Diltiazem vs Esmolol

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ethilo

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I've been bothered by this one for a while: rapid response called for patient with new onset pulmonary edema and AFRVR with stable blood pressure, so plan to rate control them, choice being dilt vs BB.

I've been warned in my residency by critical care docs of the "dilt death challenge" where administration of diltiazem actually hurts the patient in this scenario. However, in my own digging through papers the ED literature prefers diltiazem, actually.

The exact scenario I had: I was in PACU when I got called over to help an RN with some sick old guy with an old sternotomy scar on his chest s/p ERCP. Had new 10L facemask requirement satting 93% and fast HR with BP 130/80. Altered mental status pulling, at O2 mask needing restraints, looks like he is having impending respiratory failure but still maintaining sats at this time. CXR demonstrated pulmonary edema, EKG = AFRVR without STEMI. Prior EKG just AF no RVR.

What to do

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What to do
None of the above?

Seriously the guy's problem is pulmonary edema and possible sepsis vs pain post ercp: not really a scenario for dilt (which i've never seen work) vs esmolol which is equally unuseful in this scenario.
 
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Not really an answer to your question, but I have used esmolol more times than I can imagine, as it is in my cart. Dilt just on rare occasion. So its generally my go to for rate control or for svt. I find esmolol with a nice slug of neo really does the trick for both rate and pressure. Temporarily, of course.
 
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Shock him. He's unstable. I totally love shocking patients.
Alternatively, you could push some metoprolol 5 at a time since his B/P is stable.
 
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I like dilt because you can bolus, then drip, then to po. I think metop is good too for rvr but prefer to avoid when they're having respiratory issues even though they are beta1. 5 mg at a time for either one x3 then dilt or esmolol drip. But like others said, get the underlying etiology under control. Postop afib is pretty common and seems like our sicus like to amio load then transition to po when tolerating. I prefer dig because I like the contractility but sucks if they want to put him on warfarin or other medications it interacts with

Guys probably having ards from pancreatitis vs sepsis (ascending cholangitis, cholecystitis) and sympathetic excess from the inflammatory reaction likely led to afib

Pads on (probably need shock since hes altered = unstable), high flow nasal cannula (prefer to avoid intubation if possible since this guy is probably a gomer with a million problems and will be very difficult to extubate), a line, call critical care and transfer to micu. Start antibiotics as well imo, zosyn vs cefepime +/- vanc
 
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What to do

DDx: Post op delirium vs delirium 2/2 infection vs delirium 2/2 hypoperfuion vs others.

What to do depends on your workup of the DDx. Or did i miss an assumed diagnosis? we aren't even given enough information about what this guy's baseline was. What if he's always been in A fib and youre hanging your hat on that but he's actually developing something else?
 
My preference is
1. Metoprolol 5 mg IV, then 25 P.O. if responding and additional IV blouses if needed
2. Dilt 10 mg IV, then gtt if responding.
3. Amio gtt if hypotension from above

Shock if unstable, which the altered mental status if new suggests he is. He likely will do better in SR. Probably has diastolic dysfunction since he’s ancient, so you need to slow his rate way down and get him back to SR to help the heart failure. Workup for underlying cause, cardiology needs to be called anyway, since his CHADSVASC will be one million.
 
Shock him. He's unstable. I totally love shocking patients.
Alternatively, you could push some metoprolol 5 at a time since his B/P is stable.

The bp is 130/80. He is having some pulmonary edema but I wouldn't shock him.

5 of metoprolol is a lot to push at once on an old sick guy.
 
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My preference is
1. Metoprolol 5 mg IV, then 25 P.O. if responding and additional IV blouses if needed
2. Dilt 10 mg IV, then gtt if responding.
3. Amio gtt if hypotension from above

Shock if unstable, which the altered mental status if new suggests he is. He likely will do better in SR. Probably has diastolic dysfunction since he’s ancient, so you need to slow his rate way down and get him back to SR to help the heart failure. Workup for underlying cause, cardiology needs to be called anyway, since his CHADSVASC will be one million.

what is the mechanism of AF RVR causing AMS in setting of normal BP?
Shocking him will make him AAOx3 in setting of normal BP?
 
