This document discusses the pathogenesis of chest pain from three conditions: myocardial infarction, unstable angina, and pericarditis. It explains that chest pain from myocardial infarction and unstable angina is caused by a reduction in oxygen supply to the heart muscle due to blockages in the coronary arteries limiting blood flow, especially during periods of increased demand. It describes the pathophysiologic processes involved like plaque rupture and thrombus formation. For pericarditis, it states that chest pain occurs when the inflamed layers of the pericardium rub together during heart contractions, often with audible friction sounds.
This document discusses the pathogenesis of chest pain from three conditions: myocardial infarction, unstable angina, and pericarditis. It explains that chest pain from myocardial infarction and unstable angina is caused by a reduction in oxygen supply to the heart muscle due to blockages in the coronary arteries limiting blood flow, especially during periods of increased demand. It describes the pathophysiologic processes involved like plaque rupture and thrombus formation. For pericarditis, it states that chest pain occurs when the inflamed layers of the pericardium rub together during heart contractions, often with audible friction sounds.
This document discusses the pathogenesis of chest pain from three conditions: myocardial infarction, unstable angina, and pericarditis. It explains that chest pain from myocardial infarction and unstable angina is caused by a reduction in oxygen supply to the heart muscle due to blockages in the coronary arteries limiting blood flow, especially during periods of increased demand. It describes the pathophysiologic processes involved like plaque rupture and thrombus formation. For pericarditis, it states that chest pain occurs when the inflamed layers of the pericardium rub together during heart contractions, often with audible friction sounds.
This document discusses the pathogenesis of chest pain from three conditions: myocardial infarction, unstable angina, and pericarditis. It explains that chest pain from myocardial infarction and unstable angina is caused by a reduction in oxygen supply to the heart muscle due to blockages in the coronary arteries limiting blood flow, especially during periods of increased demand. It describes the pathophysiologic processes involved like plaque rupture and thrombus formation. For pericarditis, it states that chest pain occurs when the inflamed layers of the pericardium rub together during heart contractions, often with audible friction sounds.
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Myocardial Infarction
Unstable Angina Pericarditis Pathogenesis of Chest Pain
Normal coronary arteries mediate changes in
coronary blood flow in response to changes in myocardial oxygen demand (MV0 2 ). When the demands of the heart increases (during exercise)
the coronary arteries dilate to allow
increased blood flow to meet these demands Pathogenesis of Chest Pain
When a coronary artery
becomes narrowed by greater than 70%, its blood flow is by approximately 90%. Pathogenesis of Chest Pain
In this setting, maximal coronary vasodilation
occurs and allows for enough blood flow to meet the metabolic demands of the resting heart
However, during periods of increased myocardial
demand (exercise), the artery is unable to dilate further, resulting in inadequate coronary blood flow and ischemia Pathogenesis of Chest Pain caused by Reduction in oxygen supply Increase in myocardial oxygen demand superimposed on an atherosclerotic coronary plaque, with varying degrees of obstruction Four pathophysiologic processes 1. Plaque rupture or erosion with superimposed nonocclusive thrombus the most common cause 2. Dynamic obstruction Coronary spasm (Prinzmetal's variant angina) 3. Progressive mechanical obstruction Rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention 4. Secondary UA related to increased myocardial oxygen demand and/or decreased supply Tachycardia, anemia Fissue or ruptures Tissue factor plaque is released Coronary exposure of with the atheroscleros Crack or sub- arterial injury is an essential fissure in the endothelial ext Occlusive part of the diseased matrix coagulation thrombus process in arterial wall elements cascade and most patients platelet promotes activation and formation of thrombus fibrin formation , the 2 layers of the pericardium are separated by a pericardial space that contains 50 mL of clear fluid The fluid lubricates the pericardium and prevents friction between the two layers during caridiac contraction Pericarditis is marked by infiltration of the pericardium by polymorphonuclear leukocytes with eventual The inflamed pericardial layers deposition of fibrin in the rub against each other during pericardial space each cardiac contraction, often resulting in pain and an audible friction rub