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The Physiologic Effects of a Conducted Electrical Weapon in Swine
TRAUMA/ORIGINAL RESEARCH
The Physiologic Effects of a Conducted Electrical Weapon in Swine Amanda O. Esquivel, MS Elizabeth J. Dawe, DVM Javier A. Sala-Mercado, MD, PhD Robert L. Hammond, PhD Cynthia A. Bir, PhD
From Biomedical Engineering, College of Engineering (Esquivel, Bir), Surgical Research Services, College of Medicine (Dawe), and Physiology, School of Medicine (Sala-Mercado, Hammond), Wayne State University, Detroit, MI.
Study objective: By using an animal model, we determine whether repeated exposures to a conducted electrical weapon could have physiologic consequences. Methods: Exposures to the Stinger S-400 conducted electrical weapon were applied to 10 healthy, anesthetized, Yorkshire-cross, male swine by attaching probes from the cartridge to the sternal notch and anterolateral thorax at a distance of 21.5 cm. The standard pulse generated by the Stinger S400 during the normal application was applied 20 times during 31 minutes. To evaluate the health effects of the exposures, key physiologic characteristics were evaluated, including arterial pH, PCO2, PO2, blood lactate, cardiac output, ECG, pulse rate, mean arterial pressure, central venous pressure, pulmonary artery pressure and airway pressure, and the cardiac marker troponin I. Results: There were notable changes in pH, PCO2, blood lactate, cardiac output, and mean arterial pressure after 1 or more sets of exposures, all of which normalized during the next few hours. Troponin I, PO2, pulse rate, mean arterial pressure, central venous pressure, pulmonary artery pressure, and airway pressure did not change markedly during or after the shocks. Three premature ventricular contractions occurred in one animal; all other ECG results were normal. Conclusion: Repeated exposures to a conducted electrical weapon result in respiratory acidosis, metabolic vasodilation, and an increase in blood lactate level. These effects were transient in this study, with full recovery by 4 hours postexposure. The Stinger S-400 appears to have no serious adverse physiologic effects on healthy, anesthetized swine. [Ann Emerg Med. 2007;50:576-583.] 0196-0644/$-see front matter Copyright © 2007 by the American College of Emergency Physicians. doi:10.1016/j.annemergmed.2007.05.003
INTRODUCTION Background Law enforcement and military agencies are increasingly called on to neutralize potentially life-threatening situations without using lethal force. As a result, these agencies have experimented with and deployed to various degrees a number of presumably less-lethal weapons. There are several different types of lesslethal technologies that are being developed and used; one type is a conducted electrical weapon. These weapons deliver brief pulses of high-voltage electricity across wires, using the human body to complete the circuit. This voltage is pulsed and variable, depending on the resistance in the skin layers. The goal is to contract skeletal muscle, rendering the individual motionless and dispensing pain, which assists with submission. 576 Annals of Emergency Medicine
Initial concerns about the safety of these devices were raised because of the lack of adequate investigations.1-3 The most recent of these was a 2005 report by the Canadian Police Research Center, which found that 151 deaths in North America occurred after the use of a conducted electrical weapon.1-3 A medical panel reviewed these cases and consistently found that the cause of death was multifactorial rather than attributable to the conducted electrical weapon alone.3 To examine the relationship between conducted electrical weapon use and blood gas variations, it was recommended that blood pH, carbon dioxide, and “other factors” be analyzed.3 These concerns have prompted the need to assess the physiologic effect of such devices in a controlled environment. Volume , . : November
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Physiologic Effects of Conducted Electrical Weapons Editor’s Capsule Summary
What is already known on this topic Case reports of individuals who died in police custody after receiving electroshocks have raised questions about the safety of the law enforcement devices that deliver these shocks. What question this study addressed How devices designed to provide “neuromuscular incapacitation” by electric shock affect physiologic characteristics. What this study adds to our knowledge After being subjected to 20 shocks, 10 healthy pigs experienced transient respiratory acidosis, metabolic vasodilation, and an increased concentration of blood lactate. All normalized during the next hour. How this might change clinical practice This trial should not change clinical practice, because it is a first-phase investigation in an animal model.
Recently, a new conducted electrical weapon was developed by Stinger Systems, Inc. (Tampa, FL). The Stinger S-400 device varies from the previously tested TASER X26 in a variety of ways, including peak voltage, pulse duration, energy per pulse, and total power output. Importance Preliminary research about the use of conducted electrical weapons has provided brief insights into the potential concerns related to the use of these devices for less-lethal applications.4-9 An early investigation evaluated patients exposed to a Taser device by police and found several complications, including torsion of the testis (0.5%), minor rhabdomyolysis (1%), and lacerations, abrasions, and contusions (38%).9 McDaniel et al6 completed a trial with 10 animals and examined the cardiovascular responses to the device only; pulmonary or blood chemistry information was not garnered. A more detailed study probed the potential physiologic responses resulting from TASER X26 applications.5 The data showed an increased blood lactate and pCO2 level and a decrease in blood pH after the exposures.5 Because this study collected data only for 60 minutes after the exposures, it was unable to determine when these physiologic characteristics returned to baseline. Changes in troponin I level were not statistically significant.5 However, cardiac markers are not increased in such a short time (60 minutes).10 One human study, conducted at the TASER International training facility, examined the cardiac effects of 1 TASER X26 application to 66 adult human subjects.11 These subjects were monitored for 24 hours after the exposure. This study concluded that there were no adverse cardiologic effects. Volume , . : November
However, this study examined the effects of 1 exposure and not the cumulative effects of several exposures. Goals of This Investigation Given the current controversy surrounding the use of conducted electrical weapons and differences between the previously tested TASER X26 and the newly manufactured Stinger S-400, the current study was conducted. The goal of this investigation was to determine whether repeated exposures to this device had adverse cardiac or pulmonary effects in an anaesthetized swine model as a surrogate for the healthy, resting adult man.
