There is little information available concerning the 104 cardiac sequelae in survivors of electrical shock. Electrocardiographic patterns typical of acute myocardial infarction have been reported immediately after resuscitation, but it has been suggested that in long-term survivors these resolve completely. To our knowledge, only one previous report has provided any direct information concerning cardiac function in such patients. Lewin et al reported the noninvasive cardiac findings in a 19-year-old who was successfully resuscitated following an electrical injury. An echocardiogram performed at the time of cardiac enzyme elevation and striking ECG abnormalities demonstrated severe global left ventricular hypokinesis. However, a follow-up echocardiogram three days later showed significantly improved ventricular function, and a gated blood pool scan performed at that time demonstrated an ejection fraction of 69 percent. A repeat echocardiogram at one year was entirely normal. In contrast, the two patients described herein had persistent abnormalities of left ventricular function. In one, although there was a marked reduction in the extent of dysfunction noted initially, left ventricular apical dyskinesis persisted. In addition, two months later, a thallium scan demonstrated a fixed perfusion defect consistent with apical infarction. In the second patient, there was severe biventricular dysfunction that persisted until death at day 6.
There are two principal mechanisms by which electrical shock can cause myocardial damage. Although the heart is protected by body tissues that function as an infinite series of resistances, thermal injury to the heart may occur as a direct result of the transcardiac passage of current. A second mechanism is ischemic injury precipitated by arrhythmia-induced hypotension. In the two cases reported herein, it is likely that ischemic insult played a major role. In the second case, this contention is supported by the cardiac findings at autopsy as well as by the clinical and pathologic evidence of anoxic brain damage. Also in keeping with the hypothesis of ischemic damage is the apical location of the infarction in our first patient, ie, within the most vulnerable coronary watershed region.
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Direct comparison among each of our patients and the patient who was reported by Lewin et al is impossible. However, it is of interest that all patients were young, presumably free of coronary disease, and injured under similar circumstances. In our second patient as well as the patient whose case was reported by Lewin et al, there was prompt initiation of CPR, while in our first patient the commencement of CPR was delayed. Although all three patients had evidence of severe left ventricular dysfunction on initial echocardiogram, there was significant return of function only in the two who quickly received basic life support measures. These observations are not surprising given current knowledge in the area of ischemic myocardial injury.
It might be argued that later follow-up in our second patient might have demonstrated resolution of even the apical wall motion abnormality. However, we believe that this is unlikely given the fixed apical defect demonstrated on thallium scanning at two months, and the fact that abnormal wall motion was evident at three weeks, beyond the time required for the return of function in “stunned” myocardium.
In summary, this report describes two survivors of electrical injury in whom there was irreversible left ventricular dysfunction. Features of these cases support the concept of an ischemic basis for these abnormalities and suggest that a major factor in determining the final outcome in such cases is the time from acute insult to the initiation of CPR. cialis canadian pharmacy