The electrophysiology of electrocution.

Electrocution is a death caused by an application of electrical current to the human body. Our present understanding of electrocution-as the induction of ventricular fibrillation (VF)-followed a nearly century-long path of misunderstandings and speculation primarily focused on hypotheses of asphyxia as well as central nervous system trauma. It is hard for us today to appreciate the past mystery of an unexpected sudden death usually bereft of visible trauma. Even today, a false dogma exists that direct-current shocks can cause asystole instead of VF. A lightning discharge (up to 500 megavolts) is differentiated because it can cause substantial acute and chronic neural effects leading to other cardiac arrest rhythms. The human heart is exquisitely sensitive to alternating currents, and VF can be induced with currents of one-eighth that required for mere pacing. Because of these low currents, this effect obtains only in the TQ interval, and low-power electrocution does not involve the vulnerable period. If a current is strong enough to electrocute, generally it will do so in 1-2 seconds; longer shocks do not tend to be more dangerous. Regardless of concomitant drug dosing, the electrocution cardiac arrest rhythm is still VF, suggesting that electrocution is a stand-alone cause of death; the electrical current does not potentiate the effects of the drug. The experimental and clinical data supporting VF as the mechanism for electrocution are provided.

Output of Electronic Muscle Stimulators: Physical Therapy and Police Models Compared.

INTRODUCTION: Both physical therapists and police officers use electrical muscle stimulation. The typical physical therapist unit is attached with adhesive patches while the police models use needle-based electrodes to penetrate clothing. There have been very few papers describing the outputs of these physical therapy EMS (electrical muscle stimulator) units. METHODS: We purchased 6 TENS/EMS units at retail and tested them with loads of 500 Ω, 2 kΩ, and 10 kΩ. RESULTS: For the typical impedance of 500 Ω, the EMS units delivered the most current followed by the electrical weapons; TENS units delivered the least current. At higher im-pedances (> 2 kΩ) the electrical weapons delivered more current than the EMS units, which is explained by the higher voltage-compliance of their circuits. Some multi channel EMS units deliver more calculated muscle stimula tion than the multi-channel weapons. CONCLUSION: Present therapeutic electrical muscle stimula-tors can deliver more current than present law-enforcement muscle stimulators.

Electrical weapons and rhabdomyolysis.

It has been suggested that an application of a conducted electrical weapon (CEW) might cause muscle injury such as rhabdomyolysis and an acute inflammatory response. We explored this hypothesis by testing the effects of electrical weapons on circulating markers of inflammation and muscle damage. In a prospective study, 29 volunteers received a full-trunk 5-s TASER® X26(E) CEW exposure. Venous blood samples were taken before, 5 min after, and at 24 h following the discharge. We tested for changes in serum levels of C-reactive protein (CRP), alkaline phosphatase (ALP), myoglobin, albumin, globulin, albumin/globulin ratio, aspartate and alanine aminotransferase, creatine kinase, total protein, bilirubin, and lactic acid dehydrogenase. Uncorrected CRP and myoglobin levels were lower in the immediate post exposure period (CRP levels 1.44 ± 1.39 v 1.43 ± 1.32 mg/L; p = 0.046 and myoglobin 36.8 ± 11.9 v 36.1 ± 13.9 µg/L; p = 0.0019) but these changes were not significant after correction for multiple comparisons. There were no changes in other biomarkers. At 24 h, CRP levels had decreased by 30% to 1.01 ± 0.80 mg/L (p = 0.001 from baseline). ALP was unchanged immediately after the CEW application but was reduced by 5% from baseline (66.2 ± 16.1 to 62.7 ± 16.1 IU/L; p = 0.0003) at 24 h. No other biomarkers were different from baseline at 24 h. A full-trunk electrical weapon exposure did not lead to clinically significant changes in the acute phase protein levels or changes in measures of muscle cellular injury. We found no biomarker evidence of rhabdomyolysis.

Electrical weapons, hematocytes, and ischemic cardiovascular accidents.

BACKGROUND: There have been case reports following the use of a conducted electrical weapon (CEW) suggesting that these devices might affect coagulation or thrombosis in at-risk individuals. The aim of this manuscript therefore is firstly to explore this hypothesis by reviewing each of these cases and secondly to report the results of a prospective study exploring a priori the effects of electrical weapons on hematocytes in a group of human volunteers. METHODS: First, we systematically reviewed all cases of adverse outcomes following CEW discharge that could be due to an effect on coagulation or thrombosis, with particular focus on the clinical scenario and its relationship with the weapon discharge. Second, we assessed hematocyte levels in venous blood from 29 volunteers before, 5 min after, and 24 h after receiving a full-trunk 5-s TASER® X26(E) CEW exposure. RESULTS: Following extensive review of the literature, we found 3 relevant case reports of possible vascular thromboembolic clinical events after CEW exposure, specifically a case of ischemic stroke, and 2 cases of ST-segment elevation myocardial infarctions. Review of these published cases failed to establish a plausible linkage to the CEW beyond a temporal association with significant emotional and physiological stress from a violent struggle. Our prospective study of biomarker change following CEW discharge revealed acutely increased values for WBC (white blood cells), specifically lymphocytes and monocytes, and a raised platelet count. Neutrophil levels decreased as a percentage of WBC. While these changes were statistically significant at 5 min, all results remained within established reference ranges. At 24 h, all values had returned to baseline except total WBC which decreased to slightly below baseline but was still within the normal reference range. CONCLUSIONS: A review of clinical cases, of ischemic or thrombotic events revealed no direct association with the CEW discharge. A full-trunk electrical weapon exposure did not lead to hematocyte changes beyond normal clinically expected variations in similar acute response scenarios. The case report and biomarker data do not support the hypothesis that a CEW discharge is associated with changes likely to promote coagulation or thrombus formation.

