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Epi drip


akroeze

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I prefer an epi drip for any patient with a lousy pressure and one step away from cardiac arrest. I mix 4 mg of 1::1,000 in a 250 bag of NSS. 15cc/hr is 4mcg/min and you can titrate up from there although once you hit 8mcg/min and have not achieved the desired effect you need to think of something else like adding levophed to the epi or going to isuprel.

Live long and prosper.

Spock

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I might be wrong, but I remember (way back) an Epi drip was easier to adm. if no pump was available. Back then very rarely did we have a pump on board. And with Dopamine, anything less than 7-8mcg/kg/min. just produced renal dilation and frequently had to be increased. That's per another ACLS Inst. I taught with, who learned me a lot while teaching with him.

Like I said, I could be wrong. Too many brain cells have gone bye-bye I guess.

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I am re-writing our protocol for cardiogenic shock. Our medical director wants me to include Dobutamine (preload), Dopamine (afterload) and Epi drip for use of an increased vasopressor, and for bradycardia.

R/r 911

This is also true with sepsis... If your patient is in septic shock, after inital fluid boluses of NACL or LR you want to give a pressor. Dopamine is the most common choice, and can be started immediatly after a couple of isotonic boluses. However you may want to start dobutamine soon after ( if you start it 1st, expecially with pedi patients you can have a significant decrease in MAP initially, the Dopamine will "blunt" this effect somewhat) but you may have to move on to EPI or Levo to get a good Alpha Response eg. clamp them down to raise MAP.... Just another good use for an epi drip...

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I am re-writing our protocol for cardiogenic shock. Our medical director wants me to include Dobutamine (preload), Dopamine (afterload) and Epi drip for use of an increased vasopressor, and for bradycardia.

R/r 911

Just a qiestion for you about this... Is the medical director at all worried about the Beta 1 effects of an EPI drip in cardiogenic shock? Ovibously you want to increase pre/after load, and get + ino/chronotropic effects, but what about epi's cardiotoxic effects? Couldn't this stress the myocardium too much by increase MVO2 demand? At what point does he want to start an epi drip on these patients??? Not saying he/she's wrong, just wondering...

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If the patient is in cardiogenic shock, they need the beta 1 effects, and dopamine or epi would be indicated. Dobutamine or milrinone would be okay too, except if they are in shock, you'd have to add a second agent as a vasoconstrictor as well such as phenylephrine or vasopressin. Any agent with beta-1 effects, to include epi, dopamine, dobutamine, or norepinephrine, will increase myocardial oxygen demand, and there will be the potential for arrhythmia.

Epi drip is something I rarely do in adults (and usually when I've got them on several other pressors), but do more frequently in children who need a pressor. Kids tend to handle the epi drips better than adults do. I agree with with p3medic on using it on a severe anaphylaxis, though none of my anaphylaxis patients have yet needed one.

Contrary to your statement, saboats, we use norepinephrine more commonly here in adult sepsis than dopamine. Dobutamine is not indicated as a first line or second line drug for sepsis. It may actually be counterproductive due to the vasodilation that it causes which you alluded to. Children tend to get more myocardial depression with sepsis, so something inotropic is indicated like dopamine or epi.

If the patient is catecholamine depleted, such as what happens after a prolonged period of adrenergic stimulation, then dopamine won't be effective, so I go with norepi or epi if the patient is refractory to dopamine.

'zilla

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Thanks

Cardiogenic shock protocol here......

1: basic protocol 2

2: Cannulate

3: Treat disrhythmias if present

4: ADRENALINE infusion if pulse rate 50-150/min and poorly perfused with BP < 80 mmHg systolic

5: Pain management

6: Consider urgent transport

Stay Safe

Craig

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  • 2 weeks later...
Refractive bradycardia I believe.
Could you explain what that is and how to identify it? I've seen it mentioned in a few places now.

I might be wrong, but I remember (way back) an Epi drip was easier to adm. if no pump was available. Back then very rarely did we have a pump on board. And with Dopamine, anything less than 7-8mcg/kg/min.
Just as a training exercise for those not in medic school, yet, anyone want to go through calculating and setting up doses for epi and dopamine? NO ONE here uses them (they say b/c of the math)...and I never want that limit me...

If the patient is catecholamine depleted, such as what happens after a prolonged period of adrenergic stimulation, then dopamine won't be effective, so I go with norepi or epi if the patient is refractory to dopamine.
Why won't dopamine be effective after prolonged adrenergic stimulation? Dopamine doesn't bind directly to receptors, it uses body's adrenergic chemicals?
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Could you explain what that is and how to identify it? I've seen it mentioned in a few places now.

Just as a training exercise for those not in medic school, yet, anyone want to go through calculating and setting up doses for epi and dopamine? NO ONE here uses them (they say b/c of the math)...and I never want that limit me...

Why won't dopamine be effective after prolonged adrenergic stimulation? Dopamine doesn't bind directly to receptors, it uses body's adrenergic chemicals?

Good question. In many cases where we have people on high doses of pressors, the dynamics of their receptors change. Remember, the ultimate effect of or pressor of choice is the stimulation of an adrenergic receptor. (Alpha and Beta in most cases) You actually get a down regulation of the receptor. In basic terms, the receptor becomes overwhelmed and by the high levels of adrenergic substances and cease to function properly. They in essence say, "why the hell do I need to do anything with all of this stimulation, screw you guys I am going home." Sort of like insulin resistance if you will.

So, you see these people develop hypotension and bradycardia along with other problems in spite of being on massive doses of pressors. Their receptors simply cannot respond to stimulation, they are over stimulated and cannot perform anymore. hehe :D

How do we fix this?:

A few ways may help:

1) Try another pathway. Vasopressin (ADH) may help because Vasopressin has it's own receptors.

2) Stop the pressors and give the receptors a break. You may hear old school ICU nurses talk of "Pressor Holidays." This is what they mean when they use that term.

3) Give steroids. steroids can actually enhance how the receptors respond to pressors and enhance the creation of new pressor sensitive receptors.

Take care,

chbare.

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