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what is the mechanism of AF RVR causing AMS in setting of normal BP?
Shocking him will make him AAOx3 in setting of normal BP?

Altered mental status suggests cerebral hypoperfusion. Blood pressure is a surrogate for perfusion, having normal numbers does not mean normal blood flow to vital organs. We push neo for hypotension all the time but does it really improve perfusion in the microcirculation (what we really care about)? probably not and it's likely detrimental but we do it anyway.
 
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Altered mental status suggests cerebral hypoperfusion. Blood pressure is a surrogate for perfusion, having normal numbers does not mean normal blood flow to vital organs. We push neo for hypotension all the time but does it really improve perfusion in the microcirculation (what we really care about)? probably not and it's likely detrimental but we do it anyway.

yes but in setting of new a fib with rvr and AMS, what is the mechanism of A fib w rvr in setting of stable Bp causing cerebral hypoperfusion? it shouldn't be O2 since it's 93%, co2??
 
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Probably a combination of lots of cytokines from inflammation, encephalopathy from sepsis, tachycardia, decreased o2 in combination.
 
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yes but in setting of new a fib with rvr and AMS, what is the mechanism of A fib w rvr in setting of stable Bp causing cerebral hypoperfusion? it shouldn't be O2 since it's 93%, co2??

Good point, just reread the original post, I agree the AMS is unlikely from hypotension. But he is acutely SOB, so I would probably still consider him unstable.
 
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what is the mechanism of AF RVR causing AMS in setting of normal BP?
Shocking him will make him AAOx3 in setting of normal BP?
Probably won’t make him AAOx3, but will most likely make him much better. Probably significantly help his SOB.
 
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If he's an old guy, are you sure his AF is new onset? Might not want to shock someone with potential paroxysmal AF 2/2 risk of emboli stroke. Really doesn't sound like the AF is the issue if his BP is 130/80 (of course compare with baseline).

Regarding dilt, it's been studied and it increases risk of cardiac events long term in patients with reduced EF and those with pulmonary congestion, which maybe why some people don't like it. Maybe for short term use it's fine.
-The effect of diltiazem on mortality and reinfarction after myocardial infarction. The Multicenter Diltiazem Postinfarction Trial Research Group. N Engl J Med. 1988;319:385–92.

From the packet insert for dilt: https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/020062s040lbl.pdf
"CONTRAINDICATIONS: [...] patients with acute myocardial infarction and pulmonary congestion documented by x-ray on admission."

Do you have an old echo? If he has a sternotomy scar, maybe he has cardiac history of ischemia or valvular disease. Careful with giving dilt or BB to someone who may be in acute heart failure, which it sounds like this person may have (vs plain old volume overload), as you may make it worse with negative inotropes. Consider bipap, diuretic. If you really think AF is precipitating it, try dig load or amio. I also think the esmolol phenyl combo is great.
 
Really? Bipap in a old guy with questionable mental status from his afib with rvr and you don't want to use beta blockers or cc blocker? Yeah it might be heart failure but unlikely in a guy who is probably vasodilated from his pancreatitis/cholangitis. This guy is already at increased risk of cardiac events and mortality as it is.
 
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If he's an old guy, are you sure his AF is new onset? Might not want to shock someone with potential paroxysmal AF 2/2 risk of emboli stroke. Really doesn't sound like the AF is the issue if his BP is 130/80 (of course compare with baseline).

Regarding dilt, it's been studied and it increases risk of cardiac events long term in patients with reduced EF and those with pulmonary congestion, which maybe why some people don't like it. Maybe for short term use it's fine.
-The effect of diltiazem on mortality and reinfarction after myocardial infarction. The Multicenter Diltiazem Postinfarction Trial Research Group. N Engl J Med. 1988;319:385–92.

From the packet insert for dilt: https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/020062s040lbl.pdf
"CONTRAINDICATIONS: [...] patients with acute myocardial infarction and pulmonary congestion documented by x-ray on admission."

