it’s a kind of ischemia and necrosis precipitated by a sudden occlusion of a coronary artery resulting from the formation or spasm of a thrombus. we know what all these words mean, yes? we know that ischemia means a cutting off of blood supply to something, and necrosis means the subsequent death of tissue, and occlusion means a blockage, and thrombus means a piece of hardened blood that can block things and cause the occlusion, and spasm means….. i guess, a sudden movement of something that was once in an okay position but is now in a not okay position? yes, so we’re all on the same page here, basically, pretty much.
previously the risk factors for acute MI are hypertension, diabetes, dyslipidemia, tobacco use, male sex, age, and cocaine use. don’t use coke unless you want that spasm. the spasm (in the context of other risk factors leading to a thrombus being formed) is going to lead to that ischemic event!
the thing that gets occluded is a coronary artery, which is the artery that supplies blood to the muscles of the heart itself. i always thought that was kind of meta, that there are blood vessels which originate from the heart and supply the thing itself. funny….the snake eating its own tail or something….. we don’t have to philosophize about it. it’s pretty self-evident, i should think. just imagine it. and then you’re good.
anyway, the ummmm, yes, the occlusion of the cornony artery is usually due to a cholesterol polymer eruption from an ulcerated plaque which causes platelets to stick together and release vasoactive substances that induce clotting. so basically, like….. so basically….. cholesterol erupts from somewhere… you got too much cholesterol in your blood….. it erupts, somehow,,,,, it erupts from a plaque that had been formed…. so like… lemme rewind, actually… you got too much cholesterol in you, and it deposits itself inside of your blood vessels, and it makes these collections that we call plaques. but sometimes the plaques can no longer be self contained… or they just like… they split open somehow, and the cholesterol itself leaks out, and this is when you getttttt you get platelets trying to close off the plaque where it broke, you get platelets, those very things that try to step in when you have a wound on your skin for example, and they tell your body to recruit all kinds of little sticky things to getty the hole all sealed off nicely, and then you have the, ummm…. you have…. now……. in the setting of the inside of a vessel… you have all these things starting to aggregate in a place that is already close quarters, and then suddenly you got your platelets recruiting all these folks to come in, and suddenly we got way too many cooks in the kitchen of the artery, and then, boom, we have an occlusion, and then, boom, ischemia, then necrosis, and that’s the nature of a heart attack for you, folks…… pretty nasty stuff.
so what does it feel like? chest discomfort that can feel like pressure, then there’s aching and pain, a sense of heaviness, shortness of breath like you can’t breathe all the way in,,,,,,, ,, and then fatigue and other things like that. the pain can radiate to the neck, shoulders, jaw, arms, and back…. you can get pain that feels like heartburn, which makes sense, pretty logical isn’t it,, that if the muscle is necrosing you would get pain in the area that makes you think of your heart. your chest. your heart. heartburn, but literally. it’s literal heart burn. this is more common in inferior MI, as in, the lower part of your heart gettinggggg necrosed. this kind of pain is also associated with sweating, nausea/vomiting, and a sense of impending doom. that lower half of your heart, if it gets fucked up, is going to make you think you’re dying.
and now i see that the flag has untethered itself from the adjacent tree….. it’s now just lying limp at half mast, and who knows why it’s half mast in the first place. there’s a always a reason for flags to be half mast in this fuckass country. anyway.
we know this well by this point, but symptoms of acute MI may be atypiacal in women. they can also be atypical in diabetics and the elderly.
when we’re examining the potentially heart attacked patient, we can look for facial cues like grimacing, and behavioral cues like clutching the chest, sweating, s4 gallop, or evidence of vascular disease - like optic fundi, carotid/abdominal bruits (swooshing sounds in the neck or abdomen that suggest a kind offffff, you know, a kind of tuturbulent motion of the blood through the vessls), orrrrrrrrr neck vein distension, rales,,,, wheezes……. if you hear a s3 gallop this might mean that CHF is complicating the MI.
also on the differential would be unstable coronary syndrome, pulmonary embolism, aortic dissection, spontaneous pneumothorax, GERD, pneumonia, biliary colic, musculoskeletal pain syndrome, and pericarditis.
our diagnosis is supported by certain cardiac biomarkers. in other words, things that we can find in the blood that come from the heart and tell us that it’s under duress. for example, the big ones are troponin and creatinine kinase (CK). we can also look for acute changes on the ECG including ST segment elevation (which causes our favorite and most popular kind of heart attack, the STEMI) or non-ST elevation (NSTEMI), which we have to diagnose using the protein markers rather than relying fully on the ECG.
