Brief Report

Does weight force application to the lower torso have an influence on inferior vena cava and cardiovascular parameters?

Astrid Krauskopf MD^a,?, Marius Mayerhoefer MD^b, Felicitas Oberndorfer MD^a,

Bayda Salameh MD^c, Andreas Bur MD^d, Barbara Schneider PhD^e, Daniele Risser MD^a

^aDepartment of Forensic Medicine, Medical University of Vienna, 1090 Vienna, Austria

^bDepartment of Radiology, Medical University of Vienna, Austria, 1090 Vienna, Austria

^cClinical Department of occupational medicine, Medical University of Vienna, 1090 Vienna, Austria

^dDepartment of Emergency Medicine, Medical University of Vienna, 1090 Vienna, Austria

^eSection of medical statistics, Medical University of Vienna, 1090 Vienna, Austria

Received 18 July 2007; revised 13 August 2007; accepted 13 August 2007

Abstract

Objective: The aim of this study was to determine whether weight force application to the lower torso can lead to impairment of Inferior vena cava and cardiovascular parameters.

Methods: Using ultrasound sonography and Impedance cardiography, the effects of a weight force application of 5, 10, 15, and 25 kg to the lower torso, placed in prone position, on IVC diameter and maximal blood flow, mean artery pressure, stroke volume, heart rate, cardiac index, cardiac output, oxygen saturation (SpO2), and acceleration index were investigated in 6 healthy volunteers.

Results: The following parameters showed a statistically significant correlation with the amount of weight force applied: IVC diameter: r=-0.83, P b .001; IVC maximal blood flow: r=-0.76, P b .001;

cardiac index: r=-0.33, P b .05; and cardiac output: r=-0.32, P b .05.

Conclusion: Application of moderate weight force to the lower torso can lead to major changes in IVC parameters and minor changes in cardiovascular parameters.

(C) 2008

Introduction

The term inferior vena cava syndrome is used to describe obstruction or compression of the inferior vena cava , which consequently leads to a decreased preload and

* Corresponding author.

E-mail address: [email protected] (A. Krauskopf).

impaired cardiac performance. The IVC syndrome can occur during the Third trimester of pregnancy and is also associated with pathologic processes such as Renal cell carcinoma and deep vein thrombosis. Symptoms include edema of the lower extremities, tachycardia, and dyspnea, as well as circulatory collapse caused by a reduced venous return to the heart [1].

Cardiorespiratory consequences during a restraint posi- tion have been previously investigated by Roeggla et al [2], who found dramatic decreases in cardiac output (CO). Cases

0735-6757/$ - see front matter (C) 2008 doi:10.1016/j.ajem.2007.08.017

of traumatic asphyxia, in which there is evidence of increased thoracic pressure, were first reported in 1971 [3]. Increased abdominal pressure can also lead to a significant decrease in cardiac output as a result of a compression of the IVC and other large veins, which consequently leads to a decreased preload and impaired cardiac performance, venous stasis, and thrombosis [4].

To date, it is not known whether pressure applied to an individual’s back during a restraint process can lead to an IVC compression and, hence, to the aforementioned effects on cardiac output. Because of the higher demand for venous return in situations of stress, pressure on the back of an individual may thus further increase the risk of circulatory collapse.

The goal of this pilot study was to investigate the impact of different amounts of weight force, applied to the lower torso in a prone position, on IVC and cardiovascular parameters. On the basis of a case history of sudden death during a restraint position in a 32-year-old man [5], we hypothesized that a prolonged external compression of the lower torso during the fixation process may cause a severe impairment in cardiac output as a result of the narrowing or even obliteration of the IVC. A case report of a woman found dead in an unusual Body position also suggested that a reduced venous return to the heart can have severe cardiovascular consequences [6].

Materials and methods

Patients and study design

Six male volunteers (age range, 22-31 years; body mass range, 60.5-88.2 kg; Body height range, 162.2-190 cm; body mass index range, 22-24; body fat range, 9.6%- 16.6%; abdominal girth range, 80-89 cm) participated in the pilot study, which was approved by the local institutional review board. Written informed consent was obtained from the volunteers. All subjects had an unremarkable medical history and normal findings at physical examination,

performed at the beginning of the study, with no findings suggestive of cardiovascular diseases or abnormalities and no medical treatment.