Do you have an old echo? If he has a sternotomy scar, maybe he has cardiac history of ischemia or valvular disease. Careful with giving dilt or BB to someone who may be in acute heart failure, which it sounds like this person may have (vs plain old volume overload), as you may make it worse with negative inotropes. Consider bipap, diuretic. If you really think AF is precipitating it, try dig load or amio. I also think the esmolol phenyl combo is great.

I agree you never want to convert someone with like chronic AF, which makes cardioversion and amio gtt less desirable in general.

In terms of negative ionotropes, beta blockers and CCBs are both negative ionotropes, both can cause hypotension, both contraindicated in decompensated heart failure. I would not be concerned about increased cardiac events with dilt. I would be concerned about increased cardiac events in someone left very tachycardia for a long time.

Digoxin load someone mentioned above is going to take a while to work, if it even does anything.
 
Really? Bipap in a old guy with questionable mental status from his afib with rvr and you don't want to use beta blockers or cc blocker? Yeah it might be heart failure but unlikely in a guy who is probably vasodilated from his pancreatitis/cholangitis. This guy is already at increased risk of cardiac events and mortality as it is.

Agreed that bipap with encephalopathy isn't ideal, but if it helps the desats while diuretics kick in, you can avoid intubation. Bipap is great for CHF and volume overload.

I didn't say not to use CCB or BB, just be careful. Why would heart failure be unlikely in someone with arrhythmia and pulmonary edema and elderly with probable cardiac history? Agreed that pt could have post ERCP SIRS type response.

Agreed dig isn't a first line option, but it does exist and good option for heart failure.
 
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Agreed that bipap with encephalopathy isn't ideal, but if it helps the desats while diuretics kick in, you can avoid intubation. Bipap is great for CHF and volume overload.

I didn't say not to use CCB or BB, just be careful. Why would heart failure be unlikely in someone with arrhythmia and pulmonary edema and elderly with probable cardiac history? Agreed that pt could have post ERCP SIRS type response.

Agreed dig isn't a first line option, but it does exist and good option for heart failure.

did you become an attending? i swear your status said resident not long ago
 
Crit care. Thought about cardiac, some regret now that I'm job hunting and see how marketable cardiac is and not marketable ICU is
 
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This can be a difficult case, even for those of us trained for these type of patients.
This case is especially difficult because we don't have enough information.
The OP says a prior EKG showed rate-controlled Afib. Was that EKG from long ago? Was the patient in Afib upon arrival and through the case? Or was he in sinus or intermittently in Afib?
When did the RVR start? Was it abrupt, in PACU? Or was the rate slowly increasing during the whole case?
What's the volume status? Was he completely stable and then just tipped over in the PACU or has this been brewing for a long time?
What was the indication for the ERCP?
etc etc.
Each of these answers changes manangement significantly.

That said, answers involving "just call cardiology" or "CHADS scores" are just wrong.

HH
 
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I'm surprised nobody's mentioned Mag. Good evidence in the perioperative setting, almost no downside. Plus there's the LOMAGHI trial published this year.

Mag.
Ketamine till he co-operates.
CPAP.
Esmolol.
Dig load.
+/- GTN.
Bedside TTE.

But definitely esmolol over dilt. Just turn it off if you run into trouble.

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.
 
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Shocking permenant or persistent AF doesn't really work. And I'd be hesitant to do it without a TEE or some information about his anti-coagulation. Amiodarone runs into the same trouble with chemical cardioversion.
 
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Careful administration of precedex could be helpful in this situation. He's probably air hungry vs post-op delirium (cerebral perfusion is adequate w/ BP 130), both of which may be helped w/ precedex. Pts with enough pulm edema to be satting 93 on 10L can still feel distress due to feeling like they're unable to take adequate breaths. Precedex may make him able to tolerate BiPap while you work on the pulm edema. Side effects include bradycardia, and hypertension in the bolus period - perfect here.

