OBJECTIVE: Electromuscular incapacitation (EMI) devices are being used and evaluated by both military and law enforcement agencies. Although the gross muscular response is obvious, physiological responses to these devices are poorly understood. We hypothesized that the intense, repetitive, muscle contractions evoked by EMI devices would cause dose-dependent metabolic acidosis, accompanied by neuromuscular or cardiac injury. METHODS: Using an approved protocol, 26 Yucatan mini-pigs (22 experimental animals and 4 control animals) were anesthetized with ketamine and xylazine. Experimental animals were exposed to MK63 (Aegis Industries, Bellevue, Idaho) discharges over the left anterior hind limb for 10, 20, 40, or 80 seconds. Electrocardiograms, electromyograms, troponin I levels, blood gas values, and electrolyte levels were recorded before and 5, 15, 30, and 60 minutes and 24, 48, and 72 hours after discharge. Skin, muscle, and nerve biopsies were taken from the shocked and contralateral sides. RESULTS: Core body temperature significantly decreased (1.0-1.5 degrees C) in all shocked animals but not in sham-treated control animals. No cardiac dysrhythmias or deaths were seen, and heart rate was unaffected. No clinically significant changes were seen in troponin I, myoglobin, or creatine kinase-MB levels. Central venous blood pH decreased, whereas carbon dioxide pressure and lactate levels increased for 60 minutes after discharge. All values returned to normal by 24 hours after discharge, and no significant histological or electromyographic changes were found. CONCLUSIONS: Changes in blood chemistry were observed but were of little clinical significance, and no neuromuscular damage was detected. Therefore, within the limitations of this model, it appears that EMI can safely be achieved by using this device, even for lengthy periods, without causing significant injury.
OBJECTIVE: Electromuscular incapacitation (EMI) devices are being used and evaluated by both military and law enforcement agencies. Although the gross muscular response is obvious, physiological responses to these devices are poorly understood. We hypothesized that the intense, repetitive, muscle contractions evoked by EMI devices would cause dose-dependent metabolic acidosis, accompanied by neuromuscular or cardiac injury. METHODS: Using an approved protocol, 26 Yucatan mini-pigs (22 experimental animals and 4 control animals) were anesthetized with ketamine and xylazine. Experimental animals were exposed to MK63 (Aegis Industries, Bellevue, Idaho) discharges over the left anterior hind limb for 10, 20, 40, or 80 seconds. Electrocardiograms, electromyograms, troponin I levels, blood gas values, and electrolyte levels were recorded before and 5, 15, 30, and 60 minutes and 24, 48, and 72 hours after discharge. Skin, muscle, and nerve biopsies were taken from the shocked and contralateral sides. RESULTS: Core body temperature significantly decreased (1.0-1.5 degrees C) in all shocked animals but not in sham-treated control animals. No cardiac dysrhythmias or deaths were seen, and heart rate was unaffected. No clinically significant changes were seen in troponin I, myoglobin, or creatine kinase-MB levels. Central venous blood pH decreased, whereas carbon dioxide pressure and lactate levels increased for 60 minutes after discharge. All values returned to normal by 24 hours after discharge, and no significant histological or electromyographic changes were found. CONCLUSIONS: Changes in blood chemistry were observed but were of little clinical significance, and no neuromuscular damage was detected. Therefore, within the limitations of this model, it appears that EMI can safely be achieved by using this device, even for lengthy periods, without causing significant injury.