table comparing pressor agents?

[SuperflyMD]

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I'm looking for a good article and/or table comparing common pressor agents like dopamine, levophed, and neo.

I'd prefer something on the web, but I'll take what I can get.

Thanks,

SF

 

[bulgethetwine]

I'm looking for a good article and/or table comparing common pressor agents like dopamine, levophed, and neo.

I'd prefer something on the web, but I'll take what I can get.

Thanks,

SF

I would try Up-to-Date if you have access. As I recall, there is a great article that has a succinct chart as well as more copious info in you're so inclined. If you have trouble finding it on UTD by searching for pressors or the like, try a search term like Shock.

 

[OSUdoc08]

I'm looking for a good article and/or table comparing common pressor agents like dopamine, levophed, and neo.

I'd prefer something on the web, but I'll take what I can get.

Thanks,

SF

"Levophed = Leave 'em Dead"

- Paramedic Cardiology Course Instructor (RN, CCEMT-P)

 

[bulgethetwine]

"Levophed = Leave 'em Dead"

- Paramedic Cardiology Course Instructor (RN, CCEMT-P)

That's the mantra....

.... but not the science.

 

[southerndoc]

That's the mantra....

.... but not the science.

Norepi seems to be the agent of choice for treatment of septic shock at my institution. We use dobutamine for low central venous sats.

 

[Apollyon]

That's the mantra....

.... but not the science.

If you look, there's a dearth of science in critical care medicine - mostly case studies, retrospective studies, or case reports. The double-blind RCT is the holy grail (and just as elusive). The point with "leave 'em dead" is that the people that get it are essentially dead already - so, are we starting too late? That was the deal with the oscillator at Duke - when they started using it (before the data), it was being put on too late - it only kept people alive as long as it was on, and they died when it came off. then, more data came down, and, now, although results are still not great, they're not completely dismal.

 

[OSUdoc08]

If you look, there's a dearth of science in critical care medicine - mostly case studies, retrospective studies, or case reports. The double-blind RCT is the holy grail (and just as elusive). The point with "leave 'em dead" is that the people that get it are essentially dead already - so, are we starting too late? That was the deal with the oscillator at Duke - when they started using it (before the data), it was being put on too late - it only kept people alive as long as it was on, and they died when it came off. then, more data came down, and, now, although results are still not great, they're not completely dismal.

As I understood it, it was more based on the fact that Levophed has both peripheral and central alpha-adrenergic properties, which doesn't allow for any part of your body to recieve adequate circulation, due to diffuse vasoconstriction.

Obviously when contrasted with epinephrine, where only the peripheral vessels are constricted and central vessels are dilated, you can clearly see the problem with Levophed.

Of course, this is how this particular instructor presented it to us.

 

[Jeff698]

"Levophed = Leave 'em Dead"

Yep, that's what I was also taught in paramedic school (in 1987). In medical school, however, I was taught to use it. In residency, I'm being taught it is the pressor of choice for septic shock.

Several of the docs I've spoken with about this were also taught the essential baddness of norepi back in the day. That was common teaching. Much like several amps of bicarb as first line therapy for all cardiac arrests. And 'renal' doses of dopamine. And......

Anyway, you get the picture. Times change and practice is updated as science progresses (or the wind changes).

Take care,
Jeff

 

[fuegofrio17]

Levophed is first line treatment in the critical care unit we work at. Vasopressin is then added at 0.04 as a second line agent if the patient is still hypotensive at 6-8 mcg/min of Levophed. Phenylephrine is then added as a third agent if the patient is still hypotensive and maxed out on levophed. Lastly, an epi drip is started as a last ditch 4th agent if the patient has retractable hypotension. Vasopressin in not titrated, just turned either on or off. It is usually the last agent to remove after you titrate down off of levophed.

 

[OSUdoc08]

Yep, that's what I was also taught in paramedic school (in 1987). In medical school, however, I was taught to use it. In residency, I'm being taught it is the pressor of choice for septic shock.

Several of the docs I've spoken with about this were also taught the essential baddness of norepi back in the day. That was common teaching. Much like several amps of bicarb as first line therapy for all cardiac arrests. And 'renal' doses of dopamine. And......

Anyway, you get the picture. Times change and practice is updated as science progresses (or the wind changes).

