Asphyxiants

Abstract

Asphyxiants deprive the body of oxygen. Simple asphyxiants displace oxygen from the lungs, whereas systemic asphyxiants interfere with transport of oxygen by hemoglobin or with mitochondrial oxidative phosphorylation. Asphyxiants may be gases, liquids, or solids, or their metabolites. The typical clinical picture of asphyxiant poisoning is one of progressive mental status changes, alteration of breathing, progressively abnormal vital signs, coma, seizures, and eventually cardiovascular collapse and death. Treatment of asphyxiant poisoning is aggressive supportive care, with control of the airway and ventilation and maintenance of cardiac output. Supportive care is often enhanced by the administration of specific antidotes.

Hazardous Chemical Emergencies and Poisonings

“…Asphyxiant exposures cause tissue hypoxia, with profound neurologic and cardiovascular effects. 57,58 Simple asphyxiants (e.g., nitrogen and methane) act primarily through physical displacement of oxygen from inspired air, resulting in arterial hypoxemia. Some systemic or chemical asphyxiants (e.g., carbon monoxide and methemoglobin inducers) interfere with oxygen transport, and some (e.g., carbon monoxide, hydrogen sulfide, cyanide, phosphine, and azides) interfere with oxidative metabolism, leading to tissue hypoxia with a shift to anaerobic metabolism and result-ing in metabolic acidosis and hyperlactatemia.…”

“…61,62 Some asphyxiants are considered to be potential terrorist threats. 57 In the most severe exposures, particularly with carbon monoxide, cyanide, and hydrogen sulfide, rapid knockdown may occur, with a sudden loss of consciousness, collapse, and progressive cardiovascular compromise. The asphyxiant (knockdown) toxidrome ranges from severe effects, such as seizures, coma, hypotension, bradycardia, and apnea, to milder findings, including headache, dizziness, fatigue, tachycardia, dyspnea, nausea, and vomiting.…”

“…Cyanide exposure is associated with inhalation of smoke from house fires; additional sources of exposure include industrial and laboratory accidents, sodium nitroprusside therapy, cyanogenic chemical and plant ingestion, suicide attempts, and criminal or terrorist activity. 57,58,[66][67][68][69] Cyanide inhibits mitochondrial cytochrome oxidase and thus oxidative phosphorylation, with asphyxiant clinical effects, metabolic acidosis, and hyperlactatemia (Fig. 1).…”

“…68 Management of asphyxiant poisoning begins with removal to fresh air, dermal decontamination for liquid exposures, advanced life support with 100% oxygen as the respired gas, and correction of metabolic acidosis. 1,57,58,69 Gastrointestinal decontamination may be considered for cyanide and azide ingestion, particularly ingestion of cyanogenic compounds (e.g., acetonitrile and amygdalin). Oxygen, which is used for hypoxemia associated with simple asphyxiants, enhances carboxyhemoglobin elimination and, despite cytochrome oxidase inhibition, appears to be beneficial in managing the toxic effects of cyanide and hydrogen sulfide.…”

“…Oxygen, which is used for hypoxemia associated with simple asphyxiants, enhances carboxyhemoglobin elimination and, despite cytochrome oxidase inhibition, appears to be beneficial in managing the toxic effects of cyanide and hydrogen sulfide. 1,57,58 Hyperbaric oxygen therapy, if immediately available, may mitigate neurocognitive sequelae of clinically significant carbon monoxide toxicity 63,64,71 ( Table 1).…”