Overview of Myocardial Infarction (MI)
Sudden restriction of blood supply to a portion of the heart causing ischemia and death to the muscle tissue
- Myocardial infarction literally translates into “heart muscle death” and is the result of a complete loss of blood flow, or perfusion to the heart.
- Oxygen supply can’t meet oxygen demand
- Is often caused by atherosclerotic plaque breaking off of the vessel wall and causing acute loss of blood flow through the coronaries.
- Chest pain
- Burning, squeezing, crushing, etc
- Radiation of pain
- Shortness of breath
- Irregular heart rate
- Altered Vital Signs:
- Hypertension vs Hypotension (shock)
- Abnormal EKG
- Low O2 Saturation
- Altered Labs:
- Lipid profile
Myocardial Infarction Therapeutic Management
- Antiplatelet and Anticoagulant Medications
- Prevent platelet aggregation and reduce viscosity of blood
- Aspirin and IV heparin
- Vasodilatory Agents
- Nitroglycerin, Morphine
- Time is Tissue: PCI (Percutaneous Coronary Intervention) should be performed within 90 minutes
- To cath lab to attempt coronary artery stenting to restore blood flow
- CABG (Coronary Artery Bypass Grafting)
- In both emergent or non-emergent situations if PCI is unsuccessful
- High-dose statin
- Vital Sign and Lab Monitoring
Patient Education for Myocardial Infarction
- Smoking Cessation
- Taking new medications as prescribed
- Follow up
Hey guys, my name is Brad and welcome to nursing.com. And in today’s video, what we’re going to be discussing are MI’s also known as myocardial infarctions. We’re going to discuss some of the patho behind myocardial infarctions, as well as the patient presentation and how we might treat the patients. So without further ado, let’s dive in.
So whenever we’re talking about MI’s or myocardial infarction, I like to break it down like this, it helps it make sense. Myo, meaning muscle. Cardio, referring to the heart itself. So we’re talking about the heart muscle. And we’re talking about an infarction, which is permanent cell death.
Now MI’s are the result of a lot of various different factors, right? We’re talking about prolonged hypertension, prolonged constriction of these vessels that feed blood into the heart, as well as the deposition of atherosclerotic plaque in the heart, right? Which eventually leads to a blocked artery. We spoke about this a lot in angina, the way in which the narrowing of these vessels results in less fluid, less blood being delivered to the tissues of the heart.
But the way in which I like to think about this, right, I like to think about this nice pool, this nice pond at the end of this river, right? This is the way I think about it. And let’s imagine we’ve got these little fat beavers, right? I like to think about that, like little fatty beavers coming in and building a dam. They’re slowly building a dam and they’re slowly depositing fat across this river. Now what’s going to happen? Imagine that this pond here is the heart, okay. This is where all of this flow is going. And this is one of our coronary vessels. These little fat beavers are depositing this atherosclerotic plaque across this river. And what’s going to happen over time? Eventually, if this river completely gets blocked off and that dam gets built, we’re going to lose flow through that coronary artery to that heart. And this is what ends up resulting in the myocardial infarction, a complete loss of blood flow to an area of that myocardium. Kind of like we see here.
So how is our patient going to present? Well, the first thing that we’re going to see is chest pain. That’s the primary reflective indicator that this patient is experiencing, or maybe experiencing a myocardial infarction. You can imagine, as that heart is hypoperfused and not getting the blood it needs, it’s going to cause chest pain. Chest pain, again, can be described in a lot of different ways, such as stabbing or burning. It can also radiate throughout different parts of the body, down the arms to the jaw, through the back into the shoulder blades.
Shortness of breath is also something that’s not uncommon with patients who experienced MI’s. Think about it. A portion of that heart muscle, like we saw in that previous slide, is damaged. It’s not getting the oxygen it needs, or the heart starts pumping harder in the attempt to compensate for that loss. And as a result, we have an increased myocardial oxygen demand. So a patient is going to end up being short of breath as a result.
So some of the other things that a patient may present with are abnormal EKGs. We specifically look at the ST wave, right? What you’re used to seeing in patients who have MI’s are ST elevation or ST depression. Make sure you freshen up on our EKG course, if you’re unsure what I’m talking about. But this change in our ST wave is directly reflective of either cardiac ischemia, lack of blood flow, or actual infarction. We could also see an irregular heart rate or rhythm.
