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When do you folks like to give medications to speed up bradycardias?
Are you comfortable with a patient in 40s , but with normal BP or do you give glyco or something to speed it up? What is your reasoning?
I see many different practice styles in this
Too many variables..
Depends on age and comorbid conditions
Depends on blood pressure
Depends on type of surgery and whether you expect vagal responses
That being said, there's nothing wrong with giving a small dose of glyco.
Shouldn't need to think twice or question yourself with a relatively benign action like that.
55 yr old patient in sepsis on norepi and epi infusion for open bowel resection (perf). in the OR, rhythm suddenly went from sinus at 90 to sinus with prolonged pr w rate of 45. however BP improved after this occured and i lowered the vasopressors by 30%.
...and throw a probe in.
For that? I get being penny wise but pound foolish...but there'd be a few loose ends to chase down before that, I'd think...
He said it was sinus. Where did you get the loss of atrial kick from?Well what do you think is the etiology? Could be demand ischemia, takotsubo, dilated cardiomyopathy maybe rv failure or pe stretching the fibers causing conduction abnormalities, sinus node problems, inadvertent bblocker administration, electrolyte abnormality etc. I wold give some atropine to temporize, get a gas and throw a probe in. I think that losing the atrial kick isn't fantastic for your cardiac output even if the bp is higher.
Also no need to be penny wise but pound foolish. Neo is maybe 60 dollars depending on where you are and each glyco 0.2 is around 10 but I never consider that when I am taking care of patients.
He said it was sinus. Where did you get the loss of atrial kick from?
To me it shows that there was not enough trike for filling with such a fast HR. Older stiffer hearts need more filling time and slower HRs. That’s probably why this BP improved.
Same thing typing and autocorrecting to “trike” instead of time.From reading on my phone from while being distracted heh
I give it if they are concurrently hypotensive. That’s my most common reason to give it.When do you folks like to give medications to speed up bradycardias?
Are you comfortable with a patient in 40s , but with normal BP or do you give glyco or something to speed it up? What is your reasoning?
I see many different practice styles in this
Well what do you think is the etiology? Could be demand ischemia, takotsubo, dilated cardiomyopathy maybe rv failure or pe stretching the fibers causing conduction abnormalities, sinus node problems, inadvertent bblocker administration, electrolyte abnormality etc. I wold give some atropine to temporize, get a gas and throw a probe in. I think that losing the atrial kick isn't fantastic for your cardiac output even if the bp is higher.
Also no need to be penny wise but pound foolish. Neo is maybe 60 dollars depending on where you are and each glyco 0.2 is around 10 but I never consider that when I am taking care of patients.
He said it was sinus. Where did you get the loss of atrial kick from?
To me it shows that there was not enough trike for filling with such a fast HR. Older stiffer hearts need more filling time and slower HRs. That’s probably why this BP improved.
Diastolic dysfunction is what I was trying to get at in my earlier reply.i was a bit impressed with how much his BP improved with bradycardia. hes only 55, and TTE done 2 days ago was fairly unremarkable, most significant for ef of 45%
Why did another Anesthesiolgist come into your room? To give you a lunch break?isnt it like 40 bucks for glyco?
anyway just curious what people are thinking in those circumstances.
recently had a case of 55 yr old patient in sepsis on norepi and epi infusion for open bowel resection (perf). in the OR, rhythm suddenly went from sinus at 90 to sinus with prolonged pr w rate of 45. however BP improved after this occured and i lowered the vasopressors by 30%. another anesthesiologist came in and was very concerned w a HR of 40s and felt strongly about atropine. so that got me thinking
Maybe sepsis induced sick sinus syndrome?
I’m a little more liberal with glyco if I’m using a non-invasive cuff since I’m waiting relatively longer to see if BP is holding up.
But if I have an art line (which I assume you do in this patient) and HR is 40, BP is stable, I’m not really “fixing” anything by making the heart beat faster. If anything it’s just creating more demand and more oxygen consumption in an already stressed CV system.
Diastolic dysfunction is what I was trying to get at in my earlier reply.
A lot middle aged people have it in this country because of obesity and HTN.
Why did another Anesthesiolgist come into your room? To give you a lunch break?
And what did you do? So what if he has 1st degree AVB? Since when was that something cardiologists placed a pacemaker for?Yes, mild DD per TTE
No just to see if needed help since it was an emergency case
His reasoning of giving atropine is bc there is sinus brady now but PR is prolonged, so 1st av block, giving atropine would reduce PR interval.
isnt it like 40 bucks for glyco?
anyway just curious what people are thinking in those circumstances.
recently had a case of 55 yr old patient in sepsis on norepi and epi infusion for open bowel resection (perf). in the OR, rhythm suddenly went from sinus at 90 to sinus with prolonged pr w rate of 45. however BP improved after this occured and i lowered the vasopressors by 30%. another anesthesiologist came in and was very concerned w a HR of 40s and felt strongly about atropine. so that got me thinking
Any chance someone pushed through the norepi line or gave a bunch of neo? Might explain a sudden increase in BP w/ reflex brady.
