Primacor drip

[Genista]

Had a new order for Primacor IV drip today (milrinone). This is the first time I have ever heard of the drug, or given it to a pt. Cardiologist wrote order for med, but no parameters for monitoring (pt already on tele floor w/ routine tele orders). Primary MD was on floor shortly thereafter, and we asked for parameters to monitor. I think he was going to write for Q2H vs. I am curious what is standard monitoring, if you have given this drug? This was not titrated, but just a maintenance infusion rate. I've read my drug books, so I know we are watching pt's electrolytes, creat clearance, vs and tele. Just wondering what your protocol is. Thanks for your input.

[xjhoxwex]

In our hospital primacor is mainly used with our open hearts, and is tirated to CI > 2.2 and svo2 >60 . I prefer primacor over dobutamine, as it has a lesser effect on HR and BP. When titrating you normally turn off primacor first because the half life of primacor is 2-3 hours, where as dobutamine is minutes. Our primacor dosing goes from .375mcg/kg/min - .75mcg/kg/min (max dose). In my opinion primacors vasodiliatory effect is very minimal, and most times pressors are not required (levo, dopa, etc).

[elvis pringles]

If it was an acute problem that has been resolved, and the only hemodynamic issue is hypotension, I'd probably vote to wean it... but. Depends what the PA pressures are, what the cause of hypotension is (if undervolumed, this needs to be corrected first; if there's RV compromise leading to reduced LV stroke volume, I'd leave the inotrope on for a while).

The pa pressures were high

[NurseLay]

We use this drug a lot in the PICU, in the cardiac patients. Mostly it is used for the patients with heart failure waiting for a cardiac transplant. We just take vitals q1hr.

[Apollopepe]

:eek:we had an anuric dialysis patient with a pic line with the order to start primacor drip "for the rest of his life" ( family's quote) at our nursing home.

has any body experienced this? is this acceptable? feasible? liable ?

Our medical director declined the infusion since his cardiologist and discharge hospital are 90 miles away. Should we have started it?

can some body provide me with studies that show it is done in nursing home for chronic out patient? We believe this was done to shift the economical burden to the NH.

Any comments?

[ghmccart]

this positive inotrope is also a prodysrhthmic so watch for that! it vasodilates especially in the pulmonary vasculature, and is often used for folks who have pulmonary hypertension and are in need of a medication to help with contractility, lots of times levophed is added to increase the tone that is lost with the primacor. One important thing to know about this medication is that it has a long half life, so when you make a change to the dose, you wont know the effects for 1-4 hours after you do it, so watch out, they may drop after a while, even if you think they tolertated it well. Good luck!

[mtwedt]

It's interesting to read everyone else's experiences. For the Home Health RN who reactivated the thread, I would think that whatever protocol you have in place for home Dobutamine would be acceptable for home Milrinone. Proper discharge teaching for the patient and family would be critical here. A collaborative protocol between yourselves and the discharging cardiologists should be established. My concerns would be for various forms of hypotension: hypovolemic, orthostatic etc. You could run into problems if the patient has big increase in his diuretic dose or becomes ill and dehydrated. Again, patient teaching and a collaborative protocol would be key here.

I use Milrinone only in the acute setting, immediately post OHS, and it is employed only when the patient fails to separate from CPB with more standard cocktails led by Dobutamine. It's general purpose in this setting is to kick up CO but it is also an excellent vasodialator, especially in the pulmonary beds. Since it is not our first line inotrope and the patient has now been on CPB for an extended amount of time, Milrinone's vasodialating properties can become problematic and require a pressor in the form of Neo or Vaso to support SVR and therefore BP. This vasodialating impact becomes less and less as the patient moves farther away from a long pump run and the CPB induced levels of vasodialating mediators begins to fall off.

The key difference between Milrinone and Dobutamine is that while both are inotropes, Milrinone is a non-catecholamine. Being a phosphodiesterase inhibitor, it directly increases available cyclic AMP to the myocardium and does not utilize the beta andrenergics as Dobutamine does. Since beta andrenergic receptors are finite in the heart, although with dysfunction based changes in distribution and density, Dobutamine has an ultimate end point of effect. Once all beta andrenergic receptors have been recruited, that is that. Higher doses of Dobutamine will not help and, unknown to many, can have an alpha pressor effect in high doses (>10mcg/kg). Milrinone's effect is not limited by beta andrenergic availability and therefore may be preferred by some cardiologists who feel their patients might already be at maximum levels of beta andrenergic recruitment, hence Milrinone seems to "work better".

Both drugs are inotropes, Dobutamine is a superior chronotrope, in my opinion, and the lusitropic ( diastolic relaxation) effect of these drugs as compared to one another is debated in the literature. I have read that chronic Dobutamine for end stage CHF will certainly improve quality of life, but shorten it as well. I do not know if the same holds true for Milrinone.

[ghillbert, MSN, NP]

I have read that chronic Dobutamine for end stage CHF will certainly improve quality of life, but shorten it as well. I do not know if the same holds true for Milrinone.

I believe it does - REMATCH certainly showed that there was extremely poor survival for ESHF on inotropes/medical therapy - 25% at 1 year and just 8% at 2 years.

In addition, the PROMISE trial (Prospective Randomized Milrinone Survival Evaluation) was terminated early after demonstrating a clear adverse mortality risk in patients receiving oral milrinone versus placebo (plus conventional HF medical therapy).