Health and medicine
- Heart disease and heart attacks
- Stenosis, ischemia and heart failure
- Thromboemboli and thromboembolisms
- What is coronary artery disease?
- Risk factors for coronary artery disease
- Heart attack (myocardial infarction) pathophysiology
- Heart attack (myocardial infarct) diagnosis
- Heart attack (myocardial infarct) medications
- Heart attack (myocardial infarction) interventions and treatment
- Healing after a heart attack (myocardial infarction)
- Complications after a heart attack (myocardial infarction)
Heart attack (myocardial infarct) medications
Created by Vishal Punwani.
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- Would it make sense to take statins just as a preventive measure to slow down the buildup of plaques? I mean, even if you are not at risk currently (e.g. young).(3 votes)
- All medications carry a certain amount of risk. Statins inhibit the formation of mevalonic acid, which is a product made during cholesterol synthesis. While mevalonic acid is used to create cholesterol, it is also the precursor to many different products that our body needs to function, especially in the muscles. The pathways get a bit complicated from here.
One of the major side effects of statin use is muscle pain and a condition called rhabdomyolysis, or the breakdown of muscle. The reason there are so many different statins (lipitor, crestor, etc.) is because each one has the potential to cause these side effects. I could take lipitor, and have rhabdomyolysis, but take crestor and not have it. Both of these drugs work EXACTLY the same, but they have different effects on different people.
Because of these effects, and the potential consequences of having deficient levels of mevalonic acid, use of statins in younger (especially growing) individuals is usually contraindicated. This also does not inhibit the ingestion of cholesterol. Making positive lifestyle changes is usually recommended to prevent plaque build up. Eat right and stay active.
DISCLAIMER: This website is not for medical advice. I have no knowledge of your medical history, not your family's medical history. I am making no claims as to what you should do in terms of medical treatment. If you are concerned about your cholesterol levels, future issues involving cholesterol, or any health issue, please consult your family physician.(13 votes)
- I've been taught about MONA (Morphine, Oxygen, Nitrate, Aspirin) in my classes, but I've also heard conflicting ideas about prioritizing them. What order would you put these interventions in when caring for an MI patient?(3 votes)
- So the reason why we all call it MONA is because it's an easy mnemonic to remember (instead of something silly like OANM). In theory, I'd give O2, then nitro/ASA, and then morphine.
From clinical experience....it depends. Generally speaking, you always want to keep your "ABCs" (airway, breathing, circulation) at the top in terms of priority. Aspirin and Nitro may or may not go down at the same time - it also depends on whether this is pre-hospital or in-hospital. Remember that nitro has a blood pressure cut-off (SBP >90mmHg is the usual cut-off, but that's somewhat imperfect for reasons that don't pertain to your question), so if the patient doesn't meet that criteria, you might not give nitro. However, if you can't give the patient anything PO (if they're altered), you can still give nitro (paste) but no ASA. Morphine is called for in some cases but if they're anxious and the nitro takes care of the pain, you might skip the morphine.
So yeah, order (and which pieces are included) are essentially patient specific. Each component has scientifically proven benefit in patients with AMI, but that doesn't mean that each should be given to every patient in the exact same order every time.(4 votes)
- How often do doctors use morphine? I would guess not very often as it is addictive.(3 votes)
- Physicians try to avoid opiates like morphine when possible because it is addictive. There are situations when it is appropriate, namely when a patient is in severe pain and is often used post-operatively. It is classically part of therapy when a patient has a heart attack (there is an acronym called MONA, where the M is for morphine, which is commonly used by medical students when learning how to treat a heart attack - you can google it for more information).
Opiates are also used for chronic pain management (like chronic back and and several syndromes which have chronic pain as a complaint), and is subject to much debate among practitioners.(4 votes)
- Do people who haven't had a heart attack, take the medications listed in the video to help prevent a MI? I've heard of people taking asprin daily, but that's about it.(2 votes)
- Aspirin is only indicated in high risk groups and prevention of secondary acute cardiac events. There is no benefit in taking aspirin daily if you are not at risk initially.(2 votes)
- What about NSTEMI's or unstable angina?(2 votes)
- NSTEMI is treated depending on the patient's risk for worse outcomes (using a risk grade tool like TIMI or GRACE). The lower the risk score, the better the predicted outcomes, and so we'll be more conservative in the treatment (called "ischemia-guided therapy") so as to avoid doing more harm than good to these patients with our invasive strategies (like cardiac catheterization or coronary artery bypass graft). In patients with higher risk scores, we'll move to more invasive strategies.
