Mag Sulfate.

NomadicMedic

NomadicMedic

I know a guy who knows a guy.
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Does anyone here have Mag in protocols for refractory VF/VT?
(NOT TdP!!!)
 
We do here. Once we get to round 4 of VF/VT, we throw all kinds of crap at them.
 
Is 2 grams your dose? Does it do anything other than give you something else to push aside from amio and Epi?
 
Our dose is 1g, but we're giving 1.5mg/kg of Lidocaine, and 15mg metoprolol at the same time. Next round is procainamide. I honestly think the thought is throw something at it and hope it works, because nothing else has.

I joke that once we get to round 5, we're just trying to seal the deal since we're blocking nearly every ion channel into the heart.
 
Haha. My wife refers to that point as using "injectable kitchen sink"
 
Nope just for Torsades. 2grams.
 
Sacramento does not use Mag Sulfate at all in a code situation. When I first learned ACLS, we used Epi, Lido, Bretylium, Mag, Procainamide. When Amio was introduced, we could use it in place of Lido. Now, it's just Epi (3 rounds) and Amio (2 rounds), do CPR 20 minutes and cease efforts. I don't think Sacramento County's had mag in their "cardiac arrest" protocol since at least 2001...

I would hazard a guess that Sacramento doesn't use mag at all, actually.
 
We only have it for TDP unfortunately.

I was wondering about that, STX. Once you start throwing multiple antidysrhythmics at someone, especially in the same round, that block different ion channels how the hell do we expect them to come back? Amiodarone is primarily a potassium channel blocker but works on all the channels, lidocaine is a sodium channel blocker. So giving amio then giving lido has effectively blocked the sodium potassium pump, no? Add mag to the equation and you've suppressed contractility as well...

I can see using a class III OR class I plus mag making sense with the reduced contractility and slowing of the sodium potassium pump reducing excitability because the myocardium cannot depolarize as rapidly with the exchange of ions suppressed.

Maybe I'm understanding it wrong.
 
I don't want to jack your thread but I'll leave it up to you. I was wondering what people are doing for these refractory VF/VT arrests? anyone doing double synchronous defibrillation?

Like I said I don't want to steal your thread so I won't be offended if you delete it or move it. Seemed somewhat relevant though.
 
That's exactly my thought as well. By round 5, we've given a 1a and 1b sodium channel blocker, a beta blocker, and a K channel blocker. Not much left... Then I guess we're trying to rebuffer the sodium potassium pump with mag. Acidosis is "neutralized" with bicarb. And contractility and further membrane stabilization with CaCl. Then to top it all off, we shock the hell out of them with double sequential defibrillation (to answer your second post). The entire time said patient has been being cooled with intra-arrest hypothermia.

If all of that fails, they'll get transported to the ED where they'll basically repeat everything we just did. We were originally hoping for our cath labs to accept these refractory VF patients with high suspicion for cardiac etiology, and they were initially all for it. We quickly realized they weren't as accepting as they'd initially said (they never accepted anybody), so now the ED is just left throwing the same sink at the patient.
 
Robb said:
I don't want to jack your thread but I'll leave it up to you. I was wondering what people are doing for these refractory VF/VT arrests? anyone doing double synchronous defibrillation?

Like I said I don't want to steal your thread so I won't be offended if you delete it or move it. Seemed somewhat relevant though.
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Funny you ask that. I haven't had the opportunity yet, but I plan on asking a hopefully amenable doc for orders for double sequential defibrillation when I get a chance. I think we're in a good position to do that here since every cardiac arrest will have two LP15s available on scene, but I don't know how many of our local med control docs would go along with it. Now all I need is a viable cardiac arrest that is in something other than asystole or some funky and unshockable PEA...Believe it or not, I haven't defibrillated one patient since I've been in Delaware.
 
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STXmedic said:
That's exactly my thought as well. By round 5, we've given a 1a and 1b sodium channel blocker, a beta blocker, and a K channel blocker. Not much left...
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You aren't blocking nearly enough Na channels to prevent cellular depolarization, though. With lidocaine, even at doses much higher than 3 mg/kg, toxicity is from nervous system effects, not cardiac. You can give a couple hundred mg to someone with a normal rhythm and it shouldn't effect it at all.
 
STXmedic said:
Out of curiosity, what leads you to suspect hypomagnesemia?
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Malnutrition, alcoholics, (maybe DKA) and maybe GI diseases that prevent absorption or increase secretion (crohns/UC/chronic diarrhea?)

I really only think about drunks/homeless
 
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