Carbon Monoxide Poisoning
Clinical Snapshot
Carbon monoxide (CO) poisoning is a toxicologic emergency caused by inhaling a colourless, odourless, non-irritating gas produced whenever a carbon-based fuel burns incompletely — a gas that is, by design, impossible to detect without an alarm, which is exactly why recognition here depends entirely on clinical suspicion rather than on how a patient or their environment "seems."[1] CO is absorbed through the lungs and binds haemoglobin with roughly 200-250 times the affinity of oxygen, forming carboxyhaemoglobin (COHb) and sharply reducing the blood's oxygen-carrying capacity; it also left-shifts the oxyhaemoglobin dissociation curve, impairing the release of whatever oxygen the blood is still carrying to the tissues.[1] CO does not stop at haemoglobin — it also binds myoglobin and, directly and independently of any haemoglobin effect, the mitochondrial enzyme cytochrome c oxidase, poisoning cellular respiration itself. The heart and brain, the two most oxygen-hungry organs, bear the brunt of this combined carrying-capacity-plus-cellular-poisoning injury.[2][1]
The single most dangerous pitfall in this chapter is not clinical, it is instrumental: a standard pulse oximeter cannot distinguish carboxyhaemoglobin from oxyhaemoglobin and will report a falsely normal or near-normal SpO2 in a patient who is, in reality, profoundly hypoxic at the tissue level; a routine arterial blood gas is equally misleading, since its reported oxygen saturation is typically calculated rather than directly measured.[1] The only way to actually detect CO poisoning is to specifically order co-oximetry for a directly measured carboxyhaemoglobin — a test that must be requested by name, because nothing about a normal-looking pulse oximeter or a normal-looking arterial blood gas will ever prompt it on its own.
In Canada, CO poisoning causes an estimated 300 deaths and 200 hospitalizations every year, with almost two-thirds of emergency department presentations occurring in the fall and winter and close to a quarter involving children under 4.[3] Faulty furnaces, portable generators run indoors or in an attached garage, poorly ventilated space heaters, and house fires are the classic, recurring Canadian winter sources.[3][2] Management is emergency-department- and, for more severe cases, ICU- or hyperbaric-unit-level care, never an outpatient decision — the pharmacist's core role is rapid recognition (especially the vague, flu-mimicking presentation and household clusters), getting 100% oxygen started immediately, and knowing exactly which patients need urgent hyperbaric oxygen referral.
Recognize the Condition
The classic — and classically missed — presentation
Acute CO poisoning most often begins with a vague, nonspecific triad of headache, nausea (with or without vomiting), and dizziness or generalized malaise — a picture that is genuinely difficult to distinguish from a viral illness on history alone, and is exactly why CO poisoning is so often missed, especially during cold-and-flu season when both conditions are circulating.[1] As exposure and COHb rise, the picture progresses to confusion and altered mental status, chest pain from myocardial ischemia, dyspnea, syncope, seizures, and coma.[1] "Cherry red" skin is taught as the classic sign of CO poisoning, but in practice it is rare, appears late, and is unreliable at the bedside — it is described far more often as a postmortem finding than as something a clinician can count on to make the diagnosis in a living patient. Do not wait for it.[1]
The clue that actually catches it: the household cluster
The single most useful pattern-recognition clue for CO poisoning is more than one occupant of the same building (household members, coworkers, campers — even pets) presenting with a similar vague picture at the same time, especially when symptoms improve on leaving the building (work, school, a night away) and recur on returning. A pharmacist hearing "my whole family has had headaches and felt sick for a few days" should think of CO poisoning specifically and prompt urgent assessment, not reassure the patient that "it's probably just a bug going around."
Chronic, low-level exposure
Chronic or intermittent low-level exposure — a poorly tuned furnace, a leaking chimney — produces a subtler picture: recurring headache, fatigue, and cognitive complaints that are easy to misattribute to depression, migraine, or a recurring viral syndrome across several visits before CO is ever considered. A history of symptoms that consistently track with time spent at home, or that improve on vacation, should prompt specific questions about home heating and appliance maintenance.