MATERIALS AND METHODS Study Design All animals were sedated with an intramuscular injection of a combination of 0.02 mg/kg atropine (international nonproprietary names atropine), 1.1 mg/kg acepromazine (international nonproprietary names acepromazine), and 22 mg/kg ketamine (international nonproprietary names ketamine). A catheter was inserted into the ear vein for intravenous access, and 6.6 mg/kg thiopental sodium (international nonproprietary names thiopental sodium) was administered as needed. After endotracheal intubation, anesthesia was maintained with 2% to 3% isoflurane (international nonproprietary names isoflurane). A Norm-OTemp Model 11 warming mat (Cincinnati Sub-Zero Products, Cincinnati, OH) was placed under the animal to maintain a normal body core temperature (assessed by a rectal thermometer). Ventilation was controlled with a HEMC Model 2000 volume ventilator (Hallowell EMC, Pittsfield, MA) initially set at a respiratory rate of 12 breaths/min and a tidal volume of 10 to 15 mL/kg. The baseline ventilatory settings were established by serial arterial blood gas analyses. Lactated Ringer’s injection (Baxter Healthcare Corporation, Deerfield, IL) was given intravenously at 5 mL/kg per hour. Under a surgical plane of anesthesia, the right carotid artery and right external jugular vein were surgically exposed. The right carotid artery was cannulated with a Tygon S-54-HL 20gauge flexible plastic-tubing catheter (Norton Performance Plastics Company, Akron, OH) for systemic arterial blood pressure and blood samples. A 7-Fr Swan Ganz thermodilution catheter (Edwards Lifesciences, Irvine, CA) was inserted into the right external jugular vein to measure cardiac output, central venous pressure, and pulmonary arterial pressure. The catheters were connected to an Abbott Transpac IV pressure transducer (Abbott Laboratories, Ontario, Canada). A cardiac output computer (American Edwards Laboratory 9520A) was used to determine cardiac output by thermodilution. ECG electrodes were secured on the distal aspect of all 4 extremities, whereas the leads and transducers were connected to the appropriate signal conditioners (Gould 2600S recorder; Gould Instruments, Valley View, OH). The data were recorded digitally and stored for subsequent analysis at a sample rate of 200 to 300 Hz (Dataq Instruments, Akron, OH). Annals of Emergency Medicine 577
Physiologic Effects of Conducted Electrical Weapons A washout period of 2.25 to 2.50 hours was used between the use of the induction agents and application of the conducted electrical weapon to minimize their effects. Exposures were applied to the specimen by attaching probes from the cartridge to the sternal notch and anterolateral thorax at a distance of 21.5 cm. The standard pulse generated by the conducted electrical weapon during the normal application was applied. A total of 20 exposures, 4 sets of 5 exposures 5 minutes apart, were applied to each specimen to evaluate any cumulative effects. Each exposure within the set of 5 was given 1 minute apart. Selection of Participants Before commencement of the study, approval was garnered from the Institutional Animal Care and Use Committee. All procedures involving animals were in compliance with the Guide for the Care and Use of Laboratory Animals, prepared by the National Academy of Sciences and published by the National Institutes of Health (NIH publication No. 85-23, revised 1996). All animals were obtained, housed, and tested in an Association for Assessment of Laboratory Animal Care International–accredited facility. A power analysis was conducted to determine the appropriate sample size, using cardiac output as the measured outcome. Based on an expected minimum difference of 20% (5% SD), a total of 10 animals were used, for a power of 0.998. Ten Yorkshire-cross male swine (Sus scrofa domestica), with an average weight of 42.6 kg⫾2.0 kg, were included in the study. The size of the pigs was chosen to reflect a similar size in heart and torso to the adult man.12 The use of this animal model for this type of evaluation has been previously established.5-8 Two additional animals were included, one as a “sham” (45.4 kg) to observe the effects of anesthesia and surgical instrumentation only and another (41.4 kg) subjected to an infarction to investigate the sensitivity of troponin I detection. Methods of Measurement To evaluate the health effects of the exposures, key physiologic characteristics were evaluated. These included pH, PCO2, PO2, blood lactate level, cardiac output, ECG, pulse rate, mean arterial pressure, central venous pressure, pulmonary artery pressure and airway pressure monitoring, and the cardiac marker troponin I. To monitor pH, PCO2, PO2, and lactate levels, 1 mL of blood was drawn from the carotid artery after each set of 5 exposures and at hourly intervals thereafter. Cardiac output was recorded after each set of 5 exposures and again after 4 hours. Troponin I levels were also monitored with 3 mL of arterial whole blood after all 20 exposures and again at 1-, 2-, 3-, and 4-hour postexposure intervals, using the RAMP System (Response Biomedical Corporation, British Columbia, Canada). Cardiac and pulmonary characteristics, including cardiac output, ECG monitoring, pulse rate, mean arterial pressure, central venous pressure, pulmonary artery pressure, and airway pressure, are common measurements used to assess cardiovascular and pulmonary physiologic conditions. Cardiac 578 Annals of Emergency Medicine
Esquivel et al and pulmonary monitoring was continued throughout the entire testing period. To further evaluate cardiac safety, pathologic and histopathologic assessments were conducted on each of the 10 hearts and the sham heart postmortem. Incisions were made in each heart from the apex, creating 4 sections (apex⫽section 1). Tissue was extracted from the anterior wall of the left ventricle in section 2, the septum of section 3, and the posterior wall of the left ventricle in section 4. The tissue was stained using hematoxylin and eosin and Masson’s trichrome methods and examined microscopically. The assay identified to measure troponin I values had previously been used on humans only, and its cross-reactivity with swine needed to be evaluated. To determine whether the troponin I levels were accurately predicting the presence of myocardial injury in swine, a coronary occlusion to the distal segment of the left anterior descending coronary artery was performed on 1 Yorkshire-cross female swine weighing 41.4 kg before all testing. An angioplasty balloon catheter (2-mm diameter; 15-mm length) was advanced over a 0.014-inch guidewire (0.08 inch diameter; 0.59 inch length) to the distal segment of the left anterior descending coronary artery. After a 50-mg intravenous lidocaine bolus, the balloon was inflated at 4 bars to occlude coronary flow in this segment. Through a guiding catheter positioned into the left coronary ostium intracoronary, injection of contrast medium (Ioversol) was performed to confirm the absence of flow distal to the balloon. The balloon was deflated after 1 hour of occlusion. Three milliliters of arterial blood to record blood gas levels and troponin I were drawn at 1-hour intervals for 4 hours postocclusion. This procedure has been validated, and detailed methods are provided in previous studies.13,14 One sham animal was included to examine the effects of the anesthetic agents. The same induction agents and anesthesia were used, along with the surgical instrumentation described above. Three milliliters of arterial blood to analyze blood gas levels and troponin I were drawn at 1-hour intervals for 4 hours. The animal was not subjected to any exposures by the Stinger S-400 and was killed 4 hours after surgery. Primary Data Analysis Data collected from the whole-blood samples of the exposed animals for pH, PCO2, PO2, lactate level, and troponin I level were evaluated by MANOVA (P⬍.05) to determine statistical significance. Cardiac output was recorded 3 times at each point, the average of the 3 values was recorded as the cardiac output for that point, and those values were analyzed by MANOVA for statistical significance. Pulse rate, central venous pressure, pulmonary artery pressure, and airway pressure were continuously monitored and were evaluated by taking an average of 10 to 20 seconds of data at baseline after each set of exposures and at 30-minute intervals for 4 hours after the exposures. The goal was to average 20 seconds of data; however, this was not always possible, because of the effects of the device on the data acquisition system. These averages were recorded at Volume , . : November
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Table. Baseline physiologic values.
Specimen
Arterial pH
Arterial PCO2, mm Hg
Sham Mean, exposed animals SD, exposed animals Range, exposed animals Normal value, mean Normal range
7.42 7.45 0.02 7.43–7.49 7.48 7.4–7.53
45 41 2 38–44 40 35–44
Lactate, mM/L
Cardiac Index, mL/min/kg
Total Peripheral Resistance, mm Hg/L/min
Mean Arterial Pressure
NA 1.3 0.4 0.7–2.1 1.0 0.5–1.5
127 109 20 84–150 147 123–188
11.1 14.4 2.1 11.4–17.3 NA NA
64 66 8 57–76 102 86–123
NA, Not applicable. Average baseline values for arterial pH, PCO2, and lactate and baseline values for cardiac index, total peripheral resistance, and mean arterial pressure for exposed animals and 1 sham animal. Also shown are normal values for conscious swine and the range.15
a baseline level, before and after each set of exposures, and every half hour for 4 hours. Values were also recorded for the sham animal at baseline and at 30-minute intervals for 4 hours. These data were then analyzed by MANOVA (P⬍.05) to determine statistical significance. Pairwise comparisons were made between the baseline values and the values at all other points (P⬍.05) with the Sidak’s correction for preventing inflation of type I errors. All statistics were completed with SPSS 14.0 for Windows (SPSS, Inc., Chicago, IL). ECG recordings for each animal were evaluated by a cardiologist for abnormalities.
