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Carbonmonoxide (CO) is a colorless, non-irritating and odorless gas.
CO is produced by incomplete oxidative combustion and also from reaction between CO2 absorber and anesthetic agents.

CO binds to Hb to form carboxyhemoglobin (COHb) at 200-250 times of O2 and carries no O2 which causes shift in Oxy-Hb curve to the left.

CO binds to intracellular heme proteins e.g. myoglobin and cytochrome aa3 (especially in cardiac) to inhibit O2 uptake and metabolism.

Clinical symptoms : Headache (CO level of 10 %), N/V (20%), visual disturbance (30%), coma (50%) and death (60%). The Classic signs, “Cherry-red” and retinal hemorrhage, are rarely observed.

COHb level correlates poorly with clinical manifestation, so the treatment should be guided by signs and symptoms.

The pulse oximetry is unreliable and overestimates OxyHb in the presence of COHb.

The factors that influence the amount of CO production with anesthesia machine are :
  • Anesthetic agents : Des >> En > Iso >> Hal = Sevo
  • The absorbent dryness ; especially Monday morning cases
  • Type of absorbent ; Baralyme > Na Lime
  • Temperature ; increased temp -> increased production
  • Anesthetic concentration ; increased conc -> increased production.

    • Toxicity of CO is believed to be due to lack of O2 delivery and direct CO mediated damage at cellular level. Both of these induce cellular hypoxia.

    In smokers, CO level is about 10 -15 % while normal patients < 1 %.

    Treatment
    -Hyperbaric O2 : Coma (absolute indication) ,
    Relative indications :- CO > 40% in non pregnant,
    > 15 % in pregnant,
    > 20% in patients with IHD.
    -Normobaric O2 (administer 100% O2). This will reduce t1/2 of CO from 4-6 hours (room air) to 40-80 minutes.