Pulmonary Disease and Critical Care· Topic 16.2 Occupational and environmental lung disease· 16.2.8

Carbon monoxide poisoning

Carbon monoxide poisoning follows inhalation of a colorless, odorless combustion product that binds hemoglobin roughly 200 to 300 times more avidly than oxygen, producing tissue hypoxia that pulse oximetry cannot detect. Diagnosis requires co-oximetry on a blood gas to measure carboxyhemoglobin. Treatment is immediate high-flow 100% oxygen, escalated to hyperbaric oxygen for loss of consciousness, neurologic or cardiac ischemia, or pregnancy.

13 min read2 practice questions8 key factsSubscriber article
  • Topic review
    The full article, organized the way the exam asks it.
  • ABIM-format MCQs
    Vignettes with an explanation for every wrong answer.
  • Key facts
    The numbers and thresholds worth memorizing, up front.
  • AI tutor
    MedBrain answers the question you're stuck on.

What this article covers

  • Overview

    What it is: inhalation of carbon monoxide (CO), a colorless, odorless, tasteless gas from incomplete combustion; sources include vehicle exhaust, structural fire smoke, and faulty fuel-burning…

  • Epidemiology

    A leading cause of poisoning death: among the most common causes of poisoning death worldwide, and the leading cause of death in the first 24 hours after a fire.

  • Risk factors

    Enclosed or poorly ventilated space: running an engine, generator, or fuel-burning appliance indoors or in an attached garage concentrates CO far above ambient levels.

  • Pathophysiology

    Competitive hemoglobin binding: CO binds the same heme iron site as oxygen with an affinity roughly 200 to 300 times that of oxygen, so it progressively displaces oxygen and forms carboxyhemoglobin.

  • Clinical features

    Mild-to-moderate exposure: headache (often the earliest symptom), nausea, dizziness, malaise, and myalgias that can be mistaken for a viral illness.

  • Differential diagnosis

    Cyanide poisoning: can co-occur in an enclosed-space fire, but shows a markedly elevated lactate and anion gap acidosis out of proportion to COHb, since toxicity comes from cytochrome oxidase blockade rather than hemoglobin displacement.

  • Diagnosis

    The diagnosis is established by measuring carboxyhemoglobin on co-oximetry from an arterial or venous blood gas: standard pulse oximetry and a routine calculated saturation cannot distinguish…

  • Management

    First, remove the patient from the source and secure the airway: move to fresh air, apply cardiac monitoring, and intubate for depressed mental status, seizure, or airway compromise from smoke inhalation.

  • Complications

    Hypoxic-ischemic brain injury: ranges from transient confusion to permanent cognitive and motor deficits, most closely tied to loss of consciousness during exposure.

  • Prognosis

    Neurologic and cardiac findings at presentation, not the peak COHb level, drive prognosis: because cytochrome oxidase inhibition contributes independently of hemoglobin binding, outcome correlates poorly with a single COHb number.

  • Prevention

    Home carbon monoxide detectors: install on every level and outside each sleeping area, testing monthly; a triggered alarm should prompt immediate evacuation, not investigation from inside the home.

Read the whole article

Subscribing to Internal Medicine opens every article, the full question bank and MedBrain, on the web, iPhone and Android.