Share your very low EF induction

[MoMoGesiologist]

As I learned from a CRNA recently, just give propofol 50mg to a low EF 30s 80 year old patient. They’ll be fine.

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[deleted697535]

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

I'd recommend everyone be comfy ish with these drugs as boluses. You can keep a big mac alive with them
Norepi put 4mg vial in 100ml bag so 40mcg per mil, take 1 mil and dilute into 10ml syringe so 4mcg per ml. 1 or 2 ml then push at a time


Epi put 1mg in 100ml bag that's 10mcg per mil. Push 1 to 3 mls at a time in a crashing patient. No more crash


Vaso is 20unit in a vial of 20ml. Push half a mil at time. Approx equipotent to 10mcg of epi in my limited experience

Milrinone push half an mg or 1mg at a time. Comes in 1mg per ml vial. With a vaso chaser of half to 1 unit. Works great too

As for the crna pushing 50mg propofol lol. A resident did that last year when I allowed too much trust. Never again. Propofol is a lethal weapon around these people

 

[DrZzZz]

I'd recommend everyone be comfy ish with these drugs as boluses. You can keep a big mac alive with them
Norepi put 4mg vial in 100ml bag so 40mcg per mil, take 1 mil and dilute into 10ml syringe so 4mcg per ml. 1 or 2 ml then push at a time


Epi put 1mg in 100ml bag that's 10mcg per mil. Push 1 to 3 mls at a time in a crashing patient. No more crash


Vaso is 20unit in a vial of 20ml. Push half a mil at time. Approx equipotent to 10mcg of epi in my limited experience

Milrinone push half an mg or 1mg at a time. Comes in 1mg per ml vial. With a vaso chaser of half to 1 unit. Works great too

As for the crna pushing 50mg propofol lol. A resident did that last year when I allowed too much trust. Never again. Propofol is a lethal weapon around these people

I've never seen vaso in a 20ml vial. I've only seen 20U in 1 ml vials, which requires dilution.

 

[vector2]

I can think of no situation where pushing a milrinone 1/8 to 1/4 loading dose (~6-12 mcg/kg) is warranted.

Even in a situation like a protamine reaction with severe pulm HTN and acute right ventricular failure, you're likely going to cause the pt to arrest if you push some milrinone. Vasopressin chaser or not, milrinone boluses can still cause profound hypotension which (to say the least) is not ideal in a scenario where you want to maintain aortic diastolic blood pressure so an acutely overpressurized RV can maintain luxury systolic and diastolic perfusion.

 

[MoMoGesiologist]

I can think of no situation where pushing a milrinone 1/8 to 1/4 loading dose (~6-12 mcg/kg) is warranted.

Even in a situation like a protamine reaction with severe pulm HTN and acute right ventricular failure, you're likely going to cause the pt to arrest if you push some milrinone. Vasopressin chaser or not, milrinone boluses can still cause profound hypotension which (to say the least) is not ideal in a scenario where you want to maintain aortic diastolic blood pressure so an acutely overpressurized RV can maintain luxury systolic and diastolic perfusion.

I feel like small epi boluses work great. No matter the situation. Just a dab will do ya!

 

[dhb]

4mcg norepi is a baby dose
I put 4mg in a 250ml bag which gives 16mcg/ml, start with 8mcg bolus to test response and move up from there

 

[anbuitachi]

I can think of no situation where pushing a milrinone 1/8 to 1/4 loading dose (~6-12 mcg/kg) is warranted.

Even in a situation like a protamine reaction with severe pulm HTN and acute right ventricular failure, you're likely going to cause the pt to arrest if you push some milrinone. Vasopressin chaser or not, milrinone boluses can still cause profound hypotension which (to say the least) is not ideal in a scenario where you want to maintain aortic diastolic blood pressure so an acutely overpressurized RV can maintain luxury systolic and diastolic perfusion.

only pushed milrinone 1mg at a time once... ended up giving like 5mg total. and it worked well. n=1...

 

[vector2]

only pushed milrinone 1mg at a time once... ended up giving like 5mg total. and it worked well. n=1...

What was the scenario

 

[anbuitachi]

What was the scenario

honestly dont even remember. such a long time ago. it was a sick patient with phtn rv failure and they were doing a bronch i believe..

 

[deleted697535]

I can think of no situation where pushing a milrinone 1/8 to 1/4 loading dose (~6-12 mcg/kg) is warranted.

