Metabolic Acidosis in Restraint‐associated Cardiac Arrest

We read with interest the recent article by Dr. Hick et al. about metabolic acidosis in restraint-associated cardiac arrest. We commend the authors for their case series, which addresses the important issue of sudden death in association with vigorous physical activity and restraint, and the possible role of severe metabolic acidosis. We would, however, recommend caution in interpreting the observations made in this series of five patients. The contribution of restraint struggle and body position to the profound acidosis reported in these patients remains unclear. First, a good portion of the metabolic acidosis may have simply been due to cardiopulmonary arrest, as blood gas sampling seems to have taken place after the initial arrest and resuscitation efforts on these patients. Second, it is unlikely fully restrained individuals, even with struggling, are capable of generating oxygen consumptions (VO2) sufficient to generate a profound acidosis. Generally, exercise involving antigravity muscles plus movement of the extremities produces the highest VO2 levels. All subjects described in this series were in a state of heavy physical exertion from fighting or fleeing immediately prior to being physically restrained. Generation of a portion of the observed metabolic acidosis from high VO2 and anaerobic metabolism more likely occurred during this exertion rather than struggle after being restrained. Third, the role of cocaine in these cases cannot be overstated. All five patients had evidence of cocaine on toxicologic screening, and their behavior (which ultimately led to their physical restraint) was consistent with sympathomimetic intoxication or even what has been termed ‘‘toxic’’ or ‘‘excited delirium.’’ In states of catecholamine excess (endogenous and exogenously administered), impaired oxidative phosphorylation leading to metabolic acidosis has been demonstrated. As the authors note themselves, stimulant drug use, particularly when combined with physical exertion, can lead to profound metabolic acidosis without physical restraint. Regardless of the etiology of the acidosis, there is currently no evidence to support the authors’ speculation that prone and hobble body positioning ‘‘may significantly impact . . . [the] ability to develop a compensatory respiratory alkalosis’’ as evidenced by a ‘‘20%’’ drop in ‘‘maximal ventilatory volume’’ [sic] referenced to our study. We exercised subjects well beyond anaerobic threshold to a mean heart rate of 169 beats/min and pH 7.28. During 15-minute rest periods in the sitting and hobble positions, there were no differences in heart rate recovery, PaCO2 (as reported), or pH levels (7.33 vs 7.34, respectively). Moreover, none of the five victims reported in this case series were in the hobble position. Four were restrained prone, a position in which we found a much smaller (15%) drop in maximal voluntary ventilation, or MVV (and only slightly more than the 10% drop seen in the supine position). The remaining fifth victim was ‘‘on his side’’ when he suffered a sudden, ultimately fatal cardiac arrest. This case casts doubt on the authors’ recommendation that ‘‘emphasizing side rather than prone positioning may eliminate some of the problems.’’ Finally, there are several errors in the content of a number of citations. The authors’ claim that Pudiak and Bozarth placed cocaine-injected rats in restraint cylinders such that they did not have ‘‘freedom to turn around’’ is misleading. In that study, the rats had enough room to move and reverse their position, a less restrictive condition that ‘‘might better be described as confinement stress.’’ A small subgroup of rats (n = 5, outside the study’s main methodology and for which no statistical data were provided) were placed in more restrictive confines, but even in that group, ‘‘ample space was provided for normal respiration.’’ The high mortality rate seen in both groups of rats suggests changes in respiratory function do not play a role in the pathophysiology of restraint deaths. The authors’ reference to the article by Bell et al. attributing deaths of subjects in a ‘‘hobbled position’’ to positional asphyxiation is also in error. No victim in that case review was described as being restrained in the hobble or hog-tie position. In summary, there is little evidence that respiratory changes associated with specific body positions significantly contribute to the metabolic derangements and pathophysiology of sudden death in restrained individuals. More likely, as shown in this case series, a multitude of other factors may explain both the profound metabolic acidosis and sudden deaths seen in these individuals.—THEODORE C. CHAN, MD, TOM NEUMAN, MD, and GARY M. VILKE, MD, Department of Emergency Medicine, JACK CLAUSEN, MD, Division of Pulmonary Medicine, Department of Internal Medicine, and RICHARD F. CLARK, MD, Division of Toxicology, Department of Emergency Medicine, University of California—San Diego, San Diego, CA