Toxicology – Carbon Monoxide

Core concept

Carbon monoxide (CO) is a colorless, odorless, tasteless gas produced by incomplete combustion of carbon-containing fuels.

The classic poisoning syndrome is:

Headache + dizziness + nausea → confusion/syncope → coma/seizures/cardiac ischemia

The organs most vulnerable are the:

Brain + heart

because of their high oxygen requirements.

The key management principle is:

Suspected CO poisoning → immediately give 100% oxygen

Do not wait for the carboxyhemoglobin (COHb) result.

Severe poisoning may warrant hyperbaric oxygen therapy (HBOT), but the evidence for HBOT preventing long-term neurocognitive injury remains mixed. The 2025 ACEP clinical policy concludes that selected symptomatic patients may benefit, with the decision individualized according to severity and practical availability.

Sources of Carbon Monoxide

CO is generated whenever carbon-containing fuel burns incompletely.

Common sources include:

• Portable generators
• Faulty furnaces
• Gas or oil heaters
• Water heaters
• Fireplaces
• Charcoal grills
• Propane stoves
• Gasoline-powered tools
• Cars/trucks
• Internal-combustion engines
• Boats
• Structure fires

Running combustion engines or generators in enclosed or poorly ventilated spaces can rapidly generate lethal concentrations.

Important Noncombustion Source – Methylene Chloride

Methylene chloride (dichloromethane) is metabolized in the liver to carbon monoxide.

It has historically been present in:

• Paint removers
• Industrial solvents
• Degreasers

This exposure is distinctive because:

Methylene chloride → continued hepatic metabolism → continued CO production even after exposure ends

Therefore:

COHb may continue rising or rebound for hours after the patient leaves the exposure.

These patients may require more prolonged oxygen therapy and observation than ordinary combustion-related CO exposures.

Epidemiology

The older estimate of up to 8,000 U.S. deaths annually is not representative of current accidental non-fire CO epidemiology.

Current CDC information reports that each year in the United States:

• >400 people die from unintentional non-fire CO poisoning
• >100,000 ED visits occur
• >14,000 hospitalizations occur

CO remains an important and highly preventable toxicologic emergency.

Pathophysiology

CO poisoning is much more than simply “low blood oxygen.”

1. Carboxyhemoglobin Formation

CO binds hemoglobin with approximately 200-fold greater affinity than oxygen.

This produces:

CO + hemoglobin → carboxyhemoglobin

leading to:

↓ available hemoglobin for O₂ transport

2. Left Shift of the Oxyhemoglobin Dissociation Curve

CO also increases the oxygen affinity of the remaining unoccupied hemoglobin sites.

Therefore:

COHb formation + left shift → impaired O₂ carriage + impaired O₂ unloading

So even the oxygen still bound to hemoglobin is released less effectively to tissue.

3. Myoglobin Binding

CO binds cardiac and skeletal-muscle myoglobin.

This contributes to:

• Myocardial dysfunction
• Reduced cardiac oxygen reserve
• Skeletal muscle injury

4. Mitochondrial Toxicity

CO binds heme-containing mitochondrial proteins, including cytochrome systems.

Therefore:

CO → impaired mitochondrial respiration → cellular oxygen-utilization failure

This partly explains why clinical toxicity may be much worse than predicted by COHb alone.

5. Oxidative and Inflammatory Injury

CO also initiates:

• Nitric oxide–related injury
• Free-radical formation
• Lipid peroxidation
• Endothelial dysfunction
• Apoptosis
• Immune-mediated inflammation

These mechanisms are thought to contribute particularly to delayed neurologic injury. The current ACEP policy emphasizes that CO poisoning produces both hypoxic and inflammatory/immunologic cellular damage.

6. Anaerobic Metabolism

Severe tissue hypoxia causes:

Anaerobic glycolysis → lactate elevation → metabolic acidosis

A high lactate supports severe physiologic stress but does not correlate perfectly with COHb.

Risk Groups

Patients particularly vulnerable to CO include:

• Pregnant patients and fetuses
• Infants
• Young children
• Older adults
• Patients with coronary artery disease
• Patients with anemia
• Patients with significant respiratory disease

Patients with coronary disease may develop ischemia at CO exposures tolerated by otherwise healthy individuals.

Clinical Features

Symptoms depend on:

CO concentration × duration of exposure

plus the patient’s underlying physiology.

Importantly:

COHb concentration does not correlate reliably with symptom severity or outcome.