To investigate the impact of weight force on IVC and cardiovascular parameters, volunteers were placed in a prone position. The assessment of the IVC and cardiovas- cular parameters was performed with and without weight force, generated by sand-filled bags of 5, 10, 15, and 25 kg, applied to the lower torso. The contact area of the bags on the torso was approximately 136 cm² (17 x 8 cm). To avoid the possible effects of adaptation, the application of weights was randomized and was always followed by a Recovery time of 5 minutes, whereas measurements of the IVC and cardiovascular parameters (see below) were repeated. Thus, a total of 24 measurements for zero weight force application and 6 measurements each for 5-, 10-, 15-, and 25-kg weight force application was available for further analysis.

Assessment of the IVC and cardiovascular parameters

Inferior vena cava parameters were determined by ultra- sound B-mode scans using an Acuson Sequoia 512 system (Siemens Medical, Mountain View, Calif) equipped with a 6.0-MHz transabdominal transducer. The inner diameter of the IVC was measured with the transducer placed on the subject’s right flank using a longitudinal, coronal, or slightly oblique coronal imaging plane parallel to the long axis of the IVC. Using the same transducer position, the maximum flow

velocity (V?max, in m/s) of the IVC was extracted from its

double-peak Doppler frequency spectrum (see Fig. 1). Finally, the maximal blood flow (MBF, in m/s per square centimeter) in the IVC was calculated from its diameter and maximal flow velocity: MBF = V?max x (? x d²/4).

Cardiovascular parameters, measured noninvasively by impedance cardiography (Niccomo, Medis Medizinische Messtechnik GmbH, Ilmenau, Germany) with 4 dual disposable sensors placed on the neck and chest (Fig. 2), were mean artery pressure (in mm Hg); stroke volume (SV;

Fig. 1 Sonographic assessment of IVC parameters, using an oblique coronal imaging plane. First, the diameter of the IVC is measured on the longitudinal view of the vessel (A). Then, the maximum flow velocity of the IVC is extracted from its characteristic double-peak frequency spectrum (B).

Fig. 2 Volunteer in prone position with a sand-filled bag of 5 kg placed in his lower torso. For assessment of cardiovascular parameters, 4 disposable impedance cardiography sensors are placed on the subject’s neck and chest. For assessment of IVC parameters, the Transabdominal ultrasound transducer is placed on the subject’s right flank, using a longitudinal, frontal imaging plane parallel to the long axis of the IVC.

defined as CO/heart rate [HR] [in mL]); HR (in beats per minute); cardiac index (CI, defined as cardiac output per unit time divided by body surface area, in L/min per m²); CO (defined as SV x HR, in L/min), oxygen saturation (SpO2 [%]); and acceleration index (in 1/100 per square second).

Statistical analysis

For all statistical analyses, the SPSS for Microsoft Windows workstation v.11.0.0 (SPSS Inc, Chicago, Ill) was used. To determine the relation between the IVC and cardiovascular parameters, on the one hand, and the influence of weight force application to the lower torso on these parameters, on the other hand, Pearson Correlation coefficients were calculated, which were interpreted as follows: 0 to 0.25, negligible or no correlation; 0.26 to 0.50, fair correlation; 0.51 to 0.75, moderate to good correlation; 0.76 to 1.0, very good to excellent correlation [7].

Table 1 Descriptive statistics (median and range) for IVC and cardiovascular parameters, assessed under a weight force application of 0, 5, 10, 15 and 25 kg to the lower torso

For further analysis of the effects of weight force application, the Mann-Whitney U test was used to compare the medians of IVC and cardiac parameters, obtained without weight force application, with those obtained under a weight force application of 5, 10, 15, and 25 kg, respectively (Table 1). A 5% significance level was specified for all group comparisons.

