neurogenic shock arrest w/ atropine

[Mateo_1387]

I see Matty's point...(With blood flowing towards gravity then you need to roll them over every couple of minutes...right? ), and your original point is outstanding.

Exactly !

Using atropine does not eliminate the release of acetylcholine from the CNS, or the preganglionic sympathetic nervous system. It will reduce the effects of acetylcholinesterase in the neuromuscular junction resulting in less breakdown of the Ach, but it does not stop it from functioning. The neurotransmitter functions will still be present as atropine works predominantly at the muscarinic receptor site, not in the NMJ.

I have a question about the above. Does atropine affect how acetylcholinesterase processes Ach? I was under the impression (from what I was taught, and what I have read) that Atropine's mechanism of action is to block the muscarinic receptor site to promote Sympathetic nervous system control.

I respect your post AZCEP, as this is not an attack on my part, but an effort to understand what you are saying, as I have not heard of this.

[AZCEP]

Atropine will preferentially affect the muscarinic use of Ach by limiting the neuromuscular junction's ability to reabsorb the acetylcholine that is released. When this happens in PNS nerve fibers the response is a blunting of effects.

[medicv83]

Rest assured, I am in no position to validate anything. The medical world is much much bigger than me and my little mind. Initially, it was a question simply about the basic effects of atropine use in the neuro shock, arrest patient. Would it, or would it not be beneficial. With that, I have totally learned alot just reading everyones input here, and I appreciate everyone responding. So far I have gathered that I will have to delve into the deeper aspect of the pharmacodynamics of Atropine.

My thought was that, Atropine, being the parasympatholytic that it is, would cut off the only source of autonomic tone to the body, and with that, would not be beneficial. Thats all. No validation, no nothing, simply trying to discern the actions.

[ccmedoc]

I was just trying to understand the conversation..I probably could have worded it differently, but the discussion seemed to be getting more and more clouded. I guess I thought there was a point I was missing..

Oh well, live and learn.. 8)

[medicv83]

I think I was totally off, well, was to vague with my impression of Atropine's effects on the parasympathetic nervous system.........So the impression here is that, with Neurgenic shock, administration of Atropine in the Cardiac arrest setting will not adversly effect resuscitation?

Shall I even ask the question of the alive Neuroshock patient and the use of atropine?

[DwayneEMTP]

I was just trying to understand the conversation..I probably could have worded it differently, but the discussion seemed to be getting more and more clouded. I guess I thought there was a point I was missing..

Oh well, live and learn.. 8)

No, I think you're right regarding the original post, it just seemed to me that we ended up more in an exploration of the physiology than a cut and dried discussion of the question.

Your post was very clear, but I think the thread had ended up playing with the question at that point as opposed to simply answering it. To tell the truth I haven't even consider much of that information in months....it was a welcomed slap in the face that a serious review is necessary. :wink:

No offense intended with my reply. I simply wanted to make it clear to the poster that whether he was right, wrong, or completely whacked as judged by the responses, that his post was interesting, educational and absolutely appropriate.

As it turns out, he's perfectly capable of taking care of himself...He didn't really need support from the peanut gallery.

Have a great day all.

Dwayne

[chbare]

Another bit of information that may help us understand the confusion behind the physiology of atropine. The primary action of atropine is competitive in nature. It simply competes with AcH at the postganglionic receptor.

This makes sense when we consider another condition. Consider Organophosphate exposure. What occurs at the level of the receptor? Cholinesterase is inhibited and AcH accumulates without anything to break it down. Thus, these people typically require large and often repeated doses of atropine because we have so much AcH to compete with.

I hope this helps.

Take care,

chbare.

[AZCEP]

So the impression here is that, with Neurgenic shock, administration of Atropine in the Cardiac arrest setting will not adversly effect resuscitation?

Correct. By eliminating the PNS effects, the SNS will be able to have more effect. Chances are in the neurogenic shock patient, the SNS will be eliminated as well, but eliminating the PNS from the equation will not be a detrimental action.

Shall I even ask the question of the alive Neuroshock patient and the use of atropine?

The situation doesn't change too much. You would still be trying to eliminate the cholinergic effects so the adrenergic could have an effect.

[medicv83]

Makes perfect sense! Thanks again for everyones input!

[firedoc5]

I've had experience with this one. Had a pt. PEA (EMD for you old farts) showing 2nd degree block type one (Wenke-bach). At first Gene and I looked at each other and shrugged our shoulders. Both Epi and Atropine did work, but for very shortly. Medical control couldn't believe the rhythm we were getting so when we got to the hosp. we showed them the strip and said "told you so". Even a pulmo. doc said he'd never seen it. The pt. had a CVA hence the neurogenic shock. Would I do it again? Don't know. Ask your medical director what he/she thinks.