Acute forces required for fatal compression asphyxia: A biomechanical model and historical comparisons.

Background Fatalities from acute compression have been reported with soft-drink vending machine tipping, motor vehicle accidents, and trench cave-ins. A major mechanism of such deaths is flail chest but the amount of force required is unclear. Between the range of a safe static chest compression force of 1000 N (102 kg with earth gravity) and a lethal dynamic force of 10-20 kN (falling 450 kg vending machines), there are limited quantitative human data on the force required to cause flail chest, which is a major correlate of acute fatal compression asphyxia. Methods We modeled flail chest as bilateral fractures of six adjacent ribs. The static and dynamic forces required to cause such a ribcage failure were estimated using a biomechanical model of the thorax. The results were then compared with published historical records of judicial "pressing," vending machine fatalities, and automobile safety cadaver testing. Results and conclusion The modeling results suggest that an adult male requires 2550 ± 250 N of chest-applied distributed static force (260 ± 26 kg with earth gravity) or 4050 ± 320 N of dynamic force to cause flail chest from short-term chest compression.

Evaluation of the ventilatory effects of a restraint chair on human subjects.

BACKGROUND: Combative individuals often require physical restraint in the prehospital and law enforcement setting. Specialized restraint chairs have been utilized for this purpose in the latter case, but concern has arisen that restrained individuals are at risk for ventilatory compromise and asphyxiation. OBJECTIVE: We sought to determine if placement in a restraint chair results in alterations of respiratory or ventilatory function. METHODS: We conducted a randomized, cross-over, controlled experimental trial in 10 healthy human volunteers performed at a university exercise physiology laboratory. After exercise on a cycle ergometer to 85% of the age-predicted maximal heart rate, subjects were randomized to either a sitting position or restraint chair with arms, legs, and chest secured using standard law enforcement protocol. Subjects remained in each position for 30 min, during which pulmonary function testing of maximal voluntary ventilation (MVV) was performed at 11 and 30 min. Arterial oxygen saturation (O(2)sat) and end-tidal PCO(2) levels (PETCO(2)) were monitored continuously. Subjects repeated the experimental trial in the alternate position after a 45-min rest period. Measures between restraint and sitting positions were compared using a paired t-test at each time measurement. RESULTS: There was no evidence of hypoxemia. Mean PETCO(2) levels were not statistically different between the two groups at any time (p > 0.05), and there was no evidence of hypercapnia. CONCLUSION: In healthy subjects, placement in a restraint chair resulted in a small decrease in MVV, but did not result in any changes in O(2)sat or PETCO(2).

Ventilation-perfusion inequality in the human lung is not increased following no-decompression-stop hyperbaric exposure.

Venous gas bubbles occur in recreational SCUBA divers in the absence of decompression sickness, forming venous gas emboli (VGE) which are trapped within pulmonary circulation and cleared by the lung without overt pathology. We hypothesized that asymptomatic VGE would transiently increase ventilation-perfusion mismatch due to their occlusive effects within the pulmonary circulation. Two sets of healthy volunteers (n = 11, n = 12) were recruited to test this hypothesis with a single recreational ocean dive or a baro-equivalent dry hyperbaric dive. Pulmonary studies (intrabreath V (A)/Q (iV/Q), alveolar dead space, and FVC) were conducted at baseline and repeat 1- and 24-h after the exposure. Contrary to our hypothesis V (A)/Q mismatch was decreased 1-h post-SCUBA dive (iV/Q slope 0.023 +/- 0.008 ml(-1) at baseline vs. 0.010 +/- 0.005 NS), and was significantly reduced 24-h post-SCUBA dive (0.000 +/- 0.005, p < 0.05), with improved V (A)/Q homogeneity inversely correlated to dive severity. No changes in V (A)/Q mismatch were observed after the chamber dive. Alveolar dead space decreased 24-h post-SCUBA dive (78 +/- 10 ml at baseline vs. 56 +/- 5, p < 0.05), but not 1-h post dive. FVC rose 1-h post-SCUBA dive (5.01 +/- 0.18 l vs. 5.21 +/- 0.26, p < 0.05), remained elevated 24-h post SCUBA dive (5.06 +/- 0.2, p < 0.05), but was decreased 1-hr after the chamber dive (4.96 +/- 0.31 L to 4.87 +/- 0.32, p < 0.05). The degree of V (A)/Q mismatch in the lung was decreased following recreational ocean dives, and was unchanged following an equivalent air chamber dive, arguing against an impact of VGE on the pulmonary circulation.

Physiologic effects of the TASER after exercise.

