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Clarification of cyanide’s effect on oxygen transport characteristics in a canine model
  1. Julius Cuong Pham1,
  2. David T Huang2,
  3. Francis T McGeorge3,
  4. Emanuel P Rivers4
  1. 1Department of Emergency Medicine, Department of Anesthesia and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
  2. 2CRISMA Laboratory, Department of Critical Care Medicine, Department of Emergency Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
  3. 3Department of Emergency Medicine, William Beaumont Hospital, Beaumont, Michigan, USA
  4. 4Department of Emergency Medicine, Henry Ford Health System, Detroit, Michigan, USA
  1. Correspondence to:
 Dr Julius Cuong Pham
 Department of Anesthesia and Critical Care, Johns Hopkins University School of Medicine, Johns Hopkins Hospital, Meyer 297, 600 N Wolfe Street, Baltimore, MD 21287, USA; jpham3{at}jhmi.edu

Abstract

Objective: To clarify the cardiovascular mechanisms of cyanide poisoning by evaluating oxygen transport characteristics using a canine model.

Methods: A prospective controlled experiment was performed at a hospital-based animal laboratory. Five male beagle (17 (2) kg) dogs were anesthetised with α-chloralose, paralysed with pancuronium bromide and mechanically ventilated. Potassium cyanide was infused at 0.045 mg/kg/min for 110 min. Heart rate, blood pressure, cardiac output, oxygen delivery (Do2), oxygen consumption (Vo2) and oxygen extraction ratio (OER) were measured every 10 min for 140 min. Do2 was measured by an indirect calorimeter.

Results: Cyanide and lactate levels peaked at 1.52 (0.25) mg/l and 9.1 (1.5) mmol/l, respectively. Systolic blood pressure remained relatively constant whereas diastolic blood pressure decreased by 19%. Cardiac output, heart rate and Do2 increased to a maximum of 6%, 10% and 10%, respectively, at 40 min, after which they declined to a low of 32%, 28% and 30% below baseline, respectively. Stroke volume remained constant. Oxygen consumption initially increased by 5%, then decreased to 24% below baseline. The OER initially declined to 35% below baseline, then increased throughout the rest of the study.

Conclusion: Cyanide poisoning in the canine model showed two phases of injury. The first (compensated) phase had a mechanism consistent with a traditional global oxygen consumption defect. The second (decompensated) phase had a mechanism consistent with heart failure. This heart failure was due to bradycardia. These data suggest chronotropy as an avenue of further study in the temporary treatment of cyanide poisoning.

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Footnotes

  • Competing interests: None declared.

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