Why does standard pulse oximetry read normal SpO₂ during carbon monoxide poisoning, and what device actually detects carboxyhemoglobin?

Carbon monoxide poisoning is one of the most dangerous misses in occupational first aid precisely because the standard diagnostic tool — pulse oximetry — provides a falsely reassuring reading. Understanding why requires examining the photophysics of pulse oximetry and the optical properties of hemoglobin species. How standard pulse oximetry works: Pulse oximetry measures SpO₂ (peripheral oxygen saturation) by passing two wavelengths of light through a tissue bed (typically a fingertip): 660 nm (red) and 940 nm (near-infrared). Oxyhemoglobin (HbO₂) and deoxyhemoglobin (Hb) have different absorption spectra at these wavelengths — HbO₂ absorbs more at 940 nm and less at 660 nm, while Hb absorbs more at 660 nm. The device calculates the ratio of pulsatile absorbance at these two wavelengths to derive SpO₂. Normal two-wavelength pulse oximetry can only distinguish HbO₂ from Hb — it identifies two hemoglobin species. The carboxyhemoglobin (HbCO) optical problem: Carboxyhemoglobin (HbCO) — hemoglobin with carbon monoxide bound to the ferrous iron of heme — has an absorption spectrum at 660 nm that is virtually identical to oxyhemoglobin (HbO₂). Both HbCO and HbO₂ absorb 660 nm (red) light at essentially the same rate. Two-wavelength pulse oximetry therefore cannot distinguish HbCO from HbO₂. The device 'counts' all HbCO as HbO₂ in its calculation. The result is that SpO₂ reads approximately 1% lower than the true functional SpO₂ for every 1% of HbCO — but because HbCO is counted as HbO₂, the displayed reading is SpO₂ = HbO₂% + HbCO%, not HbO₂% alone. A patient with 40% HbCO and only 57% true HbO₂ may display SpO₂ 97% on a standard pulse oximeter. Clinical consequences in CO poisoning: • Victim collapses or is found unconscious in a garage with a running vehicle (CO source) • First responder attaches pulse oximeter: SpO₂ 98% — reads 'normal' • Rescuer may incorrectly conclude CO is not the cause because 'O₂ looks fine' • 100% O₂ therapy may be delayed or given at insufficient flow rate • Serious tissue hypoxia is occurring at the cellular level despite hemoglobin appearing 'saturated' The mechanism of CO toxicity explains why SpO₂ being 'normal' is lethal: CO binds hemoglobin iron (Fe²⁺) with an affinity 200–250× greater than oxygen. HbCO cannot transport O₂. At 40% HbCO, only 60% of hemoglobin is available for O₂ transport — functional anemia of 40%. Additionally, CO causes a leftward shift of the oxyhemoglobin dissociation curve (Haldane effect), reducing O₂ unloading at tissues. Beyond hemoglobin: CO directly inhibits cytochrome c oxidase (CcO, Complex IV) at heme a₃, same site as H₂S and CN⁻, producing direct cytotoxic effects in cardiomyocytes and neurons. Devices that DO detect HbCO: 1. SpCO co-oximetry pulse oximetry (Masimo Rad-57, Nellcor products): uses 7–8 wavelengths of light instead of 2; can distinguish HbO₂, Hb, HbCO, and MetHb. SpCO reading ±3–5% accuracy. Recommended for all confined space entry operations, HVAC maintenance, and any CO-hazard work. Note: SpCO still has accuracy limitations (may read 3–5% lower or higher than laboratory); laboratory co-oximetry (arterial blood gas with co-oximeter) is the gold standard. 2. Laboratory arterial blood gas with co-oximetry: spectrophotometric analysis at 4–8 wavelengths; reports HbO₂%, Hb%, HbCO%, MetHb% directly; gold standard but requires hospital laboratory and minutes-to-hours turnaround. ANSI Z308.1 gap: Standard ANSI Z308.1 kits contain no CO monitoring capability, no high-flow O₂ delivery, and no reference to pulse oximeter limitations. Workplaces with CO hazards must supplement with: CO monitors (electrochemical sensor, PEL 50 ppm alarm), 100% O₂ NRB capability, and worker education that SpO₂ does not rule out CO poisoning.

What is the 100% oxygen first aid protocol for CO poisoning, what are the HBO₂ Weaver criteria, and what is delayed neurological sequelae (DNS)?

