Nicardipine drip

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VentdependenT

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How many of you use this stuff and in what clinical scenerios (besides a noggin bleed) do you favor it?

Seems like a great option to me and seems pretty straight forward to titrate.

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The stuff works great but I mostly use it in heads. It gives you rapid control of BP and it can also be used as a bolus in a syringe, which I really like. Also my favorite way of using NTG, in a syringe.
 
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militarymd said:
I've never used it, so I don't miss it.

I've never used it either.

But I agree with you, Noy,

I'm a syringe dude.

Epi (5ug, 10ug, whatever)

NTG (100ug, 200ug, whatever)

Tell me about nicardipine.

How do I use it as a syringe cowboy?

How do you drip it?

Why is it better than labetolol boluses with a NTG infusion kicker?
 
jetproppilot said:
I've never used it either.

But I agree with you, Noy,

I'm a syringe dude.

Epi (5ug, 10ug, whatever)

NTG (100ug, 200ug, whatever)

Tell me about nicardipine.

How do I use it as a syringe cowboy?

How do you drip it?

Why is it better than labetolol boluses with a NTG infusion kicker?

Its better than Labetolol because you can turn it off and it gone unlike the labetolol.

For Rapid BP control: Infusion style
start at 50ml/hr (5mg/hr)
increase rate by 25ml/hr (2.5mg/hr)every 5 min (it works that fast as an infusion) up to 150ml/hr (15mg/hr)or until desired effect, then decrease rate to 30ml/hr 93mg/hr).

For rapid BP control: "syringe cowboy" style
Draw up a 10cc syringe from the bag (conc 10ml=1mg)
Give 1-2 cc bumps til you get to the desired BP or until you know how this amount will effect the pt then increase accordingly.

For gradual Bp control:
start infusion at 50ml/hr and increase by 25ml/hr every 15minutes until desired effect. This way is too slow for my taste.

Jet, I really only use it for cerebral aneurysms and on rare occasions when I can't get a pts BP down in PACU with labetolol or NTG/nipride (only once).

Don't use with critical aortic stenosis. 😱

Try it, you'll like Mikey
 
Noyac said:
Its better than Labetolol because you can turn it off and it gone unlike the labetolol.

For Rapid BP control: Infusion style
start at 50ml/hr (5mg/hr)
increase rate by 25ml/hr (2.5mg/hr)every 5 min (it works that fast as an infusion) up to 150ml/hr (15mg/hr)or until desired effect, then decrease rate to 30ml/hr 93mg/hr).

For rapid BP control: "syringe cowboy" style
Draw up a 10cc syringe from the bag (conc 10ml=1mg)
Give 1-2 cc bumps til you get to the desired BP or until you know how this amount will effect the pt then increase accordingly.

For gradual Bp control:
start infusion at 50ml/hr and increase by 25ml/hr every 15minutes until desired effect. This way is too slow for my taste.

Jet, I really only use it for cerebral aneurysms and on rare occasions when I can't get a pts BP down in PACU with labetolol or NTG/nipride (only once).

Don't use with critical aortic stenosis. 😱

Try it, you'll like Mikey

Nice info, Noy.

Thanks.
 
VentdependenT said:
How many of you use this stuff and in what clinical scenerios (besides a noggin bleed) do you favor it?

Seems like a great option to me and seems pretty straight forward to titrate.

We use it in the CAB population quite frequently. Of course, we do it the standard way on the pump 🙂 as a continuous infusion. It is great because if you have a pt with a labile bp, the half life is very short.
 
It was slow to catch on the CTICU where I used to work. It was heavily promoted by pharm. reps as a safer alternative to SNP (no CN toxicity, less acute hypotension from overzealous titration) but cost was a hindrance, as was the need for the instant gratification that nipride provided.
 
we've had the sales reps try to come detail us on this drug again and again and again and again and again... you get the picture. no one is really adopting it in our neck of the woods, at least for pure anesthesia purposes. it probably is a great drug at the oddball case of extreme unexplained peri-operative htn not amenable to other agents at our disposal - namely our anesthetic. but, other than specific cases and as mentioned above, i just really don't see a big use for this stuff. will be really surprised if it catches on.
 