Results

We observed a significant negative correlation between the amount of weight force applied and the IVC diameter (r=-0.83, P b .001). We also observed a significant, negative correlation between the amount of weight force, and the maximum blood flow (MBF) in the IVC (r=

-0.76, P b .001).

With regard to the IVC diameter, the Mann-Whitney U test revealed a statistically significant difference between measurements performed with zero weight force, and measurements performed with 5 (P b .05), 10 (P b .01), 15 (P b.001), and 25 kg (P b.001). With regard to the MBF, on the other hand, we only found a statistically significant difference between measurements performed with zero weight force, and measurements performed with 15 (P b

.001) and 25 kg (P b.001), but not with 5 or 10 kg (P N .05). Of the cardiovascular parameters, only the CI and the CO showed a fair, statistically significant, negative correlation with the amount of weight force, with r=-0.33 (P b.05) and r=-0.32 (P b .05), respectively. None of the cardiovascular parameters showed a significant difference between mea- surements performed without weight force application and measurements performed with weight forces of 5, 10, 15, or

25 kg applied to the lower torso.

Discussion

It was our study hypothesis that external compression of the lower torso would have a significant effect on the IVC or

0 kg		5 kg	10 kg	15 kg	25 kg
IVC diameter (cm)	2.4 (1.9-2.7)	2.2 (1.5-2.4)	1.8 (1.2-2.3)	1.3 (1.0-1.7)	1 (1-1.6)
IVC MBF (m/s per cm2)	2.9 (2.1-3.8)	2.4 (1.2-3.5)	1.8 (0.8-3.8)	0.9 (0.5-1.6)	0.6 (0.4-1.4)
MAP (mm Hg)	86 (67-93)	83.5 (67-91)	85 (77-94)	87.5(74-90)	84.5 (68-88)
SV (ml)	95 (51-119)	93 (57-113)	89 (59-105)	88 (60-112)	79 (54-102)
HR (1/min)	65.5 (43-90)	62.5 (45-85)	60.5 (47-82)	60.5 (39-76)	64.5 (44-84)
CI (L/min per m2)	2.7 (2.2-3.7)	3 (2.2-3.3)	2.6 (2.3-3.2)	2.6 (2.2-3.0)	2.5 (2.1-3.1)
CO (L/min)	5.5 (4.4-7.4)	5.1 (4.5-6.5)	4.9 (4.7-6.4)	4.9 (4.3-6.1)	4.6 (4.4-6.2)
SpO2 (%)	96 (95-97)	96 (96-98)	96.5 (95-97)	97 (96-98)	96 (96-97)
ACI (1/100 per s2)	106.5 (78-139)	106.5 (64-119)	110 (65-126)	114 (69-137)	101 (60-111)
MAP, mean artery pressure; ACI, acceleration index.

cardiovascular parameters. The results of this study partly support this hypothesis, particularly with regard to the IVC parameters (diameter, MBF). We observed a very good correlation of these IVC parameters with the amount of weight force applied, and we also found a highly significant difference between measurements obtained without weight force application and measurements obtained under a weight force application of 15 and 25 kg for both parameters.

On the other hand, of the 7 cardiovascular parameters, only CO and CI showed a significant correlation with the amount of weight force applied, which was only fair. There was also no significant difference between measurements performed with and without weight force application for any of the cardiovascular parameters, not even between zero weight force and a weight force of 25 kg.

There are several possible explanations for these results. First, heavier weights, such as may appear in the field setting, may have to be used to cause a significant or even life- threatening effect on cardiovascular parameters. Second, our selection of 6 nonobese volunteers, which was done in order to create the best possible study conditions for sonographic measurement of the diameter and flow of the IVC, resulted in

5 of 6 individuals who were very athletic and, hence, probably were in a better cardiovascular condition than the average individual. Third, as this was a laboratory physiol- ogy study, no additive conditions, which are common in cases of sudden death during a restraint position, were reproduced, such as drug application, struggle, trauma, or other stress. Finally, changes in IVC parameters may, per se, be less clinically important than previously suggested.