RESULTS Main Results Baseline values for pH, PO2, PCO2, lactate, cardiac output, total peripheral resistance, and mean arterial pressure were recorded for each animal and compared with normal values previously reported for conscious swine15 (Table). All values for pH and PCO2 for this study were in the normal range. Approximately half the values recorded at baseline for lactate and cardiac index were in the normal range. All the values for MAP were below the normal range. The coronary occlusion substudy produced an infarction that induced an increase of 0.6 ng/mL in troponin I 4 hours after occlusion (Figure 1). This increase was greater than any change in troponin I level for this study. There was no statistically significant change in troponin I level at any point after the exposures (Figure 1). Three isolated premature ventricular contractions were observed in one specimen at 16, 99, and 117 minutes after the first exposure. Contractions were not observed in any subsequent tests. The remainder of the ECG results was normal. Cardiac index increased continuously after each set of the first 3 sets of exposures (Figure 2). The increase in cardiac index after each set of exposures was statistically different from the baseline value. Although the average value was slightly increased after 4 hours, it was not statistically different from the baseline value. The mean arterial pressure was statistically different from the baseline after the first set of exposures (Figure 3). In between each set, it increased to or above the baseline level and decreased Volume , . : November
Figure 1. Values of troponin I at baseline (time 0), after all exposures, and at rest 4 hours (60-minute intervals) after the exposures for exposed animals (white bars), a sham animal (black bars), and the animal subjected to an infarction (gray bars). Error bars are ⫹/⫺ one standard deviation from the mean.
after each set of exposures, although these changes were not statistically significant. There was a steady decrease in pressure after all exposures were given. The total peripheral resistance was calculated by dividing the mean arterial pressure by the cardiac output (Figure 2). This value decreased significantly after the first set of exposures and was still significantly different from the baseline value 4 hours after the last exposure. All values measured were included in the statistical analysis for pH, PCO2, and lactate. Two data points for 1 animal were not recorded for PO2, because of equipment malfunction. The data were graphed, showing the mean values ⫾1 SD from the mean. The pH decreased significantly during the exposures (Figure 4). The average lowest value for pH was 7.34, which occurred after the third set of exposures. It had the greatest relative decrease after the first 5 exposures. There was no significant difference between the baseline value and the value 1 hour after exposures. Annals of Emergency Medicine 579
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Figure 2. Values of cardiac index and total peripheral resistance at baseline (time 0), after each set of exposures, and at rest 4 hours after the exposures for exposed animals (white bars) and a sham animal (black bars). Error bars are ⫹/⫺ one standard deviation from the mean.
Figure 4. Values of pH, PCO2, and lactate at baseline (time 0) after each set of exposures and at rest for 4 hours (60-minute intervals) after the exposure for exposed animals (white bars) and a sham animal (black bars). Error bars are ⫹/⫺ one standard deviation from the mean.
Figure 3. Value of mean arterial pressure at baseline (time 0), after each set of exposures, and at rest for 4 hours (30-minute intervals) after the exposures for exposed animals (white bars) and a sham animal (black bars). Error bars are ⫹/⫺ one standard deviation from the mean.
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The carbon dioxide pressure increased significantly during the exposures (Figure 4) to 52.5 mm Hg. It had the greatest relative increase after the first 5 exposures. It returned to the normal range 2 hours after the last exposure, although it was still statistically increased from the baseline value and continued to decrease slightly until the end of the experiment. Blood lactate values increased significantly after the first set of exposures (Figure 4). These levels increased cumulatively with each set of exposures up until 15 exposures to 4.0 mmol/L and then exhibited a slight decreasing trend to 3.5 mmol/L, although it was still statistically increased from baseline. There Volume , . : November
Esquivel et al was no statistically significant difference between the baseline value and the values obtained 1 hour after the exposures. In addition to troponin I, there was no statistically significant change measured in oxygen pressure, pulse rate, mean arterial pressure, central venous pressure, pulmonary artery pressure, and airway pressure. All values remained statistically unchanged from the baseline at all points. Gross examination of the hearts did not reveal any damage, and histopathologic analysis of the anterior wall of the left ventricle, septum, and posterior wall of the left ventricle did not show any structural changes in any animals.
LIMITATIONS The size of the animal has been shown to affect the safety of the conductive conducted electrical weapon. One previous study outlined above showed a strong correlation between size and the safety of the device; as the size of the animal decreased, the “safety index” decreased,3 which indicates that these devices, although safe to use on healthy average-sized adults, could have more serious health effects on small adults or children. A study examining the effect of size on the safety of conducted electrical weapons should be completed. This study examined the effects of a conducted electrical weapon on healthy, anesthetized animals. It is possible that persons with cardiac abnormalities or arrhythmias could exhibit a more serious response to the device. In addition, normal aging and other underlying cardiac or pulmonary disturbances such as coronary artery disease, congestive heart failure, chronic obstructive pulmonary disease, or other chronic health issues may also have a contributing effect. Persons who are subjected to repeated exposures of a conducted electrical weapon are most likely in an agitated or combative state. This stimulation could lead to a phenomenon known as excited delirium, defined as the onset of a temporary disruption in awareness and cognition, along with aggressive or violent actions.16 Most cases are associated with methamphetamine or cocaine drug use, whereas some are related to mental illness.16 The types of physiologic effects resulting from the combination of excited delirium and the use of conducted electrical weapons are unknown. Some signs used to describe excited delirium include an increased pulse rate, hyperthermia, hypotension, dehydration, and catecholamine release, causing added stress on the heart.16 In addition, strenuous physical activity (eg, struggle with or running from police) has been shown to cause an increase in norepinephrine and epinephrine, as well as stimulation of ␣- and -receptors.16 Two studies have tested a conducted electrical weapon on swine in an abnormal state.7,8 Lakkireddy et al7 examined the effects of a single high dose (8 mg/kg) of cocaine given during a 30minute period before conducted electrical weapon exposure. They found that exposure to cocaine and a conducted electrical weapon did not cause ventricular fibrillation.7 A single dose of cocaine may not capture the effects observed in the field on habitual cocaine users. Nanthakumar et al8 investigated the cardiac effect of a pharmacologic stress (infusion of epinephrine) Volume , . : November
Physiologic Effects of Conducted Electrical Weapons with conducted electrical weapon exposure. The authors found that this corresponded with episodes of tachycardia and ventricular fibrillation.8 Future research should include a more comprehensive model to study the exposure to a conducted electrical weapon in a physiologic stressful state. The repeated use of this device on an animal in a conscious state would impose unnecessary pain and suffering, so anesthesia was imperative. The use of ventilation and anesthesia in this study may have limited the effects of the conducted electrical weapon on the animals by minimizing the hypoventilation that occurs during conducted electrical weapon exposure and possibly diminishing any compensatory hyperventilatory response to increased pCO2 afterward.
