RSI: Critical Decision Making (Advanced Provider response requested)

[NomadicMedic]

I was surprised when I first saw it too, but yes Anectine can be used at low-dosage for defasciculation. One of the flight programs in northern IL uses 0.5 mg/kg Anectine as defasciculating agent before the regular full dose.

That really doesn't make sense to me. Depolarazing agents will cause fasciculations. Why would you give one to stop them?

 

[8jimi8]

Do you include lidocaine as part of your RSI? Nitrogen washout?

 

[Aidey]

Sorry this may be reposted, because i hit send, but the I couldn't find my thread.


So I am doing my RSI homework and reading drug profiles.

Concerning paralytics, what do you consider prior to choosing your paralytic. Do you have more than one option? Is it only a depolarizing or nondepolarizing? Do you have a choice between benzylquinolinium compounds or aminosteroidal compounds?

I see the various duration of actions, time of onset, side effects (histamine release, hypotension, tachycardia, increase in SBP, potentiation of hyperkalemia, bradycardia, increased intraocular pressure, among many others), 25% recovery times

Is it easy to make a decision because of protocols, or do you have autonomy and an excellent tool box?

We have Anectine, Vecuronium and technically Rocuronium. The only reason we have the Roc is because of the Succs shortage a few months ago. I don't think any of the ambulances have Roc on them now that Succs is back in stock. Succs is our first line drug, and we are only supposed to use the Vec after calling for orders or after the patient is successfully intubated and we have more than a 20 minute trip to the hospital. We can also use it if Succs is contraindicated.

We have Etomidate, Versed and Fent for sedatives. Thus far I think I like Etomidate better, as I have had a couple of patients burn through Versed stupid quickly.*

So in short, it is an easy decision because of protocols. Like you, I was recently reviewing other RSI drug profiles and I have no idea why we didn't just totally replace Succs with Roc. I suspect it has something to do with the concern of failed intubations, but that is just a guess. From talking with different ER MDs none of them seem to be a fan of Succs for in hospital RSI.

Like Linuss my biggest debate is "Should I do this?". None of my tubes have been questioned by the ER MDs or my Med Director, but I still wonder "is the patient as sick as I think they are?".



Question for those with Ketamine, do you administer it alone or with a benzo?



*One of these patients needed 10mg of Versed just to get though a head CT, it was pretty crazy.

 

[8jimi8]

We have Anectine, Vecuronium and technically Rocuronium. The only reason we have the Roc is because of the Succs shortage a few months ago. I don't think any of the ambulances have Roc on them now that Succs is back in stock. Succs is our first line drug, and we are only supposed to use the Vec after calling for orders or after the patient is successfully intubated and we have more than a 20 minute trip to the hospital. We can also use it if Succs is contraindicated.

We have Etomidate, Versed and Fent for sedatives. Thus far I think I like Etomidate better, as I have had a couple of patients burn through Versed stupid quickly.*

So in short, it is an easy decision because of protocols. Like you, I was recently reviewing other RSI drug profiles and I have no idea why we didn't just totally replace Succs with Roc. I suspect it has something to do with the concern of failed intubations, but that is just a guess. From talking with different ER MDs none of them seem to be a fan of Succs for in hospital RSI.

Like Linuss my biggest debate is "Should I do this?". None of my tubes have been questioned by the ER MDs or my Med Director, but I still wonder "is the patient as sick as I think they are?".



Question for those with Ketamine, do you administer it alone or with a benzo?



*One of these patients needed 10mg of Versed just to get though a head CT, it was pretty crazy.

One of the ideas I have been trying to consider is... the decrease in oxygen demand by a provider taking over the work of breathing.

 

[MSDeltaFlt]

Are you able to pre-medicate with a defasciculating round of either low dose anectine or a non-depolarizing paralytic?

Yes you can. However I've rarely needed to do so. If you give the full doses of your pre-intubation sedatives and analgesiacs, there's a good chance you won't need a paralytic at all. If hemodynamics might be an issue, open the fluids up. Even in a head injury on an adult, 1 bag of fluids won't do any harm.

Now as far as lidocaine is concerned, there's not much in the way of any good use listed.

 

[M3dicDO]

Our Intensive Care Paramedics can use Ketamine as an adjunct to morphine in patients with severe traumatic pain associated with:
- A. Fracture reduction and splinting
- B. Multiple or significant fractures requiring facilitated extricatin

Dosages (IV)

Adult - 10-20mg repeated every 2-3 minutes- total max dose 1mg/kg

Paed- ( = or above 1 years) 100mcg/kg repeated every 2-3 minutes- total max dose 1mg/kg

Fascinating! I can see how Ketamine would be a much better anesthetic for severe trauma than other stronger alternatives like Diprivan. Maybe you guys should come here to the U.S. and influence our medical directors to allow Ketamine for pre-hospital use ^_^

That really doesn't make sense to me. Depolarazing agents will cause fasciculations. Why would you give one to stop them?

