ganglionic blocker and tachycardia

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tarsuc

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So if a patient is given a ganglionic blocker like Hexamethonium, it abolishes the predominant autonomic tone: Hence SANS is abolished for vessels and sweat glands, and PANS abolished for the heart and everything else.

So how do explain the tachycardia seen with hexamethonium?

a) As predominant PANS (bradycardia) is abolished, the opposite SANS (tachy) comes into effect.
How is this possible? isnt the ganglia ( both SANS & PANS) blocked?

b) the tachycardia of hexamethonium is because the heart tends to beat at its own intrinsic rhythm, after PANS is abolished.

i know b) is the right answer, then how do we explain constipation and urinary retention etc with hexamethonium? 🙁
 
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The parasympathetics rules the nodal cells, hence tachy. The parasympathetics also rule bladder, hence retention.
 
The parasympathetics rules the nodal cells, hence tachy. The parasympathetics also rule bladder, hence retention.
So when you abolish the predominant tone, it automatically jumps to the opposite one; even thought the ganglia is blocked?
 
So when you abolish the predominant tone, it automatically jumps to the opposite one; even thought the ganglia is blocked?

Well, both are blocked so there is no reflex. HR is intrinsic. Where do you see tachycardia from? I've not read that as a side effect / toxicity of hexamethonium.

Urinary retention is a parasympatholytic side effect (M3) not because of increased alpha1.

At least this is my understanding.
 
Yeah, lytic effects. Know the predominant tone... eliminate, leads to opposite response.

Nodal cells are run by PS... lyse in ganglionic blockade.

Bladder predominant is PS... same idea.

Keep it simple.
 
So when you abolish the predominant tone, it automatically jumps to the opposite one; even thought the ganglia is blocked?

Abolishing what is the strongest thing means the strongest thing has less effect. There are only 2 ways to go. You aren't activating anything.
 
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