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Case #47 The Medical Train Wreck Rate Topic: -----

#41 User is offline   Speed 

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Posted 04 March 2009 - 01:13 AM

View PostMike MacKinnon, on Mar 3 2009, 06:32 PM, said:

But why then are we seeing ischemia on the EKG? (explain the physiology of why this happened related to the AS)


That's kind of a "shotgun" question, I'll give you a "shoot from the hip" answer. The blockage isn't sudden, this is over time so as gradually as the resistance builds the heart is doing things to compensate. It pushes harder to get it out therefore the muscle is getting bigger, this requires more O2, and more and more over time. Usually the supplying vessels will engorge to allow more flow, but remember the opening to them is on the outside or "behind" the blockage, so this might not happen as much as it could to help out; there is one aspect of the "off-balance" supply and demand. With the stenosis sometimes the anatomy can be altered so that the opening to the coronary arteries doesn't function perfectly the way they were intended. A lot of this flow depends on the valves working right to "snap" with back pressure on closing and providing that push at the end of a cycle, the way a IABP augments flow. So low coronary filling pressures, and add an elevated rate... killer. Also, there is the internal stress inside the heart trying to push the load through, high internal pressures, stress, and the end result of the fluid backing up every where, a lot of work and stress. On top of all of that is the alterations to picking up of O2 by "drowning" alveoli, hence ischemia.


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With Suxx what are some "relative" contraindications in a non-emergency intubation (where seconds count)?

Does this patient meet any of those risks? If so what would you use instead, if not why?


My cut-offs are usually an open globe injury, hx of serious glaucoma, high K incidences, hx of MH, hmmm.... I think that's it, hard to remember unless you throw something in front of me that turns a switch on somewhere. Relative ones, or the ones I really don't think about are kidney, liver, heart disease? If I'm using succs it's usually because death is near. I have short transports times and people are using CPAP on both ends now. I guess liver being what you're looking for maybe? Pregnancy is in there somewhere I think? If I go off of my ATLS stuff I'd say I'd use it if mom needed an airway anyway.
Mike Williams CCEMT-P/FP-C
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#42 User is offline   jwalshfan 

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Posted 04 March 2009 - 02:58 PM

View PostSpeed, on Mar 3 2009, 07:13 PM, said:

....That's kind of a "shotgun" question, I'll give you a "shoot from the hip" answer. The blockage isn't sudden, this is over time so as gradually as the resistance builds the heart is doing things to compensate. It pushes harder to get it out therefore the muscle is getting bigger, this requires more O2, and more and more over time. Usually the supplying vessels will engorge to allow more flow, but remember the opening to them is on the outside or "behind" the blockage, so this might not happen as much as it could to help out; there is one aspect of the "off-balance" supply and demand. With the stenosis sometimes the anatomy can be altered so that the opening to the coronary arteries doesn't function perfectly the way they were intended. A lot of this flow depends on the valves working right to "snap" with back pressure on closing and providing that push at the end of a cycle, the way a IABP augments flow. So low coronary filling pressures, and add an elevated rate... killer. Also, there is the internal stress inside the heart trying to push the load through, high internal pressures, stress, and the end result of the fluid backing up every where, a lot of work and stress. On top of all of that is the alterations to picking up of O2 by "drowning" alveoli, hence ischemia.
....


VERY well worded. Alot of people would have over-complicated that response.

Warren, RN/LP
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#43 User is offline   MSDeltaFlt 

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Posted 04 March 2009 - 03:25 PM

View PostMike MacKinnon, on Mar 3 2009, 07:32 PM, said:

Some additions:
YES!

AS requires high perfusion pressures to get CO through the stenosis. But why then are we seeing ischemia on the EKG? (explain the physiology of why this happened related to the AS)
With Suxx what are some "relative" contraindications in a non-emergency intubation (where seconds count)?

Does this patient meet any of those risks? If so what would you use instead, if not why?


