Overview of the distribution of TASER electronic control device (ECD) output within the body
The ADVANCED TASER[1] M26 and TASER X26 devices generate significantly less charge and energy than other medical devices, such as external defibrillators and ablation RF generators, which are approved and deemed safe for medical use.
- The charge carried by the first, also the highest, current peak of the TASER M26, or by the main phase of the TASER X26 device, is, by a wide margin, significantly below charge-based thresholds known to be capable of inducing ventricular fibrillation in humans.
- When applied to various areas of the body, only non-dangerous fractions, if any, of the voltage, current and charge generated by the M26 or the X26 TASER ECDs reach the heart.
- With a reasonable degree of medical probability, the voltage, current or charge developed by the M26 and X26 TASER devices are very unlikely to trigger fatal cardiac arrhythmias.
- With a reasonable degree of medical probability, the voltage, current or charge developed by the M26 and X26 TASER devices are sufficient to activate motor nerves involved in temporary neuromuscular incapacitation, but are not sufficient, by a very wide margin, to produce skeletal muscle damage.
- Theoretical upper limits for critical risk levels associated with use of TASER ECDs are lower than risks estimated for daily or recreational activities such as crossing a street, or swimming, than probabilities of death during car accidents, or than risks accepted by clinical use of United States Federal Drug Administration (FDA)-approved medical devices.
Electrical Output Characteristics of the ADVANCED TASER M26 and TASER X26 Devices
The output of a TASER M26 device is characterized by peak arcing voltages of about 50 kilovolts (kV), an internal energy of about 1.76 joules (J)/pulse, at a rate of 20 +/- 25% pulses/s and an internal electrical power level of about 26 watts (W). After the initial arc, at the load end (i.e., in the subject's body), these values decrease considerably: the peak voltage becomes approximately 5 kV (with 1500 V average over duration of the main phase), with a delivered energy per pulse of about 0.5 J/pulse. Only about 10 W of electrical power are delivered externally. The duration of the first peak is about 10 microseconds (µs), with a total active waveform duration of 40 µs. This main phase delivers a charge of approximately 85 microcoulombs. Given its dampen sinusoidal waveform, subsequent current peaks are biphasic, negative followed by positive peaks.
Similarly, the output of a TASER X26 ECD is characterized by peak arcing voltages of about 50 kV, an internal energy of about 0.36 J/pulse, at a rate of 19 pulses/s and an internal electrical power level of about 7 W [1-5]. After the initial arc, the peak voltage becomes approximately 1.2 kV (or 400 V average over the duration of the main phase), with a delivered energy per pulse of about 0.07 J/pulse. Only about 1.3 W of electrical power are delivered externally. The total active waveform duration of 100 µs. The waveform delivers a charge of approximately 100 microcoulombs. Table I summarizes the specifications of M26 and X26 TASER ECDs.
Link to Specifications of ADVANCED TASER M26 and X26 TASER ECDs.
By comparison, some external defibrillator devices, medically approved to resuscitate patients, put out peak voltages in the 2-5 kV range, peak currents well in excess of 20 amperes (A), with durations of typically 5 milliseconds (ms). The total output energy usually exceeds 200 J [6-8]. Similarly, some of the FDA-approved cardiac or liver ablation RF generators have maximum output power ratings of 100 W, or more, and maximum output current ratings of 1-2 Arms [9, 10]. These generators can deliver power and current to the heart, or liver, for durations that exceed 60 s. These output ratings are significantly larger than the output of M26 and X26 TASER devices. Yet, such devices are approved for medical use and are widely considered to be safe in terms of not producing undesirable long-term damage to cardiac or to liver structures.
Current Distribution inside the Human Thorax and Probable Effects on the Heart
Previous research I conducted on ventricular (de)fibrillation and defibrillator and pacing devices [6, 11-12], showed that even under optimal electrode placement configurations, a low fraction of the current that entered the human thorax reached the heart. For example, we found that more than 66% of the input voltage dropped across portions of the thorax within 4 centimeters (cm) under cardiac electrodes that were optimally placed [6, 11]. For the same optimal electrode cardiac placement, less than 10% of the input voltage dropped across the left ventricle [12]. The high resistances of the skin, the fat layer and the thoracic cage reduced the voltage gradient across the heart. Consequently, the current density at the heart level was significantly reduced with respect to values measured at electrode levels.
Koning presented that in order to successfully defibrillate a heart (defibrillation, the reverse of fibrillation, is a process whereby electrical currents resynchronize the cardiac cells) charge levels of at least 42 microcoulombs/gram (g) were required. The ratio is with respect to the mass of the heart [7]. For a heart of 485 g, such as that of some of the suspects involved in-custody-death disputes, 42*485 microcoulombs = 20,370 microcoulombs would be required for a successful defibrillation. The charge carried by the active or main phase of the current delivered by TASER ECDs can be estimated at less than 100 microcoulombs [1-3]. While defibrillation currents are usually larger than currents required for triggering fibrillation, still the ratio between required defibrillation charge and the TASER ECD charge, 20370/100, is greater than 203 times.
