Instatewaiter]

I have yet to see anyone (even cardio) doing that [re acei in cardiogenic shock]

You need new cardiologists.

I wouldn’t ever give a long acting vasodilator to someone in cardiogenic shock. Not all sick hearts can actually increase cardiac output in response to reduced afterload, and you just end up stinking up the coronary perfusion.

I do it frequently. If you are concerned enough about it use captopril as it is short acting. I prefer nipride to hydral/isdn then convert to ace/arb/arni. Rare to find the dreaded vasodilated cardiogenic shock patient- they're pretty screwed anyway...

FYI I am a heart failure/transplant/mcs doc.

Cardiology did it very frequently where I trained for residency. And it should usually only be cardiology doing that, like the quote below states, this is something to titrate in the unit.


Have you ever used enalaprilat for IV titration? The rationale given to me was that it is more similar to the medication that will eventually be started, and possibly a bit less reflex tachycardia. Although our cardiac intensivists in residency did use both nitroprusside and enalaprilat in the CCU.

Universally I find significant hypotension with enalaprilat. Personally I don't see a need for it's use, basically ever. Nitroprusside is a wonderful drug though

 

[Radetzky]

You need new cardiologists.



I do it frequently. If you are concerned enough about it use captopril as it is short acting. I prefer nipride to hydral/isdn then convert to ace/arb/arni. Rare to find the dreaded vasodilated cardiogenic shock patient- they're pretty screwed anyway...

FYI I am a heart failure/transplant/mcs doc.


Universally I find significant hypotension with enalaprilat. Personally I don't see a need for it's use, basically ever. Nitroprusside is a wonderful drug though

I usually start some SNP first to prove it works. I’ve seen too many times the consequences of over-zealous vasodilation.

 

[CluvK]

I’ve read more about concern for chemical cardioversion here than I have ever seen in practice or from cardiology. Maybe it is related to the cardiology guys where I work inpatient? People aren’t shy to start amiodarone around my local hospital if the typical metoprolol or diltiazem rate control tactics are not the best play.

I have the same question as well. Is anyone willing to share your thoughts?

 

[Make Or Break]

I have the same question as well. Is anyone willing to share your thoughts?

I’ve seen high dose amio drips used >7 days on patients and that hypersensitivity/interstitial pneumonitis happens pretty frequently. It can be a nasty drug.

 

[CluvK]

I’ve seen high dose amio drips used >7 days on patients and that hypersensitivity/interstitial pneumonitis happens pretty frequently. It can be a nasty drug.

I agree amio is a nasty drug and ideally should not be used for long time. But it would be reasonable just to use it for short-term RVR control after failure of rate control, right?