A 25-year-old previously well man lost consciousness when he touched an electrical wire. At least ten minutes elapsed before cardiopulmonary resuscitation (CPR) was initiated. On arrival at the hospital he was successfully defibrillated after several DC countershocks but he never regained consciousness. Although physical examination subsequently revealed stable vital signs and normal results of cardiac examination, findings from neurologic examination and diagnostic testing were consistent with severe anoxic brain damage. The electrocardiogram (ECG) revealed sinus tachycardia with poor R-wave progression in V, through Ve. His creatine kinase value was 9,800 units/L with 5 percent MB. A two- dimensional echocardiogram revealed severe biventricular hypoki- nesis with left ventricular apical dyskinesis (Fig 1). The left ventricular ejection fraction calculated by gated blood pool scanning was 15 percent. A repeat echocardiogram four days later was unchanged. A rest thallium study revealed apical, inferior, and septal defects. The patients neurologic status deteriorated and he died six days later.
An autopsy, there was extensive left ventricular subendocardial infarction believed to be seven to ten days old. In addition, there were focal areas, occasionally transmural, of contraction band necrosis and eosinophilia. The right ventricle showed similar but less extensive changes. The epicardial coronary arteries were normal while many of the intramyocardial vessels contained thrombi. These findings were all believed to be consistent with myocardial injury due to severe hypotension at the time of cardiac arrest rather than as a direct result of electrical injury. Examination of the brain revealed evidence of anoxic encephalopathy.
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FIGURE 1. End-diastolic (laeft panel) and end-systolic (right panel) and parasternal long axis echocardio¬grams recorded in a 15-year-old patient resuscitated from an acute electrical injury. Note the severe left ventricular hypokinesia
A 25-year-old previously well man lost consciousness when the ladder he was holding struck a 7200-V line. Cardiopulmonary resuscitation was immediately initiated. On arrival at the hospital, he was found to be in ventricular fibrillation. Over the next 30 minutes, he received seven DC countershocks until stable sinus rhythm was achieved. The following day, his vital signs and results of neurologic and cardiac examinations were normal. The ECG showed sinus rhythm with diffuse nonspecific ST and T changes. Initial and 12-hour postadmission creatine kinase values were 4,295 units/L (6 percent MB) and 4,275 units/L (12 percent MB), respectively. An echocardiogram at the time of hospital admission revealed globally severe biventricular hypokinesis with dyskinesis of the left ventricular apex. Two days later, the ECG revealed T-wave inversion in leads 1, 2, aVL, aVF, V4, V5, and Ve, and a repeat echocardiogram revealed slightly improved left ventricular (unction with pesistent apical dyskinesis. A follow-up echocardiogram three weeks later showed marked improvement in basal and midventricular function with persistent apical dyskinesis. At the time of stress testing two months later, the patient reached his predicted maximum heart rate without symptoms. The resting ECG showed the previously noted T-wave abnormalities; with exercise there was no change. Thallium imaging revealed a fixed apical defect consistent with scar. buy cialis soft tabs