| pubmed-article:1119384 | pubmed:abstractText | Electrocardiographic and hemodynamic correlates were recorded before and after a standardized nonpenetrating blow to the chest in 9 anesthetized control dogs (Group I), 5 dogs, pretreated with alcohol, 0.4 g/kg intravenously (Group II), and 12 dogs undergoing chest trauma after alcohol infusions (Group III). In animals in Group I, transient major arrhythmias, including complete heart block and ventricular tachycardia, occurred immediately after impact. One animal died with ventricular fibrillation. In the eight survivors these disturbances were accompanied by acute reductions in aortic pressure and cardiac index; values for both variables gradually increased after restoration of sinus mechanism. Alcohol alone (Group II) produced no significant alterations in either hemodynamic performance or electrical activity, but when combined with nonpenetrating chest injury (Group III) it caused a mortality rate of 92 percent, the majority of animals dying with electromechanical dissociation. Mean survival time in Group III was 23.1 plus and minus 6.5 (standard error of the mean) minutes compared with 80.3 plus and minus 9.6 minutes in Group I. At autopsy, minor cardiac lesions of either the pericardium or myocardium were observed in all animals in Groups I and III, but none were considered lethal. It is concluded that administration of alcohol, even in small doses, can effect catastrophic reductions in mechanical performance in the presence of otherwise nonfatal cardiac injury secondary to nonpenetrating chest trauma. The clinical implications of this association are discussed. | lld:pubmed |
