kayak

I had a chance to play around with the advanced medical model a bit with some friends; we had a pretty good time with it. Aside from a few quirks that are to be expected (I can infuse thousands of CC's of Ringer's or saline through someone quickly and without issue, I don't have to worry about plasma or blood stability etc.), I have only been legitimately confused by one aspect of the model so far: atropine. What is the idea behind having atropine induce such significant bradycardia? Every time I have given atropine, its either been indicated for stable bradycardia (0.5 - 1 mg) or organophosphate issues (2-4 mg). I have never given atropine for suspected nerve exposure, but our protocol is a Mark 1 kit with 2 mg of atropine. I do know in the military atropine (in the form of DuoDotes) is the catch-all for chemical attacks with SLUDGEM; I have no experience on the medical side of the military so I can't speak for anything more in depth there. I know there have been a few studies of paradoxical bradycardia from low doses of atropine in some individuals, but it is generally self-resolving unless paired with other drugs or with neurogenic or cardiovascular issues. For the scope of ACE, it seems atropine would not be given in a low enough dose to cause symptomatic bradycardia and should only fit into the medical model for chemical issues, as I don't imagine ACE seeks to simulate escape rhythms or certain heart blocks (especially in the field). If the current effect is in place to deter people from giving atropine incorrectly, you could place other side effects in lieu of bradycardia - there are some pretty annoying ones like blurred vision, nausea and (rarely) confusion and hallucinations. You could also throw in severe tachycardia and really tank people if you were feeling froggy enough.