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Posted

I thought vasopressin (ADH) worked by stimulating V1 & V2 receptors when we talk about vasoconstriction? (Vascular & Renal) I understand V1 receptor activation is very similar to alpha stimulation? In addition, I think vasopressin can cause vasodilation of the renal, pulmonary, and cerebral vascular beds. The mechanism seems to be related to nitric oxide. I can appreciate how this effect could benefit the arrest patient. In addition, the peripeties of AHD make it a good choice wen treating patients in shock states that do not respond to adrenergic agents. (septic shock for example)

Take care,

chbare.

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Posted
i am not one to be redundant but the outlook so far is cook book, i agree with the current ACLS guidlines that state to use it in place of first or second dose of epi however i have heard alot that people are using epi first because it is easier and this is bull.

Which is easier, to open a vial and withdraw the medication or screw together a prefilled syringe? How exactly is it "bull"? I disagree with following protocols by rote, but faster is faster regardless of which drug you are using.

what is the most important thing to a pt in cardiac arrests? CPR if this is going on then you have time for getting the appropriate drugs. And as to which one to use, treat it based on how the drugs work, if you dont know how a drug works dont push it.

You need to take your own advice on this one.

Epi is a beta and alpha stimulator...

In the doses used for cardiac arrest the alpha effects predominate. Beta effects are more useful for someone needing smooth muscle relaxation, not cardiac stimulation.

where vasopressin is a sellective alpha stimulator, in the protocol for V fib you are giving your first dose as a pressor to increase vascular resistance and you are already dealing with and irritable heart so why increase your automaticity with epi. however in asystole you are dealing with no automaticity so increase it with epi. dont be a cookbook medic, think every call through, and know exactly how the drug that your are going to give a pt is going to work.

Here again, take your own advice. Vasopressin has no alpha effects. That is a sympathetic nervous system receptor site that will not respond to an anterior pituitary hormone. Vasopressin has it's own receptors which chbare already discussed. Every dose of epinephrine and vasopressin are used as pressors. You will get the same response from the two drugs no matter how many times you give them.

Posted

Growing up old school, my love was always for Epi. Now that I've had some success with Vasopressin, it's difficult to decide. I agree that Epi has some great features (ease of dosing, shelf-life, and cost to say a few) but Vasopressin has been better to me over the last year.

Posted
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That is a sympathetic nervous system receptor site that will not respond to an anterior pituitary hormone. Vasopressin has it's own receptors which chbare already discussed. Every dose of epinephrine and vasopressin are used as pressors. You will get the same response from the two drugs no matter how many times you give them.

Actually its the posterior pituitary, just saying. :lol: AZ makes many good points as usual.

Posted
Epinephrine does not have any dopaminergic effects. That is an entirely different mechanism and does not belong here.

I was meaning dromotropic, not dopaminergic.

With the short time frame you are suggesting, allowing the pump to come back on its own would be much preferred. Dopamine is not necessarily recommended for someone that can maintain perfusion, as this situation probably could. There is a big difference between unstable and need to treat. You would be able to support perfusion with fluid boluses for a while, as you are watching this patient's MAP.

Great point. There defiantly is a difference between unstable and need to treat. When I said unstable I mean the patient in shock that is about to code again. The Dopamine in the case would be to maintain profusion to the brain long enough to get the patient to a Cath lab to correct the blockage.

Posted

To all that picked my last posting apart i appretiate it because i made me re learn the effects of vasopressin, unfortunately my instructor tried to simplify it and in essence taught it incorrectly. On a different not i wanted to defend my position on the use of epi though. I can appreciate that the primary function is peripheral vaso-constriction, my only argument was that it does have in some cases such as VF unwanted Beta 1 effects, ie automaticity. Last but not least, my only reason for commenting on the cookbook medicine and knowing your drugs is due to the fact that many people tend to look at EMS as if this than do that, because my protocols say so, We all need to be clinicians.

Posted

Good post, Bryan. Despite the minor technical inaccuracies in your previous post, I understood what you are getting at. And I think both AZCEP and myself would agree with that bottom line.

Regarding the "easier" to administer theory being bull, I would also agree with that. I understood your point to be not that epi wasn't easier, but that easier simply was not a sufficient reason to justify it.

The whole irritability and automaticity issue is exactly why I have always felt that vasopression was a more intuitive first choice in post MI arrest. And, even in the absence of the in-depth pharmacology, the fact that Vasopressin is recommended in VF, but not asystole, should give us a clue as to the rationale. In asystole, you've got nothing to work with. Your only hope is to stimulate some irritability and automaticity with a beta-1 agonist. But in VF, irritability is what got you into this jam in the first place. If at all possible, you want to absolutely avoid increasing that.

Now, where the scenario changes is after a good ten to twenty minutes of VF, when that nice jagged pattern starts turning fine -- and assuming you have corrected respiratory insufficiencies -- then beta-1 stimulation becomes a good thing as you struggle to maintain some kind of electrical activity to work with. V-fib sucks, but it still beats the hell out of asystole. That's why we don't jump right to epi when we have the choice of vasopressin on hand.

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