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

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.

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

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.

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???

Few things to examine here. 1. Any variation in cardiac conduction, even with AMI do not necessarily appear right away. As a matter of fact, these changes can take up to 4 hours into the patients cardiac problem to be noticed on the EKG. 2. A pt presents with all the signs and symptoms of an MI. We are talking classic case. ------------DO AN 18 LEAD---------- If you dont know how to do this, find out, because it will help you determine the nature of the problem, specifically stating that the problem could be a RIGHT sided MI, AND, if you decide to treat this cardiac pt with the typical protocol (MONA), the effects of the Nitro could be devastating to the pt.

Awesome, I think that answered generally what I was looking for. I figured it correlated to sizes. Just didnt know why the jump between letters I guess.

I need to find out in a giant, huge, super, big way why oxygen tanks are labeled with the prefix of a single letter such as D, E, M, H......What is the significance of the nomenclature for the o2 tanks. Any help will be appppppppreciated, thanks.

I see a lot of "no" replies to this question. In reality, thinking solely on the medics ability to determine if in fact a patients mentation/condition is a viable one to maintain their own airway, then the understanding, and cognitive medic will have the ability to isolate the patients airway prior to the airway becoming impregnable. Such as in a burn patient with inhalation injuries where the airway is swollen, and ready to shut down. The medic, with an RSI protocol is the only thing that stands in the way of a warranted patients airway closing off.

I think, personally, and I kinda am a rookie to all of this, that one, if you can absorb and retain, truely retain the information to apply it. That one could go directly from basic to medic school. I myself went from basic, to intermediate, and will be in "P" school starting January. I have never worked on an ambulance or anything, except for my Intermediate and Basic clinical hours