This guy is stable enough for you to go look at his chart (previous echo, how much fluid during procedure, etc.) before giving anything. Rate control with the drug you're most comfortable with - I can't see how it could matter which drug you pick, as long as you monitor effect and adjust accordingly.
 
The exact scenario I had: I was in PACU when I got called over to help an RN with some sick old guy with an old sternotomy scar on his chest s/p ERCP. Had new 10L facemask requirement satting 93% and fast HR with BP 130/80. Altered mental status pulling, at O2 mask needing restraints, looks like he is having impending respiratory failure but still maintaining sats at this time. CXR demonstrated pulmonary edema, EKG = AFRVR without STEMI. Prior EKG just AF no RVR.

What to do

I would probably deal with the impending respiratory failure first with either CPAP or reintubation and then see what the hemodynamics look like when he isn't altered and freaking out. If he's on a facemask with that low of a sat and altered, his CO2 is probably pretty high.
 
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I would probably deal with the impending respiratory failure first with either CPAP or reintubation and then see what the hemodynamics look like when he isn't altered and freaking out. If he's on a facemask with that low of a sat and altered, his CO2 is probably pretty high.

Wait a minute - you mean you'd fix the Airway and Breathing issues before addressing the Circulation?? What a novel concept. ;):prof:

Personally, I've never seen B-blockers work for controlling AF RVR. I have seen dilt work time and time again. If someone was too unstable for dilt, I'd try a nice slug of phenylephrine first. That being said, it's amazing how the BP improves with dilt once the HR isn't 160 anymore.
 
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I’m EM and CCM. I deal with this regularly, so I can speak to that literature as you addressed in the OP, but that’s a very different issue than postoperative.

The first thing is to assess whether this is a primary cardiac dysrhythmia vs a symptom of another disease (e.g. always in afib but now septic, in pain, etc). There is clear data saying if you treat the afib and it’s a symptom, the patient will do worse/you’ve done harm.

You’re asking the wrong question. The comparator isn’t dilt vs. esmolol. It’s dilt vs. metop. That’s what’s given IV push in the ER and the ICU. No one does esmolol bonuses without drips. The studies comparing the two are both very small and of marginal quality (usually 50-300 pts). The gist of the research shows that metop probably works slightly worse than dilt at some set interval (I think an hour-ish) somewhere on the order of 40-60% vs. 50-65% (pulling those numbers out of my head). Both are poorly efficacious. You see more hypotension with dilt, hence the reticence. Esmolol is so short acting it’s in a different camp. It also can only be administered in a drip, so we try to avoid it in the ER because it means you have to go to the unit. As far as shocking this patient, if they have chronic afib, what’s the point? You’re not going to restore sinus rhythm.

Regarding the bipap in encephalopathy, we do it all the time in the ER and the ICU. You can’t do it on the floor, but it’s fine temporarily in a monitored setting. I have no qualms about putting a patient who flashed on bipap, giving them some nitro and then taking it off 30m later when they perk right up or a hypercarbic COPDer.
 
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I’m EM and CCM. I deal with this regularly, so I can speak to that literature as you addressed in the OP, but that’s a very different issue than postoperative.

The first thing is to assess whether this is a primary cardiac dysrhythmia vs a symptom of another disease (e.g. always in afib but now septic, in pain, etc). There is clear data saying if you treat the afib and it’s a symptom, the patient will do worse/you’ve done harm.

You’re asking the wrong question. The comparator isn’t dilt vs. esmolol. It’s dilt vs. metop. That’s what’s given IV push in the ER and the ICU. No one does esmolol bonuses without drips. The studies comparing the two are both very small and of marginal quality (usually 50-300 pts). The gist of the research shows that metop probably works slightly worse than dilt at some set interval (I think an hour-ish) somewhere on the order of 40-60% vs. 50-65% (pulling those numbers out of my head). Both are poorly efficacious. You see more hypotension with dilt, hence the reticence. Esmolol is so short acting it’s in a different camp. It also can only be administered in a drip, so we try to avoid it in the ER because it means you have to go to the unit. As far as shocking this patient, if they have chronic afib, what’s the point? You’re not going to restore sinus rhythm.