Take care,
Jeff

Yes, it certainly makes sense for septic shock, as the mechanism is so different than the other types of shock. What other things can it be used to treat?

 

[OSUdoc08]

Levophed is first line treatment in the critical care unit we work at. Vasopressin is then added at 0.04 as a second line agent if the patient is still hypotensive at 6-8 mcg/min of Levophed. Phenylephrine is then added as a third agent if the patient is still hypotensive and maxed out on levophed. Lastly, an epi drip is started as a last ditch 4th agent if the patient has retractable hypotension. Vasopressin in not titrated, just turned either on or off. It is usually the last agent to remove after you titrate down off of levophed.

Why is there no mention of dopamine here? I would think this should be near the top of the list.

 

[jojo14]

I'm looking for a good article and/or table comparing common pressor agents like dopamine, levophed, and neo.

I'd prefer something on the web, but I'll take what I can get.

Thanks,

SF

I found the table in the green Tarascon Critical Care pocket book with the pressors listed helpful for my ICU rotation. It doesn't discuss when you use what though.

From my limited ICU experience, we use levophed quite a bit as a first line agent. I was taught that expression of "leave em dead" was pretty dated and applies to when higher doses of levophed were routinely used, but doesn't really apply now because we don't use such high doses any more. My attendings didn't really like dopamine at all for some reason I don't really understand besides that they said it didn't work as well.

 

[jojo14]

If anyone cares-

I just reviewed some of this stuff again, norepinephrine is actually synthesized from dopamine. I recall my attending saying it was easier to just skip a step and give the norepi. Plus, I think you have to use higher doses of dopamine to achieve pressor levels. Somebody with more knowledge should maybe step in here...

 

[bartleby]

If you were going to be stuck in Desert Island Hospital with only one pressor to choose from, Dopamine would be your choice. Why? Because with varying doses you can stimulate your choice of receptors. For example, in moderate doses it predominantly stimulates B1 adrenergic receptors (increases heart rate and contractility) but at high doses it begins to add alpha receptor effects (vasocontriction).

Why not just use Dopamine and dial in the desired effect? Because that beta agonism can have some undesirable effects in septic patients with preserved cardiac output but whose BP is low due to a lack of vascular tone (low SVR) from bacterial toxin and immune mediator-related factors. Norepinephrine give you the "squeeze" you need to get their BP up after judicious volume replacement without the unnecessary cardiac stimulation. This can be of particular clinical consequence in the elderly and those with coronary artery disease who will not tolerate the tachycardia associated with moderate to high doses of dopamine.

The bottom line is that you need to understand the cause of the shock you are attempting to treat and pick the appropriate pressor for that case. The old standby (The ICU Book, by Marino) covers this nicely.

Why is there no mention of dopamine here? I would think this should be near the top of the list.

 

[12R34Y]

OSUdoc,

I as well being a medic from the past was taught leveophed "leave 'em dead".

This is no longer the case.

Levophed is most commonly the first line preferred agent in septic shock and gets used a whole bunch in the ICU's.

gotta remember alot of that stuff in medic school you learned years ago no longer applies 😉

 

[12R34Y]

OH, and Marino is good (I thought) and the Taracson's ICU little book also has a nice table as mentioned above.

dopamine was almost never used in the MICU, b/c they preferred norepi, phenylephrine, vasopressin and epi drips for hypotension.

However, in the CCU dopamine flowed like crazy. Makes sense because often treating cardiogenic shock as opposed to sepsis.


later

 

[bulgethetwine]

OH, and Marino is good (I thought) and the Taracson's ICU little book also has a nice table as mentioned above.

dopamine was almost never used in the MICU, b/c they preferred norepi, phenylephrine, vasopressin and epi drips for hypotension.

However, in the CCU dopamine flowed like crazy. Makes sense because often treating cardiogenic shock as opposed to sepsis.


later

This is a GREAT thread! It's got me thinking and reviewing the latest evidence, too, especially the Up-to-date stuff and the Rivers' body of research (did everyone get the Surviving Sepsis Campaign Guidelines mail shot again this month? -- Great stuff).

I see 5 drugs being mentioned the most. Plus a 6th if you include milrinone...