During the last 20 years, various reports have suggested different theories for cases of sudden death during a restraint position, with regard to the possible mechanisms of death. Terms such as positional asphyxia, restraint asphyxia, and traumatic asphyxia have been coined, mostly relating to cases of sudden death in police custody, care institutions, or accidents.

The diagnosis of positional (postural) asphyxia is essentially based on 3 criteria: the body position must obstruct normal Gas exchange, it must be impossible to move to another position, and other causes of death must be excluded [8]. Historically, death attributed to positional asphyxia has always been accidental but was also mislead- ingly used for cases of restraint asphyxia.

The term restraint asphyxia, first proposed in 1993, expands the concept of positional asphyxia to include the process of subduing and either physically or mechanically restraining an individual (usually in a hobble or hog-tie position) [9]. This process of “taking down” contains the potential for compression and restriction of chest movement by placement of pressure (usually knee or hand) on the back of the thorax in the prone position while the subject is being subdued and initially restrained [5]. Thus, as positional asphyxia deaths are caused by “passive entrapment,” restraint asphyxia deaths are related to being physically or mechanically entrapped by another person. Pathologic

findings in death attributed to positional and restraint asphyxia usually do not reveal any signs of suffocation or other significant autopsy findings.

In contrast, the Perthes syndrome [10,11], a term first coined by Ollivier [12] in 1837, also known as traumatic asphyxia, is characterized by 3 factors: subconjunctival hemorrhages, cervicofacial petechiae, and cyanosis. The term is usually used to describe compressive asphyxia that results from the application of extreme weight force on the chest or abdomen of the individual [13-18]. Different pathomechan- isms for the development of the symptoms have been formulated in the literature [19-22]. This concept of killing a person by the application of body weight to the thorax, causing a form of mechanical asphyxia, was the underlying principle in the murders of Burke and Hare in the 19th century [23].

The impact of restraint position on Respiratory function has been discussed controversially [24-29]. Several cases of death during a restraint position, coupled with excited delirium, have been described [30-32]. Other possible factors associated with sudden death, such as drug abuse, underlying heart disease, severe metabolic acidosis, and hyperthermia, have also been subject to discussion [9,33]. Finally, as already mentioned, a dramatic decrease in cardiac output during a restraint position has been reported by Roeggla et al

[2] in 1997.

Conclusion

To better understand cases of sudden death during a restraint position that have been reported in the literature, we investigated the impact of weight force application to the lower torso on the IVC and cardiovascular parameters. Based on our findings, we conclude that weight force applied to the lower torso in prone position leads to significant changes in diameter and maximum blood flow of the IVC but only to minor changes in the cardiac index and output. Other cardiovascular parameters were not at all influenced by weight force application.

Thus, additional experiments with weight forces of more than 25 kg are necessary to determine whether more clinically relevant changes can be provoked in that way.

Acknowledgments

The authors would like to thank Mag Beatrix Krauskopf and Patrick Schatz for their experimental assistance.

