Clinical meaning
Cyanide (CN-) is a rapidly acting cellular asphyxiant that binds to cytochrome c oxidase (Complex IV) in the mitochondrial electron transport chain, halting aerobic metabolism. Despite adequate oxygen delivery, cells cannot utilize oxygen for ATP production, forcing reliance on anaerobic glycolysis. This produces profound lactic acidosis (type A -- tissue hypoxia despite adequate oxygen delivery) and cellular death within minutes of significant exposure. Sources include: smoke inhalation (combustion of synthetic materials releases hydrogen cyanide -- #1 cause in developed countries), industrial exposure (electroplating, mining, photography), ingestion of cyanogenic compounds (amygdalin in bitter almonds, apricot pits, cassava), and sodium nitroprusside metabolism (prolonged infusion produces cyanide). The classic finding is bright red/cherry-red venous blood (oxygen-rich because tissues cannot extract oxygen).
Diagnosis & workup
Diagnostics & workup: - Clinical diagnosis based on presentation and context (do NOT wait for confirmatory levels before treating) - Venous blood gas: elevated venous PaO2 and decreased arterio-venous O2 difference (tissues cannot extract oxygen) - Serum lactate: severely elevated (>8 mmol/L in significant poisoning; hallmark is lactic acidosis with normal/high PaO2) - Whole blood cyanide level: >0.5 mcg/mL toxic, >3 mcg/mL lethal; results often take hours -- treat empirically - ABG: high anion gap metabolic acidosis - Co-oximetry: if concurrent CO poisoning from smoke inhalation (carboxyhemoglobin level) - Serum methemoglobin level if hydroxocobalamin given (can interfere with some assays) - Pulse oximetry may be UNRELIABLE: normal SpO2 despite cellular hypoxia (oxygen is in the blood, just not being used)