: High blood pressure, high cholesterol, smoking, diabetes, and family history.
| Complication | Timing | Clues | |--------------|--------|-------| | | First 24–48h | Hypotension, cool extremities, oliguria, lactate ↑ | | LV thrombus | 2–14 days | Systemic emboli (stroke, limb ischemia) | | Ventricular aneurysm | Weeks–months | Persistent ST elevation, CHF, arrhythmias | | Ventricular septal rupture | 3–7 days | Harsh holosystolic murmur, thrill, sudden shock | | Papillary muscle rupture | 2–7 days | Acute severe MR, murmur (may be soft), pulmonary edema | | Ventricular tachycardia/fibrillation | First 24–48h | Pulseless, unstable | | Pericarditis (Dressler’s) | Weeks | Pleuritic chest pain, rub, fever |
: The gold standard; levels rise within hours of injury and can stay elevated for up to 14 days. anterior myocardial infarction
| Finding | Detail | |---------|--------| | | V2–V4 (classic); often extends to V1, V5, V6, I, aVL | | Reciprocal ST depression | II, III, aVF (inferior leads) | | Q waves | New Q waves in V2–V4 (develop hours to days) | | Poor R wave progression | In precordial leads | | Hyperacute T waves | Tall, symmetric T waves (earliest sign, before ST elevation) |
Without oxygen, heart muscle cells begin to die (necrosis) within minutes. : High blood pressure, high cholesterol, smoking, diabetes,
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An is a life-threatening medical emergency caused by a sudden interruption of blood flow to the front wall of the heart. It is widely considered one of the most severe forms of heart attack because it typically involves the left ventricle's largest muscular portion, which is responsible for pumping oxygenated blood to the entire body. Causes and Pathophysiology
: Elevation in precordial leads V1 through V4 . Lead V1-V2 : Suggests septal involvement. Lead V3-V4 : Indicates the anterior wall.
: Shortness of breath, cold sweats (perspiration), nausea, and radiating pain to the jaw, neck, or left arm. 2. ECG Findings