Interesting run recently

Epi-do

I see dead people
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We were dispatched for an overdose and show up onscene with PD. Our patient is a mid-50s female that took 10 ativan and 25-30 Coreg. Her initial BP was 60's/30's, pulse was 70's, and resp. rate was 16-18. She was complaining of dizziness and nausea. She was in a sinus rhythm.

I had to start an EJ, because she had absolutely nothing else to stick. I then pushed 3 mg of glucagon. Her pressure slowly began to rise and she was in the low 80's systolic when we got to the ER. I gave them a heads up to let them know what I had. When giving report to the RN at the ER, apparently she wasn't aware of glucagon being the treatment for beta blocker OD, and asked why I gave it and if the patient had low blood sugar.

I was also able to find out that the hospital was going to start a glucagon drip and an epi drip on the patient.

From what I can find out, glucagon has positive inotropic and chronotropic effects upon the heart. At the same time, however, it can cause vasodilation. By using the glucagon receptors in the heart, you are more or less "going in the back door" since the beta receptors are blocked.

Until I researched this, I didn't even know there were glucagon receptors in the heart. I have always wondered why it worked, but could never get an answer from anyone. So, since I learned something new, interesting, and important to understand, I thought I would pass it along so others who didn't know had a very simplistic understanding of what was happening and why it worked.
 
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Strangely enough, I was just reading up on glucagon and it's used for anaphalyxis. Granted this one wasn't anaphalyxis, it had the same general idea.


From my schools page

Understanding the role of glucagon in anaphylaxis requires knowledge of specific cellular biochemistry. Cyclic adenosine monophosphate (cAMP) is a nucleotide (protein molecule) that plays an important role in many biological processes. Located in the cell’s fluid, cAMP is a secondary messenger, which means it relays a signal in the cell to transfer effects for a specific hormone. When a large amount of cAMP is produced in the cell’s fluid, hormones such as epinephrine or glucagon work more effectively.

Epinephrine acts on beta-2 receptor sites of smooth muscles in the airways. When the beta-2 receptors are stimulated, cAMP is produced, relaxing the smooth muscle cells and opening the airways. If a patient is currently taking a beta blocking agent—especially a noncardioselective type, such as propranolol, naldolol, or sotalol—epinephrine may not effectively utilize beta-2 receptors. In these cases, cAMP is not produced, the bronchial smooth muscle cannot relax, and the patient’s airway remains compromised. To achieve bronchodilation and subsequent effective air exchange in a patient on beta blockers, 1 mg of IM or IV glucagon may be administered. Glucagon works by stimulating higher cAMP levels and overrides the alpha and beta receptors so that epinephrine does not require those receptor pathways to work. Glucagon has documented positive inotropic and chronotropic effects on the heart.

Patients treated with glucagon require close monitoring of their blood glucose levels because glucagon elevates serum glucose. Although current research has not directly studied its effects in anaphylaxis, glucagon acts independently of alpha and beta receptors and can counteract the systemic effects of anaphylaxis. Emergency care providers should consider glucagon therapy when treating the anaphylactic patient who is taking a beta blocker or is refractory to epinephrine.
 
Just curious here but did you give glucagon because it was in your protocol or did you do it because you found information regarding glucagon and your scenario?

Sounds like a good job on your part - I'm just weary of going outside of protocol on weird situations, if that's the case.
 
Just curious here but did you give glucagon because it was in your protocol or did you do it because you found information regarding glucagon and your scenario?

Sounds like a good job on your part - I'm just weary of going outside of protocol on weird situations, if that's the case.

It is in our protocols. I didn't finally find some information that explained how it worked to me until after the run. (I know, I know.....) Although I had asked about it in the past, everyone I asked could only tell me that they know it works, but not why it works. I finally, after this run, decided to be more proactive in finding the info and did a search on the net to find out the answer to "why."
 
Strangely enough, I was just reading up on glucagon and it's used for anaphalyxis. Granted this one wasn't anaphalyxis, it had the same general idea.


From my schools page
Learn something new everyday.... Thanks Linus
 
Oh god, I'm geting old! Each new generation that comes along finds out about the wonders of glucagon, and I feel like I've seen them all! ^_^

That said, sounds like a good job Epi. It's interesting that it is actually in your protocol as it isn't a 'that' commonly encountered issue.
 
We have glucagon for BB overdose in protocol as well. I always heard the dose required for BB OD was more then what is typically carried. It's nice to read a scenario and get an idea what dose works to what degree.
 
Up to 5mg 5 minutely which is typically a lot more than is carried in most rigs.
 
On the Paramedic Units I run on with school they carry 4mg on each unit.
 
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