The purpose of this study was to determine if alcohol worsens arrhythmias produced by nonpenetrating cardiac impact. Twenty-three dogs were studied. Twelve underwent nonpenetrating cardiac impact alone at 12 m/sec with a contact compression of 2 cm. Eleven underwent cardiac impact after having received intravenous alcohol (blood level of 197 ± 37 mg/100 ml) (mean ± SD). Three dogs experienced ventricular fibrillation immediately after impact and died: of these, two underwent impact alone and one underwent impact following ethanol. These three dogs were eliminated from the study. All of the dogs had some form of complex arrhythmia during the first 10 minutes of observation, the average cumulative duration of which during the first 10 minutes following trauma was greater among dogs that received ethanol. No complex arrhythmias other than ventricular premature contractions or ventricular tachycardia were observed after the first 10 minutes following impact. During the first 2 hours of observation following cardiac impact, dogs that received alcohol before trauma showed more single premature ventricular contractions (p<0.03), couplets (p<0.01), triplets (p<0.02), runs of 4-20 beats (p<0.05), and total number of premature ventricular contractions (p<0.05) than dogs that underwent trauma alone. Following the first 10 minutes, ventricular irritability increased with time until approximately 1 hour, and then there was a gradual reduction of the frequency of arrhythmias in both dogs that received alcohol and those that did not. In conclusion, nonpenetrating cardiac impact in dogs that previously received ethanol was associated with greater ventricular irritability than in dogs that underwent impact alone.