Cardiology

Myocardial Infarction - Complications song

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Myocardial Infarction - Complications

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Post-MI ventricular free wall rupture typically occurs 3–5 days after STEMI, presenting with sudden hemopericardium, cardiac tamponade, and pulseless electrical activity (PEA).
Interventricular septal rupture presents with a new harsh holosystolic murmur at the left sternal border with a left-to-right shunt, confirmed by oxygen step-up on right heart catheterization.
Papillary muscle rupture — most commonly the posteromedial papillary muscle (supplied solely by the PDA) — causes acute mitral regurgitation with a holosystolic murmur at the apex and flash pulmonary edema.
Dressler syndrome (post-MI pericarditis) occurs weeks to months after MI, presenting with fever, pleuritic chest pain, and pericardial friction rub; treated with NSAIDs or aspirin.
Early pericarditis (within 1–3 days of transmural MI) results from direct pericardial inflammation overlying infarcted myocardium and is managed with high-dose aspirin.
Left ventricular aneurysm forms weeks after large anterior MI (LAD territory), presents with persistent ST elevation, heart failure, and is a nidus for mural thrombus and ventricular arrhythmias.
Mural thrombus complicates anterior MI and akinetic LV segments; anticoagulation with warfarin or heparin is indicated to prevent systemic embolization and stroke.
Cardiogenic shock post-MI is defined by persistent hypotension (SBP <90 mmHg), elevated PCWP (>18 mmHg), and reduced cardiac output; intra-aortic balloon pump or revascularization is the priority.
Right ventricular infarction complicates inferior MI (RCA occlusion), presenting with hypotension, elevated JVP, and clear lungs; nitrates and diuretics are contraindicated — treatment is aggressive IV fluids.
Ventricular fibrillation is the most common cause of death in the first 24–48 hours post-MI and is an indication for immediate defibrillation; sustained VT post-MI warrants ICD placement for secondary prevention.