neurogenic shock arrest w/ atropine

[medicv83]

Wondering what peoples input is on the use of Atropine in the now brady PEA pt, with known neurogenic shock as the cause?

My thing is that with the typical brady PEA, per ACLS 1 mg Atropine IV q 3 - 5 minutes until its max blah blah blah. BUT, with the neurogenic shock pt, this application will render the pt unable to respond to any and all resuscitative efforts. Is this the general idea across the board???

[Mateo_1387]

I am not really clear what you are meaning by "this application." Is the Atropine supposed to be rendering the resuscitative efforts futile, or is it the neurogenic shock?

I have another question, why are you working a trauma code? To have these injuries is it not likely they have other internal injuries that just cannot be fixed in the field?

As far as working the code, the use of normal resuscitative efforts may or may not be applicable. Being in neurogenic shock, his arteries have dilated and the blood pooled towards gravity. To me, a logical recourse (if I were working the code by some chance) would be to get the blood up to the core. This may mean loading with epinephrine to cause vasoconstrictions causing and increase in pressure so that oxygen could be circulated. Maybe the use of some Antishock trousers would be indicated.

Overall, to me, I think that the above scenario would be a case of fixing the underlying problem of why the person is in cardiac arrest, which is that the blood is not able to be circulated due to no pressure (I know, I know, its ultimately due to the spinal injury, but I am talking about what we could possibly fix). After or while that is being fixed the use of vasopressors and atropine to increase rate would be indicated.

[medicv83]

This is the thing, your correct with the pathophysiology of blood pooling and vasodilation and all that, but its cause is due to an obstruction of the sympathetic nervous transmition with an un-impeding flow of acetylcholine causing the vasodilation. So all in all, the only portion of this patients autonomic nervous system viable at this time for conduction is the parasympathetic nervous system. If the neurogenic shock patient codes, and we administer atropine, we will essentially block out the parasympathetic tone in this patients body. If we do not administer atropine, and utilize epi as normal, and maybe say a dop drip to help constrict it is essentially treating the arrest, and the underlying cause.

[Kaisu]

its cause is due to an obstruction of the sympathetic nervous transmition with an un-impeding flow of acetylcholine causing the vasodilation. So all in all, the only portion of this patients autonomic nervous system viable at this time for conduction is the parasympathetic nervous system.

Are you sure about that? how can a spinal injury selectively block one half of the autonomous nervous system and not the other?

[medicv83]

The way it is broken down is, the Parasympathetic Nervous System stems from the Cranial Nerves, and some residual ganglia in the Sacral portion of the spine. The regulatory functions though come from the cranial nerves. Specifically cardioregulation and vasomotor control (parasympathetic control, not sympathetic). Sympathetic control stems from pre - ganglionic nerves in the thoraco-lumbar area of the spine. A patient in neurogenic shock has the sympathetic conduction essentially blocked off, while the parasympathetic, being above the level of the spine is still conducted outside of the spinal tract uninhibited. Hence the early hypotension and bradycardia seen with these spinal cord injured patients. Adrenal innervation from the symp nervous system is interrupted and you dont have the release of catecholamines below the level of the injury - again, that is why you have the warm and dry skin below the level of the injury, and the systemic vasodilation. There is no counter for parasymp tone in the body. If you admin atropine, and negate the parasymp NS, you have wiped out the only functional part of the patients Autonomic NS

[chbare]

Partially true. Neurogenic shock can be seen in injuries above the level of T6. From our A&P, we remember that the sympathetic nerves branch off from the thoracic vertebrae. So, in this case, we essentially cut off the sympathetic nervous system. This allows unopposed parasympathetic stimulation. Hence, the bradycardia and hypotension. We must also remember that much of our parasympathetic outflow is from the vagus nerve. This is actually a cranial nerve.

I am not sure where we are going with the atropine question. Are we arguing that atropine is contraindicated with the neurogenic shock patient?

Take care,

chbare.

[chbare]

The way it is broken down is, the Parasympathetic Nervous System stems from the Cranial Nerves, and some residual ganglia in the Sacral portion of the spine. The regulatory functions though come from the cranial nerves. Specifically cardioregulation and vasomotor control (parasympathetic control, not sympathetic). Sympathetic control stems from pre - ganglionic nerves in the thoraco-lumbar area of the spine. A patient in neurogenic shock has the sympathetic conduction essentially blocked off, while the parasympathetic, being above the level of the spine is still conducted outside of the spinal tract uninhibited. Hence the early hypotension and bradycardia seen with these spinal cord injured patients. Adrenal innervation from the symp nervous system is interrupted and you dont have the release of catecholamines below the level of the injury - again, that is why you have the warm and dry skin below the level of the injury, and the systemic vasodilation. There is no counter for parasymp tone in the body. If you admin atropine, and negate the parasymp NS, you have wiped out the only functional part of the patients Autonomic NS

Ok, I think I see where you are going. I think you are a little confused about how atropine works. Using your logic of atropine wiping out the parasympathetic nervous system, I could argue that atropine should be used as a paralytic. Remember, the Ach receptors at the neuromuscular junction are part of the parasympathetic nervous system. (Nicotinic receptors) Since, I do not see people developing neuromuscular blockade after receiving atropine, this medication must be a bit more specific than you think. Go back and review the physiology of the nervous system and atropine, and you should see how they interact in a new light.

Take care,

chbare.

[DwayneEMTP]

MedicV83...

First of all, welcome to the City! It is too rare that we get an honest to goodness pharmacology/pathophysiology question with a well thought out, logical core. And to get one from a 24 year old without a chip on their shoulder...well....unheard of.

Great start man...

I have this thing...I hate to research answers before answering on the board...But I have no friggin Idea! I'll give my immediate thoughts, which are going to expose me for an idiot, but am going to have to go to the books for an intelligent answer.

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

PEA at this point means that you're getting the electrical stimuli that you need for the heart to beat, but there are conditions that are not allowing it to do so. Now, we know that if you throw it out on the sidewalk it will beat for a bit....so there is something else going on with this patient's heart that is not linked to the neurological issue. Certainly that is an issue, but I don't see how it can directly be responsible for the mechanical failure that is being described here...see what I mean?

Hey! Did you try poking him in the eye! I think he's faking!

I have to go for now, but very much look forward to watching this thread play out. Another cool thing about these subjects? Only the smart people want to play....grin (Which is why I'm hiding behind the couch as I type this...)

Thanks for posting...I can see you're going to be a treat. (Also, without fail when I am impressed by a new person they almost immediately go and make an ass of themselves in their next thread...Any chance you can do your best to break my streak?)

Dwayne

[chbare]

Allow me to clarify my prior post before somebody calls me on it? Most people consider voluntary muscle movement part of the somatic branch. However, the AcH receptors at the neuromuscular junction are nicotinic receptors. This is why I called it part of the parasympathetic system. We are talking about the receptors. Hope that clears up any confusion.

Take care,

chbare.

[AZCEP]

If you eliminate the muscarinic stimulation, where atropine exerts it's effect, you will leave the SNS unopposed. Doing so would not be contraindicated in a neurogenic shock patient, but it will probably not give you the result you are looking for either.

When using atropine, we are assuming the SNS is able to function. The atropine does not induce an increased heart rate by itself, it merely allows the sympathetic system to exert an effect unimpeded.