My hosptial likes it for stroke patients, and hypertensive emergencies. Easy to titrate so the BP doesn't go too low, and less steal syndrome than nitroprusside.
 
Use it often for my off pump CABG's. Great arterial dilator, including coronary dilator, without the nitro-like drop in preload due to concurrent venodilation. Rarely see a reflex tachycardia with the continuous infusions and I have used it very frequently for coronary vasospasm that is refractory to NTG. Also, large doses tend NOT to bottom out the patient, so even if you give more than you wanted to, you will not drop the patient's pressure through the floor, assuming they aren't dry as a chip.

Disclaimer: I am about to become a lecturer for nicardipine so I am definitely biased.
 
UTSouthwestern said:
Use it often for my off pump CABG's. Great arterial dilator, including coronary dilator, without the nitro-like drop in preload due to concurrent venodilation. Rarely see a reflex tachycardia with the continuous infusions and I have used it very frequently for coronary vasospasm that is refractory to NTG. Also, large doses tend NOT to bottom out the patient, so even if you give more than you wanted to, you will not drop the patient's pressure through the floor, assuming they aren't dry as a chip.

Disclaimer: I am about to become a lecturer for nicardipine so I am definitely biased.

So I guess we should erase the eloquent paragraph before your disclaimer.

What are you, Norm, 31? 32?

Don't fall into the trap of promoting some s hit if youre biased.

Its not worth it; youre gonna be a millionairre either way.

Tell us if you clinically like the s hit.

Or if you don't.
 
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I think there are misconceptions about nicardipine IV. It actually demonstrates three half lives - the first is an early distribution phase which is indeed short - about 3 minutes. The second one, which is what you are probably familar with is the intermediate phase - about 45 minutes. But there is a third one, usually seen with long infusions which is a slow terminal (elimination) half life of 14 hours.

Nicardipine is 95% protein bound - only unbound drug is active. So, the "bumps" you see when you dose it reflects the rapid distribution & protein binding. If you only run a short infusion or bolus the drug, about 50% of "given" drug will be gone in 4 hours. However, longer infusions will follow the slow terminal phase half life.

The dilemma is when you think it is a short acting drug, have your case go on longer than you might anticipate, prescribe a post-op antihypertensive of some kind & not realize you still have nicardipine hanging around which will take some hours to get rid of. Then you have trouble hours after you think all is well. In comparison to others, it has a relatively large peak to trough difference in blood pressure effect. Others here could give more insight into how often this occurs for them clinically, but academically, it is there.

IMO, it is not a good candidate for outpt therapy (it is available orally too!) because it has demonstrated a dose dependent increase in thyroid hyperplasia & neoplasia.

All this doesn't mean it doesn't have a place....you just have to be aware of all the phases of its kinetics. As far as reality, its still expensive relative to others, but occasionally used.
 
sdn1977 said:
I think there are misconceptions about nicardipine IV. It actually demonstrates three half lives - the first is an early distribution phase which is indeed short - about 3 minutes. The second one, which is what you are probably familar with is the intermediate phase - about 45 minutes. But there is a third one, usually seen with long infusions which is a slow terminal (elimination) half life of 14 hours.

Nicardipine is 95% protein bound - only unbound drug is active. So, the "bumps" you see when you dose it reflects the rapid distribution & protein binding. If you only run a short infusion or bolus the drug, about 50% of "given" drug will be gone in 4 hours. However, longer infusions will follow the slow terminal phase half life.

The dilemma is when you think it is a short acting drug, have your case go on longer than you might anticipate, prescribe a post-op antihypertensive of some kind & not realize you still have nicardipine hanging around which will take some hours to get rid of. Then you have trouble hours after you think all is well. In comparison to others, it has a relatively large peak to trough difference in blood pressure effect. Others here could give more insight into how often this occurs for them clinically, but academically, it is there.

IMO, it is not a good candidate for outpt therapy (it is available orally too!) because it has demonstrated a dose dependent increase in thyroid hyperplasia & neoplasia.

