Bedside Snapshot

Normal / Therapeutic
Nonsmoker: <3% (<0.03)
Smoker: up to 10% (up to 0.10)
Toxic Thresholds
Exposure: ≥3% nonsmoker, >10% smoker
Critical: ≥25% (typical; lab- and center-specific)
No level rules poisoning out; severity is clinical
Toxicity Looks Like
Headache, nausea, dizziness, confusion; syncope, seizures, coma; chest pain, ischemia, arrhythmia; a flu-like illness shared by a household
Antidote / Definitive Care
100% oxygen regardless of SpO₂; hyperbaric oxygen for serious poisoning; hydroxocobalamin if smoke victim with suspected cyanide
Act Now If
Loss of consciousness, neurologic signs, ischemia, severe acidosis, pregnancy or COHb ≥25%: 100% oxygen, 12-lead and troponin, call hyperbaric center or poison center
Watch Out For
Normal SpO₂ and a low COHb after oxygen do not exclude CO poisoning: standard pulse oximetry reads COHb as oxygen

Reference & Critical Ranges

Lab-specific ranges: Every lab sets its own interval, by analyzer and by population. Trust the range on your report. The values below are typical only.

Reference ranges

PopulationConventionalSINotes
Adult, nonsmoker
<3%
<0.03 (fraction of total Hb)
Small amounts of CO are made in the body from heme breakdown.
Adult, smoker
Up to 10%
Up to 0.10
Smokers typically run about 3–8% (heavy smokers up to about 10% or more) and are often asymptomatic.
Pregnancy
Same as adult
Same as adult
Maternal COHb underestimates fetal exposure (see Special Populations).
Children
Same as adult
Same as adult
Children take up and clear CO faster than adults.

Severity & critical values

LevelConcentrationWhen to drawMeaning
Normal
<3% (smoker up to 10%)
As soon as possible after exposure; note the time oxygen started
No exposure shown, but a normal level after delay or oxygen does not exclude CO poisoning.
Elevated
≥3% nonsmoker; >10% smoker
Same sample; repeat only to follow a rising source (methylene chloride)
Exogenous CO exposure. CO poisoning = exposure + symptoms; severity is judged clinically, not by the number.
Critical
≥25% (typical; lab- and center-specific)
First available sample
Hyperbaric oxygen (HBO) referral is reasonable even with mild symptoms; also a risk factor for delayed sequelae.
Serious signs at any level
Any COHb
Do not wait for the result
Loss of consciousness, neurologic signs, cardiovascular dysfunction or severe acidosis: refer for HBO regardless of COHb.
Critical values: No lab has a universal panic value for CO. Treat COHb ≥25% as critical. Treat any elevated COHb as critical when it comes with loss of consciousness, neurologic signs, cardiac ischemia, severe acidosis or pregnancy. Critical means 100% oxygen and a call to the hyperbaric center.

Conversion: COHb % × 0.01 = COHb fraction of total hemoglobin (SI)

Causes of Abnormal Results

Sources & routes of exposure

Every exposure comes in through the lungs. Methylene chloride is the exception: it is also absorbed, and the liver turns it into CO.

SourceSettingBedside clue
Structural fire smoke
Enclosed-space fires
Soot in the mouth or nose, altered mental status; assume cyanide co-poisoning
Faulty fuel-burning heaters
Furnaces, boilers, water heaters, fireplaces and stoves
Heating season; several people in one home with headache, nausea or dizziness
Engines in enclosed spaces
Generators after power cuts, vehicles in garages, boats, small gasoline tools
Exposure history; may be intentional (vehicle exhaust)
Charcoal burned indoors
Grills used for heating, or as a suicide method
Sealed or taped-off room, note; screen for co-ingestants
Wood pellet storage
Pellet stores and silos
Collapse on entering a storage room
Hookah (water pipe)
Hookah smoking, especially indoors
Syncope or headache after a session
Methylene chloride
Paint strippers and degreasers
COHb keeps rising for hours after exposure ends
Fire victims: Smoke carries CO and hydrogen cyanide together. Persistent altered mental status, hypotension or lactate ≥10 mmol/L after smoke inhalation points to cyanide co-poisoning. Cyanide needs its own antidote.