DISCUSSION There were several metabolic changes that occurred during the study, including an increase in cardiac output caused by the exercise-like nature of the muscle contractions induced by the device. Metabolic vasodilation was observed and caused a decrease in total peripheral resistance and mean arterial pressure after each set of exposures. In addition, lactic acid, a by-product of energy production during exercise, increased during the exposures. There was not a clear pattern of change in troponin I level for the exposed animals of this study. The maximum change between a baseline value and one observed after the exposures was 0.16 ng/mL. This value was well below the increase observed in the infarcted animal. Seventy percent of the animals had no change from the baseline level at 4 hours postexposure. The sensitivity of the assay technique for the troponin I level was confirmed for the species tested by a coronary occlusion technique to create a known infarct. The tetanic muscle contractions that were created with the application of the device during this experiment are similar to those observed during exercise and therefore created a similar physiologic response. Hastings et al17 reported cardiac indices of 238 mL/kg per minute for “steady-state” exercise and 274 mL/ kg per minute for exhaustive exercise in pigs. The highest value recorded for any animal was 190 mL/kg per minute, whereas the average value after 3 sets of exposures was 132 mL/kg per minute. It was also reported by Hastings et al17 that during steady-state exercise the swine pH dropped from 7.5 to 7.48 and to 7.35 during exhaustive exercise, and the lactic acid values increased from 2.0 mM/L preexercise to 17.8 mM/L postexercise. For this study, the average pH decreased to 7.34 during the exposures, whereas the lactic acid level increased to 3.99 mM/L, indicating that for this study the effect of the conducted electrical device on these factors was less than that of either steady state or exhaustive exercise. The animals became slightly hypotensive immediately after each set of exposures because of a decrease in total peripheral resistance (vasodilation). A compensatory increase in cardiac output was observed because of this decrease in vascular resistance. During the 5-minute recovery period before the next Annals of Emergency Medicine 581
Physiologic Effects of Conducted Electrical Weapons set of exposures, vasoconstriction began to occur and the blood pressure returned to baseline or slightly increased levels. During the 4 hours after the exposures, the animals exhibited additional hypotensive behavior. Isoflurane, the anesthesia used, has been shown to produce a decrease in mean arterial pressure. One study examining the cardiovascular effects of anesthesia on human volunteers showed a decrease from 85 mm Hg to 55 mm Hg.18 The decrease in mean arterial pressure because of isoflurane is caused by the decrease in vascular resistance and not the cardiac output. Because of the effect of isoflurane on vascular resistance, and in turn mean arterial pressure, the total peripheral resistance did not return to the baseline value 4 hours after the exposures. In addition, the one animal subjected to the surgery and 4-hour anesthetic period only (sham) exhibited a decrease in mean arterial pressure similar in magnitude to that of the exposed animals. Therefore, we speculate that this finding was an effect of the anesthesia and not the exposures. The baseline PCO2 values recorded were within the normal average values previously reported for swine (35 mm Hg to 44 mm Hg).15 The average PCO2 increased from 41.4 mm Hg to 52.5 mm Hg. The PCO2 did not return to the baseline value within the 4 hours of the study. However, it did return to near normal after 1 hour and continued to decrease for the duration of the study to 43.6 mm Hg. Visual observation of the animals during exposures showed that the muscle contractions caused impaired ventilation. When ventilation is impaired, the lungs do not eliminate carbon dioxide as quickly as the body produces it, leading to a buildup in the tissues. The decrease in pH, combined with an increase in carbon dioxide pressure, indicates acute respiratory acidosis.19 The normal physiologic values previously reported for arterial blood pH in conscious pigs (7.4 to 7.53) is higher than that of humans (7.35 to 7.45).15 Jauchem et al5 reported an average decrease in pH from 7.4 to 7.0 after Taser exposure. These values did not return to baseline within the 1-hour period of the experiment. The pH values from this study did not decrease at same rate as those reported by Jauchem et al.5 However, a decrease in pH to 7.34 may still be physiologically significant because of the slightly more basic normal pH value of the pig. In the current study, arterial blood pH was not significantly different from the baseline value 1 hour after the last set of exposures. The difference in values between the current study and that by Jauchem et al5 could be attributed to the difference in protocols and timing and total number of exposures. Although the swine in the Jauchem et al5 study were exposed 18 times in 3 minutes, the current study used a total of 20 exposures in 31 minutes, which could have allowed the animals to recover between exposures. Blood lactate levels increased cumulatively with each set of exposures until 15 exposures. The relative greatest increase was observed between the baseline and after the first 5 exposures. A decrease was observed after the third set of exposures. This decrease is due to the onset of acute respiratory acidosis. Several studies examining the effect of respiratory acidosis on blood 582 Annals of Emergency Medicine
Esquivel et al lactate increases during exercise found that subjects breathing 5% carbon dioxide in air to induce respiratory acidosis had lower blood lactate values compared with subjects who breathed normal air.19,20 Jauchem et al5 recorded lactate values exceeding 15 mmol/L. The highest value observed in this study was 6.52 mmol/L, whereas on average the increase was to 3.99 mmol/L. Again, this difference could either be a function of the device used (Taser versus Stinger S-400) or the difference in protocol. Blood lactate levels in the current study returned to baseline 2 hours postexposure. In summary, according to this analysis of the data for the characteristics studied, the Stinger S-400 appears to have no serious adverse physiologic effects in healthy anesthetized pigs. Changes in pH, carbon dioxide pressure, and blood lactate level were observed but decreased to baseline or very near it within the 4-hour period of the experiment. The animals did become acidotic after the exposures but returned to normal after 1 hour. Cardiac index increased after each set of exposures, but this increase was less than that recorded for strenuous exercise. Other cardiac characteristics, including the biologic marker troponin I and ECG recordings, did not show any significant irregularities. It is unlikely that exposures from the Stinger S-400 conducted electrical weapon would cause cardiac damage to healthy, resting adults, and any changes in other metabolic factors seem to mimic those of exercise. However, the combination of a physiologic stressful state such as agitation or strenuous physical activity, along with the use of a conducted electrical weapon, could lead to further acidosis or impaired respiration. We thank the Ballistics Group in the Department of Biomedical Engineering at Wayne State University, especially Marianne Wilhelm, PhD, Hai-chun Chen, MS, Erin Hanlon, MS, and Samantha Staley, BS, for their assistance. In addition, we would like to thank Petar Prcevski, MD, for performing the coronary artery occlusion and Donna Shepherd, LVT, and Janine Matthei, LVT, for surgical support. We thank Bulent Ozkan, MA, for his statistical analysis of the results. Supervising editor: Stephen R. Thom, MD, PhD Author contributions: CAB conceived the study and obtained research funding. EJD, RLH, and CAB designed the trial. AOE, EJD, JAS-M, and RLH supervised the conduct of the trial and data collection. AOE and RLH collected the data. AOE analyzed the data. JAS-M examined the ECGs. AOE drafted the article, and all authors contributed substantially to its revision. AOE takes responsibility for the paper as a whole. Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article, that might create any potential conflict of interest. See the Manuscript Submission Agreement in this issue for examples Volume , . : November
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of specific conflicts covered by this statement. This study was supported by Stinger Systems Inc. for funding of the technical costs of the study. The authors had sole responsibility for the study design, data collection, data analysis, data interpretation, and preparation of the article. None of the authors have any financial interest in Stinger Systems Inc., nor have they received any financial support from Stinger Systems Inc. outside of the grant.
9. 10. 11.
Publication dates: Available online August 23, 2007.
12.
Address for reprints: Cynthia Bir, PhD, Biomedical Engineering, 818 W Hancock, Detroit, MI 48201; 313-577-3830, fax 313577-8333; E-mail [email protected].
13.
