Share your very low EF induction

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What do you mean in a bad way? humor me and explain to me what's wrong with a narcotic induction.
One big thing, that will bite you: prolonged loss of sympathetic response. So you may get them high enough to be able to intubate them without reflex tachycardia and hypertension (hence no ischemia), but then you may need sympathetic agonists for hours. The same way you wouldn't push 2 mg of dilaudid in the ASA 4 patient at the beginning of the case (but try 0.2 first and see what happens, and then 0.2 more etc.), why push a lot of fentanyl?

I don't do cardiac but, for my non-cardiac cases, I rarely use more than 50-100 mcg of fentanyl for intubation. Beyond that (and proper doses of propofol), I use esmolol for tachycardia. It's much easier (and appropriate) to use a short-acting drug specifically for a short-acting stimulus.
 
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if patients are coding from a narcotic induction then they were either

A) going to code anyway from any induction.
B) it was just coincidence (nothing to do with the drug choice) and the induction was simply mismanaged

It's not inherently a more risky induction. Although it's rare, in CT we do identify patients who will likely arrest on induction and establish peripheral CPB wires or even the the cannulas themselves under local anesthesia (done this approximately once in 7 years). If you recognize a patient like this presenting for non-CT anesthesia, then you have to either do the case with local and light sedation or not at all.
 
High dose opioid is great for preventing tachycardia and myocardial ischaemia on induction.
It’s great for aortic stenosis.

It’s counterproductive for patients in which tachycardia is tolerable and sympathetic tone is desirable.

I see trainees give heavy doses of fentanyl to shocked patients, and they argue it’s cardiovascularly stable.

Nope. Some patients need (and can tolerate) maximal sympathetic tone... its an evolutionary adaptive strategy !
 
if patients are coding from a narcotic induction then they were either

A) going to code anyway from any induction.
B) it was just coincidence (nothing to do with the drug choice) and the induction was simply mismanaged

I think this fatalist thinking keeps people from changing their style of practice.

Coding on induction is usually due to too much of something. (Sometimes too little, like insufficient oxygenation, insufficient ventilation, insufficient periop fluid balance)

If a patient coded during a narcotic induction, it was probably because of too much fentanyl.

Post-intubation coding is another deal and could be from decreased cardiac output from increased intrathoracic pressure, or, again, too much of something like fentanyl or propofol.
 
High dose opioid is great for preventing tachycardia and myocardial ischaemia on induction.

The 30 seconds worth of ischemia-prevention is not worth the 2 hours of ischemia risk from prolonged post-induction hypotension.

Esmolol makes a lot more sense here.


And let's not fool ourselves here, most cardiac patients don't really have much of an endogenous reserve of catecholamines that would push them over the edge.
 
I think this fatalist thinking keeps people from changing their style of practice.

Coding on induction is usually due to too much of something. (Sometimes too little, like insufficient oxygenation, insufficient ventilation, insufficient periop fluid balance)

If a patient coded during a narcotic induction, it was probably because of too much fentanyl.

Post-intubation coding is another deal and could be from decreased cardiac output from increased intrathoracic pressure, or, again, too much of something like fentanyl or propofol.

It’s fatalistic to understand and be able to identify which patients have an unacceptably high risk of arrest on induction?

I don’t think you really understood my post. You can’t “refine your practice” to get around the fact that a massive acute PE is very likely to arrest on induction even if you “preserve their sympathetic tone” by just giving them etomidate or ketamine.
 
Once again, I haven’t read all the responses.
These pts are surprisingly tolerant. Right up until they aren’t.
My preferred method for CABG on or off pump was a touch of versed while I slipped in an A line. Then roc and sufenta.
For hips, 1mg of versed and assess the response while doing other things ( moving to the room, Aline, monitors etc) if drowsy then 5-10-15mg ketamine. Position for isobaric spinal or push roc whichever the plan is.
I may give a touch of new in these pts with induction and I always have a dilute syringe of epi.
 
Or 10 mg of midaz on induction.

Curious what the concern is here? Hemodynamically stable and very little sequelae. If you’re getting an LVAD, you’re not exactly on the fast track pathway.
 
a whole lot depends on pre op vital signs and clinical picture.
same two patients with 15% EF
one with normal BP, normal HR, normal volume status, no CHF low risk procedure where LMA is an option, is very different than the same 15% EF in sepsis or major surgery or difficult airway or poor volume status...

monitors, technique, airway, case for using regional techniques will all play a role here.

it is amateurish to lock yourself into a default technique based on just a low EF. Flexibility is key.