Risk factors for toxicity

  • Greater susceptibility: pregnancy (fetus), infants and children, older adults, coronary or other heart disease, and anemia.
  • Worse prognosis: any loss of consciousness, age over 60, underlying cardiovascular disease, and severe acidosis; an initial pH <7.2 is linked to markedly higher mortality.
  • Delayed neurologic sequelae (DNS) risk: age ≥36 years, COHb ≥25%, exposure ≥24 hours, loss of consciousness, low Glasgow Coma Scale (GCS) or cognitive score, and an abnormal brain CT.
  • Intentional exposure: frequent co-ingestion, mainly alcohol; obtain a toxicology screen.

Acute vs chronic exposure

FeatureAcuteChronic or intermittent
Typical exposure
Single high exposure: fire, generator, suicide attempt
Low-level exposure over more than 24 hours, often intermittent (faulty heater)
Presentation
Headache, vomiting, syncope, confusion, seizures, coma, chest pain
Recurrent headache, fatigue, dizziness, poor concentration; easily mistaken for a viral illness
COHb
Often high if drawn early
May be only modestly raised or normal

Low COHb

A low COHb tells you nothing on its own. The only danger is false reassurance. That happens when the blood is drawn late or after oxygen.

Interpretation & Bedside Approach

Step-by-step approach

  1. Is the level believable? Confirm it is co-oximetry, and note the time since exposure and since oxygen started; a low level after either does not exclude poisoning.
  2. How sick is the patient? Look for loss of consciousness, confusion, ataxia, seizures, chest pain, arrhythmia and hypotension; severity is clinical.
  3. Check the heart and the acid-base status: 12-lead ECG and troponin in moderate to severe poisoning, as the ACEP 2017 clinical policy recommends, plus pH and lactate.
  4. Calculate the saturation gap: compare SpO₂ with the co-oximetry SaO₂ (formula below).
  5. Look for co-toxicants: cyanide after smoke inhalation, alcohol and drugs after intentional exposure, and a dyshemoglobin such as methemoglobin.
  6. Classify and escalate: CO poisoning = exposure + symptoms. Serious signs, COHb ≥25% or pregnancy → call a hyperbaric center or poison center (1-800-222-1222).
  7. Dispose: see Management Priorities; find the source and other exposed people.
Saturation gap
Gap = SpO₂ (pulse oximeter) − SaO₂ (co-oximetry)

A big gap with a normal PaO₂ points to a dyshemoglobin. That is COHb or methemoglobin, and standard oximetry cannot see either one.

Pattern recognition

PatternSuggests
SpO₂ and PaO₂ normal, co-oximetry SaO₂ low, COHb high
CO poisoning: oxygen content is low despite normal-looking numbers
SpO₂ near 85% that does not rise with oxygen, MetHb high
Methemoglobinemia (oxidant drugs, nitrites), not CO
Smoke victim with lactate ≥10 mmol/L, hypotension or persisting coma
Cyanide co-poisoning; give hydroxocobalamin without waiting for confirmation
Several people from one dwelling, nonspecific symptoms, low COHb after oxygen
CO poisoning is still likely; treat on history and have the dwelling checked
COHb that keeps rising after removal, paint-stripper use
Methylene chloride metabolized to CO

COHb does not follow symptoms. It does not predict long-term outcome. Trend the patient, not the number.