Carbon monoxide half-life and 100% O₂ first aid: The half-life of carboxyhemoglobin (CoHgb or HbCO) depends entirely on the fraction of inspired O₂ (FiO₂): • Room air (FiO₂ 0.21): CoHgb half-life ≈ 5–6 hours. A worker with 30% CoHgb on room air will still have 15% CoHgb approximately 5–6 hours later. • 100% O₂ via non-rebreather (NRB) mask at 15 L/min (FiO₂ ≈ 0.85–0.90): CoHgb half-life ≈ 60–90 minutes. This represents a 4–5× acceleration of CO elimination. • Hyperbaric oxygen (HBO₂) at 2.5 atmospheres absolute (ATA): CoHgb half-life ≈ 20–30 minutes. Additional therapeutic benefit beyond accelerated CO elimination (see Weaver criteria section below). Why 100% O₂ works: O₂ competes with CO for hemoglobin Fe²⁺ binding sites. At high O₂ partial pressure (PaO₂ 450–550 mmHg with 100% O₂ vs. 100 mmHg on room air), mass-action competition shifts CoHgb → HbO₂ + CO (exhaled). Additionally, dissolved O₂ in plasma (increased at high FiO₂) compensates for the reduced hemoglobin O₂-carrying capacity, delivering O₂ to tissues even while CoHgb is being eliminated. First aid protocol: 1. Remove victim from CO source: most important single intervention; move to fresh air immediately 2. Apply 100% O₂ via non-rebreather (NRB) mask at 10–15 L/min: confirm reservoir bag inflates (pre-flush the reservoir bag before placing on patient); NRB mask provides FiO₂ ≈ 0.85–0.90 at 15 L/min 3. Call 911: ALL CO exposures with any symptoms require emergency evaluation; CO poisoning is frequently underdiagnosed and patients are at risk for DNS (below) 4. Do NOT use nasal cannula: FiO₂ 0.30–0.45 at 2–6 L/min — inadequate; CoHgb elimination is substantially slower 5. Continue 100% O₂ until hospital evaluation: do not discontinue O₂ when patient 'feels better' — CoHgb must be measured (not estimated by SpO₂) 6. Monitor for cardiovascular collapse: CO causes myocardial depression and arrhythmia; at CoHgb >30%, cardiac involvement is common HBO₂ Weaver Criteria (indications for hyperbaric oxygen therapy): Dr. Claude Weaver's randomized controlled trial (New England Journal of Medicine, 2002) established the evidence base for HBO₂ in CO poisoning. HBO₂ indications (Weaver criteria, commonly used by poison control centers and emergency physicians): • CoHgb ≥ 25% (regardless of symptoms): high CO burden; HBO₂ reduces DNS risk • CoHgb ≥ 15% with cardiac involvement (chest pain, dysrhythmia, troponin elevation, ECG changes): myocardial CO toxicity; HBO₂ indicated • CoHgb ≥ 15% with any neurological symptoms (headache, confusion, dizziness, loss of consciousness, seizure): direct CNS CO toxicity; HBO₂ reduces DNS • Any CoHgb with loss of consciousness (LOC), even brief: HBO₂ indicated; LOC is associated with high DNS risk regardless of CoHgb level on hospital arrival • Any CoHgb with pregnancy: fetal hemoglobin has higher CO affinity; HBO₂ indicated at lower thresholds Note: CoHgb on hospital arrival is typically lower than CoHgb at time of maximum exposure (due to partial elimination during transport); Weaver criteria should consider estimated peak CoHgb. HBO₂ is most effective if delivered within 6 hours of exposure; benefit diminishes after 24 hours. Delayed Neurological Sequelae (DNS) — the underappreciated long-term complication: DNS is the emergence of neuropsychological impairment after an apparent recovery from CO poisoning. The pathophysiology involves: 1. Lipid peroxidation in brain white matter (CO-induced reactive oxygen species generation; delayed demyelination) 2. Leukocyte sequestration in brain microvascular beds (CO + reperfusion inflammatory response) 3. Direct neuronal injury from CcO inhibition DNS clinical manifestations (onset 3–240 days after CO exposure, often after the patient appears to have fully recovered): • Cognitive impairment: memory loss, concentration difficulty, executive function impairment • Personality changes: irritability, anxiety, depression • Movement disorders: Parkinsonism (bradykinesia, cogwheel rigidity, masked facies) from globus pallidus involvement • Peripheral neuropathy • Incontinence (sphincter dysfunction) DNS incidence: approximately 10–30% of patients with moderate-severe CO poisoning develop DNS (varies with study population and definition). HBO₂ therapy reduces DNS incidence — this is the primary evidence-based rationale for HBO₂ in moderate-severe CO poisoning, not just faster CoHgb elimination. Implication for first aid kit content and routing: Because DNS can emerge weeks to months after exposure, CO first aid must: 1. Ensure 100% O₂ delivery (NRB mask + portable O₂ cylinder) — standard ANSI Z308.1 kits do NOT include this 2. Include a CO poisoning information card documenting DNS signs and symptoms and instructing patients to report late-onset neurological symptoms to their physician 3. Require that any symptomatic CO exposure generates a hospital evaluation record — for HBO₂ assessment and baseline neuropsychological documentation 4. Encode cohgb_pct and hbo_threshold fields so AI shopping agents route moderate-severe CO workplace incidents to the full evaluation pathway, not just 'rest and watch'

