Is this a cardiac patient or not?

[HERBIE1]

Don't be lulled into a false sense of security. This could very well be an MI. There was a study in Annals of Emergency Medicine in 2002 that showed that only 53% of people presenting to the ER had chest pain. Studies have also shown that cardiac pain can be relieved by a GI cocktail (I beleive it was something like 10% of people with MIs had relief with a GI cocktail, can't find the study right now). As for using nitro to decide of something is cardiac or not, another study (Henrickson CA et al. "Chest pain relieved by nitroglycerin does not predict active coronary artery disease." Ann Intern Me;d, 2003 Dec 16: 139: 979-86) showed that nitro has a sensitivity of 35% and specificity of 59%.

Cardiac disease is the great imitator.

Had the "classic" alternative presentation the other day with a 50 year old female- general fatigue, mild nausea- no pain. Had a massive STEMI going on.

When I had my MI, my only symptom was mild heartburn. Drank some water, went away. Came back worse a few minutes later, then I realized it was not heartburn.

[Richard B the EMT]

Annie, perhaps this is one of those instances where BLS and ALS follow the same rule of thumb: When in doubt, treat for the worst, and hope for the best, as one can never be in trouble for over treating, but can be in trouble for under treating.

(Just as a reminder, I am a semiretired BLS person)

[DwayneEMTP]

...

The Pt was complaining of Abd pain...

Oh! You mean the reason for the call?

...Note: Warfarin inhibits Vitamin K dependant clotting factors. ASA/Plavix inhibit Platelet aggregation.

Working on different parts of the clotting cascade, I am unaware of any debate on witholding ASA with Coumadin use.

I didn't mean to imply that there was serious debate, just that when talking to an ER doc about it he claimed that it wasn't harmful but not really beneficial with Coumadin pts. Verified with another doc, that he felt the same, but that's as deep as my research went..

...Not too sure if you're talking to me anymore, but I will answer

I'm always talking to you when you're feeling kind enough to answer...

...I would give the Nitro based on the global picture.

This scenario reads cardiac (as you mentioned). The Nitro as given by me, is on a trial basis.

If epigastric pain relieved and SOB subsides... Cardiac

If there is no effect on epigastric pain...... GI.

I'm guessing that you don't mean this to sound nearly as clear cut as it appears. I think someone posted something once that shows that relief of pain with nitro isn't necessarily showing cardiac relief, as many of us have believed, as it will also commonly relieve the bronchospasm, and I believe in some cases even muscle spasm, that was actually causing the pain. I have no reference for this though...But I am confident that my index of suspicion is really high for bronchospasm in this gent. Be interesting to see his ETCO2 wave form.

I don't think it was harmful, but I would put no real stock in it's benefit regardless of pts reported changes. Placebo, relief of issues not acute, etc could retard your ability to determine any real changes as the things you are trying to effect are completely pt reported. Now, significant 12 lead change would likely shut me up...but not much short of that I think. I think that there is just too much going on with this guy, and too many effects possible from the Nitro for it to be used as a significant diagnostic aid.

...I have no concrete reason to stop at 2 sprays of Nitro before going to MS. In my mind, if there is no change after 2 sprays, and I am not sure of this even being Cardiac, moving to Morphine seems right.

Yeah, fair enough. I wasn't really questioning whether or not it was appropriate so much as looking to see if you had a physiologic benchmark to be guided by. Sometimes you just do it if there seems to be the likelihood of benefit with very little chance of detriment....I get that.

Great discussion from a lot of really smart folk...Thanks to you all for participating!

Dwayne

[Bieber]

I'm guessing that you don't mean this to sound nearly as clear cut as it appears. I think someone posted something once that shows that relief of pain with nitro isn't necessarily showing cardiac relief, as many of us have believed, as it will also commonly relieve the bronchospasm, and I believe in some cases even muscle spasm, that was actually causing the pain. I have no reference for this though...But I am confident that my index of suspicion is really high for bronchospasm in this gent. Be interesting to see his ETCO2 wave form.

I don't think it was harmful, but I would put no real stock in it's benefit regardless of pts reported changes. Placebo, relief of issues not acute, etc could retard your ability to determine any real changes as the things you are trying to effect are completely pt reported. Now, significant 12 lead change would likely shut me up...but not much short of that I think. I think that there is just too much going on with this guy, and too many effects possible from the Nitro for it to be used as a significant diagnostic aid.

I believe nitro also relieves esophageal spasm, if I'm not mistaken. Although that brings up a good question that I hadn't questioned nearly as much as I should have. What IS the correct dosing for nitro? If pain relief isn't indicative of effectiveness (though my protocols say nitro till relief of pain), then when and to what end should nitro be given, if at all? Wasn't there a study that said nitro doesn't improve mortality/morbidity?