Management Priorities

Emergency: Suspected CO poisoning

  1. Protect and remove: Rescuers need respiratory protection. Alert the fire department.
  2. Oxygen now: Start 100% oxygen whatever the SpO₂ says. Pick your route: nonrebreather at 15 L/min, CPAP, high-flow nasal cannula, or FiO₂ 1.0 by bag-mask or tube. Never titrate to SpO₂.
  3. Airway and monitoring: Lost protective reflexes? Intubate. Keep the ECG and blood pressure running the whole time.
  4. Labs: Draw co-oximetry COHb before any hydroxocobalamin. Add a blood gas with pH and lactate, troponin, a 12-lead ECG and a pregnancy test. Order a toxicology screen if the exposure was intentional.
  5. Escalate: Serious signs, COHb ≥25% or pregnancy: call a hyperbaric center early.

Emergency: Smoke inhalation with suspected cyanide

  1. Recognize: Enclosed-space fire, soot and altered mental status. Seizures, hypotension, apnea, arrest or lactate ≥10 mmol/L may come with it.
  2. Treat empirically: Hydroxocobalamin (table below) goes on its own IV line, alongside 100% oxygen. Don't wait for the lactate or a cyanide level.
  3. Avoid nitrites: With CO on board, sodium or amyl nitrite makes methemoglobin. That cuts oxygen delivery even further.

Medications

DrugAdult dosePediatric dose (max)Onset / key notes
Oxygen 100%
100% by nonrebreather 15 L/min (a tight-fitting mask delivers less than 100%; use bag-mask, CPAP or tube for true FiO₂ 1.0 when sicker), or FiO₂ 1.0 by bag-mask or tube, until symptom-free and COHb <3% (titrate to effect: no fixed max)
100% by nonrebreather, high-flow nasal cannula or bag-mask; FiO₂ 1.0 if intubated, same end points (no fixed max)
COHb t½ about 74 min on nonrebreather; reaching normal usually takes up to about 6 hr. Do not titrate to SpO₂.
Hydroxocobalamin (Cyanokit)
Suspected cyanide: 5 g IV over 15 min; second 5 g over 15 min to 2 hr if needed (max total 10 g)
70 mg/kg IV over 15 min (max 5 g/dose); may repeat once (max total 140 mg/kg, not over 10 g). Label: pediatric safety and effectiveness not established; 70 mg/kg comes from non-US experience, and the repeat dose and total are protocol-based
Reconstitute 5 g in 200 mL diluent; separate IV line; incompatible with sodium thiosulfate and sodium nitrite. Draw COHb and other labs first: the red color makes co-oximetry unreliable and interferes with many colorimetric lab tests. Monitor BP (transient hypertension is common); watch for allergic reaction. Can trigger dialysis machine alarms. Expect red skin and urine.
Hyperbaric oxygen (HBO)
2.5–3 ATA; best-studied regimen is 3 sessions within 24 hr (first at 3 ATA)
Not routinely used (consult): hyperbaric center decides case by case
Hyperbaric team decision. Start early: within 6 hr preferred in German guidance; the landmark trial treated within 24 hr.

Doses vary by protocol; follow local protocols and medical direction.

Definitive care & disposition

  • HBO referral: transient or prolonged unconsciousness, neurologic signs, cardiovascular dysfunction or severe acidosis, regardless of COHb (UHMS); COHb ≥25% is a reasonable trigger; pregnancy with poisoning, or fetal distress even if the mother is well.
  • Evidence is contested: ACEP 2025 gives only a Level C recommendation: selected patients may benefit, judged on severity and on distance and time to a chamber. One landmark trial cut 6-week cognitive sequelae from 46% to 25%. Later meta-analyses show no clear benefit.
  • Admit or observe: every symptomatic patient. Disposition follows protocol. Asymptomatic patients with a normal exam, a normal ECG and a low COHb after a brief observation period are often discharged. Offer admission to pregnant patients and children.
  • Before discharge: source made safe, working CO alarm, psychiatric assessment after intentional exposure.
  • Follow-up: teach DNS warning signs (onset 2–40 days); cognitive assessment at 4–6 weeks; cardiac follow-up after myocardial injury.

Doses are typical references. Follow local protocols, medical direction and institutional policy.

