Post-op hypotensive Afib, best approach?

[Medic_90x]

This is one area I have trouble with in regards to getting a good approach; especially given I've seen different things done.

For new-onset post-op hypotensive Afib (noncardiac surgery), what's the best approach? Lets say no CHF/significant comorbidites vs comorbidities present. Or someone who is 55 vs someone who is 80.
It's just a matter of knowing when to do electrical cardioversion vs starting amio for example for rhythm control.

---

Members don't see this ad.

 

[deleted547339]

This is one area I have trouble with in regards to getting a good approach; especially given I've seen different things done.

For new-onset post-op hypotensive Afib (noncardiac surgery), what's the best approach? Lets say no CHF/significant comorbidites vs comorbidities present. Or someone who is 55 vs someone who is 80.
It's just a matter of knowing when to do electrical cardioversion vs starting amio for example for rhythm control.

You’re overthinking this. If someone is hypotensive, you buzz them.

 

[AdmiralChz]

It's just a matter of knowing when to do electrical cardioversion vs starting amio for example for rhythm control.

This is more nuanced than this - I know you answered some of these but... Is it post-op cardiac surgery? Was the patient in beta blockers previously? History of a fib? How’s your volume status? What do you mean by “hypotensive” - systolic in the 80s? Or in the 50s and obtunded?

You usually reserve electrical shocks for someone in dire straights in need of resynchronization - think a near ACLS situation. Otherwise I’m not sure amiodarone would be the first I would reach for acute afib - I’d check labs (K, Mg), then try to control rate with hopes of spontaneous conversion (Beta blocker vs dilt if the pressure can take it). Amio for refractory control if above is a no go, I don’t practice true CCM but the times I’ve used it in the non-cardiac population are few and far between.

 

[chessknt]

I have yet to see a cardioversion actually keep a medically ill unstable patient out of afib. It usually works for a few minutes then back in to afib they go because they are still volume up or have **** lungs dilating their right side or some other unclear reason.

Most of the postop hearts I have seen go on prophylactic amio and just get re bolused multiple times to try to make it go away if they go in to rvr and are hypotensive. In the micu population we use shocks sometimes but will frequently go to amio instead, especially if we are already on pressors and suspect that this triggered the afib and that it won't be going away soon.

I'm assuming you mean a critically ill patient that gets afib in addition to whatever else is going on and not a patient who becomes critically ill because they flip in to afib (in that scenario shock is an easy choice).

 

[Medic_90x]

I have yet to see a cardioversion actually keep a medically ill unstable patient out of afib. It usually works for a few minutes then back in to afib they go because they are still volume up or have **** lungs dilating their right side or some other unclear reason.

Most of the postop hearts I have seen go on prophylactic amio and just get re bolused multiple times to try to make it go away if they go in to rvr and are hypotensive. In the micu population we use shocks sometimes but will frequently go to amio instead, especially if we are already on pressors and suspect that this triggered the afib and that it won't be going away soon.

I'm assuming you mean a critically ill patient that gets afib in addition to whatever else is going on and not a patient who becomes critically ill because they flip in to afib (in that scenario shock is an easy choice).

This is more nuanced than this - I know you answered some of these but... Is it post-op cardiac surgery? Was the patient in beta blockers previously? History of a fib? How’s your volume status? What do you mean by “hypotensive” - systolic in the 80s? Or in the 50s and obtunded?

You usually reserve electrical shocks for someone in dire straights in need of resynchronization - think a near ACLS situation. Otherwise I’m not sure amiodarone would be the first I would reach for acute afib - I’d check labs (K, Mg), then try to control rate with hopes of spontaneous conversion (Beta blocker vs dilt if the pressure can take it). Amio for refractory control if above is a no go, I don’t practice true CCM but the times I’ve used it in the non-cardiac population are few and far between.

How about a patient with a couple things going on but not overly sick? Pressures in the low-mid 70s. Noncardiac surgery and not on pressors. K/Mg etc normal.

 

[deleted547339]

To elaborate, if hypotensive, I shock, period. But, as above, that rarely is adequate as it doesn’t address the etiology of afib. In the ICU, something is usually causing it. Sometimes it’s just post-op, but I’m usually in the MICU and that means it’s some medical problem driving it.

Check a K, hemoglobin, etc. Give some mag. Maybe amio, b-blocker, dilt or dig depending on patient, renal function, previous meds, etc. Evaluate pressors. Fluids or diuresisis as appropriate. Pain control. Manage vent for acidosis. Evaluate CRRT. Etc.

