Fast Mag for stroke alert

daedalus

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My area, i found out yesterday, seems to be conducting a study on the use of field magnesium in suspected ischemic/hemorrhagic stroke. Now, I also read that the "use of neuroprotective agents is currently NOT recommenced in CVA".
Is anyone else doing this? Or is this really a brand new study in the use of magnesium?
 
we only use mag on torsodes de pointes. In a stroke caused by blockage of blood vessels (ischemic stroke) receive clot-dissolving (thrombolytic) medications and heparin...mostly at the hospital with proper diagnosis.;)
 
never heard of it, only torsades and eclampsia here
 
Never heard of it being used for that. Like people have mentioned above, use it for tosades and elcampsia.

But I guess that is why it is called a study.
 
I wonder what reason(s) they are wanting to use Mg+ for CVA? If you have more information please post.

Mg+ has multiple and many uses. I personally administer it for status Asthmaticus as well. It has varied responses and no real scientific reason on why it works, but anecdotally has been demonstrated on several of my patients. I also use Mg+ for severe Alcoholic, dehydrated, patients as well as some chest pains ( hx of dialysis) and of course pre & even post eclampsia patients should be considered.

R/r 911
 
yeah, haven't personally used it for status asthmaticus but have heard that it is a bit of a smooth muscle relaxant. our protocols are to try it as a bit of a last ditch effort if duo nebs, epi, CPAP etc. aren't working.... wow that was way off topic
 
I wonder what reason(s) they are wanting to use Mg+ for CVA? If you have more information please post.

Mg+ has multiple and many uses. I personally administer it for status Asthmaticus as well. It has varied responses and no real scientific reason on why it works, but anecdotally has been demonstrated on several of my patients. I also use Mg+ for severe Alcoholic, dehydrated, patients as well as some chest pains ( hx of dialysis) and of course pre & even post eclampsia patients should be considered.

R/r 911

Per the lit I could access from their website (I don't seem to have access to much of the actual lit, this is from their propaganda):

Apparently Mg has antagonistic effects on the NMDA receptor, as well as presynaptically inhibiting GLU release in the first place. I suspect this is the initial reason they looked at Mg specifically, as a good part of stroke research at the moment is the search for a safe and effective NMDA/GLU receptor antagonist to prevent excitotoxicity. I guess they also found that it caused some local cerebral vasodialtion and some other metabolic effects involving inhibition of Ca++ release via blocking the ion channel.

Translations:

NMDA = a synthetic analogue of Glutamate (GLU), binds only to specific NMDA GLU receptors in the brain, to which GLU will bind, but GLU binds to all GLU receptors, not just the NMDA GLU receptors.

Glutamate = excitatory neurotransmitter (as opposed to inhibitory neurotransmitter) which depolarizes a neuron which possesses a GLU receptor (aka moves it closer to firing).

excitotoxicity: over stimulation of neurons by an excitatory neurotransmitter (E.g. GLU acting on NMDA receptors). This is one of the primary pathological processes in stroke, the accumulation of GLU is a result of ischemia and results in overstimulation of a neuron and then neuronal death due to accumulation of Ca++ in the cell.

Thus: the idea is to stop the overactivation of a cell which posesses a GLU receptor in an ischemic episode. This is accomplished by antagonizing (blocking) the GLU receptor (specificially the NMDA class of GLU receptors in this case) and thus blocking the overstimulation of cells, and therefore hopefully saving the neuron.
 
Thanks for the information. I kinda wonder if they are s-t-r-e-t-c-h-i-n-g it maybe. If it works, great !

R/r 911
 
yeah good piece of info to know, thanks for the heads up...even though my protocols won't pick up on it any time soon.
 
I wonder what reason(s) they are wanting to use Mg+ for CVA? If you have more information please post.

Mg+ has multiple and many uses. I personally administer it for status Asthmaticus as well. It has varied responses and no real scientific reason on why it works, but anecdotally has been demonstrated on several of my patients. I also use Mg+ for severe Alcoholic, dehydrated, patients as well as some chest pains ( hx of dialysis) and of course pre & even post eclampsia patients should be considered.

