Which IV med is safer and more effective? IV cardizem or IV lopressor? I am not talking about a drip but the initial treatment in ER or on the floor.
Afib with RVR
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deleted547339
Tiny studies, but anecdotally (cringe) it seems to work better.
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For completely stable Afib RVR -- when a little rate control is needed -- and then you are going to walk away -- likely not needeing a drip -- I don't think it matters much if you choose dilt or metop.
I think the more interesting question is when you think a few pushes are going to be needed and a drip is immenent:
Which do you choose: diltiazem or ESMOLOL?
I used esmolol a bit in residency, some more as an attending in the ED, and now am really working on reaching for esmolol EVERY time I would have previously ordered dilt drips.
This isn't true, of course, if the patient has just missed three days of their outpatient CCB and are now in RVR. In that case, I just replace with CCB.
Why do people not use esmolol when a drip is immenent? Especially with oral Bb so commonly used for rate control at baseline (other beneficial effects too).
HH
I think the more interesting question is when you think a few pushes are going to be needed and a drip is immenent:
Which do you choose: diltiazem or ESMOLOL?
I used esmolol a bit in residency, some more as an attending in the ED, and now am really working on reaching for esmolol EVERY time I would have previously ordered dilt drips.
This isn't true, of course, if the patient has just missed three days of their outpatient CCB and are now in RVR. In that case, I just replace with CCB.
Why do people not use esmolol when a drip is immenent? Especially with oral Bb so commonly used for rate control at baseline (other beneficial effects too).
HH
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Lack of familiarity I'm sure.
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Has to do more with floor capabilities when they get admitted. First, you have to be at an institution that has Esmolol which is typically the larger centers. If you are then staffing becomes an issue. ED and ICU nurses have the expertise and time to appropriately titrate an Esmolol gtt. At my institution, Esmolol is not allowed on general and intermediate floors so it is not uncommon for it to be d/c and then switched to a Cardizem gtt since run of the mill A. Fib with RVR frequently doesn't need an ICU.
Same issue with Cleviprex for BP control.
I never realize how great I have it in the ED and ICU until I go back to a general or subspecialty medicine service.
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Second this. Cardizem gtt = tele floor. Esmolol gtt = step down at the hospital that has a step down, ICU for the two hospitals that don't
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If they're in shock and a fib then electricity is better.....
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deleted547339
Dig ain't bad either.
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Never seen it actually work in someone with shock. Increased vagal tone ain't going to overwhelm the amount of catecholamines they have fueling that RVR.
I like amio or electricity.
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deleted547339
Obviously in frank shock I buzz the patient. In hypotensive afib with RVR that looks OK but BP is too low to use b/ca channel blocker, I'll use dig. I've had pretty good success with her but it takes a while.
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You can also try Mag. Give two grams as a 30 second push. You can repeat two more times. Really benign and does work for PAF. Doesn't drop the blood pressure. Awake patients don't like the associated skin flushing and hot flash.
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Dude, you're back. You told your wife, "Pick: JDH71 and SDN, or no JDH71 at all!"
Glad to have you back.
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I wouldn't say I'm back yet. Just I think mag is a strong consideration in hypotensive but not actively dying. Just doing a bit of lerking today.
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For RVR when they get hypotensive, I like the combination of Ca Chloride and Dilt. I don't know why it works. Whenever I order that the pharmacy calls and says it is voodoo, but it works like a damn charm.
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I don't usually add the CaCl with it, but Dilt is also my go-to... minimal peripheral activity as compared to the dihydropyridine CCBs, as well as Lopressor (which, even as B1 selective, still has some B2 activity).
Plus, I always question the hypotension etiology; namely, if due to RVR causing impaired diastolic filling and thus decreased CO, then rate control of any kind ought help. Consequently, using the agent I feel has the least peripheral activity to accomplish this seems prudent.