The basis for my technique for induction like most people is slow, titrated induction, so I have time to catch up and treat if needed. I keep it simple: pre op versed, lidocaine, prop, fentanyl, phenylephrine and esmolol in hand, rocuronium...I dont do anything in hurry with these patients.

traumas or emergencies are a little different, but then again, liability is a little different also.
 
Curious what the concern is here? Hemodynamically stable and very little sequelae. If you’re getting an LVAD, you’re not exactly on the fast track pathway.

Very little sequelae is a matter of opinion, at least when I'm one the one rounding in the CTICU on pts presenting with delirium and pump head. A ton of versed is fine for the 40 year old endocarditis valve replacement or 45 year old diabetic smoker with premature CAD, but on average I minimize opioids and benzos as much as possible in the cardiac OR (since the average patient is a 60-65+ with likely undiagnosed concomitant cerebrovascular disease), and I preferentially run precedex throughout the case and leave it running for transport to ICU.
 
Curious what the concern is here? Hemodynamically stable and very little sequelae. If you’re getting an LVAD, you’re not exactly on the fast track pathway.
This is not a question of induction stability. In these patients who are often elderly and often develop an AKI secondary to hypoperfusion during their pump run, midazolam may not be the best choice. Benzodiazepines in general are implicated in postoperative delirium (and long term postoperative decline), especially in elderly folks. Postoperative delirium is associated with increased mortality.

Your induction will be more stable. The patient's postoperative course may not be. This includes LVADs.
 
Most low EF inductions aren't too concerning and don't need a long process with infusions, microdrippers, 5 drugs, etc. Lighten your doses, keep a careful eye on the pressure. Judicious epi as needed. We did a lot of VADs in training, almost all got induced with propofol and a bit of epi.
Critical left main is a lot more concerning for an arrest on induction and I take more time with those, sometimes put defib pads on. Inhaled induction is great. I'll usually breathe them down maybe 4-5% on the sevo dial until they no longer respond to voice/touch (usually about a minute, maybe less), then give 20-50mg prop, maybe some phenylephrine, and paralyze. Still doesn't take too much time.

If you have an awake art line and a critical induction, watch the waveform during induction, not the displayed number. The number averages the last few seconds (how many probably depends on the monitor brand & setting) but if you can read the trace based on the scale, you'll know significantly earlier if your left main induction is tanking their pressure and heading for a code. Was SBP 150 and over 4 beats has dropped to 100? Give pressor now before SBP's 70. If they're just a nonischemic dilated cardiomyopathy, dropping their afterload isn't the worst thing for them, may improve stroke volume for a time, and can be pretty well tolerated. Keep in mind high LVEDP can reduce CPP but again if they don't have really critical coronary lesions, transient hypotension isn't a major problem.

Without an art line, I'd probably be more conservative and slower with dosing.
 
I’m surprised not more people say etomidate. What do you guys think of using etomidate for low EF induction?

Board answer would be etomidate as it’s the most hemodynamically stable drug and that’s what they teach you in residency
 
I’m surprised not more people say etomidate. What do you guys think of using etomidate for low EF induction?

Board answer would be etomidate as it’s the most hemodynamically stable drug and that’s what they teach you in residency

I don't use etomidate. Never have.
 
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I’m surprised not more people say etomidate. What do you guys think of using etomidate for low EF induction?

Board answer would be etomidate as it’s the most hemodynamically stable drug and that’s what they teach you in residency
Actually that is NOT the oral board answer. 😉

The oral board answer is slow-controlled induction with what you have available. If you say etomidate, you come across as the CRNA++, not the savvy anesthesiologist. They want you to be safe AND flexible, hence they will tell you that there is an etomidate shortage. The best anesthesiologists can do everything in many different ways (just read all the unusual inductions above).
 
I use a lot of etomidate personally
I was just trying to teach XRanger that etomidate is not the magic oral boards answer everybody thinks it is (although they will probably get away with it). In my opinion, everybody should use the drug(s) they have mastered.

I got lucky; there were many drug shortages during my residency, and we had to improvise a lot.
 
I was just trying to teach XRanger that etomidate is not the magic oral boards answer everybody thinks it is (although they will probably get away with it). In my opinion, everybody should use the drug(s) they have mastered.

I got lucky; there were many drug shortages during my residency, and we had to improvise a lot.

