Silent MI

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LEB343

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We had a pt the other day that had a "silent MI" ie no chest pain. Pt had a history of a past MI 20+ yrs ago and on this day pt was nauseous/vomiting and was pale and diaphoretic. Pt had ST elevation in V1-V3 and depression in III and aVF. My question is: would you give this pt nitro if he wasn't experiencing CP? I don't remember his BP but I do remember it would have supported giving him nitro. We gave pt ASA but not nitro because of no CP. What would you have done?


ETA: I am an EMT basic that worked with 2 medic on this call. The lead medic did not want to give nitro when my partner did. That's where the conflict comes in.
 
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Our protocols would have us giving this patient NTG SL q5 minutes until his ST elevation resolved (Believe me, I know the debate behind this), his BP plummeted, or we arrived at the ED/Cath Lab. We'd also apply one inch of transdermal NTG paste. If it were up to me, I'd probably trial one or two SL NTG dependent on his pressure and possible right sided involvement, then stop if that wasn't improving his symptoms, which I wouldn't really expect it to.
 
Per my protocols, no NTG. I would be limited to giving zofran, fluid, ASA. I would prefer to hang a NTG drip for a pt like that though
 
This sounds like a nice discussion. I guess in theory, nitroglycerin is suppose to decrease the preload therefore decreasing how hard the heart has to work and it's oxygen demand, which is why it reduces pain. Key thing is decreasing the workload and oxygen demand of the myocardium supposedly slowing down tissue death.

I've been told it has minimally dilates the coronary arteries; doesn't really do squat to the coronary arteries.

I think nitroglycerin overall hasn't been proven to improve the outcome of MI patients. I'm not even sure if it saves heart tissue. It can cause ST changes on the 12-lead so maybe it does save tissue?

There was a study done on morphine and MI patients. When pain was reduced by morphine, it is believed that providers treated MI less aggressively, and it increased mortality. I'm not sure if a similar study was done with nitroglycerin, or if that's maybe why it hasn't been shown to benefit them either?

Awhile ago, somebody asked something about alcohol and nitroglycerin, and through research, found out that nitroglycerin would use up aldehyde dehydrogenase, which I guess is suppose to break down free radicals. We talk about oxygen being an issue with MI patients because of free radicals and reperfusion damage. I wonder if that's the case with aldehyde dehydrogenase too? Maybe aldehyde dehydrogenase is specific like for acetaldehyde so it's really not an issue during an MI?

I'd administer it if not contraindicated to reduce preload to reduce the cardiac workload and oxygen demand of the myocardium. If the patient has chest pain and the nitroglycerin successfully reduces it, that's a +1.
 
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The most important drug in this instance would be ASA which has been shown to reduce mortality. Nitro is good for relieving pain and therefore some anxiety, but this patient wasn't in pain. I am personally unaware of any literature showing nitro reduces mortality or myocardial damage, but that doesn't mean such research doesn't exist.

Getting an IV and then some ASA and zofran would be most helpful, along with a quick ride to the hospital.
 
As always its easy to sit here and arm chair quarterback, and its hard to possibly discuss pt treatments without actually being there.

MY personal only thoughts are:
- did you do a right sided 12 lead? or 15 lead?

and if so what was it showing? and do you have a picture of the 12 lead? if so can ya post it? sounds like a possible interesting case due to his extensive cardiac HX.
 
LEB343 said:
We had a pt the other day that had a "silent MI" ie no chest pain. Pt had a history of a past MI 20+ yrs ago and on this day pt was nauseous/vomiting and was pale and diaphoretic. Pt had ST elevation in V1-V3 and depression in III and aVF. My question is: would you give this pt nitro if he wasn't experiencing CP? I don't remember his BP but I do remember it would have supported giving him nitro. We gave pt ASA but not nitro because of no CP. What would you have done?


ETA: I am an EMT basic that worked with 2 medic on this call. The lead medic did not want to give nitro when my partner did. That's where the conflict comes in.
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Question is moot. Follow your protocols.

General observation: pain is a subjective sign and it is documented and taught that not everyone experiences or complains of it before needing CPR.
 
medic38209 said:
As always its easy to sit here and arm chair quarterback, and its hard to possibly discuss pt treatments without actually being there.

MY personal only thoughts are:
- did you do a right sided 12 lead? or 15 lead?

and if so what was it showing? and do you have a picture of the 12 lead? if so can ya post it? sounds like a possible interesting case due to his extensive cardiac HX.
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Anterolateral MI's can have inferior reciprocal changes( anteroseptal in this case, but still V2 and V3 involvement). The OP stated STE in V1-V3, with reciprocal changes in III and aVF. That's a confirmed STEMI. The 15-lead or v4R are useful when someone has a clinical presentation suggesting an MI, but NSTEMI on the 12. You're hoping to catch a STEMI that the 12 missed, to get the pt rapid PCI. On second thought, with any inferior changes, I would do a v4R before giving NTG.

For the general discussion, if the pt has a clinical presentation suggesting an MI (but a denial of Cx discomfort), and a STEMI (not inferior with a positive v4R), and have an acceptable BP, I'll give NTG. How many patients have neuropathy, or referred pain only? Diabetics are at increased risks for strokes and MI's, and diabetics can develop neuropathy, so an MI is high on my list of differentials for the diabetic pt with unexplained dyspnea, N&V, fatigue, etc. Our guidelines also allow for NTG admin for a suspected MI, NSTEMI, w/o Cx discomfort.
 
