RSI question for an old newbie

[yappy]

Back in the day when I was training in the AF we were given an RSI protocol that didn't make complete sense to me and it's been bugging me ever since.

Well, it was pretty standard in that we used versed (2.5-5mg) or etomidate (0.3mg/kg) as an induction agent. Then prior to giving succ (1.5mg/kg) and tubing we were told to give 1.5 mg/kg of lidocain. Then vecc. after positive placement was confirmed. All IVP.

What was the lidocain for? Why would you give this prior to intubating a patient as a standard protocol? The only rational I was able to get was that it would prevent arrhythmia but all our patients were young athletic males. Is that a legit answer? what would be the mechanism? Was the whole lido thing BS lol.

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[Bertelman]

Back in the day when I was training in the AF we were given an RSI protocol that didn't make complete sense to me and it's been bugging me ever since.

Well, it was pretty standard in that we used versed (2.5-5mg) or etomidate (0.3mg/kg) as an induction agent. Then prior to giving succ (1.5mg/kg) and tubing we were told to give 1.5 mg/kg of lidocain. Then vecc. after positive placement was confirmed. All IVP.

What was the lidocain for? Why would you give this prior to intubating a patient as a standard protocol? The only rational I was able to get was that it would prevent arrhythmia but all our patients were young athletic males. Is that a legit answer? what would be the mechanism? Was the whole lido thing BS lol.

Blunts the sympathetic response to DL. Important if you are leaving narcotic out of your cocktail.

 

[turkeyjerky]

Blunts the sympathetic response to DL. Important if you are leaving narcotic out of your cocktail.

Is that really true, I thought it was a myth. I don't think there's great evidence for any of the pre-treatment agents. My understanding is that lidocaine diminishes the reflexive rise in ICP due to DL/intubation and is thus recommended for patient's w/ possibly increased ICP (in addition to reducing the risk of bronchospasm, so that it's also recommended for asthma patients). Opiods, on the other hand, have been found to decrease the htn/tachycardic response to intubation.

Neither of these agents are recommended routinely.

There's a couple of other problems w/ your protocol. One, the versed is underdosed--correct induction dosing is .1-.3 mg/kg (http://www.ncbi.nlm.nih.gov/pubmed/12670846). Also, the lidocaine is a pretreatment agent, it should be given prior to induction.

 

[Bertelman]

There is controversy with nearly everything we do surrounding an RSI. From my brief review, the benefits of IV lidocaine may include suppressing cough, which in turn limits ICP increases; attenuating tachycardia, HTN with DL.

Whether it truly attenuated ICP with RSI in TBI, I don't know, but I also don't know in what circumstances the OP was doing RSI. I think there is certainly enough evidence to suggest it blunts the hemodynamics response to DL @ 1.5 mg/kg, thus if I were restricted from using an opiate during induction, I would probably include it in my plan. And yes, it is s pre-treat.

 

[pgg]

Blunts the sympathetic response to DL. Important if you are leaving narcotic out of your cocktail.

If that's the objective, I think esmolol is probably a better choice. (Allowing for the fact that some RSIs are getting RSI'd for reasons involving shock, or they may have other reasons to not get a beta blocker.)

I'm not really impressed with IV lidocaine's claimed ability to blunt the sympathetic response to DL.


I was taught that a "true" RSI didn't include any narcotic, but I give fentanyl or alfentanil to almost everyone now.

 

[Magnus67]

In reviewing for Orals ive come across the IV lidocaine in numerous sources for blunting sympathetic response to DL and extubation. Kind of suprising since I have never used it routinely myself.

To quote a prior attending...I prefer to provide adequate anesthesia........I dont need "tricks" like muscle relaxants, lidocaine, etc..

 

[sevoflurane]

While it may blunt the sympathetic response to laryngoscopy a tiny, little bit.... pushing 100mg IV before pushing propofol will decrease the uncomfortable feeling of your IV burning form the propofol in some patients. This, in and of itself, may decrease sympathetic outflow (and may or may not be related to laryngoscopy).

Does anybody use lido to potentiate your non-depolerizer at the end of a case...?

As in... at the end of an abdominal case where your surgeon is closing fascia and your patient starts to display respiratory effort.... I remember reading/hearing about this and don't know how true it is.

I actually prefer 30-70mg of propofol in these situations.

 

[Bertelman]

If that's the objective, I think esmolol is probably a better choice. (Allowing for the fact that some RSIs are getting RSI'd for reasons involving shock, or they may have other reasons to not get a beta blocker.)

I'm not really impressed with IV lidocaine's claimed ability to blunt the sympathetic response to DL.