Risk Factors
- Faulty, poorly maintained, or improperly vented furnaces, water heaters, and other fuel-burning household appliances.
- Portable generators run indoors, in a garage (even with the door open), or near a window or door — a classic, recurring source during winter storm-related power outages.[3]
- Poorly ventilated or malfunctioning space heaters, wood stoves, and fireplaces.
- Motor vehicle exhaust in an attached or enclosed garage.
- House fires and smoke inhalation — the most common cause of fire-related death.[2]
- Charcoal briquettes or a propane/gas barbecue used indoors or in an enclosed space such as a tent.[3]
- Occupational exposure — indoor combustion-engine equipment (e.g. forklifts), welding, firefighting.
- Hookah/shisha use in a poorly ventilated space.
- No functioning, correctly certified carbon monoxide alarm in the home.[4]
- Pre-existing cardiac or cerebrovascular disease, chronic anemia, pregnancy, and the extremes of age all increase the risk of serious harm at a given level of exposure, even though they do not increase the risk of exposure itself.
Red Flags & Refer
Carbon monoxide poisoning is never an outpatient-management condition — any of the following (or simply a convincing exposure history with symptoms) means immediate emergency referral, treated as a poison-control/ER emergency, not a "see how you feel and call back" situation:
- Any loss of consciousness, confusion, or other altered mental status at any point during or after the exposure.
- Chest pain, dyspnea, palpitations, or syncope — evaluate for CO-related myocardial ischemia or dysrhythmia.
- Seizure.
- COHb over 25% at any time regardless of current symptoms — or over 15% in a pregnant patient or a child, a materially lower threshold.[2]
- Symptoms that have not resolved after 4 hours of high-flow oxygen.[2]
- More than one person (or a pet) in the same household presenting with a similar picture — this is an environmental emergency as well as a medical one; involve the fire department/gas utility in addition to arranging care, and do not let anyone return to the building until the source has been found and corrected.
- Smoke inhalation with hypotension, coma, or lactic acidosis out of proportion to the measured COHb — evaluate urgently for concomitant cyanide toxicity (see Pharmacologic Treatment Options).
- Any suspected CO exposure in pregnancy — apply the lower (over 15%) hyperbaric-oxygen threshold and involve obstetrics given the substantially higher fetal risk (see Special Populations).
Assessment & Diagnosis
The test that actually makes the diagnosis
Carbon monoxide poisoning is diagnosed by directly measuring carboxyhaemoglobin with co-oximetry on a venous or arterial blood sample — a specific test that must be ordered by name. A standard pulse oximeter and a standard (non-co-oximetry) arterial blood gas are both unreliable here: pulse oximetry cannot distinguish COHb from oxyhaemoglobin, and a routine ABG's reported oxygen saturation is typically calculated rather than measured, so both can look reassuringly normal in a genuinely poisoned patient.[1] Baseline COHb is roughly 1-3% in non-smokers and can run as high as 10-15% in heavy smokers — worth confirming smoking status for when interpreting a borderline result, though this should never be used to talk yourself out of treating a symptomatic patient with a convincing exposure history.
Supporting investigations
- ECG and high-sensitivity troponin in essentially every symptomatic patient — myocardial injury from CO poisoning is common and is often clinically silent until specifically looked for.[2]
- Venous or arterial lactate — a markedly elevated lactate in a smoke-inhalation victim, especially one out of proportion to the COHb level, should raise concern for concomitant cyanide toxicity.
- Pregnancy test in every patient of reproductive age — it changes the oxygen-duration and hyperbaric-referral thresholds (see Special Populations).
- Head CT if there is a focal neurologic deficit, prolonged or unexplained altered mental status, or diagnostic uncertainty.
- Trend COHb serially once oxygen therapy has started rather than relying on a single value — COHb falls quickly on high-flow oxygen, so a normal repeat level reflects treatment working, not that the original exposure was mild.
