Direct current shocks to the heart generate free radicals: an electron paramagnetic resonance study.

OBJECTIVES: We sought to demonstrate that direct current (DC) shocks to the heart generate free radicals. BACKGROUND: Although it is a lifesaving maneuver, defibrillation is known to have myocardial toxicity. The mechanism of this toxicity is unknown. If DC shocks generate free radicals, free radicals could be a mechanism of myocardial injury. METHODS: In a canine model, DC shocks of 10 to 100 J were delivered to the epicardium of both beating and fibrillating hearts, and 200-J transthoracic shocks were administered in dogs with beating hearts. Ascorbate free radical (AFR) concentration was measured in arterial blood and blood continuously withdrawn from the coronary sinus. In some dogs, the antioxidant enzymes superoxide dismutase (15,000 U/kg) and catalase (55,000 U/kg) (SOD/Cat) were administered before shocks. RESULTS: Ascorbate free radicals were generated by DC shocks. A peak AFR increase of 14 +/- 2% (mean +/- SEM) was seen 5 to 6 min after 100-J epicardial shocks. A peak AFR increase of 7 +/- 5% occurred after transthoracic shocks. There was a significant linear relation between the shock energy and peak percent AFR increase: %AFR increase = 0.18 (Shock energy) + 2.9 (r = 0.73, p < 0.0001). Shocks delivered to hearts in ventricular fibrillation (30 s) resulted in generation of AFR equal to but not greater than that observed during similar shocks delivered to beating hearts in sinus rhythm. Multiple successive shocks (100 J delivered twice or five times) did not result in a greater AFR increase than single 100-J shocks, indicating that peak, not cumulative, energy is the principal determinant of AFR increase. Animals receiving SOD/Cat before shock administration showed significant attenuation of the AFR increase. CONCLUSIONS: Direct current epicardial and transthoracic shocks generate free radicals; antioxidant enzymes reduce the free radical generation by shocks.

Prolonged coronary artery occlusion-reperfusion sequences reduce myocardial free radical production: an electron paramagnetic resonance study.

Our purpose was to determine whether prolonged myocardial ischemia attenuates free radical production after early reperfusion. Twenty-two mongrel dogs underwent left anterior descending coronary artery occlusion for 20, 40, or 60 minutes followed by 30 minutes of reperfusion. Electron paramagnetic resonance spectroscopy was used to measure ascorbate free radical in the coronary vein effluent. Ascorbate free radical production during reperfusion was significantly (p < 0.05) reduced in the dogs undergoing 60 minutes of coronary artery occlusion compared with the dogs undergoing 40 and 20 minutes of occlusion. We conclude that prolonged myocardial ischemia results in less free radical production on reperfusion than do shorter periods of ischemia followed by reperfusion.

Effect of electrode position and gel-application technique on predicted transcardiac current during transthoracic defibrillation.

STUDY OBJECTIVE: In transthoracic defibrillation, the American Heart Association (AHA) recommends wide separation of electrodes and avoidance of gel smearing between electrodes. Few data support this recommendation. Our objective was to determine the importance of electrode placement and gel-application technique on transcardiac defibrillation current and the effect of changes caused by postexercise vasodilation and sweating. METHODS: Our subjects were 10 normal adults, 5 men and 5 women, who ranged in age from 22 to 48 years. We determined interelectrode impedance (Z) using a validated test-pulse method that does not require shock delivery. Electrode placement/gel-application techniques were varied among four types: (1) AHA-recommended technique (apex-to-anterior electrode placement, no smearing of gel between electrodes); (2) parasternal-to-anterior placement, electrodes within 2 cm of each other, no smearing of gel between electrodes; (3) parasternal-to-anterior placement, electrodes within 2 cm of each other with smearing of gel between electrodes (worst-case scenario); and (4) apex-to-anterior placement, smearing of gel between electrodes. To assess the effect of cutaneous vasodilation and sweating on interelectrode impedance, we repeated these measurements after the subjects performed 12 to 18 minutes of treadmill exercise. The ratio of predicted transcardiac current of the AHA technique to that of the nonstandard technique was estimated with this formula: square root of Z, non-standard technique divided by square root of Z, AHA technique. RESULTS: Resting interelectrode impedance declined 38% from 58 +/- 10.3 omega (AHA-recommended technique) to 36 +/- 7.6 omega (electrode paddles adjacent, gel smeared between) (P < .01). Predicted transcardiac current ratio was reduced to .78 +/- .09 (P < .01), a 22% reduction. We noted no change in the results after exercise. CONCLUSION: Adjacent placement of electrodes and smearing of gel between electrodes creates a low-impedance pathway along the chest wall, which shunts current away from the heart. Thus improper application of electrodes and gel substantially degrades transcardiac current and may result in failed defibrillation. Sweating and vasodilation did not cause a similar problem.