Mild–Moderate Poisoning

Common symptoms:

• Headache
• Dizziness
• Weakness
• Fatigue
• Nausea
• Vomiting
• Difficulty concentrating
• Lightheadedness
• Dyspnea
• Chest discomfort

A classic clue is:

Several people in the same building developing “flu-like” symptoms without fever.

Pets may also become ill.

Neurologic Toxicity

Progressive toxicity may cause:

• Confusion
• Impaired judgment
• Ataxia
• Syncope
• Altered consciousness
• Seizures
• Coma

Patients may be unable to recognize that they are being poisoned and therefore may fail to escape the environment.

Cardiovascular Toxicity

CO can cause:

• Sinus tachycardia
• Hypotension
• Dysrhythmias
• Myocardial ischemia
• Myocardial infarction
• Transient cardiomyopathy
• Cardiogenic shock
• Cardiac arrest

Cardiac injury may occur even in individuals without obstructive coronary disease.

In one major cohort of moderate/severe poisonings, myocardial injury occurred in approximately 37% and was associated with substantially higher long-term mortality.

Therefore:

Cardiac toxicity is not a secondary curiosity—it is a major prognostic feature.

Respiratory

Possible findings include:

• Tachypnea
• Dyspnea
• Hypoxemia from associated pulmonary disease
• Pulmonary edema

Severe exposures may also be complicated by:

• Aspiration
• Smoke-inhalation injury
• ARDS

CO itself generally causes tissue hypoxia rather than primary airway injury, so prominent airway burns or bronchospasm should prompt consideration of additional smoke toxicants.

Skin Findings

The classic:

“Cherry-red skin”

is not a useful clinical sign.

It is uncommon in living patients and is more often described in severe or postmortem cases.

Do not wait for it.

Musculoskeletal / Renal

Severe poisoning, particularly with prolonged coma, may cause:

• Muscle necrosis
• Elevated CK
• Rhabdomyolysis
• Myoglobinuria
• Acute kidney injury

Pressure injury from prolonged immobilization may coexist.

Diagnosis

Diagnosis is based on:

Compatible exposure + clinical syndrome + blood carboxyhemoglobin measurement

but treatment should begin before laboratory confirmation.

Carboxyhemoglobin Measurement

The preferred confirmatory test is:

Blood COHb measured by multiwavelength co-oximetry

Either:

• Venous blood
• or
• Arterial blood

may be used.

An arterial sample is not required solely to measure COHb.

Interpretation of COHb

CDC guidance states that:

• ≥2% in a nonsmoker
• >9% in a smoker

strongly supports CO exposure.

However:

COHb is an exposure marker—not a severity score.

A critically ill patient may have a relatively low measured COHb if:

• Exposure ended hours earlier
• EMS already administered oxygen
• The patient received oxygen before blood was drawn

Therefore:

Treat the patient, not the COHb number.

Smokers

Smokers may have chronically elevated baseline COHb.

Thus, a mild elevation must be interpreted in context.

The old statement that smokers routinely reach 12% should not be used as a universal “normal smoker value”; current CDC guidance instead considers >9% supportive of CO poisoning when the clinical context fits.

Conventional Pulse Oximetry – Major Pitfall

A normal SpO₂ does not exclude CO poisoning.

Standard two-wavelength pulse oximeters cannot reliably distinguish:

Oxyhemoglobin from carboxyhemoglobin

and may therefore display a falsely reassuring saturation such as:

SpO₂ 99%

in a significantly poisoned patient.

Therefore:

Normal pulse oximetry does not rule out carbon monoxide poisoning.

PaO₂ Can Also Be Normal

Another important pitfall:

Arterial PaO₂ measures dissolved oxygen in plasma.

It does not tell you how much hemoglobin is occupied by CO.

Therefore a patient can have:

Normal PaO₂ + dangerous COHb + severe tissue hypoxia

A standard ABG alone does not diagnose CO poisoning unless co-oximetry is performed.

Pulse CO-Oximetry

Noninvasive devices can estimate COHb as SpCO.

However, ACEP has recommended that:

Pulse CO-oximetry should not be used to definitively diagnose or exclude CO toxicity.

Blood co-oximetry remains the confirmatory method.

Essential Investigations

For clinically significant poisoning obtain:

• Blood COHb by co-oximetry
• Bedside glucose
• Electrolytes
• Bicarbonate
• BUN/creatinine
• ECG

In moderate/severe poisoning also consider:

• Troponin
• Lactate
• Blood gas
• CK
• Urinalysis

Cardiac Testing

For moderate or severe CO poisoning:

ECG + cardiac biomarkers are important.

