The effects of shock energy, propranolol, and verapamil on cardiac damage caused by transthoracic countershock

Abstract

Myocardial damage by transthoracic countershocks was assessed by observation for electrocardiographic loss of R waves and elevation of ST segments, creatine kinase depletion, and histologic evidence of necrosis in damaged areas, and by excision and examination, 3 days later, of all tissue macroscopically observed to be damaged. When 4000 J of stored energy was passed across the chest of dogs anesthetized with pentobarbital sodium (30 mg/kg), more damage was caused when the energy was divided among 10 shocks than when it was applied in 20 or 40 shocks (at intervals of 0.5 min). The prior intravenous administration of verapamil (1 mg/kg) reduced the weight of damaged myocardium, the extent of histologic change, and creatine kinase depletion caused by 10 x 400 J shocks. Propranolol (0.4 mg/kg) had no effect. These results give further evidence for the role of calcium accumulation in cardiac necrosis after direct current countershocks. Multiple low-energy shocks cause less cardiac damage than do a few high-energy shocks of similar total energy.