neurogenic shock arrest w/ atropine

[logos]

By what mechanism do you propose that atropine would make the situation worse?

Atropine is a parasympatholytic.

The simplified version of the pathophys is that that you have unopposed parasympathetic tone causing excessive vasodilation. Blocking the parasympathetic input, which causes smooth muscle relaxation, would likely tend to help the situation more than harm. The reality however, is that someone like this likely has very little parasympathetic output owing to the hypotension.

[medicv83]

Ok, I have to hit the reset button, because this will go off on a tangent, which in and of itself is a good thing to study and understand in its entirety. Specifically, the question is....In the brady PEA of a Neurogenic Shock patient (who subsequently arrested), would the use of Atropine be warranted, CONSIDERING its effects on the parasympathetic Nervous system? Two ways to think about the pharmacodynamics of Atropine - 1. It essentially blocks the effects of acetylcholine at parasymp junctions, including vagal introduction into the heart, as well as vasomotor effects. This in turn can help maybe (in my little mind), considering this patient is in cardiac arrest. Logic - he is dead anyways, and the effects of blocking the parasympathetic NS may help with vasopressors and improving vasoconstriction and an increase in inotropy, dromotropy and chronotropy. 2. The administration of Pressors will not work and if Atropine is administered will render the parasymp NS useless, and now we have both portions of the Autonomic NS useless....Which we all know that we need those for resuscitative efforts.

[medicv83]

"Blocking the parasympathetic input, which causes smooth muscle relaxation, would likely tend to help the situation more than harm. The reality however, is that someone like this likely has very little parasympathetic output owing to the hypotension"....logos

Realize you have to have a functional Symp NS if you block out the PNS for vasoconstriction to occur. Blocking the PNS will do nothing without a functional SNS

[logos]

Ok, I have to hit the reset button, because this will go off on a tangent, which in and of itself is a good thing to study and understand in its entirety. Specifically, the question is....In the brady PEA of a Neurogenic Shock patient (who subsequently arrested), would the use of Atropine be warranted, CONSIDERING its effects on the parasympathetic Nervous system? Two ways to think about the pharmacodynamics of Atropine - 1. It essentially blocks the effects of acetylcholine at parasymp junctions, including vagal introduction into the heart, as well as vasomotor effects. This in turn can help maybe (in my little mind), considering this patient is in cardiac arrest. Logic - he is dead anyways, and the effects of blocking the parasympathetic NS may help with vasopressors and proving vasoconstriction and an increase in inotropy, dromotropy and chronotropy. 2. The administration of Pressors will not work and if Atropine is administered will render the parasymp NS useless, and now we have both portions of the Autonomic NS useless....Which we all know that we need those for resuscitative efforts.

Two thoughts:

1. Why will pressors not work?

These are soluble catacholamines infused directly into the circulation, akin to endogenous production of epinephrine by the adrenal glands. That is to say that the receptors for catecholamines are located on the end organs (like the vascular smooth muscle and heart). While the SNS may no long be able to produce catecholamines because of denervation, the tissues will still be able to respond to catecholamines, unless of course we have given him medications to block those receptors...say...to control his hypertension. Alpha or beta blockers would likely make the hypotension worse in someone like this, however, administration of a bunch of adrenergic agonists plus high endogenous production will eventually overcome this.

2. The idea that the parasympathetic NS will not function.

While it is true that you are blocking the PNS, keep in mind that in this pt the PNS dosent have any function that is helpful to you. On the other hand, it can do some things to work against you, namely decrease peripheral vascular tone and slow the heart rate.

I guess one other thought:

Neurogenic shock should probably not be the first thing that pops into ones head in a scenario with hypotension and then cardiac arrest following a traumatic injury. While certainly possible, there are other causes that would likely deserve a higher position on your differential. Neurogenic shock is probably the most rare form of distributive shock. Further, it generally should be transient and relatively mild in terms of the degree of the hypotension owing to several means of physiologic compensation...soluble catecholamines and decreased parasympathetic output in response to hypotension.

Hope this clarifies a little. All the best.