Differential diagnosis
Because the classic presentation mimics a viral illness so closely, actively consider CO poisoning — rather than simply treating empirically for the more common alternative — in a patient with headache, nausea, and malaise, particularly with any of: symptom onset that clusters with time spent at home, more than one affected household member, a recent change in heating or generator use, or a picture that does not quite fit a documented local viral illness pattern. Migraine, acute coronary syndrome, viral gastroenteritis, and viral meningitis/encephalitis are the most common alternative diagnoses actually being excluded when the differential is not obvious.
Treatment Targets
- Recognize CO poisoning promptly, especially in its vague, flu-mimicking form and in a household-cluster presentation, rather than defaulting to a viral-illness diagnosis.
- Remove the patient — and any other affected occupants — from the source immediately, and do not allow re-entry until the source has been found and corrected.
- Start 100% oxygen immediately in any patient with a plausible exposure and consistent symptoms, before co-oximetry results are back, not after.
- Identify every patient who meets hyperbaric oxygen referral criteria and refer without delay — this is a genuinely time-sensitive decision.
- Screen for and manage cardiac injury, which is common and often clinically silent.
- Recognize and treat concomitant cyanide toxicity in smoke-inhalation victims with disproportionate shock, coma, or lactic acidosis.
- Apply the lower COHb and referral thresholds that specifically apply to pregnancy and to children, rather than the general adult criteria.
- Counsel every patient on the real possibility of delayed neurological/neuropsychiatric sequelae and arrange follow-up before discharge.
- Counsel on carbon monoxide alarm installation, certification, and maintenance as secondary prevention — for the patient and, where a household cluster is involved, for the whole affected household.
Choose Initial Treatment
100% oxygen now, for everyone — then decide who needs hyperbaric oxygen
Every patient with suspected or confirmed CO poisoning start 100% oxygen immediately — via a tight-fitting non-rebreather mask at minimum, escalating to high-flow nasal cannula, CPAP/BiPAP, or intubation as clinically needed — regardless of the SpO2 reading and before co-oximetry results are available. Do not wait for confirmatory testing to start treatment.[2]
Then assess every patient against the hyperbaric oxygen therapy (HBOT) referral criteria below. Meeting any one criterion is enough to refer:
- Loss of consciousness at any point during or after the exposure.
- Cardiac involvement — ischemia, a dysrhythmia, or syncope.
- New or persistent neurologic findings.
- COHb over 25% at any time regardless of current symptoms — or over 15% in a pregnant patient or a child.
- Symptoms that persist after 4 hours of high-flow oxygen.
[2] Do not delay: outcomes are best when hyperbaric oxygen is started within 6 hours of exposure, though it remains reasonably considered up to about 24 hours — contact the regional hyperbaric unit or poison control centre immediately once a criterion is met, rather than completing a full local workup first.[2][5]
A patient who meets none of these criteria and is improving can continue on high-flow oxygen alone — see Non-Pharmacologic Treatment for oxygen-duration and discharge criteria, and Special Populations for the separate pregnancy and pediatric pathways.
Non-Pharmacologic Treatment
Scene safety and source removal
Remove the patient — and every other occupant, including pets — from the source immediately, and involve the fire department or gas utility to identify and correct it before anyone is allowed to re-enter. This is not a detail to leave to the patient to sort out later: a patient discharged back into an uncorrected source will simply be re-poisoned.
Oxygen delivery
Deliver 100% oxygen by non-rebreather mask at minimum, escalating to high-flow nasal cannula, CPAP/BiPAP, or intubation for a patient who cannot protect their airway or maintain adequate ventilation. Continue until COHb has fallen to 3% or less and symptoms have resolved — in practice, this generally means a minimum of 6-8 hours of high-flow oxygen for a symptomatic adult before considering discharge.[2] Oxygen sharply shortens the COHb half-life — from roughly 4-6 hours on room air to about 40-90 minutes on 100% oxygen — which is exactly why serial COHb, not a single value, is what actually tells you treatment is working.[1]
Hyperbaric oxygen therapy
Hyperbaric oxygen further shortens the COHb half-life to roughly 15-30 minutes, and is believed to work through mechanisms that go well beyond simply clearing CO faster — increasing plasma-dissolved oxygen delivery, reducing CO binding to cytochrome c oxidase and myoglobin, and limiting the lipid-peroxidation/inflammatory cascade thought to drive delayed neurological injury.[2][1] The best-known randomized trial protocol delivered 3 hyperbaric sessions at 2.8 atmospheres absolute — an initial 90-minute session followed by two 60-minute sessions on the following two days — though the exact number and timing of sessions is set by the treating hyperbaric unit's own protocol.[5] Evidence for a mortality or long-term-outcome benefit from hyperbaric oxygen is genuinely mixed across the available randomized trials, but current North American practice still refers patients who meet the criteria above given the plausible benefit for delayed neurocognitive outcome and the low risk of a short, monitored hyperbaric course.[5]
Supportive care in severe poisoning
- Continuous cardiac monitoring for any patient with cardiac involvement or significant exposure.