I totally agree with you n7lxi. It didn't make sense to me either, but they've had this defasciculating option for many years as part of their RSI protocol, with much success....

The best explanation I can come up with is that a small dose of Anectine would partially depolarize many but not all Ach receptors. It would cause minor fasciculations (if any) but not as drastic (or complete) as would a full dose of Anectine. Once the NM junction is partially concentrated with the Anectine, giving the full dose would complete occupying the remaining Ach receptors hence causing a negligible fasciculation. So in summary, it's like breaking down the fasciculations into smaller pieces. But it's not going to be half of the complete fasciculation (i.e. it's not 1+1=2) because the NM junction has an exponential physiology rather than linear.

If you give the full doses of your pre-intubation sedatives and analgesiacs, there's a good chance you won't need a paralytic at all.

Amen! I only used Versed, Etomidate and Fentanyl for RSI, for many years on an ALS ambulance. Our protocols allowed us to stack all three, if needed to achieve proper sedation. And it always worked Paralytics are indeed a great asset for an RSI, not a requirement.

 

[8jimi8]

the NM junction has an exponential physiology rather than linear.

please elaborate.




I hope that this isnt outdated information. According to

http://emcongress.org/2007/presentations/18Gibbs.pdf

There is no evidence that succinylcholine worsens outcomes in at risk ICP patients.

Also there is no evidence that defasciculating doses improve outcomes for at risk patients.


Maybe there just needs to be a study.

 

[M3dicDO]

http://emcongress.org/2007/presentations/18Gibbs.pdf

There is no evidence that succinylcholine worsens outcomes in at risk ICP patients.

Also there is no evidence that defasciculating doses improve outcomes for at risk patients.

Maybe there just needs to be a study.

Thanks for sharing this presentation. It's a really good read!

please elaborate.

Sorry I tried to cut corners and didn't give a full explanation. Well, consider skeletal muscular depolarization. As you have the wave of depolarization reach the contractile units of the muscle, the translation of the electrical activity into contraction is mediated by the eflux of Ca from the sarcoplasmic reticulum. As you may already know about the nature of Ca in electrochemical activity, increasingly higher concentrations of Ca causes faster and greater release of even more sequestered stores of Ca in the muscle cells. This phenomenon is referred to as "Calcium induced Calcium release." (This similar physiology is seen in pre-synaptic neurons as well, where calcium is used by the neurotransmitter vesicles as a means of "sticking" to the pre-synaptic membrane and mediating neurotransmitter release, to some extent).

What I mean by this is that small doses of Anectine translates to small release of Ca from the sacroplasmic reticulum and hence less Ca to interact with troponin, and so on. If on the other hand a large dose of Anectine is given, the Ca release is so huge (due to a large wave of incoming depolarization) that the a large storm of the ion causes fasciculations. But you can achieve occupying Ach receptors without inducing the "Calcium induced Calcium release," by giving a small dose of Anectine as a premedicating defasciculator, and so the upcoming full dose will not cause the fasciculations normally expected.......since many of the Ach receptors are already occupied. I guess, you can make two 0.5 mg/kg doses suffice (in theory), but giving the full 1-1.5 mg/kg doses as the second dose is a way of being certain you've achieved a definite paralyzation.

Oh, I forgot to address the "exponential" vs. "linear" physiology. If you were to graph the Ca release (and thus muscle contraction) vs. Ach stimulation, you would expect to see a steeper curve as more and more Ach receptors are recruited.

Please let me know if I missed anything....

 

[8jimi8]

Thanks for sharing this presentation. It's a really good read!



Sorry I tried to cut corners and didn't give a full explanation. Well, consider skeletal muscular depolarization. As you have the wave of depolarization reach the contractile units of the muscle, the translation of the electrical activity into contraction is mediated by the eflux of Ca from the sarcoplasmic reticulum. As you may already know about the nature of Ca in electrochemical activity, increasingly higher concentrations of Ca causes faster and greater release of even more sequestered stores of Ca in the muscle cells. This phenomenon is referred to as "Calcium induced Calcium release." (This similar physiology is seen in pre-synaptic neurons as well, where calcium is used by the neurotransmitter vesicles as a means of "sticking" to the pre-synaptic membrane and mediating neurotransmitter release, to some extent).

What I mean by this is that small doses of Anectine translates to small release of Ca from the sacroplasmic reticulum and hence less Ca to interact with troponin, and so on. If on the other hand a large dose of Anectine is given, the Ca release is so huge (due to a large wave of incoming depolarization) that the a large storm of the ion causes fasciculations. But you can achieve occupying Ach receptors without inducing the "Calcium induced Calcium release," by giving a small dose of Anectine as a premedicating defasciculator, and so the upcoming full dose will not cause the fasciculations normally expected.......since many of the Ach receptors are already occupied. I guess, you can make two 0.5 mg/kg doses suffice (in theory), but giving the full 1-1.5 mg/kg doses as the second dose is a way of being certain you've achieved a definite paralyzation.