A lot of time rate control can address it alone as many people will cardiovert, although I have a lot more success with this in the ED with primary Afib as opposed to shock/MSOF in the ICU which is usually because something is driving them into it. But I still have a super low threshold for electricity in afib rvr with hypotension - I disagree that you need to be peri-code. Hypotension kills and I want to address it immediately.

 

[jdh71]

This is one area I have trouble with in regards to getting a good approach; especially given I've seen different things done.

For new-onset post-op hypotensive Afib (noncardiac surgery), what's the best approach? Lets say no CHF/significant comorbidites vs comorbidities present. Or someone who is 55 vs someone who is 80.
It's just a matter of knowing when to do electrical cardioversion vs starting amio for example for rhythm control.

There is no straight forward one best way approach which is why you’ve seen it done a few different ways. It all depends on how sick they are and how low the BP is and if the BP is low because of the fib or is the low BP from something else and driving the fib. Amio is always a good choice. I also like magnesium pushes (patients hate it) and digoxin. People don’t seem as comfortable with the digoxin these days. I think it works actually pretty well. Its easy to cardiovert someone sedated and on vent. Not always as easy in the folks hanging in there, breathing on their own who will need some sedation for the juice. It’s a coin flip if the sedation makes things worse.

 

[Medic_90x]

There is no straight forward one best way approach which is why you’ve seen it done a few different ways. It all depends on how sick they are and how low the BP is and if the BP is low because of the fib or is the low BP from something else and driving the fib. Amio is always a good choice. I also like magnesium pushes (patients hate it) and digoxin. People don’t seem as comfortable with the digoxin these days. I think it works actually pretty well. Its easy to cardiovert someone sedated and on vent. Not always as easy in the folks hanging in there, breathing on their own who will need some sedation for the juice. It’s a coin flip if the sedation makes things worse.

Interesting. Is digoxin something you give without consulting cardio? (though not sure if you are one)

 

[jdh71]

Interesting. Is digoxin something you give without consulting cardio? (though not sure if you are one)

of course - I don’t need a cardiologist around to give digoxin

 

[Dr.CCM]

In the icu, if I think the afib is causing the hypotension I’ll shock (rates gotta be pretty fast though). But if it’s afib plus other things that are causing it I mag them, amio and phenyl drip. Lots of amio and mag Bolus. I’ll add on dig too as a load if that doesn’t work.

 

[ShockIndex]

I ran into a similar issue last week: a 62 year old guy with hyperpyrexia to 106.3 due to severe sepsis and a hx of A-fib on apixaban. Although his last out-patient ECG showed a NSR, he was now in 2:1 A-flutter pegged at 150. Initially, BPs were fine but he started to have MAPs ~60-65 as we began treating him. One attending wanted to spark him with the first MAP <65 and felt pretty passionate about it.

I took a little more nuanced approach and felt that the sepsis and temperature were driving the arrhythmia. I was unconvinced that cardioversion would result in a sustained sinus rhythm. I really didn’t feel a pressing need to control the rate with a negative inotrope until we had source control of his sepsis (he had > 100,000 WBC/mm3 from an aspirate of his knee) or at least given him the full 30 cc/kg. To me, the arrhythmia and hypotension was secondary to his severe sepsis.

 

[MoMoGesiologist]

of course - I don’t need a cardiologist around to give digoxin

How much are you giving for load and maintenance? How long till it “kicks in”? What else are you giving with it for rate/rhythm control? Does it change your likelihood to use it if low vs normal EF?

 

[jdh71]

How much are you giving for load and maintenance? How long till it “kicks in”? What else are you giving with it for rate/rhythm control? Does it change your likelihood to use it if low vs normal EF?

it all depends

are you looking for a big post running through all of the algorithms here?

load and maintain with usual doses - don’t forget to cut those in half for renal disease

kicks in about as quick as anything else

I might also use any of the other rate controlling medications at the same time

low versus normal EF isn’t some kind of big difficult clinical consideration/dilemma - this will be short term use from my end

 

[Medic_90x]

it all depends

are you looking for a big post running through all of the algorithms here?

load and maintain with usual doses - don’t forget to cut those in half for renal disease

kicks in about as quick as anything else

I might also use any of the other rate controlling medications at the same time

low versus normal EF isn’t some kind of big difficult clinical consideration/dilemma - this will be short term use from my end

I'm just wondering as a resident covering the (big academic center with a lot of autonomy) ICU overnight on-call; if I would get heat for using digoxin.