- Fever prevention/treatment — hyperthermia appears to worsen CO-related neurologic injury.
- Maintain adequate cardiac output and ventilation; manage seizures if they occur (see Pharmacologic Treatment Options).
- Evaluate every smoke-inhalation victim for concomitant cyanide toxicity, particularly with unexplained shock, coma, or a disproportionately elevated lactate — see Pharmacologic Treatment Options for empiric hydroxocobalamin.
Discharge readiness
A patient is ready for discharge once COHb is 3% or less, symptoms have resolved, any indicated cardiac workup is reassuring, and — critically — the source has actually been found and corrected and the home confirmed safe for re-entry. See Monitoring & Follow-Up for delayed-neurological-sequelae counseling and CO alarm counseling, both of which belong in this same discharge conversation, not as an afterthought.
Special Populations
Pregnancy
Pregnancy meaningfully changes this chapter's thresholds, not just its footnotes. Fetal haemoglobin's own affinity dynamics and the placental transfer of CO mean fetal COHb tracks toward, and can exceed, maternal levels, while fetal COHb elimination takes roughly 3-5 times longer than maternal elimination once the mother is on oxygen.[6] That single fact drives two concrete changes to management: apply the lower HBOT threshold (COHb over 15%, not 25%), and continue oxygen for a minimum of 24 hours with fetal assessment, not the shorter adult course.[2] Reported fetal mortality in severe maternal CO poisoning exceeds 50%, which is why the threshold for both oxygen duration and hyperbaric referral is deliberately set lower than the general adult criteria rather than simply applying the same numbers to a pregnant patient.[2] Involve obstetrics/maternal-fetal medicine for any pregnant patient with a confirmed or strongly suspected exposure, not only once hyperbaric oxygen is already being arranged.
Pediatrics
Children use the same lower HBOT threshold as pregnancy — COHb over 15%, not 25% — reflecting their higher metabolic rate and oxygen consumption relative to body size.[2] Presentation in young children is often nonspecific (irritability, poor feeding, lethargy) rather than a reported headache, which likely contributes to children under 4 accounting for close to a quarter of CO-related emergency department visits captured in Canadian surveillance data.[3] Maintain a low threshold to test any young child with vague, non-localizing symptoms and any plausible household exposure history.
Older adults and pre-existing cardiac or cerebrovascular disease
The same COHb level causes more harm in a patient with reduced cardiac or cerebrovascular reserve — obtain an ECG and troponin routinely in this group even with modest symptoms, and hold a lower threshold for hospital-level observation.
Smokers
Baseline COHb runs higher in smokers (up to roughly 10-15%, versus roughly 1-3% in non-smokers), which can make a modestly elevated level look falsely reassuring — interpret the result in light of the clinical picture and exposure history, not the raw number in isolation, and never use smoking status alone to withhold treatment from a symptomatic patient.
Household and cluster presentations
Any suspected case should prompt an evaluation of every other occupant of the same building, including pets — pets can show signs before people do and are a genuinely useful early clue. A pharmacist who identifies this pattern in the community should treat it as an emergency for the whole household, not only for the person in front of them.
