Morphine in UA/nSTEMI

Melclin

Melclin

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The AHA recommends that morphine be used with caution in UA/nSTEMI because of the association between its administration and increased mortality:

Meine TJ, Roe MT, Chen AY, Patel MR, Washam JB, Ohman EM, Peacock WF, Pollack CV, Jr, Gibler WB, Peterson ED. Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. Am Heart J. 2005;149:1043–1049.

Firstly, I've lost my university journal access (shattered) now that I'm a workin' man, so if anyone has the full text of this article and would like to send it to me, PM away.

Secondly, does this study affect the admin of morphine in UA/nSTEMI in your practice? Why or why not do you take notice of this idea? What about it says, "Nah useless", or "Yeah definitely something I take notice of" to you.

I assume fentanyl is the only alternative in most cases. If its opioid induced hypocortisolism is behind the troubles with morphine, doesn't fent still create the same problems? If you're using fent instead, what pushed you to do so? Do you worry about fent's interactions with amiodarone if your pt becomes rhythmically challenged? (Please no, 'My protocols say 1mcg/kg fent in chestpain after nitro x2 so I do" unless it comes with a reason why your protocols say that. That is the point of this sub forum after all).
 
I don't know if this is the same study I read, but there was one a while back that mentioned the correlation between morphine administration and mortality in ACS patients. However, they made it very clear that they couldn't prove cause and effect. Is it the morphine causing the mortality, or it that more serious ACS patients have more pain?
 
What aidey said. The study itself (it's been a while since I read it, I'll try to find a copy) I think admitted that there was no causal relationship established, merely that it is an interesting avenue for more research.

Logically it would seem that sicker patients are both more likely to die because they are sicker, and more likely to get pain relief.

So the short answer for me is "no" it hasn't changed my practice. I still feel that pain relief is an important and fundamental aspect of out of hospital care.
 
Ah, okay. The abstract didn't seem quite so equivocal.



Logically it would seem that sicker patients are both more likely to die because they are sicker, and more likely to get pain relief.
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Hasn't there been some evidence published showing no link between extremity of pain and infarct size, etc? Thats not rhetorical, I actually can't remember.

From the abstract I couldn't really tell, but it seemed maybe the pts receiving morph were those with pain refractory to nitrates (essentially comparing pts refractory to nitrates with those that weren't), but I have to admit the abstract confused me a bit. So I'd still like to read the full text if anyone digs it up.
 
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It's an observational study, from a large registry (n = 57,000 total; 17,000 receiving MS). So, it's not randomised. They used inhospital death, reinfarction, CHF and cardiogenic shock as endpoints.

They first compared patients who received morphine versus those who didn't. Both unadjusted OR and OR adjusted for baseline CV risks (e.g. prior CHF, HTN, smoking, etc.) showed significantly higher values for patients treated with morphine for all endpoints.

They recognised that morphine administration might be a marker for patients who were sicker, so they reasoned that patients receiving IV nitroglycerin were probably pretty sick as well --- so they then compared patients receiving IV NTG vs patients receiving MS. These patients had higher odds ratios as well (although a couple of 95% CIs just crossed unity).

They also found significantly increased odds ratios in patients receiving NTG + MS, versus those just receiving NTG.

There were obvious differences in the composition of the groups receiving MS, no-MS, IV NTG, and IV NTG+MS, as you might expect. These included higher use of plavix, glycoprotein inhibitors, and interventions such as PCI, CABG.

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The authors point out a number of hypotheses, roughly (1) MS use might be a marker for suboptimal care, (2) that MS might be a marker for sicker patients, (3) morphine might be bad for UA/NSTEMI patients.

They suggest (1) is unlikely as a greater percentage of patients receiving MS had cardiologist care. They argued against (2) by pointing out that there was no difference in the presence of CHF at presentation between the two groups, and that NTG+MS patients did worse than NTG-only patients. They support (3) with reference to animal studies of coronary blood flow and infarct size.

