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The administration of magnesium ion (Mg++) has been reported to defibrillate the ventricles and to decrease the incidence of arrhythmias after cardiopulmonary bypass. In a prospective study of 76 randomly selected patients undergoing coronary artery bypass grafting, patients received either no Mg++, 0.25 mEq/kg of Mg++ during cardiopulmonary bypass with the aorta clamped, or 0.375 mEq/kg of Mg++ before cardiopulmonary bypass. Spontaneous resumption of a cardiac rhythm or spontaneous defibrillation during reperfusion was not significantly affected by Mg++ administration. However, the number of shocks to initial and to sustained defibrillation and the energy required for the last direct-current shock was greatest in patients who received Mg++ before bypass and in those whose plasma Mg++ was greater than 2.26 mg/dl. Thus, the administration of Mg++ may have adverse effects on the heart if intraoperative plasma Mg++ exceeds 2.26 mg/dl.

In a prospective survey employing conventional devices that stored 400 joules or less, direct-current shocks that delivered 194 +/- 11 joules (1.8 joules/kg) to the chest wall terminated 45 of 46 episodes of ventricular fibrillation in 11 of 12 patients weighing 91 to 225 kg. Patients with coronary disease defibrillated more easily than patients without coronary disease. Weight did not determine outcome. The 98% defibrillation efficiency occurred at only half the energy predicted for 50% efficiency from retrospective data. Human defibrillation not only occurred at one third the untested level recommended by proponents of high-energy defibrillation, but also at one fourth the energy, defibrillating 69% of comparably heavy animals. Thus, the costly defibrillators delivering 400 to 800 joules now sold by 11 of 14 American manufacturers are superfluous, untested, potentially lethal devices with which to attempt ventricular defibrillation.

The efficacy of lidocaine during myocardial reperfusion in coronary artery bypass surgery was evaluated in 20 patients randomly assigned to a control group (n = 10) or to receive lidocaine, 1 mg/kg intravenously 5 min before aortic unclamping and cardiac reperfusion, followed by infusion at 40 micrograms X kg-1 X min-1 (n = 10). We recorded ECG leads II and V5 continuously, and number, energy, and current of direct current (DC) shocks starting at 1 joule. The number of low energy DC shocks to sustained defibrillation (5.5 +/- 2.0 vs 3.5 +/- 2.0, mean +/- SD, P less than 0.05) decreased significantly with lidocaine infusion. The energy (11.0 +/- 6.3 vs 5.6 +/- 3.9 joules, P less than 0.05) and current (12.7 +/- 4.2 vs 8.9 +/- 4.7 amperes, not significant) likewise decreased with lidocaine infusion. Energy and current for the first successful shock, although lower in the lidocaine group, were not statistically significantly lower than in the control group. Initial reperfusion rhythm was not influenced by lidocaine. Plasma electrolyte levels, arterial blood gas tensions, myocardial temperature, and surgical technique--factors known to influence defibrillation--were similar in all patients. Administration of lidocaine during myocardial reperfusion allows defibrillation with fewer DC shocks of lower energy and current.

In a study demonstrating 95% success in achieving defibrillation in 94 resuscitative events in adult patients, the authors find that weight did not determine that success and that the results were obtained at significantly low rates of energy output. Diagnosis was the key, they conclude, and they view the expensive high-energy defibrillators marketed today as unnecessary, potentially lethal, and economically wasteful.