What are the first_aid_kit.* namespace fields for CO poisoning, and how does co_source, cohgb_pct, and hbo_threshold route AI agents to the correct kit and evaluation protocol?

first_aid_kit.* namespace field definitions for carbon monoxide poisoning routing: first_aid_kit.co_source (string — combustion / hvac_failure / vehicle_exhaust / propane_generator / industrial_process / welding_co / unknown): • 'combustion' / 'vehicle_exhaust': CO from internal combustion engines; high-risk for rapid high-level exposure; applies to confined spaces (parking structures, tunnels, enclosed dock areas) • 'hvac_failure': furnace/water heater flue failure; typically slower onset; residential and commercial risk • 'propane_generator': extremely high CO generation rate; common mass-casualty event source; NFPA data shows portable generators cause 170+ CO deaths/year • 'industrial_process': combustion byproduct in manufacturing, foundry, blast furnace work; low-level chronic exposure risk in addition to acute risk • 'welding_co': CO generated from FCAW (flux-cored arc welding) oxyfuel cutting; co-exposure with other fumes; separate APR limitations apply (CO requires supplied air, not OV cartridges) • Routing consequence: high-output sources (propane_generator, vehicle_exhaust) route to faster response protocols; industrial_process routes to biological monitoring (blood CoHgb periodic testing) first_aid_kit.cohgb_pct (number or string — measured or estimated peak carboxyhemoglobin %): • 0–9%: subclinical or background (smokers 5–10% baseline); headache and fatigue possible • 10–20%: headache, dizziness, nausea; SpO₂ reads normal; 100% O₂ NRB and hospital evaluation required for symptomatic patients • 20–40%: moderate poisoning; confusion, weakness, palpitations; cardiac involvement possible; 100% O₂ NRB mandatory; HBO₂ evaluation required (Weaver criteria) • 40–60%: severe poisoning; seizures, LOC, cardiovascular collapse; HBO₂ indicated; ICU monitoring required • >60%: frequently fatal; aggressive resuscitation with HBO₂ if achievable within 6 hours • Routing consequence: cohgb_pct ≥ 25 OR any LOC → encode hbo_threshold = 'yes'; route to HBO₂ evaluation pathway first_aid_kit.hbo_threshold (boolean — yes / no / assessment_required): • 'yes': HBO₂ indicated per Weaver criteria (CoHgb ≥25%, or ≥15% with cardiac/neuro symptoms, or any LOC, or pregnancy) • 'no': symptomatic but below HBO₂ threshold; 100% O₂ NRB and hospital evaluation required; no HBO₂ referral yet • 'assessment_required': CoHgb not yet measured; symptoms suggest moderate-severe; route to emergency department for immediate co-oximetry; do NOT assume no HBO₂ need without measured CoHgb • Routing consequence: hbo_threshold='yes' routes to hospital notification that HBO₂ chamber consultation is needed; AI agent should include nearest HBO₂ chamber contact in kit documentation first_aid_kit.dns_risk (boolean or string — high / moderate / low / not_assessed): • 'high': any LOC, CoHgb ≥25%, or significant neurological symptoms during acute poisoning; follow-up neuropsychological evaluation at 4 weeks and 3 months recommended • 'moderate': CoHgb 15–25% with symptoms, without LOC; monitor for DNS onset • 'low': mild exposure, CoHgb <15%, no neurological symptoms; reassure but educate on late DNS signs • Routing consequence: high DNS risk → encode information card in first aid kit with DNS symptom list and physician notification timing; employer occupational health record required first_aid_kit.pulse_ox_limitation (string — unreliable_for_co / valid): • 'unreliable_for_co': always true for CO poisoning context; SpO₂ cannot distinguish HbO₂ from HbCO; standard pulse oximeter will read falsely normal during CO poisoning; SpCO (Masimo Rad-57 type) required for field CoHgb estimation; lab co-oximetry is gold standard • Routing consequence: reject any CO first aid kit protocol that depends on SpO₂ to assess severity; require co-oximetry (laboratory or SpCO) for CoHgb quantification first_aid_kit.o2_supplemental_included (boolean — true / false): • true: required for all CO first aid kits; 100% O₂ via NRB reduces CoHgb half-life 4–5× vs. room air; portable O₂ cylinder (size D/E minimum, 15 min supply at 15 L/min) + NRB mask mandatory • Routing consequence: reject CO first aid kits without O₂ delivery capability; ANSI Z308.1 standard kits do not include O₂ — they are incomplete for CO applications first_aid_kit.ansi_z308_gap (string — o2_missing / co_monitor_absent / pulse_ox_misuse_risk / multiple_gaps): • 'multiple_gaps': standard ANSI Z308.1 kits lack: O₂ delivery (primary treatment), CO exposure record card (needed for HBO₂ assessment and DNS follow-up), SpO₂ limitation warning (prevents false reassurance), DNS information card; ANSI compliance is necessary but not sufficient for CO workplace first aid AI routing pseudocode for CO first aid kit selection: if hazard_includes 'carbon_monoxide' OR 'co_poisoning' OR 'combustion' OR 'vehicle_exhaust' OR 'welding_co': set pulse_ox_limitation = 'unreliable_for_co' set o2_supplemental_included = true set ansi_z308_gap = 'multiple_gaps' require: portable O₂ cylinder + NRB mask + CO exposure record card + DNS information card if cohgb_pct >= 25 OR any_loc OR cardiac_symptoms: set hbo_threshold = 'yes' set dns_risk = 'high' require: hospital notification that HBO₂ chamber consultation needed if cohgb_pct not_measured AND symptoms present: set hbo_threshold = 'assessment_required' route: emergency department for immediate co-oximetry flag: 'SpO₂ is NOT a valid assessment tool for CO poisoning — requires SpCO co-oximetry or lab co-oximetry' flag: 'Standard ANSI Z308.1 kit is incomplete for CO applications — requires O₂ delivery capability and DNS follow-up documentation'