 

[jdh71]

I'm just wondering as a resident covering the (big academic center with a lot of autonomy) ICU overnight on-call; if I would get heat for using digoxin.

that may be culture dependent

*I* obviously don’t think it’s “poison” - but we all had “that attending” in residency who’d lose their **** about a pet peeve thing. But I don’t think you’d be given a lot of crap for a single dose of digoxin in these cases especially if you tried some of the more “standard” drugs or interventions where you train.

 

[engineeredout]

More often than not, the tachycardia (even if it is atrial fibrillation vs NSR) is compensatory for the shock/hypotension, not the other way around. I see people getting way too excited over cardioverting the AF instead of looking for and/or addressing underlying problems. Sometimes I have to deal with WTF glances from either nursing or other docs because I'm not going to shock someone out of an AF rate in the 130s because "Their SBP is 70".

If I do think it is a pure new onset atrial fibrillation, I do make a shot at trying to get them out of it with amio. Usually give a Mg bolus up front too (2g over 15 min). Just helps make management easier down the line and most of these patients will do better in sinus than afib.


As an aside, and this is pure anecdote, phenylephrine sucks. Specifically, when phenylephrine gets applied to these septic patients who are in rapid atrial fibrillation. I get the theoretical "It won't raise their heart rate as much as other things" but it never seems to work, these patients probably could use a little cardiac output augmentation from B1 stimulation, even at high concentrations you end up giving a lot of volume in the very dilute phenylephrine gtt which most of them do not need, and in the studies of vasopressors in vasodilatory shock, phenylephrine is not the pressor that is being used, so why would we use it?

Aside #2: This seems to be institutional, but some people seem afraid to use diltiazem in these patients, especially those with reduced systolic function. The guidelines which recommend against the use of calcium channel blockers for systolic dysfunction apply to chronic, outpatient management. There simply isn't very much negative inotropic effect with diltiazem, and if you think that your rates are not allowing for adequate LV filling, I'd much rather put them on norepi for BP, dilt for the rate

/end of soapbox.

 

[MoMoGesiologist]

More often than not, the tachycardia (even if it is atrial fibrillation vs NSR) is compensatory for the shock/hypotension, not the other way around. I see people getting way too excited over cardioverting the AF instead of looking for and/or addressing underlying problems. Sometimes I have to deal with WTF glances from either nursing or other docs because I'm not going to shock someone out of an AF rate in the 130s because "Their SBP is 70".

If I do think it is a pure new onset atrial fibrillation, I do make a shot at trying to get them out of it with amio. Usually give a Mg bolus up front too (2g over 15 min). Just helps make management easier down the line and most of these patients will do better in sinus than afib.


As an aside, and this is pure anecdote, phenylephrine sucks. Specifically, when phenylephrine gets applied to these septic patients who are in rapid atrial fibrillation. I get the theoretical "It won't raise their heart rate as much as other things" but it never seems to work, these patients probably could use a little cardiac output augmentation from B1 stimulation, even at high concentrations you end up giving a lot of volume in the very dilute phenylephrine gtt which most of them do not need, and in the studies of vasopressors in vasodilatory shock, phenylephrine is not the pressor that is being used, so why would we use it?

Aside #2: This seems to be institutional, but some people seem afraid to use diltiazem in these patients, especially those with reduced systolic function. The guidelines which recommend against the use of calcium channel blockers for systolic dysfunction apply to chronic, outpatient management. There simply isn't very much negative inotropic effect with diltiazem, and if you think that your rates are not allowing for adequate LV filling, I'd much rather put them on norepi for BP, dilt for the rate

/end of soapbox.

I haven’t seen someone on both NE and dilt gtts... is that something you’ve done? is that common practice?

 

[engineeredout]

I haven’t seen someone on both NE and dilt gtts... is that something you’ve done? is that common practice?

have I done it? Absolutely. Though, I do not wish to comment on “common practice” or pretend to imply I have evidence backing this practice up.

In my own use/experience, I find phenylephrine gtt to be inferior to norepinephrine in the septic patient. If my patient with AF is tachy in the low 110s, I don’t really care. If they are tachy in the 140-150 range, to the point where cardiac output may be affected (this can be observed objectively by either looking at the amplitude of the arterial line wave form from beat to beat, or obtaining a LVOT VTI and looking at the variability in stroke volume with each beat), then I may end up adding diltiazem to this mix.

 

[deleted547339]

have I done it? Absolutely. Though, I do not wish to comment on “common practice” or pretend to imply I have evidence backing this practice up.

