Lectures

Acute Coronary Syndrome

by Carlo Raj, MD
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    00:01 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.

    00:48 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 then as we move towards the apex of the heart, then you start thinking about V3 and V4, aren’t you? I am hoping that you have a pretty good idea as to what the leads of an EKG is going to be representing on the heart. And if you don't, that is quite alright because we will be paying attention to this as move further. Acute coronary syndrome is which you are seeing here as a bracket. Before we get into acute coronary syndrome, which will be a combination of unstable angina, acute MI and I cannot have you memorize this. It is a buildup of atherosclerosis. Let us go back to the concept of supply and demand. Do you remember that? Well, supply, what then happen? The coronary arteries underwent occlusion and there was a progressive occlusion that was taking place that eventually resulted in pain in the chest even, at rest and what about before that? Well before that it was stable angina and you keep this out of the discussion of acute coronary syndrome. Take a look at stable angina, who is your patient? Coronary arterial disease, atherosclerosis head to toe. Remember we talked about this with cardiovascular disease including peripheral vascular disease, cerebrovascular accident and our topic at hand, which is coronary arterial disease. Under stable angina, the precordial chest pain is exacerbated by either stress or exercise. Now, by stress, there are a couple of ways that we can get induced ,can’t we? What does that mean? Well your patient let us say it is 67-year-old female and she tells you "Hey doc, I am having chest pain when I am walking a few blocks here, when I am walking up the stairs. When I stop, the chest pain goes away." You do an EKG at rest. What happens? Everything comes back to normal. You say bye bye. Have a nice day. No. My goodness. You want to stay in practice right and so therefore you have to then induce a stress test. Now if your patient has arthritis and is debilitating, please don’t be a masochist and put your patient on a treadmill. That sounds very nice. Be nice to your patient. So we will get into what is known as your chemical stress test because that is incredibly important. And what kind of changes which you expect to see an EKG when you induce a stress. We will talk about that coming up.

    04:20 Now once this patient is giving you such a history, what would you want to give that patient automatically? You give this patient something in which there is going to be relief from the chest pain. Correct? What does that mean to you? It means underneath the tongue anytime that there's chest pain, you place nitroglycerin correct? Sublingual. So when you place sublingual and it then dissolves and enters your circulation, what is it going to do your veins? Good. Vasodilate. When you vasodilate your veins, what is that effect? Preload or afterload please. Good. Preload.

    04:57 You are going to decrease preload and so therefore you are going to decrease demand, aren’t you? Of the heart for oxygen exactly what you are going for and then what about afterload? Well, it also causes arteriolar vasodilation. When you have arteriolar vasodilation, you are going to decrease TPR. Let us move on. So now with stable angina, what does this mean to you? What kind of changes? In the very beginning, we looked at the pathogenesis of an atherosclerotic plaque. Do you remember that? We talked about how there might be endothelial injury? We talked about how there was a thrombotic event. We also referred to your monocytes coming in and smooth muscle cells that are being recovered from the intima coming into the media and all this is then forming a fibrous cap and what happen in the middle? A necrotic core of LDL, foam cells and such. If that atherosclerotic plaque continues to build, what may then happen? 90 percent occlusion. We are moving towards to what kind of angina? Unstable angina. What does that mean to you? "Hey doc, I am having chest pain." When? Even at rest. Not good. Now this comes under what? This comes under the category of acute coronary syndrome. Is that clear? Is this is a myocardial infarction? Not at all. Is that clear? Are you going to find elevated cardiac enzymes? What's your gold standard please for cardiac enzyme? You all should know troponin I, not C. Is that clear. Troponin I. We are going to find troponin I with unstable angina, yes or no? Good. No. Is that clear? It is that crystal clear for you to differentiate between unstable angina a.k.a. crescendo. What are you crescendoing towards? Crescendoing towards leaving this planet. What does that mean? It means you are moving towards myocardial infarction. You won't want that. Is that clear? So another name for unstable angina. We will never forget that. You have a crescendo. You are moving towards the myocardial infarction. How can you tell the difference? In myocardial infarction obviously that gold standard cardiac enzyme is troponin I. In unstable angina, yes you are going to have chest pain at rest. But this is not a myocardial infarction and you can come from that, how? Without finding any cardiac enzymes. Or you are going to find changes on EKG, you could.