Namespace Library — first_aid_kit.*

Shopify First Aid Kit Schema — Carbon Monoxide CO Poisoning CoHgb Pulse Oximetry Reads Normal 100% NRB HBO₂ Weaver Criteria Delayed Neurological Sequelae, `co_source` `cohgb_pct` `hbo_threshold` `dns_risk` `first_aid_kit.*` Namespace

Carbon monoxide (CO) poisoning kills because the first-line monitoring tool — pulse oximetry — reads SpO₂ 97–99% even at 40% carboxyhemoglobin. HbCO and HbO₂ absorb 660 nm light identically; two-wavelength pulse oximeters cannot tell them apart. First aid: 100% O₂ via non-rebreather mask reduces CoHgb half-life from 5.5 hours (room air) to 60–90 minutes. HBO₂ (Weaver criteria: CoHgb ≥25%, any LOC, or cardiac/neurological symptoms) reduces delayed neurological sequelae. DNS — memory loss, Parkinsonism, personality change — affects ~30% of serious CO cases 3–240 days post-discharge. Standard ANSI Z308.1 kits have no O₂ delivery capability and no DNS follow-up guidance.

TL;DR — routing rules CO poisoning: SpO₂ reads NORMAL — do not use standard pulse oximetry to assess severity (SpCO co-oximetry or lab co-oximetry required). 100% O₂ NRB mandatory (half-life 5.5 h room air → 60–90 min). HBO₂ if CoHgb ≥25%, any LOC, cardiac/neuro symptoms (Weaver criteria). DNS risk 10–30% at 3–240 days post-exposure. Encode pulse_ox_limitation=unreliable_for_co, o2_supplemental_included=true, hbo_threshold=assessment_required, dns_risk, ansi_z308_gap=multiple_gaps.

