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Questions and Answers
What is the most common complication associated with myocardial infarction that occurs within the first 24 hours?
Which complication occurs 2-7 days after a myocardial infarction and can lead to severe mitral regurgitation?
What is a major risk associated with a ventricular free wall rupture occurring 5-14 days after a myocardial infarction?
Which treatment is included for unstable angina/NSTEMI management?
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Which complication that occurs several weeks after a myocardial infarction is characterized by an autoimmune response?
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Study Notes
Myocardial Infarction Complications
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Cardiac arrhythmias are a common complication of myocardial infarction (MI), occurring within the first few days and peaking within the first 24 hours. They are a leading cause of death before reaching the hospital.
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Postinfarction fibrinous pericarditis develops typically 1-3 days after MI, characterized by a friction rub.
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Papillary muscle rupture can occur 2-7 days after MI, with the posteromedial papillary muscle being more vulnerable due to its single blood supply from the posterior descending artery. This complication can lead to severe mitral regurgitation.
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Interventricular septal rupture commonly occurs 3-5 days after MI, resulting from macrophage-mediated degradation of the infarcted septum. This leads to a ventricular septal defect (VSD), causing increased oxygen saturation and pressure in the right ventricle.
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Ventricular pseudoaneurysm formation can develop 3-14 days after MI, representing a contained free wall rupture. This can lead to decreased cardiac output, an increased risk of arrhythmias, and potential emboli from mural thrombi.
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Ventricular free wall rupture is a life-threatening complication that occurs 5-14 days after MI. It involves a complete rupture of the ventricular wall, resulting in cardiac tamponade. Left ventricular hypertrophy and prior MI can offer protection against free wall rupture. The acute form of this complication often leads to sudden death.
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True ventricular aneurysm occurs 2 weeks to several months after MI, forming an outward bulge with impaired contraction, known as "dyskinesia." This aneurysm is associated with fibrosis.
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Dressler syndrome, an autoimmune phenomenon, can develop several weeks after MI, presenting as fibrinous pericarditis. It can be triggered by left ventricular infarction, VSD, free wall rupture, or papillary muscle rupture with mitral regurgitation.
Acute Coronary Syndrome Treatments
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Unstable angina and non-ST-segment elevation myocardial infarction (NSTEMI) are treated with anticoagulants (e.g., heparin), antiplatelet agents (e.g., aspirin, clopidogrel), beta-blockers, ACE inhibitors, and statins. Pain management is achieved with nitroglycerin and morphine.
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ST-segment elevation myocardial infarction (STEMI) requires reperfusion therapy along with the treatments mentioned for unstable angina and NSTEMI. Percutaneous coronary intervention (PCI) is the preferred method of reperfusion over fibrinolysis.
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Description
Explore the various complications that can arise from myocardial infarction, such as cardiac arrhythmias, postinfarction fibrinous pericarditis, and papillary muscle rupture. Understand the timing and nature of these complications, along with their potential consequences. This quiz will help deepen your knowledge of post-MI patient management.