McDaniel et al. found that the blood pressure of animals stimulated with TASER devices was within normal range, an indication that no critical cardiac tachycardias took place [4, 5]. Furthermore, they found that more than 2000 microcoulombs of charge were required to fibrillate animals with a mass of 117 kilograms (kg) (mass range was 74 to 126 kg in a study of 20 cases of excited delirium death associated with struggle and restraint that were witnessed by emergency medical services (EMS) personnel [13]). This charge level represented a significant margin of safety with respect to the charge of the TASER M26 or X26.
Deale and Lerman studied the ratio of transcardiac to transthoracic threshold currents in dogs [14]. They reported that the thoracic cage shunted 82% of the input current and that the lungs shunted 14%. Only the remaining 4% of the input current passed through the heart.
The references cited above indicate that only a small fraction of the input current generated by external devices reaches the heart. Other layers of tissue, such as the thoracic cage, fat, and intercostal muscles divert most of the current away from the heart. It is commonly accepted that the amount of charge deposited in myocytes is the main contributor to the onset of ventricular fibrillation. Work cited above shows that the charge generated by TASER ECDs is below fibrillation thresholds by a wide margin of safety. It is also important to emphasize that there are no significant changes noted in blood pressure levels during TASER device applications [4, 5].
Review of TASER M26 Electrical Output with Respect to Requirements of Standard IEC 479-1 and –2
The International Electrotechnical Commission (IEC) 479 standard deals with effects of current on human beings and livestock [15, 16]. As stated in IEC 479-1, section 3, page 39, and section 4, page 49, describe the effects of sinusoidal alternating currents with frequencies between 15 hertz (Hz) and 100 Hz and of direct currents passing through the human body, respectively [15]. The effects of non-sinusoidal currents of higher frequencies are covered by IEC 479-2. Section 4.4 describes the thresholds of ventricular fibrillation for impulses of short duration [16]. It states that "for 50% probability of fibrillation, Fq is of the order of 0.005 [amperes/second] As." Fq is defined as the charge of the impulse. By the definition of current, charge and time units of measurement, the quantity 0.005 As is equal to 5000 microcoulombs. As presented in 3.2.1, the TASER M26 and X26 ECDs current (and by far the largest) carry charges less than or about 100 microcoulombs. This is at least 50 times less than the threshold indicated by IEC 479-2 for a 50% probability of ventricular fibrillation induction.
Finite Element Modeling of TASER ECD Current Distribution in the Human Body
It is known that after the onset of ventricular fibrillation (VF) the blood pressure drops precipitously within a few seconds. As a result, the subject would lose consciousness within several seconds, certainly less than a minute, and also lose physical strength, control of gait and balance. Given the fact that most suspects reportedly had the physical strength to resist arrest even after they were exposed to TASER devices, it would be highly improbable that their hearts experienced VF caused by currents delivered by the TASER device. Although the TASER electrode could be applied to various parts of the body, including frontal chest – straight over the heart, based on information presented above, only an insignificant amount of current, if any, would reach the suspect’s heart, making it highly unlikely that TASER currents trigger cardiac arrhythmias or VF. In addition to the current attenuation that increases with distance from the electrode, the skin, the fat and the skeletal muscle layers play a significant role in diverting currents away from deeper tissue layers, such as away from the heart. To further validate these statements, I developed finite element models (FEM) of a male body, approximating the relative physical attributes of certain suspects (176 cm length neck-feet and 76 cm shoulder width - 5' 9" long neck-feet and 30" wide). Finite element modeling is a known mathematical technique that provides numerical approximations to solutions of differential equations, such as those governing electrical current distributions through the thorax [6]. The following tissue regions were modeled:
· Muscle (neck, shoulder, limbs)
· Bone (spine, ribcage)
· Heart
· Lungs
· Skin/Fat
· Abdomen
Fig. 1. Mesh of the finite element model.
The model consisted of 8460 hexahedral elements. Tissue resistivities were assigned using values published in previous work [6, 11-12]. Figure 1 shows the finite element (FE) mesh with its corresponding regions. Voltage type boundary conditions of 1000 V were applied at various body locations. The current density inside the finite element volume corresponding to the heart region was then computed and compared against threshold known to cause VF or capture, temporarily, the heart. Table II summarizes the electrode spacing and body locations, the maximum current density values in the heart volume and the safety margins with respect to VF and heart-capture thresholds.