All this doesn't mean it doesn't have a place....you just have to be aware of all the phases of its kinetics. As far as reality, its still expensive relative to others, but occasionally used.


We use it as an alternative to nipride for HTN, primarily because it is safer on the renal system (at least that's what they tell us-let me know if that is not correct). I will say I have seen in several of my patients where they had significant HTN I couldn't get controlled with the Nitro, so I start some Cardene. Within 30 minutes the Nitro is off and I'm happy because I've got my bp exactly where I want it, but your post makes complete sense to me because sometimes, we'll start trending down with the bp and I'll end up off the gtt. A few of these patients have been hypotensive for a day or so after, independent of any other changes (fluid status, diuresis, CO/CI/SVR) that would affect thier bp, and I've wondered if it was the Cardene that did it. Of course, everyone I work with says no, the cardene should be gone in about 15 minutes, but I found that hard to believe.

I also wonder with it being 95% protein bound, if some of our patients who come nutritionally deficit with low albumin levels are at a higher risk for the problems with it that you describe. If they don't have as much protein for the drug to bind to, then I would hypothesize there will be more free cardene active. What do you think?
 
SilverStreak said:
We use it as an alternative to nipride for HTN, primarily because it is safer on the renal system (at least that's what they tell us-let me know if that is not correct). I will say I have seen in several of my patients where they had significant HTN I couldn't get controlled with the Nitro, so I start some Cardene. Within 30 minutes the Nitro is off and I'm happy because I've got my bp exactly where I want it, but your post makes complete sense to me because sometimes, we'll start trending down with the bp and I'll end up off the gtt. A few of these patients have been hypotensive for a day or so after, independent of any other changes (fluid status, diuresis, CO/CI/SVR) that would affect thier bp, and I've wondered if it was the Cardene that did it. Of course, everyone I work with says no, the cardene should be gone in about 15 minutes, but I found that hard to believe.

I also wonder with it being 95% protein bound, if some of our patients who come nutritionally deficit with low albumin levels are at a higher risk for the problems with it that you describe. If they don't have as much protein for the drug to bind to, then I would hypothesize there will be more free cardene active. What do you think?

Silver - I only mentioned protein binding because its high % allows the proteins to become drug reservoirs. As the free drug is metabolized & eliminated, bound drug dissociates from proteins, thus becoming free. Binding is usually nonselective which allows other drugs to readily knock it off the proteins, which also allows more free drug into the circulation. These interactions & how they affect target organ levels, elimination, etc...are complex & not germain to this discussion, especially since it is a drug which is titrated. No one cares what the actual level is as long as the effect is what is sought.

However, there are more proteins in the blood than albumin & it is only the very acidic ones which are bound tightly to albumin, so trying to guess a dose of a drug like nicardipine based on the serum albumin is not a good idea. For your malnourished pt, I'm guessing there are greater issues with pts who are nutritionally compromised than drug binding which would affect drug choice & dose. Critically dosed drugs in which you are not titrating to effect might change (think aminoglycosides..)
 
sdn1977 said:
However, there are more proteins in the blood than albumin & it is only the very acidic ones which are bound tightly to albumin, so trying to guess a dose of a drug like nicardipine based on the serum albumin is not a good idea. For your malnourished pt, I'm guessing there are greater issues with pts who are nutritionally compromised than drug binding which would affect drug choice & dose. Critically dosed drugs in which you are not titrating to effect might change (think aminoglycosides..)

Your expertise is much appreciated here, SDN.

I have some thoughts with regard to the above statement, however. If the albumin is low then the rest of the proteins are usually low as well. Albumin is used to help determine the overall protein state as well as liver fxn as you well know. An acidotic state will also affect protein binding ( I know you know that as well). 👍

i
 
Noyac said:
Your expertise is much appreciated here, SDN.

