02.03 Myocardial Infarction (MI)

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Included In This Lesson

Study Tools

Myocardial Infarction- Management (Mnemonic)
MI Pathochart (Cheat Sheet)
MI Locations (Cheat Sheet)
MONA MI Intervention (Cheat Sheet)
Anterior MI (Cheat Sheet)
Inferior MI (Cheat Sheet)
Nitroglycerin (Image)
Myocardial Infarction (Image)
Inferior STEMI (Image)
Normal Sinus Rhythm (Image)
Stemi Myocardial Infarction 12 Lead EKG (Image)
Myocardiac Infarction Heart Attack Cardiac (Image)
Myocardial Infarction Heart Attack Cardiac (Image)
63 Must Know Lab Values (Book)

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In this lesson we’ll be talking about Myocardial Infarction, which is a sudden restriction of blood supply to a portion of the heart - causing ischemia and death to the muscle tissue.

When you think about a Myocardial Infarction (or MI), I want you to think Vascular Disorder. If you remember from the anatomy module, we have coronary arteries that supply the heart muscle with blood. If one of them gets blocked with plaque or a clot, it can occlude blood flow. As you can see here, the blood cannot flow past the occlusion and therefore the muscle beyond the occlusion is dying. The problem is in the vessels, so think Blocked Vessels = Blocked Blood Flow.

So how do the patients present? The classic sign is crushing chest pain or chest pressure - they may even say they feel like an elephant is sitting on their chest or that their chest is in a vice grip. If this chest pain is relieved by nitrates, we call it angina. But if this is an MI, the nitrates will be ineffective. This pain can also radiate, usually to the left arm, back, or left shoulder. In women it can present differently. Sometimes they have epigastric pain or heartburn, or they complain of jaw pain. Patients will often be short of breath, pale, diaphoretic, or nauseous. And many times they will be very anxious or report palpitations. It’s important to note that the pain shouldn’t be sharp, worsen with breathing, or be related to eating at all. **Kevin Smith** When your patient presents with these symptoms, do a thorough pain assessment, get a set of vital signs, listen to their heart and lungs, and call the doctor with your findings. They will likely order a set of cardiac enzymes and a 12-lead EKG, as well as medications. We’ll talk about the specifics as we go along.

There are two types of MI, an ST-Elevation MI (or STEMI) and a Non ST-Elevation MI (or NSTEMI). BOTH will have the crushing chest pain and other symptoms and BOTH will have elevated cardiac enzymes, but only the STEMI presents with the ST Elevation on the 12-lead EKG. The ST Elevation that you see on the EKG will be specific to the location of the infarction. This gives us a way to know which coronary artery is involved. A STEMI means complete occlusion of the coronary artery and requires immediate intervention. This will be either thrombolytics or surgical intervention. Most of the time, these patients will be in the cath lab within 60 minutes of arrival for an angioplasty and possibly stenting. With a Non ST-Elevation MI, they do not have ST Elevation on the 12-lead. Instead you may see ST depression or T-wave inversion, or possibly no changes at all. Either way these changes are considered nonspecific. You can’t really tell where the problem is until you get ST Elevation. These patients will need pharmacologic therapy like nitrates, beta blockers, etc., and will likely go to the cath lab within 24-48 hours, depending on how stable they are.

When we’re talking about diagnostics... These are a few of the enzymes we look at to determine cardiac muscle damage. Troponin I, CK-MB, and Myoglobin. There’s also Troponin T and CK, but the main one you’ll be looking at is Troponin I. It is the most sensitive to cardiac muscle damage. It peaks in about 12 hours, so you will be drawing these enzymes every few hours for the first 12-16 hours. CK-MB is less specific than Troponin, but can still give us an idea of cardiac muscle damage, as long as there is no skeletal muscle damage present (like if they were in a car accident or fell), and it peaks in 10-24 hours. Lastly we use Myoglobin - it’s not specific to cardiac infarction at all because it’s released with any muscle damage, but because it peaks in only 2 hours, it’s useful to us to determine the severity of the damage sooner.

The second diagnostic we use is a 12-lead EKG. When we look at a 12-Lead, and see ST-Elevation, we can determine where the infarction is occurring. We don’t teach that much about 12-leads in detail in the Academy because it’s not something you need to know thoroughly as a new grad. However, we want you guys to be able to look at one and have a general idea of what’s going on. Looking at this image, you have the 12 lead or images laid out in 3 x 4. Lead I, II, and III, aVR, aVL, and aVF (I remember the name “Ralph”), then V1 through V6. I like it this way because it makes it easier to remember. So - leads II, III, and aVF down here are your inferior leads. I remember this because it looks like a boot or a foot. Then, V1 through V4 are your anterior leads. I remember this because it looks like the front of a shirt. Here’s the torso and the sleeve. aVR doesn’t give us a specific enough reading so we cross it out (I think “no one cares about Ralph”), then the leads you have leftover (I, aVL, and V5/V6) are your lateral leads - leftover...lateral. So, boot - inferior, shirt - anterior, no one cares about Ralph, and leftovers are lateral.

So when you have a STEMI, it will look something like this. You’ll notice I have ST Elevation in II, III, and aVF. Those are my inferior leads. You’ll also notice that you have what we call reciprocal changes in opposite leads. It’s seeing the damage from the opposite side. So leads I, aVL, V2, V3, and V6 are all showing T-wave inversion or ST depression. This confirms for us that this is an Inferior MI. It’s important to note this because Inferior MI’s require different interventions.

So what ARE our interventions for this patient. In the Angina lesson we talked about MONA, so I won’t go into too much detail. You can also grab the Cheatsheet to have with you in clinicals. So just remember Morphine for pain and decreased workload, Oxygen for oxygenation, Nitrates for vasodilation, and Aspirin for anti-platelet action. But here’s where it’s important to have a general knowledge of 12-leads. I said before that Inferior MI’s get treated differently. That’s because they tend to involve the right side of the heart. And if you remember from the Hemodynamic lesson, the right side is where we measure Preload. So these Inferior MI patients are HIGHLY dependent on their preload to have a good cardiac output. So if we vasodilate them, they lose their Preload, can bottom out their blood pressure, and lose cardiac output. So that’s why Morphine and Nitrates are actually contraindicated in Inferior MI. Instead, we give them lots of fluids to boost their Preload and improve their Cardiac Output.

Just to review - an MI is a vascular problem. Blocked vessels = Blocked Blood Flow. Remember the delivery truck driver analogy. If they can’t get through, the packages don’t get delivered. Second, when you have a patient with chest pain, do a thorough nursing assessment and anticipate orders for labs, meds, and a 12-lead EKG - then possibly the cath lab. Third, check your 12-lead for an Inferior MI and advocate for your patient to receive fluids instead of morphine and nitrates. Remember that a STEMI is an emergency and needs intervention immediately. And finally, always remember MONA and give fluids if it’s Inferior.

I hope this helps you better understand MI’s and how to recognize and treat them. In the next lesson we’ll talk about surgical interventions. Until then, go out and be your best self. Happy Nursing!

Mention Kevin Smith - “I felt like I just couldn’t catch my breath - I never really had pain. But turns out my LAD was 90% blocked. If I had just laid down instead of calling 911, I would have died.”
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