Torsades Treatment

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jroyster06

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Have a company meeting with our MD this evening. Our protocol states in Cardiac arrest Tx for Torsades is mag, duh! Question is our protocol states to give it over 10 min. I have googled other protocols and they state give 2mg over 2 min. Seems like in a full arrest, 10 min is too long. I want to bring this up at the meeting but was curious what others thoughts were.
 
Well first off, I doubt 2mg of mag is really going to do anything... ;) But in response to your question: All of my systems use 1-2g over about a minute. The infusion is used more for treatment of asthma.
 
haha dang it i ment 2g
 
for torsads in cardiac arrest we give 2g bolus, for eclampsia we give 2g over 5min.
 
here is an excerpt from some of my notes taken from the current AMLS book related to the treatment of hypomagnesemia/torsades.

In the emergency setting for the patient showing severe S/S, infuse 2-4g magnesium sulfate over 5-10 minutes. DO NOT GIVE MAG SULFATE AS A BOLUS: doing so has been associated with severe side effects, including bradycardia, heart block, and hypotension.
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this is, of course, in a "perfect world" scenario.. in the full arrest setting, with minimal manpower - a diluted SIVP would more than likely suffice...
 
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I have never given anyone mag yet, i imagine i will for asthma within the near future but in NYC, we give 1-2g in 50-100ml of NS over 10 min for asthma/eclampsia and 2g bolus over 2 min for torsades.
 
Curious to some of your math. Isnt Mag supposed to only be given in a 10% solution, infusions and SIVP I mean. Cardiac IE torsades and refractory ectopy and respiratory distress (recently removed) is 1 - 2g and PIH with symptoms and eclampsia is 2 - 4g both in 10% solutiom given over 20min. I know our protocol dictates it and I was under the impression that it was standard of care in both the prehospital and in hospital setting.
 
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2g (1g/2mL) given over 5 mins in a 15gtt/mL set=12 gtt/minute

Right?

If so, doing med math after out at the bar all night....
 
Corky said:
Curious to some of your math. Isnt Mag supposed to only be given in a 10% solution, infusions and SIVP I mean. Cardiac IE torsades and refractory ectopy and respiratory distress (recently removed) is 1 - 2g and PIH with symptoms and eclampsia is 2 - 4g both in 10% solutiom given over 20min. I know our protocol dictates it and I was under the impression that it was standard of care in both the prehospital and in hospital setting.
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10%???? 10% solution of what? Its supposed to be in a 0.9% NS solution.



Has anyone actually had torsades and pushed mag for it? I know it is extremely rare.
 
I have pushed Mag before, although it was after 2 rounds of amiodarone failed to convert the patient.

The mag worked, which leads me to believe it was either a case of very subtle Torsades that I did not identify, or alternatively, a very blatant case of Torsades I did not identify.

I would like to say that we pushed 1g over 5 minutes, but I am sure it was a bit faster than that. We did take care though to try and push it slowly. More reasonably we probably pushed it over 3 minutes or so. 5 minutes is an extremely long time for sure, although it is the minimum time required for administration that I have been able to find in any reference, even in the case of full arrest.

Also, Mag is packaged 2 ways that I have seen. I have seen 50% Mag (1g/2mL) and 10% Mag (packaged in resuscitation ampule, dark brown box.)

If you are using the 50%, it is imperative that you dilute the Mag to below 20% prior to administration (10% is best). It is rough on the vasculature, and higher concentrations are associated with increased complications in hemodynamic status, respiratory status, etc. 0.9% NS or 5% Dextrose in water can be used without noticeable difference.
 
TheGodfather said:
^^ Can I have your brain please?
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Sure you can, one post at a time... It will probably take around 5 minutes to get through the useful information and make it to the stored YouTube videos of squirrels water skiing! :D
 
Dumb question but I'm a newbie. If a prolonged qti is a risk for torsades and hypocalcemia is causes a prolonged at would it be appropriate to give calcium or is it presumed that if you have torsades its hypomagnesium(sp) also we do not have mag so would Amil be appropriate? And could someone please explain overdrive pacing for torsades to me?
 
d_miracle36 said:
Dumb question but I'm a newbie. If a prolonged qti is a risk for torsades and hypocalcemia is causes a prolonged at would it be appropriate to give calcium or is it presumed that if you have torsades its hypomagnesium(sp) also we do not have mag so would Amil be appropriate? And could someone please explain overdrive pacing for torsades to me?
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If the QT prolongation is a congenital thing you'd want to definitely get the HR above 100 in order to shorten your QTc.

The term "overdrive" pacing is at times somewhat of a misnomer (when you have the option of VVI, AAI, or DDD mode) because a lot of the time, you "overdrive" pace at a rate slower than the actual tach, but that's ok because we're pacing asynchronously. With the TCP, you're wanting to pace as fast or faster than the rhythm. Never done it with an external pacemaker, only with the epicardial wires or tvp in place, so someone else who's done it with a TCP may be of more help in that regard. Anywho, the point of overdrive pacing is to allow us to tap into the tachycardia's circuit, interfere, and eventually cause the entrainment of the rhythm.

This is a gross oversimplification but picture this:
Think back to those old western movies where a wild mustang takes off super fast across a valley (usually with some poor damsel in distress aboard). Then the cowboy takes off on his horse and runs equally as fast or sometimes faster, catches up to the wild mustang, tosses a rope around it and then gradually slows it down to where it is now under control and the cowboy's horse is now setting the pace, eventually slowing down to a manageable, less dangerous speed.


I don't know to what you're referring when you say "Amil."

As far as the other stuff, without writing two pages of cardiac action potential (which i assume everyone here already has a good grasp on), the basic premise is that a lack of calcium (and usually potassium as well) means it takes cells longer to repolarize which is identified as a prolonged QT. This can cause early afterdepolarizations (inward depol current is > outward repol current in late phases). Mag lowers the amplitude of the EADs (presumably) via the sodium-potassium ATPase. Vene can expound on this in great detail I'm sure.

You can play with your Nernst equation and see how the varying degrees of your intracellular and extracellular ions affect potential.
 
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TatuICU said:
Vene can expound on this in great detail I'm sure.
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Thanks,

but as I find cardiology to be the single most boring subject in medicine, I will save myself and everyone else the pain of it :)
 
I guess what I'm wondering is treatment for torsades without mag. Ours is defibrilation but what's next in line for pharmacology
 
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