What is the management of carbon monoxide (CO) poisoning?

Management of Carbon Monoxide Poisoning

Immediate Oxygen Administration

Administer 100% oxygen immediately via non-rebreather mask or endotracheal tube to all patients with suspected CO poisoning, even before obtaining carboxyhemoglobin levels. 1

• Do not delay oxygen therapy while waiting for laboratory confirmation—this is critical to prevent disability and mortality 1
• Oxygen reduces the COHb elimination half-life from 320 minutes on room air to approximately 74 minutes 1
• Continue 100% normobaric oxygen until COHb normalizes and the patient becomes asymptomatic, typically requiring approximately 6 hours of treatment 1

Diagnostic Confirmation

Obtain carboxyhemoglobin level via CO-oximetry on venous or arterial blood immediately. 1

• Standard pulse oximetry is completely unreliable—it will show falsely normal SpO2 readings (>90%) even with COHb levels as high as 25% because it cannot differentiate between oxyhemoglobin and carboxyhemoglobin 1, 2
• Older blood gas analyzers without CO-oximetry capabilities may calculate SaO2 based only on PaO2 and pH, reporting falsely normal oxygen saturation despite high COHb levels 2
• Critical pitfall: PaO2 typically remains normal in CO poisoning because it measures dissolved oxygen in plasma, which is unaffected by CO binding to hemoglobin—this creates a dangerous clinical scenario where patients appear well-oxygenated but are experiencing severe tissue hypoxia 2
• COHb levels correlate poorly with symptoms or prognosis and serve primarily to confirm exposure, not to guide treatment intensity 1

Cardiac Monitoring and Assessment

Obtain 12-lead ECG and initiate continuous cardiac monitoring for all patients with moderate to severe poisoning. 1

• CO causes direct myocardial injury through tissue hypoxia and cellular damage, with cardiac complications possible even at relatively low COHb levels 1
• Patients with ischemic heart disease may experience chest pain and decreased exercise duration at COHb levels between 1% and 9% 3
• Monitor for cardiac arrhythmias or arrest, particularly with prolonged hypoxia from high CO levels 4

Hyperbaric Oxygen Therapy Decision Algorithm

Consider HBO therapy at 2.5-3.0 atmospheres absolute pressure for patients with ANY of the following high-risk features: 1

• Loss of consciousness at any point
• Ischemic cardiac changes on ECG
• Neurological deficits
• Significant metabolic acidosis
• COHb level >25%
• Pregnancy with significant CO exposure

HBO reduces COHb half-life to approximately 20 minutes 1. While the use of hyperbaric oxygen remains controversial in the literature 5, 4, 3, one randomized trial demonstrated that HBO-treated non-comatose patients had significantly fewer electroencephalogram abnormalities and better cerebral blood flow reactivity at 3 weeks compared to normobaric oxygen alone 6.

Special Clinical Scenarios

Suspect concomitant cyanide poisoning if the CO source is a house fire. 1

• Consider empiric cyanide treatment if arterial pH <7.20 or plasma lactate >10 mmol/L 1
• House fires produce both CO and cyanide from combustion of synthetic materials

Pregnant patients require special attention. 2

• Fetal hemoglobin has higher affinity for CO than maternal hemoglobin, placing the fetus at greater risk 2
• Lower threshold for HBO therapy in pregnancy 1

Consider CPAP or non-invasive ventilation for patients with pulmonary edema resulting from CO-induced cardiac dysfunction. 2

Pathophysiologic Mechanisms Driving Treatment

CO causes tissue hypoxia through multiple mechanisms beyond simple hemoglobin binding 2:

• CO binds to hemoglobin with an affinity approximately 220 times greater than oxygen, directly reducing oxygen-carrying capacity 2
• CO shifts the oxyhemoglobin dissociation curve to the left, further reducing tissue oxygen delivery despite normal PaO2 values 2
• CO binds to intracellular heme proteins including myoglobin and cytochrome oxidase, impairing mitochondrial ATP production 2
• CO triggers nitric oxide generation, peroxynitrite production, lipid peroxidation, mitochondrial oxidative stress, and immune-mediated injury 2

This explains why clinical severity does not correlate with COHb levels—patients may have significant toxicity despite relatively low COHb percentages 2.

Source Identification and Prevention

Do not discharge without identifying and eliminating the CO source to prevent re-exposure. 2

• Common sources include poorly functioning heating systems, indoor propane-powered equipment, indoor charcoal burning, gasoline-powered generators in enclosed spaces, and vehicle exhaust 3
• Obtain information about ambient CO levels from emergency personnel if available—elevated environmental levels confirm CO poisoning even if patient COHb is low due to time elapsed or oxygen treatment already administered 2

Follow-Up Care

Schedule follow-up in 4-6 weeks to screen for delayed neurologic sequelae (DNS) in accidental poisoning cases. 1

• DNS can develop after a lucid interval of 2-40 days, presenting with diffuse demyelination, lethargy, behavior changes, forgetfulness, memory loss, and parkinsonian features 3
• Seventy-five percent of patients with DNS recover within 1 year 3
• White-matter damage in the centrum semiovale and periventricular area and abnormalities in the globus pallidus are most commonly seen on MRI following CO exposure 3