Field & Transport Considerations

Point-of-care testing

A standard pulse oximeter reads COHb as oxyhemoglobin, so SpO₂ looks normal. Multiwavelength pulse CO-oximeters estimate SpCO. A 2023 meta-analysis found sensitivity 77%, specificity 83% and limits of agreement about −7 to +9 percentage points against blood COHb. ACEP advises against using SpCO to diagnose CO toxicity. Use a high reading to raise suspicion. A low one never rules poisoning out.

Before and during interfacility transport

SettingConsideration
Scene (EMS)
Bag-mounted CO alarm sounding: leave and request fire department. Note time found, exposure duration and time oxygen started.
Early blood sample
Where protocol allows, draw venous blood before or as oxygen starts and hand it over labeled with the time.
Destination
Nearest suitable hospital; the receiving team decides on secondary transfer to a hyperbaric center.
Interfacility
Send COHb with draw time, ECG, troponin, pH and lactate, pregnancy status and serial neurologic exams. Keep 100% oxygen running en route. For air transport, keep cabin altitude as low as practicable (pressurize to sea level where possible), because lower inspired oxygen pressure reduces delivery. An untreated pneumothorax is a contraindication to HBO: confirm it is excluded or treated, and tell the hyperbaric team if one is present.
Re-check
Neurologic status and rhythm throughout; a falling COHb en route is expected.

Scope notes

Who screens with SpCO and who draws blood depends on protocol. Sending a patient for HBO is a call for medical direction and the hyperbaric physician.

Timing & Kinetics

ParameterValueClinical implication
COHb t½, room air
About 4–5 hr (reported 249–320 min)
Untreated, levels stay high for many hours
COHb t½, 100% O₂ by nonrebreather
About 74 min (range 26–148)
Shorter with a higher PaO₂; poor ventilation or low cardiac output prolongs it
COHb t½, high-flow nasal cannula
Reported shorter than nonrebreather in small studies; evidence limited
Faster clearance; outcome benefit unproven
COHb t½, HBO 2.5–3 ATA
Often quoted 15–30 min
Fastest clearance, but HBO is chosen for neurologic protection, not speed
Fetal COHb
Clears about 1.5 times slower than maternal
Fetal levels can exceed maternal; maternal COHb underestimates fetal exposure
Methylene chloride
COHb can rise for hours and stay high 1–2 days
Repeat COHb; levels may rebound after oxygen stops
Oxygen end point
Symptom-free and COHb <3% (about 5 half-lives, roughly 6 hr)
Do not stop early because COHb is falling
Delayed neurologic sequelae
Onset 2–40 days
Discharge teaching; cognitive check at 4–6 weeks
Back-calculation misleads: Symptoms run on their own clock, not on COHb clearance. The level proves exposure. The patient tells you how sick they are and whether HBO is on the table.

Special Populations

PopulationWhat changesClinical implication
Neonates & infants
Fetal hemoglobin (60–85% at birth, falling over the first year) binds CO avidly; symptoms may be only poor feeding or irritability
Low threshold to test; a neonate has been asymptomatic at 22% COHb, so the level does not grade severity
Children & adolescents
Faster uptake and elimination; symptoms at lower levels, mimic a viral illness without fever; syncope more common and ECG changes less common than in adults
Treat with 100% oxygen; HBO is a case-by-case decision (UHMS: can be safe; German guidance: individual cases only)
Pregnancy
Fetal COHb can exceed maternal and clears about 1.5 times slower; severe poisoning threatens fetal survival and development
Maternal COHb underestimates fetal risk. HBO is safe in pregnancy and recommended in German guidance; consider it for fetal distress even if the mother is well. Involve obstetrics.
Older adults
Age >60 predicts worse outcome; age ≥36 raises DNS risk
Lower threshold for admission, ECG, troponin and HBO discussion
Heart disease or anemia
Less reserve for reduced oxygen delivery
Ischemia and arrhythmia at lower exposures; serial ECG and troponin
Smokers
Baseline COHb up to 10%
Interpret modest elevations against the smoking history
No separate pediatric reference range: The COHb ranges hold at every age. Find pediatric hydroxocobalamin dosing in Management Priorities, then check weight-based dosing.