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incapacitating device discharges. J Am Coll Cardiol. 2006;48:798-804. Ordog GJ, Wasserberger J, Schlater T, et al. Electronic gun (Taser) injuries. Ann Emerg Med. 1987;16:73-78. Ammann P, Pfisterer M, Fehr T, et al. Raised cardiac troponins. BMJ. 2004;328:1028-1029. Ho JD, Miner JR, Lakireddy DR, et al. Cardiovascular and physiologic effects of conducted electrical weapon discharge in resting adults. Acad Emerg Med. 2006;13:589-595. Swindle MM, Smith AC. Comparative Anatomy and Physiology of the Pig. Beltsville, MD: United States Department of Agriculture; 2000. Spears JR, Henney C, Prcevski P, et al. Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction. J Invasive Cardiol. 2002;14:160-166. Spears JR, Prcevski P, Xu R, et al. Aqueous oxygen attenuation of reperfusion microvascular ischemia in a canine model of myocardial infarction. ASAIO J. 2003;49:716-720. Hannon JP, Bossone CA, Wade CE. Normal physiological values for conscious pigs used in biomedical research. Lab Anim Sci. 1990;40:293-298. Di Maio TG, Di Maio VJM. Excited Delirium Syndrome: Cause of Death and Prevention. Boca Raton, FL:Taylor & Francis Group; 2006. Hastings AB, White FC, Sanders TM, et al. Comparative physiological responses to exercise stress. J Appl Physiol. 1982; 52:1077-1083. Malan TP Jr, DiNardo JA, Isner RJ, et al. Cardiovascular effects of sevoflurane compared with those of isoflurane in volunteers. Anesthesiology. 1995;83:918-928. Ehrsam RE, Heigenhauser GJ, Jones NL. Effect of respiratory acidosis on metabolism in exercise. J Appl Physiol. 1982;53:6369. Kemp G. Lactate accumulation, proton buffering, and pH change in ischemically exercising muscle. Am J Physiol Regul Integr Comp Physiol. 2005;289:R895-R901; author reply R904-910.
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Annals of Emergency Medicine 583
The Physiologic Effects of a Conducted Electrical Weapon in Swine Amanda O. Esquivel, MS Elizabeth J. Dawe, DVM Javier A. Sala-Mercado, MD, PhD Robert L. Hammond, PhD Cynthia A. Bir, PhD
From Biomedical Engineering, College of Engineering (Esquivel, Bir), Surgical Research Services, College of Medicine (Dawe), and Physiology, School of Medicine (Sala-Mercado, Hammond), Wayne State University, Detroit, MI.
Study objective: By using an animal model, we determine whether repeated exposures to a conducted electrical weapon could have physiologic consequences. Methods: Exposures to the Stinger S-400 conducted electrical weapon were applied to 10 healthy, anesthetized, Yorkshire-cross, male swine by attaching probes from the cartridge to the sternal notch and anterolateral thorax at a distance of 21.5 cm. The standard pulse generated by the Stinger S400 during the normal application was applied 20 times during 31 minutes. To evaluate the health effects of the exposures, key physiologic characteristics were evaluated, including arterial pH, PCO2, PO2, blood lactate, cardiac output, ECG, pulse rate, mean arterial pressure, central venous pressure, pulmonary artery pressure and airway pressure, and the cardiac marker troponin I. Results: There were notable changes in pH, PCO2, blood lactate, cardiac output, and mean arterial pressure after 1 or more sets of exposures, all of which normalized during the next few hours. Troponin I, PO2, pulse rate, mean arterial pressure, central venous pressure, pulmonary artery pressure, and airway pressure did not change markedly during or after the shocks. Three premature ventricular contractions occurred in one animal; all other ECG results were normal. Conclusion: Repeated exposures to a conducted electrical weapon result in respiratory acidosis, metabolic vasodilation, and an increase in blood lactate level. These effects were transient in this study, with full recovery by 4 hours postexposure. The Stinger S-400 appears to have no serious adverse physiologic effects on healthy, anesthetized swine. [Ann Emerg Med. 2007;50:576-583.] 0196-0644/$-see front matter Copyright © 2007 by the American College of Emergency Physicians. doi:10.1016/j.annemergmed.2007.05.003
INTRODUCTION Background Law enforcement and military agencies are increasingly called on to neutralize potentially life-threatening situations without using lethal force. As a result, these agencies have experimented with and deployed to various degrees a number of presumably less-lethal weapons. There are several different types of lesslethal technologies that are being developed and used; one type is a conducted electrical weapon. These weapons deliver brief pulses of high-voltage electricity across wires, using the human body to complete the circuit. This voltage is pulsed and variable, depending on the resistance in the skin layers. The goal is to contract skeletal muscle, rendering the individual motionless and dispensing pain, which assists with submission. 576 Annals of Emergency Medicine
Initial concerns about the safety of these devices were raised because of the lack of adequate investigations.1-3 The most recent of these was a 2005 report by the Canadian Police Research Center, which found that 151 deaths in North America occurred after the use of a conducted electrical weapon.1-3 A medical panel reviewed these cases and consistently found that the cause of death was multifactorial rather than attributable to the conducted electrical weapon alone.3 To examine the relationship between conducted electrical weapon use and blood gas variations, it was recommended that blood pH, carbon dioxide, and “other factors” be analyzed.3 These concerns have prompted the need to assess the physiologic effect of such devices in a controlled environment. Volume , . : November
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Physiologic Effects of Conducted Electrical Weapons Editor’s Capsule Summary
What is already known on this topic Case reports of individuals who died in police custody after receiving electroshocks have raised questions about the safety of the law enforcement devices that deliver these shocks. What question this study addressed How devices designed to provide “neuromuscular incapacitation” by electric shock affect physiologic characteristics. What this study adds to our knowledge After being subjected to 20 shocks, 10 healthy pigs experienced transient respiratory acidosis, metabolic vasodilation, and an increased concentration of blood lactate. All normalized during the next hour. How this might change clinical practice This trial should not change clinical practice, because it is a first-phase investigation in an animal model.
Recently, a new conducted electrical weapon was developed by Stinger Systems, Inc. (Tampa, FL). The Stinger S-400 device varies from the previously tested TASER X26 in a variety of ways, including peak voltage, pulse duration, energy per pulse, and total power output. Importance Preliminary research about the use of conducted electrical weapons has provided brief insights into the potential concerns related to the use of these devices for less-lethal applications.4-9 An early investigation evaluated patients exposed to a Taser device by police and found several complications, including torsion of the testis (0.5%), minor rhabdomyolysis (1%), and lacerations, abrasions, and contusions (38%).9 McDaniel et al6 completed a trial with 10 animals and examined the cardiovascular responses to the device only; pulmonary or blood chemistry information was not garnered. A more detailed study probed the potential physiologic responses resulting from TASER X26 applications.5 The data showed an increased blood lactate and pCO2 level and a decrease in blood pH after the exposures.5 Because this study collected data only for 60 minutes after the exposures, it was unable to determine when these physiologic characteristics returned to baseline. Changes in troponin I level were not statistically significant.5 However, cardiac markers are not increased in such a short time (60 minutes).10 One human study, conducted at the TASER International training facility, examined the cardiac effects of 1 TASER X26 application to 66 adult human subjects.11 These subjects were monitored for 24 hours after the exposure. This study concluded that there were no adverse cardiologic effects. Volume , . : November
However, this study examined the effects of 1 exposure and not the cumulative effects of several exposures. Goals of This Investigation Given the current controversy surrounding the use of conducted electrical weapons and differences between the previously tested TASER X26 and the newly manufactured Stinger S-400, the current study was conducted. The goal of this investigation was to determine whether repeated exposures to this device had adverse cardiac or pulmonary effects in an anaesthetized swine model as a surrogate for the healthy, resting adult man.
