Thoracic weighting of restrained subjects during exhaustion recovery causes loss of lung reserve volume in a model of police arrest

Campbell, Mark; Dakin, Roslyn; Stowe, Symon; Burton, Kira; Raven, Brianna; Mapani, Malitela; Dawson, J. W.; Adler, Andy

doi:10.1038/s41598-021-94157-w

Cited by 2 publications

(1 citation statement)

References 26 publications

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“…Prolongation of this situation will result in continued carbon dioxide accumulation. Campbell has demonstrated that prone positioning results in increased work of breathing [88]. Moreover, hyperventilation requires substantial work, with the work of breathing increasing geometrically with the need.…”

Section: Discussionmentioning

confidence: 99%

Prone restraint cardiac arrest in in‐custody and arrest‐related deaths

Weedn

Steinberg²,

Speth³

2022

Journal of Forensic Sciences

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We postulate that most atraumatic deaths during police restraint of subjects in the prone position are due to prone restraint cardiac arrest (PRCA), rather than from restraint asphyxia or a stress-induced cardiac condition, such as excited delirium. The prone position restricts ventilation and diminishes pulmonary perfusion. In the setting of a police encounter, metabolic demand will be high from anxiety, stress, excitement, physical struggle, and/or stimulant drugs, leading to metabolic acidosis and requiring significant hyperventilation.Although oxygen levels may be maintained, prolonged restraint in the prone position may result in an inability to adequately blow off CO 2 , causing blood pCO 2 levels to rise rapidly.The uncompensated metabolic acidosis (low pH) will eventually result in loss of myocyte contractility. The initial electrocardiogram rhythm will generally be either pulseless electrical activity (PEA) or asystole, indicating a noncardiac etiology, more consistent with PRCA and inconsistent with a primary role of any underlying cardiac pathology or stress-induced cardiac etiology. We point to two animal models: in one model rats unable to breathe deeply due to an external restraint die when their metabolic demand is increased, and in the other model, pressure on the chest of rats results in decreased venous return and cardiac arrest rather than death from asphyxia. We present two cases of subjects restrained in the prone position who went into cardiac arrest and had low pHs and initial PEA cardiac rhythms. Our cases demonstrate the danger of prone restraint and serve as examples of PRCA. K E Y W O R D Sprone restraint, in-custody deaths, arrest-related deaths (ARDs), police-involved deaths, restraint asphyxia, positional asphyxia, excited delirium, sudden cardiac death, metabolic acidosis, George Floyd, forensic pathology, autopsy Highlights• Prone restraint deaths result from metabolic acidosis, not hypoxic asphyxia.• Metabolic demand is increased by stimulant drugs, physical exertion, and stress.• Metabolic acidosis requires hyperventilation to "blow off" carbon dioxide (CO 2 ).• Prolonged restraint in the prone position may prevent adequate elimination of CO 2 .• An initial ECG rhythm of PEA or asystole after a cardiac arrest is generally inconsistent with a primary cardiac etiology.How to cite this article: Weedn V, Steinberg A, Speth P. Prone restraint cardiac arrest in in-custody and arrest-related deaths.

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Section: Discussionmentioning

confidence: 99%

Prone restraint cardiac arrest in in‐custody and arrest‐related deaths

Weedn

Steinberg²,

Speth³

2022

Journal of Forensic Sciences

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Response to “Scrutinizing the causal link between excited delirium syndrome and restraint – a commentary on: ‘The role of restraint in fatal excited delirium: a research synthesis and pooled analysis’ by E.M.F. Strömmer, W. Leith, M.P. Zeegers and M.D. Freeman”

Freeman

Strömmer

Leith

et al. 2023

Forensic Sci Med Pathol

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Abstractde Boer et al. criticize the conclusions in our 2020 paper on the validity of Excited Delirium Syndrome (ExDS) as “egregiously misleading.” Our conclusion was that there “is no existing evidence that indicates that ExDS is inherently lethal in the absence of aggressive restraint.” The basis for de Boer and colleague’s criticism of our paper is that the ExDS literature does not provide an unbiased view of the lethality of the condition, and therefore the true epidemiologic features of ExDS cannot be determined from what has been published. The criticism is unrelated to the goals or methods of the study, however. Our stated purpose was to investigate “how the term ExDS has evolved in the literature and been endowed with a uniquely lethal quality,” and whether there is “evidence for ExDS as a unique cause of a death that would have occurred regardless of restraint, or a label used when a restrained and agitated person dies, and which erroneously directs attention away from the role of restraint in explaining the death.” We cannot fathom how de Boer et al. missed this clearly stated description of the study rationale, or why they would endorse a series of fallacious and meaningless claims that gave the appearance that they failed to grasp the basic design of the study. We do acknowledge and thank these authors for pointing out 3 minor citation errors and an equally minor table formatting error (neither of which altered the reported results and conclusions in the slightest), however.

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Thoracic weighting of restrained subjects during exhaustion recovery causes loss of lung reserve volume in a model of police arrest

Cited by 2 publications

References 26 publications

Prone restraint cardiac arrest in in‐custody and arrest‐related deaths

Prone restraint cardiac arrest in in‐custody and arrest‐related deaths

Response to “Scrutinizing the causal link between excited delirium syndrome and restraint – a commentary on: ‘The role of restraint in fatal excited delirium: a research synthesis and pooled analysis’ by E.M.F. Strömmer, W. Leith, M.P. Zeegers and M.D. Freeman”

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