Dennis Andrew J, Valentino Daniel J, Walter Robert J, Nagy Kimberly K, Winners Jerry, Bokhari Faran, Wiley Dorion E, Joseph Kimberly T, Roberts Roxanne R
Department of Trauma, Stroger Hospital of Cook County, Rush University Medical Center, Chicago, Illinois, USA.
J Trauma. 2007 Sep;63(3):581-90. doi: 10.1097/TA.0b013e3180683c16.
Very little objective laboratory data are available describing the physiologic effects of stun guns or electromuscular incapacitation devices (EIDs). Unfortunately, there have been several hundred in-custody deaths, which have been temporally associated with the deployment of these devices. Most of the deaths have been attributed to specific cardiac and metabolic effects. We hypothesized that prolonged EID exposure in a model animal system would induce clinically significant metabolic acidosis and cardiovascular disturbances.
Using an Institutional Animal Care and Use Committee-approved protocol, 11 standard pigs (6 experimentals and 5 sham controls) were anesthetized with ketamine and xylazine. The experimentals were exposed to two 40-second discharges from an EID (TASER X26, TASER Intl., Scottsdale, AZ) across the torso. Electrocardiograms, blood pressure, troponin I, blood gases, and electrolyte levels were obtained pre-exposure and at 5, 15, 30, and 60 minutes and 24, 48, and 72 hours postdischarge. p values <0.05 were considered significant.
Two deaths were observed immediately after TASER exposure from acute onset ventricular fibrillation (VF). In surviving animals, heart rate was significantly increased and significant hypotension was noted. Acid-base status was dramatically affected by the TASER discharge at the 5-minute time point and throughout the 60-minute monitoring period. Five minutes postdischarge, central venous blood pH (6.86 +/- 0.07) decreased from baseline (7.45 +/- 0.02; p = 0.0004). Pco2 (94.5 mm Hg +/- 14.8 mm Hg) was significantly increased from baseline (45.3 mm Hg +/- 2.6 mm Hg) and bicarbonate levels significantly decreased (15.7 mmol/L +/- 1.04 mmol/L) from baseline (30.4 mmol/L +/- 0.7 mmol/L). A large, significant increase in lactate occurred postdischarge (22.1 mmol/L +/- 1.5 mmol/L) from baseline (1.5 mmol/L +/- 0.3 mmol/L). All values returned to normal by 24 hours postdischarge in surviving animals. A minor, nonsignificant increase in troponin I was seen at 24 hours postdischarge (0.052 ng/mL +/- 0.030 ng/mL, mean +/- SEM).
Immediately after the discharge, two deaths occurred because of ventricular fibrillation. In this model of prolonged EID exposure, clinically significant acid-base and cardiovascular disturbances were clearly seen. The severe metabolic and respiratory acidosis seen here suggests the involvement of a primary cardiovascular mechanism.
关于电击枪或肌肉麻痹装置（EIDs）的生理效应，现有的客观实验室数据非常少。不幸的是，已有数百起在押人员死亡事件，这些事件在时间上与这些装置的使用相关。大多数死亡归因于特定的心脏和代谢效应。我们假设在模型动物系统中长时间暴露于EID会诱发具有临床意义的代谢性酸中毒和心血管紊乱。
采用经机构动物护理和使用委员会批准的方案，用氯胺酮和赛拉嗪对11头标准猪（6头实验猪和5头假对照猪）进行麻醉。实验猪的躯干接受来自EID（泰瑟X26，泰瑟国际公司，亚利桑那州斯科茨代尔）的两次40秒放电。在暴露前以及放电后5、15、30和60分钟以及24、48和72小时获取心电图、血压、肌钙蛋白I、血气和电解质水平。p值<0.05被认为具有统计学意义。
电击枪暴露后立即观察到两例因急性心室颤动（VF）死亡。在存活的动物中，心率显著增加，出现明显的低血压。在5分钟时间点以及整个60分钟监测期内，电击枪放电对酸碱状态有显著影响。放电后5分钟，中心静脉血pH值（6.86±0.07）从基线值（7.45±0.02；p = 0.0004）下降。二氧化碳分压（94.5 mmHg±14.8 mmHg）较基线值（45.3 mmHg±2.6 mmHg）显著升高，碳酸氢盐水平较基线值（30.4 mmol/L±0.7 mmol/L）显著降低（15.7 mmol/L±1.04 mmol/L）。放电后乳酸水平较基线值（1.5 mmol/L±0.3 mmol/L）大幅显著升高（22.1 mmol/L±1.5 mmol/L）。存活动物在放电后24小时所有值均恢复正常。放电后24小时肌钙蛋白I有轻微、无统计学意义的升高（0.052 ng/mL±0.030 ng/mL，平均值±标准误）。
放电后立即有两例因心室颤动死亡。在这个长时间暴露于EID的模型中，明显观察到具有临床意义的酸碱和心血管紊乱。此处所见的严重代谢性和呼吸性酸中毒提示存在原发性心血管机制。
