amicar

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joncmarkley

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anyone using amicar for opcabs?

What dose are you using for pump cases?

Thanks

just want to see what others are doing

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only for pump cases...

5 gms the first hour, 1 gm an hour after that.
 
anyone using amicar for opcabs?

What dose are you using for pump cases?

Thanks

just want to see what others are doing

Most of my attendings want me to give either a full loading dose of amicar or at least 5 gm, in case it is realized that the case needs to be on pump.

For on pump, we give 1 gm/10 kg body weight as a loading dose, followed by 1 gm/hr. Most attendings stop giving it after we come off pump, but one of our attendings (our chairman) likes to keep giving it on an hourly basis until the end of the case.
 
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It's very hard to find any official dosing regimens. Probably because it isn't approved for this and there is not money in it anyway...

We do not use it for OPCAB. I don't see why one would.

We currently do 100mg/kg bolus at skin incision (unless with an unstable plaque and then only after heparinization) up to 10 grams, start a 1 g/hr infusion and load 10 g on CPB pump. We stop it on sternal closure.

This is pretty much a hybrid of two other institutions I have worked at, and was acceptable to the surgeons. It is similar to a dosing regimen that was used in some small studies, I believe, from Duke.
 
I had a fairly wise and experienced CRNA tell me recently that the initial Amicar bolus is to be given over 15 minutes. I've always just been just shooting the bolus in. Any thoughts?
 
The CRNA is right. You should bolus it over at least a few minutes.

I have seen hypotension when bolusing fast. The main fear is that by rapidly filling the RA with 10g of Amicar, you could cause spontaneous thrombosis in the RA or CS, which would ruin your day. Probably won't happen though.

Here's the part from the package insert:

"Rapid intravenous administration of the drug should be avoided since this may induce hypotension, bradycardia, and/or arrhythmia.

Inhibition of fibrinolysis by aminocaproic acid may theoretically result in clotting or thrombosis. However, there is no definite evidence that administration of aminocaproic acid has been responsible for the few reported cases of intravascular clotting which followed this treatment. Rather, it appears that such intravascular clotting was most likely due to the patient's preexisting clinical condition, e.g., the presence of DIC. It has been postulated that extravascular clots formed in vivo may not undergo spontaneous lysis as do normal clots."
 
we give 10 prepump, 10 on pump, then another 10 post pump all in boluses not infusions
 
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