Table II. TASER electrode locations, maximum heart current density and safety margins.
|
Electrode separation and position |
Maximum current density in the heart |
Safety margin with respect to VF threshold |
Safety margin with respect to capture threshold |
|
8"- over dorsal area |
0.064 mA/cm2 |
1421 times |
69 times |
|
8" - left nipple to left thigh |
0.24 mA/cm2 |
379 times |
18 times |
|
3" - frontal chest, straight over heart |
2.7 mA/cm2 |
33 times |
1.7 times |
Figure 2(a) shows the voltage distribution on the body surface for the frontal probe locations. To find actual voltage values, the color legend values have to be multiplied by 10. On the dorsal side, the voltage boundary conditions were applied at locations about 8", consistent with likely inter-probe distances for situations when the TASER device were fired from close range. Figure 2(b) shows the voltage distribution in V for the dorsal probe locations. It is important to note that the electric field drops rapidly with the distance from the TASER probes. Figure 2 also shows the actual voltage boundary condition locations, which simulated the locations of the TASER probes.
Fig. 2(a). Voltage distribution on the surface of the body. Electrodes applied about 3" apart, right over the heart volume. For actual voltage values multiply color legend by 10.
Fig. 2(b). Voltage distribution on the surface of the body. Electrodes applied about 8" apart on the dorsal side of the body. Actual voltage values shown.
Figures 3 (a) - (d) illustrate the current density distribution at the heart level for boundary condition locations shown in Table II. For reference, the FEM volume simulating the heart is drawn with a white outline. In Fig. 3(a), the maximum current density in the heart volume was 0.064 mA/cm2. In Fig. 3(b), the maximum current density in the heart volume was 0.24 mA/cm2. Figure 3(c) shows the current density distribution on the surface of the FEM with boundary conditions corresponding to locations at the left nipple and left thigh. In Fig. 3(d), the maximum current density at elements representing the heart was 2.7 mA/cm2. Based on published myocyte rheobase and chronaxie values (i.e. 7 mA/cm2 and 1.2 ms, respectively), and based on the specifics of the TASER devices current waveform (e.g. duration of the main current peak of 10 µs for M26 and 100 microseconds for X26) the current density required to induce VF is estimated at about 91 mA/cm2[17-19]. Consequently, current densities seen in the heart volume for the above TASER probe locations (i.e. 2.7, 0.24 and 0.064 mA/cm2, respectively) are significantly lower, by a very wide margin, than the required current density for VF induction of 91 mA/cm2. The safety margin ranges between 1421 times the VF threshold, for the dorsal electrode placement, and 33 times, for the frontal placement. The condition shown in Fig. 3(d) is representative of a worst-case scenario because it uses electrode locations in immediate proximity to the heart. Thereby, the resulting current density is representative of highest achievable theoretical values. On this basis, with a reasonable degree of medical probability, I find that currents delivered by TASER ECDs are highly unlikely to induce VF. The FEM assumes an electrical resistivity of the heart region of 450 W·cm, situated at the higher end of values reported in the literature [6, 11]. Based on this resistivity number, the corresponding maximum electrical field strengths are limited on the upside to approximately 1.2 V/cm (the electrical field strength is computed by multiplying the corresponding current density and resistivity values). This value corresponds to the frontal TASER probe placement. The myocyte excitation threshold is reported to be between 2-5 V/cm [20-22]. Consequently, even considering the lower end of the interval, 2 V/cm, the current density values in the heart region, as predicted by the FEM, are significantly lower than the threshold required to locally capture the heart. The safety margin varies between 69 times the capture threshold, for the dorsal placement, and 1.7 times, for the frontal probe placement. On this basis, with a reasonable degree of medical probability, I find that currents delivered by TASER ECDs are highly unlikely to capture the heart.
Fig. 3(a). Current density distribution at the heart level. The TASER probes were applied about 8" apart, on the dorsal area. The current density decreases rapidly with distance from electrode. Current density values are in A/cm2.
Fig. 3(b). Current density distribution at the heart level with electrodes at the left nipple and left thigh locations. The left nipple electrode location is colored in red, as it corresponds to the maximum current density in the model. Current density values are in A/cm2.
Fig. 3(c). Current density distribution on the surface of the FEM with electrodes located at the left nipple and left thigh. This view also shows the location of the voltage boundary condition nodes. Current density values are in A/cm2.
Fig. 3(d). Current density distribution at the heart level. The TASER probes were applied about 3" apart, on the frontal chest area, right over the heart. The current density decreases rapidly with distance from electrode. Multiply the color legend by 10 to obtain actual current density values in A/cm2.
These results are consistent with recent animal research reports that show TASER devices could not induce VF in swine [23]. Lakkireddy et al. studied five TASER electrode locations. At none of these locations the currents were high enough to induce VF. No metabolic or hemodynamic changes were observed after X26 TASER discharge.
The FE modeling results presented above support data discussed in section 3.1.2 and indicate with reasonable medical probability that insignificant, if any, TASER currents reach a suspect’s heart during a confrontation with law enforcement officers. If any TASER currents reach the heart, their magnitude would likely be insufficient to trigger cardiac arrhythmias.