I understand I was just offering that I actually like etomidate and think it’s a good drug. Sometimes I think people on this board make it a weird matter of pride to use a strong vasodilator like propofol in sick people
 
I understand I was just offering that I actually like etomidate and think it’s a good drug. Sometimes I think people on this board make it a weird matter of pride to use a strong vasodilator like propofol in sick people
I'd rather use a good induction agent that happens to cause hypotension if you don't use it appropriately in certain circumstances
 
My attendings were mostly of the opinion that etomidate might be poison and shouldn't be used outside the ER (where they didn't have or weren't comfortable pushing pressors). That's probably an overblown fear but I'm a product of my professional childhood. I think the last time I used it was as a fellow when an attending made me.
 
Actually that is NOT the oral board answer. 😉

The oral board answer is slow-controlled induction with what you have available. If you say etomidate, you come across as the CRNA++, not the savvy anesthesiologist. They want you to be safe AND flexible, hence they will tell you that there is an etomidate shortage. The best anesthesiologists can do everything in many different ways (just read all the unusual inductions above).

It is for the written board 🙂

But I agree real life scenarios are not black and white and there are multiple ways to approach this. I myself have used different methods like versed/ketamine, inhalation, slow prop titration with neo and etomidate. I still use etomidate frequently in low EF pts and I think it’s a good drug.
 
This is not a question of induction stability. In these patients who are often elderly and often develop an AKI secondary to hypoperfusion during their pump run, midazolam may not be the best choice. Benzodiazepines in general are implicated in postoperative delirium (and long term postoperative decline), especially in elderly folks. Postoperative delirium is associated with increased mortality.

Your induction will be more stable. The patient's postoperative course may not be. This includes LVADs.

This seems pharmacologically improbable. The half life of a versed bolus is about 1.5 hours. As an infusion in the ICU it makes total sense, but I think this is an example of inappropriate extrapolation of ICU data to the OR. There is actually a multicenter clinical trial looking at this exact issue. (Benzodiazepine-free Anesthetic for Reduction of Delirium (B-Free) - Full Text View - ClinicalTrials.gov)
 
Hey guys!

Just curious. What would be your induction for a 50–60 yo 70 kg patient with severely depress EF (lets say 15%). Let's just skip all the other considerations say she is not decompensated and has optimal medical management on board. Just focus on the induction for a GA with intubation. Pre–induction arterial line for sure.

And what about if its ischemic CM?

Would you start with vasopressors on board?

Thanks in advance for sharing!
midazolam
 
He's saying as an infusion it makes sense that versed would cause delirium in the ICU, but that intraop boluses of versed don't affect POCD in the ICU

Exactly. It’s like the difference between three beers on a Friday night and going on a seven day bender.
 
High dose opioid is great for preventing tachycardia and myocardial ischaemia on induction.
It’s great for aortic stenosis.

It’s counterproductive for patients in which tachycardia is tolerable and sympathetic tone is desirable.

I see trainees give heavy doses of fentanyl to shocked patients, and they argue it’s cardiovascularly stable.

Nope. Some patients need (and can tolerate) maximal sympathetic tone... its an evolutionary adaptive strategy !

Nice! Its easy to forget this and get carried away by "the recipe" of Fentanil+Propofol+NMBD

Thats why I was asking about low EF with and without CAD. Next time I'll try the titrated propofol (no fentanyl) and sux for the low EF without CAD and go heavy on the fentanyl with not much else on the CAD patient. Art line preinduction is kind of a must for me in these escenarios.

Anyway, thanks EVERYONE for your amazing feedback.
 
Nice! Its easy to forget this and get carried away by "the recipe" of Fentanil+Propofol+NMBD

Thats why I was asking about low EF with and without CAD. Next time I'll try the titrated propofol (no fentanyl) and sux for the low EF without CAD and go heavy on the fentanyl with not much else on the CAD patient. Art line preinduction is kind of a must for me in these escenarios.

Anyway, thanks EVERYONE for your amazing feedback.
Personally, I’ve found going light on everything is best. It’s fine if their systolics go to 160-180s during intubation. It’ll be gone after a minute. Dealing with hypertension >>> hypotension.

Compare the ratio of your inductions that you deal with hypertension vs hypotension. I’ve found I’m dealing with post-induction low BPs much much more frequently than high BPs aka, at least for me, there’s always room to give less.
 
I’m surprised not more people say etomidate. What do you guys think of using etomidate for low EF induction?

Board answer would be etomidate as it’s the most hemodynamically stable drug and that’s what they teach you in residency
I can go the rest of my career, as a cardiac anesthesiologists, and never touch etomidate. It was one of the first “always-isms” of residency I threw out the window.
 