I have some thoughts with regard to the above statement, however. If the albumin is low then the rest of the proteins are usually low as well. Albumin is used to help determine the overall protein state as well as liver fxn as you well know. An acidotic state will also affect protein binding ( I know you know that as well). 👍

i

Yep, yep...but, you get the pt how you get him - no matter the protein state, so you start dosing....the purpose is not to saturate the proteins, the purpose is to lower the bp (but you do saturate the proteins in the process). So....you do what you described...start with whatever dose you know, then bump & bump, etc...However, in treating the bp, when you know the first phases of the drug are distribution & binding phases, then you know if there is any change in that reservoir, you can anticipate the need to change the dose. You aren't really dosing to keep a blood level (as you would for an aminoglycoside...keep above.....), you are dosing to keep bp within a range.

In your situation in the OR (or ER for example), the major serum protein changes would be hemorrhage. I don't know your field well enough to know for sure, but I don't think you replace with albumin. So....if you get a bad bleed, for sure you can expect a bp drop from the fluid loss, but if you had absolutely no time on your hands ( :laugh: ) & got to thinking about what is happening to the nicardipine, you would expect the free drug is now being bound to the newly infused albumin & you've lost your previous drug reservoir of bound albumin from the bleed, so your desired effect is less....but you're trying to fix the bleed outcome & not thinking about drug binding.

This is not so much an OR/ER thing....but, many years ago (20 😱 ) we had physicians "treat" low serum albumins in the ICU. Daily they would write to infuse 2 or 3 units of albumin - it brought the serum albumin up, then it would redistribute to the tissues, & that night we'd be left with low albumins again. The drug effects of highly bound drugs would follow.. There were fewer of them which were titrated by nursing at that time & I have no personal experience with nicardipine - just academic with similarly tagged drugs in the lab. UT could tell you if this happens in actual practice.

Sorry....I may not be clear...don't want to hijack the thread with drug metabolism & pharmacodynamics. Plus.....I gotta go to work 😳 ......See ya all later!
 
sdn1977 said:
Yep, yep...but, you get the pt how you get him - no matter the protein state, so you start dosing....the purpose is not to saturate the proteins, the purpose is to lower the bp (but you do saturate the proteins in the process). So....you do what you described...start with whatever dose you know, then bump & bump, etc...However, in treating the bp, when you know the first phases of the drug are distribution & binding phases, then you know if there is any change in that reservoir, you can anticipate the need to change the dose. You aren't really dosing to keep a blood level (as you would for an aminoglycoside...keep above.....), you are dosing to keep bp within a range.

In your situation in the OR (or ER for example), the major serum protein changes would be hemorrhage. I don't know your field well enough to know for sure, but I don't think you replace with albumin. So....if you get a bad bleed, for sure you can expect a bp drop from the fluid loss, but if you had absolutely no time on your hands ( :laugh: ) & got to thinking about what is happening to the nicardipine, you would expect the free drug is now being bound to the newly infused albumin & you've lost your previous drug reservoir of bound albumin from the bleed, so your desired effect is less....but you're trying to fix the bleed outcome & not thinking about drug binding.

This is not so much an OR/ER thing....but, many years ago (20 😱 ) we had physicians "treat" low serum albumins in the ICU. Daily they would write to infuse 2 or 3 units of albumin - it brought the serum albumin up, then it would redistribute to the tissues, & that night we'd be left with low albumins again. The drug effects of highly bound drugs would follow.. There were fewer of them which were titrated by nursing at that time & I have no personal experience with nicardipine - just academic with similarly tagged drugs in the lab. UT could tell you if this happens in actual practice.

Sorry....I may not be clear...don't want to hijack the thread with drug metabolism & pharmacodynamics. Plus.....I gotta go to work 😳 ......See ya all later!

We do routinely give our hearts volume with albumisol post op. I know it's a diluted form of albumin, but still they can potentially get up to a liter of albumisol.
 
sdn1977 said:
Yep, yep...but, you get the pt how you get him - no matter the protein state, so you start dosing....the purpose is not to saturate the proteins, the purpose is to lower the bp (but you do saturate the proteins in the process). So....you do what you described...start with whatever dose you know, then bump & bump, etc...However, in treating the bp, when you know the first phases of the drug are distribution & binding phases, then you know if there is any change in that reservoir, you can anticipate the need to change the dose. You aren't really dosing to keep a blood level (as you would for an aminoglycoside...keep above.....), you are dosing to keep bp within a range.

