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Management of Angina and Myocardial Infarction

by Carlo Raj, MD
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    Let us take a look at the management of your patient who has stable angina, acute coronary syndrome. Let us go back to quickly our discussion. If it is stable, exertion, angina, pain. If it is acute coronary syndrome, then the plaque has gotten so big that the pain is going to be at rest. Myocardial infarction, acute, we've walked through in great detail in our previous lectures. What is the two immediate goals? Let us go back to the physiology that we talked about where we are addressing the demand and we are addressing the supply. What do you want to do? If you know that your heart is compromised due to whatever reason, in this case the atherosclerosis, then would that make sense to try to decrease the demand of the heart. So, therefore, what kind of receptor does the heart have in which its activity is pretty much controlled or influenced? Beta-1 receptor. When I try to control the beta receptors, why not administer some calcium channel blockers? Those are the thing that you pay attention, now be careful though because if you administer too much or if you have your patient going into massive MI, then the heart has no chance of recovering, you’re going to kill your patient so be careful when you are giving such drugs. Or what about the supply? We know that the supply has already been compromised when I try to get in there and try to remove that clot and by doing so, aren’t you addressing both goals? By decreasing myocardial oxygen demand, we have beta-blockers, slows down the heart rate. Remember the two major factors or components or constituents of your work of the heart demand depended on heart rate and the ability to pump. The heart rate when...

    About the Lecture

    The lecture Management of Angina and Myocardial Infarction by Carlo Raj, MD is from the course Ischemic Heart Disease. It contains the following chapters:

    • Management of Angina and MI
    • NSTEMI / STEMI: Treatment
    • Contraindications to Thrombolytics
    • After (N)STEMI: Treatment & Complications

    Included Quiz Questions

    1. Pain reduction leads to a reduction in adrenergic drive which lowers the oxygen demand of the heart.
    2. The only purpose of morphine is to provide pain control for the patient to improve their comfort.
    3. Morphine works as a direct vasodilator in addition to pain control.
    4. Morphine induces clot breakdown by an unknown mechanism.
    5. Pain control is needed to ensure patient compliance.
    1. Inhibition of ADP-mediated activation of glycoprotein IIb/IIIa thereby irreversibly inhibiting platelet aggregation.
    2. Inhibition of ADP-mediated activation of glycoprotein IIb/IIIa thereby reversibly inhibiting platelet aggregation.
    3. Irreversible inactivation of COX enzyme, thereby suppressing production of thromboxanes and prostaglandins.
    4. Inactivation of thrombin and factor Xa by binding to anti-thrombin III
    5. Inhibiting the synthesis of vitamin K-dependent clotting factors.
    1. Inactivation of thrombin and factor Xa by binding to anti-thrombin III
    2. Inhibiting the synthesis of vitamin K-dependent clotting factors.
    3. Irreversible inactivation of COX enzyme, thereby suppressing production of thromboxanes and prostaglandins.
    4. Inhibition of ADP-mediated activation of glycoprotein IIb/IIIa thereby irreversibly inhibiting platelet aggregation.
    5. Reversible inhibition of COX enzyme, thereby suppressing production of thromboxanes and prostaglandins.
    1. Tissue plasminogen activator
    2. Heparin
    3. Aspirin
    4. Beta blocker
    5. Warfarin
    1. History of hemorrhagic stroke 2 years ago.
    2. History of head trauma - 1 year ago.
    3. Uncontrolled coagulation defects.
    4. History of gastrointestinal bleeding 8 months ago.
    5. History of non-hemorrhagic stroke 1 year ago.
    1. Immediate pericardiocentesis.
    2. Immediate fluid resuscitation.
    3. Sublingual nitroglycerin.
    4. Bed rest with leg elevation.
    5. Intravenous administration of diuretics.
    1. Ventricular septal defect murmur due to ventricular septal rupture .
    2. Mitral valve regurgitation murmur due to papillary muscle rupture.
    3. Atrial septal defect murmur due to left ventricular systolic dysfunction.
    4. Mitral valve stenosis murmur due to progressive atherosclerosis.
    5. Aortic valve regurgitation murmur due to thickened left ventricle.

    Author of lecture Management of Angina and Myocardial Infarction

     Carlo Raj, MD

    Carlo Raj, MD


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    Significant Gaps in Management
    By Hamed S. on 18. February 2017 for Management of Angina and Myocardial Infarction

    The lecture on management was extremely superficial and not suitable for board exams. No mention of: Newer agents such as ticagrelor/prasugrel When you would choose PCI vs thrombolysis risk stratification of NSTEMI patients with the TIMI score and subsequent angio When you would use CABG first line This talk I feel is more step 1 then step 2. Step 2 needs to focus more on decision making rather than lengthy talk on the basic pathophys I had to go back to references to Toronoto Notes to fill this gap