And, if they continue to crump or are resistant, well, Dr. Edison is always available for a consult. d=)
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per AHA/ACC, BB is preferable to CCB unless there is a specific reason why you don't want BB (severe reactive airway dx, etc)
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because calcium chloride is considered one of the reversal agents to calcium channel blockers.... ????????
if you're dealing with RVR and the patient becomes unstable, you should be thinking about electrical cardioversion
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Amio is nice in pressor-induced arrhythmia as BB is counterproductive. I’ve used dig a couple of times, but never continued it after the arrhythmia broke - good with right sided CHF.
Haven’t tried mag
Haven’t tried mag
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Agree with most of this, except let's say you cardiovert your patient x 3 with permanent afib, and surprise, it doesn't work. Now what? In my experience, afib with severe tachycardia with associated hypotension can be ridiculously difficult to manage in some of these patients. You throw amio at them, and magnesium, and dig, and even consider beta blocking while they're on norepinephrine or other beta agonists, and of course treat the underlying driver of their high adrenergic state, but sometimes nothing works. Sometimes they seem to do okay, othertimes if they have severe diastolic dysfunction or AS, they just can't tolerate it.
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Why are we rate/rhythm controlling most of these compensatory a-fib RVR ICU patients to begin with? I get it if you have evidence of clear diastolic dysfunction, the HR is >160 that isn't improving with fluids, or if you are going 2-3 days of HR>130-140 after the patient has been appropriately tanked up and on appropriate therapy for the reason they are in a-fib w/ RVR. What I don't get is getting the septic a-fibber from the ER with the borderline BP and lactate of 6 and immediately starting them on a diltiazem drip for their HR of 140. I see this daily from individuals outside the ER. The heart rate is compensatory. A-fibbers get their heart rates into the 150s during exercise with similar exercise tolerance to their normal sinus rhythm counterparts. They don't need rate control, they need source control. There was actually an ER study from 2015 in annals of EM demonstrating worse outcomes in individuals receiving rate or rhythm control for secondary causes of a-fib/flutter compared to those who received no therapy for their a-fib. Adverse event rates were 6x higher in the treatment group which matches with my experience. Also, rate and rhythm control obviously works poorly in this group.
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Scheuermeyer FX et al. Emergency Department Patients With Atrial Fibrillation or Flutter and an Acute Underlying MedicalIllness May Not Benefit From Attempts to Control Rate or Rhythm. Ann Emerg Med. 2015 May;65(5):511-522
(If anyone else is looking for it.)
What if the HR is greater than 130-140, say its 180 or 190, don't you think in those patients they are going so fast that poor end diastolic filling is exacerbating their cardiac output and contributing to their hypotension and shock state? I agree with you in a patient with permanent AF who is in septic shock some of their AF with RVR and a HR in the 130s is basically the patient's version of compensatory tachycardia. However a rate above 130-140 probably needs to be controlled.
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Your question was already addressed in my post
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Here is a thought: If the patient was on a BB before admission, try restarting the BB, and bridge with esmolol-- Beta Blocker withdrawal is a really entity?!?!
Sure but what if the pt has soft blood pressure or is frankly in shock and cardioversion is unsuccessful (patient has been in permanent AF since forever)? What is your weapon of choice? Amio? Dig? BB or CCB anyways hoping that lowering rate might improve pressure? Pressor + some combination of the above? I feel like years ago when I was a resident in the CVICU I would see the intensevists use Levophed + amio or Levophed + cardizem; but this always seemed like a contradicting pattern of pharmacy.
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Why is amio with levophed conflicting in pharmacology? BB with levo sure
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Even though it’s classified as a potassium channel blocker on the Vaughan Williams system it actually causes sodium, beta, potassium, and calcium channel blockade. At least I think that’s what the concern was in the previous post? Still seems as though it’s other effects would be useful?
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deleted171991
Phenylephrine gtt titrated to effect. Increase in MAP with reflex decrease in HR. Or phenylephrine with your favorite rate control drug. Both can be given peripherally. Nice and easy.
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deleted547339
Levo and B.B. isn’t contradictory. Epi and B.B. is.
If you give mostly alpha with levo and mostly anti-beta with B.B. that makes perfect sense. I probably wouldn’t give levo and metop, but levo and esmolol is reasonable. Also just using neo for some (potential) reflex bradycardia is reasonable.