1. Dopamine - lots of talk about the dose dependency effect which may or may not have any effect on the kidney (theoretical) based on differential receptor effects (this is the established science part). Good to use if you're not afraid of a little cardiac beta-agonism. High heart rate or CAD? Not so much...

2. Dobutamine - might improve conditions attributable to depressed cardiac function, but the problem, as I interpret it is the potential to expose one to low volume... it will give ya more squeeze, but the sink gets bigger (peripheral dilation).

3. Norepi (Levophed) - This is the choice in septic shock because of the dilated peripheral circulation -- you get the cardiac squeeze but also tightening of the peripheral circulation. In theory.

4. Phenylephrine (Neo-synephrine) - Similar to levophed in that it has more alpha agonist then dopamine and thus might be ideal for tachycardic/CAD patients. I'm not sure what the advantage over levophed is, though. Is it duration of action? Would the levophed studies (although Apollyon points out these aren't *great*) have the same results if they were repeated with this?

5. Vasopressin - Of particular use in patients with refractory shock and may have a synergistic effect with other pressors. Rivers' points out you replace them in physiologic replacement doses, not high dose "as traditionally used".

... and for the hell of it, I'm gonna throw in milrinone - it's a phosphodiesterase inhibitor. So it should, like dobutamine, kick up the cardiac output... but it lasts a lot longer than the latter - and again, Rivers' points out it accumulates in renal patients).

Ok, let the whacking start -- let's kick this around some more!

 

[fuegofrio17]

There's a good powerpoint presentation I found on the web regarding Inotropic and Vasoactive Agents. It also goes into detail about the use of dopamine and its varied negative effects.

http://www.cgi.ualberta.ca/emergency/rounds/files/InotropicandVasoactiveDrugs.ppt

 

[NinerNiner999]

Low-Dose Dopa (2-5) is excellent for CHF patients with poor renal function who may need assistance clearing their Lasix (due to its dilatory effect on the renal vaculature). Dobuatamine works well here to. At higher levels of Dopamine (greater than 10) adrenergic effects become more prominent. Dopamine in theory can go to much higher doses, but it typically should be limited to doses in the 18-25 range. At this point, I prefer switching over to Levo (NE) at low doses (2) and titrating up to effect, while at the same time weaning down the dopamine. It is because of this "balancing act" that many people prefer to use Levo as a first-line agent to treat sepsis.

Using these three pressors is usually effective. Moving to higher adreniergic agents such as Neo can cause a desired effect, but must be watched closely because it can quickly lead to distal extremity necrosis (due to its extreme alpha-1 effects). As with any pressor, it is imperative that they are run through a central line to avoid local peripheral vasoconstriction as can happen through a PIV.

 

[12R34Y]

I thought the "renal dose" of dopamine (2-5mcg/kg/min) went out the window several years ago! Are you still doing this? 😕

 

[jojo14]

I thought the "renal dose" of dopamine (2-5mcg/kg/min) went out the window several years ago! Are you still doing this? 😕

I thought so too. There's actually a current thread about renal dose dopamine in the anesthesiology forum (not like, I go there a lot or anything) where they site this study from Lancet 2000 saying it dopamine doesn't show any significant renal protection.

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=PubMed&list_uids=11191541&dopt=Abstract

I agree, this is a great thread, I'm actually learning stuff while procrastinating.

 

[deleted52758]

from april critical care medicine
Does dopamine administration in shock influence outcome? Results of the Sepsis Occurrence in Acutely Ill Patients (SOAP) Study

 

[roja]

I have a table that was made by one of our attendings when he was a chief resident. It is really amazing. I can try and scan it and post it for you...

 

[SuperflyMD]

I have a table that was made by one of our attendings when he was a chief resident. It is really amazing. I can try and scan it and post it for you...

That'd be great. Thanks.

BTW: are you headed back to Texas after residency? I'm a UTHSCSA grad too, and I can't wait to get back down South.

 

[OSUdoc08]

I just took a refresher ACLS course today, with the new guidlines.

The only mention of dopamine was with stable symptomatic bradycardias.

After atropine and TCP, it looked like an epi or dopamine drip is the next treatment if the former do not work.

The algorithm shows epi preferred first and then dopamine, but it was explained to us that since dopamine is premixed, it will be the most common to be used.

They also made a big emphasis on using amiodarone instead of lidocaine as the first-line anti-arrythmic.

