Anaphylaxis!

akulahawk- You can give Epi IV (I assume for Allergic reactions, since thats what the convo is about) But you cant give it IM?!?!?!?!?!? That doesnt make a whole lotta since to me...

I know some places give it IV for Allergic Reactions, but they (your system) thinks that is safer then IM?!?!?!?!?!
 
akulahawk- You can give Epi IV (I assume for Allergic reactions, since thats what the convo is about) But you cant give it IM?!?!?!?!?!? That doesnt make a whole lotta since to me...

I know some places give it IV for Allergic Reactions, but they (your system) thinks that is safer then IM?!?!?!?!?!

We give IM first IV second. I don't see how IV would be more 'dangerous' provided your giving at the correct concentration. If you're at the point of giving it IV the patient is in a bad state.
 
We give IM first IV second. I don't see how IV would be more 'dangerous' provided your giving at the correct concentration. If you're at the point of giving it IV the patient is in a bad state.

There's a difference in absorption and peak plasma levels. If we give 300 ug (0.3mg) IM, it has to diffuse through the connective tissue, into a capillary, into the venous circulation, etc. and it takes a while for it to get into the circulation. Case in point, slower onset and longer duration of pain relief with IM morphine.

If I give an IV dose of epinephrine, e.g. 100ug (0.1mg) of 1:10,000 IV, I get instant absorption, by definition, and I'm giving a huge pressor dose of epinephrine in one go (consider a normal epinephrine drip is 0.5 - 10 ug/min -- This is the dopamine equivalent of giving 200ug / kg in one minute, if you want to think about it another way).

So the coronaries, the heart, and the cerebral circulation are going to get exposed to much higher concentrations of epinephrine than they'll see if you give even a much larger amount IM.

This means you now have a hugely elevated risk for coronary vasospasm, cardiac arrhythmia, and a very sudden hypertension. The bonus is that the plasma concentrations will fall very rapidly, so this will probably be short-lived. But there's definitely associated risks.

* Anecdote. I had a near-death anaphylaxis patient, profoundly desaturated, SpO2 reading 68% (for whatever that's worth - we all know the accuracy is questionable at that level), with no palpable radials, ST @ 180 with multifocal PVCs, and intermittent hypoxic seizures. Horrible compliance. Two doses of 0.1 mg epinephrine 1:10,000 IVP later, and I've still got a train wreck, but I now have improved compliance, an SpO2 of 82%, radial pulses and a pressure of 190 / 120. [End result an ETT, another 0.8 mg of epinephrine IM, some benadryl, sedation, analgesia, MDI ventolin, etc.].

IV administration is there for the near death patient where there's minimal perfusion to the muscular tissues, and we can't wait for the effects of IM epinephrine to take place. I've heard of people giving very high doses of epinephrine IV, e.g. 0.3-0.5 mg doses to people in moderate distress, because "I have the IV, so why not?". This isn't smart, it's exposing the patient to a very unnecessary risk.
 
Glucagon 0.5mg IVP, IM?

Is this standard protocol anywhere that anyone knows of?

Nice call.
 
akulahawk- You can give Epi IV (I assume for Allergic reactions, since thats what the convo is about) But you cant give it IM?!?!?!?!?!? That doesnt make a whole lotta since to me...

I know some places give it IV for Allergic Reactions, but they (your system) thinks that is safer then IM?!?!?!?!?!
Late response, I know... but yes, IV epi is base order only. That's 0.1mg epi slow IVP, only for stridor and hypotension. They want us to manage those patients with Subcut. Epi, Benadryl IM, 2.5mg albuterol and saline... unless you're doing an IFT and your patient presents with anaphylaxis with stridor and hypotension. You can then simply do the 0.3mg subcut, 50mg Benadryl IM, start a line, and begin 0.1mg epi slow IVP as soon as you think it's clinically indicated. IFT is treated differently in the protocols.
 
I'm with systemet on this one. IM use of Epi is a compromise between SQ and IV. You get faster action than SQ, but a drawn out administration that reduces cardiac risk. We are permitted to give IV only for FTD patients.
 
it is in our protocols. 1mg glucagon IVP q5 if they are on b-blockers.

I believe i've been told it will take a bit more Glucagon than that to reverse a beta blocker overdose. Its more like 3+ milligrams as a first dose and then keep pushing til you get a good response. I'm finishing up my intermediate, and Glucagon is in my scope, so the question gets brought up a lot in class.
 
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I believe i've been told it will take a bit more Glucagon than that to reverse a beta blocker overdose. Its more like 3+ milligrams as a first dose and then keep pushing til you get a good response. I'm finishing up my intermediate, and Glucagon is in my scope, so the question gets brought up a lot in class.

I think you're probably right, and the dosing is going to be limited in most ambulances by the amount of glucagon on the ambulance, which is probably going to be < 5 mg total. But you're going to need less to reverse the effects of the patient's prescription beta-blocker compared to an overdose with a much larger quantity of beta blocker on board. There's also the question of whether a small improvement with glucagon might allow you to avoid using a more dangerous drug / therapy.
 
I never would have though about the Glucagon.

I know it can be used in beta-blocker OD's but I have just one question of clarification.

So in a patient taking betablockers in which epi isn't working you should consider Glucagon? Or is there more to it?
 
I never would have though about the Glucagon.

I know it can be used in beta-blocker OD's but I have just one question of clarification.

So in a patient taking betablockers in which epi isn't working you should consider Glucagon? Or is there more to it?

The way it was explained to me and it may have even been in this thread, I don't remember, is that glucagon opens a "back door" so to speak. It bypasses the second messenger system of the cells which bypasses the beta blockade and allows for the desired effects of the beta stimulating meds.

Someone please correct me if I'm wrong.
 
The way it was explained to me and it may have even been in this thread, I don't remember, is that glucagon opens a "back door" so to speak. It bypasses the second messenger system of the cells which bypasses the beta blockade and allows for the desired effects of the beta stimulating meds.

Someone please correct me if I'm wrong.

This is the essence of it. Strictly, it would be more correct to say that glucagon activates a separate non-beta receptor (the glucagon receptor), that's coupled to the same second messenger system, and results in similar downstream responses.
 
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