R/r 911
On the website for the study, there is a list of participating hospitals. I frequented almost every single one of them in my old service. I forgot about where I had heard this from, but I looked it up the next day. Im not sure if it is still going on or not. Apparently, Magnesium exhibits neuroprotective qualities, improves blood flow to the area of infarct, and "reduces size of stroke". I have never heard of such a thing, so curiosity lead me to post here to determine if others have heard about this, and most importantly the study was experimenting with administration by paramedics in the field. The participating agencies include(d) LA City Fire and County Fire.
 
Per the lit I could access from their website (I don't seem to have access to much of the actual lit, this is from their propaganda):

Apparently Mg has antagonistic effects on the NMDA receptor, as well as presynaptically inhibiting GLU release in the first place. I suspect this is the initial reason they looked at Mg specifically, as a good part of stroke research at the moment is the search for a safe and effective NMDA/GLU receptor antagonist to prevent excitotoxicity. I guess they also found that it caused some local cerebral vasodialtion and some other metabolic effects involving inhibition of Ca++ release via blocking the ion channel.

Translations:

NMDA = a synthetic analogue of Glutamate (GLU), binds only to specific NMDA GLU receptors in the brain, to which GLU will bind, but GLU binds to all GLU receptors, not just the NMDA GLU receptors.

Glutamate = excitatory neurotransmitter (as opposed to inhibitory neurotransmitter) which depolarizes a neuron which possesses a GLU receptor (aka moves it closer to firing).

excitotoxicity: over stimulation of neurons by an excitatory neurotransmitter (E.g. GLU acting on NMDA receptors). This is one of the primary pathological processes in stroke, the accumulation of GLU is a result of ischemia and results in overstimulation of a neuron and then neuronal death due to accumulation of Ca++ in the cell.

Thus: the idea is to stop the overactivation of a cell which posesses a GLU receptor in an ischemic episode. This is accomplished by antagonizing (blocking) the GLU receptor (specificially the NMDA class of GLU receptors in this case) and thus blocking the overstimulation of cells, and therefore hopefully saving the neuron.
I had read that, and than from an AHA document read that it dilates blood vessels in the brain leading to increasing perfusion.
 
Yup, LA County is doing an experimental trial with FastMag, though I've yet to see it used.

You have to have very clear uni-lateral symptoms of stroke and be within a specific age range and it must be given with a specific time frame (so unwitnessed events where patient is unable to communicate don't work).

A lot of the time medics don't even remember to use it, though.
 
As long as were on the Mag topic, does anyone ever use or have the time to use for say long ETA's Magnesium Sulfate for refractory status asthmaticus? i have heard of using a slow infusion over 15-30 minutes with a 2g max. i guess you could use Methylprednisolone but i don't think anyone here would have a good enough reason to carry it on their rig.
 
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Actually I give Mg+ for status asthmaticus a lot in the field. Especially on some of our "known" asthma patients it is the only med that will break it. I mix 2gm in 50 ml and infuse over 15 to 30 minutes, usually ending as we are arriving in the ER. As well, our protocol on all asthma and COPD patents is Solu-Medrol is 125 -300mg IVP. Why not carry it? Treatment is treatment in or out of the rig! It takes upto 20 minutes to work, so why wait? Waiting, especially in asthma = death. One has to be agressive in care for airway constrictions.

There is no REAL proof Mg+ works in all asthma patients. Anecdotal, I have seen it work in about 50%. Another medication I have seen work well is Morphine Sulfate, it acts upon the smooth muscles and releases histamines.

I have even placed Decadron in a nebulized form to reduce swelling in the alveoli.. one has to think outside the box on asthmatics. They will die!

R/r911
 
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To continue on what Rid said... Anything to reduce the severity of an asthma attack is a great thing. Even if they aren't knocking on death's door, fast ALS treatment (steroids, etc) in the field may reduce or eliminate an inpatient stay for that patient. This is in the best interest of the patient, as well as reducing strain on the hospital's inpatient capacity.
 
I am sure our friend & EMT Life Pulmonologist -Vent can be more detailed and maybe start a thread on some new and current treatment of Asthma..

R/r 911
 
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