I believe so. Some possible contraindications with succs is tachyarrythmias and impaired cardiovascular function. With his AS and right/inf ischemia going on, he is at risk going into full blown Rt side AMI.

If I read the tuturials correctly, I'd like to go ahead with some Rocc. If I didn't read them correctly. I wouldn't. <_<
Mike Hester, RRT/NRP/FP-C
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#44 User is offline   Mike MacKinnon 

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Posted 04 March 2009 - 03:57 PM

Excellent responses.

For the ischemia think more about AS.

You give them a beta blocker AND a venodilator so preload reduces. Overall pressure reduces and so CO reduces. This is even MORE complicated by severe AS.

Have to ask if the pt has mild, mod or severe AS. Anything below a Aortic valve of 1 (2-3 is ~ normal) is at HIGH risk of becoming ischemic and coding if any drugs are given which can dump the pressure. No pressure, no ability to overcome AS not CO no filling of the coronary arteries at the aortic ostia = ischemia. coupled with tachycardia and you have a severely compromised coronary filling time.

This is someone you would consider inducing with ketamine or etomidate and avoiding anything that will decrease BP or increase HR.

With Suxx think more about his physician condition. He has been immobile now for years, what is the risk of giving suxx to this patient?
Mike MacKinnon MSN CRNA
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It's what we know for sure that just ain't so" - Mark Twain
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#45 User is offline   EMT-I2RN 

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Posted 04 March 2009 - 04:04 PM

With Suxx think more about his physician condition. He has been immobile now for years, what is the risk of giving suxx to this patient?

Something along the lines of a massive release of K. I don't remember who told me that.
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#46 User is offline   Speed 

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Posted 04 March 2009 - 05:22 PM

View PostMike MacKinnon, on Mar 4 2009, 09:57 AM, said:

This is someone you would consider inducing with ketamine or etomidate and avoiding anything that will decrease BP or increase HR.

With Suxx think more about his physician condition. He has been immobile now for years, what is the risk of giving suxx to this patient?


I know the K dump would be exaggerated being immobile, but do you think it would be enough to avoid it? Sure, the Etomidate only sounds fine and with his "feeble" state would probably be enough. With the unknown extent of the contractures and severity of the chest wall and diaphragm affected I wouldn't want him to be paralyzed for 45 minutes (vec is the only other one I carry) as I was learning his only "flexibility was what little he could do with what was left in the diaphragm only, and I'm stuck with a rigid or non-flexible "shell". I know if severe you'll get asystole, but I just haven't seen it happen in similar invalids, of course it can. And of course we would do damage control if it happened. I was expecting some "MacKinnon pearl of wisdom" with toxic Fe and succs?
Mike Williams CCEMT-P/FP-C
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#47 User is offline   JLP 

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Posted 05 March 2009 - 03:37 AM

View PostEMT-I2RN, on Mar 4 2009, 11:04 AM, said:

With Suxx think more about his physician condition. He has been immobile now for years, what is the risk of giving suxx to this patient?

Something along the lines of a massive release of K. I don't remember who told me that.


depends on the specific nature of the immobility. Muscular dystrophy patients notoriously store up K in defective muscle tissue, and still have acetylcholine receptors that can trigger a K dump - tend to have more, in fact, since the muscle responds to its inactivity by upregulating ACh receptors. Likewise patients with paralysis due to spinal injury - the muscles react to loss of signal by increasing their ability to respond, expressing lots more ACH receptors, while K is also stored since it's never released. Patients with wasting disorders, likely not so much as they tend to have very little muscle to store up K, and myasthenia gravis patients have few ACh receptors left so SUXX tends to paralyse them for ages but not much K response. For a CP patient, I can only guess that muscle mass would have some effect - I've seen CP patients with so little muscle that there likely isn't enough K in them to cause a blip.
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#48 User is offline   Mike MacKinnon 

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Posted 05 March 2009 - 07:46 PM

good questions speed.