And what did you do? So what if he has 1st degree AVB? Since when was that something cardiologists placed a pacemaker for?
Hope you said, Thank you, but I am good.
There have been papers showing that in Sepsis, sometimes giving b blockers concurrently with the pressors to slow the HR down and increase filling time is helpful. Sometimes the compensatory HR can be too high to help the matter. Doesn’t sound like this was your case as we are only talking two pressors. And he slowed down on his own. So unless he continues to deteriorate with that slower rate, I would thank my lucky stars. Maybe them taking out the offending agent dit it? Usually doesn’t happen that quickly though.
What’s his baseline EKG when not septic?
Yes. If you apparently don’t give a minimum dose of 0.5mg or something.i believe sinus w bundle branch. i refused the speed up.
arent there also potential for paradoxical effects from atropine
Yes. If you apparently don’t give a minimum dose of 0.5mg or something.
I have never honestly given atropine anyway outside of when we were short on neostigmine and had to use physo? pyrido? And once or twice in a code. Because I was always taught that it messes with people’s heads. Just use glyco if needed. Since you almost always have to use it for reversal anyway.
Very well could be. Never seen it.Paradoxical bradycardia from atropine is a myth.
Paradoxical bradycardia from atropine is a myth.
Kids who got bradycardic from hypoxia secondary to airway mismanagement.where did this mythical creature come from?
Our supplier sells for $0.99 per 200mcg vialisnt it like 40 bucks for glyco
isnt it like 40 bucks for glyco?
anyway just curious what people are thinking in those circumstances.
recently had a case of 55 yr old patient in sepsis on norepi and epi infusion for open bowel resection (perf). in the OR, rhythm suddenly went from sinus at 90 to sinus with prolonged pr w rate of 45. however BP improved after this occured and i lowered the vasopressors by 30%. another anesthesiologist came in and was very concerned w a HR of 40s and felt strongly about atropine. so that got me thinking
This should show you that there are situations where NEO is a better pressor than LEVO.
Most patients requiring pressor support are going to be tachy to begin with. Neo attenuates this HR response and gives more time for filling, less strain on the heart. Still tachy, but not severely tachy. But for some reason the surgical intensivists will ALWAYS change in back to levo after the case and struggle, then add vasporession, ugh...
In general I give glyco when HR is low 40s in a patient with no reason for that, targetting a HR of 60s
But what do they charge the patient? I bet something ridiculous.Our supplier sells for $0.99 per 200mcg vial
Depends on the patients cardiomyopathy. If their EF is low then a straight alpha agonist is not going to help the situation. Now in addition to another hand I agree with.This should show you that there are situations where NEO is a better pressor than LEVO.
Most patients requiring pressor support are going to be tachy to begin with. Neo attenuates this HR response and gives more time for filling, less strain on the heart. Still tachy, but not severely tachy. But for some reason the surgical intensivists will ALWAYS change in back to levo after the case and struggle, then add vasporession, ugh...
In general I give glyco when HR is low 40s in a patient with no reason for that, targetting a HR of 60s
Paradoxical bradycardia from atropine is a myth.
so you would give glyco w HR in 40s even if BP is elevated? say 160s, to bring it to ~60
this entire time i thought you meant neostigmine when you say neo, but im guessing you mean phenylephrine?
other than cost, you prefer phenylephrine over vasopressin?
Depends on the patients cardiomyopathy. If their EF is low then a straight alpha agonist is not going to help the situation. Now in addition to another hand I agree with.
Septic cardiomyopathy is common enough.
If I have someone under 1 MAC of anesthesia with SBP 160s and a HR of 40, they are getting hydralazine or a nitroglycerin like medication, to achieve both the goals of lowering the SBP and increasing HR.. This combo of HTN and bradycardia could mean an intracranial injury
If this particular septic person has a SBP of 160s, my first move would be to turn down the levophed. On a good amount of levo and still HR 40 I would have in the back of my mind this could be heart block and we may need to pace, rare but its a thought in my mind
You must be facile at controlling any and all hemodynamic parameters...between Beta blockers, Nitrates, Phenylephrine, glyco, Ephedrine, levophed/epi - you should be able to make anyones numbers anything you want.
I rarely use vasopressin (only when extreme doses of neo/epi not going the job which is very very rare)
What hemodynamics do I want for a septic person?
I want MAP 50-60. I want HR 90-130. I want Fio2 as high as it can be and HCT > 25 at least.