Either way, patients with NSTEMI/UA are treated with the same initial steps as a STEMI - oxygen if they need it (O2 saturations <90% or signs of hypoxia), morphine for vasodilation/pain relief/destress, nitroglycerine for coronary artery dilation and ischemic pain relief, and aspirin to begin prevention of clot formation/compounding.
Beyond that, we use medications that prevent formation of new clots or compounding of current ones (like heparins, glycoprotein IIb/IIIa inhibitors, P2Y12 inhibitors, and aspirin). We don't give the clot-busters in NSTEMI because the block, wherever it is, is not completely blocking the blood flow and so the risks involved with thrombolytic therapy outweigh the potential benefit. Again, as mentioned above, we might still decide to perform an intervention (like a balloon cath with or without a stent, or maybe a coronary artery bypass graft) but it would be based on the patients mortality/morbidity risk.(1 vote)
- How are Clot-Busters actually working and why are they only effective on "STEMI-clots"? What's the difference between "STEMI-clots" and "NSTEMI-clots"/unstable-angina-clots?(2 votes)
- In a nutshell, "clot-busters" work by breaking down the fibrin network of a clot (sort of like scissors cutting through a fishing net).
So the difference between a STEMI and an NSTEMI by definition is that in an NSTEMI, there is no ST-segment elevation. Remember that ST-segment elevation correlates with heart muscle injury meaning that blood flow (and therefore oxygen delivery) has been cut off long enough for irreversible damage to begin. This is why we need to break open the clot (either with "clot-buster" drugs or surgical placement of a stent, if a cath lab is available). In an NSTEMI, the blockage is big enough to cause damage (there will be a rise in cardiac enzymes indicating that there is damage occuring), but it's not severe enough to fully occlude the artery.
In the end, the major reason we don't use thrombolytics in NSTEMI is because of a question of risk v. benefit. Thrombolytics are not target-specific (they will act whenever and wherever they are present) which can result in severe consequences for the patient. For patients with both NSTEMI/STEMI, the preferred option is always going to be PCI (the stenting procedure) if it's available, but we're willing to use thrombolytics in STEMI because the benefits may outweigh the risks (although we do have a number of contraindications to work through before we're comfortable with saying that).(1 vote)
- What dose of aspirin should be administered and when?
When someone's having heart attack, is it OK to give him 300 mg right away at home (in non retard form)? Would 500 mg be too much? And latter to put him on a daily 100 mg (or 75 mg) once per day?(1 vote)
- This site is not for medical advice; ask your doctor. That being said, 325mg ASA is typically recommended for a heart attack.(3 votes)
- can doctor's not start treatment until they have gone through all three things?(1 vote)
- Do you mean the diagnostic tests? That's a pretty complicated question, and the answer isn't cut and dry. They will start oxygen, nitoglycerin, aspirin and morphine (google MONA for more info about that protocol) pretty much immediately once MI is suspected. The more heavy hitting interventions (cardiac cath, angioplasty, thrombolytics, etc. depending on what hospital they're in) won't occur until they've verified what they're dealing with.(2 votes)
- How can not having a healthy teeth can affect your heart?(1 vote)
- As a dentist should I operate on someone who has a history of myocardial infarct?(1 vote)
- [voiceover] The main idea in treating myocardial infarcts is to limit the damage that happens to your heart, and to minimize complications that might crop up. The treatment has to address the clot that caused the myocardial infarct in the first place. And it has to restore the balance between the myocardial oxygen supply and demand. So there are some treatment aspects that are common to all of the types of acute coronary syndromes. But there's some really important differences in the approach to patients who present with a STEMI, or an ST elevation myocardial infarct; compared to unstable angina and N STEMI, non-st elevation myocardial infarct. And we'll talk about those. Unstable angina and N STEMI's they're usually treated in the same way. Whereas STEMI's are treated a little bit differently because they're more serious. So what happens? Well any patient who comes to a hospital with a suspected heart attack, with a suspected myocardial infarct, will first be admitted to an intensive care setting. They would be under continuous ECG monitoring for arrhythmias, or abnormal heart rhythms. Remember