The effect of cocaine on the physiologic response to hemorrhagic shock

Bradycardia is thought to be an uncommon and abnormal response to acute blood loss. A review of trauma patients (n = 84) admitted during a 1-year period with a systolic blood pressure of less than 100 mm Hg revealed that 45% had relative bradycardia (heart rate < 100 beats/minute). Cocaine use was recorded more often in this group (76% versus 26%; p < 0.05) compared with patients with tachycardia (heart rate > or = 100 beats/minute). We investigated the effect of cocaine use on the response to acute blood loss in an animal model of hemorrhagic shock.

Rats were given intraperitoneal cocaine 20 mg/kg/day for 14 days (n = 10) or saline solution (n = 10). The rats were bled until 30% of their blood volume was shed; they were resuscitated 30 minutes later.

Cocaine-treated rats showed a decreased 24-hour survival rate (50% versus 100%; p < 0.05), a relative bradycardic response compared to baseline heart rate (-8.9% +/- 6.4% versus 7.5% +/- 3.5%; p < 0.05), and a greater drop in mean arterial blood pressure (-55.5% +/- 4.8% versus -37.0% +/- 5.5%; p < 0.05) by 5 minutes of shock. Cocaine-treated rats were more acidotic after shock compared to controls (pH 7.36 +/- 0.03 versus 7.44 +/- 0.02; p < 0.05).

Cocaine had a deleterious effect on experimental hemorrhage. The bradycardic response observed in our trauma patients may be due, in part, to cocaine abuse, and we postulate that chronic cocaine use alters the normal adrenergic response to blood loss.