ACEP specifically recommends ECG and cardiac biomarker testing to identify acute myocardial injury because cardiac injury predicts poorer outcome.

Consider echocardiography for:

• Shock
• Elevated troponin
• Significant ECG abnormalities
• Suspected cardiomyopathy

Lactate

Lactate may rise because of:

• Tissue hypoxia
• Seizures
• Shock
• Catecholamine response

A markedly elevated lactate in a patient with structure-fire smoke exposure should also raise concern for:

Concurrent cyanide poisoning

because fire victims can have both:

CO + cyanide toxicity

simultaneously.

Neuroimaging

CT or MRI is not required for every mild exposure.

Consider neuroimaging for:

• Persistent altered consciousness
• Focal neurologic findings
• Severe poisoning
• Alternative intracranial diagnosis

Possible abnormalities include:

• Globus pallidus injury
• Cerebral edema
• White-matter abnormalities

A normal scan does not exclude significant CO poisoning or future delayed neurologic sequelae.

Differential Diagnosis

Toxicologic

Consider:

• Cyanide
• Hydrogen sulfide
• Simple asphyxiants
• Opioids
• Sedative-hypnotics
• Ethanol
• Toxic alcohols
• Other smoke-inhalation toxins

Medical

Consider:

• Viral illness
• Hypoglycemia
• Stroke
• Intracranial hemorrhage
• Sepsis
• Migraine
• Acute coronary syndrome
• Seizure/postictal state

Treatment

1. Remove From Exposure

Immediately move the patient to uncontaminated air.

Rescuers must not enter a dangerous enclosed atmosphere without appropriate respiratory protection.

Also remember:

Multiple victims may still be in the same environment.

Emergency services should identify and eliminate the source.

2. Give 100% Oxygen Immediately

This is the fundamental treatment.

Administer:

100% oxygen by a tightly fitting non-rebreather mask

using sufficient flow to keep the reservoir inflated.

If intubated:

FiO₂ = 1.0

should initially be used.

CDC recommends 100% oxygen until symptoms resolve, commonly approximately 4–5 hours in uncomplicated cases, while performing serial neurologic examinations.

COHb Elimination

Approximate COHb half-life:

Room air

~5 hours

100% high-flow oxygen

~60–90 minutes

Hyperbaric oxygen

~20–30 minutes

The 2025 ACEP policy cites approximately 5 hours, 85 minutes, and 20 minutes, respectively.

Thus:

High-concentration oxygen dramatically accelerates CO elimination.

Oxygen and COPD

The older suggestion that COPD-associated CO₂ retention is a contraindication to 100% oxygen is misleading.

In clinically important CO poisoning:

Do not withhold high-concentration oxygen because the patient has COPD.

If hypercapnia is a concern:

• Monitor ventilation
• Obtain blood gas when needed
• Provide ventilatory support

The immediate threat from CO-mediated hypoxia outweighs theoretical concern about oxygen-induced hypercapnia.

Treatment Endpoint

Do not treat to a specific COHb concentration alone.

Continue oxygen until:

• Symptoms have resolved or clearly improved
• Neurologic examination is reassuring
• Cardiac/hemodynamic abnormalities are addressed
• Hyperbaric treatment is initiated when selected

A falling COHb does not necessarily mean cellular injury has resolved.

Hyperbaric Oxygen Therapy

HBOT provides oxygen at increased atmospheric pressure, producing:

• Faster COHb dissociation
• Very high dissolved plasma oxygen concentrations
• Improved tissue oxygen delivery
• Potential effects on inflammatory/oxidative pathways

However:

The long-term neurocognitive benefit remains controversial.

The 2025 ACEP clinical policy found no Level A or Level B recommendation supporting routine HBOT for all CO-poisoned adults.

Its Level C recommendation is:

Selected symptomatic patients may benefit from HBOT according to clinical severity and availability, including transport distance/time.

This is an important modernization of the older textbook’s relatively rigid HBO criteria.

When to Strongly Consider HBOT

Current CDC clinical guidance recommends considering HBOT when there is:

• COHb >25–30%
• Transient or prolonged loss of consciousness
• Significant neurologic impairment
• Abnormal neuropsychological testing
• Cardiac involvement
• Severe acidosis

and notes that HBOT may be appropriate at lower COHb concentrations when clinical severity warrants it.