Monitoring & Follow-Up
Continue oxygen and reassess until COHb is 3% or less and symptoms have resolved — trend COHb serially rather than relying on a single value, since it falls quickly once oxygen therapy starts.[2] Repeat troponin and ECG before discharge for anyone with initial cardiac involvement.
Delayed neurological sequelae
Counsel every patient — this is not optional, and it is easy to forget once the acute presentation has resolved — that delayed neurological/neuropsychiatric sequelae occur in roughly a quarter to just under half of hospitalized or significantly symptomatic patients, typically emerging 2 to 40 days after apparent recovery, and can include memory and concentration problems, mood changes, movement disorders, and personality change.[1][2] Arrange a follow-up contact and, where available, neuropsychological assessment at roughly 2-6 weeks, and give explicit return precautions for any new cognitive, mood, or motor symptom in that window rather than leaving the patient to decide on their own whether it is "just stress" from the original event.
Source correction and household safety
Confirm before discharge — not after — that the CO source has actually been identified and corrected and that the home has been cleared as safe for re-entry, typically by the fire department or gas utility.
Carbon monoxide alarm counseling
Recommend a correctly certified CO alarm — look for the CSA, cUL, ULC, or cETL mark — installed outside every sleeping area and on every level of the home, and confirm any existing alarm is actually certified and not simply a smoke alarm alone, since an uncertified device may fail to operate correctly.[4] Alarms should be tested regularly and replaced on the manufacturer's schedule.[4] Provide the regional poison control centre's number for any future concern — in Ontario, the Ontario Poison Centre is available 24 hours a day at 1-800-268-9017.[7]
Common Errors to Avoid
- Trusting a normal pulse oximetry reading to exclude CO poisoning — standard pulse oximetry cannot distinguish carboxyhaemoglobin from oxyhaemoglobin.[1]
- Relying on a routine arterial blood gas's calculated oxygen saturation instead of specifically ordering co-oximetry for a directly measured COHb.[1]
- Waiting for "cherry red" skin as a diagnostic sign — it is rare, late, and unreliable, and is described far more often after death than in a patient you can still treat.
- Attributing a household cluster of vague, flu-like symptoms to a circulating viral illness without specifically considering CO, especially when symptoms improve away from home.
- Delaying 100% oxygen while waiting for co-oximetry confirmation, rather than starting it immediately on clinical suspicion.[2]
- Applying the general adult COHb threshold (25%) to a pregnant patient or a child instead of the lower 15% threshold that actually applies to them.[2]
- Discharging a pregnant patient after the standard adult oxygen course instead of the required minimum 24 hours with fetal assessment.[2]
- Missing concomitant cyanide toxicity in a smoke-inhalation/fire victim presenting with shock or a disproportionately elevated lactate.
- Allowing a patient to return to a home where the CO source has not actually been confirmed corrected.
- Discharging without counseling on delayed neurological sequelae and without arranging follow-up.
- Treating CO alarm counseling as optional patient education rather than a core part of the discharge plan.
Clinical Decision Algorithm
Drug Tables
How to use this table: Doses are adult doses and require patient-specific confirmation, including pregnancy/pediatric and renal/hepatic adjustment where relevant. Select any drug name to open its complete Pharmasist Drug Database page. There is no pharmacologic antidote for carbon monoxide itself — oxygen, escalating to hyperbaric oxygen where indicated, is the actual treatment; the agents below are symptomatic/supportive care, or address the specific, real co-toxicity of cyanide in smoke-inhalation victims.
