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Ischemic Heart Disease: Stable Angina, Unstable Angina & Myocardial Infarction

by Carlo Raj, MD
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    Let us continue our discussion of ischemic heart disease and now we'll take a look at acute coronary syndrome. What does that mean to you? It means that we are one step closer to having a myocardial infarction, but not completely. So acute coronary syndrome, we understand that our patient has pain and may require rest and before we get into all of those, just make sure that we understand some simple basic anatomy because as we get to the tail end of our lecture series I will have you take a look at EKGs. This is that you know clearly the difference between what is known as STEMI an ST elevation myocardial infarction versus a non-STEMI. Before we get to any of that, there we are going to build a pathology and our understanding so that we would be able to clearly see this. First, we have the aorta, but then we have the left coronary artery. After left coronary artery that which is moving down between the ventricle. It would be your left anterior descending as you should know from anatomy. That left anterior descending if it underwent major mass of atherosclerosis and had an area in which there was myocardial infarction. You have any ideas to what leads of your EKG that you might be paying attention to? What is important for you to understand? And we will when the time is right. But just to give you an idea, if it is anterior 2/3rds of the interventricular septum that the left anterior descending is supplying and it is also supplying the lateral aspect of the heart a little bit. Then what might you be thinking about? The interventricular septum you still thinking about things like V1 and V2 leads. Does that make sense to you? And...

    About the Lecture

    The lecture Ischemic Heart Disease: Stable Angina, Unstable Angina & Myocardial Infarction by Carlo Raj, MD is from the course Ischemic Heart Disease. It contains the following chapters:

    • Acute Coronary Syndrome
    • Stable & Unstable Angina
    • Ischemic Heart Disease
    • Coronary Steal Syndrome
    • Mycardial Infarction

    Included Quiz Questions

    1. Leads V1 and V2 - which supply the anterior 2/3 of the interventricular septum.
    2. Leads V3 and V4 - which supply the anterior 2/3 of the interventricular septum.
    3. Leads V1 and V2 - which supply the apex of the heart
    4. Leads I and II - which supply the apex of the heart
    5. Leads V3 and V4 - which supply the posterior aspect of the heart.
    1. Venous vasodilation reduces preload and arteriolar vasodilation reduces afterload .
    2. Arteriolar vasodilation reduces preload and venous vasodilation reduces afterload.
    3. Venous vasodilation ALONE reduces preload.
    4. Arteriolar vasodilation ALONE reduces afterload.
    5. Venous vasodilation ALONE reduces afterload.
    1. Chest pain at rest OR myocardial infarction.
    2. Any chest pain associated with the heart.
    3. Myocardial infarction ONLY.
    4. Chest pain on exertion, Chest pain at rest OR myocardial infarction.
    5. STEMI, Non-STEMI OR stable angina.
    1. Voltage-gated sodium channels.
    2. Ligand-gated sodium channels.
    3. Slow calcium channels.
    4. Ligand-gated potassium channels.
    5. Beta-adrenergic receptors.
    1. Myocardial infarction will have positive troponin I.
    2. Myocardial infarction will have positive troponin C.
    3. Unstable angina will subside with a longer rest period.
    4. Only unstable angina will have an ST depression on EKG.
    5. Only myocardial infarction will show ST elevation on EKG.
    1. Lateral aspect
    2. Apex
    3. Interventricular septum
    4. Posterior aspect
    5. Medial aspect
    1. Cardiac stress test showing ST changes
    2. EKG at rest
    3. Chest pain at rest
    4. Chest pain on exertion
    5. Positive cardiac enzymes
    1. Positive cardiac enzyme - troponin I AND ST depression on EKG
    2. ST depression on EKG
    3. Positive cardiac enzyme - troponin C AND ST elevation on EKG
    4. ST elevation on EKG
    5. Positive cardiac enzyme - troponin I AND ST elevation on EKG
    1. Pain worsens with leaning backwards and on inspiration and improves on leaning forward.
    2. Pain worsens with leaning forward and on inspiration and improves on leaning backwards.
    3. Pain improves on expiration and leaning forward.
    4. Pain improves with rest and nitroglycerin.
    5. Pain is improved on inspiration and with rest.
    1. Papillary muscle rupture and free wall rupture.
    2. Fibrinous pericarditis and Dresslers syndrome
    3. Fibrinous pericarditis and free wall rupture
    4. Free wall rupture and autoimmune pericarditis
    5. Papillary muscle rupture and fibrinous pericarditis
    1. Dressler's syndrome caused by autoimmune pericarditis.
    2. Fibrinous pericarditis caused by inflammatory processes.
    3. Dressler's syndrome caused by inflammatory processes.
    4. Fibrinous pericarditis caused by neutrophil infiltration.
    5. Fibrinous pericarditis caused by macrophage infiltration.
    1. Endocardium is closest to the lumen, then the myocardium which are both supplied by arterioles and the arteries supply the pericardium at the surface of the heart.
    2. Pericardium is closest to the lumen, then the myocardium in the middle, which are both supplied by arterioles and arteries supply the endocardium at the surface of the heart.
    3. Endocardium is closest to the lumen and supplied by the arteries, the arterioles supply the myocardium in the middle and the pericardium which is the surface of the heart.
    4. Myocardium is closest to the lumen and supplied by the arterioles, the arteries supply the endocardium in the middle and the pericardium which is the surface of the heart.
    5. Pericardium is closest to the lumen and supplied by arteries, the arterioles supply the myocardium in the middle and the endocardium which is the surface of the heart.
    1. A non-STEMI involves a subendocardial infarction due to occlusion of coronary arterioles .
    2. A non-STEMI involves transmural infarction and represents occlusion of the coronary arterioles.
    3. A non-STEMI involves subendocardial infarction due to occlusion of the coronary arteries.
    4. A STEMI involves a subendocardial infarction due to occlusion of the coronary arteries.
    5. A STEMI involves a transmural infarction due to occlusion of the coronary arterioles.
    1. Vasodilation in vessels near the occlusion causes further ischemia of occluded areas.
    2. Vasodilation of coronary vessels increases blood flow to coronary vasculature causing reperfusion injury.
    3. Chemically induced vasoconstriction of blood vessels induces chest pain and EKG changes.
    4. Exercise induced vasoconstriction of blood vessels causes EKG changes.
    5. Vasoconstriction of vessels near the occlusion causes blood to pool near the occlusion.
    1. II, III, aVF
    2. V1-V4
    3. V5, V6, I, aVL
    4. II, III, aVL
    5. V2, V3
    1. subendocardial
    2. apex
    3. septum
    4. pericardium
    5. base

    Author of lecture Ischemic Heart Disease: Stable Angina, Unstable Angina & Myocardial Infarction

     Carlo Raj, MD

    Carlo Raj, MD


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    Amazing Lecturer !
    By Monu A. on 02. December 2016 for Ischemic Heart Disease: Stable Angina, Unstable Angina & Myocardial Infarction

    Dr Raj, Is amazing at teaching. I have never gained as much knowledge in a short space of time and retained it. Thank you