Practical high-risk features

Urgent hyperbaric/toxicology consultation is particularly reasonable with:

• Coma
• Persistent altered consciousness
• Syncope attributable to CO
• Seizures
• Focal neurologic deficits
• Significant myocardial ischemia/injury
• Severe metabolic acidosis
• Hemodynamic instability after stabilization
• Severe exposure with persistent symptoms
• Pregnancy

Do Not Use COHb Alone to Decide HBOT

A patient can be critically poisoned with a modest COHb if:

• Oxygen was already administered
• Presentation was delayed

Conversely, an awake clinically well patient may have had a relatively high measured COHb.

Therefore:

HBOT decisions are primarily clinical—not based on one cutoff.

Timing of HBOT

When HBOT is selected, consultation and transfer should occur early.

Potential benefit is generally considered greatest when treatment is initiated during the early hours after poisoning, but exact protocols vary by hyperbaric center.

Do not delay:

• Airway management
• Hemodynamic stabilization
• High-flow oxygen

while arranging chamber therapy.

HBOT Regimen

There is no single universally mandated regimen.

Treatment centers commonly use oxygen at approximately:

2–3 atmospheres absolute (ATA)

with treatment duration and repeat sessions individualized by:

• Clinical severity
• Neurologic response
• Center protocol

The old fixed protocol of exactly 2.7 ATA for 30 minutes followed by 2.2 ATA for 90 minutes should not be treated as the universal contemporary standard.

HBOT Risks

Potential complications include:

• Middle-ear barotrauma
• Sinus barotrauma
• Claustrophobia
• Oxygen-induced seizure
• Pulmonary barotrauma
• Transport-related deterioration

The 2025 ACEP policy specifically emphasizes that the risks of transfer to a distant chamber and deterioration during transport must be incorporated into the decision.

Untreated pneumothorax

An untreated pneumothorax is a major/absolute contraindication to entering a hyperbaric chamber until treated.

Hemodynamic instability

The older blanket statement that hemodynamic instability is a contraindication is too simplistic.

Severe cardiac injury may itself favor HBOT consideration, but an unstable patient must be adequately stabilized and transported only when the chamber can safely support critical care.

Pregnancy

Pregnancy deserves special treatment because the fetus is at disproportionately high risk.

CO crosses the placenta.

Fetal hemoglobin:

• Has greater affinity for CO
• Accumulates CO more readily
• Eliminates CO more slowly

Fetal COHb may therefore exceed the maternal level, and fetal clearance may be several times slower.

Therefore:

A reassuring maternal COHb does not guarantee fetal safety.

HBOT in Pregnancy

CDC currently states that:

Hyperbaric oxygen is the treatment of choice in pregnant patients with CO poisoning, even when maternal poisoning appears less severe.

Thus pregnancy should prompt:

Early toxicology/hyperbaric consultation at a lower threshold than in a nonpregnant adult.

Consider:

• Obstetric consultation
• Fetal assessment/monitoring when gestationally appropriate

Do not rely on the old single cutoff of:

COHb >15%

as the only indication for HBOT in pregnancy.

Cardiac Toxicity Treatment

Treatment begins with:

• 100% oxygen
• Correction of shock
• Continuous ECG monitoring

Treat true acute coronary syndrome according to standard cardiac principles when appropriate.

However, recognize that CO may cause:

• Myocardial stunning
• Demand ischemia
• Direct myocardial toxicity

even without obstructive coronary disease.

Patients with myocardial injury deserve close follow-up because it is associated with increased long-term mortality.

Hypotension / Shock

Treat according to contemporary shock principles:

• Judicious isotonic crystalloid if fluid responsive
• Vasopressor therapy if hypotension persists

Norepinephrine is generally a reasonable first-line vasopressor for persistent shock.

The historical preference for:

• Trendelenburg positioning
• Dopamine as the default first vasopressor

is outdated.

Seizures

Treat with:

Benzodiazepines first-line

Examples:

• Lorazepam
• Midazolam
• Diazepam

For refractory seizures, escalate according to standard status-epilepticus/toxicologic seizure management.

Maintain:

• 100% oxygen
• Adequate ventilation
• Glucose
• Temperature control

Rhabdomyolysis

If prolonged coma or seizures occur:

• Check CK
• Check renal function
• Monitor potassium
• Monitor urine output

Treat rhabdomyolysis according to standard principles.