 

[Jeff698]

are you headed back to Texas after residency? I'm a UTHSCSA grad too, and I can't wait to get back down South.

Come on back to the homeland, ye wayward Texans. I did my time out of state (NY 1990-1992) and got my little Texas butt home as soon as I could. I enjoyed my 'vacation' away but learned a valuable lesson. I may like other places, but Texas is my home.

Come on home. You'll be glad you did.

Doesn't that sound like a commercial? I oughtta be paid for this...

Take care,
Jeff

 

[BKN]

from april critical care medicine
Does dopamine administration in shock influence outcome? Results of the Sepsis Occurrence in Acutely Ill Patients (SOAP) Study

Meaningless, a observatoinal study that did not assign patients randomly to dopamine or no dopamine. Sure the dopamine group had a higher mortality-they were probably treated with it cause they were worse on average.

We still await meaningful vasopressor research after all these years.🙁

 

[NinerNiner999]

Or perhaps there was a larger patient population 👎 who recieved dopamine as a first-line agent compared to others...

 

[bulgethetwine]

I just took a refresher ACLS course today, with the new guidlines.

The only mention of dopamine was with stable symptomatic bradycardias.

After atropine and TCP, it looked like an epi or dopamine drip is the next treatment if the former do not work.

The algorithm shows epi preferred first and then dopamine, but it was explained to us that since dopamine is premixed, it will be the most common to be used.

They also made a big emphasis on using amiodarone instead of lidocaine as the first-line anti-arrythmic.

But don't forget that these are "guidelines" ... not hard and fast rules. This is where the fun part of being a doctor comes in. The relative merits of dopamine or dobutamine are going to be different or different patients -- not to mention different docs seeing the same patients with the same presentatoin!

Plus, logistics and "reality" always play a role -- illustrated by the explanation that dopamine is premixed.

There IS a big emphasis on amiodarone instead of lidocaine -- but there are two things important here, too: One, lidocaine works faster. This matters if your patient is unstable and you're at least some minutes away from being set up to give electricity. (Disclaimer: Many will retort that amio works PLENTY fast. If you give it in high enough dose.... which the re-retort will point out, how much is too much ) Second, amio is much more $$$$. This matters in some peripheral hospitals and health networks.

Guidelines to the sidelines, sometimes... 😀

 

[12R34Y]

But don't forget that these are "guidelines" ... not hard and fast rules. This is where the fun part of being a doctor comes in. The relative merits of dopamine or dobutamine are going to be different or different patients -- not to mention different docs seeing the same patients with the same presentatoin!

Plus, logistics and "reality" always play a role -- illustrated by the explanation that dopamine is premixed.

There IS a big emphasis on amiodarone instead of lidocaine -- but there are two things important here, too: One, lidocaine works faster. This matters if your patient is unstable and you're at least some minutes away from being set up to give electricity. (Disclaimer: Many will retort that amio works PLENTY fast. If you give it in high enough dose.... which the re-retort will point out, how much is too much ) Second, amio is much more $$$$. This matters in some peripheral hospitals and health networks.



Guidelines to the sidelines, sometimes... 😀

There was actually a article in the last annals about how HORRIBLE lidocaine is at converting monomorphic V-tach and amiodorone only converts monomorphic V-tach in like 30% of the time! It's dismal.

The best drug to terminate monomorphic stable V-tach is procainamide. If we had IV sotalol that would be the best, but it's only oral.

Of course if they become unstable just shock 'em.

but, bottom line of that article plus an editorial is that lidocaine may be the worst drug and amio not much better, but it's all we've got.

later

 

[OSUdoc08]

There was actually a article in the last annals about how HORRIBLE lidocaine is at converting monomorphic V-tach and amiodorone only converts monomorphic V-tach in like 30% of the time! It's dismal.

The best drug to terminate monomorphic stable V-tach is procainamide. If we had IV sotalol that would be the best, but it's only oral.

Of course if they become unstable just shock 'em.

but, bottom line of that article plus an editorial is that lidocaine may be the worst drug and amio not much better, but it's all we've got.

later

Too bad procainamide has been dropped from the ACLS algorithm.

(I'm assuming that since the ECC 2005 was from an international consensus, that it is in fact the best protocol, right?)