I wouldn't argue against any of those points, just providing some justification as to why someone might be taught to use lido.

I also wouldn't ever consider 30 mg of Midaz for an RSI.

 

[pgg]

I also wouldn't ever consider 30 mg of Midaz for an RSI.

Well if you did, then it wouldn't matter if the ICU nurses didn't get the sedation drip started until after snack time ...


As a brand new CA1 with a brand new attending, I once did a midazolam induction for an outpatient, just for the hell of it. She had to be admitted postop and lost the entire day's worth of memory.

 

[Hamhock]

I have never heard of giving lido between the induction agent and NMB.

I see very little good reason to use lido, especially in head trauma. And the idea of giving lido as proophylaxis for arrhythmia doesn't even make sense to me.

Given pretty much no benefits for lido in RSI pre-treatment, I think more focus should be on the risks. Then I think everyone would agree, it's not a great idea.

Love opioids for peri-RSI.

I have previously wondered after watching 100mg of lido being pushed by anesthesiologists prior to induction with propofol two things:

1. Given that is idea is to decrease local pain at the IV site from the profol burning, is 100mg really necessary? Couldn't a much smaller dose be used?

2. I wonder if the surgeon (especially ortho) is incorporating this into their plans, given the risks of local anesthetic toxicity.

HH

 

[Noyac]

I think you guys are missing the point.
If I remember right, the AF uses nurses for their anesthesia.
Therefore, it's not supposed to make sense.

At least, not to us.

 

[periopdoc]

I use 100 mg mixed with 50 mg propofol as I am hooking the patient up to the monitors. Significantly less burning than straight propofol.

To test this in residency, I would lean down whenever I was inducing a opiate addict and say, this may burn in the IV a lot. It can be pretty painful etc. Even with the coaching, few complained of any pain from the propofol. Doesn't completely eliminate it, but reduces it significantly. Interestingly, it does not reduce the burn from the induction dose of straight propofol that I give subsequently, but by that point they are stunned enough that they don't remember it.

It supposedly helps to reduce SUX induced myalgias although I haven't looked at the data recently.

- pod

 

[yappy]

It was worse than that man - I was a field guy - not even a RN. We had great trauma training but we skimmed over alot of the background info because all together our training was only 2 years and included alot more than medical interventions.

Thanks for the debate. I hope I never hurt anyone by following that protocol!

I think you guys are missing the point.
If I remember right, the AF uses nurses for their anesthesia.
Therefore, it's not supposed to make sense.

At least, not to us.

 

[fakin' the funk]

I have never heard of giving lido between the induction agent and NMB.

Where I'm at, we mostly use lido pre-propofol, but some advocate that instead of using for that purpose, you'll get the most out of its "sympathetic-outflow-reducing" effect by giving it right before laryngoscopy, since it is quick-acting and short-lived. So this is at least a feasible plan.

I personally think it reduces propofol pain quite a bit.

 

[fakin' the funk]

1. Given that is idea is to decrease local pain at the IV site from the profol burning, is 100mg really necessary? Couldn't a much smaller dose be used?

Yep

 

[fakin' the funk]

Back in the day when I was training in the AF we were given an RSI protocol that didn't make complete sense to me and it's been bugging me ever since.

Just want to reiterate to any young'uns out there, such as this OP, that RSI is all about timing and not at all about individual drug selections.

That is, giving etomidate and sux 5 minutes apart ain't an RSI, but giving etomidate/alfentanil/lidocaine/sux nearly simultaneously is.

For an RSI all you need is an induction agent and a quick time from hypnosis to laryngoscopy/intubation. Neuromuscular blockade is nice, but not necessary.

 

[Bertelman]

I use 100 mg mixed with 50 mg propofol as I am hooking the patient up to the monitors. Significantly less burning than straight propofol.

You've got to mix it.

 

[WholeLottaGame7]

You've got to mix it.

Mix it, or let it sit in the vein for a little bit, like a poor man's mini-Bier block. I'll try to find the paper I read on that once I recover from my week of nights.

 

[Bertelman]

Mix it, or let it sit in the vein for a little bit, like a poor man's mini-Bier block.

yeah, that sounds like a lot of work.

 

[Planktonmd]

It seems that the OP is referring to what RSI means in the minds of ER physicians not anesthesiologists.
ER guys think that RSI is any intubation where you give a muscle relaxant before you intubate.
RSI from anesthesia point of view is an intubation done in the shortest time possible after induction regardless of the medications used.
The usual sequence is: Induction agent followed immediately by Succinylcholine and intubate as soon as the fasciculation of the face stops usually in less than 10 seconds.
Rocuronium can be used to replace Sux but nothing works as fast as sux.
Many people still incorporate cricoid pressure in this process although we now know it is ineffective in preventing aspiration.
There is no need for any other medication but people do have different styles.

