Angina Pectoris vs Myocardial Infarction

This was taught in my EMT calss. (the difference that is) The pain of an AMI/MCI is porologed and does not go away with rest. Pain from an Angina subsides with rest (and of coruse nitro)
 
Melclin said:
Speaking of education, how exactly would a PE 'make its way to her heart'? You are talking about a pulmonary embolism aren't you? Explain to me how that happens.
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hmm, what causes a PE? generally a blood clot.... what are diabetics known for? having poor circulation in their extremities. Clot goes from the traumatic toe injury to the heart, causes cardiac arrest. sometimes it goes to the lung and causes a PE, other times it goes to the heart and causes an MI. Either way, it sucks for the patient.

Silent MIs happen. some people live for years without even knowing they had an MI. I will not say that atypical MIs don't occur because we both know that is not true.

I never said this patient shouldn't be treated. but every time you walk into a MD's office they don't throw you on a monitor just in case you are having a silent or a typical MI. ditto every clinic. the doctors use the appropriate tools to describe the symptoms.

so ask you self, for every toe pain that you get that turns out to be an MI, how many any just toe pain? maybe 1000:1? 10000:1? greater odds?
 
DrP... PE means Pulmonary Embolism... meaning an embolis (or blood clot) in the pulmonic circulation. It's no longer in the heart.

It's impossible to have a PE in the heart, just as it's impossible to have a stroke in the lungs.
 
The capillaries in the lungs makes a pretty good filter to make sure that blood clots starting in the venous system doesn't reach the coronary circulation. Hence any clots larger than, say, a red blood cell, from the veins will cause a PE before it even gets close to anywhere where it can cause a MI.
 
DrParasite said:
hmm, what causes a PE? generally a blood clot.... what are diabetics known for? having poor circulation in their extremities. Clot goes from the traumatic toe injury to the heart, causes cardiac arrest. sometimes it goes to the lung and causes a PE, other times it goes to the heart and causes an MI. Either way, it sucks for the patient.

Outstanding. Now hop on wiki, or pick up a middle school science text to see why that is about as likely as me getting a date with Megan Fox.

Silent MIs happen. some people live for years without even knowing they had an MI. I will not say that atypical MIs don't occur because we both know that is not true.

I never said this patient shouldn't be treated. but every time you walk into a MD's office they don't throw you on a monitor just in case you are having a silent or a typical MI. ditto every clinic. the doctors use the appropriate tools to describe the symptoms.

Yes, quite. But a doctor has the book learnin to know when it is appropriate and when its not - this is my point - an EMT (often) doesn't. It is pretty clear to an educated person that this woman was a good candidate for an atypical MI, given her medical history and the other aspects of her clinical presentation. This is why I feel that patients deserves that the HCPs who arrive in an ambulance have a greater knowledge regarding cardiovascular problems than simply, CP=nitro+aspirin+transport. The fact that you thought a clot can move to eitherthe lungs or the heart is quite frankly absurd and indicative of the fact you need to be hitting the books.

so ask you self, for every toe pain that you get that turns out to be an MI, how many any just toe pain? maybe 1000:1? 10000:1? greater odds?

Again, this isn't just toe pain, and a good medic shouldn't need an ECG to be at least considering the possibility of an MI, given the particulars of the clinical presentation. If you're looking at that scenario and thinking, 'yep, can't see that this is anything but toe pain', then you really want to be heading back to school mate.
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10 characters
 
daedalus said:
Hi Melcin,

No, the differences between angina and MI are not taught to United States EMT students. Sad, huh?
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Oh yes it is! I most definitely learned it.

But as others have mentioned, you are not to diagnose. AMI = heart attack. Easy enough.
 
Soon to be medics, better start learning to diagnose!
 
reaper said:
Soon to be medics, better start learning to diagnose!
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Yeah...I'm nervous about that. It just bothers me to know I'll start diagnosing soon.
 
I'm surprised that nobody's mentioned Troponin yet. In this part of the world it's the only univerally accepted way to tell the difference between NSTEMI and unstable angina.
 