Even in a situation like a protamine reaction with severe pulm HTN and acute right ventricular failure, you're likely going to cause the pt to arrest if you push some milrinone. Vasopressin chaser or not, milrinone boluses can still cause profound hypotension which (to say the least) is not ideal in a scenario where you want to maintain aortic diastolic blood pressure so an acutely overpressurized RV can maintain luxury systolic and diastolic perfusion.

Ok it's a high dose but I've seen it quite a bit and I got it from our chief cardiac anesthesia prof. He would use it on difficult weans from cpb.
I guess the idea of my post should have been more to stimulate a conversation on this as opposed to how I worded it as a prescription...

 

[T-burglar]

Mi”rinone only causes major hypotension if you’re not expecting it to work (make the heart snap more).

This is something that I believe many don’t understand. If you give milrinine to a heart with some contractility reserve, the increased stroke vigor balances the vasodilation. If you’re looking at a dead heart that probably won’t snap any harder (large areas of ischemic myocardium), then of course giving milrinone will mostly cause vasodilation with no CO to balance it.

Don’t give milrinone unless you think the myocardium that isn’t snapping is likely to snap harder. Or if something else will prevent an increase in cardiac output like AS or pulmonary artery hypertension/ obstruction

 

[AdmiralChz]

Being comfy with pushes is in our wheelhouse, for sure. I agree with the can’t imagine case for milrinone bonus camp - sounds like a great way to bottom out the pressure. If you’re really struggling and need an ionotrope for the RV (think acute PE) - think EPI.

 

[anbuitachi]

Being comfy with pushes is in our wheelhouse, for sure. I agree with the can’t imagine case for milrinone bonus camp - sounds like a great way to bottom out the pressure. If you’re really struggling and need an ionotrope for the RV (think acute PE) - think EPI.

what about RV due to pHTN? milrinone isn't going to get rid of the PE and fix the pulmonary issue, but it helps with pHTN

 

[vector2]

what about RV due to pHTN? milrinone isn't going to get rid of the PE and fix the pulmonary issue, but it helps with pHTN

pHTN is a catchall term which should probably be differentiated before you push some milrinone. Is the pHTN pre-capillary or post-capillary? What's the transpulmonary gradient? Do you have any evidence that the pt still has intact vasoreactivity? Has a RHC with a pulm vasodilator challenge been performed? What's the patient's current biventricular function and their systemic to PA ratio?

My main point is that 'high PA pressures' on its own does not automatically mean milrinone is beneficial or even indicated.

 

[AdmiralChz]

what about RV due to pHTN? milrinone isn't going to get rid of the PE and fix the pulmonary issue, but it helps with pHTN

Start an infusion instead if you feel like it’s warranted, and use vasopressin for hypotension rather than phenylephrine. But it’s so easy to overreact to “pulmonary HTN” as a number.

 

[deleted171991]

Mi”rinone only causes major hypotension if you’re not expecting it to work (make the heart snap more).

This is something that I believe many don’t understand. If you give milrinine to a heart with some contractility reserve, the increased stroke vigor balances the vasodilation. If you’re looking at a dead heart that probably won’t snap any harder (large areas of ischemic myocardium), then of course giving milrinone will mostly cause vasodilation with no CO to balance it.

Don’t give milrinone unless you think the myocardium that isn’t snapping is likely to snap harder. Or if something else will prevent an increase in cardiac output like AS or pulmonary artery hypertension/ obstruction

This is so basic knowledge that, if anyone didn't know this BEFORE reading your post, they should not even consider playing with advanced inotropes and pressors.

 

[deleted171991]

Start an infusion instead if you feel like it’s warranted, and use vasopressin for hypotension rather than phenylephrine. But it’s so easy to overreact to “pulmonary HTN” as a number.

There is so much "pulmonary HTN" due to left heart disease (e.g. diastolic dysfunction) that's misdiagnosed, even by pulmonary docs. The RV may be "failing" because the LV is failing (more frequently than one would think). It's the so-called biventricular HF reflex (from the Manual for Pulmonary and Critical Care Medicine by Landsberg):

If one looks at the red arrows, one can see that a lot of it is neurohormonal, not hydrostatic. Before one plays with pulmonary vasodilators, one should make sure that the left heart is A-OK, and that the pulmonary venous pressures are normal.