when we know someone’s having a STEMI, or we strongly suspect it, we give them aspirin, nitroglycerin, oxygen, morphine sulphate, and clopidogrel. we consider giving them beta blockers and primary percutaneous coronary intervention (PIC) (aka stent angioplasty).
when we suspect NSTEMI, we still give them the MONA treatment (morphine oxygen nitro and aspirin) but we don’t do primary PCI because NSTEMI implies that there’s not a full blockage, so getting in there with a catheter isn’t going to be as therapeutic as it would be in the case of a STEMI.
if you think somebody’s heart attacking because of cocaine use, DON’T use beta blockers!!! because that’ll cause an unopposed alpha effect which just worsens vasoconstriction.
all of that to say in terms of summary. let’s see what kinds of weeds we can get into now.
so yeah, we said that it’s precipitated by a sudden occlusion of a coronary artery as a result of thrombus formation or spasm. we also said that criteria for diagnosing MI can include abnormal biomarkers, like an elevated troponin, as well as evidence of acute ischemia of the heart tissue.
in terms of epidemiology, about one and a half million people present with an acute myocardial infarction every year. that’s a lot. it seems like a lot. way more than AAA, right? i guess it makes sense. MI is such a common thing in our collective unconscious, and i guess this is telling us that it’s common in our minds for good reason.
on the bright side, people die from heart attacks way less now that we’ve discovered aggressive thrombolytic therapy. thrombolytic means destroying the clots. the blood clots we talked about earlier.
it’s the most common cause of death in adults. you’re most likely, if you’re an adult, to die from a heart attack. i’m sorry to say it. i hate to be the bearer of bad news. but i suppose we don’t have to think of it as all bad. it’ just the way things are. the way of the world. not good and not bad.
the kind of disease that leads to MI develops 7-10 years later in women than in men. shoutout to all the beautiful queens out there. you deserve to live longer. you go through so much………. can i fuck? lol just kidding. i’m kidding. all of this talk about beautiful queens is quite tongue in cheek. shoutout to women, of course, all the same, but i hope you also …. er…… i’m not…. i’m trying to be respectful. i love women. shoutout to yall. enjoy those additional years of disease free life and slaying. keep slaying ladies. love yall.
before age 60, men have ischemic heart disease four times as much as women. after 75, though, women become the majority of those affected by ischemic heart disease, and they often present with atypical symptoms.
men and women must be managed in a similar fashion according to a european study that they did. in spite of it all, we still treat heart attacks the same no matter what you got going on in your sex cells and chromosomes and genitals and whatever other markers we’re using these days to define ‘biological sex.’
the risk factors for a heart attack are always going to start with hypertension. that’s always going to be the number one risk factor. then close behind is diabetes, and then there’s dyslipidemia (some kind of imbalance of fat in your blood), tobacco use, male sex, age, and cocaine use.
we’ve talked about the pathogenesis sufficiently, i think. pathogenesis, of course, just meaning how it happens that an MI develops. but let’s talk about it anyway. it’s an acute occlusion, yes, from an erupted cholesterol plaque, of course, then platelets stick together, right, and vasoactive substances come in and clot things up, right. we’ve been there.
the myocardium, or the heart muscle, is the place where we first see signs of ischemia. it’s the place that gets necrosed first. of all the territory supplied by an occluded coronary artery, we’ll see the damage first in the muscle (i should think, probably, that that’s because the muscle is using more of the oxygen that the blood is carrying, it’s trying to work, and it’s trying so hard, and it’ll notice the lack of blood and oxygen before any of the other kinds of tissues).
when the occlusion is not addressed right away, we see more necrosis and more scarring. scarring, if it’s significant, can then lead to mechanical and electrical abnormalities in the heart that make it harder for the heart-having person to survive.
there are different types of MI. one of them is called type 1. this one is caused by coronary artery disease, like those plaques that come from cholesterol, and it starts when you disrupt those atherosclerotic plaques. the criteria include symptoms of acute ischemia, ischemic changes on ECG, pathological Q waves on ECG, imaging showing loss of viable myocardium or new regional wall motion abnormality, and a coronary thrombus identified by angiography.
but what about type 2? this is due to a mismatch of oxygen supply and demand, not necessarily due to an atherosclerotic plaque disruption. it’s different!!! it doesn’t always have to be a plaque causing the ischemia. the criteria for type 2 MI include symptoms of acute ischemia, new ischemic changes on ECG, pathological Q waves, imaging showing loss of viable myocardium or wall motion abnormality, just like with type 1. but the other criteria are where we further define it. they include evidence of imbalance of myocardial oxygen supply and demand, like i said, not related to thrombus found on angiography.
