ORIGINAL ARTICLE

Clarification of cyanide’s effect on oxygen transport characteristics in a canine model

Julius Cuong Pham¹, David T Huang², Francis T McGeorge³ and Emanuel P Rivers⁴

¹ Department of Emergency Medicine, Department of Anesthesia and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
² CRISMA Laboratory, Department of Critical Care Medicine, Department of Emergency Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
³ Department of Emergency Medicine, William Beaumont Hospital, Beaumont, Michigan, USA
⁴ Department of Emergency Medicine, Henry Ford Health System, Detroit, Michigan, USA

Correspondence to:
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

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 -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.

Abbreviations: OER, oxygen extraction ratio

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