So Im a new EMT, just got my Arizona license a few days ago, and I got into a sort of discussion with my uncle, who was an EMT-i years ago (1980's). We got to talking about Angina Pectoris vs Myocardial Infaction's and I was wondering, is there a way to tell the difference?
Angina Pectoris vs Myocardial Infarction
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Melclin
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I'm not having a go at you..but is that not taught in the EMT course? Golly.
An infarction is localised cell death caused by an occlusion of the blood supply to that area. It can be caused by a number of things and happen in many places throughout the body, though some are more prone than others. Its most infamous manifestation is the Acute Myocardial Infarction.
Angina pectoris is descriptive of a set of symptoms (central, retrosternal pain, tightness, SOB ) that form a syndrome, not a particular disease process and it can be caused by a number of things, most common of which is narrowing or the arteries because of atherosclerotic plaque.
The typical AMI has it's origins early in life. Some have even suggested that plaque begins to form on the artery's walls in the womb, but it any case, it starts young. The details of its birth and formation you can read for yourself in any good pathophys textbook, but in short a plaque is a thrombogenic lipid rich interior encased in a more robust collagen cap. As plaques expand into the lumen of the artery, they take up space where blood is supposed to be flowing. This happens concurrently, all over the body, but the heart and brain are the most susceptible to reduced blood flow. The narrowing means that the heart gets less blood, which means less O2 (at the same time because of the narrowing/hardening or arteries, it has to use more O2, to work harder to get blood around the body, so its a double whammy). Often a person in the later stages of this disease may experience pain on exertion, which then dissipates when they rest. This is because while exercising, the heart needs more O2...O2 which it cannot get, so it 'screams' in pain/tightness/discomfort. But when the person rests, so can the heart and so it requires less O2. Now that the heart is less demanding, the O2 supply its getting through the narrowed arteries is just enough again, so the pain goes away. This is stable angina, or angina pectoris.
Now in a case where one of these plaques burst and the thrombogenic interior is exposed to the blood stream, it does just that...it generates thrombi, which block the supply of blood. There are a number of ways in which this happen, but in a general sense, the vast majority of infarcts are caused by complete (or near enough) blockages like this. It is relatively sudden and complete, so the areas that can't get O2, failing some fine diagnosis and expeditious treatment, will die. This is an AMI.
The world is never so simple though; UA/nSTEMIs can provide a world of confusion to you if you are simply trying to break things down to angina and infarct, but that can come later.
With any chest pain, you should be asking the pt (amongst other things) about when the pain came on, what they were doing when it did and if anything made the pain better/was it constant.
The picture of angina is typically someone who experiences chest pain and excessive SOB while they were doing exercise, but when they sat down it went away. Angina is also more responsive to treatments like nitro and O2. It also tends not last for two long. Some say 5 mins, some say 10, the AHA says a maximum of 20; but put it this way, if a person has had the same crushing chest pain for an hour now....its not stable angina/angina pectoris.
Unstable angina and MIs on the other hand can come on at rest (although they can come on anytime) and tend not to improve when they sit down and take a breather. They tend not to be as responsive to treatment, sometimes not at all. The pain remains in intensity or may get worse. Often pt will have a history of angina that has been getting worse lately; this is a big warning sign and one of the criteria for upgrading a diagnosis of stable angina/angina pectoris, to unstable angina, which, if you are only having two buckets, goes in the 'heart attack' bucket rather than the 'plain old angina' bucket.
I'm told few people ever conform to the classic picture of a heart attack, but those rules above should do you well in general.
Some reading...
Angina Pectoris
http://www.merck.com/mmpe/sec07/ch073/ch073b.html
AMI
http://www.merck.com/mmpe/sec07/ch073/ch073c.html
An infarction is localised cell death caused by an occlusion of the blood supply to that area. It can be caused by a number of things and happen in many places throughout the body, though some are more prone than others. Its most infamous manifestation is the Acute Myocardial Infarction.
Angina pectoris is descriptive of a set of symptoms (central, retrosternal pain, tightness, SOB ) that form a syndrome, not a particular disease process and it can be caused by a number of things, most common of which is narrowing or the arteries because of atherosclerotic plaque.