Edit: The ACLS algorithm was only for the first 10 minutes of a code, as I later learned, which explains why there was no mention of procainamide in my course.

 

[roja]

That'd be great. Thanks.

BTW: are you headed back to Texas after residency? I'm a UTHSCSA grad too, and I can't wait to get back down South.

I have to find a scanner but I will post it when I can.


I am not sure about heading back. I am starting a 2 year fellowship in july. So who knows... 🙂

 

[BKN]

Too bad procainamide has been dropped from the ACLS algorithm.

As I told Keith, who did the study referred to, the purpose of the procainamide in stable V tach is to widen the QRS and drop the pressure so that you can feel good about heating up the paddles for this awake patient. 😀

 

[12R34Y]

As I told Keith, who did the study referred to, the purpose of the procainamide in stable V tach is to widen the QRS and drop the pressure so that you can feel good about heating up the paddles for this awake patient. 😀

that's hysterical!!

 

[12R34Y]

Too bad procainamide has been dropped from the ACLS algorithm.

(I'm assuming that since the ECC 2005 was from an international consensus, that it is in fact the best protocol, right?)

Procainamide has most definately NOT been dropped from ACLS. Just because its not in the little algorithm boxes doesn't mean it isn't in the full set of guidelines for the 2005 changes which is very very long document.

The below is pasted from the new 2005 guidelines:

Procainamide
Procainamide hydrochloride suppresses both atrial and ventricular arrhythmias by slowing conduction in myocardial tissue. One randomized trial (LOE 2)47 indicated that procainamide is superior to lidocaine in terminating spontaneously occurring VT. Procainamide may be considered in the following situations:


As one of several drugs that may be used for treatment of stable monomorphic VT in patients with preserved ventricular function (Class IIa)46

One of several equivalent drugs that can be used for control of heart rate in atrial fibrillation or atrial flutter in patients with preserved ventricular function

One of several drugs that can be used for acute control of heart rhythm in atrial fibrillation or atrial flutter in patients with known pre-excitation (WPW) syndrome and preserved ventricular function

One of several drugs that can be used for AV reentrant, narrow-complex tachycardias such as reentry SVT if rhythm is uncontrolled by adenosine and vagal maneuvers in patients with preserved ventricular function

Procainamide hydrochloride for non-VF/VT arrest may be given in an infusion of 20 mg/min until the arrhythmia is suppressed, hypotension ensues, the QRS complex is prolonged by 50% from its original duration, or a total of 17 mg/kg (1.2 g for a 70-kg patient) of the drug has been given. Bolus administration of the drug can result in toxic concentrations and significant hypotension. The maintenance infusion rate of procainamide hydrochloride is 1 to 4 mg/min, diluted in D5W or normal saline. This should be reduced in the presence of renal failure.

Procainamide should be used cautiously in patients with preexisting QT prolongation. In general it should be used with caution if at all in combination with other drugs that prolong the QT interval (consider obtaining expert consultation). Monitor the ECG and blood pressure continuously during administration of procainamide.

Sotalol
Sotalol is not a first-line antiarrhythmic. Sotalol hydrochloride is an antiarrhythmic agent that, like amiodarone, prolongs action potential duration and increases cardiac tissue refractoriness. It also has nonselective ß-blocking properties. One randomized controlled trial (LOE 1)48 indicated that sotalol is significantly more effective than lidocaine for terminating acute sustained VT. This agent may be used in the following circumstances with expert consultation:


To control rhythm in atrial fibrillation or atrial flutter in patients with pre-excitation (WPW) syndrome and preserved ventricular function when the duration of the arrhythmia is 48 hours. But the intervention of choice for this indication is DC cardioversion.

For monomorphic VT.

IV sotalol is usually administered at a dose of 1 to 1.5 mg/kg body weight, then infused at a rate of 10 mg/min. Side effects include bradycardia, hypotension, and arrhythmia. The incidence of torsades de pointes following a single dose of sotalol for treatment of VT is reportedly 0.1%.45 Use of IV sotalol is limited by the need to infuse it relatively slowly.


read the full guidelines.

not just the algorithm boxes.

 

[BKN]

Too bad procainamide has been dropped from the ACLS algorithm.

(I'm assuming that since the ECC 2005 was from an international consensus, that it is in fact the best protocol, right?)