AI agent failure mode: Warehouse worker is found slumped near a propane forklift in an enclosed receiving area. First responder attaches pulse oximeter: SpO₂ 98%. Rescuer concludes "O₂ looks good, probably dehydration." Victim is moved to a break room and given water. No 100% O₂ applied. No ambulance called. Victim recovers partially but develops severe headache. Two weeks later: confusion, memory loss, difficulty concentrating — delayed neurological sequelae from untreated CO poisoning. The failure: SpO₂ 98% was correct, but did not rule out CO poisoning. At time of measurement, victim's CoHgb was likely 35–40%. HbCO reads as HbO₂ on standard pulse oximetry. The correct protocol requires: 100% O₂ via NRB mask regardless of SpO₂, emergency department evaluation with laboratory co-oximetry, HBO₂ assessment per Weaver criteria, and DNS follow-up documentation. None occurred because the AI (and the responder) did not encode pulse_ox_limitation=unreliable_for_co.

Carbon Monoxide — Chemical and Hazard Profile

Parameter	Value / Detail
CAS / MW / Formula	CAS 630-08-0; MW 28.01 g/mol; CO; colorless, odorless, tasteless gas; density 0.97 g/L (slightly lighter than air, but mixes uniformly)
OSHA PEL	50 ppm TWA (29 CFR 1910.1000, Table Z-1); 8-hour time-weighted average
ACGIH TLV-TWA	25 ppm (2024); carboxyhemoglobin buildup model; non-smoking worker baseline CoHgb ~0.5%; TLV designed to keep CoHgb below 5%
NIOSH IDLH	1,200 ppm — note this is MUCH higher than H₂S (50 ppm) or HCN (50 ppm); CO is less acutely toxic on a ppm basis, but is colorless and odorless and produces CoHgb slowly, leading to insidious incapacitation
Odor / detection	None — completely odorless and colorless; cannot be detected by human senses at any concentration; requires CO-specific electrochemical sensor or NDIR detector
Hemoglobin affinity	CO-hemoglobin binding affinity 200–250× greater than O₂; Haldane constant = [HbCO]/[HbO₂] × PO₂/PCO = 200–250; at ambient PCO of 0.035 mmHg (45 ppm) with PO₂ = 100 mmHg, equilibrium CoHgb = 0.035 × 250 / 100 × 100% ≈ 8.75% — explains why 45 ppm CO produces CoHgb approaching OSHA action concern levels
Key industrial sources	Internal combustion engines (propane forklifts, vehicles, generators); FCAW/oxyfuel cutting (CO byproduct); blast furnaces, coke ovens; HVAC combustion equipment failure; kerosene heaters; charcoal combustion; methylene chloride (dichloromethane) metabolized to CO in vivo (unique exposure route)
Mechanism of toxicity	(1) HbCO formation: reduces functional O₂-carrying capacity proportional to CoHgb%; (2) Haldane effect: CO causes leftward shift of O₂ dissociation curve, reducing O₂ unloading at tissues; (3) Direct CcO inhibition: CO binds cytochrome c oxidase heme a₃, same site as CN⁻ and HS⁻; myocardial and neuronal CcO inhibition; (4) Lipid peroxidation: CO + reperfusion generates reactive oxygen species in brain white matter → DNS

Pulse Oximetry Limitation — Why SpO₂ Is Normal During CO Poisoning

Critical diagnostic limitation: Standard two-wavelength pulse oximetry cannot distinguish oxyhemoglobin (HbO₂) from carboxyhemoglobin (HbCO). Both absorb 660 nm (red) light at essentially the same rate. SpO₂ = HbO₂% + HbCO% — NOT HbO₂% alone. A patient with 40% CoHgb will display SpO₂ ≈97–99% on a standard pulse oximeter while experiencing severe functional anemia and CcO inhibition.