References

1. Pschyrembewl: Klinisches Worterbuch. 260th ed. Berlin: Walter de Gruyter; 2004. p. 1902.
2. Roeggla M, Wagner A, Muellner M, et al. Cardiorespiratory consequences to hobble restraint. Wien Klin Wochenschr 1997; 109:359-61.
3. Haller Jr JA, Donahoo JS. Traumatic asphyxia in children: pathophysiology and management. J Trauma 1971;11:453-7.
4. Epelman M, Soudack M, Engel A, et al. Abdominal compart- ment syndrome in children: CT findings. Pediatr Radiol 2002;32: 319Q22.
5. Krauskopf A, Oberndorfer F, Hudabiunigg K, et al. Is the vena cava inferior syndrome a possible pathomechanism in sudden death during restraint position? [scientific poster]. 4th European Academy of Forensic Science Meeting, June 13-16, 2006, Helsinki.
6. Falk J, Riepert T, Iffland R, et al. Death due to unusual position of the body-an explanation for the consequence of reduced venous reflux to the heart. Arch Kriminol 2004;213:102-7.
7. Colton T. Statistics in medicine. Boston: Little, Brown and Company; 1974.
8. Belviso M, De Donno A, Vitale L, et al. Positional asphyxia: reflection on 2 cases. Am J Forensic Med Pathol 2003;24:292-7.
9. O’Halloran RL, Lewman LV. Restraint asphyxiation in excited delirium. Am J Forensic Med Pathol 1993;14:289-95.
10. Brinkmann B. Traumatic asphyxia: pathophysiology and pathomor- phology. Z Rechtsmed 1978;81:79-96.
11. Perthes G. Uber Druckstauung”. Dtsch Z Chir 1900;55:384-92.
12. Ollivier DA. Relation medicale des evenements survenus au Champ- de-Mars- le 14 juin, 1837. Ann Hyg 1837;18:485-9.
13. Gosling T, Schmidt U, Herzog T, et al. Perthes syndrome. The classical symptom triad as a rarity in trauma surgery practice. Unfallchirurg 2001;104:191-4.
14. Wardrope J, Ryan F, Clark G, et al. The Hillsborough tragedy. BMJ 1991;303:1381-5.
15. Byard RW, Wick R, Simpson E, et al. The pathological features and circumstances of death of lethal crush/traumatic asphyxia in adults-a 25-year study. Forensic Sci Int 2006;159:200-5.
16. DeAngeles D, Schurr M, Birnbaum M, et al. Traumatic asphyxia following stadium crowd surge: stadium factors affecting outcome. WMJ 1998;97:42-5.
17. Madzimbamuto F, Madamombe T. Traumatic asphyxia during stadium stampede. Cent Afr J Med 2004;50:69-72.
18. Reay DT. Death in custody. Clin Lab Med 1998;18:1-22.
19. Tardieu A. Relation medico-legalede l’accident survenu au pont de la condorde, a Paris, le 15 aout 1866, pour servir a l’histoire de la mort par suffocation. Ann d’hyg 1866;2:338.
20. Bolt RA. Traumatic asphyxia-report of a case. Cleve Med J 1908;7:647-59.
21. Williams JS, Minken SL, Adams JT. Traumatic asphyxia-reap- praised. Ann Surg 1968;167:384-92.
22. Thompson Jr A, Illescas FF, Chiu RC. Why is the lower torso protected in traumatic asphyxia? A new hypothesis. Ann Thorac Surg 1989;47:247-9.
23. McDonald SW. Glasgow resurrectionists. Scott Med J 1997;42:84-7.
24. Reay DT, Howard JD, Fligner CL, et al. Effects of positional restraint on oxygen saturation and heart rate following exercise. Am J Forensic Med Pathol 1988;9:16-8.
25. Reay DT, Fligner CL, Stilwell AD, et al. Positional asphyxia during law enforcement transport. Am J Forensic Med Pathol 1992;13:90-7.
26. Chan TC, Vilke GM, Neuman T, et al. Restraint position and positional asphyxia. Ann Emerg Med 1997;30:578-86.
27. Chan TC, Vilke GM, Neuman T. Reexamination of custody restraint position and positional asphyxia. Am J Forensic Med Pathol 1998;19:201-5.
28. Chan TC, Neuman T, Clausen J, et al. Weight force during prone restraint and respiratory function. Am J Forensic Med Pathol 2004;25:185-9.
29. Michalewicz BA, Chan TC, Vilke GM, et al. Ventilatory and metabolic demands during aggressive physical restraint in Healthy adults. J Forensic Sci 2007;52:171-5.
30. Stratton SJ, Rogers C, Brickett K, et al. Factors associated with sudden death of individuals requiring restraint for excited delirium. Am J Emerg Med 2001;19:187-91.
31. Brodsky MA, Sato DA, Iseri LT, et al. Ventricular tachyarrhythmia associated with psychological stress. The role of the sympathetic nervous system. JAMA 1987;257:2064-7.
32. Di Maio G, Di Maio VJ. Excited delirium syndrome: cause of death and prevention. 1st ed. London: Taylor & Francis Group; 2005.
33. Hick JL, Smith SW, Lynch MT. Metabolic acidosis in restraint- associated cardiac arrest: a case series. Acad Emerg Med 1999; 6:239-43.