Can someone explain why so many posts are suggesting using phenylephrine in this example? My fear would be increasing afterload in a patient with a heart that is already struggling to eject that SV. I can't recall ever using phe on CT. Wouldn't small doses of epi on induction be far superior? Sure with EFs 30%+ it probably doesn't matter, but 10-15%?
 
Can someone explain why so many posts are suggesting using phenylephrine in this example? My fear would be increasing afterload in a patient with a heart that is already struggling to eject that SV. I can't recall ever using phe on CT. Wouldn't small doses of epi on induction be far superior? Sure with EFs 30%+ it probably doesn't matter, but 10-15%?

Venous constriction returns more blood to heart, which increases preload and increases stroke volume, so heart doesn't have to work as hard so less oxygen consumption.

Low dose phenylephrine good. If you need higher dose, you should probably get more inotropy augmentation instead.
 
Can someone explain why so many posts are suggesting using phenylephrine in this example? My fear would be increasing afterload in a patient with a heart that is already struggling to eject that SV. I can't recall ever using phe on CT. Wouldn't small doses of epi on induction be far superior? Sure with EFs 30%+ it probably doesn't matter, but 10-15%?


It’s one of the least energetically costly ways to maintain perfusion pressure as it does not directly increase myocardial oxygen consumption.
 
Bolusing phenylephrine probably improves the arterial pressure numbers while increasing afterload and myocardial work. Does this matter? Who knows. A phenylehprine infusion supposedly has a different physiology than a bonus and will over time (a short time) recruit the unstressed volume and increase preload.

Is any of this proven? Does any of it really matter? Nobody knows

I personally bonus norepi for push dose circulatory support unless epi or Vaso is indicated based on these assumptions
 
Can someone explain why so many posts are suggesting using phenylephrine in this example?

Our anesthetics are for the most part, vasodilators. Phenylephrine corrects the anesthetic induced vast-dilation. No one is advocating for pushing Neo until the BP is 200/100.

The other thing to keep in mind is that if you think their EF sucks now, wait till that myocardium gets ischemic. You need to maintain that BP to maintain coronary perfusion pressure. Also, any increase in after load is offset by the decrease in HR which has a much more significant effect on myocardial O2 consumption.
 
Bolusing phenylephrine probably improves the arterial pressure numbers while increasing afterload and myocardial work. Does this matter? Who knows. A phenylehprine infusion supposedly has a different physiology than a bonus and will over time (a short time) recruit the unstressed volume and increase preload.

Is any of this proven? Does any of it really matter? Nobody knows

I personally bonus norepi for push dose circulatory support unless epi or Vaso is indicated based on these assumptions

Agree with the norepinephrine bolus. Works great. Hypertension >>>>>>>hypotension. If the blood pressure is high the patient won’t be dead (assuming they don’t have an aneurysm)
 
. Benzodiazepines in general are implicated in postoperative delirium (and long term postoperative decline), especially in elderly folks. Postoperative delirium is associated with increased mortality.

provide your source please.
 
provide your source please.

Hi!

Without knowing which point you take umbrage with it's hard to target some citations to interest you and engage in a discussion, but here are a few, including various primary sources and meta-analyses.

Benzodiazepine use and postoperative delirium:



Postoperative delirium and perioperative mortality:

POSTOPERATIVE DELIRIUM (yes, a repeat!)

Before getting into the weeds with this stuff, I'd love to understand what your particular quibble is in that quote so we can chat about it. I am not saying this is you, but if I hear "I've never heard of any randomized, double-blinded, placebo controlled trial that shows 2-5 mg of midaz pre-op causes delirium!!" (typically stated while pushing it in a completely chill, non-anxious 85 year old getting an arterial line), one more time, I am going to scream.
 
I prefer to titrate roc in until they don't respond to my voice. Usually 20-30 mg. If you go slow it is much more entertaining. Then I slip in the LMA real gentle-like to avoid stimulating them. Take your time and don't rush it. I like to keep them spontaneously breathing so as not to affect their preload. I cycle the NIBP q 5 minutes, but may skip one or two cycles because the worst thing for these patients is yo-yo anesthesia. Overreacting and getting the blood pressure too high or low is bad. I sometimes put in the A-line after the case is started if I get bored. It is important to keep your skill set up and not neglect it.
 
Agree with the norepinephrine bolus. Works great. Hypertension >>>>>>>hypotension. If the blood pressure is high the patient won’t be dead (assuming they don’t have an aneurysm)

Could you give us some numbers (mg) for the boluses? Honestly, I've only used norepi as an infusion :/
 
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