Is dopamine contraindicated in acute stage myocardial infection???

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resender

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Hi every one:)
I'm happy to join such a forum
I'm new here
by the way I'm a new resident in hospital
I have a question and I'll be happy if anyone experience help me in it:love:

41 years old female was presenting to us with severe chest pain radiating to back after ECG revealed acute stage MI (ST elevation in 4 contagious chest leads) ; BP: was undetected!!!
so in such cases does dopamine has a role in mangement or it is contraindicated????:confused:

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Levophed is better then dopamine in cardiogenic shock. Check out the NEJM article from early March.
 
41 years old female was presenting to us with severe chest pain radiating to back after ECG revealed acute stage MI (ST elevation in 4 contagious chest leads) ; BP: was undetected!!!
so in such cases does dopamine has a role in mangement or it is contraindicated????:confused:

While the mention of 4 contiguous leads suggests otherwise, I'd consider inferior w/ RVI as a reason for the hypotension and start with fluids.

If I didn't think preload was an issue, I'd go with levo as well to avoid the increased beta with dopamine.

Take care,
Jeff
 
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I agree with the above responses. Not to mention that an intra-aortic balloon pump is likely in the patient's near future if they survive to cath lab.
 
41 years old female was presenting to us with severe chest pain radiating to back after ECG revealed acute stage MI (ST elevation in 4 contagious chest leads) ; BP: was undetected!!!

I shouldn't really be pointing this out but really... At first I was amused to read the title of the thread but then I assumed it must have been a typo (infection instead of infarction) but then I read this.
 
Agree as above. Cardiogenic shock = levo as first line. Dopamine if you have no levo on hand and are in pinch. Loved seeing this thread, had a STEMI who waited 20 hrs after onset of pain to come in last night with a BP dipping between the low 60's and high 70's, levo time my friend.
 
any dissection risk factors?
 
hey all I'm so thankful to all ur posts
actually I was not aware about NEJM
thanx to all
and keep in touch
 
how many of you are doing central lines on all your patients that are started on levo? I use to do it all the time in residency but in the community, they seem to infuse it as long as you have at least a 20 gauge peripheral.
 
how many of you are doing central lines on all your patients that are started on levo? I use to do it all the time in residency but in the community, they seem to infuse it as long as you have at least a 20 gauge peripheral.

I tend to put in a line in all my patients who I put on pressors. The complications of running pressors through a peripheral IV can be pretty bad. One hospital I work at tried to institute a pressors via cental line policy for a while but the docs (not the EM docs) complained too much and got it removed.
 
I tend to put in a line in all my patients who I put on pressors. The complications of running pressors through a peripheral IV can be pretty bad. One hospital I work at tried to institute a pressors via cental line policy for a while but the docs (not the EM docs) complained too much and got it removed.

We have that policy. It's a real pain sometimes. Can get around it by ordering a PICC line on the non-emergent patient who's a bit hypotensive.
 
I've seen people run levo through a peripheral...but, it always makes me a little uncomfortable because as a student I took care of a patient who had his arm amputated to his shoulder after Levo infiltrated from his peripheral site. As a result, I tend to put in a central line. With that said, I am a resident and am not single coverage in the community.
 
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I can't believe no one has side tracked this thread by pointing out that the title says "myocardial infection". When I read it I hear gomer pyle's voice in my head saying "citizayun's arrayust! He's havin uh my-cardjul eenfecshun!"

I put in a CVL or use a picc in my patients on pressors unless the unit is whisking them away in the next 15 minutes in which case their residents can do it.
 
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Don't forget to pace them if they brady down. Preload-dependent RCA infarcts often hit the SA node, and trancutaneously pacing while making cath arrangements may help decrease the amount of pressors used.
 
Aren't neosynephrine and dopamine safe peripherally?

That's another issue, access when you are in a pinch.
 
Aren't neosynephrine and dopamine safe peripherally?

That's another issue, access when you are in a pinch.


Google dopamine extravasation images.

You use what you have until you get central access. Getting that access is pretty high on the priority list. Iatrogenic pressor injuries are lawsuit slamdunks.

In our hospital we usually do not use dopamine for cardiogenic hypoperfusion because it increases O2 demand and is dysrhythmogenic.

We do use Levo, Neo, and Dobutamine.
 
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Aren't neosynephrine and dopamine safe peripherally?

That's another issue, access when you are in a pinch.

Neo seems like a really, really bad idea to me - especially given peripherally!:scared:

Also, regarding access: I am just a resident and have consequently never worked solo; that is, there is always someone to toss in a central line (how long does it really take anyway?...it may not be a sterile line, but a subclavian can be placed in a jiffy, if needed).

However, even if there is not time for a central line, why not just a quick IO drill to the tibia? Immediate central access for all pressors except neo.

Am I missing something?
(I guess not everyone has an IO drill, but why not a 'clean' subclavian?)
HH
 
Neo seems like a really, really bad idea to me - especially given peripherally!:scared:

Also, regarding access: I am just a resident and have consequently never worked solo; that is, there is always someone to toss in a central line (how long does it really take anyway?...it may not be a sterile line, but a subclavian can be placed in a jiffy, if needed).