so then how do you get a type 2? we’re all a little confused. you can have a source from the coronary artery, just like a spasm, or you could have a fixed atherosclerosis that just gets in the way of the blood pumping without a disruption of the plaque, or you could get an embolism, as in, a piece of clotted blood that comes from some other source, elsewhere in the body… or it could be due to a dissection of something. like one of your vessels gets ripped. it could also arise from hemodynamic instability including sustained tachycardia, severe bradycardia, severe hypertension, or hypotensive shock. could also result from respiratory failure or severe anemia. all these things make sense, right? like if your heart is working too hard it might not work hard enough to meet the demand. and similarly if we don’t have enough blood in us, the demand won’t be met. got it?
we also have type 3 MI. this is cardiac death with symptoms that suggest ischemia associated with ECG changes of ischemia or ventricular fibrillation. these patients die before we can obtain biomarkers.
there’s also type 4 and 5, which we have even less to say about. these types are associated with coronary artery procedures like PCI or bypass grafting.
when you’re asking someone about their MI symptoms, you should specifically ask about chest discomfort (which people can describe as, again, pressure, or aching, or pain, or heaviness, or shortness of breath, or fatigue…. pain is different for different people, people!). you also want to ask about if the pain is radiating up to the shoulders, jaw, neck, or across to the arms or back. ask them if they have heartburn, which again is concerning for inferior MI. ask if they’ve been sweating, if they’ve felt like vomiting, if they feel a sense of doom. if it’s a woman, ask more subtle and careful questions, because she will be more likely to have atypical symptoms. the website offers no additional information here like what those symptoms may be, but maybe they’ll tell us later?
if someone’s having shortness of breath in addition to fatigue, nausea, abdominal discomfort, or passing out, you should consider acute coronary syndrome, which i’m sure we’ll talk about later.
while you’re taking such a great and thorough history, you should ask them if the pain is burning and if it gets worse with meals or while lying down. if the answer is yes, they probably just have GERD. ask them if the pain is relieved when sitting forward and worse with deep breathing. if it is, then they probably have pericarditis. ask if their pain radiates in between their shoulder blades and feels like ripping. if so, that’s aortic dissection.
once you’ve taken the history, then you look at and touch the patient. you’re looking very specifically again for those facial and behavioral cues to let you know they’re in real pain, as well as sweating, S4 gallop when you use that stethoscope, evidence of vascular disease like optic fundi or carotid/abdominal bruits like i said before. you also want to check their peripheral pulses and see if their neck veins are distended or they have other evidence of CHF. congestive heart failure. we’ll talk about it i’m sure.
the reason you’re checking pulses is because you might find rhythm disturbances, which might signal life threateningness early in the course of a MI. okay, so now we’ve talked to and looked at and touched the patient. we wanna make that diagnosis. how we do it is ordering labs. look for those biomarkers. troponin is the big one. myocardial injury has occurred if you have troponin levels above the 99th percentile. troponin will increase an hour after symptom onset and remain elevated for days. CK is less sensitive and specific for diagnosis. you can also look at coagulation studies, electrolytes, BUN, creatinine, liver function tests, magnesium, and blood count.
if the labs aren’t enough for you, you can also get an ECG. you should get an ECG, actually, for any patient who seems like they’re going through acute coronary syndrome. a vague term, intentionally vague. half of patients with ACS will have an initial non-diagnostic ECG, which is why we do serial ECGs at 15-30 minute intervals. don’t trust that first benign ECG, brother.
STEMI, of course, is diagnosed how the name suggests. ST segment Elevation. that’s it. look at the ECG. you’ll know it when you see it.
NSTEMI is about the protein markers, like i said before. just reaffirming that. you won’t see it on ECG in that same obvious way as you do with STEMI.
while you’re looking at the ECG, you might see some ST segment deviation that is not consistent with STEMI but perhaps is indicating left ventricle hypertrophy, pericarditis, or brugada syndrome.
an echocardiogram can be helpful if you’re looking to rule out a complication of MI like papillary muscle rupture which has led to acute mitral regurgitation or ventricular septal defect.
you can get a chest xray if you want.
you can get a chest CT if you’re worried about pulmonary embolism or aortic dissection. you’d be worried about the former if there’s coughing and shortness of breath, and the latter if you have that ripping pain in your back.
