# Reflex Bradycardia with Atropine



## kindofafireguy (Jun 10, 2014)

I couldn't find this exact question anywhere, but if it's already answered somewhere please forgive me.

Had this question on my paramedic homework:
.  Your patient is in sinus bradycardia at a rate of 36 beats per minute when you arrive.  She relates that she has been feeling weak and dizzy but otherwise seems fine.  You determine to start an IV and administer 0.5 mg of atropine.  Immediately after administration, your patient’s heart rate drops to 16 beats per minute and she loses consciousness.
	a.  what mistake did you must likely make?
	b.  what should you do to correct the situation?

I'm assuming it's a reflex bradycardia of some sort but I'm confused on the action. If it's obvious, I'm going to beat myself.


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## blindsideflank (Jun 10, 2014)

Dunno if we are supposed to help with homework but I would also look I to 2nd degree blocks and what happens when you speed up the rate


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## DesertMedic66 (Jun 10, 2014)

Also look up what happens if you give too much or too little.


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## joshrunkle35 (Jun 10, 2014)

blindsideflank said:


> Dunno if we are supposed to help with homework but I would also look I to 2nd degree blocks and what happens when you speed up the rate




The question says "sinus bradycardia" not just a "bradycardic rate".


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## joshrunkle35 (Jun 10, 2014)

I'm a pretty new medic, so take this with a grain of salt:

I may be misreading the question, but I know one problem would be giving the wrong dose of Atropine. If you give too little, it could cause reflex bradycardia. One mistake that could be made would be that while you "determined" to give .5 mg of atropine, you did not. You should immediately determine how much you actually did give and correct the dosage. Switching away from drugs and going to TCP might be another way to try to fix the situation until you get to definitive care or they self-correct. Some studies have shown no discernible advantage with pacing over drugs, one way or the other. 

Other things, I would want a BP, to rule out high BP/head injury/ICP, and give O2. Should do a 12 lead instead of just a 3 lead as well if you can. 

Obviously, in the real world, it takes time to get a monitor hooked up, get an IV started, etc. I would be politely and calmly firing question after question about history, dizziness, recent injury, etc.


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## Handsome Robb (Jun 10, 2014)

I'd bet the mistake you made is you gave 0.5 mL instead of 0.5mg. 

Since they're now severely symptomatic they're going to get transcutaneous pacing unless it's a transient change that corrects itself quickly. 

I've looked for the answer to what causes the reflex bradycardia before and never been able to find a good explanation. usually just listed as a side effect if too low (<0.5mg) is given to an adult.


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## joshrunkle35 (Jun 10, 2014)

Also:

"The decision point for ACLS intervention in the bradycardia algorithm is determination of adequate perfusion. For the patient with adequate perfusion, you should observe and monitor. If the patient has poor perfusion, preparation for transcutaneous pacing should be initiated, and an assessment of contributing causes (H’s and T’s) should be carried out."

https://acls-algorithms.com/bradycardia

Feeling weak and dizzy could be signs of inadequate perfusion, assuming no other history. I guess according to ACLS, you should use TCP first.


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## Bearamedic (Jun 10, 2014)

You missed the iv? You didnt flush the iv site and failed at giving the entire dose? 
(Which would be .5ml of a 1mg/1ml vial at my workplace)


I would be slightly torn if this would have happened to me, a small part of me would want to flush the iv (finishing the atropine dose if its a flush issue), and the other part would want tcp and then start a new iv and dc the old one

Id probably prefer tcp. 


As to the cause of paradoxical bradycardia, i was taught (but dont entirely trust) was that the little bit of atropine blocks the vagal acetylcholine (slow down) response by blocking acetylcholine receptors at the sa node which increases the amount of acetylcholine in the synapse for more stimulation of other muscarinic acetylcholine receptors at the same synapse in the sa node. Atropine doesnt lower the total sa node muscarinic receptor activations until more muscarinic receptors are antagonized. 

I tried to simplify some of the verbs for comprehension.


