Electrocardiographic and serum enzymic alterations associated with cardiac alterations induced in dogs by single transthoracic damped sinusoidal defibrillator shocks of various strengths.

The safety margin between the strength of shock needed to defibrillate the ventricle and shocks which produce cardiac damage has not previously been reported. This study quantitates the shock intensity required to produce ECG alterations, serum alpha-1LDH and MB CPK isoenzyme elevation and myocardial damage using single transchest damped sinusoidal defibrillator shocks. Shocks of 1 to 20 amperes per Kg. of body weight were applied. Fifty-six dog weighing 2.4 to 15 kilograms were shocked with defibrillator pulses via 10 centimeter diameter electrodes applied to the thorax. Electrocardiograms were taken to be analyzed for arrhythmias, S-T segment changes, and T wave changes. Serum enzyme levels were determined in 25 dogs. Macroscopic and histopathologic studies were conducted on the hearts. Transchest single damped sine wave shocks did not produce microscopically detectable cardiac damage until at least a threefold current overdose was applied. No macroscopic morphologic alterations were observed until at least a sixfold current overdose was applied and no deaths occurred until a twelvefold or greater current overdose was delivered. Incidence and severity of ECG changes, increase in serum enzyme activity, incidence and severity of cardiac damage, and incidence of mortality all correlated positively with shock strength. However, these four adverse effects did not correlate well with each other. Transient ECG changes were very frequent following shock application regardless of the morphologic damage produced, and hence the transient changes have little value as indicators or predictors of damage. Persistent ECG changes were predictive of morphologic changes but were not sensitive enough to detect damage in mildly injured hearts. Likewise, elevated serum cardiac isoenzyme activity was a reliable but insensitive indicator of damage.