Regarding the bipap in encephalopathy, we do it all the time in the ER and the ICU. You can’t do it on the floor, but it’s fine temporarily in a monitored setting. I have no qualms about putting a patient who flashed on bipap, giving them some nitro and then taking it off 30m later when they perk right up or a hypercarbic COPDer.
I'd say esmolol push is pretty common in the pacu
 
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The first thing is to assess whether this is a primary cardiac dysrhythmia vs a symptom of another disease (e.g. always in afib but now septic, in pain, etc). There is clear data saying if you treat the afib and it’s a symptom, the patient will do worse/you’ve done harm.
.


This
 
I was speaking to the ER and ICU. I’ve never heard of someone doing that in those settings.
I have in the unit as a BB challenge before committing to metoprolol. Can't remember the exact situation, but my attending was concerned about how the pt was going to tolerate beta blockade, I thought they'd do fine. I gave a bolus of esmolol, he tolerated it well, pressure actually improved, HR back up a few minutes later, gave 5mg metoprolol.

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Thats exactly what esmolol is great for. You can be wrong as hell for 10 mins but who cares. instant answer... its great... bolus the **** out of it
 
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Altered mental status suggests cerebral hypoperfusion. Blood pressure is a surrogate for perfusion, having normal numbers does not mean normal blood flow to vital organs. We push neo for hypotension all the time but does it really improve perfusion in the microcirculation (what we really care about)? probably not and it's likely detrimental but we do it anyway.

I disagree with this statement. We push neo for hypotension that we have caused with our anesthetic. It is an alpha receptor stimulant causing contraction of smooth muscles. My understanding is that the amount of smooth muscles exists in a decreasing manor, arteries >arterioles > capillaries and that this creates greater vasoconstriction in the larger vessels and therefore better perfusion.
 
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I was speaking to the ER and ICU. I’ve never heard of someone doing that in those settings.
I appreciate your input (as always) but this isn’t the ER. We use esmolol all the time as others have said. It is a fantastic drug for determining quickly if your assessment and approach is on the right track.
It also seems somewhat short sighted to say that “In the ER we don’t use esmolol because it requires a drip and then they must go to the ICU”. I’d say, do what’s best for the pt then decide what’s next.
 
My perspective is this:
1) determine what is the most pressing issue at this moment. I’d say it’s his AMS. Deal with that first whether it’s respiratory or perfusion. I’m thinking he could use some lasix and CPAP
2) IF he has a history of AF but came to me in sinus I’d give it a go to try to convert him chemically. Personally, I like dilt. I will frequently give 50mg of esmolol push just to see what happens. Plus some neo. If nothing happens then I go to Dilt. assuming he isn’t a CHF pt. If so then I use digoxin. I don’t particularly like to mix longer acting betablockers (metoprolol) and Ca Ch blockers. Risk of AV block.
3) don’t crucify me here but I would also consider a gentle carotid massage in the beginning if he wasn’t a complete vasculopath.
 
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I appreciate your input (as always) but this isn’t the ER. We use esmolol all the time as others have said. It is a fantastic drug for determining quickly if your assessment and approach is on the right track.
It also seems somewhat short sighted to say that “In the ER we don’t use esmolol because it requires a drip and then they must go to the ICU”. I’d say, do what’s best for the pt then decide what’s next.

It’s not that we never do it, it’s just that we do our best to avoid it. And you’re absolutely right, we have to do what’s best for the patient regardless of what’s convenient - the problem is that if you put them on a drip, then they’re committed to needing an icu bed. In the ideal world, you have icu beds, could try a couple IV doses, start a drip, ship them to the icu then let them titrate off/start PO and transfer to the floor. In reality, putting them on a drip in the ER at a lot of places usually means they wait in the for many hours to days and get their work up for afib and management delayed for hours to days - so it’s kind of a catch 22.

The other crappy thing about esmolol is the tachyphylaxis.
 