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## kindofafireguy (Jun 10, 2014)

This is research homework, and the instructions say that not all answers will be in our books. Therefore, we need to research, use the internet, doctors, preceptors, etc. to find the answers. Medicine is, after all, a field of research. If you don't know the answer, find it.

Also, I don't have the option of TCP as this is pharmacology homework.

I also feel like there is a lot missing from the question to make any judgments about the answer, but my clinical coordinator thinks its reflex bradycardia in compensation for MI, and that atropine is knocking out the compensatory mechanism. 

Seems like a fair enough answer, based on what little provided.


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## rmena (Jun 10, 2014)

http://www.cob.org/cob/policies.nsf/0/7D3BC1D24BDAAE72882574D40064E06B

If given too slowly Atropine will actually cause greater bradycardia. That is probably what they are looking for. Its under adverse effects on the above website as well as on medex. Hope this helps


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## kindofafireguy (Jun 10, 2014)

Thanks. That's probably exactly what they're looking for.


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## Handsome Robb (Jun 10, 2014)

Bearamedic said:


> You missed the iv? You didnt flush the iv site and failed at giving the entire dose?
> (Which would be .5ml of a 1mg/1ml vial at my workplace)
> 
> 
> ...




It would've been easier to read without the simplification haha but that actually makes some sense if I'm understanding what you're getting at correctly.


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## blindsideflank (Jun 11, 2014)

joshrunkle35 said:


> The question says "sinus bradycardia" not just a "bradycardic rate".



And?...


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## rmena (Jun 11, 2014)

indicating that the Brady is coming from the sa node as opposed to an av block.


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## rmena (Jun 11, 2014)

Or junctional rhythm


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## Christopher (Jun 11, 2014)

joshrunkle35 said:


> Also:
> 
> "The decision point for ACLS intervention in the bradycardia algorithm is determination of adequate perfusion. For the patient with adequate perfusion, you should observe and monitor. If the patient has poor perfusion, preparation for transcutaneous pacing should be initiated, and an assessment of contributing causes (H’s and T’s) should be carried out."
> 
> ...



If the patient is in sinus bradycardia the jump to TCP is a bit extreme.


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## joshrunkle35 (Jun 11, 2014)

Christopher said:


> If the patient is in sinus bradycardia the jump to TCP is a bit extreme.




Yet, apparently, ACLS says that perfusion is the key factor in decision making.


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## NomadicMedic (Jun 11, 2014)

joshrunkle35 said:


> Yet, apparently, ACLS says that perfusion is the key factor in decision making.



While perfusion is the breakpoint, the ACLS algorithm still recommends atropine as the first intervention.


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## rmena (Jun 11, 2014)

yep atropine first unless its an av brady then go straight to pacing. you can try atropine on a block but it wont work


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## Christopher (Jun 11, 2014)

rmena said:


> treat the pt not the monitor



Treat the patient _and the monitor_. It provides exceedingly useful information...like you know...what the patient's heart is doing. A fairly important piece of information during bradycardia.

Use the patient's history, presentation, *and ECG* with the mnemonic "DIES(SS)" for bradycardia: Drugs, Ischemia, Electrolytes, Sinus Nodal Dysfunction/Sick Sinus Syndrome.


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## Bearamedic (Jun 11, 2014)

blindsideflank said:


> And?...




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.


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## Carlos Danger (Jun 11, 2014)

Bearamedic said:


> 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?


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## Bearamedic (Jun 11, 2014)

Remi said:


> 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


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## Carlos Danger (Jun 12, 2014)

Bearamedic said:


> 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?


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## VFlutter (Jun 12, 2014)

Bearamedic said:


> 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?


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## Anjel (Jun 12, 2014)

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.


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## Carlos Danger (Jun 12, 2014)

"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


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## kindofafireguy (Jun 12, 2014)

Does anyone have any explanation for the mechanism by which pushing atropine slowly causes reflex bradycardia?


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## Bearamedic (Jul 6, 2014)

Remi said:


> 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.


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## Bearamedic (Jul 6, 2014)

Chase said:


> Huh?



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.


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