 

[dhb]

Blunts the sympathetic response to DL

This is clearly the intent although it's just a clearly a myth. The only lido that suppresses the hemodynamic response to DL is the one that you spray on the cords.

Second lidocaine (as do other local anesthetics) blocks the kinine/kalikreine reaction induced by the propofol solvent which is responsible for the burning caused upon injection.
Of course if you do the mini bier block it will work, just easier for me to mix and inject. I get a complaint maybe twice a year.

 

[Bertelman]

I add the lido b/c it balances the pH of Propofol, which is quite basic. That's my understanding of the mechanism. That and injecting slowly. I also typically get a few complaints/yr.

 

[dhb]

I add the lido b/c it balances the pH of Propofol, which is quite basic. That's my understanding of the mechanism. That and injecting slowly. I also typically get a few complaints/yr.

Not true

Here are he studies that i've posted a couple of times already over the years:

http://www.ncbi.nlm.nih.gov/pubmed/10211027
http://www.ncbi.nlm.nih.gov/pubmed/10655909

 

[Idiopathic]

Just want to reiterate to any young'uns out there, such as this OP, that RSI is all about timing and not at all about individual drug selections.

That is, giving etomidate and sux 5 minutes apart ain't an RSI, but giving etomidate/alfentanil/lidocaine/sux nearly simultaneously is.

For an RSI all you need is an induction agent and a quick time from hypnosis to laryngoscopy/intubation. Neuromuscular blockade is nice, but not necessary.

just to offer an alternate viewpoint, for a true RSI you plan on rapid achievement of optimal intubating conditions, which almost universally involves fast acting neuromuscular blockade. it all depends on what your indications are for "RSI", I suppose.

 

[Hamhock]

Many people still incorporate cricoid pressure in this process although we now know it is ineffective in preventing aspiration.

Please provide some data for this that a "typical anesthesiologist" will believe.

I don't use cricoid in the ED during RSI and the respiratory techs and anesthesiologists flip out.

I can't seem to convince them to keep their hands off the neck, even if it is ruining the resident's view.

HH

 

[Bertelman]

Not true

Here are he studies that i've posted a couple of times already over the years:

http://www.ncbi.nlm.nih.gov/pubmed/10211027
http://www.ncbi.nlm.nih.gov/pubmed/10655909

Actually, it is true. And ironically, the second study you posted acknowledges the fact that lidocaine lowers the pH in a vial of propofol, which brings more propofol out of the aqueous solution, which is the fraction of propofol responsible for the pain on injection.

I suspect that means you never actually read the study, which is why you posted the PubMed abstract instead of the actual article in the BJA.

You can start with this thread, where Noy takes us to school on the proposed mechanisms, quoting the 1999 BJA study above.

My orientation to this topic began with this article in the BJA which determined that lidocaine effectively reduces the pH of a propofol emulsion, decreasing the concentration of propofol in the aqueous phase. They adjusted the pH of propofol equally with lidocaine or HCl, and determined either of those adjustments significantly lowered pain on injection v. propofol + saline.
"...pain is known to be related to the aqueous concentration of propofol in the emulsion."
"Addition of 1% lignocaine to 1% Diprivan caused propofol to migrate from the aqueous phase of the 1% Diprivan emulsion into its lipid phase. This migration was accompanied by a change in pH...An increased proportion of propofol in the lipid phase caused less pain on injection."
"The results showed that the addition of HCl to 1% Diprivan produced pain relief and that local anesthesia by lignocaine was the less important factor for pain relief.

Now on to your 1999 BJA reference. That paper is actually like 10 studies in one, but they effectively compare the ability of lidocaine v. nafamostat, a bradykinin inhibitor, to reduce the pain of injection when mixed with propofol.
"...speculated that pain is caused by activation of the kallikrein-kinin system in plasma by contact with propofol, consequently generating ...bradykinin."
"...the effect of nafamostat on propofol-induced pain may be attributed to systemic inhibition of kallikrein activity."
"..propofol causes more pain on injection than lipid solvent alone. Thus bradykinin is not the only factor inducing pain on injection."
"Also, the reduced pain on injection of propofol diluted with lipid solvent is attributed to decreased concentrations of aqueous phase propofol." ...ahem...lidocaine...cough.
"As documented in this study, complete elimination of propofol-induced pain cannot be achieved, even if generation of bradykinin is repressed completely."