Effects of TASER ECD Electric Fields on Nerve and Muscle
It is important to understand the electrical attenuating effects of the skin, fat and skeletal muscle layers. Additionally, the speculation has been raised that TASER currents could produce skeletal muscle damage. To address these concerns, I generated an FEM that analyzed current density and electric field distributions inside skeletal muscle [24]. The models analyzed herein describe skeletal muscle and motor nerve activation, cell electroporation, and current and electric field distributions.
In general, skeletal muscle activation by electrical stimulation is elicited by excitation of a-motor neurons which innervate such muscle fibers. This fact often comes as a surprise, in that skeletal muscle cells are themselves excitable. Skeletal muscle excitability, however, is less than that of motor neuron cells in that both rheobase and chronaxie values of skeletal muscle are higher than those of the myelinated nerve axons which innervate them. Therefore, immediately adjacent to TASER dart locations it is possible that skeletal muscle fibers might be “directly” stimulated but any significant distance away from the darts one would expect skeletal muscle to be “indirectly” activated through its nervous innervation. Sensations of pain or discomfort in response to TASER stimuli would be expected to result from a host of sensory nerve fiber types, to some extent dependent upon the specific locations of TASER dart attachment to the body (as well as the specific tissues located between and near the darts in what might be called the “capture” zone of the darts where excitable cells are activated). To elicit muscle activation then, each TASER pulse has to inject current through darts such that the electric fields created in the body capture sufficient volume of skeletal muscle, through indirect stimulation via motor nerves. At the same time, to avoid direct tissue damage, the current densities (J) and electric field strengths (E) have to be lower than, for example, thresholds that may produce cell electroporation. Based on existing modeling and experimental literature, we have assumed the following J and E thresholds for excitation:
– Motor neurons: chronaxie ~ 140 µs, rheobase E field ~ 0.06 to 0.15 V/cm for excitation at axon terminations such as motor end-plates [4];
– Strength-duration correction of needed E field strength for the M26: (1 + 140/10)x(0.06 to 0.15 V/cm) = 0.9 to 2.25 V/cm
– Strength-duration correction of needed E field strength for the X26: (1 + 140/70)x(0.06 to 0.15 V/cm) = 0.18 to 0.45 V/cm
By comparison to these expected field strength values needed for neuromuscular activation, Gehl et al. have reported that for reversible and irreversible electroporation field strengths of 450 V/cm and 1600 V/cm are needed, respectively [25].
Based on these values, it is estimated that the E field required to successfully activate motor nerves with the M26 and X26 has to exceed 0.18-2.25 V/cm, whereas to avoid electroporation E has to be less than 450-1600 V/cm. This yields a worst-case range for the E field strength of 2.25-450 V/cm, to insure successful activation with either device while also avoiding electroporation.
To understand the J and E distributions generated by TASER electrodes, we introduce a FE model with the following characteristics:
· Regions:
Ø Epidermis – 3 mm
Ø Dermis – 6 mm
Ø Fat – 5 mm
Ø Muscle – 6 mm
Ø Electrodes – 9-mm long, 2-mm diameter
· Nodes: 45360
· Elements: 41080 hexahedral elements
· Model: 15-cm long, 5-cm wide, 2-cm deep
· Dart electrodes 10-cm apart
· Voltage boundary conditions: 1000 V
· Steady-state solution
The FEM models the electrodes based on dimensions provided in [1-3] and considers them fully penetrated. The inter-electrode distance is at the minimal end of reported actual-use separations [1-3]. The FE material properties are as reported in the literature [6]:
· Epidermis – 1 MW·cm
· Dermis – 500 W·cm
· Fat – 2200 W·cm
· Muscle – anisotropic layer
u rx = ry = 200 W·cm (longitudinal)
u rz = 1000 W·cm (transversal)
· Dart electrodes – 0.001 W·cm
Note that the thickness of the fat layer is also at the low end of reported values. Therefore, the conditions above represent a worst-case scenario for J and E distributions in the muscle layer. Actual-use values would not be expected to exceed the FEA prediction results.
Figure 4 shows an example mesh of the FEM, its regions, as well as the overall current density distribution.
Fig. 4. FEM mesh and overall current density distribution. The current density is expressed in A/mm2.
The magnitude of J is listed in A/mm2. Figure 5 presents a close-up of the current distribution values in the layers proximal to and under the electrode for the sample mesh. These layers are exposed to higher J and E values.
Fig. 5. FEM current density distribution.
As shown in Fig. 5, the highest normal Jz and Ez seen in the muscle layer, where the nerve density is presumably higher than in other layers, are 15.63 mA/cm2 and 15.63 V/cm, respectively. Note that J decreases dramatically 2-mm away from the electrode.
Fig. 6. FEM electric field strength distribution.