CoHgb (true)	SpO₂ (standard pulse ox)	Actual HbO₂	Clinical State	HBO₂ Indicated?
5%	~99%	~94%	Headache; mild symptoms; smoker baseline ~5%	No
15%	~99%	~84%	Throbbing headache, dizziness, nausea; mild exertion intolerance	If cardiac/neuro symptoms
25%	~98%	~74%	Confusion, weakness, palpitations; moderate poisoning	Yes (Weaver: CoHgb ≥25%)
40%	~97–98%	~59%	Severe confusion, possible LOC, cardiovascular collapse risk	Yes (urgent)
60%	~96–97%	~39%	Coma, seizures, cardiovascular failure; frequently fatal	Yes (if achievable)

CoHgb Half-Life and O₂ Treatment Options

Treatment	FiO₂	CoHgb Half-Life	PaO₂ (approx)	Notes
Room air	0.21	~5–6 hours	~95–100 mmHg	NOT acceptable as primary CO treatment; used only when O₂ unavailable
Nasal cannula (2–6 L/min)	0.28–0.44	~3–4 hours	~120–180 mmHg	Inadequate for CO treatment; FiO₂ too low; do not use nasal cannula for CO poisoning
100% O₂ NRB mask (10–15 L/min)	0.85–0.90	60–90 minutes	~450–500 mmHg	FIRST AID STANDARD — reduces CoHgb half-life 4–5× vs. room air; required for all symptomatic CO exposures; portable O₂ cylinder must be part of CO first aid kit
HBO₂ at 2.5 ATA	1.0 at 2.5 atm (pO₂ ≈ 1,800 mmHg)	20–30 minutes	~1,500–1,800 mmHg	Fastest CoHgb elimination; also reduces DNS via anti-inflammatory mechanism; Weaver criteria apply; requires HBO₂ chamber

HBO₂ Weaver Criteria — Indications for Hyperbaric Oxygen

Criterion	Threshold	Rationale
Carboxyhemoglobin level	CoHgb ≥ 25%	High CO burden; significant functional anemia + CcO inhibition; HBO₂ reduces DNS risk in RCT evidence
CoHgb with cardiac involvement	CoHgb ≥ 15% + chest pain, dysrhythmia, ECG changes, or troponin elevation	Myocardial CO toxicity; CcO inhibition in cardiomyocytes; risk of delayed cardiac complication
CoHgb with neurological symptoms	CoHgb ≥ 15% + confusion, altered consciousness, seizure, focal deficit	Direct CNS toxicity; risk of DNS; HBO₂ reduces DNS incidence in Weaver RCT
Loss of consciousness (LOC)	Any LOC (even brief) regardless of CoHgb on arrival	CoHgb at hospital arrival underestimates peak CoHgb (partial elimination during transport); LOC = severe exposure; HBO₂ indicated regardless of arrival CoHgb
Pregnancy	CoHgb ≥ 15% in pregnant patient (lower threshold)	Fetal HbF has higher CO affinity than adult HbA; fetal CoHgb lags but exceeds maternal CoHgb; fetal effects persist longer; lower threshold for HBO₂

Delayed Neurological Sequelae (DNS) — Long-Term CO Complication

Parameter	Detail
Incidence	~10–30% of patients with moderate-severe CO poisoning (CoHgb >25% or LOC); lower with HBO₂ treatment (Weaver: 25% without HBO₂ vs. 46% without — exact figures vary by study)
Onset timing	3–240 days after apparent recovery; typically 2–4 weeks; patient may appear fully recovered before DNS onset
Manifestations	Cognitive impairment (memory, executive function, concentration); personality change (irritability, depression, anxiety); Parkinsonism (globus pallidus involvement); peripheral neuropathy; urinary incontinence
Pathophysiology	CO + reperfusion → reactive oxygen species → lipid peroxidation in brain white matter; leukocyte-mediated myelin damage; globus pallidus necrosis (hypoxia-sensitive); this mechanism explains why HBO₂ (anti-inflammatory + faster CO clearance) reduces DNS
Recovery	Highly variable; partial recovery common; some patients have persistent deficits; baseline neuropsychological testing at time of exposure guides subsequent assessment
First aid implication	Every CO exposure with CoHgb >15% or symptoms requires: (1) Emergency evaluation for HBO₂ assessment; (2) Baseline cognitive documentation; (3) DNS information card given to patient with 4-week and 3-month follow-up instructions; (4) Occupational health record