In my own use/experience, I find phenylephrine gtt to be inferior to norepinephrine in the septic patient. If my patient with AF is tachy in the low 110s, I don’t really care. If they are tachy in the 140-150 range, to the point where cardiac output may be affected (this can be observed objectively by either looking at the amplitude of the arterial line wave form from beat to beat, or obtaining a LVOT VTI and looking at the variability in stroke volume with each beat), then I may end up adding diltiazem to this mix.

You’d probably be better off with amio or esmolol.

 

[jdh71]

You’d probably be better off with amio or esmolol.

why?

 

[deleted547339]

why?

Less alpha effect. If you’re having problems with tachyarrhythmias and hypotension, giving something that has a stronger hypotension promoting profile seems like shooting yourself in the foot.

Also, people always seems to forget that amio is a mild beta-blocker.

 

[jdh71]

Less alpha effect. If you’re having problems with tachyarrhythmias and hypotension, giving something that has a stronger hypotension promoting profile seems like shooting yourself in the foot.

Also, people always seems to forget that amio is a mild beta-blocker.

diltiazem has more ALPHA effect than amio or esmolol?

 

[deleted547339]

diltiazem has more ALPHA effect than amio or esmolol?

Sorry. Fair. More hypotensive effects. You know what I mean.

 

[betamale]

Dig 0.25 mg IV if soft BP. check istat K+, Ca++ first though. We use to give on the floor frequently as a resident; didn't have issues. We mostly use Esmolol and Diltiazem in the ER though

 

[jdh71]

Sorry. Fair. More hypotensive effects. You know what I mean.

Is diltiazem more hypotension inducing though??

I’m not trying to be difficult here. But we all wander around with certain dogmas and anecdotes. Is there good data that diltiazem causes more hypotension? *In my experience* I’ve run into more hypotensive effects from esmolol than diltiazem for instance (not to mention the large IV fluid load of esmolol). I reach for amio and digoxin in these kinds of situations in part because of this but also because I have sense of how these drugs work “better” because of frequency of use and also in part because of my training.

And now I’m just musing here but let’s say it did drop BP a bit. You’re running a pressor. So what? I’m not trying to be flip here either. Let’s say you go up on your norepi by 0.02 or 0.04 but now you’ve got a more stable heart rate with the fib situation. So. ****ing. What?

The thing is. And I don’t know exactly why but some fib only responds well to one medication. You throw everything you usually use at it. Maybe even try cardioversion a few times and finally give the mast drug you use and things get better. Did that situation need time, ALL of the drugs, or just that last drug?

This is fog of war stuff. And this is why EBM is largely unhelpful in the ICU. So when you or I or anyone else says, “you’re probably better off . . .” to anything, is that *actually* true?

 

[deleted547339]

Is diltiazem more hypotension inducing though??

I’m not trying to be difficult here. But we all wander around with certain dogmas and anecdotes. Is there good data that diltiazem causes more hypotension? *In my experience* I’ve run into more hypotensive effects from esmolol than diltiazem for instance (not to mention the large IV fluid load of esmolol). I reach for amio and digoxin in these kinds of situations in part because of this but also because I have sense of how these drugs work “better” because of frequency of use and also in part because of my training.

And now I’m just musing here but let’s say it did drop BP a bit. You’re running a pressor. So what? I’m not trying to be flip here either. Let’s say you go up on your norepi by 0.02 or 0.04 but now you’ve got a more stable heart rate with the fib situation. So. ****ing. What?

The thing is. And I don’t know exactly why but some fib only responds well to one medication. You throw everything you usually use at it. Maybe even try cardioversion a few times and finally give the mast drug you use and things get better. Did that situation need time, ALL of the drugs, or just that last drug?

This is fog of war stuff. And this is why EBM is largely unhelpful in the ICU. So when you or I or anyone else says, “you’re probably better off . . .” to anything, is that *actually* true?

There are several studies in the EM literature showing that beta blockers are less efficacious in rare controlling afib, but also less likely to cause hypotension. You can argue with anyone of them, but I think that in aggregate they support my point. This seems to fit with my clinical experience in the ED and ICU. Also, how many times have you had patients with aortic pathology on an esmolol drop with crazy systolic hypertension? Decent rate control med, crummy BP Med in my opinion.

 

[jdh71]

There are several studies in the EM literature showing that beta blockers are less efficacious in rare controlling afib, but also less likely to cause hypotension. You can argue with anyone of them, but I think that in aggregate they support my point. This seems to fit with my clinical experience in the ED and ICU. Also, how many times have you had patients with aortic pathology on an esmolol drop with crazy systolic hypertension? Decent rate control med, crummy BP Med in my opinion.