"Thus both these results support our hypothesis that the lipid solvent for propofol activates the plasma kallikrein-kinin system and produces bradykinin which subsequently modifies the local vein, increases contact between the aqueous phase propofol and the free nerve endings and aggravates pain on injection."



Major Points:
1) You can just as easily reduce the pain of propofol by adding HCl, effectively lowering the pH, thus the propofol concentration of the aqueous phase, which is known to be the irritating part.
2) Bradykinin modifies the local vein, making it more susceptible to irritation.
3) Lidocaine reduces the concentration of bradykinin, but it also reduces the aqueous phase concentration of propofol.

 

[Magnus67]

Actually, it is true. And ironically, the second study you posted acknowledges the fact that lidocaine lowers the pH in a vial of propofol, which brings more propofol out of the aqueous solution, which is the fraction of propofol responsible for the pain on injection.

I suspect that means you never actually read the study, which is why you posted the PubMed abstract instead of the actual article in the BJA.

You can start with this thread, where Noy takes us to school on the proposed mechanisms, quoting the 1999 BJA study above.

My orientation to this topic began with this article in the BJA which determined that lidocaine effectively reduces the pH of a propofol emulsion, decreasing the concentration of propofol in the aqueous phase. They adjusted the pH of propofol equally with lidocaine or HCl, and determined either of those adjustments significantly lowered pain on injection v. propofol + saline.
"...pain is known to be related to the aqueous concentration of propofol in the emulsion."
"Addition of 1% lignocaine to 1% Diprivan caused propofol to migrate from the aqueous phase of the 1% Diprivan emulsion into its liquid phase. This migration was accompanied by a change in pH...An increased proportion of propofol in the lipid phase caused less pain on injection."
"The results showed that the addition of HCl to 1% Diprivan produced pain relief and that local anesthesia by lignocaine was the less important factor for pain relief.

Now on to your 1999 BJA reference. That paper is actually like 10 studies in one, but they effectively compare the ability of lidocaine v. nafamostat, a bradykinin inhibitor, to reduce the pain of injection when mixed with propofol.
"...speculated that pain is caused by activation of the kallikrein-kinin system in plasma by contact with propofol, consequently generating ...bradykinin."
"...the effect of nafamostat on propofol-induced pain may be attributed to systemic inhibition of kallikrein activity."
"..propofol causes more pain on injection than lipid solvent alone. Thus bradykinin is not the only factor indusing pain on injection."
"Also, the reduced pain on injection of propofol diluted with lipid solvent is attributed to decreased concentrations of aqueous phase propofol." ...ahem...lidocaine...cough.
"As documented in this study, complete elimination of propofol-induced pain cannot be achieved, even if generation of bradykinin is repressed completely."

"Thus both these results support our hypothesis that the lipid solvent for propofol activates the plasma kallikrein-kinin system and produces bradykinin which subsequently modifies the local vein, increases contact between the aqueous phase propofol and the free nerve endings and aggravates pain on injection."



Major Points:
1) You can just as easily reduce the pain of propofol by adding HCl, effectively lowering the pH, thus the propofol concentration of the aqueous phase, which is known to be the irritating part.
2) Bradykinin modifies the local vein, making it more susceptible to irritation.
3) Lidocaine reduces the concentration of bradykinin, but it also reduces the aqueous phase concentration of propofol.

Dude just got pwned oral board style

 

[dhb]

I suspect that means you never actually read the study, which is why you posted the PubMed abstract instead of the actual article in the BJA.


Major Points:
1) You can just as easily reduce the pain of propofol by adding HCl, effectively lowering the pH, thus the propofol concentration of the aqueous phase, which is known to be the irritating part.
2) Bradykinin modifies the local vein, making it more susceptible to irritation.
3) Lidocaine reduces the concentration of bradykinin, but it also reduces the aqueous phase concentration of propofol.

Thanks for the study and the love

Couple of points:

The reduction of aqueous phase propofol with lido is 20% while clinically pain reduction is close to 100%.
They injected 2ml of propofol over 30seconds (not very relevant clinically) to determine pain which not surprisingly is 2/10 in the saline group
Very puzzling that you can mix 2ml of a pH 8 solution to 0.1ml of a pH 6.75 solution and end up with a final pH of 6.57 where did those extra H+ come from?
I doubt it is as easy to add a 0.0064mol/l solution of HCl than 2ml of lido

But ok maybe there is a contribution of lowering the pH, it would be interesting to repeat the experiment with other acidic solutions in a clinically relevant manner.