Essentials of low-power electrocution: established and speculated mechanisms.

Even though electrocution has been recognized--and studied--for over a century, there remain several common misconceptions among medical professional as well as lay persons. This review focuses on "low-power" electrocutions rather than on the "high-power" electrocutions such as from lightning and power lines. Low-power electrocution induces ventricular fibrillation (VF). We review the 3 established mechanisms for electrocution: (1) shock on cardiac T-wave, (2) direct induction of VF, and (3) long-term high-rate cardiac capture reducing the VF threshold until VF is induced. There are several electrocution myths addressed, including the concept--often taught in medical school--that direct current causes asystole instead of VF and that electrical exposure can lead to a delayed cardiac arrest by inducing a subclinical ventricular tachycardia (VT). Other misunderstandings are also discussed.

The stability of electrically induced ventricular fibrillation.

The first recorded heart rhythm for cardiac arrest patients can either be ventricular fibrillation (VF) which is treatable with a defibrillator, or asystole or pulseless electrical activity (PEA) which are not. The time course for the deterioration of VF to either asystole or PEA is not well understood. Knowing the time course of this deterioration may allow for improvements in emergency service delivery. In addition, this may improve the diagnosis of possible electrocutions from various electrical sources including utility power, electric fences, or electronic control devices (ECDs) such as a TASER(®) ECD. We induced VF in 6 ventilated swine by electrically maintaining rapid cardiac capture, with resulting hypotension, for 90 seconds. No circulatory assistance was provided. They were then monitored for 40 minutes via an electrode in the right ventricle. Only 2 swine remained in VF; 3 progressed to asystole; 1 progressed to PEA. These results were used in a logistic regression model. The results are then compared to published animal and human data. The median time for the deterioration of electrically induced VF in the swine was 35 minutes. At 24 minutes VF was still maintained in all of the animals. We conclude that electrically induced VF is long-lived--even in the absence of chest compressions.

Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure.

BACKGROUND: Sudden death from cardiac causes remains a leading cause of death among patients with congestive heart failure (CHF). Treatment with amiodarone or an implantable cardioverter-defibrillator (ICD) has been proposed to improve the prognosis in such patients. METHODS: We randomly assigned 2521 patients with New York Heart Association (NYHA) class II or III CHF and a left ventricular ejection fraction (LVEF) of 35 percent or less to conventional therapy for CHF plus placebo (847 patients), conventional therapy plus amiodarone (845 patients), or conventional therapy plus a conservatively programmed, shock-only, single-lead ICD (829 patients). Placebo and amiodarone were administered in a double-blind fashion. The primary end point was death from any cause. RESULTS: The median LVEF in patients was 25 percent; 70 percent were in NYHA class II, and 30 percent were in class III CHF. The cause of CHF was ischemic in 52 percent and nonischemic in 48 percent. The median follow-up was 45.5 months. There were 244 deaths (29 percent) in the placebo group, 240 (28 percent) in the amiodarone group, and 182 (22 percent) in the ICD group. As compared with placebo, amiodarone was associated with a similar risk of death (hazard ratio, 1.06; 97.5 percent confidence interval, 0.86 to 1.30; P=0.53) and ICD therapy was associated with a decreased risk of death of 23 percent (0.77; 97.5 percent confidence interval, 0.62 to 0.96; P=0.007) and an absolute decrease in mortality of 7.2 percentage points after five years in the overall population. Results did not vary according to either ischemic or nonischemic causes of CHF, but they did vary according to the NYHA class. CONCLUSIONS: In patients with NYHA class II or III CHF and LVEF of 35 percent or less, amiodarone has no favorable effect on survival, whereas single-lead, shock-only ICD therapy reduces overall mortality by 23 percent.

Seasonal variation of mortality in the Antiarrhythmics Versus Implantable Defibrillators (AVID) study registry.

OBJECTIVES: We postulated that the pattern of death would be nonrandom with respect to temporal variables. BACKGROUND: Previous studies have demonstrated increased sudden death is associated with periods of relative stress, and overall mortality is associated with temporal variables. METHODS: In the Antiarrhythmics Versus Implantable Defibrillators (AVID) registry, vital status was obtained for 4,450 patients (who had a recent episode of sustained ventricular arrhythmias or unexplained syncope and inducible ventricular tachycardia) through the National Death Index Service as of December 31, 1997 (follow-up 25.5 +/- 13.7 months). RESULTS: Mortality was not associated with the day of the week or with holidays but was associated with season (P = .033). Seasonal variation was present both in northern and southern sites. Mortality was higher during the winter months compared to the remaining months (111.2% in winter vs 96.5% in other months, P = .036). In addition, increased mortality was associated with a high-risk season variable defined (prior to evaluation of treatment arm associations) as spring in the north and winter in the south (P < .001). The hazard ratio for death associated with this "high-risk season" measured 1.25 (P = .001) compared to the other seasons in each region. A test of interaction between "high-risk" season and implantable cardioverter-defibrillator (ICD) status suggested that the group with ICDs experienced reduced mortality during the "high-risk season" compared to the group without ICDs (P = .047). CONCLUSIONS: Mortality was higher in the winter months and in the respective regional "high-risk" seasons. Furthermore, seasonal variation in mortality may have been due to variation in sudden arrhythmic death, and associated increases in mortality were reduced by ICD therapy.