Read keith's article and the accompanying editorial. The last paragraph in the latter says it best.

Annals EM March? 2006

 

[BKN]

that's hysterical!!

and true.

 

[OSUdoc08]

Read keith's article and the accompanying editorial. The last paragraph in the latter says it best.

Annals EM March? 2006

My ACLS class this week decided to omit lidocaine from the algorithm, contrary to my previous class 2 years ago. It seemed as though they were in love with amiodarone, and wouldn't even let me use lidocaine during my megacode. Instead of asking for an amp of lidocaine, I had to order 300mg (6ml) of Amiodarone mixed with 14ml of D5W. That order works well in a code, now doesn't it?

Upon further investigation, it was revealed to me that the ACLS class was based upon the first 10 minutes of a code only, and they did not cover the later antiarrythmics after amiodarone.

So, I must ask, what order do most people use?

300mg Amiodarone --> 150mg Amiodarone --> ?? (1 mg lidocaine?)

Or does anyone actually use amiodarone for codes?

 

[NinerNiner999]

Usually, the first ten minutes of a code is just long enough to give a couple of rounds of epi, atropine, and vasopressin. Throw in some calcium, bicarb, and magnesium, and then - if you get a rhythm from asystole - you can jump on the amiodarone/other antidysrhythmic road...

 

[southerndoc]

I had my first asystolic resuscitation the other day. A MICU "border" was in the SICU. The patient went asystolic. The MICU residents were downstairs in the ED admitting another patient. I ran the code. 2 mg of epi and 1 mg of atropine -> sinus tach with a pressure of ~180 systolic with a minute or so run of VT. The nurses were trying to get me to give amio for the VT (with a pulse), but I refused. Luckily my suspicions of it being secondary to the epi were correct. It resolved after about a minute.

I and the MICU team gave me/myself a pat on the back. It was the first asystolic code that I have resuscitated. (The patient was subsequently extubated and sent to the floor, neurologically intact.)

 

[12R34Y]

My ACLS class this week decided to omit lidocaine from the algorithm, contrary to my previous class 2 years ago. It seemed as though they were in love with amiodarone, and wouldn't even let me use lidocaine during my megacode. Instead of asking for an amp of lidocaine, I had to order 300mg (6ml) of Amiodarone mixed with 14ml of D5W. That order works well in a code, now doesn't it?

Upon further investigation, it was revealed to me that the ACLS class was based upon the first 10 minutes of a code only, and they did not cover the later antiarrythmics after amiodarone.

So, I must ask, what order do most people use?

300mg Amiodarone --> 150mg Amiodarone --> ?? (1 mg lidocaine?)

Or does anyone actually use amiodarone for codes?

We've been giving amio in the field on the ambulance since 2000. It's not that hard. It comes in 150 vials. Just draw 2 vials up in a syringe and push.

Yes, the order was typically epi, 300 amio, epi, 150 amio, epi, by that time you are at least 10 minutes into the code. So after that nothing much matters anyway.

Of course, the new guidelines focus more on good CPR for 2 minute stints uninterrupted then shock.........2 minutes CPR.........shock..........2minutes CPR then worry about the drugs.

later

 

[OSUdoc08]

Usually, the first ten minutes of a code is just long enough to give a couple of rounds of epi, atropine, and vasopressin. Throw in some calcium, bicarb, and magnesium, and then - if you get a rhythm from asystole - you can jump on the amiodarone/other antidysrhythmic road...

I don't think we are talking about an asystole code which converts to Vfib/Vtach.

We instead are talking about a Vfib/Vtach code. You would not use atropine in this code unless it turned into asystole.

The algorithm would be Shock --> Epi --> Shock --> Amiodarone OR Lidocaine.

You wouldnt throw in the Mag unless you have Torsades or labs back, and the Bicarb would be late in the code, unless you had a long down time.

 

[OSUdoc08]

We've been giving amio in the field on the ambulance since 2000. It's not that hard. It comes in 150 vials. Just draw 2 vials up in a syringe and push.

Yes, the order was typically epi, 300 amio, epi, 150 amio, epi, by that time you are at least 10 minutes into the code. So after that nothing much matters anyway.

