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Published byLillian Jennings Modified over 9 years ago
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Arteriosclerosis - “hardening of the arteries”. Atherosclerosis – build up of plaque (atheroma) on the lining of arteries. End results for both are the same Stenosis of the lumen of artery Ulceration of plaque Rupture of plaque with thrombus formation Obstruction of blood flow Ischemia of tissue distal to thrombus
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Left Coronary Artery. Anterior Descending (LAD) Left Circumflex (LCx) Right Coronary Artery
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Inflammatory response secondary to injury is mostly widely accepted theory for development of atherosclerosis. Endothelial injury from shearing stresses, radiation, chemicals, hyperlipidemia Inflammatory response Beginning of atheroma
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Atherosclerosis Vasospasm Thrombus or embolus Atheroma Coronary Artery:
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Slow obstruction: Fat plaque formation Thrombosis – formation of blood clot Sudden obstruction: Embolism – separated blood clot
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Non-modifiable Risk Factors Contributing To CAD Heredity Increasing age Gender During reproductive years, women have a much lower incidence of Coronary Heart Diseases (CHD) compared to men of similar age. The reason for this due to the protective effect of oestrogen.
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Modifiable Major Risk Factors 1- Elevated Serum lipids: An elevated ”total” cholesterol level is major component of atherosclerotic plaque build up which causes the development of an acute MI. 2- Hypertension: This related to the shearing stress, causing denuding injuries of the endothelial lining. Atherosclerosis, in turn, causes narrowed, thickened arterial walls and decreases the distensibility and elasticity of vessels.
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3. Cigarette smoking: includes increases of plasma cholesterol Triglycerides and fibrinogen, and platelet aggregation and decreases high –density lipoprotein (HDL). 4. Physical Inactivity: Physical active people have increased HDL levels, and exercise enhances fibrinolytic activity, thus reducing the risk of clot formation.
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5. Obesity: Obesity increases risk for CAD through increased level of LDL, which are strongly implicated in arteriosclerosis” and hypertension. 6- Diabetes mellitus: Arterial wall exposure to abnormally high levels of circulating insulin causes proliferation of smooth muscle cells inhibition of glycolysis and synthesis of cholesterol, triglyceride and phospholipids.
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7- Stress and behavior patterns: Several behavior patterns have been correlated with CAD. Type A behaviors include protectionism and a hard working, driving personality. 8- Psychological traits: Depression, anxiety, and hostility have been demonstrated to be associated with the risk of coronary artery disease and of adverse outcomes after acute coronary events.
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Definition Clinical syndrome characterized by episodes of discomfort or pressure in the upper chest Result of ischemia Atherosclerosis is most common cause Factors Known To Precipitate Typical Angina. Physical exertion Exposure to cold Eating a heavy meal Stress or emotional situation
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1. Stable angina: pain that occurs on exertion and is relieves by rest or nitrate. The discomfort is usually relieves within 2- 10 minutes by rest. 2. Unstable angina: the discomfort has become more frequent, more easily triggered, more severe or prolonged or less responsive to nitrate therapy, and lasting more than 20 minutes.
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3. Variant angina (Prinzmetal’s angina): This discomfort tends to be prolonged, severe and not readily relieved by nitroglycerin. Variant angina is caused by spasm of the coronary arteries and can be accompanied by transient elevation of the segment. 4. Nocturnal angina: It occurs only at night but not necessary when the person is in the recumbent position or during sleep.
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5- Angina decubitus: It is chest pain that occurs only while the person is lying down and is usually relieved by standing or sitting. 6- Silent ischemia: Approximately 70% of ischemic episodes in patients with CHD are silent, making silent ischemia a more common occurrence than angina. In addition, up to 30% of symptomatic myocardial infarctions are silent.
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Heaviness, squeezing, pressure, tightness in upper chest Choking or smothering sensation Indigestion or gas Radiation to neck, jaw, shoulders and arms
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Feeling of weakness or numbness in arms, wrists or hands Associated symptoms Dyspnea Diaphoresis Dizziness N/V Anxiety
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Diagnosis often made by evaluating clinical manifestations and history 12 lead ECG May show T-wave inversions and ST segment depressions in the electrocardiograpgic leads Stress test with or without nuclear scan or ECHO Cardiac catheterization
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Objectives of Medical Management of Angina *Decrease oxygen demands of myocardium or myocardial oxygen consumption * Increase oxygen supply Treatment of Angina Pharmacologic therapy Control risk factors Revascularization Invasive interventional procedures Coronary artery bypass grafting (CABG)
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Nitrates – mainstay of treatment Dilate veins – decreases preload Dilate arteries – decreases afterload as well as dilates coronary arteries Administer- spray, sublingually, PO, IV, topically Side effects – hypotension, HA, flushing, tachycardia Ex: Nitrostat SL or Tridil (nitroglycerin), DO NOT administer with Viagra
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Beta blockers Reduce myocardial oxygen consumption by decreasing heart rate, contractility and blood pressure Monitor heart failure clients for worsening failure Side effects – hypotension, bradycardia, bronchial spasm, masks hypoglycemia Ex: Lopressor or Toprol (metoprolol), Inderal (propranolol), Tenormin
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Calcium channel blockers Dilate arteries which decreases workload and O2 consumption Decrease heart rate and myocardial contractility – decreases O2 consumption Side effects - hypotension, bradycardia, constipation, edema, AV blocks Ex: Adalat or Procardia (nifedipine), Cardene (nicardipine), Cardizem (diltiazem)
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Antiplatelet medications Prevent platelet aggregation on atheroma or thrombus EX: Aspirin and ticlopidine. side effects: GI irritation, bleeding, increased bruising Anticoagulants (Heparin) * Given IV in acute situations or subcutaneous in non-acute situation * Monitor partial thromboplastin time (PTT) * Observe bleeding precautions
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Anticoagulants (warfarin) * Used long term; given PO Effects do not occur for 3-5 days Oxygen therapy Administered usually at 2 L/min per nasal cannula Increases amount of O 2 delivered to myocardium
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