Combined Carbon Monoxide and Cyanide Poisoning
- 1 April 1995
- journal article
- critical care-and-trauma
- Published by Wolters Kluwer Health in Anesthesia & Analgesia
- Vol. 80 (4) , 671-677
- https://doi.org/10.1097/00000539-199504000-00004
Abstract
During fires, victims can inhale significant carbon monoxide (CO) and cyanide (CN) gases, which may cause synergistic toxicity in humans.Oxygen therapy is the specific treatment for CO poisoning, but the treatment of CN toxicity is controversial. To examine the indication for treatment of CN toxicity, we have established a canine model to delineate the natural history of combined CO and CN poisoning. In seven dogs (24 +/- 3 kg), CO gas (201 +/- 43 mL) was administered by closed-circuit inhalation. Then, potassium CN was intravenously (IV) infused (0.072 mg centered dot kg-1 centered dot min-1) for 17.5 +/- 3.0 min. Cardiorespiratory measurements were conducted before and after these toxic challenges. Despite significant CO poisoning (peak carboxyhemoglobin fractions [COHb] = 46% of total hemoglobin [Hb]; elimination t1/2 = 114 +/- 42 min) with attendant decrease in blood O2 content, CO had essentially little effect on any hemodynamic or metabolic variable. On the other hand, CN severely depressed most hemodynamic and metabolic functions. Compared to baseline values, CN caused significant (P < 0.01) decreases in cardiac output (6.4 +/- 2.0 to 3.1 +/- 0.5 L/min) and heart rate (169 +/- 44 to 115 +/- 29 bpm) and decreases in oxygen consumption (VO2) (133 +/- 19 to 69 +/- 21 mL/min) and carbon dioxide production (VCO2) (128 +/- 27 to 103 +/- 22 mL/min). However, these critical hemodynamic and metabolic variables recovered to baseline values by 15 min after stopping the CN infusion, except lactic acidosis which persisted for at least 25 min after the CN infusion. The elimination half-life of CN in the blood was 129 min and significant blood [CN] persisted at least 25 min after the CN infusion. We suggest that, after extraction of a victim from a fire, mechanical ventilation alone should facilitate the return of critical body functions, and that the presence of persistent blood [CN] and lactic acidosis indicate the need for specific therapy for CN toxicity. (Anesth Analg 1995;80:671-7)Keywords
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