Oxygen Therapy
The immediate, first-line treatment for every patient with suspected or confirmed CO poisoning — start on clinical suspicion alone, never delayed for co-oximetry confirmation.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Oxygen 100% | Delivery: 100% FiO2 by tight-fitting non-rebreather mask at minimum; escalate to high-flow nasal cannula, CPAP/BiPAP, or intubation as clinically needed Minimum duration, symptomatic adult: 6-8 hours, or until COHb ≤3% and symptoms resolved, whichever is longer Minimum duration, pregnancy: 24 hours, with fetal assessment | Minimal at these durations; theoretical oxygen toxicity with very prolonged high-FiO2 use | None clinically significant | Shortens the COHb half-life from roughly 4-6 hours on room air to about 40-90 minutes. Continue until COHb ≤3% and symptoms resolve. |
| Hyperbaric oxygen | Protocol: 2.8 ATA; a representative trial protocol used an initial 90-minute session then 60-minute sessions on each of the following 2 days, per the treating hyperbaric unit's own protocol | Barotrauma (middle ear, sinus, rarely pulmonary), reversible myopia, claustrophobia, rare oxygen-toxicity seizure | None clinically significant | Shortens the COHb half-life further to roughly 15-30 minutes. Refer immediately once any HBOT criterion is met — do not complete a full local workup first; benefit is greatest within 6 hours of exposure. |
Cyanide Antidote (Suspected Concomitant Toxicity in Smoke Inhalation)
Reserve for a smoke-inhalation/fire victim with shock, coma, or lactic acidosis out of proportion to the measured COHb — give empirically, without waiting for a send-out cyanide level, alongside continued CO-directed care.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Hydroxocobalamin | Adults: 5 g IV infusion over 15 minutes; may repeat once (maximum cumulative 10 g) for a severe or inadequate response | Transient hypertension, red-orange discolouration of skin/urine/mucous membranes lasting several days, rare anaphylactoid reaction | Interferes with some colorimetric laboratory assays and with the optical monitoring of some dialysis/plasmapheresis equipment | This Drug Database entry (brand Cyanokit) is specifically the high-dose IV cyanide-poisoning antidote — an entirely different product and indication from vitamin B12 replacement therapy. |
Symptomatic and Supportive Care
Treat pain, nausea, and (if it occurs) seizure activity alongside CO-directed therapy — none of these agents treat the CO poisoning itself.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Acetaminophen | Adults: 650-1000 mg PO every 6 hours PRN, maximum 4 g/day (lower in hepatic impairment) | Hepatotoxicity with overdose or significant hepatic impairment | None significant at standard doses | Preferred first-line analgesic for headache; avoid reaching for an NSAID as a routine substitute given the added renal/cardiac stress in an already hypoxic patient. |
| Ondansetron | Adults: 4 mg IV/PO/ODT, may repeat per the product monograph | Headache, QTc prolongation at higher/repeated doses | Additive QTc prolongation with other QTc-prolonging drugs | First-line for nausea and vomiting; review other QTc-prolonging exposures before repeated dosing, particularly with concurrent CO-related cardiac involvement. |
| Lorazepam | Adults: 2-4 mg IV, may repeat | Sedation, respiratory depression, hypotension | Additive CNS/respiratory depression with other sedatives | For termination of a CO-associated seizure. A seizure is itself a new neurologic finding that independently meets hyperbaric oxygen referral criteria. |
References
- Carbon Monoxide Toxicity — StatPearls, StatPearls Publishing, National Library of Medicine (McMahon K, Launico MV). StatPearls [Internet], updated April 19, 2025
- Carbon Monoxide Toxicity: Treatment — Emergency Care BC, Provincial Health Services Authority (Andruko J, Marsden J). Emergency Care BC Clinical Summary, reviewed October 27, 2020
- Poisonings and injuries related to carbon monoxide exposure — Government of Canada, Health Canada Consumer Product Safety Program (Canadian Hospitals Injury Reporting and Prevention Program). Health Infobase DataLab, Government of Canada, updated August 24, 2023
- When purchasing smoke or carbon monoxide alarms, look for the Canadian certification mark — Health Canada. Government of Canada Recalls and Safety Alerts, posted May 12, 2021, updated May 17, 2021
- Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning — New England Journal of Medicine (Weaver LK, Hopkins RO, Chan KJ, et al.). N Engl J Med 2002;347(14):1057-1067
- The biological effects of carbon monoxide on the pregnant woman, fetus, and newborn infant — American Journal of Obstetrics and Gynecology (Longo LD). Am J Obstet Gynecol 1977;129(1):69-103
- Carbon Monoxide — Ontario Poison Centre, The Hospital for Sick Children. Ontario Poison Centre Patient Fact Sheet
Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.