Reflex Bradycardia with Atropine



It is *possible* for a 2nd degree block mobitz II (below av node) to be almost indistinguishable from any sinus rhythm (more so in a single lead (II), and for a short strip while brady). Atropine could disrupt the av node (and then below), which could lead to a 3rd degree block. Which would also cause a massive drop in pulse as per the question. (And would be visible on the monitor which the question avoided by just saying pulse)

The questioning about the interpretation of sinus brady (vs a brady mobitz II) seemed relevant given that a mistake had been made in this hypothetical.
 
It is *possible* for a 2nd degree block mobitz II (below av node) to be almost indistinguishable from any sinus rhythm (more so in a single lead (II), and for a short strip while brady). Atropine could disrupt the av node (and then below), which could lead to a 3rd degree block. Which would also cause a massive drop in pulse as per the question. (And would be visible on the monitor which the question avoided by just saying pulse)

The questioning about the interpretation of sinus brady (vs a brady mobitz II) seemed relevant given that a mistake had been made in this hypothetical.

How does atropine disrupt the AV node?
 
How does atropine disrupt the AV node? [...and then below...]


By blocking the vagal (parasympathetic/muscarinic/slow down) innervation, increasing the AV node rate past what the bundle of his (the below) can metabolically sustain while it is experiencing (whatever is causing the) mobitz II
 
By blocking the vagal (parasympathetic/muscarinic/slow down) innervation, increasing the AV node rate past what the bundle of his (the below) can metabolically sustain while it is experiencing (whatever is causing the) mobitz II

So it doesn't "disrupt" the AV node at all, it simply speeds up its intrinsic rate?
 
increasing the AV node rate past what the bundle of his (the below) can metabolically sustain while it is experiencing (whatever is causing the) mobitz II

Huh?
 
I was taught if you push atropine too slow that it causes reflexive bradycardia.

As far as high degree AV blocks you are to go to pacing but can push atropine while getting the pacer set up. It's not contraindicated and it's not gonna cause bradycardia.
 
"This interesting physiologic study demonstrated that very low doses of atropine, dosed on a per- kilogram basis, of 0.0036 mg/kg (3.6 ug/ kg) or less may cause a mild slowing of heart rate."

"The most markedly affected children were the 7- to 12-year-olds who had an average decrease in heart rate from 79 to 70 beats per minute; above this dos- age, heart rate was increased by atropine."

"This effect was later demonstrated to be a result of blockade of M1 muscarinic receptors, whereas the familiar tachycardic response is a result of blockade of the M2 and M3 receptors."

"It seems that the strict, universal, often-repeated, minimum absolute dose of atropine is derived from an unsupported and irrational statement."

"This approach to atropine dosing may be dangerous......A dose of 0.1 mg would be toxic for some of our neonatal patients."

The Myth of a Minimum Dose for Atropine
 
Does anyone have any explanation for the mechanism by which pushing atropine slowly causes reflex bradycardia?
 
So it doesn't "disrupt" the AV node at all, it simply speeds up its intrinsic rate?

I disagree with this simplification. The significant functions of the AV node seem to be in creating a pause to allow complete filling of the ventricles, and to serve as a backup pacemaker.

I disagree with your assessment, that during the hypothetical of atropine being given during a second degree type II which resulted in a 3rd degree block, atropine simply speeds up the intrinsic rate.

I argue, that by preventing the ability of the av node to introduce a pause between the atria and ventricular contractions, and by preventing the ability of the AV node to serve as a pacemaker, atropine, in this instance has disrupted the function of the av node.
 

Atropine, which typically (and generally) functions to speed up the heart, usually increases the: oxygen demand, the glucose demand, the electrolytic demands, etc, of the parts of the heart (electrophysiologically) distal (but not limited to) from the SA and AV nodes.

During a 2nd degree type II block, the bundle of HIS is where the disfunctionality typically is. The bundle of HIS shares it's blood supply (obviously) with parts of the heart that also are stressed upon atropine administration.

During the possibility that atropine causes a 3rd degree block, while the heart is in a second degree type II block, it is likely that the bundle of his was [activated] at a rate past what the bundle of his could metabolically tolerate.
 
Last edited by a moderator:
Back
Top