Oh, I forgot to address the "exponential" vs. "linear" physiology. If you were to graph the Ca release (and thus muscle contraction) vs. Ach stimulation, you would expect to see a steeper curve as more and more Ach receptors are recruited.

Please let me know if I missed anything....

Thanks!

 

[8jimi8]

Yes you can. However I've rarely needed to do so. If you give the full doses of your pre-intubation sedatives and analgesiacs, there's a good chance you won't need a paralytic at all. If hemodynamics might be an issue, open the fluids up. Even in a head injury on an adult, 1 bag of fluids won't do any harm.

Now as far as lidocaine is concerned, there's not much in the way of any good use listed.

You didn't mention the nitrogen washout, i'm curious if in the most critically emergent patient's you take time to bag them for 3 minutes.


Also,

Do you disagree with this statement below from ACEP?
Focus On: Rapid Sequence Intubation Pharmacology
http://www.acep.org/Content.aspx?id=49401

When used as a pretreatment agent, lidocaine is dosed at 1.5 mg/kg intravenously, and the duration of action is approximately 10-20 minutes.1 Lidocaine offers protection in two clinical scenarios: 1) prevention of increase in ICP caused by RSRL, and 2) bronchodilation in reactive airway disease

 

[MSDeltaFlt]

You didn't mention the nitrogen washout, i'm curious if in the most critically emergent patient's you take time to bag them for 3 minutes.


Also,

Do you disagree with this statement below from ACEP?
Focus On: Rapid Sequence Intubation Pharmacology
http://www.acep.org/Content.aspx?id=49401

When used as a pretreatment agent, lidocaine is dosed at 1.5 mg/kg intravenously, and the duration of action is approximately 10-20 minutes.1 Lidocaine offers protection in two clinical scenarios: 1) prevention of increase in ICP caused by RSRL, and 2) bronchodilation in reactive airway disease

As stated in my quote, "not much..."

"Robinson and Clancy in the Emergency Medicine Journal published a literature review showing that although this agent does blunt the RSRL-caused ICP increase, there is no evidence of improved neurologic outcome when using lidocaine in head-injured patients"

Besides, there is a difference here that some don't seem to realize. And it's a phylosophy as well that depends on one's medical control. And that, my friend is Rapid "Sequence" Intubation vs Drug "Assisted" Intubation.

The operative words here (depending on you OLMC) is "sequence' in RSI: once you start the sequence, you complete the sequence, and "assisted" in DAI: if your pt stops breathing and loses a gag before you've given your paralytic, go ahead and pass the tube.

This is where the true nature of the original title of this thread lies: critical thinking.

Look at your patient. Assess and reassess. Never say never. Never say always.

 

[usalsfyre]

You didn't mention the nitrogen washout, i'm curious if in the most critically emergent patient's you take time to bag them for 3 minutes.

If at all possible I absolutely denitrogenate a patient prior to making any attempt to pass a tube, drug assisted or not. The only times I haven't (since I stopped tubing arrest) are the two times I've used a paralytic with no sedative as I noted in another thread (bradycardiac hypoxic patient we couldn't BVM and a head injury with trismus who had puke coming through his teeth, manual airway maneuvers wouldn't work on either one).

 

[NomadicMedic]

This has been one of the most fascinating threads on EMTlife.

Thanks to everyone who's taken part.

 

[M3dicDO]

I've used a paralytic with no sedative.....

Interesting approach. Does your protocol allow you to skip sedation? :glare: Or did a physician approve this method via OLMC? Can you share with us "the two times" you did this?

 

[usalsfyre]

Interesting approach. Does your protocol allow you to skip sedation? :glare: Or did a physician approve this method via OLMC? Can you share with us "the two times" you did this?

I shared the two times in the same post, immediately after the line you quoted. Yes it was based on guideline, if you'll look up the National Emergency Airway Algorithms(Dr. Walls guidelines) this is an accepted technique called crash airway. Both of these patients were deeply unconscious and both had midazolam administered with in a minute or two post-intubation for sedation/retrograde amnesia. Both of these cases were headed rapidly for a bad outcome, and waiting the extra minute or so to draw up and administer the Etomidate wasn't in the cards. This would be absoloutely idiotic technique to place under OLMC as it's intended for situations where you don't have time for a sedative, as by that time I a doc on the phone here I could sedate 20 times. I've never worked in a system where RSI has been online anyway.

No, it's not a technique I think is appropriate on 99.99% of patients, it's something where critical thinking applies. I sedate first always, excepting these two specific cases. So there's no need to glare .

