Cardiovascular Toxicology

, Volume 18, Issue 5, pp 436–449 | Cite as

On the Efficacy of Cardio-Pulmonary Resuscitation and Epinephrine Following Cyanide- and H2S Intoxication-Induced Cardiac Asystole

  • Annick Judenherc-HaouzI
  • Takashi Sonobe
  • Vikhyat S. Bebarta
  • Philippe Haouzi


This study was aimed at determining the efficacy of epinephrine, followed by chest compressions, in producing a return of spontaneous circulation (ROSC) during cyanide (CN)- or hydrogen sulfide (H2S)-induced toxic cardiac pulseless electrical activity (PEA) in the rat. Thirty-nine anesthetized rats were exposed to either intravenous KCN (n = 27) or H2S solutions (n = 12), at a rate that led to a PEA within less than 10 min. In the group intoxicated by CN, 20 rats were mechanically ventilated and received either epinephrine (0.1 mg/kg i.v. n = 10) followed by chest compressions or saline (n = 10, “control CN”) when in PEA. PEA was defined as a systolic pressure below 20 mmHg and a pulse pressure of less than 5 mmHg for 1 min. In addition, seven spontaneously breathing rats were also exposed to the same CN protocol, but infusion was stopped when a central apnea occurred; then, as soon as a PEA occurred, epinephrine (0.1 mg/kg IV) was administered while providing manual chest compressions and mechanical ventilation (CPR). Finally, 12 rats were intoxicated with H2S, while mechanically ventilated, and received either saline (n = 6, “control H2S”) or epinephrine (n = 6) with CPR when in PEA. None of the control-intoxicated animals resuscitated (10 rats in the control CN group and 6 in the control H2S group). In contrast, all the animals intoxicated with CN or H2S that received epinephrine followed by chest compressions, returned to effective circulation. In addition, half of the spontaneously breathing CN-intoxicated animals that achieved ROSC after epinephrine resumed spontaneous breathing. In all the animals achieving ROSC, blood pressure, cardiac output, peripheral blood flow and \( {\dot{\text{V}}} \)O2 returned toward baseline, but remained lower than the pre-intoxication levels (p < 0.01) with a persistent lactic acidosis. Epinephrine, along with CPR maneuvers, was highly effective in resuscitating rodents intoxicated with CN or H2S. Since epinephrine is readily available in any ambulance, its place as an important countermeasure against mitochondrial poisons should be advocated. It remains critical to determine whether the systematic administration of epinephrine to any victims found hypotensive following CN or H2S intoxication could prevent PEA, decrease post-ischemic brain injury and increase the efficacy of current antidotes by improving the circulatory status.


Cyanide Hydrogen sulfide Acute cardiac failure Toxic pulseless electrical activity Epinephrine 



This work was in part supported by the National Institutes of Health Office of the Director (NIH OD), and the National Institute of Neurological Disorders and Stroke (NINDS), Grant Numbers R21 NS090017 and R21 NS098991.

Author Contributions

A. J-H contributed to the design of the experiments, the analysis of the data and the writing and edition of the manuscript, T.S. performed some of the experiments and contributed to the design of experiments, V.B. contributed to the analysis of the data and the writing and editing of the manuscript, P.H. provided the original idea for the study, performed some of the experiments, supervised the study, contributed to the design of the experiments, to the analysis of the data, to the writing of the first and last draft and editing of the manuscript.

Compliance with Ethical Standards

Conflict of interest

All authors declare that they have no conflict of interest.


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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  • Annick Judenherc-HaouzI
    • 1
  • Takashi Sonobe
    • 2
  • Vikhyat S. Bebarta
    • 3
  • Philippe Haouzi
    • 2
  1. 1.Heart and Vascular InstituteHersheyUSA
  2. 2.Division of Pulmonary and Critical Care Medicine, Department of Medicine, College of MedicinePennsylvania State UniversityHersheyUSA
  3. 3.Department of Emergency MedicineUniversity of Colorado School of MedicineAuroraUSA

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