B is the correct answer. Why?

Explanation

Cyanide is a common byproduct of combustion, and cyanide poisoning is a common finding in people rescued from house fires. Cyanide’s toxic effects are the result of it binding to cytochrome oxidase (specifically the ferric ion cytochrome a3) in the mitochondria, which leads to cessation of the electron transport chain and thus cessation of cellular respiration. The cells resort to anaerobic metabolism despite sufficient oxygen levels. Laboratory studies will show a high anion gap metabolic acidosis and elevated lactate levels. Cyanide toxicity was traditionally reversed by the two-step sodium nitrite and sodium thiosulfate kit. This method involved administration of a nitrite (IV or inhalant) to induce methemoglobinemia. The iron molecule in hemoglobin would change from the Fe²⁺ to the Fe³⁺ state, which has a much higher affinity for cyanide, thus pulling it off the electron transport chain. Subsequently, a thiosulfate was given via IV, which would donate a sulfur unit to the cyanide molecule, neutralizing it. This treatment regimen is still an option, however, it should be avoided in patients with possible concomitant carbon monoxide poisoning. More recently, a single 5 g administration of hydroxocobalamin (vitamin B12a) is given intravenously, which has a central cobalt molecule with higher affinity for binding cyanide than the electron transport chain. It converts into cyanocobalamin, which is nontoxic, and reestablishes oxidative metabolism.

While airway edema (A) can evolve quickly and necessitates preventative intubation in an unresponsive patient, this patient has a patent airway at the present time, and a better reason for his distress is smoke inhalation toxicity. Pulmonary edema (C) can be a late-onset injury due to significant alveolar damage by heat and toxic irritants from house fire smoke inhalation. In this acute phase of injury, the more likely cause of injury is cyanide or carbon monoxide toxicity. Ventilation-perfusion mismatch (D) can develop from shunting, alveolar damage, or low perfusion. However, in cyanide toxicity, the patient will have persistently poor aerobic metabolism despite adequate supplemental oxygen levels.