MATERIALS AND METHODS Study Design All animals were sedated with an intramuscular injection of a combination of 0.02 mg/kg atropine (international nonproprietary names atropine), 1.1 mg/kg acepromazine (international nonproprietary names acepromazine), and 22 mg/kg ketamine (international nonproprietary names ketamine). A catheter was inserted into the ear vein for intravenous access, and 6.6 mg/kg thiopental sodium (international nonproprietary names thiopental sodium) was administered as needed. After endotracheal intubation, anesthesia was maintained with 2% to 3% isoflurane (international nonproprietary names isoflurane). A Norm-OTemp Model 11 warming mat (Cincinnati Sub-Zero Products, Cincinnati, OH) was placed under the animal to maintain a normal body core temperature (assessed by a rectal thermometer). Ventilation was controlled with a HEMC Model 2000 volume ventilator (Hallowell EMC, Pittsfield, MA) initially set at a respiratory rate of 12 breaths/min and a tidal volume of 10 to 15 mL/kg. The baseline ventilatory settings were established by serial arterial blood gas analyses. Lactated Ringer’s injection (Baxter Healthcare Corporation, Deerfield, IL) was given intravenously at 5 mL/kg per hour. Under a surgical plane of anesthesia, the right carotid artery and right external jugular vein were surgically exposed. The right carotid artery was cannulated with a Tygon S-54-HL 20gauge flexible plastic-tubing catheter (Norton Performance Plastics Company, Akron, OH) for systemic arterial blood pressure and blood samples. A 7-Fr Swan Ganz thermodilution catheter (Edwards Lifesciences, Irvine, CA) was inserted into the right external jugular vein to measure cardiac output, central venous pressure, and pulmonary arterial pressure. The catheters were connected to an Abbott Transpac IV pressure transducer (Abbott Laboratories, Ontario, Canada). A cardiac output computer (American Edwards Laboratory 9520A) was used to determine cardiac output by thermodilution. ECG electrodes were secured on the distal aspect of all 4 extremities, whereas the leads and transducers were connected to the appropriate signal conditioners (Gould 2600S recorder; Gould Instruments, Valley View, OH). The data were recorded digitally and stored for subsequent analysis at a sample rate of 200 to 300 Hz (Dataq Instruments, Akron, OH). Annals of Emergency Medicine 577
Physiologic Effects of Conducted Electrical Weapons A washout period of 2.25 to 2.50 hours was used between the use of the induction agents and application of the conducted electrical weapon to minimize their effects. Exposures were applied to the specimen by attaching probes from the cartridge to the sternal notch and anterolateral thorax at a distance of 21.5 cm. The standard pulse generated by the conducted electrical weapon during the normal application was applied. A total of 20 exposures, 4 sets of 5 exposures 5 minutes apart, were applied to each specimen to evaluate any cumulative effects. Each exposure within the set of 5 was given 1 minute apart. Selection of Participants Before commencement of the study, approval was garnered from the Institutional Animal Care and Use Committee. All procedures involving animals were in compliance with the Guide for the Care and Use of Laboratory Animals, prepared by the National Academy of Sciences and published by the National Institutes of Health (NIH publication No. 85-23, revised 1996). All animals were obtained, housed, and tested in an Association for Assessment of Laboratory Animal Care International–accredited facility. A power analysis was conducted to determine the appropriate sample size, using cardiac output as the measured outcome. Based on an expected minimum difference of 20% (5% SD), a total of 10 animals were used, for a power of 0.998. Ten Yorkshire-cross male swine (Sus scrofa domestica), with an average weight of 42.6 kg⫾2.0 kg, were included in the study. The size of the pigs was chosen to reflect a similar size in heart and torso to the adult man.12 The use of this animal model for this type of evaluation has been previously established.5-8 Two additional animals were included, one as a “sham” (45.4 kg) to observe the effects of anesthesia and surgical instrumentation only and another (41.4 kg) subjected to an infarction to investigate the sensitivity of troponin I detection. Methods of Measurement To evaluate the health effects of the exposures, key physiologic characteristics were evaluated. These included pH, PCO2, PO2, blood lactate level, cardiac output, ECG, pulse rate, mean arterial pressure, central venous pressure, pulmonary artery pressure and airway pressure monitoring, and the cardiac marker troponin I. To monitor pH, PCO2, PO2, and lactate levels, 1 mL of blood was drawn from the carotid artery after each set of 5 exposures and at hourly intervals thereafter. Cardiac output was recorded after each set of 5 exposures and again after 4 hours. Troponin I levels were also monitored with 3 mL of arterial whole blood after all 20 exposures and again at 1-, 2-, 3-, and 4-hour postexposure intervals, using the RAMP System (Response Biomedical Corporation, British Columbia, Canada). Cardiac and pulmonary characteristics, including cardiac output, ECG monitoring, pulse rate, mean arterial pressure, central venous pressure, pulmonary artery pressure, and airway pressure, are common measurements used to assess cardiovascular and pulmonary physiologic conditions. Cardiac 578 Annals of Emergency Medicine
Esquivel et al and pulmonary monitoring was continued throughout the entire testing period. To further evaluate cardiac safety, pathologic and histopathologic assessments were conducted on each of the 10 hearts and the sham heart postmortem. Incisions were made in each heart from the apex, creating 4 sections (apex⫽section 1). Tissue was extracted from the anterior wall of the left ventricle in section 2, the septum of section 3, and the posterior wall of the left ventricle in section 4. The tissue was stained using hematoxylin and eosin and Masson’s trichrome methods and examined microscopically. The assay identified to measure troponin I values had previously been used on humans only, and its cross-reactivity with swine needed to be evaluated. To determine whether the troponin I levels were accurately predicting the presence of myocardial injury in swine, a coronary occlusion to the distal segment of the left anterior descending coronary artery was performed on 1 Yorkshire-cross female swine weighing 41.4 kg before all testing. An angioplasty balloon catheter (2-mm diameter; 15-mm length) was advanced over a 0.014-inch guidewire (0.08 inch diameter; 0.59 inch length) to the distal segment of the left anterior descending coronary artery. After a 50-mg intravenous lidocaine bolus, the balloon was inflated at 4 bars to occlude coronary flow in this segment. Through a guiding catheter positioned into the left coronary ostium intracoronary, injection of contrast medium (Ioversol) was performed to confirm the absence of flow distal to the balloon. The balloon was deflated after 1 hour of occlusion. Three milliliters of arterial blood to record blood gas levels and troponin I were drawn at 1-hour intervals for 4 hours postocclusion. This procedure has been validated, and detailed methods are provided in previous studies.13,14 One sham animal was included to examine the effects of the anesthetic agents. The same induction agents and anesthesia were used, along with the surgical instrumentation described above. Three milliliters of arterial blood to analyze blood gas levels and troponin I were drawn at 1-hour intervals for 4 hours. The animal was not subjected to any exposures by the Stinger S-400 and was killed 4 hours after surgery. Primary Data Analysis Data collected from the whole-blood samples of the exposed animals for pH, PCO2, PO2, lactate level, and troponin I level were evaluated by MANOVA (P⬍.05) to determine statistical significance. Cardiac output was recorded 3 times at each point, the average of the 3 values was recorded as the cardiac output for that point, and those values were analyzed by MANOVA for statistical significance. Pulse rate, central venous pressure, pulmonary artery pressure, and airway pressure were continuously monitored and were evaluated by taking an average of 10 to 20 seconds of data at baseline after each set of exposures and at 30-minute intervals for 4 hours after the exposures. The goal was to average 20 seconds of data; however, this was not always possible, because of the effects of the device on the data acquisition system. These averages were recorded at Volume , . : November
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Table. Baseline physiologic values.
Specimen
Arterial pH
Arterial PCO2, mm Hg
Sham Mean, exposed animals SD, exposed animals Range, exposed animals Normal value, mean Normal range
7.42 7.45 0.02 7.43–7.49 7.48 7.4–7.53
45 41 2 38–44 40 35–44
Lactate, mM/L
Cardiac Index, mL/min/kg
Total Peripheral Resistance, mm Hg/L/min
Mean Arterial Pressure
NA 1.3 0.4 0.7–2.1 1.0 0.5–1.5
127 109 20 84–150 147 123–188
11.1 14.4 2.1 11.4–17.3 NA NA
64 66 8 57–76 102 86–123
NA, Not applicable. Average baseline values for arterial pH, PCO2, and lactate and baseline values for cardiac index, total peripheral resistance, and mean arterial pressure for exposed animals and 1 sham animal. Also shown are normal values for conscious swine and the range.15
a baseline level, before and after each set of exposures, and every half hour for 4 hours. Values were also recorded for the sham animal at baseline and at 30-minute intervals for 4 hours. These data were then analyzed by MANOVA (P⬍.05) to determine statistical significance. Pairwise comparisons were made between the baseline values and the values at all other points (P⬍.05) with the Sidak’s correction for preventing inflation of type I errors. All statistics were completed with SPSS 14.0 for Windows (SPSS, Inc., Chicago, IL). ECG recordings for each animal were evaluated by a cardiologist for abnormalities.