[5m27medic]

was there a 15 lead done, what was his axis deviation.................

[tniuqs]

Don't be lulled into a false sense of security. This could very well be an MI. There was a study in Annals of Emergency Medicine in 2002 that showed that only 53% of people presenting to the ER had chest pain. Studies have also shown that cardiac pain can be relieved by a GI cocktail (I beleive it was something like 10% of people with MIs had relief with a GI cocktail, can't find the study right now). As for using nitro to decide of something is cardiac or not, another study (Henrickson CA et al. "Chest pain relieved by nitroglycerin does not predict active coronary artery disease." Ann Intern Me;d, 2003 Dec 16: 139: 979-86) showed that nitro has a sensitivity of 35% and specificity of 59%.

Cardiac disease is the great imitator.

Good point ... why are we not using "pink lady" in EMS ?

Why are we not using bedside troponin ? an even better query .. I have and use them !

Quoting Mobey: ..Note: Warfarin inhibits Vitamin K dependant clotting factors. ASA/Plavix inhibit Platelet aggregation.Working on different parts of the clotting cascade, I am unaware of any debate on witholding ASA with Coumadin use

There is a huge volume of studies with concomitant use of ASA and Warfarin, everything from valve replacement therapy to CVA prophylaxis in the A Fib patient ... and beyond .... rat poison.

My question (maybe I have missed something in a most excellent presentation) why is this patient on Warfarin in the first place, AFib? PE? DVT ? after that said does one have a bedside INR in there back pocket ? Nope so ASA fer sure.

[Johnboy]

It seems like this pt is having some sort of GI bleed, of which is causing him to be anemic. This would cause his shortness of breath, as well as St segment elevations, even precipitating an MI. He is on coumadin, he is not tachy probably because of his B blockers, an his urine is dark. Would not be inclined to think that the dark urine is myoglobin, (nothing in hx to point to that). His pressure is up, most likely because he is compensating, although, his pulse pressure might be narrowing. This could be because of cardiac disease, or blood loss. One would keep an eye on his pulse pressure enroute. I would placed two lines, and give high flow 02. I would probably hold the ASA on this one, but would confer with med command just to make sure. Hope this helps.

[tniuqs]

It seems like this pt is having some sort of GI bleed, of which is causing him to be anemic. This would cause his shortness of breath, as well as St segment elevations, even precipitating an MI. He is on coumadin, he is not tachy probably because of his B blockers, an his urine is dark. Would not be inclined to think that the dark urine is myoglobin, (nothing in hx to point to that). His pressure is up, most likely because he is compensating, although, his pulse pressure might be narrowing. This could be because of cardiac disease, or blood loss. One would keep an eye on his pulse pressure enroute. I would placed two lines, and give high flow 02. I would probably hold the ASA on this one, but would confer with med command just to make sure. Hope this helps.

Firstly .. a dang good first post thinking outside the [box] ... welcome.

cheers

[46Young]

First let me complement you on your thorough and diligent assessment. A lot of people never realize that the "paramedic assessment" is *much* more about diligence than it is about diagnosis.

As far as your questions:

No. ST elevation means the condition is acute. With rare exception (like in the days following a CABG), there is no such thing as "old ST elevation." Keep your STEMI mimickers in mind (LBBB, BER, LVH, pacers, etc etc etc), but real ST elevation is something to be considered as cardiac injury. Depression can be a number of things, but "cardiac depression" is caused by ischemia or is a reflective change from injury. Consider it an acute problem.

Whats the difference? What does a "cardiac" patient get that a GI patient does not? If you are worried about a AAA or some sort of GI bleed I would imagine you might be concerned about ASA (and I would too), but it seems you did the right thing by passing that decision on to on-line medical control. NTG as well. Other than that, both GI and cardiac patients get IV/Monitor/O2 and continued reassessment.

Don't forget that this patient may have both a GI problem and a cardiac problem. It is not necessarily one or the other. You can't rule out cardiac because he has problems in his belly. Take heart, though. Our job is largely the same. Prepare for something worse to happen, consult on any meds you might want to give (if any), and reassess, reassess, reassess.

+1 on the above. As far as mimickers of ST elevation, I recently asked my medical director if there was a way to diagnose STEMI with a PPM. He said there was, and that it also works for LBBB. He explained T-wave discordance. It prompted me to start this thread; it's a good read:

http://www.emtlife.com/showthread.php?t=21542&highlight=lead

Tom B. provided this link on the third page:

http://ems12lead.com/2010/12/29/excessive-discordance-as-a-marker-of-acute-stemi-in-lbbb/

[crotchitymedic1986]

your patient was in CHF. just needed alot of Lasix.