Share your very low EF induction

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First, i would like to thank you for providing sources. You've already done a lot to engage me in this nerdy conversation and i appreciate it.

My "quibble" is that a good anesthesiologist is first and foremost a good scientist. but your original quote is very misleading and does not promote good science. If you had said "it is fine to use midazolam, but weigh it against this possible weak evidence that are emerging, and only give the pt what he needs" I would be 100% behind you. but your original quote is too extreme:



X is bad. Y has some correlation but no real causation to X. Therefore Y is bad.
X has at least 10 other contributor to it (including contributors such as sleep deprivation, constantly waking pts to draw labs, foreign environment, etc). Y has an effect time of 2 hours. The surgey is often 6 hrs +. Therefore Y is not good of the pt because it causes X.
This thought process does not reflect a good scientist. It downplays the other positive effects of Y.

I am all about judicious use of drugs and not forcing midazolam if the pt doesn't need it. But @bcat85 original goal of minimizing propofol with a higher dose of midazolam is a very valid method of inducting a patient. Your claim of "the patient's post operative course may not be (stable)." has very little evidence to it. And I believe your concern of post op delirium is overblown and backed up with very weak evidence.

In just last 2 weeks, i've induced many pts in your category (70 years old +, low EF) with midazolam, sevolfourane, and fentanyl only for cases that involve cardiopulmonary bypass. On post op follow up in the ICU they all did great without any signs of delirium or increased morality during their 2-3 day ICU course. I believe good ICU management really trumps that midazolam you gave for induction. And whether or not one uses midazolam for induction matters very little.

Hence my quibble. I also want to echo the sentiment of "it's not what you use to induce, but ensuring the pt is stable during induction, that matters"

I think that we largely agree in many ways: judicious use of midazolam as an anxiolytic in a patient who is incredibly anxious pre-operatively is a justifiable therapeutic option. Especially in those patients (left main, anyone?) in whom tachycardia and hypertension would be an undesirable hemodynamic state. Are there other options? Sure. But would I fault anyone for using midazolam in that circumstance? No, even if I may personally pursue other options such a dexmedetomidine first. I also agree that maintenance of hemodynamic stability, avoidance of hypotension, and strong ICU care also do a lot to ensure a good perioperative outcome for these often frail patients.

Having said that, I strongly believe that you do not need midazolam to achieve your stated goal of minimizing propofol administration, and that is the fundamental issue I have with the original comment. I think that in general we are far, far too impatient in the operating room, and in the very low EF patient this problem is exacerbated. Why not take advantage of the pharmacokinetics of fentanyl and give it (reasonable dose here, 1-1.5 mcg/kg) before you start pre-oxygenating, so it has some time to peak? Let them breathe for a couple of minutes. Give your lidocaine. Give a whiff of propofol, 20-30 mg or so, and wait. Wait longer than you normally would. 45 seconds? A minute? Wait!! You have a fragile patient with a slow circulation time, so take your time. Elderly opiate-naive non-drinkers may even fall asleep here. Still not asleep? Give another 20-30 mg. And so on. Lid reflex disappears and you give paralytic and you're done. The key, however, is to just WAIT. I think the problem is that 45-60 seconds can at times feel like an eternity during induction, especially relative to other cases, so we get impatient. Or we give the fentanyl and immediately chase it with propofol, and end up giving more of the latter acutely to get the patient off to sleep. In either of these two scenarios, that is where you will get into trouble with overdosing propofol. I did my fellowship at a "big name" program with a very large heart failure program, and with the exception of an attending or two, we almost never gave midazolam because it simply was not needed. This was a huge change compared to my residency where everyone got 2-10 mg pre-op, and really changed the way I approach these patients. Nevertheless, you are a board certified anesthesiologist: I don't need to teach you how to induce a patient. That's my own cocktail and I recognize this is an art as much as a science. (EDIT: This is to say, in a patient who is medically optimized undergoing elective surgery. Obviously there are other things to consider in the patient with profound biventricular failure who was admitted with a hip fracture after he fell while SOB during his most recent CHF exacerbation)

However, it is curious to me that you, as a proponent that an anesthesiologist should be a scientist as well as a physician, in your closing paragraphs use your own anecdotal data about how well your few recent patients did with midazolam on board. I am glad that your patients did well for the last two weeks and stayed on the pathway leaving the ICU on time, but as you are well aware as a physician scientist, the only thing worse than "overblown and...very weak evidence" is your recent anecdata. Perhaps you do not like the studies that I have provided, but more peer-reviewed research is on the way, especially with the spotlight on POCD and resilience in the critically ill patient, and perhaps those will convince you.