Figure 6 shows the distribution of E in a transversal cross-section through the center of an electrode. The values are expressed in V/mm. The electrode-electrode line is perpendicular to the plane of this section. The maximum E values are reached within a region, with a volume of approximately 4 mm3, located about 1 mm beneath the electrode. While these values are somewhat higher than 450 V/cm, the threshold for skeletal muscle reversible electroporation, they are located in the fat layer, not the skeletal muscle layer, and are far lower than 1600 V/cm, the threshold required for irreversible electroporation [25]. The values of E in the skeletal muscle layer are all lower than 450 V/cm, the threshold for skeletal muscle reversible electroporation. The magnitude of E also decreases rapidly with distance from the electrode, dropping below the threshold for reversible electroporation within a space less than 2 mm away from electrodes. Note that the E magnitude at the interface between the fat and muscle layers decreases quickly and reaches its overall model minimum, of about 15-30 V/cm, within a depth less than 1 mm. The values of E in the muscle layer, although more than 25 times lower than the E maximum, are still greater, by a significant margin, than the threshold required to capture the motor neurons responsible for muscle activation. Because of the high resistivity of the fat layer and because of the attenuating effects of the skeletal muscle anisotropy, the results of this model show that in the skeletal muscle layer the transverse current density is less than about 15 mA/cm2 and the field strength is less that about 15-30 V/cm range. These values are greater than 2.25 V/cm – threshold to capture motor neurons, but much low lower than levels required for irreversible electroporation (1600 V/cm – Gehl et al. 1999, [33]). Table III presents the electrical shell effect provided by the fat and by the anisotropy of the skeletal muscle layer. This electrical shell effect can be summarized by the fact that more than 85% of the current is diverted away from deeper layers of tissue, such as the heart.
Table III. Electrical Shell Effect of Fat and Skeletal Muscle
|
Condition |
Jtrans [mA/cm2] |
Jlong/Jtrans |
Comments |
|
Thin body with 5-mm fat and anisotropic muscle layers |
15.63 |
8 |
Current is diverted away from deeper tissue layers by fat and longitudinal muscle electrical conduction |
|
Muscle anisotropy removed |
20.81 |
5 |
Removing muscle anisotropy increases current into deeper tissue layers by 30% |
|
Fat and muscle anisotropy removed |
45.49 |
2.9 |
Removing fat increases current into deeper tissue layers by 200% |
It is also important to understand what type of muscular contraction do TASER ECD pulses produce, once they activate motor neurons. Pulse repetition rate produces increased force production dependent upon frequency and pulse train duration. Human skeletal muscle is generally mixed in its fiber type composition. Slow motor units start to fuse at about 5 to 10 Hz and fuse by 25 to 30 Hz while fast motor units may require activation at 80 to 100 Hz to fuse completely [26]. Figure 7 shows the difference between the level of force for a twitch contraction and that achieved during a tetanic contraction with full fiber fusion [27]. The TASER ECDs pulse repetition rates of 19 Hz or 20 ± 25% Hz are set to capture most slow motor units. The resulting muscular contraction is strong enough to produce suspect’s dysreflexia, causing him/her to lose posture control and fall to ground (thereby allowing the law enforcement officer to complete the arrest procedure). However, these repetition rates are not fast enough to completely capture fast motor units. Consequently, TASER ECD are well suited to produce strong but not maximal (fused tetanus) contractions. As such, it is highly unlikely, with a reasonable medical probability, that TASER currents are capable of triggering muscular contractions that are powerful enough to cause damage to underlying skeletal structures.
Fig. 7. Production of twitch vs. tetanus force in response to an action potential [27].
In conclusion, TASER ECDs deliver currents that efficiently capture neuromuscular structures. Worst-case maximum values for TASER J and E are lower, by at least a factor of two, than levels reported to produce permanent cellular electroporation or tissue damage. The TASER ECD pulse repetition rate is efficient in producing muscular contractions that result in dysreflexia, but not high enough to produce complete fiber fusion that might have a theoretical risk of causing damage to underlying skeletal structures. TASER devices are efficient and safe in producing neuromuscular activation for temporary suspect incapacitation.
Risk Assessment of Theoretical Effects of TASER ECD Currents
TASER International, Inc. reported that ECDs were used in more than 232,000 human volunteer and 383,000 human suspects during actual law enforcement field deployments [28]. In any of these situations, no evidence was provided that TASER ECDs caused cardiac rhythm disturbances or muscular or skeletal damage. As such, the overall critical risk of using TASER ECDs is estimated at less than 1/(232000+383000) = 0.0000016
EN 60601-1 rational for acceptable levels of VF risk
The EN 60601-1 international standard stipulates accepted regulatory requirements for the safety of electrical medical devices [29]. Particularly, this standard sets the allowed threshold for the patient leakage current for medical devices that have direct contact to the patient's heart. Citing from the standard, we learn that [29]:
"The allowable value of PATIENT LEAKAGE CURRENT for TYPE CF APPLIED PARTS in NORMAL CONDITION is 10 µA which has a probability of 0.002 for causing ventricular fibrillation or pump failure when applied through small areas to an intracardiac site.