The typical AMI has it's origins early in life. Some have even suggested that plaque begins to form on the artery's walls in the womb, but it any case, it starts young. The details of its birth and formation you can read for yourself in any good pathophys textbook, but in short a plaque is a thrombogenic lipid rich interior encased in a more robust collagen cap. As plaques expand into the lumen of the artery, they take up space where blood is supposed to be flowing. This happens concurrently, all over the body, but the heart and brain are the most susceptible to reduced blood flow. The narrowing means that the heart gets less blood, which means less O2 (at the same time because of the narrowing/hardening or arteries, it has to use more O2, to work harder to get blood around the body, so its a double whammy). Often a person in the later stages of this disease may experience pain on exertion, which then dissipates when they rest. This is because while exercising, the heart needs more O2...O2 which it cannot get, so it 'screams' in pain/tightness/discomfort. But when the person rests, so can the heart and so it requires less O2. Now that the heart is less demanding, the O2 supply its getting through the narrowed arteries is just enough again, so the pain goes away. This is stable angina, or angina pectoris.
Now in a case where one of these plaques burst and the thrombogenic interior is exposed to the blood stream, it does just that...it generates thrombi, which block the supply of blood. There are a number of ways in which this happen, but in a general sense, the vast majority of infarcts are caused by complete (or near enough) blockages like this. It is relatively sudden and complete, so the areas that can't get O2, failing some fine diagnosis and expeditious treatment, will die. This is an AMI.
The world is never so simple though; UA/nSTEMIs can provide a world of confusion to you if you are simply trying to break things down to angina and infarct, but that can come later.
With any chest pain, you should be asking the pt (amongst other things) about when the pain came on, what they were doing when it did and if anything made the pain better/was it constant.
The picture of angina is typically someone who experiences chest pain and excessive SOB while they were doing exercise, but when they sat down it went away. Angina is also more responsive to treatments like nitro and O2. It also tends not last for two long. Some say 5 mins, some say 10, the AHA says a maximum of 20; but put it this way, if a person has had the same crushing chest pain for an hour now....its not stable angina/angina pectoris.
Unstable angina and MIs on the other hand can come on at rest (although they can come on anytime) and tend not to improve when they sit down and take a breather. They tend not to be as responsive to treatment, sometimes not at all. The pain remains in intensity or may get worse. Often pt will have a history of angina that has been getting worse lately; this is a big warning sign and one of the criteria for upgrading a diagnosis of stable angina/angina pectoris, to unstable angina, which, if you are only having two buckets, goes in the 'heart attack' bucket rather than the 'plain old angina' bucket.
I'm told few people ever conform to the classic picture of a heart attack, but those rules above should do you well in general.
Some reading...
Angina Pectoris
http://www.merck.com/mmpe/sec07/ch073/ch073b.html
AMI
http://www.merck.com/mmpe/sec07/ch073/ch073c.html
daedalus
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Hi Melcin,
No, the differences between angina and MI are not taught to United States EMT students. Sad, huh?
OP, Melcin gave you a good run down. Your job as an EMT is to treat all chest pain as serious. However, recognize that this is a "continuum" of sorts that chest pain of cardiac origin can be classified as. It goes from stable angina (relieved with rest/nitro at home) all the way to MI (death of heart tissue). In between there is Unstable Angina which requires cardiologist consultation at the hospital before discharge. In addition, the nomenclature for MI now includes "NSTEMI" and "STEMI". STEMI is usually caused by a complete occlusion of a coronary artery that supplies the heart tissue, and is identified because of characteristic changes on the EKG (elevation of the "ST" segment of the tracing in leads where the MI is occurring). NSTEMI may not be immediately identified on the EKG, but may be diagnosed after blood work has come back in the ER.
If you can get your hands on a paramedic textbook, it has a more detailed breakdown of what Melcin wrote above, and if you are really interested try reading the cardiology chapter in an Internal Medicine book at Borders or Barnes and Noble (something like Harrison's Internal Medicine).