If you re-read my original post, I did not say that benzodiazepines cause increased mortality in this patient population. I maintain that benzodiazepines in the elderly cause delirium, and that delirium is associated with increased mortality. A is associated with B. B is associated with C. I agree - A has not been established as a causal link to C. But to me, there is enough evidence against benzodiazepine use in elderly patients who AREN'T undergoing a pump run, ICU stay, major surgery, a likely AKI, etc., that to give them as a matter of reflex in this setting seems inappropriate. Especially if we have established that they are not needed as a propofol-sparing agent. Not to beat this horse further, but it's sort of similar to the etomidate and adrenal suppression question. Whatever your interpretation of the data (many people have many opinions), to me, there is enough smoke there that despite the uncertainty, given that we have so many other options for inducing patients in a stable fashion, why would you use it?

Cheers. Appreciate the cordial discourse.
 
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Not sure if this counts, but we just had a patient being retrieved with an EF 10-15% on .5 mcg/kg/min norepinephrine and 10 mcgs/kg/min dobutamine still cold and shocked suspected Takotsubo's (basal sparring on the bedside TTE). Attending sprayed the cords early, IV lidocaine 1mg/kg and a whiff of fentanyl. Just a whiff. 50mcgs total. I think the patient was too altered to care but it went crazy smooth.
 
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Not sure if this counts, but we just had a patient being retrieved with an EF 10-15% on .5 mcg/kg/min norepinephrine and 10 mcgs/kg/min dobutamine still cold and shocked suspected Takotsubo's (basal sparring on the bedside TTE). Attending sprayed the cords early, IV lidocaine 1mg/kg and a whiff of fentanyl. Just a whiff. 50mcgs total. I think the patient was too altered to care but it went crazy smooth.

If the attending was able to spray the cords with minimal sedation....then yes........your patient is pretty altered 🙂


Also, somewhat unrelatedly, patients with takotsubo need a comprehensive TTE (or TEE) with a particular focus on LVOT obstruction. Inotropes can make the shock worse and/or kill these patients unless you've excluded LVOTO.
 
If the attending was able to spray the cords with minimal sedation....then yes........your patient is pretty altered 🙂


Also, somewhat unrelatedly, patients with takotsubo need a comprehensive TTE (or TEE) with a particular focus on LVOT obstruction. Inotropes can make the shock worse and/or kill these patients unless you've excluded LVOTO.

In retrospect, levosimendan might've been a better choice, especially since the patient was pre-morbidly on beta-blockers.

It was not an ideal situation; we were called down to help facilitate a transfer to a bigger centre by our ED. We got him tubed, and then he was pretty much out the door thereafter.
 
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For really low EFs, I've been taught fentanyl about 5mcg/EF%, wait for four-five minutes, then prop 1-2mg/EF%, wait for sleep, bvm, some roc or cisatracurium, cords, tube, des or sevo. Works like a charm.

Sent from my LYA-L29 using SDN mobile
 
For really low EFs, I've been taught fentanyl about 5mcg/EF%, wait for four-five minutes, then prop 1-2mg/EF%, wait for sleep, bvm, some roc or cisatracurium, cords, tube, des or sevo. Works like a charm.

Sent from my LYA-L29 using SDN mobile


The waiting is the most important ingredient in that induction. You can do the same without any fentanyl. It’s what I do for my bivent ICDs.
 
In retrospect, levosimendan might've been a better choice, especially since the patient was pre-morbidly on beta-blockers.

It was not an ideal situation; we were called down to help facilitate a transfer to a bigger centre by our ED. We got him tubed, and then he was pretty much out the door thereafter.


You have levosimendan? Where are you located? Been hearing about it for years but still just a rumor in the USA.
 
