Presented in part at the 2009 Society for Academic Emergency Medicine annual meeting, New Orleans, LA, May 2009.
Effect of an Electronic Control Device Exposure on a Methamphetamine-intoxicated Animal Model
Article first published online: 2 APR 2010
© 2010 by the Society for Academic Emergency Medicine
Academic Emergency Medicine
Volume 17, Issue 4, pages 436–443, April 2010
How to Cite
Dawes, D. M., Ho, J. D., Cole, J. B., Reardon, R. F., Lundin, E. J., Terwey, K. S., Falvey, D. G. and Miner, J. R. (2010), Effect of an Electronic Control Device Exposure on a Methamphetamine-intoxicated Animal Model. Academic Emergency Medicine, 17: 436–443. doi: 10.1111/j.1553-2712.2010.00708.x
This study was funded in part by TASER International.
Conflict of Interest: Dr. Dawes and Dr. Ho are external medical consultants to TASER International and stockholders of TASER International. Dr. Ho is also the Medical Director of TASER International, Inc.
- Issue published online: 2 APR 2010
- Article first published online: 2 APR 2010
- Received August 11, 2009; revisions received October 6 and October 19, 2009; accepted October 21, 2009.
- law enforcement;
- arrhythmias, cardiac;
Objectives: Because of the prevalence of methamphetamine abuse worldwide, it is not uncommon for subjects in law enforcement encounters to be methamphetamine-intoxicated. Methamphetamine has been present in arrest-related death cases in which an electronic control device (ECD) was used. The primary purpose of this study was to determine the cardiac effects of an ECD in a methamphetamine intoxication model.
Methods: Sixteen anesthetized Dorset sheep (26–78 kg) received 0.0 mg/kg (control animals, n = 4), 0.5 mg/kg (n = 4), 1.0 mg/kg (n = 4), or 1.5 mg/kg (n = 4) of methamphetamine hydrochloride as a slow intravenous (IV) bolus during continuous cardiac monitoring. The animals received the following exposures in sequence from a TASER X26 ECD beginning at 30 minutes after the administration of the drug: 1) 5-second continuous exposure, 2) 15-second intermittent exposure, 3) 30-second intermittent exposure, and 4) 40-second intermittent exposure. Darts were inserted at the sternal notch and the cardiac apex, to a depth of 9 mm. Cardiac motion was determined by thoracotomy (smaller animals, ≤ 32 kg) or echocardiography (larger animals, > 68 kg). Data were analyzed using descriptive statistics and chi-square tests.
Results: Animals given methamphetamine demonstrated signs of methamphetamine toxicity with tachycardia, hypertension, and atrial and ventricular ectopy in the 30-minute period immediately after administration of the drug. Smaller animals (n = 8, ≤ 32 kg, mean = 29.4 kg) had supraventricular dysrhythmias immediately after the ECD exposures. Larger animals (n = 8, > 68 kg, mean = 72.4) had only sinus tachycardia after the exposures. One of the smaller animals had frequent episodes of ventricular ectopy after two exposures, including runs of delayed onset, nonsustained six- to eight-beat unifocal and multifocal ventricular tachycardia that spontaneously resolved. This animal had significant ectopy prior to the exposures as well. Thoracotomy performed on three smaller animals demonstrated cardiac capture during ECD exposure consistent with previous animal studies. In the larger animals, none of the methamphetamine-intoxicated animals demonstrated cardiac capture. Two control sheep showed evidence of capture similar to the smaller animals. No ventricular fibrillation occurred after the exposure in any animal.
Conclusions: In smaller animals (32 kg or less), ECD exposure exacerbated atrial and ventricular irritability induced by methamphetamine intoxication, but this effect was not seen in larger, adult-sized animals. There were no episodes of ventricular fibrillation after exposure associated with ECD exposure in methamphetamine-intoxicated sheep.
ACADEMIC EMERGENCY MEDICINE 2010; 17:436–443 © 2010 by the Society for Academic Emergency Medicine