Bradycardia discussion

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anbuitachi

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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

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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.
 
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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.

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
 
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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.
 
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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...
 
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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...

That's true, I was just brainstorming. It's not like I'm doing a comprehensive exam on every other bradycardia.
 
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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.
 
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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.

From reading on my phone from while being distracted heh
 
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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
I give it if they are concurrently hypotensive. That’s my most common reason to give it.
Other times is if I expect it to get lower with surgical manipulation.
 
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throw a probe in... we have no probes, and i think most hospitals dont have probes..
i didnt give anything since patient was already on epi infusion and BP improved with the slower HR.

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.

temporize the heart rate?
 
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.

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%
 
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.
 
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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%
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.
 
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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
Why did another Anesthesiolgist come into your room? To give you a lunch break?
 
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.

Yes there was an arterial line, so i just watched it. I also think its sepsis induced , he's also acidotic due to septic shock
 
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.

Yes, mild DD per TTE

Why did another Anesthesiolgist come into your room? To give you a lunch break?

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.
 
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.
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?
 
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Lance Armstrong at 40bpm - fine, and no glyco.

Vasculopath on only an ACE (no BB) and HR in 40 with no P waves - consult cardiology preop or speed it up intraop.
 
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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.
 
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Any chance someone pushed through the norepi line or gave a bunch of neo? Might explain a sudden increase in BP w/ reflex brady.

nor epi was going thru central line and the line ports were capped so highly doubt it. also he lasted in that state for rest of the case
 
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?

i believe sinus w bundle branch. i refused the speed up.
arent there also potential for paradoxical effects from atropine
 
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.
 
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.

Paradoxical bradycardia from atropine is a myth.
 
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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
 
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

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?
 
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
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.
 
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EP here.... from my standpoint only reason to treat this relative bradycardia is if there's any associated hypoperfusion. If not then leave alone.
 
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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?


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
 
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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.

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
 
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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

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.
 
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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

Intracranial injury and cushings reflex... probably not good idea to use a cerebral vasodilator? :eek::eek:
 
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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

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.
 
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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
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.
 
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Intracranial injury and cushings reflex... probably not good idea to use a cerebral vasodilator? :eek::eek:

I was thinking the same thing as soon as I saw this....Cushing’s hypertension would be a compensatory response to perfuse the brain if there is increased ICP so vasodilator could be detrimental
 
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I want MAP 50-60. I want HR 90-130. I want Fio2 as high as it can be and HCT > 25 at least

Very generalized statements with little evidence and where specific situations should dictate hemodynamic management plan.

Why MAP of 50 to 60? Would you do that for a patient with hx uncontrolled HTN and BP of 210/110?
Why HR of 90 to 130? Would you do that for a patient with severe aortic stenosis? Or at risk of CAD?
Why FiO2 of 1.0 when it is unnecessary (in the absence of blood gas monitoring it decreases your ability to guage PaO2, and arguably it is harmful over the long term)
What evidence do you have that HCT > 25 js superior to HCT > 21? Except for very specific circumstances This goes against current best practices. I'm sure blood bank will love you for raiding their blood stores.
 
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EP here.... from my standpoint only reason to treat this relative bradycardia is if there's any associated hypoperfusion. If not then leave alone.

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?
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.
 
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One mid lvl administrator to sit at meetings probably cost 150k/year. And here we are talking about sparing use of potentially life saving meds. Murica.. oy vey..or is it ai ya..
 
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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.
 
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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.

Nice. yea over here unfortunately our department doesnt have TVPs.. so i would have to consult cardiology intraop if i even want a TVP.. sad
 
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.

yea thats my usual practice too!
 
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.

When you have sepsis induced vasodilation is your preload reduced? Yes
How about rapid AF? Dehydration? Acute blood loss? A combination? Preload reduced. How often do you see those conditions?

Its not as simple as "give more fluid" you have to deliver that fluid from the vasoplegic pulmonary and systemic vascular system to the heart. Have you ever seen someone volume overloaded in sepsis who is hypotensive? Why dont they just give more fluid?

The venoconstriction with neo is greater than the afterload increase, your getting more blood out overall which is why the CO increases in preload dependent situations - which are a LOT of situations, i would argue MOST
 
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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.

The point is you want a reasonable MAP and a reasonable HCT to ensure adequate oxygen delivery to tissues.

Getting fixated on MAP 58 vs 62, Levo vs Neo, or HCT 21 vs 25 and the outrage of the blood bank over such a crime - get over it. Make the vitals look good and make sense for the clinical situation, we should all be good at achieving that.

Dont be scared to give BP medicine or give blood or give pressors which the text book may not agree with to achieve that

I do not think its super important HOW you achieve your desired vital signs when it comes down to such nuances as levo vs neo, Hr 40 vs 60, keep the big picture in mind
 
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