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So far i'm not saying i wouldn't of given NTG just getting a general impression of what was done and maybe more of a impression on the pt.

so far with the information provided my treatment plan is as follows:

IV,O2,Monitor, and 12 lead, Vitals if they can handle the NTG SL then give it if no right sided involvement (ruled out by R sided ECG) followed by ASA, reassess vitals after treatment, HAS he improved? HAS he declined?

Treat my pt not my monitor.
 
I wouldn't call an MI that presented with nausea, vomiting, and diaphoresis "silent". I'm not trying to nitpick but this is an important point.
 
TomB said:
I wouldn't call an MI that presented with nausea, vomiting, and diaphoresis "silent". I'm not trying to nitpick but this is an important point.
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A very good point, as I understand for it to be silent myocardial ischaemia there needs to be evidence of either ST segment or T wave changes eg elevation, depression or flattening
 
Over 200,000 people are "known" to have a silent MI. Some are missed until other symptoms from the damage occur. Even ECGs are not that reliable especially after the fact. But more ECGs are being done in EDs and clinics on patients who might be considered at risk just like more BGLs are being done. Several women have been wrongly diagnosed until a thorough cardiac work up was done. So, women, diabetics and the elderly would be likely candidates for a silent MI. The ECG may or may not present as a typical MI which is why serial ECGs and labs are done.
 
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medic38209 said:
Treat my pt not my monitor.
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Or you could use the qualitative and quantitative tools given to us in conjunction with a good assessment and clinical knowledge...ie clinical correlation.

:rolleyes:

Per protocol I cannot give this pt NTG. We give NTG for chest pain of suspected or confirmed cardiac etiology.

If I treated every cool, pale, diaphoretic and hypotensive pt like they were a STEMI and ignored all the other tools given to me I'd be bringing in a lot of false positives. I'm also well aware that the patient can have ischemia and/or infarction without ECG changes.

Alright now that I'm off my soap box I do agree with the rest of your post provided protocol will allow it. If you're allowed to give it without chest pain/discomfort I see no reason not to trial it in a confirmed STEMI, provided their vitals will support it. If there's a positive change then awesome keep going. No change or a negative change stop and re-assess your treatment path.

This is a topic that will always have different answers from different people until there is definitive evidence supporting or against NTG in the presence of an AMI in regards to morbidity/mortality.
 
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TomB said:
I wouldn't call an MI that presented with nausea, vomiting, and diaphoresis "silent". I'm not trying to nitpick but this is an important point.
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I agree. Personally, I would consider it ACS/STEMI with Atypical presentation rather than a true "Silent" MI.

It is pretty common, especially in diabetics and females, that patients may never experience chest pain with ACS. My favorite is a lady who came in with a history of uncontrollable hiccups x2 days and was having a gnarly posterolateral STEMI.
 
I had a friend experience an inferior MI in postop five years ago (after a TURP) which they missed. Talk about silent. Felt crappy, driven sixty miles back to the VA facility three days later, they detected enzymes, he was treated and put on cardiac rehab, and now not only feels much better but is cancer free as well.
 
If one believes that nitro is a worthy therapy (I realize there are some opposing views on this), then why would a STEMI patient with a typical presentation receive it, but a STEMI patient with an atypical presentation not receive it?

Analgesia, of course, is not the reason we give nitro. Improved pain scores may be the metric we often use as an endpoint, but they are not the goal of the therapy. Reduced MV02 and improved myocardial blood supply are the goals, and those goals remain in a STEMI patient whether they are having classic pain or not.

I wonder if there is any research comparing the outcomes of patients receiving NTG titrated to analgesic response vs. titrated to ST normalization?
 
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TomB said:
I wouldn't call an MI that presented with nausea, vomiting, and diaphoresis "silent". I'm not trying to nitpick but this is an important point.
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I'm glad you said this.

A "silent" MI to me is more like one that presents with Q waves, fatigue and maybe CHF.
 
Silent MI versus atypical MI? I'd say that, depending on protocol of course, that a MI with confirmed ST segment changes is rarely going to produce no symptoms. And these are symptoms, albeit not chest pain per se. Would love to see a 12 lead and a right sided 12 lead.

In other words, this patient gets the full work up from me. And I'd probably be more likely to consider Phenergan than Zofran, if allowed, due to some QT issues with Zofran.

So, in short, ASA, O2 titrated to effect, NTG, narcotic analgeisa PRN, fluids PRN, and anti-emetic PRN.
 
Halothane said:
If one believes that nitro is a worthy therapy (I realize there are some opposing views on this), then why would a STEMI patient with a typical presentation receive it, but a STEMI patient with an atypical presentation not receive it?

Analgesia, of course, is not the reason we give nitro. Improved pain scores may be the metric we often use as an endpoint, but they are not the goal of the therapy. MV02 and improved myocardial blood supply are the goals, and those goals remain in a STEMI patient whether they are having classic pain or not.

I wonder if there is any research comparing the outcomes of patients receiving NTG titrated to analgesic response vs. titrated to ST normalization?
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I already have a twin brother. Did my parents not me that I was a triplet?
 
Thanks for the discussion. Like I said, I'm a basic and I only have basic EKG knowledge. I've never attended an ACLS class or a 12 lead class. The system I work in is very weird to say the least. The protocols make many medics scared to do anything but drive code 3 to the ED. The treatment done were: IV, O2, monitor, ASA, and eventually zofran. The lead medic didn't really want to even give that. Also, no R sided EKG performed. It just frustrates my partner and I because we always want to do more for the patient.

Also, thanks whomever mentioned atypical MI vs silent. That makes more sense.
 
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