My residents make this mistake all the time: "EF is normal, left heart is OK". If there is a dilated LA there is diastolic dysfunction, even if not mentioned in the echo. And with low EF patients, you can BET the so-called PHTN is due to the left heart. Hence treat the left heart, not the PAP. If milrinone or dobutamine works, it's probably not because of the pulmonary vasodilator effect, it's because of the inotropic one (hence try epi first, especially since you're probably more familiar with it).

 

[T-burglar]

This is so basic knowledge that, if anyone didn't know this BEFORE reading your post, they should not even consider playing with advanced inotropes and pressors.

Lots of people don't understand why some people get very hypotensive with milrinone and others don't.

 

[deleted171991]

Lots of people don't understand why some people get very hypotensive with milrinone and others don't.

I am sticking to what I said before and you quoted.

 

[MoMoGesiologist]

The right heart was one of the most interesting things I learned about in residency. I’m still confused by it and the diagnosis and management of RV failure and PA pressures. It’s not so straight forward IMO. Or maybe I’m just dumb...

 

[vector2]

The right heart was one of the most interesting things I learned about in residency. I’m still confused by it and the diagnosis and management of RV failure and PA pressures. It’s not so straight forward IMO. Or maybe I’m just dumb...

The silverton lecture in the first link and 2016 lecture in the 2nd link are absolute gold.

RV Function - Echocardiography and Perioperative Ultrasound

Echocardiography and Perioperative Ultrasound

echo.anesthesia.med.utah.edu

Echo in Pulmonary HTN / RV Failure - Echocardiography and Perioperative Ultrasound

Echocardiography and Perioperative Ultrasound

echo.anesthesia.med.utah.edu

 

[aneftp]

If General needed. Lma is preferred over geta as long as airway and other conditions are reasonable.

 

[deleted875186]

If General needed. Lma is preferred over geta as long as airway and other conditions are reasonable.

I disagree. Paralyze, tube, keep them light.

 

[Mikkel]

I disagree. Paralyze, tube, keep them light.

LMA allows you to keep the patient light and tolerate the airway. Tubes will always be more stimulating compared to LMA.

 

[dchz]

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

Delirium is an unfortunately common complication seen during the postoperative course. Because of its significant association with physical and cognitive morbidity, clinicians should be aware of evidence-based practices relating to the diagnosis, treatment, ...

www.ncbi.nlm.nih.gov

Preoperative medication use and postoperative delirium: a systematic review

Medications are frequently reported as both predisposing factors and inducers of delirium. This review evaluated the available evidence and determined the magnitude of risk of postoperative delirium associated with preoperative medication use.A systematic ...

www.ncbi.nlm.nih.gov

Clinical risk factors associated with postoperative delirium and evaluation of delirium management and assessment team in lung and esophageal cancer patients - Journal of Pharmaceutical Health Care and Sciences

Background Delirium is an acute change in cognition and concentration that complicates the postoperative course. Patients who suffer delirium after surgery have an increased risk of persistent cognitive impairment, functional decline, and death. Postoperative delirium is also associated with an...

jphcs.biomedcentral.com

https://www.journalacs.org/article/S1072-7515(14)01793-1/pdf

Emergence delirium in adults in the post-anaesthesia care unit - PubMed

Preoperative benzodiazepines, breast and abdominal surgery and surgery of long duration are risk factors for emergence delirium.

www.ncbi.nlm.nih.gov

Risk factors for inadequate emergence after anesthesia: emergence delirium and hypoactive emergence - PubMed

Inadequate emergence after anesthesia is a frequent complication. Preventable risk factors for emergence delirium were induction of anesthesia with etomidate, premedication with benzodiazepines and higher postoperative pain scores. Hypoactive emergence was less frequent than emergence delirium...

www.ncbi.nlm.nih.gov

Postoperative delirium and perioperative mortality:

POSTOPERATIVE DELIRIUM (yes, a repeat!)