If the patient is clinically in CHF you need to treat that before attempting to correct the rate, since both beta blockers and Diltiazem will directly reduce the cardiac output.
So maybe some diuretic with an ACE inhibitor or NTG would be a good first step then you can focus on rate control and maybe consider Amiodarone.
 
.
I've been bothered by this one for a while: rapid response called for patient with new onset pulmonary edema and AFRVR with stable blood pressure, so plan to rate control them, choice being dilt vs BB.

I've been warned in my residency by critical care docs of the "dilt death challenge" where administration of diltiazem actually hurts the patient in this scenario. However, in my own digging through papers the ED literature prefers diltiazem, actually.

The exact scenario I had: I was in PACU when I got called over to help an RN with some sick old guy with an old sternotomy scar on his chest s/p ERCP. Had new 10L facemask requirement satting 93% and fast HR with BP 130/80. Altered mental status pulling, at O2 mask needing restraints, looks like he is having impending respiratory failure but still maintaining sats at this time. CXR demonstrated pulmonary edema, EKG = AFRVR without STEMI. Prior EKG just AF no RVR.

What to do
What's so hard?

BiPAP for pulmonary edema, to avoid intubation and fix the dyspnea (he's pulling at the mask because of crazy bad air hunger - he's uncontrolled like a drowning person). The patient is postop, so the chances of aspiration with BiPAP are virtually nil. While that shows up, SIT UP the patient, with his legs DANGLING on the side of the bed (decreases preload big time). In a couple of minutes, you may even fix the "AMS".

Esmolol (OR DILTIAZEM) gtt for the HR which is the real cause of the pulmonary edema. The ED lit prefers diltiazem simply because it works better than esmolol, same as my experience. Amiodarone would work, too, though not my first line. Just make sure that the AFib/RVR is not due to some accessory pathway (all these nodal blockers could kill one of those patients).

Lasix to get rid of extra fluid, if the patient is hypervolemic (enough diuresis to fix the pulmonary edema will take time - plan for it). High dose nitroglycerine gtt to decrease preload (and afterload), and temporize things some more, if needed (also my preference if the patient is hypertensive). Small dose of morphine for air hunger (careful not to sedate the patient).

Critical care is applied (patho)physiology. Understand the latter and you will know how to practice the former.
 
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what is the mechanism of AF RVR causing AMS in setting of normal BP?
Shocking him will make him AAOx3 in setting of normal BP?
The pulmonary edema means acute decompensated diastolic CHF. You could argue that makes him unstable (he may be a hypertensive guy, so that 130/80 may actually mean decreased cardiac output). Cardioversion (after sedation) would be by far the easiest and fastest way to fix his AFib, if new onset. Not a bad idea at all (especially to avoid intubation).
 
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.

What's so hard?

BiPAP for pulmonary edema, to avoid intubation and fix the dyspnea (he's pulling at the mask because of crazy bad air hunger - he's uncontrolled like a drowning person). The patient is postop, so the chances of aspiration with BiPAP are virtually nil. While that shows up, SIT UP the patient, with his legs DANGLING on the side of the bed (decreases preload big time). In a couple of minutes, you may even fix the "AMS".

Esmolol (OR DILTIAZEM) gtt for the HR which is the real cause of the pulmonary edema. The ED lit prefers diltiazem simply because it works better than esmolol, same as my experience. Amiodarone would work, too, though not my first line. Just make sure that the AFib/RVR is not due to some accessory pathway (all these nodal blockers could kill one of those patients).

Lasix to get rid of extra fluid, if the patient is hypervolemic (enough diuresis to fix the pulmonary edema will take time - plan for it). High dose nitroglycerine gtt to decrease preload (and afterload), and temporize things some more, if needed (also my preference if the patient is hypertensive). Small dose of morphine for air hunger (careful not to sedate the patient).

Critical care is applied (patho)physiology. Understand the latter and you will know how to practice the former.

All of this is spot on, but I almost never give morphine. It's associated with worse outcomes in APE as per the EAHFE and ADHERE registries. I also never give it in ACS. This goes double if they have AMS.
 
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