|Another example: whatever this guy is doing (source)|
|"Start at 5-15 µg/min"|
A recent case report might cause some EMS providers to worry about administering the appropriate IM dose of 0.3 mg. I don't think that it should - let me explain more.
"Cardiac anaphylaxis: A case of acute ST-segment elevation myocardial infarction after IM epinephrine for anaphylactic shock."
This case report describes the clinical course of a middle-aged gentleman:
A 62-year-old male smoker with no other comorbidities presented to emergency department at 6 am with complaints of generalized pruritus and shortness of breath after taking diclofenac for toothache 1 hour back. On examination, pulse was 97/min; blood pressure, 84/60 mm Hg; jvp, normal; cardiovascular system, unremarkable; respiratory system, rhonchi bilaterally.Sounds like anaphylaxis! The ECG, before epinephrine, showed:
|"Nonspecific [ECG] changes on arrival"|
A second ECG was obtained after the patient developed chest pain:
He underwent PCI, and a thrombus was sucked out of his LAD. He ended up doing well.
Was the STEMI really due to the epinephrine?
I'm not so sure - take a closer look at the initial, "non-specific," ECG:
|Close up of V1-V3|
Well, sometimes anaphylaxis itself can cause an MI. It's called Kounis Syndrome, and there a number of case reports out there:
The Bottom Line
The authors acknowledge this possibility, and also acknowledge that epinephrine-related MI is not typical.
Acute myocardial infarction (MI) following anaphylaxis ("cardiac anaphylaxis") is rare. Epinephrine causing ST elevation in these anaphylactic patients is even more rare.In this case, I wonder about the initial "nonspecific" ECG, and the role of epinephrine in causing his STEMI. Despite the authors' certainty that "high-dose epinephrine 1 mg (1:1000) IM has triggered the formation of a thrombus in the left anterior descending artery," I wonder if the STEMI was underway before they gave the epinephrine.
What do you think?