Nicotine is a cholinomimetic, similar to the -stigmines and organophosphates. Increase in ACH increases parasympathetic activity from the Nicotinic Receptors. Expect cholinergic toxidrome, but with a caveat. One of which being that atropine would not be the antidote for this, given its activity on muscarinic acetylcholine receptors and not nicotinic. Atropine may be used for some respiratory symptoms.
If we look at nicotine as something that triggers rapid neural and neuromuscular transmissions, then we can understand the end goal of its presence being the mimic of excess acetylcholine.
Therefore, we could say that functionally, the end result of a toxicity is similar to an overdose of anti-acetylcholinesterase, but there is a biphasic action in the setting of extreme overdose. First it appears to have a stimulant effect, then it will look more like cholinergic excess afterwards.
In particular, nicotinic agonists, or just nicotine alone, paradoxically leads to a constellation of cholinergic + sympathomimetic findings, since nicotinic receptors are located on postganglionic nerves in both the sympathetic and parasympathetic nervous systems. The respiratory depression is what proves to be fatal.
These cases are patients who I, or my colleagues have seen. They are de-identified and many instances have been presented in more depth in an academic setting.
These videos are not individual medical advice and are for general educational purposes only. I do not give medical advice over the internet.