Interfering Factors & Pitfalls

Collection & handling

FactorEffectWhyAvoid / fix
Oxygen given before the draw
↓
CO is cleared within hours on oxygen
Document oxygen start time; never use a low level to rule out
Delay from exposure to draw
↓
Elimination continues even on room air
Draw as early as possible; record removal time
Sample type
No effect
Arterial, venous and capillary samples are all acceptable
Venous is enough; arterial if acid-base detail is needed

Medications & supplements

FactorEffectWhyAvoid / fix
Hydroxocobalamin (Cyanokit)
False + or False − (analyzer-dependent)
Deep red color interferes with spectrophotometry
Draw COHb before the infusion
Methylene chloride exposure
↑ (true), prolonged
Ongoing hepatic conversion to CO
Repeat COHb; expect rebound after oxygen stops

Physiologic / biologic

FactorEffectWhyAvoid / fix
Tobacco or hookah smoking
↑
Inhaled CO
Smokers up to 10% at baseline

Assay & device-specific

FactorEffectWhyAvoid / fix
Standard pulse oximetry
False − (SpO₂ normal)
Two wavelengths read COHb as oxyhemoglobin
Never use SpO₂ to exclude CO; give oxygen anyway
Pulse CO-oximetry (SpCO)
False + and False −
Wide limits of agreement; both false-positive and false-negative readings occur (see Papin 2023)
Screen only; confirm with blood co-oximetry
Blood gas without co-oximetry
False − (SaO₂ normal)
SaO₂ calculated from a normal PaO₂
Ask for measured COHb and SaO₂

Common misinterpretations

  • A normal SpO₂ or PaO₂ does not mean oxygen delivery is normal.
  • A low COHb after oxygen or a delay does not rule out poisoning or delayed sequelae.
  • The COHb level does not grade severity. It does not predict neurologic outcome.
  • Skin color is unreliable. Do not wait for "cherry red" skin before you suspect CO.
Pulse oximetry is falsely reassuring: In CO poisoning, a standard oximeter still shows a normal SpO₂. Start 100% oxygen on history alone. Then confirm with co-oximetry.

Physiology & Test Basics

What it measures

Think of COHb as hemoglobin with CO stuck to it. The lab reports it as a percentage of total hemoglobin. It confirms exposure. It does not measure CO in the tissues. Injury can keep going after COHb falls.

Physiology & regulation

  • Affinity: CO grabs hemoglobin about 230–300 times harder than oxygen does. That is why even 10 ppm in air gives about 2% COHb.
  • Left shift: The hemoglobin that is left holds onto oxygen harder. It gives less of it to the tissues.
  • Tissue toxicity: CO binds myoglobin and mitochondrial cytochrome c oxidase. Cardiac and cellular energy use both suffer.
  • Inflammation: Oxidative stress and immune injury keep going after COHb clears. They underlie delayed brain injury.
  • Elimination: CO leaves unchanged through the lungs. A higher inspired oxygen and a higher pressure speed it up.

How it is measured

The method is co-oximetry, which means multiwavelength spectrophotometry. A blood gas analyzer runs it, and the same analyzer reports oxyhemoglobin, deoxyhemoglobin and methemoglobin. Draw arterial, venous or capillary whole blood into a heparinized blood gas syringe or capillary tube. No fasting. Point-of-care analyzers return results in minutes. Noninvasive SpCO is a screening estimate only.

Why it matters

CO poisoning is common, and it hides well. Its symptoms are vague, and the pulse oximeter misses it. A COHb confirms exposure. It sends you looking for the source and other victims, and it feeds the hyperbaric decision. A low result must never override a convincing history.