In your situation in the OR (or ER for example), the major serum protein changes would be hemorrhage. I don't know your field well enough to know for sure, but I don't think you replace with albumin. So....if you get a bad bleed, for sure you can expect a bp drop from the fluid loss, but if you had absolutely no time on your hands ( :laugh: ) & got to thinking about what is happening to the nicardipine, you would expect the free drug is now being bound to the newly infused albumin & you've lost your previous drug reservoir of bound albumin from the bleed, so your desired effect is less....but you're trying to fix the bleed outcome & not thinking about drug binding.

This is not so much an OR/ER thing....but, many years ago (20 😱 ) we had physicians "treat" low serum albumins in the ICU. Daily they would write to infuse 2 or 3 units of albumin - it brought the serum albumin up, then it would redistribute to the tissues, & that night we'd be left with low albumins again. The drug effects of highly bound drugs would follow.. There were fewer of them which were titrated by nursing at that time & I have no personal experience with nicardipine - just academic with similarly tagged drugs in the lab. UT could tell you if this happens in actual practice.

Sorry....I may not be clear...don't want to hijack the thread with drug metabolism & pharmacodynamics. Plus.....I gotta go to work 😳 ......See ya all later!


So with a hemorrhage you would hope not to have any cardene on board or else yo would really be fighting BP. Then giving albumin would not be a bad idea with the idea being that it would bind the active (unbound) cardene therefore resolving some of the effect.

With regard to the albumin in the ICU for low albumin states, you are right if the cause of the low albumin is sepsis or a burn or the like. But if it is liver failure I'm not totally sure if it would just 3rd space as rapidly. Maybe Mil would know this. What am I saying? Of course Mil knows. 🙂
 
jetproppilot said:
So I guess we should erase the eloquent paragraph before your disclaimer.

What are you, Norm, 31? 32?

Don't fall into the trap of promoting some s hit if youre biased.

Its not worth it; youre gonna be a millionairre either way.

Tell us if you clinically like the s hit.

Or if you don't.

In other words,

please give us The Jedi's Yay or Nay. :laugh:
 
Noyac said:
So with a hemorrhage you would hope not to have any cardene on board or else yo would really be fighting BP. Then giving albumin would not be a bad idea with the idea being that it would bind the active (unbound) cardene therefore resolving some of the effect.

With regard to the albumin in the ICU for low albumin states, you are right if the cause of the low albumin is sepsis or a burn or the like. But if it is liver failure I'm not totally sure if it would just 3rd space as rapidly. Maybe Mil would know this. What am I saying? Of course Mil knows. 🙂

You know with a hemorrhage, we wouldn't have the Cardene going in the unit to start with, but as he stated in his original post, if you've still got some hanging around post op, and we're trying to keep a bp to perfuse until the surgeon gets there to take pt to the OR, then it would be bad. We give blood of course when they're bleeding out the chest tubes, but if we're in a bind waiting on the blood, we'll give albumin in the interim until we can get the blood going. It's a interesting twist to think about the drugs we use in this way.
 
Noyac said:
So with a hemorrhage you would hope not to have any cardene on board or else yo would really be fighting BP. Then giving albumin would not be a bad idea with the idea being that it would bind the active (unbound) cardene therefore resolving some of the effect.

With regard to the albumin in the ICU for low albumin states, you are right if the cause of the low albumin is sepsis or a burn or the like. But if it is liver failure I'm not totally sure if it would just 3rd space as rapidly. Maybe Mil would know this. What am I saying? Of course Mil knows. 🙂

I knew I explained this poorly - the result of hurrying! As a pharmacist, I think of drugs as existing in "compartments" in the body. For the most part, all circulate in the plasma to a certain extent, but some will store elsewhere. Some are lipid soluble, so the fat levels are greater than the serum levels. In this situation, the storage is on the various plasma proteins. At steady state, there is an equilibrium between the free drug in plasma and that which is bound to proteins (confusing because it also seems like its all in the blood, but its not really from my perspective). If your patient already has low proteins, from whatever source, you'd dose at the lower end & titrate more conservatively. But..you'd still dose to effect - not to a particular mcg/ml level.