RESULTS Main Results Baseline values for pH, PO2, PCO2, lactate, cardiac output, total peripheral resistance, and mean arterial pressure were recorded for each animal and compared with normal values previously reported for conscious swine15 (Table). All values for pH and PCO2 for this study were in the normal range. Approximately half the values recorded at baseline for lactate and cardiac index were in the normal range. All the values for MAP were below the normal range. The coronary occlusion substudy produced an infarction that induced an increase of 0.6 ng/mL in troponin I 4 hours after occlusion (Figure 1). This increase was greater than any change in troponin I level for this study. There was no statistically significant change in troponin I level at any point after the exposures (Figure 1). Three isolated premature ventricular contractions were observed in one specimen at 16, 99, and 117 minutes after the first exposure. Contractions were not observed in any subsequent tests. The remainder of the ECG results was normal. Cardiac index increased continuously after each set of the first 3 sets of exposures (Figure 2). The increase in cardiac index after each set of exposures was statistically different from the baseline value. Although the average value was slightly increased after 4 hours, it was not statistically different from the baseline value. The mean arterial pressure was statistically different from the baseline after the first set of exposures (Figure 3). In between each set, it increased to or above the baseline level and decreased Volume , . : November
Figure 1. Values of troponin I at baseline (time 0), after all exposures, and at rest 4 hours (60-minute intervals) after the exposures for exposed animals (white bars), a sham animal (black bars), and the animal subjected to an infarction (gray bars). Error bars are ⫹/⫺ one standard deviation from the mean.
after each set of exposures, although these changes were not statistically significant. There was a steady decrease in pressure after all exposures were given. The total peripheral resistance was calculated by dividing the mean arterial pressure by the cardiac output (Figure 2). This value decreased significantly after the first set of exposures and was still significantly different from the baseline value 4 hours after the last exposure. All values measured were included in the statistical analysis for pH, PCO2, and lactate. Two data points for 1 animal were not recorded for PO2, because of equipment malfunction. The data were graphed, showing the mean values ⫾1 SD from the mean. The pH decreased significantly during the exposures (Figure 4). The average lowest value for pH was 7.34, which occurred after the third set of exposures. It had the greatest relative decrease after the first 5 exposures. There was no significant difference between the baseline value and the value 1 hour after exposures. Annals of Emergency Medicine 579
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Figure 2. Values of cardiac index and total peripheral resistance at baseline (time 0), after each set of exposures, and at rest 4 hours after the exposures for exposed animals (white bars) and a sham animal (black bars). Error bars are ⫹/⫺ one standard deviation from the mean.
Figure 4. Values of pH, PCO2, and lactate at baseline (time 0) after each set of exposures and at rest for 4 hours (60-minute intervals) after the exposure for exposed animals (white bars) and a sham animal (black bars). Error bars are ⫹/⫺ one standard deviation from the mean.
Figure 3. Value of mean arterial pressure at baseline (time 0), after each set of exposures, and at rest for 4 hours (30-minute intervals) after the exposures for exposed animals (white bars) and a sham animal (black bars). Error bars are ⫹/⫺ one standard deviation from the mean.
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The carbon dioxide pressure increased significantly during the exposures (Figure 4) to 52.5 mm Hg. It had the greatest relative increase after the first 5 exposures. It returned to the normal range 2 hours after the last exposure, although it was still statistically increased from the baseline value and continued to decrease slightly until the end of the experiment. Blood lactate values increased significantly after the first set of exposures (Figure 4). These levels increased cumulatively with each set of exposures up until 15 exposures to 4.0 mmol/L and then exhibited a slight decreasing trend to 3.5 mmol/L, although it was still statistically increased from baseline. There Volume , . : November
Esquivel et al was no statistically significant difference between the baseline value and the values obtained 1 hour after the exposures. In addition to troponin I, there was no statistically significant change measured in oxygen pressure, pulse rate, mean arterial pressure, central venous pressure, pulmonary artery pressure, and airway pressure. All values remained statistically unchanged from the baseline at all points. Gross examination of the hearts did not reveal any damage, and histopathologic analysis of the anterior wall of the left ventricle, septum, and posterior wall of the left ventricle did not show any structural changes in any animals.
LIMITATIONS The size of the animal has been shown to affect the safety of the conductive conducted electrical weapon. One previous study outlined above showed a strong correlation between size and the safety of the device; as the size of the animal decreased, the “safety index” decreased,3 which indicates that these devices, although safe to use on healthy average-sized adults, could have more serious health effects on small adults or children. A study examining the effect of size on the safety of conducted electrical weapons should be completed. This study examined the effects of a conducted electrical weapon on healthy, anesthetized animals. It is possible that persons with cardiac abnormalities or arrhythmias could exhibit a more serious response to the device. In addition, normal aging and other underlying cardiac or pulmonary disturbances such as coronary artery disease, congestive heart failure, chronic obstructive pulmonary disease, or other chronic health issues may also have a contributing effect. Persons who are subjected to repeated exposures of a conducted electrical weapon are most likely in an agitated or combative state. This stimulation could lead to a phenomenon known as excited delirium, defined as the onset of a temporary disruption in awareness and cognition, along with aggressive or violent actions.16 Most cases are associated with methamphetamine or cocaine drug use, whereas some are related to mental illness.16 The types of physiologic effects resulting from the combination of excited delirium and the use of conducted electrical weapons are unknown. Some signs used to describe excited delirium include an increased pulse rate, hyperthermia, hypotension, dehydration, and catecholamine release, causing added stress on the heart.16 In addition, strenuous physical activity (eg, struggle with or running from police) has been shown to cause an increase in norepinephrine and epinephrine, as well as stimulation of ␣- and -receptors.16 Two studies have tested a conducted electrical weapon on swine in an abnormal state.7,8 Lakkireddy et al7 examined the effects of a single high dose (8 mg/kg) of cocaine given during a 30minute period before conducted electrical weapon exposure. They found that exposure to cocaine and a conducted electrical weapon did not cause ventricular fibrillation.7 A single dose of cocaine may not capture the effects observed in the field on habitual cocaine users. Nanthakumar et al8 investigated the cardiac effect of a pharmacologic stress (infusion of epinephrine) Volume , . : November
Physiologic Effects of Conducted Electrical Weapons with conducted electrical weapon exposure. The authors found that this corresponded with episodes of tachycardia and ventricular fibrillation.8 Future research should include a more comprehensive model to study the exposure to a conducted electrical weapon in a physiologic stressful state. The repeated use of this device on an animal in a conscious state would impose unnecessary pain and suffering, so anesthesia was imperative. The use of ventilation and anesthesia in this study may have limited the effects of the conducted electrical weapon on the animals by minimizing the hypoventilation that occurs during conducted electrical weapon exposure and possibly diminishing any compensatory hyperventilatory response to increased pCO2 afterward.