At some point the HR of 140+ is counterproductive. I see people with rapid AF on levo from the ICU all the time, switch it over to neo for instantly better rate control and still able to maintain good MAPs
If I have someone under 1 MAC of anesthesia with SBP 160s and a HR of 40, they are getting hydralazine or a nitroglycerin like medication, to achieve both the goals of lowering the SBP and increasing HR.. This combo of HTN and bradycardia could mean an intracranial injury
If this particular septic person has a SBP of 160s, my first move would be to turn down the levophed. On a good amount of levo and still HR 40 I would have in the back of my mind this could be heart block and we may need to pace, rare but its a thought in my mind
You must be facile at controlling any and all hemodynamic parameters...between Beta blockers, Nitrates, Phenylephrine, glyco, Ephedrine, levophed/epi - you should be able to make anyones numbers anything you want.
I rarely use vasopressin (only when extreme doses of neo/epi not going the job which is very very rare)
What hemodynamics do I want for a septic person?
I want MAP 50-60. I want HR 90-130. I want Fio2 as high as it can be and HCT > 25 at least.
At some point the HR of 140+ is counterproductive. I see people with rapid AF on levo from the ICU all the time, switch it over to neo for instantly better rate control and still able to maintain good MAPs
This is the thinking of the surgeon/intensivist. This is the book answer. Well its an alpha agonist so its not going to help contractility.. but it actually does increase CO since it increases venous return which increases contractility. The bradycardic (relative to levo/epi) effect give more time between beats meaning more preload and more SV, also less likely to exacerbate tachyarrythmias - I love neo
Sinus Brady in the 40s with normal BP, I'm definitely not touching that. Even if there's a 1st degree AV block, that's not an indication for pacing, chemically or electrically if the patient remains HD stable. You tell me the patient has severe MR? SURE, I'll speed him up. But that's obviously not the prompt you gave us.When do you folks like to give medications to speed up bradycardias?
Are you comfortable with a patient in 40s , but with normal BP or do you give glyco or something to speed it up? What is your reasoning?
I see many different practice styles in this
Intracranial injury and cushings reflex... probably not good idea to use a cerebral vasodilator? 😱😱
I want MAP 50-60. I want HR 90-130. I want Fio2 as high as it can be and HCT > 25 at least
EP here.... from my standpoint only reason to treat this relative bradycardia is if there's any associated hypoperfusion. If not then leave alone.
You shouldn't need to do anything right? I mean not immediately. As long as vital signs are stable. Eventually, pacer is needed for mobitz type 2 or complete heart block I think.What would you do in this patient if it's mobitz heart block? Or even complete heart block, if the rate is 40 but sbp us maintained at 140, other than maybe throw pads on.. patient already has Levi and epi infusion going. Would you give atropine?
What would you do in this patient if it's mobitz heart block? Or even complete heart block, if the rate is 40 but sbp us maintained at 140, other than maybe throw pads on.. patient already has Levi and epi infusion going. Would you give atropine?
I’ll first mention what i would do if seeing that consult as it may differ from what you may do as far as intra-op management. If seeing a consult for 3rd degree AV block (or even significant 2nd set type II) if they are tolerating it well then I wouldn’t do anything acutely. Most of these will likely end up getting a pacemaker that stay, either later that day or the next day. Would prob throw some pads on in case but wouldn’t do anything differently.
As far as intra-op management if they are tolerating it well then could certainly watch it and just be ready to treat (atropine, pacing either transcutaneously or ready to throw in TVP, or maybe isuprel if sinus Brady). If this is pre-op and someone going into procedure where you may expect some vagal episodes or they previously did not tolerate the heart block then could consider a prophylactic TVP to get them through. Had one a few weeks ago like that. Some wrecked their motorcycle and was having periods of complete AV block and underlying LBBB in trauma bay associated to BP drops. Met them in OR and out in a quick TVP for the surgery.
You shouldn't need to do anything right? I mean not immediately. As long as vital signs are stable. Eventually, pacer is needed for mobitz type 2 or complete heart block I think.
From statpearls: Treatments for bradydysrhythmias are indicated when there is a structural disease of the infra-nodal system or if the heart rate is less than 50 beats/min with unstable vital signs.
This is true only to the extent that preload is insufficient. You squeeze those vessels with your neo, increase your preload and allow for a more optimal spot on the frank starling curve. You could of course give more fluids if that was your concern? This is also a very specific situation you describe. In many other situations it does make sense to use isotopes. When your EF is crap (or you have regurgitant lesions) pushing against a lot of afterload isn't a great way to go about it.
I like a lot of what you’re saying, but MAP of 50 is just too low. The literature shows 60-65 is about as low as you want to go. Maybe higher if baseline is relatively hypertensive. Dipping into the 50s means at the very least the kidneys are taking a hit, maybe the brain, liver and heart as well. The only exception would be the patient who lives with a systolic in the 90s pre-illness, they’ll probably tolerate a little less. Also no evidence that I’m aware of for crit > 21, unless patient has some sort of ACS going on as well.
Would love to hear your reasoning for the above and/or any evidence you have to support it. Not trying to be argumentative, just trying to learn.