The hemmorhage example perhaps was a bad one, but I tried to find an example in your practice with fluctuating albumin levels. You could think binding drug with new albumin might be good, but you have to think about it 45-2hr later (give or take) because the drug is not gone - its just been newly stored. This is not predictable because drug binding is competitive (usually) & is affected by all the other stuff you are giving & is dependent also upon dissociation constants of each drug (I told you it is far more information than is practical in this scenario 😉 - especially when you are trying to save a life! 😱 ) There's a time & place for drug metabolism concerns & this example was a poor one!

To clarify the ICU albumin scenario, I was poorly referring to the practice of many, many years ago of not feeding postop patients (sometimes for weeks!). We would watch the albumin levels fall, they would order albumin (treating a symptom, not a cause) then we'd watch drug levels fluctuate. Finally, they'd resort to starting TPN with added albumin which caused endless drug incompatibilities, drug level fluctuations & expense. I was not referring to albumin for fluid replacement.

I cannot speak to physiologic serum protein changes with different disease states because now you've gone beyond what I have knowledge of. I defer to those who can speak to that. Sorry for being so confusing!
 
sdn1977 said:
they'd resort to starting TPN with added albumin which caused endless drug incompatibilities, drug level fluctuations & expense. I was not referring to albumin for fluid replacement.

I cannot speak to physiologic serum protein changes with different disease states because now you've gone beyond what I have knowledge of. I defer to those who can speak to that. Sorry for being so confusing!

I know this isn't the context you brought up TPN for, but since you're here, I'll pick your brain. We had very limited central line access on a patient the other night and were trying to come up with an accepatable way to run all of our needed gtts to one line. We ended up with TPN and insulin running together, which I knew was okay. Then someone else said you can run Diprivan and TPN together because they're both lipid based. I was not okay with this for several reasons. Then someone else piped up and said well your TPN has naturally occurring things found in the body, I would think it's okay to run with stuff. We clearly have a hospital policy that states Diprivan should have a dedicated line as well as TPN. I was okay with insulin/TPN running together because I know some hospitals have insulin mixed in their TPN. Bottom line, I know there is a pharmacological reason for TPN running alone, can you tell me what it is (aside from the line being at high risk for contaminant/infection if other drugs are ran to it).
 
SilverStreak said:
I know this isn't the context you brought up TPN for, but since you're here, I'll pick your brain. We had very limited central line access on a patient the other night and were trying to come up with an accepatable way to run all of our needed gtts to one line. We ended up with TPN and insulin running together, which I knew was okay. Then someone else said you can run Diprivan and TPN together because they're both lipid based. I was not okay with this for several reasons. Then someone else piped up and said well your TPN has naturally occurring things found in the body, I would think it's okay to run with stuff. We clearly have a hospital policy that states Diprivan should have a dedicated line as well as TPN. I was okay with insulin/TPN running together because I know some hospitals have insulin mixed in their TPN. Bottom line, I know there is a pharmacological reason for TPN running alone, can you tell me what it is (aside from the line being at high risk for contaminant/infection if other drugs are ran to it).

Not really an anesthesia topic & completely off the nicardipine question, so I'll answer with a pm to not bore folks.
 
Great info, SDN! Thanks for all the insight! 👍
 
sdn1977 said:
Not really an anesthesia topic & completely off the nicardipine question, so I'll answer with a pm to not bore folks.

can one of you send me the answer too? Never really had the question...but since it was brought up - would like to know the anwer.
 
jetproppilot said:
In other words,

please give us The Jedi's Yay or Nay. :laugh:

Way yay. For short term intraop use, I have found that my OPCAB's remain more stable hemodynamically than with NTG and those patients that fluctuate on NTG stabilize after I switch to nicardipine.

Fluctuating albumin levels in the intraop clinical course does occur, but not to a great enough extent to affect medication levels, particularly those that are being continuously infused. I have yet to see a pronounced delayed effect of nicardipine so I cannot comment on that possible effect.
 
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