Cardiac damage caused by direct application of defibrillator shocks to isolated Langendorff-perfused rabbit heart.
The purpose of this study was to establish the damaging dose of defibrillator pulses. The damage caused to isolated perfused rabbit hearts by synchronized defibrillator shocks with a stored energy from 15 up to 70 joules is reported. The damage was characterized by the duration and severity of post-shock arrhythmias, changes in the elastic properties of the left ventricle, the first derivative of left ventricular pressure, morphological changes of the heart muscle, elevation of creating kinase, potassium washout, and a change in mean coronary flow rate. Varying the electrode area showed that densities of applied current and energy are major factors in damaging the heart. At current and energy densities of 0.5 amp./cm.2 and 0.6 J./cm.2, respectively, potassium washout and mild arrhythmias are seen, as is complete arrest of the ventricles at 1.2 amp./cm.2 and 1.5 J./cm.2 pulses. After 1.8 amp./cm.2, irreversible cell damage occurs, as demonstrated by CK release, and also cardiac function is reduced, measured by increased diastolic stiffness and decreased contractility. Current and energy densities exceeding 2.5 amp./cm.2 and 4.2 J./cm.2, respectively, cause changes in cardiac function incompatible with life. Accumulation of damage was observed with a series of 1.2 amp./cm.2 shocks.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology; D001794:Blood Pressure; D001810:Blood Volume; D003402:Creatine Kinase / Q000378:metabolism; D003971:Diastole; D004554:Electric Countershock; D006335:Heart Injuries / Q000209:etiology*; D006352:Heart Ventricles / Q000473:pathology / Q000648:ultrastructure; D010477:Perfusion; D011817:Rabbits; D013599:Systole
D003402:Creatine Kinase