Vasopressin vs. Levophed

[sugarmagnoliaRN]

This is kind of a newbie CCU nurse question but I'd really appreciate y'alls help understanding this! I just started in a cardiac ICU and there is a strong preference for vasopressin over levophed... I understand why Levo is good for sepsis because it jacks up your SVR and causes vasoconstriction, which are generally not things you want for cardiac patients (especially not with cariogenic shock). But doesn't vasopressin have a lot of the same effects? I will say I see it more on the post-op patients (e.g. CABG) than the pts that come in with cardiogenic shock. I'm trying to research this on my own but I'm not really finding a clear answer as to why it would be preferred over Levo. Can anyone with more experience than me shed some light on this? Thank you in advance!! :)

[BlueChocolateCat]

In my cardiac surg ICU we prefer levo as a first line. If the patient isn't responding to levo (generally requiring doses over 10 mcg/min) we will add vaso. Amoung our ICU, there is some speculation that high doses of vaso may be linked to bowel ischemia?

Also, we will utlize vaso if the patient has persistant acidosis with a ph

[offlabel]

So you pick an inotrope, inopressor, pressor (among other things as well) based on the identified cause of whatever disruption in hemodynamics you're interested in fixing.

A fall in flow (cardiac output) and blood pressure is caused by one or a combination of 4 things: impaired contractility of the heart, loss of adequate vasomotor tone, inadequate intravascular volume or a non-perfusing dysrhythmia.

To keep things to the point of this thread, NE has both a mild inotropic effect and a vasomotor tone effect, thus increasing flow and pressure by two means. Vasopressin has no inotropic effect and primarily raises blood pressure, but not CO to the extent that NE does.

A cardiac output of 9 with an MAP of 50 does not call for inotropy, it calls for an increase in vasomotor tone, so vasopressin would be the choice over NE. A Cardiac index of 1.5 and an MAP of 50 would call for more inotropy so, depending on the cause, NE could be chosen or epinephrine once intravascular volume was assessed to be optimal.

More of a complex topic than can be treated in a comm box, but hopefully that's a start.

[kalycat, BSN, RN]

So you pick an inotrope, inopressor, pressor (among other things as well) based on the identified cause of whatever disruption in hemodynamics you're interested in fixing.

A fall in flow (cardiac output) and blood pressure is caused by one or a combination of 4 things: impaired contractility of the heart, loss of adequate vasomotor tone, inadequate intravascular volume or a non-perfusing dysrhythmia.

To keep things to the point of this thread, NE has both a mild inotropic effect and a vasomotor tone effect, thus increasing flow and pressure by two means. Vasopressin has no inotropic effect and primarily raises blood pressure, but not CO to the extent that NE does.

A cardiac output of 9 with an MAP of 50 does not call for inotropy, it calls for an increase in vasomotor tone, so vasopressin would be the choice over NE. A Cardiac index of 1.5 and an MAP of 50 would call for more inotropy so, depending on the cause, NE could be chosen or epinephrine once intravascular volume was assessed to be optimal.

More of a complex topic than can be treated in a comm box, but hopefully that's a start.

Shout out for this clear and concise explanation!

[MYSTICOOKIEBEAR]

First of all you have to understand that Levo or norepinephrine is an Adrenergic Agonist that stimulates the a1, a2, B1 receptors. This will give us vasoconstriction in the peripheral vasculature thus increasing BP/MAP and increasing afterload, it will also give us a + inotropic and + chronotropic effect. So if we have a soft index and a soft map, then it is definitely indicated. But levo definitely has an emphasis on the a1 agonization more so than the a2 or B1.

Vasopressin on the other hand is Antidiuretic Hormone (ADH) which works very similarly to Adrenergic Agonists but has no effect on Adrenergic Agonist receptors. It works by keeping fluid in the vascular space. So although some consider it to be a Pressor, it technically is not, even though it gives us a very similar effect. One downside of prolonged use of vasopressin is that it can "kill your gut" due to the vasoconstriction that it causes to the Mesenteric bed. I have seen many a patient develop ischemic bowel from prolonged use of vasopressin and it's kinda sad.

One of the reasons vasopressin wil be used is if the patient was vasoplegic in the OR necessitating methylene blue, they would want to give a medication that will increase the blood pressure that will have actual efficacy until the methylene blue kicks in and the pressors start to work again.

i made a somewhat extensive and lengthy video about Pressors and pressor like medications that I made to help newer ICU nurses understand it a little bit better and also as a review for the more experienced ICU nurses.

[video=youtube;hiI-8GV-kBk]

[offlabel]

F

Vasopressin on the other hand is Antidiuretic Hormone (ADH) which works very similarly to Adrenergic Agonists but has no effect on Adrenergic Agonist receptors. It works by keeping fluid in the vascular space. So although some consider it to be a Pressor, it technically is not, even though it gives us a very similar effect. One downside of prolonged use of vasopressin is that it can "kill your gut" due to the vasoconstriction that it causes to the Mesenteric bed. I have seen many a patient develop ischemic bowel from prolonged use of vasopressin and it's kinda sad.

One of the reasons vasopressin wil be used is if the patient was vasoplegic in the OR necessitating methylene blue, they would want to give a medication that will increase the blood pressure that will have actual efficacy until the methylene blue kicks in and the pressors start to work again

Just to be clear, vasopressin at the doses used in critical care is a vasopressor and nothing else. It raises blood pressure by increasing vasomotor tone via V1 receptor mediated g protein coupling on vascular smooth muscle.

As to concerns about bowel ischemia, it has been reported but it is not any concern at all when treating acute hypotension 2/2 vasoplegia. Severe hypotension is a greater threat to bowel perfusion than vasopressin is.

[MYSTICOOKIEBEAR]

What doses are you talking about when you say "at the doses used in critical care" because I have personally used vasopressin as low as 0.01 to as high as 0.1 and have seen it as high as 0.12.

[offlabel]

What doses are you talking about when you say "at the doses used in critical care" because I have personally used vasopressin as low as 0.01 to as high as 0.1 and have seen it as high as 0.12.

What I mean by that is as opposed to the physiologic blood level of endogenous vasopressin that is excreted from the posterior hypothalamus. When we give vasopressin in critical care, we're giving hundreds of times what is being excreted and are exploiting only 1 of the 4 vasopressin responsive receptors that have been identified, those being the ones on vascular smooth muscle.

So, the doses you're citing are about 1 to 10 units an hour. 10 is pretty high, but not unheard of. I try not to go above 4, using volume and other pressors and inotropes, but going above that is not out of the realm of possibility.

For perspective, normal serum levels of vasopressin is around 4 pg/ml or less. One unit of vasopressin is equivalent to about 0.5 mcg of drug. So at even 3 units per hour, you're giving several hundred thousand times even elevated levels let alone normal ones.

[MYSTICOOKIEBEAR]

I had no idea and actually never thought to look up normal serum levels vs what we give in the Critical Care setting, cheers! Im gonna have to do a little more research myself now . Thanks for the info and helping expand my knowledge!