in terms of treatment, the first thing we’ll wanna do is reperfusion. the problem is one of perfusion, or a lack thereof, so the solution will be to reestablish blood flow to the places where it’s been lost. so we do PCI as soon as possible. it’s the primary treatment modality for patients in STEMI. do it within 12 hours of symptom onset. if you can’t do that, you should do thrombolytic therapy. ideally you’d do it within 10 minutes of the diagnosis, assuming the patient can tolerate the treatment. and then you’d still want to transfer them to a facility that can do the PCI, cuz that really is the gold standard.
you should do antiplatelet therapy on all patients as well. this is aspirin. aspirin is an antiplatelet therapy. it’s going to prevent your platelets from bunching up and getting too many cooks in the kitchen of your blood vessels. shoutout aspirin. it inhibits thromboxane synthesis. thromboxane is one of those things that tells platelets to come together.
you could use other antiplatelet therapies like P2Y12 inhibitors or clopidogrel, but i don’t want to get into those weeds here. just conceptually speaking, we know that we want to prevent platelets from aggregating. that’s sort of hitting at the root of the issue, at least closer to the root than …. something else. some other stuff. like ……..uhhh…… yeah. that’s all for that thought i guess.
anyway, back to that scenario where, say, your patient is up in the boonies and isn’t near a hospital that does PCI. you give them thrombolytics. you give them thrombolytics just as soon as you can. use a fibrin-specific product like alteplase, and administer aspirin and clopidogrel at the same time. at the same time as all that, you also wanna give them heparin (a blood thinner) until you can get that PCI performed, or until they get discharged from the hospital. you also wanna give that nitroglycerin we talked about earlier. nitro can be dangerous if the patient is having an inferior MI (the one with the nausea and sense of doom) or if the patient has hypotension. don’t give nitro to someone with hypotension! give oxygen if the patient has hypoxemia. oxygen can be dangerous if the patient has an uncomplicated MI. morphine we’re giving to reduce pain.
after you’ve given all that stuff, you’ll also want to start the patient on a statin to prevent all this from happening again. it’s gonna lower their cholesterol levels and prevent the plaques from forming. the real root of the issue, as it were.
you can give beta blockers only if there are no contraindications. you’re doing this to bring their blood pressure down. a little bit less chaos in the system this way. slow things down.
but what if they were having an NSTEMI? you do symptom management, antiplatelet thearpy, and anticoagulation. manage the symptoms with nitroglycerin (do it through the IV, or under the tongue if you can’t get IV access) if they’re not hypotensive. nitro is only helpful for symptom management, mind you. you can also give morphine for the pain, and oxygen as described above. give a beta blocker early in treatment if there are no contraindications. give them aspirin on a regular basis. higher loading dose than maintenance dose. add P2Y12 inhibitor for a year unless there is a high risk of bleeding. for anticoagulation, you’ll do that parenterally at the time of diagnosis using fondaparinux or heparin (both blood thinners). you don’t need to give thrombolytic drugs because you’re not worried about a total occlusion of the vessel. similarly you don’t need to do PCI.
but what if someone is having an MI due to cocaine? in this case, the management is the same as STEMI or NSTEMI but with the addition of aggressive benzodiazepines for getting the heart rate and blood pressure and anxiety under control. give some valium or ativan through IV. you might need a very large dose. and in these cases, you will avoid the use of beta blockers because they might make the spasm worse.
what happens when you’ve gotten the patient under control during that initial stressful period? you do some chronic management that you initiate while they’re in the hospital or right as they’re about to go home. start them on oral beta blockers if they can tolerate them, as well as ACE inhibitors, mineralocorticoid receptor blockers, statin, aspirin, dual antiplatelet therapy. you want lifestyle changes too, like exercise, cardiac rehab, weight loss, and quitting smoking.
what happens to people after they’ve had a heart attack? it depends how bad the injury to their heart is. they lost blood flow to it, so the muscle died to an extent. we say that 'time is myocardium,' so it’s really important to intervene as soon as possible once you suspect someone’s having a heart attack. as soon as you can reperfuse it, you should. that’ll give their heart the best chance at recovery. for us to consider a patient high risk, we need to see something like ongoing pain at rest for more than 20 minutes, pulmonary edema, or angina with ST changes, new/worsening mitral regurgitation murmur, S3 or rales, or hypotension.
sound good? now you know how to fix someone’s heart attack. that’s all there is to say about it right now.
i don’t feel like learning the next thing, but i guess that’s the only thing there is to do. isn’t it? or is there some other option? it’s still kind of early in the day….. what else would there be for me to do but learn about
something else?