 

[usafmedic45]

You would have thought the cramping sensation in the wrist would give 'em a clue they're going wayyy to fast

As someone who bagged a patient all the way from Pensacola to Ft. Smith, Arkansas after we had out ventilator start acting up just as we reached cruising altitude, I would agree with that.

Are you able to pre-medicate with a defasciculating round of either low dose anectine or a non-depolarizing paralytic?

Why would you waste time doing that when faced with any of the scenarios that would be amenable to RSI?

 

[M3dicDO]

Why would you waste time doing that when faced with any of the

scenarios that would be amenable to RSI?

Just like there are varying opinions on the benefits of using Lidocaine on head trauma patients, there are many practitioners out there that are firm believers in using a defasciculating round of paralytics before intubating a patient suspected of increased ICP.

I agree with you on the fact that we would "waste time doing that when faced with any of the scenarios that would be amenable to RSI" but there are many transport programs out there that either a) require a defasciculating dose as one of their pre-medications in RSI or b) strongly urge transport personnel to consider it. Defasciculating pre-medication may be an old-school (and by some, considered possibly controversial) practice but I've noticed many medical directors feel indifferent in removing therapies that prove no harm.

I shared the two times in the same post, immediately after the line you quoted.

Yes, I read it, but I was hoping you wouldn't mind doing a short case presentation on it, so we would get a more complete picture....

Yes it was based on guideline, if you'll look up the National Emergency Airway Algorithms(Dr. Walls guidelines) this is an accepted technique called crash airway.

I agree, it is a great algorithm for difficult airways. I understand that in the field, critical thinking is important in the matters of life and death, but I was asking you if you had the ability to skip sedation based on established protocols for your program. I have never heard of such leniency for any non-physician provider. I worked with a few medics and nurses that thought whatever happened behind closed doors of the aircraft stayed in the aircraft, and got away with a lot (as long as it was "properly documented.") Reminds me of the two "cowboy" flight nurses from CALSTAR in February 2008 that got nailed to the cross.....

Both of these patients were deeply unconscious and both had midazolam administered with in a minute or two post-intubation for sedation/retrograde amnesia

Deeply unconcious as in code blue? :blink: I don't mean to be picky but Midazolam has not been proven to produce effective retrograde amnesia in any patient population (1,2,3,4). I hope neither of those patients remember being gagged by the cold laryngoscope blade.

This would be absoloutely idiotic technique to place under OLMC as it's intended for situations where you don't have time for a sedative, as by that time I a doc on the phone here I could sedate 20 times

I guess it all depends on how much you would want to put your license on the line. If :censored::censored::censored::censored: hits the fan, any medical director would cover their own butt first. Seen it happen, it's not pretty.

(1) Hupp JR, Becker LE. Intensity and duration of amnesia from intravenous midazolam given for sedation, Conn St Dent Assoc J 1988;62:80-5.
(2) Oboyle CA. Benzodiazepine-induced amnesia and anaesthetic practice: a review. Psychopharmacol Ser 1988;6:146-65.
(3) Twersky RS, Hartung J, Berger BJ, et al. Midazolam enhances anterograde but not retrograde amnesia in pediatric patients. Anesthesiology 1993;78:51-5.
(4) Antoun K, Janet IM. Does Midazolam cause retrograde amnesia, and can flumazenil reverse that amnesia? Anesth Analg 1997;85:211-2.

 

[MrBrown]

Just curious, does anyone know of transport programs (w/o a physician) that use Ketamine? If so, what kind of dosage and provisions do they have?

We use ketamine for analgesia and anaesthesia (RSI).

Ketamine
• Indicated in severe pain, particularly musculoskeletal or burn pain.
Is preferably used in combination with morphine.
• Contraindicated if:
a. Age less than one year or
b. Unable to obey commands or
c. Has active psychosis or
d. Has cardiac chest pain or
e. Midazolam has already been given.
• Give oxygen via nasal prongs or acute (ordinary) mask.
• In adults:
a. If morphine or IM ketamine already given, give 5-10 mg
ketamine IV every 3-5 min.
b. If morphine or IM ketamine has not been given, give 10-20 mg
ketamine IV every 3-5 min.
c. If unable to gain IV access, give 1 mg/kg ketamine (rounded off
to nearest 10 kg) IM or oral, up to a maximum of 100 mg. This
may be repeated after 20 minutes if required. Do not use IM
route if shocked and avoid IM use in children if possible.
d. Reduce the dose if the patient is elderly, small or
physiologically unstable.
• For children, see paediatric drug dose table.
• Ketamine must be diluted to 2 mg/ml for IV use. Place 200 mg
(2 ml) of ketamine in a 100 ml bag of 5% glucose (shake well and
label).

 

[Aidey]

Nasal prongs? lol

 

[Shishkabob]

RSI scares the absolute bejeezus out of me.