Even with zero current, it has been observed that mechanical irritation can produce ventricular fibrillation. A limit of 10 µA is readily achievable and does not significantly increase the risk of ventricular fibrillation during intracardiac procedures.”
This implies that under normal device operation, the allowed maximum patient leakage current is 10 µArms. Although a 10-µArms patient leakage current has a 0.002-probability of causing VF or pump failure in humans, the standards accepts this value as being safe. Regulatory bodies, such as the US FDA or the Germany-based TUV, certify electrical medical devices as being safe for use in intracardiac clinical procedures if they comply with the patient leakage current limit above. Intracardiac procedures carry the highest risk for patients. Therefore, by accepting requirements of EN60601-1, these conservative regulatory bodies, including the US FDA, accept that a probability of causing VF of 0.002 represents an extremely low risk. This FDA-accepted probability level of 0.002 is between 12 to 200 times higher than the probability estimates for TASER-induced risk I estimated above.
Probabilities of Risk Encountered in Common Daily-Life Activities
A literature search on risk of daily-life activities showed that the average rate of car accident death in Italy in 1996 was 0.000219, while the rate of drowning in France in 1996 was 0.000016 [30]. Figure 8 tabulates certain risks per information collected by the World Health Organization [30].
Fig. 8. Risk probabilities in France, Italy and UK [30].
Similarly, another study showed that in the US about 5,700 pedestrians die every year while crossing the street [31]. Assuming a total of about 129 million pedestrians in the US, this number equates to a yearly compounded probability of dying while crossing the street of about 0.0000442. Other statistics help put things into perspective. For example, one study found that there is a probability of 0.116 of in-hospital death in patients with myocardial infarction that did not have early VF at the time of admission [32]. Another study presented that there is a probability of 0.018 of preoperative death in patients admitted for implantation of cardiac stimulators [33]. Preoperative death occurs before any implantation procedure steps are taken.
Compared to the probability values listed above, the estimated theoretical upper limit of TASER critical risk, less than 0.0000016, is lower than the probability of death while crossing a street, or than that of dying while swimming and significantly lower than probabilities of death during car accidents or during certain medical procedures.
Risks Associated with Non-Lethal Weapons or Options Available to Law Enforcement Officers
Dr. Ho studied 162 in-custody death events [34]. He learned that in 68.5% of these cases, the suspects went hands-on with the law enforcement officers. In 100% of these cases, the suspects were handcuffed [34]. By comparison, TASER devices were involved in a lower 30.1% of these deaths. Obviously, it would be a stretch of imagination to think that because all suspects died while handcuffed, handcuffs could, therefore, cause ventricular fibrillation. There is no cause-effect relationship between the use of handcuffs and onset of VF, if any, in these suspects. Similarly, Dr. Ho found that in 0% of these deaths occurred within a short time after TASER deployment [34]. Corroborating Dr. Ho’s finding with the risk assessment above, it results that it is highly likely, with reasonable degree of medical probability, that TASER ECDs are not contributory to alleged in-custody deaths.
Probable Effects of Overdose with Illegal Drugs
Suspects resisting law enforcement arrest procedures may have elevated concentrations of illegal drugs in their blood stream. These drugs can have damaging, even fatal, consequences for critical body organs such as the heart and the brain. Methamphetamine makes users aggressive and violent [35]. Twitching, jitteriness, and repetitive behavior (known as "tweaking") are common effects of methamphetamine. Methamphetamine excites specific brain systems and has a high potential for abuse and dependence. Its use releases high amounts of dopamine, a neurotransmitter, which stimulates the brain and enhances mood and body movement. Methamphetamine can cause arrhythmia and ventricular fibrillation similar to symptoms experienced during a heart attack [36]. In high concentration, delusions, hallucinations, severe chest pain, seizure, coma, even death, are likely outcomes [37]. In fact, doses above 0.5 mg/L can initiate an irreversible chain of symptoms/events that may, ultimately, result in the individual’s death [37]. Cocaine overdose is a highly probable cause of cardiac tachycardias, including ventricular fibrillation, and respiratory failure [38-40]. Intoxication with cyclobenzaprine can lead to irregular heart rhythm and troubled breathing [41]. Ephedrine overdose is a highly probable cause of heart rhythm irregularities, heart attacks, and death [41]. Promethazine overdose is known to cause breathing disturbances. Ecstasy affects the regulation of the body's internal systems and produces body overheating [41].
Chronic abuse of illegal drugs can cause dilated and hypertrophic heart. Cardiac hypertrophy is a condition known to contribute to sudden death. For example, hypertrophic cardiomyopathy is a major cause of death in young athletes who seem completely healthy but die during heavy exercise [42].