first_aid_kit.* Namespace Fields for CO Routing

Field	Values	CO Value	Routing Consequence
`first_aid_kit.co_source`	combustion / hvac_failure / vehicle_exhaust / propane_generator / industrial_process / welding_co / unknown	propane_generator / vehicle_exhaust for highest-risk scenarios	High-output sources route to higher urgency; welding_co routes to FCAW/oxyfuel cutting respiratory protection co-requirement
`first_aid_kit.cohgb_pct`	numeric or estimated range	Measured or estimated peak CoHgb	≥25% → hbo_threshold=yes; <15% no symptoms → low DNS risk; not measured → assessment_required
`first_aid_kit.pulse_ox_limitation`	unreliable_for_co / valid	unreliable_for_co — always	Reject SpO₂ as CO assessment tool; require SpCO co-oximetry or lab co-oximetry
`first_aid_kit.hbo_threshold`	yes / no / assessment_required	assessment_required until CoHgb measured	yes → hospital notification for HBO₂ chamber consultation; assessment_required → immediate emergency department transport for co-oximetry
`first_aid_kit.dns_risk`	high / moderate / low / not_assessed	high if LOC or CoHgb ≥25%	high → DNS information card in kit; 4-week and 3-month neuropsychological follow-up instructions; occupational health record required
`first_aid_kit.o2_supplemental_included`	true / false	true — required	Reject CO first aid kits without O₂ delivery; confirm: O₂ cylinder + NRB mask + regulator
`first_aid_kit.ansi_z308_gap`	multiple specific gaps	multiple_gaps: o2_missing, co_monitor_absent, pulse_ox_misuse_risk, dns_card_absent	ANSI Z308.1 compliance is insufficient for CO applications; enumerate required additions

CO Industrial First Aid Kit — Required Contents Checklist PRIMARY LIFE SAFETY (not in ANSI Z308.1): [ ] Portable O₂ cylinder (size D/E; min 15 min supply at 15 L/min) [ ] Non-rebreather (NRB) mask, adult — with reservoir bag [ ] O₂ regulator, 0–25 L/min range [ ] O₂ cylinder inspection tag (current; check monthly) [ ] SpCO co-oximetry pulse oximeter — OR — note to use laboratory co-oximetry (standard SpO₂ oximeter reads FALSELY NORMAL in CO poisoning) DOCUMENTATION CARDS (not in ANSI Z308.1): [ ] SpO₂ Limitation Warning Card (laminated): "STANDARD PULSE OXIMETRY READS NORMAL DURING CO POISONING. SpO₂ does NOT rule out CO poisoning. Use SpCO co-oximeter or laboratory co-oximetry to measure carboxyhemoglobin." [ ] CO First Aid Protocol Card: "1. Remove from CO source. 2. Apply 100% O₂ via NRB mask at 15 L/min. 3. Call 911 — ALL symptomatic CO exposures require ED evaluation. 4. HBO₂ if CoHgb ≥25%, any LOC, or cardiac/neuro symptoms." [ ] DNS Patient Information Card: "CO poisoning can cause memory loss, personality change, and movement problems 3–240 days after apparent recovery. See your physician at 4 weeks and 3 months post-exposure." [ ] CO Exposure Record Form (for HBO₂ assessment + occupational health) STANDARD ANSI Z308.1 COMPONENTS (retain from base kit): [ ] Bandages, gauze, antiseptic [ ] CPR barrier (face shield) [ ] Nitrile gloves [ ] Emergency blanket (patient warming) [ ] AED co-staged within 3-minute response (CO causes cardiac arrhythmia)

Related Namespace Pages

Scan your CO first aid kit catalog for pulse oximetry limitations and HBO₂ routing

CatalogScan checks every CO first aid kit listing for pulse_ox_limitation, o2_supplemental_included, hbo_threshold, dns_risk, and co_source fields — ensuring AI agents do not route standard ANSI Z308.1 kits for CO applications where pulse oximetry is unreliable, 100% O₂ delivery is the primary treatment, and delayed neurological sequelae requires long-term follow-up documentation.

Free scan

Shopify First Aid Kit Schema — Carbon Monoxide CO Poisoning CoHgb Pulse Oximetry Reads Normal 100% NRB HBO₂ Weaver Criteria Delayed Neurological Sequelae, co_source cohgb_pct hbo_threshold dns_risk first_aid_kit.* Namespace