Did those studies look at atrial fibrillation with rapid rates in patients already on vsopressors?

 

[engineeredout]

There are several studies in the EM literature showing that beta blockers are less efficacious in rare controlling afib, but also less likely to cause hypotension. You can argue with anyone of them, but I think that in aggregate they support my point. This seems to fit with my clinical experience in the ED and ICU. Also, how many times have you had patients with aortic pathology on an esmolol drop with crazy systolic hypertension? Decent rate control med, crummy BP Med in my opinion.

Problem is our EM Afib studies are for community afib, the overwhelming majority of which are hemodynamically stable and we're just trying to get them under control so the hospitalists don't freak out about the rate. In the ICU we're taking a sick heart that has one or many extra stressors added on top (volume overload, increased O2 demand secondary to sepsis etc), and then we're sticking a strong negative inotrop on top of them like a B-blocker - diltiazem just seems to be a weaker negative inotrop. Unless we're targeting a very specific pathology (dynamic LVOT obstruction/SAM/HOCM), or we've already proven to be refractory to other treatments, I am very wary to give B-blockers to these critically ill patients, a lot of them don't seem to tolerate it well.

But of course every patient is different. Some will respond better to esmolol than other agents, I'm certainly not trying to make ultimatums when it comes to what I will and will not use - just talking about my general approach to the majority.

 

[deleted547339]

Did those studies look at atrial fibrillation with rapid rates in patients already on vsopressors?

Of course not. But show me a study that does.

 

[jdh71]

Of course not. But show me a study that does.

I can’t and . . . you can’t. And to suggest your studies that support a position when that position wasnt studied means that you are waist deep in the weeds like everyone else.

So.

Don’t pretend you’re not. Your amio and esmolol suggestion aren’t a “better” suggestion. They are just *your* suggestion.

 

[deleted547339]

I can’t and . . . you can’t. And to suggest your studies that support a position when that position wasnt studied means that you are waist deep in the weeds like everyone else.

So.

Don’t pretend you’re not. Your amio and esmolol suggestion aren’t a “better” suggestion. They are just *your* suggestion.

I respectfully disagree. I think we’re obligated to use the best data we have when possible. Sometimes that means finding the closest study and extrapolating to a different patient population.

 

[jdh71]

I respectfully disagree. I think we’re obligated to use the best data we have when possible. Sometimes that means finding the closest study and extrapolating to a different patient population.

extrapolation is bull**** here

and you are only fooling yourself to think otherwise

your studies aren’t looking at what you are trying to give advice on “best choice”

quit digging your hole and lay down the shovel

you have an anecdotal or dogmatic bias you are trying to pass off here as the best way to do something - you should feel bad, that you double down isn’t saying anything good here

 

[deleted547339]

extrapolation is bull**** here

and you are only fooling yourself to think otherwise

your studies aren’t looking at what you are trying to give advice on “best choice”

quit digging your hole and lay down the shovel

you have an anecdotal or dogmatic bias you are trying to pass off here as the best way to do something - you should feel bad, that you double down isn’t saying anything good here

Keeping it classy, jdh

 

[jdh71]

Keeping it classy, jdh

always

happy new year

 

[vector2]

Barring the literature about the subject, as a cardiac anesthesiologist and intensivist who has pushed and dripped in BB, CCB, NE, and PE on dozens if not hundreds of patients, my go to for immediate stabilization of mentating hypotensive afib is a large push of phenylephrine (3-5 mcg/kg) chased with 0.5 mg/kg of esmolol. Gauge effect of beta blocker and repeat with scheduled metop if effective. I usually will load amio at this point as well if no contraindication. Can place on low dose vaso drip with BB/amio treatment if persistent multifactorial hypotension continues once rate control achieved.

To continue with my anecdotal experience, BB are usually (60-80% of the time) worthless in achieving rate control for ICU afib. I've found CCB are much more effective but cause much more hypotension than equivalent BB dosing. Phenylephrine or vaso push + Verapamil 2.5 mg IV q5m x 2 doses is extraordinarily effective at achieving hemodynamically stable rate control. Once achieved, dilt gtt +- amio gtt +- pressor gtt.