No, the differences between angina and MI are not taught to United States EMT students. Sad, huh?
OP, Melcin gave you a good run down. Your job as an EMT is to treat all chest pain as serious. However, recognize that this is a "continuum" of sorts that chest pain of cardiac origin can be classified as. It goes from stable angina (relieved with rest/nitro at home) all the way to MI (death of heart tissue). In between there is Unstable Angina which requires cardiologist consultation at the hospital before discharge. In addition, the nomenclature for MI now includes "NSTEMI" and "STEMI". STEMI is usually caused by a complete occlusion of a coronary artery that supplies the heart tissue, and is identified because of characteristic changes on the EKG (elevation of the "ST" segment of the tracing in leads where the MI is occurring). NSTEMI may not be immediately identified on the EKG, but may be diagnosed after blood work has come back in the ER.
If you can get your hands on a paramedic textbook, it has a more detailed breakdown of what Melcin wrote above, and if you are really interested try reading the cardiology chapter in an Internal Medicine book at Borders or Barnes and Noble (something like Harrison's Internal Medicine).
MIkePrekopa
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In my EMT-B class we were taught the difference, but we were also taught that we aren't to diagnose, just treat the symptoms and get them to the hospital asap. We were told that the pain of an MCI is much much worse, and has a tendency to stay for a lot longer than angina. also that typically, though not always, angina goes away, or feels a little better with rest where a MCI doesn't.
Shishkabob
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The main difference you need to know, in simple terms, is angina is pain brought on by insufficient oxygen supplied to the heart to meet it's needs, while infarction is the actual death of the cells if they go without oxygen for long enough.
Ischemic and injured cells (from "best" to moderate) can both be re-oxygenated with very little, if any, long term damage. Once a cell reaches the infarct stage, it's gone for good.
Now, something to keep in mind, just because there is ST-elevation does NOT mean there is an infarct happening, as there is a condition called Prinzmetals angina, which causes ST-elevation which can disappear as soon as nitro is administered, which is why medics love to have 12-leads done BEFORE nitro / morphine is administered as that is really the only way to diagnose Prinzmetals. If left untreated, there is a, I believe, 75% chance an MI will occur in the next 6 months.
Ischemic and injured cells (from "best" to moderate) can both be re-oxygenated with very little, if any, long term damage. Once a cell reaches the infarct stage, it's gone for good.
Now, something to keep in mind, just because there is ST-elevation does NOT mean there is an infarct happening, as there is a condition called Prinzmetals angina, which causes ST-elevation which can disappear as soon as nitro is administered, which is why medics love to have 12-leads done BEFORE nitro / morphine is administered as that is really the only way to diagnose Prinzmetals. If left untreated, there is a, I believe, 75% chance an MI will occur in the next 6 months.
JPINFV
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The problem is that, as a basic, you don't have the tools necessary to rule either way.
In my opinion, that is completely opposite way from how you should look at providing medical care. Now, yes, the training and education for EMT-Bs is limited. Yes, as such the diagnostic tools and treatment interventions are limited. However, you should always strive to develop a differential diagnosis or a field diagnosis for the patient. I say this for a few reasons.
One, there are signs and symptoms that have different treatments.
Two, if you start studying what different conditions are, you can catch more. All of a sudden patient A isn't really an emergency because, despite how critical the patient might look on the outside, X explains everything and is likely. Now there isn't a reason to go screaming down the road lights and sirens. On the opposite end, patient Y looks fine, but your history and physical assessment keys you to problem Z, which you know is a medical emergency and take appropriate steps.
Three. It's always good to be able to defend your treatment plans. In my time working, I think I pulled the "but but but protocol" card an entire one time and felt rather dirty afterwords. Treat the patient, not the protocol, however your treatment plan should match up with the protocol fairly well.
Four, when you become a paramedic or any other higher level provider, the expanded diagnostic tools and treatment interventions makes coming to a logical and educated conclusion vital to your success as a medical provider. It's best not to fall into the hole of "ho, hum, we only treat signs and symptoms and read off a protocol" now than to try and break it later.
