Carbon Monoxide Poisoning


Risk

  • CO is the predominant toxic gas in smoke. (COHb can reach 10% in tobacco smokers.)

  • CO poisoning is a major cause of death (early symptoms may be only headache and dizziness).

  • CO is produced by all internal combustion engines, incomplete oxidative combustion (e.g., house fires, charcoal and gas grills, malfunctioning butane/propane stoves), and endogenous sources (e.g., by the liver from exogenous exposure to paint stripper).

  • No odor, taste, or color and causes no irritation.

  • Toxicity potentiated by low inspired O 2 concentration (e.g., smoke inhalation).

  • To minimize CO in circle circuit carbon dioxide absorbers, use fresh soda lime, use sevoflurane, and minimize drying (lower FGF and stop FGF during use).

  • During GA, use semiclosed circuits, especially when machine has not been used for 2–3 d (e.g., Monday morning).

Perioperative Risks

  • Main target organs: Heart and brain

  • Heart: Effect can resemble ischemia; potentiated by CAD.

  • Brain: Acute loss of consciousness; after initial improvement (lucid window), up to 30% risk of secondary syndrome: chronic psychiatric dysfunction and cerebral and cerebellar syndromes.

Worry About

  • Seek other smoke inhalation injury.

  • Consider concomitant cyanide poisoning, which potentiates CO toxicity.

  • Be alert for CO poisoning in donor for organ transplantation.

Overview

  • CO, a colorless, nonirritating, odorless gas, is a natural byproduct of combustion.

  • CO binds avidly to Hgb (>200 times more than O 2 ) to form COHb, which carries no O 2 and causes a left shift in the oxyhemoglobin dissociation curve (decreases O 2 off-loading to tissues).

  • CO binds to intracellular hemoproteins such as myoglobin and cytochrome aa 3 (esp cardiac) to inhibit O 2 uptake and metabolism.

  • ”Classic” cherry-red complexion rarely observed (need COHb >40%; may be obscured by coexistent hypoxia and cyanosis).

  • COHb level correlates poorly with clinical condition (symptoms with “normal” COHb).

  • Treatment should be guided by symptoms and signs, not by blood COHb concentration.

Etiology

  • CO produced by incomplete oxidative combustion (e.g., house fires, malfunctioning butane/propane stoves, home heaters, all internal combustion engines)

  • Suicide attempts

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