Atropine, not for peds

[hammerpcp]

Why?

[hertzvanrental]

Depends what you are using it for. In children bradycardia is most commonly caused by hypoxia which needs rapid ABC care , not drug therapy.In the UK we are told according to JRCALC guidelines that we should only give it in cases of bradycardia caused by vagal stimulation(i.e suctioning and intubation) or for organophosphate poisoning.

[AZCEP]

Up to age 6 years, the parasympathetic nervous system is poorly formed. From 6- about 10 years, the parasympathetic begins to have more effect on the cardiovascular system.

Depending on the context in which you are considering using it, Atropine probably won't give any great response. For pre-intubation, Atropine is used to blunt the sudden increase in vagal tone created by manipulating the oropharynx. For bradycardia, the Vagus nerve is not having a direct effect unless it has somehow been stimulated through other means.

Under 6 years, kids are purely sympathetic. Running, moving, growing, then energy supplies run out, and they go to sleep where they fall.

Between 6 and 10, the parasympathetic is beginning to exert more influence. After 10, the systems are more like an adult.

[Lithium]

Cuz that's what your protocols say!

ha ... sorry, had to throw that in there

[hammerpcp]

Cuz that's what your protocols say!

ha ... sorry, had to throw that in there

PFFFTTTTT.

Azcep,

Thanks teach. So, more questions.....if the parasympathetic NS is poorly developed (namely the vagus nerve) why would there be a sudden increase in vagal tone during intubation? I wouldn't expect a poorly developed system to not have much effect under any circumstances. Also i wonder why they often give atropine to peds in hospital but it is contraindicated prehospital (as Lithium mentioned)? Any ideas?

Another question (I'll allow that this may be a dumb one), but stay with me here. So Atropine is a parasympatholytic, meaning it blocks the parasympathetic nervous system (effects on the heart at least), which means that the sympathetic nervous system can then exert its effect uninhibited or unchallenged. This leads to an increase in heart rate (hopefully). So a pediatric pt experiencing bradycardia- that can not be corrected with proper or improved oxygenation- who has a poorly developed PNS in the first place should be more effected by a blocking of the PNS. No? Is any one else confused? 8-[

[medic429]

we administer atropine for peds....

bradycardia - .02 mg/kg (min. dose .1mg)

--of course that's after ABCs......and after epi

[AZCEP]

Thanks teach. So, more questions.....if the parasympathetic NS is poorly developed (namely the vagus nerve) why would there be a sudden increase in vagal tone during intubation? I wouldn't expect a poorly developed system to not have much effect under any circumstances. Also i wonder why they often give atropine to peds in hospital but it is contraindicated prehospital (as Lithium mentioned)? Any ideas?

The vagus nerve is still there, the effects of the system really aren't fully developed. So, when we do something to stimulate the vagus nerve, it will tend to overcompensate when it responds. The adult system is being used much more often, so the sudden release of Acetylcholine won't result in as large a reduction in sympathetic effects. The use of Atropine in the hospital is more related to the amount of time they are with the patient, than a indication of parasympathetic activity. When prehospital has a kiddo with a bradycardia, we focus on the more likely reasons they are bradycardic. Oxygenation issues come first, sympathetic next. If you are with this kid long enough, and have adequately oxygenated them, and supplemented their SNS with your epinephrine, and haven't gotten a response, trying some atropine might be worth taking a look at.

Another question (I'll allow that this may be a dumb one), but stay with me here. So Atropine is a parasympatholytic, meaning it blocks the parasympathetic nervous system (effects on the heart at least), which means that the sympathetic nervous system can then exert its effect uninhibited or unchallenged. This leads to an increase in heart rate (hopefully). So a pediatric pt experiencing bradycardia- that can not be corrected with proper or improved oxygenation- who has a poorly developed PNS in the first place should be more effected by a blocking of the PNS. No? Is any one else confused? 8-

If the PNS is having little to no effect anyway, then blocking it's action is not going to gain any great result. Kids are sympathetic driven. They need oxygen to allow the mitochondria to create more ATP. They need sugar to provide the fuel for the sympathetic system to burn. Atropine can be useful in specific situations, but for most, kids only need oxygen/epinephrine/sugar.

[hammerpcp]

It's starting to make a little more sense to me now. Thanks Azcep. I will continue to read up on it though, because even all this does not satisfy me as far as why it is contraindicated for peds in our protocols. Perhaps they think we are too dumb to try other options first? I don't know.