A timely reminder to remember for those of us who can it's important to record cardiac rhythm before giving GTN, aspirin or oxygen.
The 30 seconds it will take to get an ECG means you have the basis for serial evaluation and trend analysis. So if your do have T wave changes which subsequently vanish post treatment there is still evidence that they were there.
Very handy to show the ED staff for proper triage.
The 30 seconds it will take to get an ECG means you have the basis for serial evaluation and trend analysis. So if your do have T wave changes which subsequently vanish post treatment there is still evidence that they were there.
Very handy to show the ED staff for proper triage.
wow its really been interesting getting a different perspective on things. To be honest, all 11 of my instructors all have roughly the same perspective... So there was not much room for debate there.
But really, I understand the perspective of "im not trained to diagnose, so just transport" but it also makes sense from a triage standpoint, and from just a basic care standpoint to try to make a diagnosis...
But really, I understand the perspective of "im not trained to diagnose, so just transport" but it also makes sense from a triage standpoint, and from just a basic care standpoint to try to make a diagnosis...
MIkePrekopa
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I do agree with what JPINFV said, but for me, right now, its "memorize the book so I can pass the test". I don't like the idea of just treating the symptoms and give 'em high flow diesel (in proper dosage) to definitive care, but thats what I'm to memorize for now. After I finish class, I can learn anything and everything I want, but right now I'm working on learning just what the book wants me to do. The way one of my instructors put it to me is "you go to school to learn the rules, you work in the field to see which you need to follow." Not that rules are to be broken, but does EVERY one of your patients get 15L O2 via non rebreather? We get to learn proper dosing of activated charcoal even though local protocols took it off the ambulances a few months ago.
I understand why they don't want us to diagnose in the field. With limited contact, and fewer resources than an EMT-P or hospital staff, an EMT-B is less likely to come to a correct diagnosis, and if we diagnose incorrectly, and subsequently treat incorrectly, we can do more damage than good. But at the same time learning never hurt anyone.
I suppose in my ramblings at 0500 I'm trying to say its good to be able to diagnose what your dealing with, but at the same time you need to remember local protocols. If you begin treating causes and not symptoms something will go wrong. You can learn outside your job, but in doing so, be sure your doing YOUR job properly. Don't let something you read in a EMT-P book bias you to do something beyond what your allowed.
</0500 ramblings>
Have a good night....... erm... day everyone... :blink:
I understand why they don't want us to diagnose in the field. With limited contact, and fewer resources than an EMT-P or hospital staff, an EMT-B is less likely to come to a correct diagnosis, and if we diagnose incorrectly, and subsequently treat incorrectly, we can do more damage than good. But at the same time learning never hurt anyone.
I suppose in my ramblings at 0500 I'm trying to say its good to be able to diagnose what your dealing with, but at the same time you need to remember local protocols. If you begin treating causes and not symptoms something will go wrong. You can learn outside your job, but in doing so, be sure your doing YOUR job properly. Don't let something you read in a EMT-P book bias you to do something beyond what your allowed.
</0500 ramblings>
Have a good night....... erm... day everyone... :blink:
Melclin
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PLUS ONE TO JPINFV
Sugi,
TONED OUT : 3:23PM 47 Female - Trauma; Extremity.
You're pt's foot really hurts. BLS job right? Nothing to worry about? Why does education make a difference?
She a bit pale when you get there and she's got new pit stains. Her face is dry but you notice a hankerchief in her hand. With some further questioning, she turns out to be a diabetic. Her BP is 130/90 thats within the limits of normal for the Idiot's guide to EMT-Basic book right? Still a BLS job?
This is a real case by the way. Luckily the basic here have a much better education and some good tools. Luckily they saw this for what it was and had ALS back up role L/S which was a good thing too because she arrested halfway to an appropriate PCI hospital. She lived (ALS got her back and rolled straight into the cath lab because we're cool like that B) ), but you have to wonder if she would have, if her BLS provider had simply said, "oh toe pain, I'll sit here and spinal immobilize her because protocol says it was given as trauma" and generally pis about because its just a sore leg and you don't need an education to drive people to hospital.