OBJECTIVES: Incidents of sudden death following TASER exposure are poorly studied, and substantive links between TASER exposure and sudden death are minimal. The authors studied the effects of a single TASER exposure on markers of physiologic stress in humans. METHODS: This prospective, controlled study evaluated the effects of a TASER exposure on healthy police volunteers after vigorous exercise, compared to a subsequent, identical exercise session that was not followed by TASER exposure. Subjects exercised to 85% of predicted heart rate (HR) on an ergometer and then were given a standard 5-second TASER activation. Measures before and for 60 minutes after the TASER activation included minute ventilation, tidal volume, respiratory rate, end-tidal pCO(2), oxygen saturation, HR, blood pressure (systolic BP/diastolic BP), 12-lead electrocardiogram, and arterialized blood for pH, pO(2), pCO(2), and lactate. Each subject repeated the exercise and data collection session on a subsequent data, without TASER activation. Data were analyzed using paired Student's t-tests with differences and 95% confidence intervals (CIs). Statistical significance was adjusted for multiple comparisons. RESULTS: A total of 25 officers (21 men and 4 women) completed both portions of the study. After adjusting for multiple comparisons, the TASER group was significantly higher for systolic BP at baseline (difference of 14.1, 95% CI = 8.7 to 19.5, p < 0.001) and HR at 5, 30, and 60 minutes with the largest difference at 30 minutes (difference of 7.0, 95% CI = 2.5 to 11.5, p = 0.004). There were no other significant differences between the two groups in any other measure at any time. CONCLUSIONS: A 5-second exposure of a TASER following vigorous exercise to healthy law enforcement personnel does not result in clinically significant changes in ventilatory or blood parameters of physiologic stress.

Physiological effects of a conducted electrical weapon on human subjects.

STUDY OBJECTIVE: Sudden death after a conducted electrical weapon exposure has not been well studied. We examine the effects of a single Taser exposure on markers of physiologic stress in healthy humans. METHODS: This is a prospective trial investigating the effects of a single Taser exposure. As part of their police training, 32 healthy law enforcement officers received a 5-second Taser electrical discharge. Measures before and for 60 minutes after an exposure included minute ventilation; tidal volume; respiratory rate (RR); end-tidal PCO2; oxygen saturation, pulse rate; blood pressure (systolic blood pressure/diastolic blood pressure); arterialized blood for pH, PO2, PCO2, and lactate; and venous blood for bicarbonate and electrolytes. Troponin I was measured at 6 hours. Data were analyzed using a repeated-measures ANOVA and paired t tests. RESULTS: At 1 minute postexposure, minute ventilation increased from a mean of 16 to 29 L/minute, tidal volume increased from 0.9 to 1.4 L, and RR increased from 19 to 23 breaths/min, all returning to baseline at 10 min. Pulse rate of 102 beats/min and systolic blood pressure of 139 mm Hg were higher before Taser exposure than at anytime afterward. Blood lactate increased from 1.4 mmol/L at baseline to 2.8 mmol/L at 1 minute, returning to baseline at 30 minutes. pH And bicarbonate decreased, respectively, by 0.03 and 1.2 mEq/L at 1 minute, returning to baseline at 30 minutes. All troponin I values were normal and there were no EKG changes. Ventilation was not interrupted, and there was no hypoxemia or hypercarbia. CONCLUSION: A 5-second exposure of a Taser X26 to healthy law enforcement personnel does not result in clinically significant changes of physiologic stress.

Ventilatory and metabolic demands during aggressive physical restraint in healthy adults.

We investigated ventilatory and metabolic demands in healthy adults when placed in the prone maximal restraint position (PMRP), i.e., hogtie restraint. Maximal voluntary ventilation (MVV) was measured in seated subjects (n=30), in the PMRP, and when prone with up to 90.1 or 102.3 kg of weight on the back. MVV with the heaviest weight was 70% of the seated MVV (122+/-28 and 156+/-38 L/min, respectively; p<0.001). Also, subjects (n=27) were placed in the PMRP and struggled vigorously for 60 sec. During the restrained struggle, ventilatory function (V(E)/ MVV) was 44% of MVV in the resting PMRP. While prone with up to 90.1 or 102.3 kg on the back, the decrease in MVV was of no clinical importance in these subjects. Also, while maximally struggling in the PMRP, V(E) was still adequate to supply the ventilatory needs.

Arterial gas embolism and decompression sickness.

Decompression sickness occurs when a sufficiently large gas phase forms within the tissues of the body after a reduction in ambient pressure. Arterial gas embolism occurs secondary to pulmonary barotrauma when gas is forced into the pulmonary vasculature. Although they may clinically present in a similar fashion, the underlying pathophysiology of the two conditions is quite different.