However, even if there is not time for a central line, why not just a quick IO drill to the tibia? Immediate central access for all pressors except neo.

Am I missing something?
(I guess not everyone has an IO drill, but why not a 'clean' subclavian?)
HH

I wasn't aware that an IO counts as "central access" - what are you basing this on? Is anyone else practicing this way?

NB: Please read the above as a genuine inquiry rather than an attack.
 
I wasn't aware that an IO counts as "central access" - what are you basing this on? Is anyone else practicing this way?

I saw a literature review a year or so ago about the time it took meds to hit the heart between IO and different central lines. IIRC, the times were about equivalent. Not that speed is all there is to consider, of course.

I have exactly none of these papers on hand, though.

Take care,
Jeff
 
I saw a literature review a year or so ago about the time it took meds to hit the heart between IO and different central lines. IIRC, the times were about equivalent. Not that speed is all there is to consider, of course.

I have exactly none of these papers on hand, though.

Take care,
Jeff

We've been using I/O lines a lot more for difficult IV access, and our paramedics now routinely do them. The papers you were referring to used contrast die and fluoroscopy to measure the time of infusion to central circulation. The times with I/O lines and peripheral access were similar. I would imagine a PICC line would have similar speed.

I think an I/O line is a good alternative for patients who need Levophed or pressors emergently, but there is no time for a central line, or the patient's anatomy isn't favorable for one.
 
I think an I/O line is a good alternative for patients who need Levophed or pressors emergently, but there is no time for a central line, or the patient's anatomy isn't favorable for one.

Or for the patient who is severely hypovolemic. Use the IO to get the CVP up a bit and the cental line success rate gets much better.
 
Or for the patient who is severely hypovolemic. Use the IO to get the CVP up a bit and the cental line success rate gets much better.

Exactly. There's actually a pretty good study that was published showing that if you measure the IJ using U/S and it's less than 0.7 cm the odds of success decrease and the rates of complication increase.

After putting one in the carotid artery a few months ago (yes, under U/S guidance) I'm now measuring the IJ, and if it's not favorable I look at alternative IV access like a PICC line, or I/O. A central line is not the panacea of medicine that we have always been taught.

BTW there is now emerging research that CVP can be estimated using ultrasound, potentially eliminating a few central lines placed for that purpose.
 
Did the same (with the U/S) when I was a resident.

We've actually as a group had three of them in the last four months from three different people. The reason is that we are now doing central lines almost daily (sometimes 2-3 times) to meet our sepsis protocol guidelines. Obviously with increased number of procedures there is going to be increased number of complications.
 
After putting one in the carotid artery a few months ago (yes, under U/S guidance) I'm now measuring the IJ, and if it's not favorable I look at alternative IV access like a PICC line, or I/O. A central line is not the panacea of medicine that we have always been taught.

The only one I've put in an artery (so far, *crosses fingers*) was US guided and had non-pulsating blood when I checked before advancing the wire... in a patient with an SBP > 110.

I've made the point several times in residency that central lines are not benign or without complication and should not be used willy-nilly. This opinion has not always gone over well.
 
The only one I've put in an artery (so far, *crosses fingers*) was US guided and had non-pulsating blood when I checked before advancing the wire... in a patient with an SBP > 110.

I've made the point several times in residency that central lines are not benign or without complication and should not be used willy-nilly. This opinion has not always gone over well.

Mine was the same. We've all hit carotid before and seen bright red blood, or a pulse of blood when taking the syringe off.

In this case it was a small IJ next to the carotid. The U/S seemed to show it in the IJ, had dark red blood, and barely a dribble when I took the syringe off. Everything looked venous until the CVP said 50.
 
The last IJ I did was blind and had no complications.

I too have placed an intra-carotid central line with US guidance (with my very experienced attending standing at my side).
 
The last IJ I did was blind and had no complications.

I too have placed an intra-carotid central line with US guidance (with my very experienced attending standing at my side).

Mine was with the attending, too, and I remember it clearly - he was totally spazzing. I even told him (err, asked him) to relax just a bit, because he was all over the place.
 
I luckily haven't hit a carotid yet., but how did you guys realize you had hit it if you weren't checking CVP (something we dont' do routinely at my hospital)? And how did you handle the bleeding/hematoma after dilating it? it's not like you can sandbag it and have the person lie down for 6 hours like they do with fem caths.
 
I luckily haven't hit a carotid yet., but how did you guys realize you had hit it if you weren't checking CVP (something we dont' do routinely at my hospital)? And how did you handle the bleeding/hematoma after dilating it? it's not like you can sandbag it and have the person lie down for 6 hours like they do with fem caths.

We had one patient (not mine) who spent 4 days in the ICU with a carotid line before they realized it, so it's possible not to know unless you check a CVP.

It's a bad complication to have. The worst thing you can do is remove the line, as they can get an enormous hematoma and potentially airway compromise. In any case where a line is placed, it should be left alone and explored in the OR by the vascular surgeon for possible carotid repair.
 
