Toxic Gases
General Characteristics
- Toxic gases tend to interfere with one or more of the four phases of oxygen delivery: uptake, diffusion, transport, and utilization
- Simple asphyxiants displace oxygen from the inspired gas mixture creating diminished uptake
- Pulmonary irritants cause non-cardiogenic pulmonary edema and impair oxygen diffusion across the alveolar membrane
- Chemical asphyxiants affect either transport or utilization
- Agents that disrupt oxygen utilization act at the mitochondrial level
Simple Asphyxiants
- Simple asphyxiants displace oxygen from air (carbon dioxide, nitrogen, hydrogen, methane, propane)
- When the concentration of any of gases increase, the fraction of inspired oxygen (FiO2) decreases:
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- At a FiO2 of less than 16% air, hunger, tachypnea, and changes in level of conscious occur
- At FiO2 less than 10%, loss of consciousness, seizures, or vomiting may occur
- Treatment is restoration of a higher FiO2 with supplemental oxygen discontinued exposure
Irritant Gases
- Highly water-soluble agents:
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- Highly water-soluble agents react with water in the upper respiratory tract and produce immediate irritation and discomfort
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- Ammonia, used as an industrial refrigerant, is prototypical
- Chloramine is created when bleach and ammonia are mixed together
- Warning symptoms include eye irritation and edema, burning in the throat, and constriction of the upper airway
- Treatment is aimed supplying supplemental oxygen, discontinued exposure, and monitoring the pulmonary status
- Intermediate water-soluble agents:
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- The only gas classified as intermediate in solubility is chlorine
- Chlorine reacts with water in the upper airways to produce hydrochloric and hydrochlorous acids
- Warning symptoms include burning of the conjunctiva, throat, and the bronchial tree
- Higher concentrations can produce bronchospasm, lower pulmonary injury, and delayed onset of pulmonary edema
- Treatment is aimed supplying supplemental oxygen, discontinued exposure, and monitoring the pulmonary status
- Slightly water-soluble agents:
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- Phosgene is prototypical of the slightly water-soluble gases
- At concentrations as low as 25 ppm, it can be fatal after even brief exposures
- It produces minimal warning symptoms consisting of mild irritation of the eyes and upper airways
- It slowly hydrolyzes to hydrochloric acid in the alveoli to cause delayed onset of pulmonary edema
- Treatment is supportive, including pulmonary monitoring, and intubation and ventilation as indicated
Chemical Asphyxiants
- The chemical asphyxiants react in the body to interrupt either the delivery or utilization of oxygen
- Carbon monoxide binds to hemoglobin creating carboxyhemoglobin and has 250 to 270 times the affinity of oxygen, making it incapable of binding and transporting oxygen
- Nitrites convert Fe ++ to Fe +++ (methemoglobin), making it incapable of binding and transporting oxygen:
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- Both carboxyhemoglobin and methemoglobin can be measured by co-oximetry on an arterial blood gas analyzer
- Both are treated with high concentrations of oxygen
- Hyperbaric oxygen can be used for carbon monoxide exposures with altered level of consciousness and neurologic findings
- Methemoglobinemia can be treated with methylene blue, which acts as an electron donor, and converts Fe +++ back to Fe ++
- Patients with methemoglobin levels in excess of 30% should be treated with 1 mg/kg of methylene blue as a 10% solution intravenously
- Chemical asphyxiants can interfere with the electron transport chain in the mitochondria:
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- These agents include cyanide, hydrogen sulfide, and sodium azide
- By binding to cytochrome oxidase a3, these agents disrupt aerobic metabolism and create intracellular acidosis
- Symptoms include headache, alteration of consciousness, seizures, and severe acidosis
- The cyanide antidote kit contains three components: perles of amyl nitrite, an ampoule of sodium nitrite, and an ampoule of sodium thiosulfate:
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- Either the inhaled amyl nitrite, from a crushed perle, or the intravenous sodium nitrite will induce methemoglobinemia
- Both cyanide and sulfide will bind with greater affinity to methemoglobinemia than to cytochrome oxidase, forming either cyanomethemoglobin or sulfmethemoglobin
- The cyanomethemoglobin is detoxified in the liver by the enzyme rhodanase
- Sodium thiosulfate, the third component of the cyanide antidote kit, will stimulate the conversion of cyanide to sodium thiocyanate, which can be renally excreted
- The sodium thiosulfate component is indicated only for suspected cyanide exposure, whereas the nitrite components may be used with sulfide, cyanide, or azide exposures
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