Cardiocirculatory function in the intoxicated shocked dog: acid base derangements.

The present study examined the effects of acute ethanol consumption alone or in combination with hemorrhagic shock on cardiac performance and regional blood flows in a canine model. Dogs in the alcoholic groups received 3 ml/kg body weight ethanol administered via a Salem tube placed in the jejunum (N = 26); control dogs received normal saline (N = 9). One hour after ethanol administration, blood ethanol levels were 290 +/- 6 mg/100 ml. Shock was produced by bleeding to a mean arterial blood pressure of 30-35 mmHg. The alcoholic shocked dogs were further divided into two subgroups; in one group, acid base derangements were continuously corrected with sodium bicarbonate infusion, while acid base derangements remained uncorrected in the other group. After 2 hours of sustained hypotension, shed blood was returned, and lactated Ringer's was infused (50 mlk/kg) in all shocked groups. The results indicate that ethanol in normovolemic dogs did not depress left ventricular function or regional blood flow, despite significant acidosis. Two hours of hypotension impaired cardiac function and regional perfusion to a similar extent in both intoxicated and nonintoxicated dogs. Acid base correction in intoxicated shocked dogs improved subendocardial perfusion and left ventricular performance both during shock and after fluid resuscitation from shock compared to alcoholic shocked dogs with persistent acid base derangements. Our data show that acidosis produced by acute ethanolism is exacerbated by 2 hours of hemorrhagic shock. It is likely that ethanol-depressed ventilation prevents appropriate respiratory compensation of shock-induced metabolic acidosis. Acid base correction improves subendocardial perfusion and cardiac performance, suggesting a causative role for acidosis in the reduced cardiac performance after shock resuscitation in intoxicated dogs.