JBP said:
This was taught in my EMT calss. (the difference that is) The pain of an AMI/MCI is porologed and does not go away with rest. Pain from an Angina subsides with rest (and of coruse nitro)
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In my experience and knowledge, pain from MI can subside and often does respond to GTN, unstable angina can persist despite rest and the effect of GTN isn't always that dramatic.
 
LondonMedic said:
I'm surprised that nobody's mentioned Troponin yet. In this part of the world it's the only univerally accepted way to tell the difference between NSTEMI and unstable angina.
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In hospital, yes. Very, very few services carry Istat machines on the trucks, so Troponin levels will not be known till in the ED.
 
LondonMedic said:
So do you not treat as MI with ACS until proven otherwise?
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What do you mean by "treat"? The biggest diagnosis-treatment connection here is usually diverting to a STEMI center and activating their cath lab based on ischemic findings in a field ECG. Short of this -- eg. for the BLS guys -- it usually just involves recognizing the common clinical signs, picking the right transport destination and priority, and perhaps aspirin and nitro.

Since there aren't a lot of actual field interventions, except for the relatively few ALS regions that field-administer thrombolytics, the biggest issue of mis- or non-diagnosis is usually failing to recognize the problem and transport with the appropriate speed to the appropriate facility. That's why you see a lot of bickering between medics who want to be recognized with the full authority to "declare" a STEMI in the field, and definitive care who doesn't think they have the training to do so appropriately.

The big deal is how fast we can blow up a balloon in your arteries. Everything else is a pretty distant second place.
 
Brandon Oto said:
What do you mean by "treat"? The biggest diagnosis-treatment connection here is usually diverting to a STEMI center and activating their cath lab based on ischemic findings in a field ECG. Short of this -- eg. for the BLS guys -- it usually just involves recognizing the common clinical signs, picking the right transport destination and priority, and perhaps aspirin and nitro.
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Sorry, I come to this problem as someone with access to lots of drugs, investigations, a cath lab and the facility to transfer for emergency PCI.

As you say - if it looks like an MI, smells like an MI and has ST elevation then transfer to a STEMI centre.

But, in the absence of ST elevation, we would call it Acute Coronary Syndrome and treat symptomatically with diamorph, oxygen and nitrates but load with aspirin, clopidogrel and start enoxaparin before using the trop T (or I) to make the actual diagnosis and determine subsequent management.

You're right, of course, that in EMS the issue is identifying the STEMI and getting it PCI and really that is the end of.
 
It all depends on which part of the US you're in with how they treat ACS'. Just as we can do cardiac things here that you in the UK cannot, you have a few tools that we do not.


But typically, if it's a cardiac episode, it goes to a cardiac center.
 
Linuss said:
But typically, if it's a cardiac episode, it goes to a cardiac center.
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Are they all emergency PCI centres? We 'save' those for STEMIs requiring PCI (my local one doesn't even have an ER).

Yours seems a reasonable policy except where confusion creeps in about the cause of the chest pain - I've treated plenty of '?MI' diagnoses that have lasted until a CTPA demonstrates a massive PE.
 
LondonMedic said:
But, in the absence of ST elevation, we would call it Acute Coronary Syndrome and treat symptomatically with diamorph, oxygen and nitrates but load with aspirin, clopidogrel and start enoxaparin before using the trop T (or I) to make the actual diagnosis and determine subsequent management.
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This is not too different from how I, as a Basic-level provider, would be running such a call in the field, with the obvious exception that I have no idea whether there's ST changes, since I don't have a squiggly box. I'm assessing as fully as possible and moving my butt towards definitive care (and if possible, with squiggly-box-guys arriving prior to that), with oxygen, ASA, and nitrates as my only other tools. The patient may land at the ED with a diagnosis of, say, bad heartburn, they may end up in the cath lab, or they may be somewhere in between. All I'll really know for sure is that it could have been an MI.

The medics obviously have a much better eye on the situation.
 
LondonMedic said:
As you say - if it looks like an MI, smells like an MI and has ST elevation then transfer to a STEMI centre.
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Depends... what's the machine interpretation? <_<:wacko:
 
(central, retrosternal pain, tightness, SOB )

+1 for the use of retrosternal as opposed to substernal.
 
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