Electrocardiographic changes due to subarachnoid hemorrhage (SAH) are seen frequently and this can lead to erroneous examinations and treatment, like thrombolytic or antiaggregant, which can increase the mortality. A 42-year-old female was admitted to our emergency. While planning with primary percutan transluminal coronary angioplasty (PTCA) the ECG changed to narrow QRS complex supraventricular tachycardia. Due to the normal echocardiography of the heart, lack of coronary artery disease medical history, physical examination was made again and we decided to take a non-contrast cranial computer tomography(CT) to exclude intracranial hemorrhage which could explain the electrocardiographic changes and clinical situation of the patient We presented a case with SAH whose electrocardiograph mimicked myocardial infarction. Introduction Subarachnoid haemorrhage accounts for only 5% of strokes, but it generally ocur in the young age. Hypertension, hypoxaemia, and electrocardiographic (ECG) changes, which can mimic acute myocardial infarction and lead to erroneous examinations and treatment are associated with subarachnoid haemorrhage in the acute phase(1). Electrocardiographic changes can be responsible for life-threatening arrhythmias. They are found responsible for 8 to 15% prehospital mortality rate of patients with SAH. Of deaths within the first 24 hours after SAH, 75% occur suddenly and are presumed also to be cardiac in origin(2).Aim: We presented a case with SAH, who mimicked myocardial infarction, to avoid misdiagnoses and thrombolytic therapy. Case Report A 42-year-old female was admitted to our emergency service by paramedics with asystole rhythm. After 10 minute cardiopulmonary resuscitation with intermittently epinephrine administration (3mg total) cardiac rhythm turned to torsades de pointes. She was defibrillated with 200j (biphasic defibrillator) and also 1gr MgSO4, and 300mg amiodarone were administered intravenously. The ECG changed to third degree AV block, 3 mm ST-segment elevation in DI, aVL, DII, DIII and aVF limbs and ST segment depression, T wave negativity in V1 and ST-segment elevation in V2-6 precordial limbs (Figure 1).
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