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24 Cards in this Set
- Front
- Back
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name 5 steps of MI consequences
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1) impaired rate of relaxation
2) potassium leakage 3) impaired active force development 4) rigor 5) Na/K pump inhibition |
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impaired rate of relaxation in an MI causes
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increased LVEDP
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why impaired active force development?
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limp garden hose...myofilaments no longer stretched to optimum thick and thin filament overlap
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hemodynamic consequences of acute ischemia
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reduced SV and CO
increased LVEDP reduce coronary perfusion pressure |
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why MI release of cellular potassium
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activation of ATP-sensitive K+ channels as ATP: ADP ratio falls
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what does K efflux lead to in acute ischemia?
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arrhythmias (can't conduct anymore)
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what is the leading cause of death from MI before any necrosis occurs?
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arrhythmias
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how does rigor develop
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ATP falls --> crossbridges can't dissociate
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Na/K pump inhibition leads to
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no electrical excitability
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irreversible injury
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infarction = necrosis of myocytes
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in an MI, necrosis begins
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within 20-30 mins of onset of ischemia, starting at the subendocardium
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Right coronary artery thrombosis causes
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inferior MI
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what can rupture in MI?
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papillary muscle if involved (and mitral regurg)
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LAD thrombosis causes
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anterior MI
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Left circumflex thrombosis causes
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lateral MI
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clinical features of ischemia and infarction
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chest pain, dyspnea, diaphoresis, and nausea
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what do we use to measure necrosis?
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troponin 1 and creatine kinase
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ECG of MI
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ST elevation = infarction (not always)
ST depression = ischemia |
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STEMI
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ST elevation MI
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how do we treat an MI?
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increase supply and reduce demand
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how do we treat an MI?
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aspirin and heparin = prevent more clotting
TPA = dissolve clots angeoplasty/stent = mechanically remove coronary bypass = bypass the clot |
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what do we do to acutely reduce the demand?
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rest
beta blockers nitrates ACE inhibitors |
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beta blockers
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reduce heart rate, contractility, and systolic pressure
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nitrates
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decrease venous return by venodilation
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