Energy dose for defibrillation.
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Biomedical subjects
Publications and source records attributed to W A Tacker.
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Anesthetized dogs were cooled to a core body temperature of 26 degree C. or maintained at a body temperature of 37 degree C. during periods of 5 and 10 hours of LAD coronary artery occlusion. Subsequent macroscopic dehydrogenase enzyme mapping showed that ischemic injury was 25 per cent less after 5 hours of coronary occlusion and 20 per cent less after 10 hours of occlusion in hypothermic dogs than in normothermic controls. The heart rate and left ventricular minute work in hypothermic dogs decreased to roughly half the levels measured in normothermic animals, while left ventricular contractility was 10 to 40 per cent lower in hypothermic dogs than in normothermic dogs. However, cardiac index and left ventricular end-diastolic pressure were unchanged by whole-body cooling. Thus, hypothermia appeared to diminish the oxygen requirements of the ischemic myocardium without reducing the performance of the heart as a pump. Hypothermia may be useful as a therapeutic adjunct to myocardial revascularization or pharmacologic interventions.
The threshold electrical energy for direct ventricular defibrillation was measured in 100 patients whose hypothermic hearts were fibrillated for cardiac operations. In 93 cases 10 joules or less was sufficient, and in 48 of these cases 5 joules or less defibrillated the ventricles. Because a shock of 10 joules defibrillated the heart of most of our patients, we recommend an initial shock of 5 to 10 joules rather than the 20 joules used more commonly. Until the safety margin between defibrillation threshold and damage threshold is established for direct defibrillation, use of shocks with adequate but not excessive strength may avoid unnecessary damage to the myocardium. When hearts refibrillate after defibrillation, it is unnecessary to use higher energy settings for subsequent defibrillation attempts. Instead, an antiarrhythmic drug should be administered and another shock of the same intensity that defibrillated the first time should be applied.
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The safety of open thorax defibrillation with single damped sine-wave shocks and 6-cm-diameter electrodes was evaluated in healthy anesthetized dogs. Twenty-one dogs were allotted to 6 groups: Group A were nonshocked controls and groups B through F were given single shocks of 4-, 7-, 12-, 19-, or 32-fold, respectively, greater than a defibrillation threshold dose (30 mA/g of heart). Immediate postshock death resulted in group F dogs; group A through E dogs survived and were killed after 2 days. The incidence and severity of cardiac morphologic damage increased with shock strength (mild damage occurred in 1 of 3 dogs in group C and in 3 of 4 dogs in group D and severe damage occurred in 2 of 3 dogs in group E). The cardiac lesions were characterized grossly and microscopically. In dogs that died immediately after shocking, damage was apparent as pale circular zones of edema and myofibrillar degeneration in the ventricular free walls beneath the electrode placement sites on the cardiac surface. In the dogs that survived 2 days, the defibrillator-induced areas of myocardial necrosis and calcification were concentrated in arc or ringlike patterns beneath the periphery of the electrode placement sites. All dogs that were studied 2 days after shocking had mild fibrinous pericarditis. Postshock electrocardiographic changes were not good indicators of cardiac damage because the mild epicardial inflammatory reaction associated with the surgical procedure produced large ST and T wave changes which masked any changes associated with myocardial necrosis induced by the electric shocks. It was concluded that a substantial safety margin exists between the required defibrillation threshold shock dose and the large shocks required to produce marked cardiac damage or death in healthy dogs.
The thoraces of dogs were mapped out to identify those areas where defibrillating current gains easiest access to the heart. Of all of the transchest and chest-to-back electrode locations, the lowest current dose (0.6 amp. per kilogram of body weight) was found with one electrode over the apex-beat area with transchest electrodes and slightly anterior to the apex-beat area with chest-to-back electrodes.
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Trans-chest electrical ventricular defibrillation was attempted in eight adult patients using a 400 watt-second truncated exponential decay waveform defibrillator. All attempts occurred in the immediate post-operative period after heart surgery. Five of the eight subjects were defibrillated (63% success). This success rate is similar to that of 300 watt-second damped sinusoidal waveform defibrillators.
Transthoracic direct current shock is the recommended treatment for ventricular fibrillation in children as in adults. To determine the appropriate energy dose, data were collected from 71 defibrillation attempts in 27 children. Sixty-three of the 71 shocks (89%) were successful in terminating fibrillation. Fifty-seven shocks were within 10 watt-seconds (w-sec) above or below an energy dose of 2 w-sec/kg of body weight. Fifty-two (91%) of these were effective and five (9%) were ineffective. In every case, fibrillation was ultimately terminated by a shock of 4 w-sec/kg or less. The results of these studies suggest that an energy dose of 2 w-sec/kg (or approximately 1 w-sec/lb) is adequate to defibrillate most children weighing under 50 kg. We currently use 2 w-sec/kg and double the energy dose if the first defibrillation attempt is unsuccessful.
Effectiveness of four truncated exponential waveform defibrillators for transchest ventricular defibrillation was evaluated in 27 human-sized animals. With all waveforms, effectiveness was virtually 100% for small subjects, but decreased as body weight increased. These data confirm the electrical dose concept for ventricular defibrillation and demonstrate that the truncated exponential waveform is effective only when adequate current is delivered through the subject's chest.
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