Opinions
Based on my review of the documentation listed above, as well as my professional education, experience and background, it is my opinion, to a reasonable degree of medical probability that:
- When applied to various areas of the body, only non-dangerous fractions, if any, of the voltage, current and charge generated by the M26 or the X26 TASER ECDs reach the heart.
- The ADVANCED TASER M26 and X26 ECDs generate voltages, currents and charges that are, by a wide margin, significantly below thresholds known to induce fatal cardiac rhythm disturbances.
- With a reasonable degree of medical probability, the voltage, current or charge developed by the M26 and X26 TASER ECDs are sufficient to activate motor nerves involved in temporary neuromuscular incapacitation, but are not sufficient, by a very wide margin, to produce permanent skeletal muscle damage.
- With a reasonable degree of medical probability, the pulse repetition rate of the M26 and X26 TASER ECDs is not high enough to cause muscular contractions that are so powerful that may pose a theoretical risk of producing damage to underlying skeletal structures.
- Theoretical upper limits for critical risk levels associated with use of TASER ECDs are lower than risks estimated for daily or recreational activities such as crossing a street, or swimming, than probabilities of death during car accidents, or than risks accepted by clinical use of FDA-approved medical devices.
- Abuse of illegal drugs causes significant damage, fatal under certain circumstances, to critical organs of the body, such as the heart, the brain and the lungs.
Conclusion:
Based on my review of the documentation listed above, as well as my professional education, experience and background, it is my opinion, to a reasonable degree of medical probability, that TASER ECDs are efficient in producing temporary suspect incapacitation and safe in terms of being very unlikely to trigger fatal cardiac rhythm disturbances, skeletal muscle damage and damage to underlying skeletal structures.
It is also my opinion, to a reasonable degree of medical probability, that excited delirium, or other conditions induced by abuse of illegal drugs, can result in subsequent metabolic, respiratory, hepatic, renal and cardiac failures.
References
1 TASER International, ADVANCED TASER: M26 Specifications. 2005.
2 TASER International, ADVANCED TASER: X26 Specifications. 2005.
3 TASER International, ADVANCED TASER: M-Series Operating Manual. 2005.
4 W. McDaniel, R. A. Stratbucker, M. Nerheim, and J. E. Brewer, "Cardiac safety of neuromuscular incapacitating defensive devices," PACE, vol. 28, pp. S1-S4, 2004.
5 W. McDaniel, R. A. Stratbucker, and R. W. Smith, "Surface application of Taser stun guns does not cause ventricular fibrillation in canines," Proc. IEEE-EMBS Ann. Intl. Conf., 2000.
6 D. Panescu, J. G. Webster, W. J. Tompkins and R. A. Stratbucker, "Optimization of cardiac defibrillation by three-dimensional finite element modeling of the human thorax," IEEE Trans. Biomed. Eng., vol. 42, no. 2, pp. 185–192, 1995.
7 G. Koning, "Strength-duration curves for direct ventricular defibrillation with rectangular current pulses," Proc. Cardiac Defib. Conf., pp. 75-80, Purdue University, West Lafayette, IN, 1975.
8 Zoll Medical Corporation, PD 1200 Cardiac Defibrillator, http://www.zoll.com
9 Boston Scientific Corporation, EPT 1000 XP Cardiac Ablation RF Generator, www.bostonscientific.com
10 Boston Scientific Corporation, RF 3000 Hepatic Ablation RF Generator, www.bostonscientific.com
11 D. Panescu, J. G. Webster, W. J. Tompkins and R. A. Stratbucker, "Optimization of transcutaneous cardiac pacing by three-dimensional finite element modeling of the human thorax," Med. Biol. Eng. Comput., vol. 33, no. 6, pp. 769-775, 1995.
12 D. Panescu, J. G. Webster and R. A. Stratbucker, "Modeling current density distribution during transcutaneous cardiac pacing," IEEE Trans. Biomed. Eng., vol. 41, no. 6, pp. 549–555, 1994.
13 S. J. Stratton, C. Rogers, K. Brickett and G. Gruzinski, “Factors associated with sudden death of individuals requiring restraint from excited delirium,” Am. J. Emerg. Med., vol. 19, pp. 187-191, 2001.
14 O. C. Deale and B. B. Lerman, "Intrathoracic current flow during transthoracic defibrillation in dogs," Circ. Res., vol. 67, no. 6, pp. 1405-1419, 1990.
15 International Electrotechnical Commission (IEC), "Effects of Current on Human Beingsand Livestock," CEI/IEC 479-1: General Aspects, 3rd Edition, IEC, Geneva, Switzerland, 1994.
16 International Electrotechnical Commission (IEC), "Effects of Current on Human Beingsand Livestock," CEI/IEC 479-2: Effects of currents passing through the human body, 2nd Edition, IEC, Geneva, Switzerland, 1987.
