How many times can we defibrillate a patient ?

Ventricular fibrillation (VF) is the cardiac rhythm disturbance which is the number one cause of cardiac arrest. Most common etiologic factor is the coronary heart disease [1]. VF may occur due to acute myocardial ischemia, infarction or a scar tissue formed previously because of a prior myocardial infarction (MI). Defibrillation is the first line therapy. Antiarrhythmic drugs should also be added, and the predisposing factors should be eliminated as well [2]. Sometimes multiple shocks are needed for resistant or recurrent VF. We have a case in whom we performed several times of defibrillation because of repeated VF attacks. This 38-yearold male who was resuscitated because of VF at a different center was transferred to our hospital with extensive anterior MI. Because of cardiogenic shock an intra-aortic balloon pump was placed in addition to positive inotropic therapy and mechanical ventilation. The patient was defibrillated twice in the 3th and the 5th days of MI. The condition of the patient got worse and he was transferred to our unit in the 17th day of MI with respiratory failure, acute renal failure (BUN 76 mg/dL and creatinine 5.7 mg/dL) and frequent ventricular premature beats. Because of recurrent VFs he was under amiodarone infusion. Potassium and magnesium were replaced as well. Echocardiography revealed anterior IVS (interventicular septum) mid-apical segment, apex, and anterior wall were akinetic . We performed coronary angiography which showed that left anterior descending (LAD) artery was totally occluded at its ostium. Right coronary and circumflex coronary arteries were normal. LAD was opened and two bare metal stents were placed. Soon after the intervention VF attacks started. Lidocain infusion was started in addition to amiodarone infusion. Despite the antiarrhythmic infusions VF runs continued and he was defibrillated 50 times in 9 hours. ECG showed ST depression in leads D2D3-aVF and ST elevations at precordial leads between the shocks. Reinfarction was thought and nitroglycerin and aspirin were added. At this period his blood testes was normal besides BUN and Cre. And his cardiac markers before and during attacks were CKMB:1.4, 2.3, 11.7, 18,8Myoglobin:180, 229,989,1235Throponin:4.95, 4.81, 5.09, 4.86. At echocardiography 8 hours after attacks, apex was hipokinetic and other wall motions were normal. With all these findings reperfusion injury considered as the cause of these attacks. 30 hours after attacks patient was extubated, amiodarone infusion stopped gradually and metoprolol therapy was started. CKMB, myoglobin, troponin levels decreased, renal functions improved and the patient was discharged and referred to cardiology outpatient clinic.