They didn't push hypocortisolism as a mechanism. (I think I will have to read more about this, as I don't know anything about it).

Personally, I think it's an interesting study. It's hard not to listen, when you see an association between any intervention and bad outcomes when there's 17,000 patients in the intervention arm. But it's an observational study, it's not randomised, and as such, it can only show association, and not causation. It's still possible that the MS patients were just sicker. I think that maybe the best conclusion to draw from it, is that an RCT of MS use in MI may be in order. I don't know if this is going to be ethically permissible.
 
Brown thinks there is a need for a more tightly controlled study but we still routinely give morphine to patients with ACS if the entonox doesn't touch it.

Brown has also lost Browns university journal access, shattering indeed mate.
 
Another idea proposed by one of our cardiologist groups is that when someone is medicated with morphine, their pain tends to be managed better, and they complain less. Providers might then be lulled into a false sense of security, by thinking these patients are less acute than they might be. Thus, the patients might wait longer for definitive treatment, and have a higher morbidity and/or mortality rate because of it.

Their response has been: cath early, and cath often. Some of our cardiologists have a very low threshold to do angiograms. One of our salty old guys is said (respectfully by us, I'd trust anyone in my family to him) "Dr. So-and-so would cath a ham sandwich." It removes the doubt about how advanced their heart disease is, and fixes the problem if there is one.
 
This is something that Bob Page and many of us have been preaching for decades. That their is an increased mortality rate with the use of morphine in higher risk cardiacs. Many of the services here (US) are now introducing Fentanyl in lieu of the morphine usage.
 
I'm not saying this is right or wrong, but we are currently being taught that the use of morphine in in nSTEMI is the better choice due too it's a better vasodilator than fentanyl. M.O.N.A Morphine, O2, Nitro, ASA. They are also teaching not to give O2 unless the PT is under 95% or complaining of SOB.
 
MrBrown said:
Brown thinks there is a need for a more tightly controlled study but we still routinely give morphine to patients with ACS if the entonox doesn't touch it.

Brown has also lost Browns university journal access, shattering indeed mate.
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I think the way to do this might be to randomise to either morphine or fentanyl for continuing pain. It would be nice to randomise to placebo versus morphine, but I doubt that would get past ethics.

I wonder if someone is already doing this.
 
Ridryder911 said:
This is something that Bob Page and many of us have been preaching for decades. That their is an increased mortality rate with the use of morphine in higher risk cardiacs. Many of the services here (US) are now introducing Fentanyl in lieu of the morphine usage.
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Why?

There are a couple of possible explanations for the association that have nothing to do with the particular analgesic used. As far as I can tell, they're on all on pretty much equal footing.

What about it pushes you to encourage a change in practice?

Is their any consideration of the fent interacting with amiodarone?
 
There's growing evidence that vasodilation means exactly bupkis in the treatment of AMI (look up the Mayo paper in NTG). When you honestly think about it, can you REALLY dilate past a plaque rupture, or will more platelets aggregate in the available space? PO ASA isn't immediate. Not to mention NTG has next to no effect on the coronary arteries anyway, it's main effect on chest pain is reduction of preload and resultant reduction of MvO2.

So it very well might come down to the fact we're giving NTG and opioids for pain relief (still a VERY admirable goal). Fentanyl (or hydromorphone) have a better side effect profile than morphine (remember the vaunted vasodilation is only a side effect) thereby making fentanyl a better choice. Morphine has it's place in medicine. However, due to the wide variety of patients EMS sees coupled with the reality of probably having few analgesics available I'd choose one of the above mentioned meds to stock before morphine.
 
Trevor said:
oops... I knew that... :)
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Hey, I realised I came off kinda *****y when I responded to you earlier -- Sorry about that. It was great that you'd tried to help by looking up the citation, even though it had already been posted.
 
systemet said:
Hey, I realised I came off kinda *****y when I responded to you earlier -- Sorry about that. It was great that you'd tried to help by looking up the citation, even though it had already been posted.
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no big deal, didnt seem that *****y...
 
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