ACP American College of Physicians - Internal Medicine - Doctors for Adults

Clinical Information

• PIER - Decision Support
• Guidelines
• Journals & Publications
• Additional Resources
  • Cardiology Corner
  • Adult Immunization
  • Bedside Diagnosis
  • Bioterrorism
  • Lyme Disease Initiative
  • End of Life Care
  • Explaining GFR

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:
• • 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:
• • Highly water-soluble agents react with water in the upper respiratory tract and produce immediate irritation and discomfort
  • • 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:
• • 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:
• • 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:
• • 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:
• • 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:
• • 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

• Careers at ACP
• Contact Us
• Privacy
• Site Map
• For Advertisers
• For Media
• For Governors
• For Regents