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12 Cards in this Set
- Front
- Back
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Ischemic Cascade
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Decreased oxygen availability
Decreased ATP Decreased actin-myosin unbridging, diastolic stiffness Increased end-diastolic filling Decreased contractility ECG changes Pain |
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Plaque Morphology
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Endothelial Injury
Monocyte / Macrophage infiltration LDL oxidation / Fixation Endothelial / Medial hyperplasia Fibrous Cap Central Degranulation |
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Plaque Rupture
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1. Most likely to occur when subcapular material heavily lipid laden and fibrous cap is thin
2. Shear force at bifurcations and sharp vessel bends likely to tear cap 3. Most severe stenosis may not necessarily be the plaque to rupture due to calcification of the cap 4. After rupture, exposed collagen and substrate promote platelet adherence 5. Clotting cascade initiated, along with release of growth factors and chemotaxins 6. plasmin activated simultaneously to lyse thrombus intrinsically |
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Anginal Characteristics
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Substernal heaviness or squeezing
Radiation down left arm, to jaw, or neck May occur in epigastrium Can present with dyspnea instead of pain Fatigue often follows |
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Stable Angina
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Related to Physical exertion
Predictable in occurrence Never occurs at rest Stability nor correlated to severity |
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Unstable Angina
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Any change in pattern, frequency, severity or quality of angina
New onset angina Angina at rest |
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Mixed Angina
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Component of stable angina
Component of variable threshold angina, but not in progressive pattern Often has pain variably at rest and activity |
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Crescendo Angina
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Progressively severe symptoms over a short amount of time
Requires the most aggressive therapy |
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Consequences of Coronary Ischemia
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Myocardial Infarction
Ischemic Dilated Cardiomyopathy Arrythmias (Ventricular or Supraventricular) Congestive Heart Failure Ischemic Papillary Muscle Dysfunction w/ Mitral Regurgitation |
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Myocardial Infarction
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Epi:
Eti: RF: Hypercholesterolemia, Hypertriglyceridemia, Low HDL, Hypertension, Smoking, Diabetes, Obesity, Sedentary Lifestyle, Type A Personality, Genetic Factors Path: Blockage of coronary artery leading to ischemia and myocardial death and fibrosis of tissue Sx: Angina, Pallor, Diaphoresis, Tachycardia, Radiation of Pain Px: Tx: Intravenous thrombolysis, Anticoagulants, Anti-arrythmics Note: |
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MI Physical Examination
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Appearance: Pallor, Diaphoresis, Dyspnea, Hypertensive, Mild Tachycardia
Jugular Venous Pulse: If elevated (Right Ventricular Involvement), If associated with rales or hypotension (Consider Congestive Failure) Labs: Troponin T and I are sensitive and specific markers of earliest myonecrosis (1-2 hours), Creatine Kinase elevation in MB (rises w/in 4-6 hours, peaks at 12-36 hours) ECG: ST segment elevation, Q wave may develop, T wave will invert later |
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MI Classification
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ST-Elevation Myocardial Infarct (STEMI): Usually defines transmural infarct, Usually more myocardial necrosis, Acute mortality higher than other
Non ST-Elevation Myocardial Infarction: Diagnosed with ST depression and elevated enzymes, usually less total damage, Acute mortality is low but subsequent mortality is higher than STEMI, More extensive coronary damage Hemodynamic Classifications Class one: Normal BP and cardiac output w/ normal filling pressure Class two: High filling pressure with normal cardiac output Class three: Normal filling pressure w/ reduced cardiac output Class four: Low cardiac output and high filling pressure |