Smoke-Inhalation Patients

A structure-fire victim may have several simultaneous toxicities:

CO + cyanide + airway thermal injury + pulmonary irritants

Do not assume that every abnormality is explained by CO.

Consider cyanide especially with:

• Enclosed-space fire
• Soot
• Severe altered consciousness
• Profound cardiovascular collapse
• Severe lactic acidosis

No Gastrointestinal Decontamination

Ordinary CO poisoning occurs by inhalation.

There is no role for:

• Activated charcoal
• Gastric lavage
• Whole-bowel irrigation

for CO itself.

GI decontamination is relevant only for a separate coingestant.

Antidote

The functional antidotal therapy is:

OXYGEN

at either:

• Normobaric pressure
• Hyperbaric pressure in selected patients

There is no conventional chemical antidote that binds and neutralizes CO in routine clinical use.

Delayed Neurologic Sequelae

This is one of the most important follow-up issues.

After apparent recovery, a patient may experience a lucid interval followed by new neurologic/psychiatric abnormalities.

Current ACEP material describes delayed neurologic findings developing approximately:

2–40 days after the original exposure.

Delayed Symptoms

Possible manifestations include:

• Memory impairment
• Poor concentration
• Personality change
• Depression
• Psychosis
• Apathy
• Cognitive decline
• Gait abnormality
• Tremor
• Parkinsonism
• Urinary incontinence
• Speech disturbance
• Seizures

The syndrome is sometimes termed:

Delayed neurologic sequelae (DNS)

or

Delayed neuropsychiatric syndrome

Who Is at Higher Risk of DNS?

Risk is greater after features such as:

• Older age
• Prolonged exposure
• Loss of consciousness
• Low GCS
• Significant cognitive impairment
• Higher initial COHb
• Abnormal brain imaging

but no available marker reliably predicts DNS in every patient.

Follow-Up

All discharged CO-poisoned patients should be told explicitly that neurologic or psychiatric symptoms can appear after apparent recovery.

CDC recommends:

Repeat medical and neurologic examination in approximately 2 weeks.

Earlier reassessment is warranted for:

• New confusion
• Memory problems
• Personality change
• Gait disturbance
• Tremor
• Urinary incontinence
• New weakness
• Seizure

Observation and Admission

Mild Poisoning

Patients with mild symptoms may be considered for discharge once:

• Exposure has ended
• Symptoms have resolved with oxygen
• Neurologic examination is normal
• Vital signs are stable
• No cardiac injury is identified
• The exposure source has been made safe

A specific COHb concentration alone should not determine discharge.

Hospital Admission

Admission is appropriate for:

• Persistent neurologic symptoms
• Loss of consciousness
• Seizures
• Significant cardiac injury
• Abnormal ECG/troponin
• Severe metabolic acidosis
• Persistent hypotension
• Pulmonary complications
• Significant rhabdomyolysis
• Need for continued oxygen/monitoring

Patients with severe poisoning generally require ICU-level care.

Pregnancy warrants a particularly low threshold for prolonged observation and specialty consultation.

Occupational Exposure Standards

The older occupational-standard section needs correction.

OSHA

Current federal OSHA PEL:

50 ppm as an 8-hour TWA

There is not a general OSHA 200-ppm ceiling in the standard general-industry PEL table.

NIOSH

Current NIOSH recommendations:

REL TWA: 35 ppm

Ceiling: 200 ppm

IDLH: 1,200 ppm

Therefore, the older source incorrectly attributes the 200-ppm ceiling to OSHA; it is the NIOSH ceiling recommendation.

ACGIH

Current occupational information cites:

ACGIH TLV-TWA: 25 ppm

Thus the older ACGIH 25-ppm TWA remains broadly consistent, whereas the OSHA ceiling statement does not.

Prevention

CO poisoning is highly preventable.

Important measures include:

• Install functioning CO detectors near sleeping areas
• Maintain furnaces/heaters
• Never use charcoal grills indoors
• Never operate portable generators indoors or in enclosed spaces
• Avoid running vehicles in attached or poorly ventilated garages
• Ensure combustion appliances are properly vented

CDC recommends battery-powered or battery-backup CO alarms and regular detector replacement according to manufacturer guidance.

A poisoned patient should not return to the exposure site until the CO source has been identified and corrected.

Important Pitfalls

1. Trusting the pulse oximeter

A patient with severe CO poisoning may show:

SpO₂ = 99%

because conventional pulse oximetry misidentifies COHb.

Use blood co-oximetry.

2. Trusting a normal PaO₂

PaO₂ measures dissolved plasma oxygen.