[medicv83]

All well thinking of course. I truly understand that in any case, neurogenic shock would not be an initial train of though, however a diagnosis of rule - out. BUT..........We are saying the the neuro shock pt who codes yada yada yada..........The issue is not the ability to produce catecholamines, but the ability to conduct the transmission via the nervous tracts. Yet, of course the tissues ( end organs ) once able to recieve the neurotransmitter, will be able to act, will perform the expected action. That is why initially I said I support the administration of pressor agents, as well as possibly a dopamine drip. Your input is very logical....Just trying to counter it for the sake of countering it. lol

[medicv83]

DwayneEMP.............Thank you by the way. Should have said that earlier. Rest assured, I will continually post complex, intriguing questions, that I myself am in search of answers to. I support the same notion that one must think before looking to the books for answers. Us Medics, basics, and intermediates on here know the answers to most, but are just to lazy to think sometimes.

[chbare]

I am still a little confused regarding the argument against using atropine. Atropine antagonizes the muscarinic actions of AcH and other choline ester like substances. Yes, you can argue for some nicotinic crossover when we take GI smooth muscle motility into consideration. We are not blocking the entire parasympathetic nervous system. I fail to see how this is harmful in the setting of the neurogenic shock cardiac arrest patient. You could argue that atropine may have limited effectiveness in some patients; however, contraindicated in this setting?

Take care,

chbare.

[AZCEP]

Are you arguing for the sake of argument, or do you really not understand atropine's mechanism of action and pharmacodynamics?

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.

[ccmedoc]

OK.....

Fluid for the distributive shock and possibly the cause of the PEA (relative hypovolemia ?)

Epi for the alpha and beta effects

I think since excessive vagal tone may be the source of the bradycardia, Atropine would be indicated as a vagolytic. This has nothing to do with the SCI, only control of the vagal response.

I guess I fail to see what the muscarinic, nicotinic, postsynaptic, presynaptic, etc talk has to do with anything. Other than direct damage to the vagus nerve, why should a SCI have any impact on the effect of atropine in this 'application'? Last I knew, Atropine had little effect on the CNS at these doses you speak of..

1.Atropine is absolutely indicated for rate control.

2.Fluid for the obvious effects of the SCI, and probable cause of PEA.

3.Epinepherine or Neosynepherine to increase SVR

4.Dopamine as necessary....

Either I am oversimplifying this, we are talking about different things, or you like to argue over moot points...

Just because the brain no longer controls the nerves doesn't mean they can't be stimulated by other means..

Ok, I have to hit the reset button, because this will go off on a tangent, which in and of itself is a good thing to study and understand in its entirety. Specifically, the question is....In the brady PEA of a Neurogenic Shock patient (who subsequently arrested), would the use of Atropine be warranted, CONSIDERING its effects on the parasympathetic Nervous system? Two ways to think about the pharmacodynamics of Atropine - 1. It essentially blocks the effects of acetylcholine at parasymp junctions, including vagal introduction into the heart, as well as vasomotor effects. This in turn can help maybe (in my little mind), considering this patient is in cardiac arrest. Logic - he is dead anyways, and the effects of blocking the parasympathetic NS may help with vasopressors and improving vasoconstriction and an increase in inotropy, dromotropy and chronotropy. 2. The administration of Pressors will not work and if Atropine is administered will render the parasymp NS useless, and now we have both portions of the Autonomic NS useless....Which we all know that we need those for resuscitative efforts.

Lots of big fancy words..doesn't read especially well..kind of a circular argument

What are you trying to validate? :shock:

...question with a well thought out, logical core.

With all due respect, I don't see it. :?

[DwayneEMTP]

With all due respect, I don't see it. :?

Actually, the quote you posted and my response are taken out of contest, I meant to address the OP, and should have quoted it. My fault not yours.

Secondly, other than his possible misunderstanding of the scope and/or specificity of atropine's effect on the parasympathetic nervous system, I'm still happy with my above quote, I think it was a logical theoretic question.

Also, I'm not clear on what you felt he's attempting to validate. The thread reads to me as if he's enjoying taking the mental journey through the physiology of this question, not so much attempting to defend it, as attack it and try to look at it from an unusual angle. I didn't get the feeling that he has a right point so much as he's attempting to fuel the disection of this part of the nervous system while he's got the ear of a lot of smart people...and if I'm correct I have a lot of respect for his attitude.

And lastly, anyone that starts a thread that leads to the actual naming, defining and categorizing of the nervous system and their specific neurotransmitters need some major kudos. We haven't had a medical discussion of this depth here in months...It's way past due.

Besides, this was a great review of about two weeks of college physiology in just a couple of pages...I'm on board regardless of his motivation...

Dwayne