Postoperative Delirium: Acute Change with Long-Term Implications

Delirium is an acute change in cognition and attention, which may include alterations in consciousness and disorganized thinking. While delirium may affect any age group, it is most common in older patients, especially those with preexisting cognitive ...

www.ncbi.nlm.nih.gov

Incidence of Postoperative Delirium and Its Impact on Outcomes After Transcatheter Aortic Valve Implantation - PubMed

There are limited data on the occurrence of postoperative delirium after transcatheter aortic valve implantation (TAVI). We sought to investigate the incidence of delirium after TAVI and its impact on clinical outcomes. A total of 148 consecutive patients who underwent TAVI were enrolled. Of...

www.ncbi.nlm.nih.gov

Outcome and quality of life in patients with postoperative delirium during an ICU stay following major surgery - Critical Care

Introduction Delirium is an acute disturbance of consciousness and cognition that has been shown to be associated with poor outcomes, including increased mortality. We aimed to evaluate outcome after postoperative delirium in a cohort of surgical intensive care unit (SICU) patients. Methods This...

ccforum.biomedcentral.com

A Systematic Review and Meta-analysis Examining the Impact of Incident Postoperative Delirium on Mortality

Patients who develop delirium are at increased risk of death. However, in the studies with reduced bias and adequate control for confounding, an independent association between delirium and mortality was not apparent.Supplemental Digital Content is available in the text.

anesthesiology.pubs.asahq.org

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.

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:

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 [weak evidence if any at all with midazolam. It makes as much sense as giving 1mg of esmolol to a pt on chornic metoprolol is going to improve their survival 1 year later.]. Postoperative delirium is associated with increased mortality [very true I totally agree].

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

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"

 

[vector2]

Obviously a single-center Chinese study should be taken with a grain of salt, but prospectively in patients getting TKA or THA and receiving a CSE + only prop, dex, or midaz titrated to BIS 70-80, 7 day POCD as assessed by various cognitive batteries was highest in the midaz group. The weird part is that 7 day POCD incidence was also high in the dex group which is confusing because dex is thought to be neuroprotective. The authors believe dex was neuroprotective in some of the visual-spatial tests but not most of the other tests used. Prop was the cleanest. There were no differences at 1 year.

Effects of propofol, dexmedetomidine, and midazolam on postoperative cognitive dysfunction in elderly patients: a randomized controlled preliminary trial

Postoperative cognitive dysfunction (POCD) is a serious complication after surgery, especially in elderly patients. The anesthesia technique is a potentially modifiable risk factor for POCD. This study assessed the effects of dexmedetomidine, propofol ...

www.ncbi.nlm.nih.gov

 

[MoMoGesiologist]

Is anyone giving midaz to hypotensive pts intraop so they can reduce the amount of volatile? Sometimes I see CRNAs running 0.5 MAC gas and I get worried about awareness. I’d rather run higher gas with pressors but curious if anyone is giving midaz instead

 

[deleted162650]

Sometimes I see CRNAs running 0.5 MAC gas and I get worried about awareness.

Don't be

 

[MoMoGesiologist]

Don't be

If there’s no narcotics or benzos on board, what MAC do you worry about awareness?

 

[deleted162650]

If there’s no narcotics or benzos on board, what MAC do you worry about awareness?

Depends on the patient, but I'm confident in just about everybody at 0.8% Sevo.

 

[deleted171991]

Depends on the patient and surgical stimuli. Hugely. About 0.8% Sevo (0.4 MAC) is my number, too.

On the other hand, I tend to run a balanced anesthetic, and I give opiates, decadron, lidocaine etc. so the real "MAC" is higher.

 

[deleted875186]

Depends on the patient and surgical stimuli. Hugely. About 0.8% Sevo (0.4 MAC) is my number, too.

On the other hand, I tend to run a balanced anesthetic, and I give opiates, decadron, lidocaine etc. so the real "MAC" is higher.

Where does this number come from? If it’s anecdotal experience it means nothing to me, awareness is too rare and anesthesiologists notoriously never follow up long enough after surgery to reliably catch awareness.

My number is typically 0.7 age adjusted MAC of all volatile.

 

[dchz]

Is anyone giving midaz to hypotensive pts intraop so they can reduce the amount of volatile? Sometimes I see CRNAs running 0.5 MAC gas and I get worried about awareness. I’d rather run higher gas with pressors but curious if anyone is giving midaz instead

I do both, depending on the case. Both has merits and can be carried out as a safe anesthetic. It's physician comfort that usually dictates practice.

I feel like small epi boluses work great. No matter the situation. Just a dab will do ya!

It does not work great in these following:

severe CAD

severe AS

type 1 hypersensitivity to epi

 

[Hoya11]

Where does this number come from? If it’s anecdotal experience it means nothing to me, awareness is too rare and anesthesiologists notoriously never follow up long enough after surgery to reliably catch awareness.

