Audio Article: Top High-Yield Info for Myocardial Infarction on USMLE Step 2CK with Dr. Tanner Schrank

Welcome to a unique episode of AMBOSS: Beyond the Textbook! Today, Dr. Tanner Schrank covers the most important knowledge you need to study to be prepared for myocardial infarctions, whether on the USMLE Step 2CK or in the clinic. Buckle up for a high-yield journey to the heart of medicine! And let us know if this episode style gets your blood pumping, so we can prepare more for you. 

Myocardial Infarction Article: https://next.amboss.com/us/article/wS0hbf
Myocardial Infarction Qbank Session: https://next.amboss.com/us/shared/questions/bTC20H6rP2/1 

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Transcript

Tanner 0:22

Hello, and welcome to this episode of the ambitious podcast beyond the textbook. I'm Dr. Tanner shrank. And I'll be your host today. In this unique episode, we're going to go through the high yield concepts. That are covered in the myocardial infarction article within the Ann boss library. So if you like this style of episode, where we have an audio version of an ambush article, Let us know by leaving a comment or getting in touch with us. If you go to ambass.com and make your five day free trial or log into your account, you can follow along. We'll be going through the myocardial infarction article. You could find this by searching for EMI in the search. Or it's also visible. By browsing through the library. So if you turn on high yield mode at the top, Then you'll find that the. Sections that are most high yield for us. Are the summary definition, epidemiology, etiology, pathophysiology clinical features diagnostics. Pathology. Differential diagnoses. Uh, treatment and complications. So today I set my study objective as us MLE step two CK. So my high yield and key exam info will be specific to that exam. If your study objective is a thing else, then you'll have different key exam info. For step one. Emphasis is more on understanding the underlying mechanisms, pharmacology and basic clinical manifestations. For step two CK. Expect to focus on clinical diagnosis management and prevention strategies, As well as the treatment of associated complications. No. And I turned on high yield mode and key exam info. I see the most tested information highlighted in yellow. And information I keep getting wrong in the question bank underlined in red. So this way I can focus on what's important and my weak areas. Let's focus on the highlighted yellow Starting with the definition, type one. M I is most common. It's caused by atherosclerotic plaque disruption. Or acute coronary thrombosis. Which subsequently causes sudden death of myocardial cells. Now in the U S. M I occurs more often in males. And the most common etiology is coronary artery disease In coronary artery vasospasm. If we look at the underlying pathophysiology, coronary artery occlusion Can be broken down into partial occlusion or complete occlusion. Partial usually affects the inner layer of the myocardium. And typically manifest as unstable angina. Or an N STEMI. Complete coronary artery occlusion. Usually affects the full thickness of the myocardium. And typically manifests as STEMI or St. Segment elevation, myocardial infarction. Now. For type one, am I. The atherosclerotic plaque. That's disrupted. Can be. Uh, stable plaque manifesting as stable angina. Or an unstable plaque that's lipid, rich and covered by a thin fibrous cap. Inflammatory cells in the plaque. For example, macrophages. Secrete matrix, metalloproteinases, which break down the extracellular matrix. Weakening the fibers cap. Leading to my under stress, which ruptures the cap. Exposing. The highly thrombogenic lipid core. And leads to the formation of a thrombus. Now clinically. an M I can have multiple different presentations. But the classic presentation. It would be acute retrosternal chest pain. OCDEL squeezing pain, Commonly radiating to the left chest. R shoulder, neck, jaw. And, or epigastrium. As can be precipitated by exertion or stress. And it can co-occur with dyspnea, pallor, nausea, vomiting. Diaphoresis anxiety, dizziness, lightheadedness, and syncope. Other presentations can include tech, cardio arrhythmia. Congestive heart failure. Cardiogenic shock. Or new heart murmurs on auscultation. Atypical presentations, which are more likely in women. Elderly patients and diabetic individuals. Good show no. Or minimal chest pain. Also known as a silent EMI. They can also show autonomic symptoms such as nausea and diaphoresis. And most often with an inferior wall infarction, you'll see epic gastric pain and Brady cardio. Now classically it's been taught that STEMI manifests with more severe symptoms. Then N STEMI, but that's not always the case. Now let's get to the diagnostics. Of course you've run an ECG. A 12 lead is the initial test. Findings would include a pathological Q wave. S T segment shift, And T-wave inversions. We have a handy chart on the article. For you to localize the myocardial infarct on the ECG. You can run through that and look at the specific leads, the infarct locations and the vessels involved to figure out where the. Sales are being damaged. And in a severe transmural posture while infarction, there can even be no St. Elevation. Now when we're testing to see. If the cardiac biomarkers are elevated, we would focus on. Troponin T and I. You would see a rise, six to eight hours. Maximum rise would be in 12 to 24 hours. And they normalize in seven to 10 days. C K M B on the other hand, rises four to nine hours. Maximum is also 12 to 24 hours. but CK-MB normalizes in two to three days. Myoglobin rises after an hour. It reaches a maximum four to 12 hours. And normalizes in 24, but it's non-specific so it's no longer commonly used. The most common cardiac, specific marker that