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!

Late to the party and haven’t read all the responses, so I apologize in advance.

General case NPO:
Skip the benzos

+\- 25-50 fent based on frailty or narc history

Propofol in small titrated bits starting with 2ml, most don’t need much more than 3-5 ml,

PATIENCE

paralytic when eyes closed (assuming airway fine), take over respirations and turn on gas

Titrate the epi and Have dilute push stick to use of the trend down starts

GENERAL/CARDIAC CASE FULL STOMACH
etomidate / paralytic / epi gtt @3 (before etomidate given)

Turn gtt up or down or use push dose stick of epi 4mcg at a time

Vaso/ Levo boluses depending on other pathology going on and response to epi

CARDIAC:
Epi @3, fent 250-450 , wait , prop 15 , wait , if eyes not closed prop 15, paralytic when eyes closed, gas, tube, push dose prn

A guy I worked with would start prop ketamine infusion while putting on the monitors while mask was being held, worked nicely and slowly drifted patient off


So for me...anticipate with epi , patience, titrate small doses prop, gas when eyes closed
 
We do cases like this all the time. Some of these folks actually have reasonable functional status and do well. Very important to ask what they can do at home, will give you hints to how they will do during during an anesthetic.

I think that's an important point.

Several patients can all have same EF and their response to induction can vary greatly.

EF 20 and SV 70? Big dilated heart and long standing niCM guy doing stuff around the house...

EF 20 and SV 20 w/acute insult and admitted with pulmonary edema....much different approach to induction
 
It's not only how you do it, but what you do it for and who you're doing it on.
The 85yo with an EF of 15 for an EGD is different than than the 85yo with and EF of 15 for even an inguinal hernia. Low and slow is good advice for any of these, but breaking down to the nitty gritty (do I need an aline? CVC? what induction agents etc) is where your skill will come in. I've done GI procedures on EFs of 10 with some gargled lidocaine, ketamine and inhaled nitrous. You need to think about the patient and the procedure. Does everyone need an aline, I don't think so but I would never discount someone for getting one. Also small doses of ketamine will help you in these situations, it may hinder your wakeup in quick procedures but really just getting these people through their procedure should be your goal and going fast is not the point, if anyone in the room says otherwise you need to make this known. I wouldn't do a narcotic induction, the advantages just aren't there unless you know they're staying intubated and even then I don't see it.
Also have everything you need drawn up and ready, whether you want to start infusions beforehand or not is up to you, I usually don't. What I will do and what I think is the best thing you can do is give 5-10mcg of epi before anything starts to see how responsive their receptors are, learned this from a very good ICU/cardoac anes doc, a lot of these cardiac depressed people will have no response and some will perk right up, it gives you an idea about what to expect when you want to push drugs which is important in these situations so you don't overdue it which can be harmful as well. Some of these people pressures will come right up with some phenylephrine, some need vaso/epi and knowing this beforehand will let you have some control

Edit: besides maybe young patients with viral myocarditis pretty much none of these people need a benzo
 
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I think that's an important point.

Several patients can all have same EF and their response to induction can vary greatly.

EF 20 and SV 70? Big dilated heart and long standing niCM guy doing stuff around the house...

EF 20 and SV 20 w/acute insult and admitted with pulmonary edema....much different approach to induction

I cannot like this post enough. General anesthesiologists are much better off using functional status, warm extremities, clear lungs, nl Na/Cr, and 0-1 pillow orthopnea (or the lack thereof of all those things) to titrate induction meds vs. A single number from the TTE summary report.
 
You have levosimendan? Where are you located? Been hearing about it for years but still just a rumor in the USA.

Australia. It's good stuff when it makes sense like a beta-blocked patient or in Takotsubo's where more catecholamines probably won't help. Less arrhythmogenic than dobutamine. Probably not helpful in sepsis but the LEOPARDS didn't really disaggregate people with diastolic septic cardiomyopathy -- again, useful when it makes sense.

Veli-Pekka Harjola, et al. Use of levosimendan in acute heart failure. European Heart Journal Supplements. 20(1). 2018. Use of levosimendan in acute heart failure
 
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