It's a bad complication to have. The worst thing you can do is remove the line, as they can get an enormous hematoma and potentially airway compromise. In any case where a line is placed, it should be left alone and explored in the OR by the vascular surgeon for possible carotid repair.

See, I thought this, too, but a general surgery resident told me to definitely remove it and NOT leave it in. From where do you get your information?
 
We had one patient (not mine) who spent 4 days in the ICU with a carotid line before they realized it, so it's possible not to know unless you check a CVP.

It's a bad complication to have. The worst thing you can do is remove the line, as they can get an enormous hematoma and potentially airway compromise. In any case where a line is placed, it should be left alone and explored in the OR by the vascular surgeon for possible carotid repair.

At that facility don't they confirm placement with CXR?
 
At that facility don't they confirm placement with CXR?

Would Carotid v. IJ placement show a difference on a CXR necessarily? The aortic root should lie in close proximity to the R atrium
 
I luckily haven't hit a carotid yet., but how did you guys realize you had hit it if you weren't checking CVP (something we dont' do routinely at my hospital)? And how did you handle the bleeding/hematoma after dilating it? it's not like you can sandbag it and have the person lie down for 6 hours like they do with fem caths.

I've got the subclavian artery (in med school- it was bright red blood, and when I took the syringe off the needle, there was pulsatile blood squirting 5 inches out of the needle. I immediately pulled out and the patient had no complications.

In residency, when I cannulated the carotid, it was again pulsatile. I pulled out, held pressure for 10 minutes and the patient had no adverse side effects.

I think that an arterial line could look pretty similar to a venous on a chest x-ray, although it could appear to be more deviated to the left (if it were all that obvious, you'd think one of the 4 people that saw the xray (ER resident, ER attending, rad resident and rad attending) would have noticed.
 
Re cannulating the IJ vs carotid, consider transducing with a short length of tubing held upright prior to dilating the vessel. This is something that we do routinely at my institution and there is some data indicating that this reduces the risk of carotid dilation. Also, if using US, you can visualize the guidewire in the IJ using an in plane technique prior to dilating.
 
Re cannulating the IJ vs carotid, consider transducing with a short length of tubing held upright prior to dilating the vessel. This is something that we do routinely at my institution and there is some data indicating that this reduces the risk of carotid dilation. Also, if using US, you can visualize the guidewire in the IJ using an in plane technique prior to dilating.

Interesting idea about the tubing. I have had difficulty using US to verify placement by seeing the wire or the canula in the IJ using a longitudinal view because I run out of real estate between the site and the clavicle. I can get the cross picture but the longitudinal is tough.
 
I do both of those things- IV tubing manometry or just look at the wire or slimstick sheath in the vessel with the machine - and it helps.
 
I do both of those things- IV tubing manometry or just look at the wire or slimstick sheath in the vessel with the machine - and it helps.

The introducer kits supplied by (?) company even have a stretch of sterile tubing nicely included that works well for "tubing manometry"...a nice idea when in doubt, as the Cordis is a pretty big tube to be shoving into a carotid artery. :scared:
HH
 
Google dopamine extravasation images.

You use what you have until you get central access. Getting that access is pretty high on the priority list. Iatrogenic pressor injuries are lawsuit slamdunks.

In our hospital we usually do not use dopamine for cardiogenic hypoperfusion because it increases O2 demand and is dysrhythmogenic.

We do use Levo, Neo, and Dobutamine.

quick question -- doesn't dobutamine increase O2 demand too (beta activity)?
thx.


PS - i would not start compressions; this guy was awake enough to tell you where his pain was!
 
yeah in that case i guess it depends on how attractive she is (kidding, just being a pig, kidding)
 
quick question -- doesn't dobutamine increase O2 demand too (beta activity)?
thx.


PS - i would not start compressions; this guy was awake enough to tell you where his pain was!


Yes. Any positive inotrope will increase O2 demand. Dobutamine is (theoretically) beneficial in cardiogenic shock because it reduces SVR (which is high as a compensatory mechanism to the shock state- renin, angiotensin, aldosterone, etc.) Levo, dopa, and neo increase SVR (which is low in sepsis, anaphylaxis, neurogenic shock).

I work in neuroscience ICU and ICU (trauma, medical, surgical), so honestly I don't keep up with what the latest consensus on treatment of choice for cardiogenic shock is (that's for the CCU folks). I've had only one patient in my career on dobutamine (in the neuro unit). She had a SDH after falling as a result of MI. The SDH was the reason we had her. Obviously, cardiology was following her as well as neurosurgery, but maybe she would have been on an IABP if she were in CCU. She did have a PA line (which is fairly uncommon in our units- except for the donor cases). With the management she had, she did end up with a good outcome. n=1, lol.

I have heard of patients receiving compressions when showing signs of inadequate pefusion (even though they are not completely unconscious). This was in the field though; I haven't seen it personally.
 
(how long does it really take anyway?...it may not be a sterile line, but a subclavian can be placed in a jiffy, if needed).

Is there a different kind of central line than a sterile central line? I hope not.
 
I've put an 18 ga angiocath in supraclavicular for emergent access in a couple patients who had no EJ (or anything else) to speak of. Didn't leave it there all day, but it was useful when we needed it.
 
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