Administration of electrical shock to the conotruncal area of embryonic chicks at developmental stage 24-27 induced a complex malformation, namely, double outlet right ventricle (DORV) of varying degrees of severity. The device used to apply electrical current to the heart was constructed using a 9-volt battery, a push-button switch, and a 100-ohm potentiometer with calibrated dial. This allowed a short pulse of known voltage to be applied through the electrodes to a selected area of the heart. Two different methods were chosen to administer electrical shock at the conotruncal area of the heart. One method utilized longitudinal application of electrical shock, and the other used horizontal application of electrical shock directly to the conotruncus. Three distinct types of DORV were found in the longitudinal (L) and the horizontal (H) electrical shock groups: 1) DORV without a ventricular septal defect (VSD), in which the dilated sinus of Valsalva of the aortic valve extends into the right ventricle. 2) DORV with a subaortic VSD, with variable degrees of pulmonary stenosis and a hypoplastic left ventricle. 3) DORV with a subpulmonic VSD, pulmonic stenosis and a hypoplastic right ventricle. Longitudinal stimulation produced a higher incidence of cardiovascular anomalies than horizontal stimulation (p = 0.01). Histological examination showed complete disappearance of myocardial fibers, myocardial degeneration, and the aggregation of protein material or glycogen within myocardial cells. Our Doppler findings demonstrate that relative to control embryos, peak velocity initially increased 3 minutes after electrical stimulation (p less than 0.01), and subsequently decreased significantly within 30 minutes (p less than 0.01). One may hypothesize that the marked initial increase of peak velocity was induced by tissue damage, which led to a narrowing of the conotruncal outflow tract. Evidence for contruncal narrowing was also reflected in percent window data (% W), which indicates the level of turbulence within a vessel. However, the decrease of peak velocity 30 minutes after stimulation might be caused by myocardial damage resulting in a diminished cardiac output. The relationship between cell death processes in the conotruncal area and DORV spectrum induced by electrical shock is discussed.