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40 Cards in this Set
- Front
- Back
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Myocardial Infarction (MI)
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- Focus of myocardial necrosis resulting from inadequate tissue perfusion
- Accompanied by tissue hypoxia and accumulation of deleterious metabolites |
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What are the benefits of early treatments in acute myocardial infarction?
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Early treatment results in reductions in mortality and infarct size and improvement in left ventricular function
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Which leads on a 12 lead ECG are the inferior leads?
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2
3 aVF |
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Why do at least half of people die from an acute MI within first hour?
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because of a fatal arrythmia
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What are the Acute Coronary Syndromes?
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1. Unstable Angina
2. Non ST-Elevation Myocardial Infarction (NSTEMI); (Non Q Wave Myocardial Infarction) 3. ST-Elevation Myocardial Infarction (STEMI); (Q Wave Myocardial Infarction) |
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Is the erosion pathophysiology of AMI more common in women or men?
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women
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What is the most common pathophysiology of AMI?
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plaque rupture leading to thrombosis
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What are the possible pathophysiologic causes of AMI that occur in the absence of atherosclerotic plaque thrombosis?
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- Vasospasm
- Emboli - Unexplained ( these account for less than 10% of AMI) |
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What is the pathophysiology of an AMI when associated with cocaine?
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COCAINE results in VASOSPASM
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Vasospasm
and Acute MI |
- intense and prolonged, with or without atherosclerosis;
- possibly in association with platelet aggregation. This is the likely mechanism for cocaine induced MI |
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Emboli
and Acute MI |
from the left atrium in association with:
- atrial fibrillation, - left sided cardiac thrombus or vegetation, or - paradoxical embolus |
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What do we target to interfere with thrombus formation in AMI?
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Target Glycoprotein (GP) IIb/IIIa receptor
because it is the final common pathway in platelet aggregation - GPIIb/IIIa enables binding to fibrinogen |
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Factors affecting plaque rupture/fissure
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1. Sudden changes in intraluminal pressure or tone
2. Bending and twisting of an artery during each heart contraction 3. Lipid content of plaque 4. Thickness of fibrous cap 5. Plaque shape 6. Mechanical injury |
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What are the direct thrombin inhibitors?
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bivalirudin
argatroban |
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Reprefusion
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restore myocardial flow
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What happens if myocardial perfusion is reduced beyond myocardial demand for an extended time interval?
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- myocardial infarction with extensive myocardial necrosis
- hypoxia and decreased removal of noxious metaboolites (potassium, calcium, amphiphilic lipids, and oxygen-centered free radicals) leads to impaired ventricular function and predisposition to lethal arrhythmias |
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What are the results of transient hypoxia and accumulation of metabolites in heart tissue?
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causes diminished diastolic relaxation, abnormal systolic contraction, abnormal wall motion, and diminished stroke volume.
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Where is tissue necrosis initially seen?
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at the endocardium... as time elapses, necrosis spreads to myocardium and epicardium
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What hapens with myocardial reperfusion?
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if it occurs in a timely interval, loss of cell viability may not occur
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Determinants of Myocardial Response to Acute MI
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1. Size of the vascular bed supplied by the obstructed vessel
2. Duration of coronary arterial occlusion 3. Metabolic/oxygen needs of myocardium at risk 4. Extent of collateral vessels 5. Alterations in blood pressure, heart rate, and cardiac rhythm |
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What is a Q wave?
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A negative deflection before QRS
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Clinical Presentation
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- acute onset crushing chest pain often radiating to left arm and neck with associated shortness of breath and diaphoresis
- Atypical chest or epigastric discomfort - May be clinically silent (like in diabetics) - May present with catastrophic arrhythmia(sudden death/ventricular fibrillation) - Congestive heart failure or cardiogenic shock |
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Risk Factors for CAD and Acute MI
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1. Hypertension
2. Cigarette Smoking 3. High LDL-Cholesterol 4. Low HDL-Cholesterol 5. Diabetes Mellitus 6. Family History of Premature Coronary Artery Disease (in men <45, in women <55) 7. Sedentary Lifestyle 8. Obesity 9. Age |
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What is the timeline of Creatine Kinase and MB isoenzyme?
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MB/total CK > 4%
initial rise within 4-6 hours peaks within 16-24 hours and returns to baseline within 3-4 days |
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What is the timeline of Cardiac specific troponin (T or I)?
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rise within 4-6 hours
peak within 24 hours remain elevated up to 7-14 days |
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ECG Findings of Acute MI
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in progression from ischemia to infarct:
1. ST depression or deep T wave inversions in a consistent anatomical distribution suggest ischemia 2. Hyperacute(Peaked) T waves – earliest signs of injury 3. ST elevation in a consistent anatomical distribution suggests ongoing myocardial injury 4. Diagnostic Q waves in a consistent anatomical distribution suggest prior myocardial infarct |
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What is the earliest sign of cardiac injury?
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hyperacute (peaked) T waves
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When does a ST-Elevation MI occur?
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ST-Elevation MI (Q Wave MI) occurs when occlusive thrombi persist resulting in myocardial necrosis
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When does a non-ST-Elevation MI occur?
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Non ST-Elevation MI (Non Q Wave MI) results from incomplete or spontaneously recanalized thrombotic occlusions after ischemia that is persistent enough to elicit necrosis
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What is the difference between NQMI and Q-wave MI?
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In both you have necrosis, but in the Q wave MI you have persistent occlusion leading to ST elevation (you do not have persistent occlusion in the NQMI)
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What is the difference between NQMI and UA?
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NQMI will be positive for cardiac markers whereas a patient with unstable angina will not have the markers
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Non-ST Elevation MI
(Non-Q Wave MI) |
- Total occlusion of culprit vessel much less likely vs. ST elevation MI
- More likely to have multivessel CAD - More likely to have prior Mis - More likely to have history of diabetes, hypertension, heart failure, and peripheral vascular disease - Less likely to be smokers or have dyslipidemia - Elderly patients more likely to have non-ST elevation MIs |
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LAD occlusions lead to what type of infarct (which leads show changes)?
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- Anterior (V1-V4)
- Septum and Anteroseptum (V1-V3) - Anterolateral (V4-V6, 1, aVL) |
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L circumflex occlusions lead to infarctions in this zone (ECG changes seen in these leads)?
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- Lateral (1, aVL)
- Posterior (V1-V3... look for ST depression for posterior injury) |
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RCA occlusions lead to infarctions in this zone (ECG changes seen in these leads)?
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Inferior (2, 3, aVF)
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Early prognosis of AMI
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is determined by presence of:
- arrhythmias, - sudden cardiac death, and - development of complications |
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Late prognosis of AMI
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is determined by left ventricular function
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Complications of Acute MI
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- Arrhythmias: heart block, bradycardia, or ventricular arrhythmias
- Congestive heart failure and pulmonary edema - Cardiogenic shock - Pericarditis: early or late(Dressler’s Syndrome) - Mechanical Complications: ventricular septal defect; papillary muscle rupture with development of severe mitral regurgitation; or rupture of the left ventricular free wall - Development of scar or ventricular aneurysm |
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Right Ventricular Infarcts
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RV ischemia occurs in up to half of all inferior infarcts(only 10-15% show classic hemodynamic abnormalities)
... this is bad because decrease right fxn= decrease preload for L heart RV infarction accompanying inferior infarct=significantly higher mortality(25-30%) =high priority candidate for reperfusion |
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Secondary AMI
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secondary to insufficient perfusion relative myocardial demand during certain pathologic conditions:
- Anemia - Hypoxia - Acidemia - Infection - High catecholamine state |