If you believe in good pt care, you will make the effort to go above and beyond the scope of you EMT education.
Sugi,
TONED OUT : 3:23PM 47 Female - Trauma; Extremity.
You're pt's foot really hurts. BLS job right? Nothing to worry about? Why does education make a difference?
She a bit pale when you get there and she's got new pit stains. Her face is dry but you notice a hankerchief in her hand. With some further questioning, she turns out to be a diabetic. Her BP is 130/90 thats within the limits of normal for the Idiot's guide to EMT-Basic book right? Still a BLS job?
This is a real case by the way. Luckily the basic here have a much better education and some good tools. Luckily they saw this for what it was and had ALS back up role L/S which was a good thing too because she arrested halfway to an appropriate PCI hospital. She lived (ALS got her back and rolled straight into the cath lab because we're cool like that B) ), but you have to wonder if she would have, if her BLS provider had simply said, "oh toe pain, I'll sit here and spinal immobilize her because protocol says it was given as trauma" and generally pis about because its just a sore leg and you don't need an education to drive people to hospital.
If you believe in good pt care, you will make the effort to go above and beyond the scope of you EMT education.
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Melclin
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Evidently. Or you wouldn't be here. Sorry if I sounded like I was having a go.
We're in the same position you and I, students, trying to make sense of our education without much experience. I've only had a few placements, albeit some mercifully hands on.
At my local school they just implemented a Zero to Hero coarse, which will bring you straight from nothing to Paramedic in about 2-3 years. So I got my EMT-b, but I have almost no experience in the field. Ive had my clinicals and ride alongs, but man is it a chore trying to get through a 2 year paramedic class with no experience.... So any resource I can find, i appreciate. This forums happens to seem like a great one ^_^
vquintessence
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I'll go on a limb and assume your Paramedic course is full-time (not a nights or weekend thing). If that's the case, be happy it's two full years of cirriculum. Some programs will literally piss out medics in almost 6 months... it's horrifying.
Don't worry a hell of a lot regarding "zero to hero". I can assure you the zero to hero expression largely came about from a couple groups:
1) EMT-B's who have been doing it for years and years without expanding to other arenas. Some will resent those who move up the chain of care provider "too quickly", whether its you becoming a Paramedic, RN, Phlebotomist, etc.
2) Paramedics/EMTs/RNs/MDs who hear you say "I wasn't in BLS too long so I can't be blamed for not knowing what to do". Don't EVER use that excuse, it's a weak and pathetic argument that screams of immaturity and incompetence.
Brandon O
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Lots of other reasons for ST elevation, in my understanding. In fact, injury is not even necessarily the most common cause. Some stats here -- http://ems12lead.blogspot.com/2008/10/problem-of-st-segment-elevation.html
daedalus
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I doubt that Linuss is suggesting that ST elevation automatically means injury. However, when a 12 lead spits out with some ST elevation, and the patient is clinically suggestive of ACS, my case is pretty solid. The data from studies backs that up as well.
My 12 lead EKG actually will spit out with ***Acute MI*** because of my RBBB.
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Brandon O
Puzzled by facies
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No, he was clearly indicating the opposite; we're in agreement and I was just providing some further details
In my rough and silly EMT brain it seems to me that the four main things one would look for are the ST elevation (in contiguous leads), supporting indicators like reciprocal depression, whether the ECG (or other assessments) suggest another explanation (BBB, etc), and consider their clinical presentation. If all of that lines up you're good to go; even if some of it seems wrong you may still think MI; but in the end you're going to be looking at those things anyway, since they're relevant to treatment decisions whether you believe there's ischemia or no.
But perhaps I'm wrong.
daedalus
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I have been trying to find the study on the number of false positives from field activation of the cath lab. Let me know if you guys can find them.
I think your head is in the right place Brandon.
I think your head is in the right place Brandon.
Brandon O
Puzzled by facies
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Which one -- the one mentioned at the end of the link I gave? (Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis fo acute myocardial infarction) Or some other?
I doubt that... yesterday I bumped it yet again getting out of the rig. Seems like it'd be safer somewhere less... protruding...