the ECG would also give a really good idea of what type of heart attack they might have had. They'd be made to lie down in bed to prevent their heart from working to hard. Thus, minimizing their heart muscles oxygen demand. They might be given supplemental oxygen, if it turned out that they weren't carrying enough oxygen in their blood stream. And they might be given morphine and that's to reduce the amount of chest pain that they're feeling. And to also reduce the amount of anxiety that they might be feeling. And hopefully by doing that, by reducing their anxiety they'd reduce their heart rate and even further reduce the amount of oxygen that their heart needed. Really importantly, they'd be given aspirin too. And the aspirin would reduce the development of the clot that might be causing their symptoms, that might be causing their myocardial infarct. This aspirin is actually one of the most important interventions in reducing mortality in patients with all forms of acute coronary syndrome. Okay, so all that stuff happens right away on an immediate basis. Then we have to think about sort of getting rid of that clot that caused their heart attack. And allowing blood to flow back into that area that was deprived of blood. So getting rid of that clot and allowing blood back into that part of the heart is called reperfusion. And that's the next goal. If a patient comes in and the ECG trace has determined that they have a STEMI, an ST elevation myocardial infarct and they presented to the hospital within about two hours of the onset of their symptoms. They might be given a medication to break down their clot, in a process called thrombolysis, or thrombolysis. Thrombo refers to the blood clot and lysis refers to break down. This is actually what's being referred to when you hear of clot busters. Unfortunately, no relation to Ghostbusters. So if this mediation's given early enough, there's a really high chance of restoring blood flow to the damaged part of the heart. And that actually really reduces the tissue damage that the heart would experience. Again, just to reiterate this is only for patients with STEMI's, not unstable angina or N STEMI's. And that's because the type of clots that are being busted up with clot busters, they're only found in STEMI's and not in N STEMI's. So everything that we've talked is really part of the acute management of someone who presents with an acute coronary syndrome. So all this stuff will happen in the hospital right away. Then the patient will be put on medications at the hospital that they'll then have to continue for the rest of their life. And the reason for this is because taking these medications for the rest of their lives, this has been shown in clinical trials to reduce mortality, so that's the rate of death attributed to having had a previous heart attack. Among other positive affects, they've also been shown to reduce the chance of you having another heart attack. So again, these are medications that you'll start in hospital after the sort of acute management. And then you'll need to be on them indefinitely. So what are these drugs? Well, there's drugs that try to restore that oxygen supply and demand balance. So drugs like beta blockers, beta blockers work by making the heart beat slower, so fewer beats per minute. And it also makes the heart beat with a reduced force. So over all this reduces the heart's oxygen demand, because if the muscles not working as hard it needs less oxygen. Another group of drugs you might get are nitrates. Nitrates are vasodilators, so they open up your blood vessels. They dilate your blood vessels to improve your blood flow. You'd also be given more medications to prevent the development of more clots that could block off your coronary vessels. So you're already on aspirin, but you might also be given one called heparin or warfarin. And what these do is they prevent your clotting cascade from happening as easily. So they slow down the growth of, first of all the clot that might have caused your myocardial infarct, and second any further clots that you might develop down the track. You'd probably be given a statin. Statin's reduce your blood cholesterol level. And so they decrease progression of atherosclerotic buildup in your coronary arteries. Remember plaques are filled with cholesterol, so you'd probably be given a statin to take indefinitely. Finally, you might be given an ace inhibitor. Ace inhibitor's reduce blood pressure and actually studies have shown that ace inhibitors can reduce negative structural changes that can happen in your heart after myocardial infarct. So those are the major, sort of treatments with medications that you get after having a myocardial infarct.