My number is typically 0.7 age adjusted MAC of all volatile.

ill go even lower and say 0.6% !!

but seriously that is my number when i want to keep asleep but as light as possible (putting on dressings, putting legs down, finishing sutures, etc..

 

[dchz]

I can think of no situation where pushing a milrinone 1/8 to 1/4 loading dose (~6-12 mcg/kg) is warranted.

You're coming off pump and the RV protection was questionable and the pt has Pulm HTN. you need to load your milirinone and you either give it to the perfusionist to give on pump or you push 5mg (or 1/2 vial of this yourself). Done it 3 or 4 times in residency.

 

[deleted162650]

Where does this number come from

MAC Aware is generally considered to be 0.4 MAC. I’m sure it probably comes from the early dose finding studies by Egar.

 

[anbuitachi]

0.4 mac sevo is very different when there are other agents on board like fentanyl. if only PURELY volatile, I usually go ~0.7 mac for reliable amnesia

 

[vector2]

You're coming off pump and the RV protection was questionable and the pt has Pulm HTN. you need to load your milirinone and you either give it to the perfusionist to give on pump or you push 5mg (or 1/2 vial of this yourself). Done it 3 or 4 times in residency.

If RV protection is questionable and the pt has pHTN then you instruct the perfusionist and surgeon that we're not going to be coming off pump at the usual pace. Once the cross clamp is off and everyone is ready, let the heart fill a bit and if things look terrible then start a whiff of epi to get things snapping and load your milrinone over 5 minutes while you allow the heart rest on half- or quarter-flow CPB. You're not doing anyone any favors by rushing the process if you're expecting a difficult wean.

 

[deleted697535]

Don't be

Disagree. Awareness is rare enough but if you do have a case of it and you're at 0.5 you're screwed royally

 

[dchz]

If RV protection is questionable and the pt has pHTN then you instruct the perfusionist and surgeon that we're not going to be coming off pump at the usual pace. Once the cross clamp is off and everyone is ready, let the heart fill a bit and if things look terrible then start a whiff of epi to get things snapping and load your milrinone over 5 minutes while you allow the heart rest on half- or quarter-flow CPB. You're not doing anyone any favors by rushing the process if you're expecting a difficult wean.

totally agree with not rushing off pump.

But what would be the advantage of slowly adding milrinone vs just pushing if the pt is on pump anyways. perfusionist is just sitting right there, cannulas are in? the patient needs a milirinone load if you want to start milirinone. youre prolonging the pump run by waiting for your .375 mcg/kg/min to take effect.

If you really think giving milirinone over 5 mins is that different than pushing it. I think that i would disagree.

 

[dchz]

0.4 mac sevo is very different when there are other agents on board like fentanyl. if only PURELY volatile, I usually go ~0.7 mac for reliable amnesia

how long since your last bolus do you consider fentanyl still "on board"? let's say you gave fentanyl 100mcg bolus 1 hour ago in a 64M 170cm 75kg male with HTN and DM2. do you still consider it "on board"? if 1 hour is no longer on board how long do you consider it "on board"?

 

[vector2]

totally agree with not rushing off pump.

But what would be the advantage of slowly adding milrinone vs just pushing if the pt is on pump anyways. perfusionist is just sitting right there, cannulas are in? the patient needs a milirinone load if you want to start milirinone. youre prolonging the pump run by waiting for your .375 mcg/kg/min to take effect.

If you really think giving milirinone over 5 mins is that different than pushing it. I think that i would disagree.

I do think, at least anecdotally, there is a difference between pushing 50 mcg/kg and loading it over 10 minutes. However, I don't specifically know the literature regarding the subject.

Regardless, there's not really any point pushing it or loading it if you're still on pump and cross clamped because it's not making it to the heart anyway. For pts with known bad RVs/pHTN getting complex surgery or where I anticipate a long pump run, I load milrinone 12.5 mcg/kg and start the infusion at 0.125-0.375 pre-bypass and leave the drip on during pump so I already have an adequate plasma level by the time we're coming off.

Presumably in an acute situation where you started with a normalish RV/no prepump inotropes, and you think RV protection was bad, you would wait until the cardioplegia has worn off, cross clamp is removed, and you've actually confirmed that RV or BiV function appears bad as native heart function returns.