17 R. A. Stratbucker, M. W. Kroll, W. McDaniel and D. Panescu, "Cardiac Current Density Distribution by Electrical Pulses from TASER devices," Proc. 28th IEEE EMBS Intl. Conf., New York, August-September 2006.
18 L.A. Geddes and L.E. Baker: "Principles of Applied Biomedical Instrumentation", 3rd ed., John Wiley & Sons, New York, pp. 460, 1989.
19 H. Sun, J.-Y. Wu, R. Abdallah, and J. G. Webster, "Electromuscular incapacitating device safety," Proc. IFMBE, vol. 11(1)., 3rd EMBE Conference, Prague, 2005.
20 S. B. Knisley, W. M. Smith and R. E. Ideker, “Effect of field stimulation on cellular repolarization in rabbit myocardium. Implications for reentry induction,” Circ Res., vol. 70(4), pp. 707-715, 1992.
21 S. B. Knisley, W. M. Smith and R. E. Ideker, “Prolongation and shortening of action potentials by electrical shocks in frog ventricular muscle,” Am. J. Physiol., vol. 266(6 Pt 2), pp. H2348-2358, 1994.
22 H. Bien, L. Yin and E. Entcheva, “Calcium instabilities in mammalian cardiomyocyte networks,” Biophys J., vol. Jan 6, 2006.
23 D. J. Lakkireddy, W. Kowalewski, D. W. Wallick, A. Verma, D. O. Martin, K. Ryschon, J. Butany, A. Natale and P. J. Tchou, "Cardiovascular safety profile of electrical guns (TASER): Impact of point of delivery on ventricular fibrillation thresholds," Heart Rhythm, vol. 3(5)., pp. S249, 2006.
24 D. Panescu, M. W. Kroll, I. R. Efimov and J. D. Sweeney, "Finite Element Modeling of Electric Field Effects of TASER Devices on Nerve and Muscle," Proc. 28th IEEE EMBS Intl. Conf., New York, August-September 2006.
25 J Gehl, T.H. Sorensen, K. Nielsen, P. Raskmark, S.L. Nielsen, T. Skovsgaard, and L.M. Mir, "In vivo electroporation of skeletal muscle: threshold, efficacy and relation to electric field distribution," BBA-General Subjects., vol. 1428 (2-3, pp. 233-20, 1999.
26 Burke, R.E. (1981): "Motor Units: Anatomy, physiology and functional organization." In Handbook of Physiology, Section 1: The Nervous System. Motor Control Part I, Vol. III, Motor Systems, pp. 345-422, American Physiological Society, Bethesda, Md.
27 Malmivuo, J. and R. Plonsey. Bioelectromagnetism. New York, Oxford University Press, 1995.
28 TASER International, “Facts.” Available at: http://www.taser.com/facts/index.htm
29 BS EN 60601-1:2006 Medical electrical equipment. General requirements for basic safety and essential performance.
30 European Food Information Council, Risk: "Putting activities into perspective," http://www.eufic.org/web/page.asp?cust=1&lng=en&page=ONEUFIC
31 G. Charleton, “Living the risky life?” Advance, Texas A&M, 2005, http://vpr.tamu.edu/advance/2005/risky%20life%2005_advance.pdf
32 J. W. Swayer, R. A. Archbold, P. Wilkinson, S. Ray, K. Ranjadayala and A D Timmis “Prognostic implications of ventricular fibrillation in acute myocardial infarction: new strategies required for further mortality reduction,” Heart, vol. 84, pp. 258–261, 2000.
33 "Probability of ICD Perioperative Death," Stanford University Medical Report, http://smi-web.stanford.edu/projects/scd/periop.html
34 J. D. Ho, et al. "Deaths in police custody: an 8 month surveillance study." Annals Emerg Med, vol. 46 (suppl):S94, 2005.
35 http://encyclopedia.laborlawtalk.com/Methamphetamine
36 "Methamphetamine," National Drug Intelligence Center, California Central District Drug Threat Assessment: http://www.usdoj.gov/ndic/pubs0/668/meth.htm
37 B. K. Logan, “Stimulants and driving impairment,” Forensic Laboratory Services Bureau, Washington State Patrol, 2004, www.icadts.org/T2004/pdfs/197.pdf
38 Schaffer Library of Drug Policy: http://www.druglibrary.org/schaffer/other/alc_ch8.htm.
39 Dictionary Laboratory Talk: http://encyclopedia.laborlawtalk.com/Cocaine.
40 G. E. Billman, "Cocaine: a review of its toxic actions on cardiac function," Crit. Rev. Toxicol., vol. 25(2), pp. 113-32, 1995.
41 http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202172.html
42 "Hypertrophic cardiomyopathy," Medical Encyclopedia: http://www.nlm.nih.gov/medlineplus/ency/article/000192.htm
[1] AIR TASER, M26, and X26 are trademarks of TASER International, Inc. TASER® and ADVANCED TASER® are registered trademarks of TASER International, Inc.