Quote

I know the K dump would be exaggerated being immobile, but do you think it would be enough to avoid it?


excellent question. When patients are immobilized for years (like this fellow) they may have an increase upregulation of extrajunctional nicotinic receptors which can cause a k dump. In this case, a RA/CP caused contracture and immobility is certainly a risk but it is a relative one not an absolute one (like duschannes would be). I would feel comfortable giving suxx to this person in an emergency but i wouldnt otherwise and might consider rocc to play it say not knowing how much upregulation and proliferation of extrajunctional receptors he may have.


Quote

Sure, the Etomidate only sounds fine and with his "feeble" state would probably be enough. With the unknown extent of the contractures and severity of the chest wall and diaphragm affected I wouldn't want him to be paralyzed for 45 minutes (vec is the only other one I carry) as I was learning his only "flexibility was what little he could do with what was left in the diaphragm only, and I'm stuck with a rigid or non-flexible "shell". I know if severe you'll get asystole, but I just haven't seen it happen in similar invalids, of course it can. And of course we would do damage control if it happened. I was expecting some "MacKinnon pearl of wisdom" with toxic Fe and succs?


Naw yer all over it bro. Suxx is probably safe in this patient but it cant hurt to play it safe on something not horribly emergent and use Rocc.

Now, the question is, based on his airway presentation, would yah use rocc? Or go for suxx and why?
Mike MacKinnon MSN CRNA
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It's what we know for sure that just ain't so" - Mark Twain
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#49 User is offline   Mike MacKinnon 

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Posted 05 March 2009 - 08:06 PM

well said JLP :)

View PostJLP, on Mar 4 2009, 10:37 PM, said:

depends on the specific nature of the immobility. Muscular dystrophy patients notoriously store up K in defective muscle tissue, and still have acetylcholine receptors that can trigger a K dump - tend to have more, in fact, since the muscle responds to its inactivity by upregulating ACh receptors. Likewise patients with paralysis due to spinal injury - the muscles react to loss of signal by increasing their ability to respond, expressing lots more ACH receptors, while K is also stored since it's never released. Patients with wasting disorders, likely not so much as they tend to have very little muscle to store up K, and myasthenia gravis patients have few ACh receptors left so SUXX tends to paralyse them for ages but not much K response. For a CP patient, I can only guess that muscle mass would have some effect - I've seen CP patients with so little muscle that there likely isn't enough K in them to cause a blip.

Mike MacKinnon MSN CRNA
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"What gets us into trouble is not what we don't know
It's what we know for sure that just ain't so" - Mark Twain
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#50 User is offline   viking563 

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Posted 05 March 2009 - 08:56 PM

I would like to try a nasal intubation if I have time to see if we can avoid using paralytics at all. I would use Suxx in event that I couldn't get an airway, That way if airway attempts fail, I only have to BVM for a few minutes. Hopefully I have a glidescope with me ;) At 6' and 155 lbs he probably doesn't have much for muscle mass. I would keep NaHCO3 and CaCl2 handy in case of a K+ overload. Would a defasiculation dose of Roc prevent a possible K+ overload?
Matt, NREMT-P
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#51 User is offline   Speed 

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Posted 06 March 2009 - 01:42 AM

View PostMike MacKinnon, on Mar 5 2009, 01:46 PM, said:

i wouldnt otherwise and might consider rocc to play it say not knowing how much upregulation and proliferation of extrajunctional receptors he may have.
Suxx is probably safe in this patient but it cant hurt to play it safe on something not horribly emergent and use Rocc.

Now, the question is, based on his airway presentation, would yah use rocc? Or go for suxx and why?