If it does look bad, I suppose you could just have perfusion push your milrinone after x-clamp off but still on pump at full flow, but it wouldn't be my favorite thing to do because you potentially could cause or exacerbate vasoplegia literally minutes before you're coming off. It should also be known that milrinone can precipitate tachyarrhythmias albeit at a much, much lower rate than beta agonists. So really, what is the point in you or perfusion pushing milrinone at this point since we should be letting the stunned RV rest on full flow pump for a few minutes- or doing a really, really slow wean while you titrate in / load your inotropes in a normal fashion...

 

[JWebar]

how long since your last bolus do you consider fentanyl still "on board"? let's say you gave fentanyl 100mcg bolus 1 hour ago in a 64M 170cm 75kg male with HTN and DM2. do you still consider it "on board"? if 1 hour is no longer on board how long do you consider it "on board"?

Thats a very interesting questions, and I don't think it has a single "correct" answer. As with any bolused drug, you get a peak effect (usually overshoots your desired site effect concentration) and then a slow decreasing plasma (and site effect) concentration. Both depend on previous doses and clearance of the drug (which in turn depends on a lot of different factors). We can only relay on changes over time of very indirect measurements such as a BP, HR or maybe BIS?

Indeed MAC is always changing if you are using opioids in boluses doses, even if your etGAS % is stable over time. Some people will give standard boluses of narcotic every 1–2 hrs of X mg/kg or some people will wait for changes in vital sign trends.

 

[JWebar]

By the way, even if I haven't commented all that much, I want to thank everyone for their contributions. This post is turning out to be very instructive (at least for me) and its a good reminder of why it's a good idea to check SDN regularly.

We should open another post about RV failure induction (specially for non cardiac surgery). That to be is probably the scariest induction ever.

 

[vector2]

Thats a very interesting questions, and I don't think it has a single "correct" answer. As with any bolused drug, you get a peak effect (usually overshoots your desired site effect concentration) and then a slow decreasing plasma (and site effect) concentration. Both depend on previous doses and clearance of the drug (which in turn depends on a lot of different factors). We can only relay on changes over time of very indirect measurements such as a BP, HR or maybe BIS?

Indeed MAC is always changing if you are using opioids in boluses doses, even if your etGAS % is stable over time. Some people will give standard boluses of narcotic every 1–2 hrs of X mg/kg or some people will wait for changes in vital sign trends.

As far as I know, vital sign changes have never been validated as a marker of depth of anesthesia. But that doesnt really change the fact that me and literally every other anesthesiologist in the world uses them for that purpose.

 

[anbuitachi]

how long since your last bolus do you consider fentanyl still "on board"? let's say you gave fentanyl 100mcg bolus 1 hour ago in a 64M 170cm 75kg male with HTN and DM2. do you still consider it "on board"? if 1 hour is no longer on board how long do you consider it "on board"?

yea i agree with above poster. no definite line but in this case i do still count it as on board

 

[JWebar]

As far as I know, vital sign changes have never been validated as a marker of depth of anesthesia. But that doesnt really change the fact that me and literally every other anesthesiologist in the world uses them for that purpose.

So true lol
But my point was not using it as a marker of depth of anesthesia but of narcotic effect in blunting the sympathetic response to surgical stimuli (regarding the comment of until when we consider that a dose of narcotic is still "on board").

 

[vector2]

So true lol
But my point was not using it as a marker of depth of anesthesia but of narcotic effect in blunting the sympathetic response to surgical stimuli (regarding the comment of until when we consider that a dose of narcotic is still "on board").

Huh? That on board comment I thought was in regard to sevo 0.4 plus other agents such as fentanyl "on board" vs solely sevo at 0.7, i.e. are both of those options still in safe MAC-aware territory

 

[anbuitachi]

now what about propofol infusions or tiva? what would you say is your rate to prevent awareness?

 

[Hork Bajir]

Having used Sedline w/ frontal EEG waveforms available for a great many TIVAs, I can say that there is no number of mcg/kg/min of propofol which is reliably amnestic. Some patients will be still showing beta waves at 150+, others will be in burst suppression on 70. It could be that it all has to do with pharmacokinetics, and the effect site concentration is preserved (meaning there is a “MAC equivalent for propofol)... but I would be surprised if that was the case. More likely that the dose-response curve is wider for prop than for the volatiles, at least in my anecdotal opinion. Of course, whether any combination of EEG findings reliably excludes awareness is a separate issue entirely