Remember that, that cardiac, that electrical conduction system, the SA node feeding into the AV nodes, so on and so forth, actually lives, is housed, within that heart muscle itself. So, as that blood flow to the heart muscle gets impaired, so does the perfusion to that electrical system.
Tachycardia, as we just described previously, increases myocardial oxygen demand. The brain is thinking, the heart is not getting blood flow like it needs to, let’s work harder. So tachycardia ensues.
Hypertension versus hypotension. Typically, you’ll see hypertension initially in patients experiencing MI’s. Patient is in bad pain. Sympathetic nervous system is kicked in, fight or flight response. Blood pressure goes up. But should an MI progress far enough, should the damage to that heart muscle become extensive enough, that heart muscle is then going to be greatly weakened, stunned, and its ability to pump effectively is going to be greatly reduced.
As we just described, increased myocardial oxygen demand, patients are going to be short of breath. They’re going to have low O2 SATs and are usually going to require some supplemental oxygen. And also one of the, basically the gold standard, for laboratory values are troponins. We will typically trend troponins, which is a cardiac enzyme that gets released into the bloodstream anytime that the heart sustains an insult or an injury. So trending these troponins are going to be important so that we can know the extent to which a patient’s heart may or may not be damaged.
So what are we going to use? What kind of medications or treatment modalities that we’re going to use for patients with MI’s? You’re going to see, pharmacologically speaking, anti-platelets being given such as aspirin to prevent further platelet aggregation to that clot within that coronary vessel. Also anticoagulants such as IV heparin. Again, these are medications we see all the time and the CV ICU. We would give IV heparin to try and lubricate and maintain patency of that coronary vessel.
You would also see vasodilatory agents being given such as nitroglycerin, or morphine. Again, the overall idea, we have a blocked coronary artery. It’s blocked, it’s very narrow, and it’s hard for blood to pass through. If we can dilate that vessel and we can allow more flow through that vessel to the heart.
We’re also going to treat chest pain, right? We mentioned morphine. It’s not only a coronary vasodilator, but of course we know it helps treats pain.
Now the last two bullet points here are PCI, percutaneous coronary intervention, as well as a CABG, coronary artery bypass graft. These are actual surgical interventions, invasive interventions, I should say, used to treat MI’s. We see PCI all the time where I work at. Basically they go in, threading a small catheter up through the groin or through the arm, up into the coronary vessel itself. They’re able to inflate a balloon within that vessel, which basically squishes all of that fatty beaver deposit up against the vessel wall. It squishes it up against the vessel wall, and then they deploy a stint, as we can see in this image, to keep that vessel open and maintain patency of that vessel. If PCI is unsuccessful, then you could move to a more invasive surgical option such as CABG, coronary artery bypass graft, where they actually split open the sternum and go in and take vessels, usually veins from the legs, saphenous veins, and they graft them directly on to this diseased artery to restore blood flow to that damaged heart.
Now, what kind of education are we going to provide for our patients who have sustained MIs? Of course, we’re going to express the importance of diet and exercise with the overall idea of hopefully reducing any kind of further atherosclerotic plaque deposition to hopefully prevent any recurrent MIs from occurring. Smoking cessation is definitely going to be something that you’re going to educate your patients on, should it be applicable, as smoking directly is correlated to coronary artery disease and coronary vessel vasoconstriction. Should a patient undergo PCI or CABG, there’s going to be specific kinds of educations associated with those that I’m not going to dive into in depth here, but usually they’re going to end up being prescribed a variation of medications, post intervention, whether it be anti-platelets or, anticoagulants lifelong. It’s going to be important that we educate them on the importance of adhering to these and any followup appointments that may be applicable.
So to summarize some of our key points related to MIs, remember myo – muscle, cardio -heart, heart muscle, infarction, or permanent cell death, most commonly caused by atherosclerotic plaque breaking off or forming completely across that coronary vessel. Remember our little fatty beavers and the dam that they build. A lot of the common symptoms are associated with lack of blood flow to that heart. And remember, our treatments are aimed at reperfusing that heart. We want to reestablish proper blood flow to that damaged heart. So all of our interventions, both pharmacologically, as well as procedurally, are geared at restoring that blood flow. Then the patient education, which we just discussed.
Guys, I really hope that this video helped bring clarity to the concept of MI’s and I really hope that it helps you as you move forward throughout nursing school. I hope that you guys go out there and be your best selves today and as always happy nursing.