Occasionally I may ask for some zemuron from a facility but otherwise I just have norcuron, of that type of paralytics. I can see where you're going with the cardiac effects or lack of with it versus succinylcholine, and the lack of causing hyperkalemia, but I'm looking at the duration of it versus the short lived succinylcholine. If I'm walking in my sleep on an airway, sure I'll throw down vec or zemmy on the first round (but not when I'm following protocols that don't allow that-for the lawyers), but with this guy I'd really like to be able to back out of it, maybe not though... you've thrown me with your description of the contractures "way up", almost hinting at other morbidities, not just "posturing from pain"....sneaky guy. If it's the over-emphasized histamines that succs can cause, and I think roc doesn't, usually the stimulation of intubation counters that (initially), and I just don't see it as drastic enough to change my mind.
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#52 User is offline   Mike MacKinnon 

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Posted 06 March 2009 - 01:48 AM

Nasal intubation isnt a bad idea.

On one attempt he squirms all over the place and wont be compliant, his nare is now bleeding profusely and he starts coughing up blood.

What is the mechanism by which suxx causes an increased K? That will answer your question :)


View Postviking563, on Mar 5 2009, 03:56 PM, said:

I would like to try a nasal intubation if I have time to see if we can avoid using paralytics at all. I would use Suxx in event that I couldn't get an airway, That way if airway attempts fail, I only have to BVM for a few minutes. Hopefully I have a glidescope with me ;) At 6' and 155 lbs he probably doesn't have much for muscle mass. I would keep NaHCO3 and CaCl2 handy in case of a K+ overload. Would a defasiculation dose of Roc prevent a possible K+ overload?

Mike MacKinnon MSN CRNA
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#53 User is offline   viking563 

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Posted 07 March 2009 - 03:33 AM

Quote

What is the mechanism by which suxx causes an increased K? That will answer your question :)

The defasiculation dose should block the depolarizing effect of suxx on the membranes of muscles. If the defasiculation dose is enough that should prevent the K+ overload because the intracellular K+ will not rush out of the cell because the cell will not have to repolarize because depolarization did not occur

View PostMike MacKinnon, on Mar 5 2009, 08:48 PM, said:

Nasal intubation isnt a bad idea.

On one attempt he squirms all over the place and wont be compliant, his nare is now bleeding profusely and he starts coughing up blood.

Well, now that he is activitely bleeding into the airway, I would need to suction. I would start with defasiculting dose of roc, followed by suxx. Endotracheal is plan A. Plans B & C is combitube and surgical cric respectively.
Matt, NREMT-P
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#54 User is offline   Mike MacKinnon 

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Posted 07 March 2009 - 01:55 PM

View Postviking563, on Mar 6 2009, 10:33 PM, said:

The defasiculation dose should block the depolarizing effect of suxx on the membranes of muscles. If the defasiculation dose is enough that should prevent the K+ overload because the intracellular K+ will not rush out of the cell because the cell will not have to repolarize because depolarization did not occur



Is that why it happens?

I will say that a defas dose of a NDMR will stop the post op myalgia often associated with suxx d/t fasciculations but the 0.5-1 meq K increase isnt because of them :)
Mike MacKinnon MSN CRNA
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#55 User is offline   JLP 

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Posted 07 March 2009 - 05:43 PM

View PostMike MacKinnon, on Mar 7 2009, 08:55 AM, said:

Is that why it happens?

I will say that a defas dose of a NDMR will stop the post op myalgia often associated with suxx d/t fasciculations but the 0.5-1 meq K increase isnt because of them :)


I would not trust a defasc dose to do this. To prevent the K rush you have to saturate most of the ACh receptors, which would actually require a higher NDMB dose than you use to paralyse (paralysis only requires that you occupy enough receptors to prevent effective contraction, which is well under the total number of receptors), in a patient with up-regulation of ACh receptors (e.g. duchenne MD patient's, quads) you'sd need a whopping NDMB dose - enough that sux would be unnecessary. And you'd better hope you can get that tube 'cause he'll be paralysed for while.