For ICU afib in pts with decreased EF, decreased inotropy is very, very rarely a contributing problem with regard to their hypotension unless we're talking about some massively dilated cardiomyopathy with EF 10% who has concomitant RVR. Most of these typical HFrEF folks have significant diastolic heart failure as well, and their diastolic filling (and thus stroke volume) has gone to sht in RVR, same as someone with a relatively normal heart. If anyone has ever TEE'ed one of these pts, you'll typically see a massively dilated LA and an obliterated LV cavity. Ergo, there is no need to favor NE if one needs to start a pressor, although I wouldn't necessarily avoid it either. As far as rate control for them, I stick to the recs and avoid CCB in HFrEF. Many times I'll give a token dose of BB (assuming non-decompensated HF) and go straight to amio. If still poor control after amio load x 2 (300mg), 250 mcg of dig followed by a load is reasonable, although I don't find it particularly effective for acute control.

 

[MoMoGesiologist]

Barring the literature about the subject, as a cardiac anesthesiologist and intensivist who has pushed and dripped in BB, CCB, NE, and PE on dozens if not hundreds of patients, my go to for immediate stabilization of mentating hypotensive afib is a large push of phenylephrine (3-5 mcg/kg) chased with 0.5 mg/kg of esmolol. Gauge effect of beta blocker and repeat with scheduled metop if effective. I usually will load amio at this point as well if no contraindication. Can place on low dose vaso drip with BB/amio treatment if persistent multifactorial hypotension continues once rate control achieved.

To continue with my anecdotal experience, BB are usually (60-80% of the time) worthless in achieving rate control for ICU afib. I've found CCB are much more effective but cause much more hypotension than equivalent BB dosing. Phenylephrine or vaso push + Verapamil 2.5 mg IV q5m x 2 doses is extraordinarily effective at achieving hemodynamically stable rate control. Once achieved, dilt gtt +- amio gtt +- pressor gtt.

For ICU afib in pts with decreased EF, decreased inotropy is very, very rarely a contributing problem with regard to their hypotension unless we're talking about some massively dilated cardiomyopathy with EF 10% who has concomitant RVR. Most of these typical HFrEF folks have significant diastolic heart failure as well, and their diastolic filling (and thus stroke volume) has gone to sht in RVR, same as someone with a relatively normal heart. If anyone has ever TEE'ed one of these pts, you'll typically see a massively dilated LA and an obliterated LV cavity. Ergo, there is no need to favor NE if one needs to start a pressor, although I wouldn't necessarily avoid it either. As far as rate control for them, I stick to the recs and avoid CCB in HFrEF. Many times I'll give a token dose of BB (assuming non-defompensated HF) and go straight to amio. If still poor control after amio load x 2 (300mg), 250 mcg of dig followed by a load is reasonable, although I don't find it particularly effective for acute control.

You bolus verapamil and not dilt? Haven’t used before. You find verapamil more efficacious vs dilt for rate control?

 

[vector2]

You bolus verapamil and not dilt? Haven’t used before. You find verapamil more efficacious vs dilt for rate control?

Again, not really evidenced based, but using verapamil is something I picked up from my CCM attendings. In post-OP cardiac surgery with new onset afib, many of these pts would not only get rate controlled but actually convert after a verapamil bolus.

 

[MoMoGesiologist]

Again, not really evidenced based, but using verapamil is something I picked up from my CCM attendings. In post-OP cardiac surgery with new onset afib, many of these pts would not only get rate controlled but actually convert after a verapamil bolus.

How about postop non cardiac surgery or medicine crit care pts?

 

[vector2]

How about postop non cardiac surgery or medicine crit care pts?

Verap is 40-50% effective imo for conversion in all-comers with new onset afib. Rhythm control literature with verapamil is sparse, though- mostly small studies from the 80s.

 

[drmwvr]

Don't people give fluid anymore? How fast are we talking about here?

 

[ShockIndex]

Verap is 50% effective imo for conversion in all-comers with new onset afib. Rhythm control literature with verapamil is sparse, though- mostly small studies from the 80s.

I’ve always had the impression that verap and dilt were roughly equivalent at rate control in a-fib / a-flutter, with a possible slight edge to verap at conversion to NSR. However, verap had more peripheral vasodilation leading to a higher incidence of hypotension. This has lead some to give calcium with verap to attenuate the peripheral calcium blockade.

Personally, I’ve never worked at a place where verap was part of the culture. It has always been either dilt, esmolol, or amio with an emphasis on the latter. A lot of the cardiologists like mixing neo or vasopressin with one of the previously mention agents when blood pressure is an issue and cardioversion isn’t working or in the deck of cards.