you'll encounter would be serum troponin T. And I. And additional lab study you could run would be complete blood count. Specifically looking for elevated inflammatory markers, including white blood cells and CRP. But the best test for a definitive diagnosis of acute coronary occlusion and to identify the site and degree of vessel occlusion would be coronary angiography. This can be used for concurrent interventions like PCI. And. This would be indicated if you have an acute STEMI. And important to note the most commonly occluded coronary arteries. Are the left anterior descending artery, the right coronary artery, and then the circumflex artery. Another diagnostic study you could run. It would be a transthoracic echocardiography. And this would show. Any wall motion abnormalities. This brings us to the pathology. So you can have a look at our helpful table showing the histopathological findings of EMI. Broken down by time interval. And the microscopic and macroscopic histopathological findings. You also want to check out the cellular changes section. To find out. All about reprofusion injury. After the acute coronary artery occlusion. The damaged myocytes release. Reactive oxygen species. The calcium enters the cytosol. And the myocytes hyper contract. This leads to neutrophilic infiltration, capillary obstruction, and contraction, band, necrosis of the myocardium Now for treatment, any patient with St. Elevations on ECG would require immediate evaluation for urgent revascularization. The administration of other therapies should not delay this care. All patients should be considered for emergency percutaneous, coronary intervention or PCI. Monitor with a serial 12 lead ECG, continuous cardiac monitoring and serial serum, troponin measurements. Start anti-platelet therapy in anticoagulation. If possible. Using dual anti-platelet therapy, Into coagulation can include unfractionated heparin. or molecular weight heparin. Adjunctive therapies include giving oxygen only if there's cyanosis severe dyspnea. Or. Oxygen saturation below 90%. Sublingual or intravenous nitrates can be given unless you have an inferior wall infarct. Hypotension. Or. A PDE five inhibitors, such as sildenafil has been taken within the last 24 hours. You can also give morphine. Beta blockers. And statins. And the mnemonic to remember all of this is Mona bash, morphine oxygen nitroglycerin. Antiplatelet drugs. Beta blockers, ACE inhibitors, statins and heparin. Now we get to further management. Further management includes prevention of recurrent EMI. Lifestyle modifications, lipid lowering therapy, anti platelet therapy, such as lifelong low-dose aspirin. A stent placement after PCI. And other cardioprotective drugs as indicated. Now We have a handy table again, for the overview of EMI complications. Now, this is just the most highly tested information. And the high yield info for step two CK. If we start a cubing session. We'll see some related questions that Anne boss editors have highlighted for us. Here's an example. Uh, 47 year old man comes to the physician because of severe retrosternal chest pain and shortness of breath for 45 minutes. He has dyslipidemia hypertension and type two diabetes. Current medications include hydroclorothiazide lisinopril, Metformin, and atorvastatin. He has smoked a pack of cigarettes a day for 20 years. He appears pale and diaphoretic. His temperature is 37 degrees Celsius. 98.6 degrees Fahrenheit. Pulse is one 15. Beats per minute, blood pressure is one 40 over 70. breath sounds are normal. The remainder of the exam shows no abnormalities. Now an ECG shows left ventricular hypertrophy with St. Segment elevation. In leads one AVL. N V one through V6. High dose. aspirin. Clopidigrel Metoprolol. Sublingual nitro glycerin. And unfractionated heparin are administered. As the patient awaits transport to the nearest emergency room, he collapses becomes unresponsive. His pulse and blood pressure cannot be detected. Despite resuscitative efforts. Unfortunately, the patient dies. Which of the following is the most likely cause of death in this patient. We have a papillary muscle rupture. B left ventricular failure. See. Ventricular fibrillation. D pericarditis. He free wall rupture. F septal wall rupture. N G pulmonary embolism. Our key info button says that we should focus on the. ECG findings. Our attending tip. Says the St. Segment elevations. Would lead us to think that the left anterior descending artery. Has a myocardial infarction. The patient's subsequent death within an hour of symptom onset is known as sudden cardiac death. So with this information, we should be able to figure out that. See ventricular fibrillation is the correct answer. So I can cardiac death after EMI is usually due to ventricular techie, arrhythmias. Such as Vtech or V-fib. These arrhythmias compromised, cardiac output, and ultimately lead to a systally. Patients with V-fib. And sudden cardiac death, which is the leading cause of death post M I. So this was a two out of five hammer question. Try out the other associated questions in the queue bank To test yourself and see how well you can do. That's all the high yield content we need to cover for M I. For our exam. You can expand any of the sections and turn off high yield to focus on all of the contexts. You need to know. And make sure to. Explore our clinical cases in the. And boss library to test yourself for real clinical scenarios, such as this. That's it for this audio article on myocardial infarction. Make sure to read up on the official USM, Ellie content guidelines and practice more Questions in the ambush. Q bank. Thanks so much for listening. This has been another episode of the podcast beyond the textbook. I'm Dr. Tanner shrank. Please let us know if you like this style of episode. And we'll see you next time.