Of course, the new guidelines focus more on good CPR for 2 minute stints uninterrupted then shock.........2 minutes CPR.........shock..........2minutes CPR then worry about the drugs.

later

They heavily emphasized that the 300mg of amiodarone must be mixed with 14mL of D5W, and not pushed directly.

 

[12R34Y]

They heavily emphasized that the 300mg of amiodarone must be mixed with 14mL of D5W, and not pushed directly.

I can be pushed directly has been for years.

later

 

[OSUdoc08]

I can be pushed directly has been for years.

later

Why do you think they wouldn't let us push it directly in our ACLS class?

The reason I ask, is that I also know we shocked 200-300-360 for years, and that has changed as well.

I just assumed it was a change for some reason.

 

[12R34Y]

Why do you think they wouldn't let us push it directly in our ACLS class?

The reason I ask, is that I also know we shocked 200-300-360 for years, and that has changed as well.

I just assumed it was a change for some reason.

nobody shocks 200-300-360 anymore because most defibrillators are now biphasic and you shock at 150-200.

if you've got the fancy defibrillators the machine will measure transthoracic impedance and deliver the appropriate energy level.

I can't explain your class. I've been pushing it directly for years and so do others I know. Never actually heard of mixing it up first in code blue. not gonna make a difference.

Now if you are dripping the dose of 150mg over 10 minutes to someone who is perfusing then you dilute it.

just your class instructors way of presenting and personal preference.

not the norm in my book however or at my hospital or old ambo service.

 

[OSUdoc08]

nobody shocks 200-300-360 anymore because most defibrillators are now biphasic and you shock at 150-200.

if you've got the fancy defibrillators the machine will measure transthoracic impedance and deliver the appropriate energy level.

I can't explain your class. I've been pushing it directly for years and so do others I know. Never actually heard of mixing it up first in code blue. not gonna make a difference.

Now if you are dripping the dose of 150mg over 10 minutes to someone who is perfusing then you dilute it.

just your class instructors way of presenting and personal preference.

not the norm in my book however or at my hospital or old ambo service.

I'm not familiar with any hospitals in my area using biphasic defibrillators.

Nobody shocks at 200-300-360 anymore, because the 2005 ECC protocols state that you start with one shock at 360, followed by 2 minutes of CPR.

Unfortunately, it will be a number of years before AED's are up to par with the new standards, and the stacked shocks will continue with these units.

 

[Hercules]

I'm not familiar with any hospitals in my area using biphasic defibrillators.

Nobody shocks at 200-300-360 anymore, because the 2005 ECC protocols state that you start with one shock at 360, followed by 2 minutes of CPR.

Unfortunately, it will be a number of years before AED's are up to par with the new standards, and the stacked shocks will continue with these units.

I was taught on biphasics and they've been the standard at several hospitals where I've trained. I also push the amiodarone straight.

 

[southerndoc]

I was taught on biphasics and they've been the standard at several hospitals where I've trained. I also push the amiodarone straight.

We use biphasics in my hospital. The evidence really supports their use, but it is a huge expense to convert your "fleet" of defibrillators to biphasic.

We push amiodarone diluted with 54 mL of D5W or NS. Basically use a 60 mL syringe draw up roughly 55 mL of NS or D5 (whatever is hanging, just not LR) from the IV bag, then draw up the med. Concentrations >3 mg/mL have been associated with thrombophlebitis, often severe. This isn't diluted like it's supposed to be, but it does help. However, I doubt anyone will fault you for administering it undiluted in a code situation. If there isn't a bag of fluids hanging when we go to administer the amiodarone in a code (i.e., the patient was heplocked and coded recently without time to hang fluids yet), then I certainly wouldn't delay the amio to find 6 bottles of saline flushes or a bag of fluids.

There is a big push for cardiocerebral resuscitation now. Interesting research coming out about that.

 

[12R34Y]

I'm not familiar with any hospitals in my area using biphasic defibrillators.

Nobody shocks at 200-300-360 anymore, because the 2005 ECC protocols state that you start with one shock at 360, followed by 2 minutes of CPR.

Unfortunately, it will be a number of years before AED's are up to par with the new standards, and the stacked shocks will continue with these units.

I haven't worked at a hospital OR prehospital service that didn't use biphasic in probably 5 years! where are you at?!

all lifepack 12's are biphasic which is probably one of the most commonly used prehospital and in hospital monitor/defibs.

later