    07:29 And it is called the non-STEMI. We will talk about this and now, I want to take a look at acute coronary syndrome. Are we clear about definitions? Are we clear about concepts? We now understand what is going on from the beginning of the lecture series up to where we are right now. It is all about building up this information so that you integrate across the board from biochemistry or physiopath because that is what medicine is and there was a type of question. There was type of patients walking through the door all the time. So symptoms at rest. Number 1 minimal exercise perhaps. May not be relieved by nitrates because it is really beyond the point of that type of therapy. Classified based on ECG changes.

    08:11 Now it could be STEMI or non-STEMI. If it is non-STEMI, we will talk about that being perhaps an ST-depression. A STEMI is ST elevation myocardial infarction and we will get into further detail. Not to worry at this point. Next, the distinction is essential for management is reperfusion therapy or not is dependent on whether or not your patient has STEMI. Now reperfusion is another topic that we will have to go into further detail when the time is right. This is all under acute coronary syndrome. We are going to keep repeating that so that you clearly know where we are. What is your mainstay treatment? So you have a clot. A clot is rather large, 90 percent perhaps. Let's do antiplatelet therapy. Let's do anticoagulants. Let's do, maybe the drugs are not working properly and you have to get in their percutaneous and you have to get in there with what is known as angioplasty. What does angioplasty mean? That type of intervention, percutaenous type of intervention, angioplasty is ballooning, isn't it? Maybe place a stent. Maybe in that cath lab, your cardiologist is not able to get in there putting a stent, which is your only step of management at this point. Next step of management CABG, coronary artery bypass surgery.

    09:30 Let us continue. Now if it is STEMI, ST elevation myocardial infarction, what you do? .

    09:37 What does that mean to you? You have your reperfusion type of issues that we will talk about. That is something we have to discuss in greater detail.

    09:46 Next acute coronary syndrome, myocardial infarction. What are the complications that you are worried about post-MI? Number 1 complication you worry about arrhythmias, don't you? And so therefore, you want to try to give you patient antiarrhythmics. Now post-MI, let it be your boards, clinically it might be a little bit different, but remember antiarrhythmics are quite a complicated topic, isn't it? Now we will deal with a little bit and right now your first introduction post-MI arrhythmia, your best drug to give is something like your class IB drug. B for best. In general, when you say class I antiarrhythmic, then what channel are you blocking, please? Sodium channel, good.

    10:32 What kind of sodium channel? Voltage-gated or ligand-gated? How important is that? Really important from physio. It's your oltage-gated sodium channel. Is that clear? This is something that you will be talking about and have discussed in pharmacology. All I am doing is reiterating it and clearly see where to bring all this information into play. Next beta-blockers, perhaps. Post-MI, think about metoprolol. Anti-platelet therapy drugs such as statins and so forth.

    11:01 Also, what else am I worried about with my cardiac infarction and as being a complication? How about congestive heart failure? And if it is congestive heart failure, then you do everything in your power to decrease the mortality increase survival and those are type of drugs which you are looking for, aren't you? So, therefore, those include spironolactone, metoprolol. We are also looking at drugs such as ACE inhibitors.

    11:26 Now mainstay of treatment eventually is the fact that you are trying to decrease the demand for oxygen by the heart. You are trying to increase the supply of oxygen continously.

    11:35 Nitrates perhaps and eventually once it get past the hurdle and the emergency has been properly managed, then you get into lifestyle modification. Is your patient obese? Is your patient a smoker? Those things that you cannot control, but you must educate your patient with including the fact that you have familial issues. The beautiful slide, the beautiful little explanation, a table in which it gives you really a storyline between stable angina moving into myocardial infarction and we will get into all the detail as we move through here. Quickly walk through stable angina and this


    About the Lecture

    The lecture Acute Coronary Syndrome by Carlo Raj, MD is from the course Ischemic Heart Disease.


    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 a positive troponin I
    2. Myocardial infarction will have a positive troponin C
    3. Unstable angina will subside with a longer rest period
    4. Only unstable angina will have an ST depression on ECG
    5. Only myocardial infarction will show ST elevation on ECG

    Author of lecture Acute Coronary Syndrome

     Carlo Raj, MD

    Carlo Raj, MD


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