DISCUSSION There were several metabolic changes that occurred during the study, including an increase in cardiac output caused by the exercise-like nature of the muscle contractions induced by the device. Metabolic vasodilation was observed and caused a decrease in total peripheral resistance and mean arterial pressure after each set of exposures. In addition, lactic acid, a by-product of energy production during exercise, increased during the exposures. There was not a clear pattern of change in troponin I level for the exposed animals of this study. The maximum change between a baseline value and one observed after the exposures was 0.16 ng/mL. This value was well below the increase observed in the infarcted animal. Seventy percent of the animals had no change from the baseline level at 4 hours postexposure. The sensitivity of the assay technique for the troponin I level was confirmed for the species tested by a coronary occlusion technique to create a known infarct. The tetanic muscle contractions that were created with the application of the device during this experiment are similar to those observed during exercise and therefore created a similar physiologic response. Hastings et al17 reported cardiac indices of 238 mL/kg per minute for “steady-state” exercise and 274 mL/ kg per minute for exhaustive exercise in pigs. The highest value recorded for any animal was 190 mL/kg per minute, whereas the average value after 3 sets of exposures was 132 mL/kg per minute. It was also reported by Hastings et al17 that during steady-state exercise the swine pH dropped from 7.5 to 7.48 and to 7.35 during exhaustive exercise, and the lactic acid values increased from 2.0 mM/L preexercise to 17.8 mM/L postexercise. For this study, the average pH decreased to 7.34 during the exposures, whereas the lactic acid level increased to 3.99 mM/L, indicating that for this study the effect of the conducted electrical device on these factors was less than that of either steady state or exhaustive exercise. The animals became slightly hypotensive immediately after each set of exposures because of a decrease in total peripheral resistance (vasodilation). A compensatory increase in cardiac output was observed because of this decrease in vascular resistance. During the 5-minute recovery period before the next Annals of Emergency Medicine 581
Physiologic Effects of Conducted Electrical Weapons set of exposures, vasoconstriction began to occur and the blood pressure returned to baseline or slightly increased levels. During the 4 hours after the exposures, the animals exhibited additional hypotensive behavior. Isoflurane, the anesthesia used, has been shown to produce a decrease in mean arterial pressure. One study examining the cardiovascular effects of anesthesia on human volunteers showed a decrease from 85 mm Hg to 55 mm Hg.18 The decrease in mean arterial pressure because of isoflurane is caused by the decrease in vascular resistance and not the cardiac output. Because of the effect of isoflurane on vascular resistance, and in turn mean arterial pressure, the total peripheral resistance did not return to the baseline value 4 hours after the exposures. In addition, the one animal subjected to the surgery and 4-hour anesthetic period only (sham) exhibited a decrease in mean arterial pressure similar in magnitude to that of the exposed animals. Therefore, we speculate that this finding was an effect of the anesthesia and not the exposures. The baseline PCO2 values recorded were within the normal average values previously reported for swine (35 mm Hg to 44 mm Hg).15 The average PCO2 increased from 41.4 mm Hg to 52.5 mm Hg. The PCO2 did not return to the baseline value within the 4 hours of the study. However, it did return to near normal after 1 hour and continued to decrease for the duration of the study to 43.6 mm Hg. Visual observation of the animals during exposures showed that the muscle contractions caused impaired ventilation. When ventilation is impaired, the lungs do not eliminate carbon dioxide as quickly as the body produces it, leading to a buildup in the tissues. The decrease in pH, combined with an increase in carbon dioxide pressure, indicates acute respiratory acidosis.19 The normal physiologic values previously reported for arterial blood pH in conscious pigs (7.4 to 7.53) is higher than that of humans (7.35 to 7.45).15 Jauchem et al5 reported an average decrease in pH from 7.4 to 7.0 after Taser exposure. These values did not return to baseline within the 1-hour period of the experiment. The pH values from this study did not decrease at same rate as those reported by Jauchem et al.5 However, a decrease in pH to 7.34 may still be physiologically significant because of the slightly more basic normal pH value of the pig. In the current study, arterial blood pH was not significantly different from the baseline value 1 hour after the last set of exposures. The difference in values between the current study and that by Jauchem et al5 could be attributed to the difference in protocols and timing and total number of exposures. Although the swine in the Jauchem et al5 study were exposed 18 times in 3 minutes, the current study used a total of 20 exposures in 31 minutes, which could have allowed the animals to recover between exposures. Blood lactate levels increased cumulatively with each set of exposures until 15 exposures. The relative greatest increase was observed between the baseline and after the first 5 exposures. A decrease was observed after the third set of exposures. This decrease is due to the onset of acute respiratory acidosis. Several studies examining the effect of respiratory acidosis on blood 582 Annals of Emergency Medicine
Esquivel et al lactate increases during exercise found that subjects breathing 5% carbon dioxide in air to induce respiratory acidosis had lower blood lactate values compared with subjects who breathed normal air.19,20 Jauchem et al5 recorded lactate values exceeding 15 mmol/L. The highest value observed in this study was 6.52 mmol/L, whereas on average the increase was to 3.99 mmol/L. Again, this difference could either be a function of the device used (Taser versus Stinger S-400) or the difference in protocol. Blood lactate levels in the current study returned to baseline 2 hours postexposure. In summary, according to this analysis of the data for the characteristics studied, the Stinger S-400 appears to have no serious adverse physiologic effects in healthy anesthetized pigs. Changes in pH, carbon dioxide pressure, and blood lactate level were observed but decreased to baseline or very near it within the 4-hour period of the experiment. The animals did become acidotic after the exposures but returned to normal after 1 hour. Cardiac index increased after each set of exposures, but this increase was less than that recorded for strenuous exercise. Other cardiac characteristics, including the biologic marker troponin I and ECG recordings, did not show any significant irregularities. It is unlikely that exposures from the Stinger S-400 conducted electrical weapon would cause cardiac damage to healthy, resting adults, and any changes in other metabolic factors seem to mimic those of exercise. However, the combination of a physiologic stressful state such as agitation or strenuous physical activity, along with the use of a conducted electrical weapon, could lead to further acidosis or impaired respiration. We thank the Ballistics Group in the Department of Biomedical Engineering at Wayne State University, especially Marianne Wilhelm, PhD, Hai-chun Chen, MS, Erin Hanlon, MS, and Samantha Staley, BS, for their assistance. In addition, we would like to thank Petar Prcevski, MD, for performing the coronary artery occlusion and Donna Shepherd, LVT, and Janine Matthei, LVT, for surgical support. We thank Bulent Ozkan, MA, for his statistical analysis of the results. Supervising editor: Stephen R. Thom, MD, PhD Author contributions: CAB conceived the study and obtained research funding. EJD, RLH, and CAB designed the trial. AOE, EJD, JAS-M, and RLH supervised the conduct of the trial and data collection. AOE and RLH collected the data. AOE analyzed the data. JAS-M examined the ECGs. AOE drafted the article, and all authors contributed substantially to its revision. AOE takes responsibility for the paper as a whole. Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article, that might create any potential conflict of interest. See the Manuscript Submission Agreement in this issue for examples Volume , . : November
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of specific conflicts covered by this statement. This study was supported by Stinger Systems Inc. for funding of the technical costs of the study. The authors had sole responsibility for the study design, data collection, data analysis, data interpretation, and preparation of the article. None of the authors have any financial interest in Stinger Systems Inc., nor have they received any financial support from Stinger Systems Inc. outside of the grant.
9. 10. 11.
Publication dates: Available online August 23, 2007.
12.
Address for reprints: Cynthia Bir, PhD, Biomedical Engineering, 818 W Hancock, Detroit, MI 48201; 313-577-3830, fax 313577-8333; E-mail [email protected].
13.
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Volume , . : November
Annals of Emergency Medicine 583