Citation

Haouzi P, Tubbs N, Rannals MD, Judenherc-Haouzi A, Cabell LA, McDonough JA, Sonobe T. Shock 2016; 47(3): 352-362.

Affiliation

*Division of Pulmonary and Critical Care Medicine, Department of Medicine †Heart and Vascular Institute, Pennsylvania State University, College of Medicine, Hershey, PA ‡Southwest Research Institute, San Antonio, TX.

Copyright

(Copyright © 2016, The Shock Society, Publisher Lippincott Williams and Wilkins)

DOI

10.1097/SHK.0000000000000732

PMID

27513083

Abstract

Our objective was to determine how circulatory failure develops following systemic administration of potassium cyanide (KCN). We used a non-inhaled modality of intoxication, wherein the change in breathing pattern would not influence the diffusion of CN into the blood, akin to the effects of ingesting toxic levels of CN. In a group of 300-400 g rats, CN-induced coma (CN IP, 7 mg/kg) produced a central apnea within 2-3 minutes along with a potent and prolonged gasping pattern leading to auto-resuscitation in 38% of the animals. Motor deficits and neuronal necrosis were nevertheless observed in the surviving animals. To clarify the mechanisms leading to potential auto-resuscitation versus asystole, 12 urethane-anesthetized rats were then exposed to the lowest possible levels of CN exposure that would lead to breathing depression within 7-8 minutes; this dose averaged 0.375 mg/kg/min iv. At this level of intoxication, a cardiac depression developed several minutes only after the onset of the apnea, leading to cardiac asystole as PaO2 reached value around 15 Torr, unless breathing was maintained by mechanical ventilation or through spontaneous gasping. Higher levels of KCN exposure in 10 animals provoked a primary cardiac depression, which led to a rapid cardiac arrest by pulseless electrical activity despite the maintenance of PaO2 by mechanical ventilation. These effects were totally unrelated to the potassium contained in KCN.It is concluded that circulatory failure can develop as a direct consequence of CN induced apnea but in a narrow range of exposure. In this "low" range, maintaining pulmonary gas exchange after exposure, through mechanical ventilation (or spontaneous gasping) can reverse cardiac depression and restore spontaneous breathing. At higher level of intoxication, cardiac depression is to be treated as a specific and spontaneously irreversible consequence of CN exposure, leading to a pulseless electrical activity.

Language: en