Systemic and regional hemodynamic effects of a high intravenous dose of cocaine under halothane or sevoflurane anesthesia

Background

Cocaine abuse has been linked to penetrating and blunt trauma requiring surgical treatment. Although the cardiovascular effects of cocaine are well studied, particularly its association with arrhythmia, myocardial infarction and sudden death, little is known about the effects of cocaine abuse on splanchnic perfusion and the potential undesirable interaction with volatile anesthetics. We hypothesized that halothane would elicit more circulatory adverse effects than sevoflurane in an acute model of cocaine intoxication.

Methods

Mechanically ventilated Beagle dogs (n = 14, 12.8 ± 0.3 kg) underwent anesthesia induction with intravenous propofol. They were then randomly assigned to two experimental groups: 1.5% halothane (n = 7, Halo) or 2.25% sevoflurane (n = 7, Sevo). After 30 min (Baseline), intravenous cocaine was infused as a bolus (12 mg/kg over 5 min), followed by 0.22 mg/kg/min during 30 min (BL-T35), and followed for 60 min thereafter (T35–T95). Systemic hemodynamics were determined by arterial and pulmonary artery catheters. Portal vein blood flow was measured by a transit time ultrasonic flowprobe. The PCO₂ gap (gas tonometry), blood gases, arterial lactate and cocaine levels were measured at each timepoint.

Results

See Table 1.

Table 1

Conclusions

A high dose of cocaine in anesthetized animals induces a severe, but transient, hypodynamic state, which was more pronounced under halothane anesthesia. Regional hemodynamic derangement accompanied systemic hemodynamic variations and was completely reversible.