And yes, most people forget that Amio has mild, but not entirely insignificant beta blocking effect.
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deleted171991
Levo plus beta-blocker (beta1 selective or not) = alpha-agonist, i.e. phenylephrine. 
Epi plus cardioselective beta-blocker = alpha-agonist plus beta-2 agonist. "Interesting" combo, especially as a pressor.
Epi plus nonselective beta-blocker = alpha agonist.
If levo and esmolol are "reasonable", levo and metoprolol = levo plus long-acting esmolol (i.e. esmolol gtt). Metoprolol and esmolol act on the same beta-1 receptors.
One should watch the oxygen demand and supply of the heart (i.e. HR, SV, MAP, DBP - nota bene the LV is perfused only in diastole). If all those are fine, the patient will be fine. When patients get hurt, it's many times because people sit on a HR of 140-150 with a good MAP (not just in AFib/RVR, but in various tachycardias). There is not much ventricular filling or diastolic coronary perfusion at that heart rate.
Epi plus cardioselective beta-blocker = alpha-agonist plus beta-2 agonist. "Interesting" combo, especially as a pressor.
Epi plus nonselective beta-blocker = alpha agonist.
If levo and esmolol are "reasonable", levo and metoprolol = levo plus long-acting esmolol (i.e. esmolol gtt).
Metoprolol and esmolol act on the same beta-1 receptors.One should watch the oxygen demand and supply of the heart (i.e. HR, SV, MAP, DBP - nota bene the LV is perfused only in diastole). If all those are fine, the patient will be fine. When patients get hurt, it's many times because people sit on a HR of 140-150 with a good MAP (not just in AFib/RVR, but in various tachycardias). There is not much ventricular filling or diastolic coronary perfusion at that heart rate.
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deleted547339
Levo plus beta-blocker (beta1 selective or not) = alpha-agonist, i.e. phenylephrine.
Epi plus cardioselective beta-blocker = alpha-agonist plus beta-2 agonist. "Interesting" combo, especially as a pressor.
Epi plus nonselective beta-blocker = alpha agonist.
If levo and esmolol are "reasonable", levo and metoprolol = levo plus long-acting esmolol (i.e. esmolol gtt).
One should watch the oxygen demand and supply of the heart (i.e. HR, SV, MAP, DBP - nota bene the LV is perfused only in diastole). If all those are fine, the patient will be fine. When patients get hurt, it's many times because people sit on a HR of 140-150 with a good MAP (not just in AFib/RVR, but in various tachycardias). There is not much ventricular filling or diastolic coronary perfusion at that heart rate.
I understand that metop and esmolol are similar, but just because I am willing to trial a med with a short half-life doesn’t mean I’m willing to commit to that for a longer period. If someone tolerates esmolol, sure, I’ll put them on metop.
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857937
I had a patient once who developed A. Fib RVR due to Levophed.
Stopped and started Phenylephrine.
Was about to give Digoxin but the episode resolved once Phenylephrine started in less than 5 minutes.
Stopped and started Phenylephrine.
Was about to give Digoxin but the episode resolved once Phenylephrine started in less than 5 minutes.
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deleted171991
But wait, Phenylephrine is the devil's medicine!
Which brings me to one of my pet peeves: it's just scary how many dumb people are allowed to run ICUs nowadays, even academic ones. I know of a big name academic MICU where one cannot even run a phenylephrine infusion (I assume the nurses and the administrators are too incompetent), not to mention running it peripherally (that's for us in the 21st century, not their archaic medicine).
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D
deleted547339
But wait, Phenylephrine is the devil's medicine!
Which brings me to one of my pet peeves: it's just scary how many dumb people are allowed to run ICUs nowadays, even academic ones. I know of a big name academic MICU where one cannot even run a phenylephrine infusion (I assume the nurses and the administrators are too incompetent), not to mention running it peripherally (that's for us in the 21st century, not their archaic medicine).
Uhhhhhh......what????