Normal PaO₂ does not exclude severe CO poisoning.

3. Treating the COHb number instead of the patient

COHb may already have fallen substantially before presentation.

Clinical features and exposure history matter more than a single level.

4. Waiting for a COHb result before giving oxygen

Start 100% oxygen immediately.

There is no benefit to delaying treatment for diagnostic confirmation.

5. Assuming smokers can “normally” have any high COHb

Smoking increases baseline COHb, but current CDC guidance regards:

>9% in a smoker

as strongly supportive of CO poisoning when clinically appropriate.

6. Missing myocardial injury

Obtain:

ECG + troponin

in moderate/severe poisoning.

Cardiac injury predicts important short- and long-term risk.

7. Using a rigid HBOT cutoff

Current practice does not support:

COHb ≥X% = HBO, <X% = no HBO

as an absolute rule.

The 2025 ACEP policy emphasizes selected symptomatic patients and individualized risk/availability considerations.

8. Claiming HBOT definitely prevents delayed neurologic sequelae

Evidence remains conflicting.

HBOT is an important option for selected severe poisoning, but a universal neuroprotective benefit has not been conclusively established.

9. Under-treating pregnancy

The fetus:

• Accumulates more CO
• Clears CO more slowly

Maternal improvement does not guarantee fetal recovery.

Pregnancy warrants aggressive oxygen therapy and early HBOT consultation.

10. Missing delayed neurologic disease

A patient may appear completely recovered and then deteriorate neurologically days to weeks later.

Warn every significant CO-poisoned patient before discharge.

11. Missing methylene chloride

Paint-stripper/solvent exposure may generate CO metabolically.

COHb can continue to rise after exposure ends.

12. Missing cyanide in fire victims

CO does not explain every case of:

• Profound shock
• Severe lactic acidosis
• Rapid collapse

after enclosed-space fire exposure.

Think:

CO + cyanide

13. Failing to identify the exposure source

Treating the patient without correcting:

• Faulty furnace
• Generator placement
• Vehicle exhaust
• Water heater problem

creates a major risk of repeat poisoning.

High-Yield Toxicology Pearls

Carbon monoxide = normal pulse oximeter does NOT mean normal oxygen delivery

Think:

Headache + nausea + dizziness + multiple people affected → CO until proven otherwise

Severe poisoning:

Syncope/coma + seizure + myocardial injury + acidosis

Key points:

• CO is colorless, odorless, and tasteless
• Produced by incomplete combustion
• Common sources:
• Generators
• Furnaces/heaters
• Vehicle exhaust
• Charcoal
• Structure fires
• Methylene chloride is metabolized to CO
• Main mechanism:
• COHb formation
• Left shift of O₂ dissociation curve
• Myoglobin binding
• Mitochondrial dysfunction
• Oxidative/inflammatory injury
• Brain and heart are the major target organs
• Normal SpO₂ does not exclude CO poisoning
• Normal PaO₂ does not exclude CO poisoning
• Confirm with blood co-oximetry
• Venous blood is acceptable
• COHb:
• ≥2% nonsmoker supports exposure
• >9% smoker supports exposure
• COHb correlates poorly with clinical severity
• First treatment:
• 100% oxygen immediately
• Approximate COHb half-life:
• Room air: ~5 h
• 100% O₂: ~60–90 min
• HBOT: ~20–30 min
• Do not withhold 100% O₂ because of COPD
• Moderate/severe poisoning:
• ECG + troponin
• Myocardial injury predicts poorer long-term outcome
• HBOT should be considered particularly for:
• Loss of consciousness
• Significant neurologic toxicity
• Cardiac injury
• Severe acidosis
• COHb approximately >25–30%
• Pregnancy
• HBOT evidence remains controversial
• 2025 ACEP:
• Selected symptomatic patients may benefit
• Consider severity + availability/transport
• Pregnancy:
• Fetal COHb may exceed maternal COHb
• Fetal elimination is much slower
• Early HBOT consultation is recommended
• Fire victim with severe lactic acidosis/shock → consider cyanide co-poisoning
• Delayed neurologic sequelae may appear approximately 2–40 days later
• Arrange neurologic follow-up; CDC suggests reassessment at about 2 weeks
• NIOSH:
• 35 ppm TWA
• 200 ppm ceiling
• 1,200 ppm IDLH
• OSHA:
• 50 ppm 8-hour TWA
• Prevention and elimination of the exposure source are essential