Now, this is just my extrapolation of pharmacology theory, so if someone has a different experience in real-life patients, please correct me.
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#56 User is offline   rfdsdoc 

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Posted 07 March 2009 - 09:09 PM

There is one way to avoid all this issue of whether to use sux or vec etcetcetcetc.

keep him breathing and sedate with ketamine. He cannot afford to stop breathing nor will tolerate any apnoea well at all.

Under LA insert a surgical airway using something like a seldinger kit such as the Melker.

Concept wise it is like deciding when to use an IO. IN the past it was always last resort as it seemed too hard or too cruel to screw an IO needle in so we would try multiple failed attempts at IV access, often wasting a lot of time and letting the patient deteriorate further. Same with this case, make the decision early to go with a rapid and safer technique than plan for an uncertain and risky laryngoscopy and get stuck in the multiple attempts of failed laryngoscopy trap.
Minh Le Cong
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MBBS(Adelaide), FRACGP, FACRRM, FARGP, GDRGP, GCMA
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#57 User is offline   Speed 

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Posted 07 March 2009 - 10:44 PM

View Postrfdsdoc, on Mar 7 2009, 03:09 PM, said:

keep him breathing and sedate with ketamine.
Under LA insert a surgical airway using something like a seldinger kit such as the Melker.


Now you're speaking my language, I'll ride with you.

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stuck in the multiple attempts of failed laryngoscopy trap


What's that? Excuses, excuses, cluck cluck, chicken (thems jokes)
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#58 User is offline   viking563 

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Posted 08 March 2009 - 06:53 AM

View PostMike MacKinnon, on Mar 7 2009, 08:55 AM, said:

Is that why it happens?

I will say that a defas dose of a NDMR will stop the post op myalgia often associated with suxx d/t fasciculations but the 0.5-1 meq K increase isnt because of them :)

Got it now. Suxx causes the cells to stay depolarized causing the K+ gated channels to remain open until the suxx is brokendown and the gated channels closed. Thanks for being patient.
Matt, NREMT-P
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#59 User is offline   Mike MacKinnon 

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Posted 08 March 2009 - 11:15 PM

Wicked awesome :)

I could have told yah but you wont ever forget it now :) Well done and exactly right!


View Postviking563, on Mar 8 2009, 02:53 AM, said:

Got it now. Suxx causes the cells to stay depolarized causing the K+ gated channels to remain open until the suxx is brokendown and the gated channels closed. Thanks for being patient.

Mike MacKinnon MSN CRNA
WWW.NURSE-ANESTHESIA.ORG

"What gets us into trouble is not what we don't know
It's what we know for sure that just ain't so" - Mark Twain
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#60 User is offline   Mike MacKinnon 

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Posted 08 March 2009 - 11:38 PM

Minh

Yer a 'cut to the chase' kinda guy ;)

I LOVE ketamine. The drug is incredibly underrated and should be used much more often.

I agree with everything you have said here, however most US HEMS companies do not carry special K.

So assuming we didnt have it, what would you go with?


View Postrfdsdoc, on Mar 7 2009, 05:09 PM, said:

There is one way to avoid all this issue of whether to use sux or vec etcetcetcetc.

keep him breathing and sedate with ketamine. He cannot afford to stop breathing nor will tolerate any apnoea well at all.

Under LA insert a surgical airway using something like a seldinger kit such as the Melker.

Concept wise it is like deciding when to use an IO. IN the past it was always last resort as it seemed too hard or too cruel to screw an IO needle in so we would try multiple failed attempts at IV access, often wasting a lot of time and letting the patient deteriorate further. Same with this case, make the decision early to go with a rapid and safer technique than plan for an uncertain and risky laryngoscopy and get stuck in the multiple attempts of failed laryngoscopy trap.

Mike MacKinnon MSN CRNA
WWW.NURSE-ANESTHESIA.ORG

"What gets us into trouble is not what we don't know
It's what we know for sure that just ain't so" - Mark Twain
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