Clinical Pearls

Ask about everyone in the home: Several people with headache and nausea under one roof? Think CO, especially in cold weather. Assume it until proven otherwise. Get the fire department into the dwelling before anyone goes back inside.
Prehospital: trust the alarm, not the oximeter: Hear the bag-mounted CO detector? Get out first. Then start 100% oxygen on scene, whatever the SpO₂ shows.
Hand over the clock: Report when the patient was removed and when oxygen started. Give the receiving team both times with the patient. Every COHb they see gets read against those two numbers.
Nursing: keep the oxygen on: 100% oxygen stays on until the patient is symptom-free and COHb is under 3%. Keep checking neurologic status, rhythm and lactate. A patient getting worse on oxygen is telling you about another cause.
Delayed sequelae: Watch for these after moderate-to-severe poisoning: memory loss, personality or mood change, parkinsonism, gait disturbance and psychosis. They can surface 2–40 days after an apparent full recovery. Brain MRI may show globus pallidus injury. Many patients improve over months. Some do not. Teach the warning signs at discharge and book follow-up at 4–6 weeks.

References

  1. Shih, R. D., Tomaszewski, C. A., Kaji, A., & Diercks, D. B.; American College of Emergency Physicians Clinical Policies Subcommittee on Carbon Monoxide Poisoning. (2025). A critical issue in the management of adult patients presenting to the emergency department with acute carbon monoxide poisoning. Annals of Emergency Medicine, 85(4), e45–e59. https://doi.org/10.1016/j.annemergmed.2024.12.005
  2. Wolf, S. J., Maloney, G. E., Shih, R. D., Shy, B. D., & Brown, M. D.; American College of Emergency Physicians Clinical Policies Subcommittee on Carbon Monoxide Poisoning. (2017). Clinical policy: Critical issues in the evaluation and management of adult patients presenting to the emergency department with acute carbon monoxide poisoning. Annals of Emergency Medicine, 69(1), 98–107.e6. https://doi.org/10.1016/j.annemergmed.2016.11.003
  3. Weaver, L. K. (2024). Carbon monoxide poisoning (reprinted from the Hyperbaric Medicine Indications Manual, 15th ed., 2023). Undersea and Hyperbaric Medicine, 51(3), 253–276. https://www.uhms.org/uhm-search/uhm-journal-volume-51-2024/number-3/indications-chapter.html
  4. Jüttner, B., Busch, H. J., Callies, A., Dormann, H., Janisch, T., Kaiser, G., et al. (2021). S2k guideline diagnosis and treatment of carbon monoxide poisoning. GMS German Medical Science, 19, Doc13. https://doi.org/10.3205/000300
  5. Papin, M., Latour, C., Leclère, B., & Javaudin, F. (2023). Accuracy of pulse CO-oximetry to evaluate blood carboxyhemoglobin level: A systematic review and meta-analysis of diagnostic test accuracy studies. European Journal of Emergency Medicine, 30(4), 233–243. https://doi.org/10.1097/MEJ.0000000000001043
  6. Weaver, L. K., Hopkins, R. O., Chan, K. J., Churchill, S., Elliott, C. G., Clemmer, T. P., Orme, J. F., Thomas, F. O., & Morris, A. H. (2002). Hyperbaric oxygen for acute carbon monoxide poisoning (landmark trial). New England Journal of Medicine, 347(14), 1057–1067. https://doi.org/10.1056/NEJMoa013121
  7. BTG International Inc. (2023). CYANOKIT (hydroxocobalamin for injection) for intravenous infusion: Prescribing information (DailyMed SPL version 2, published May 4, 2023; label text revised 05/2021). U.S. National Library of Medicine. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=d56fcc8d-bd64-46ab-b0c0-2124bd745a6b
  8. Agency for Toxic Substances and Disease Registry. (2017). Medical management guidelines for methylene chloride. U.S. Department of Health and Human Services. https://wwwn.cdc.gov/TSP/MMG/MMGDetails.aspx?mmgid=230&toxid=42

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