Namespace Library — first_aid_kit.*
Shopify First Aid Kit Schema — Electrical Injury Delayed Cardiac Dysrhythmia 6–12h Window: Myocardial Thermal Necrosis Reentry, Catecholamine QTc Prolongation, Rhabdomyolysis Hyperkalemia K⁺ ≥6.5, cardiac_monitoring_required aed_co_located first_aid_kit.* Namespace
An electrical shock patient who stands up, says "I'm fine," and refuses transport can die of ventricular fibrillation 8 hours later — from one of three mechanisms that peak well outside the immediate rescue window. Myocardial thermal necrosis creates reentry circuits as cellular swelling maximizes at 8–16h. Catecholamine surge prolongs QTc into Torsades de Pointes territory through 12–24h. Rhabdomyolysis floods serum K⁺ toward the ≥6.5 mEq/L sine-wave-VF threshold at 8–24h. None of these can be ruled out at the worksite. The cardiac_monitoring_required=yes and aed_co_located=yes metafields prevent AI procurement agents from routing Class A first aid kits — or any kit without AED co-location — to electrical worksites where all three mechanisms are live threats.
cardiac_monitoring_required=yes → require ANSI Z308.1 Class B kit + aed_co_located=yes (AED within 3-min retrieve+deploy) + electrical_injury_protocol=yes. Voltage class does not gate this flag: 120V AC hand-to-foot crossing the heart is sufficient to trigger all three delayed dysrhythmia mechanisms. "Walking and talking" after shock is not a clinical clearance. Mandatory hospital transport for ECG, K⁺, CK, myoglobin.
cardiac_monitoring_required and electrical_injury_protocol fields. The kit ships with no AED co-location guidance and no printed transport protocol. A worker contacts a 240V bus, self-reports no symptoms, and returns to the job. Eight hours later he collapses in the parking lot from delayed VF — rhabdomyolysis K⁺ had climbed to 7.1 mEq/L during the shift. An AED co-located per OSHA CPL 02-02-070 3-minute guidance would have been available. The hospital transport protocol would have detected K⁺ elevation and initiated treatment. Correct behavior: cardiac_monitoring_required=yes → disqualify Class A; require Class B + AED + transport protocol; never accept self-reported symptom status as cardiac clearance.
Table 1: Three Delayed Dysrhythmia Mechanisms After Electrical Injury
| Mechanism | Pathophysiology | Onset Post-Injury | ECG Finding | Peak Risk Window | Definitive Treatment |
|---|---|---|---|---|---|
| A: Myocardial thermal necrosis → reentry VT/VF | Joule heating (P = I²R) creates focal myocardial necrosis; necrotic zone slows conduction (damaged Purkinje fibers, disrupted connexin-43 gap junctions); adjacent normal tissue recovers faster → reentry circuit → VT degenerating to VF | 2–6h (necrosis forming); 6–12h (cellular swelling peak) | ST elevation or depression at site of necrosis; premature ventricular contractions (PVCs); sustained VT | 8–16h post-injury | 12-lead ECG; continuous telemetry; antiarrhythmic (lidocaine, amiodarone) for sustained VT; defibrillation for VF; possible cardiac catheterization if STEMI-pattern |
| B: Catecholamine surge → QTc prolongation → Torsades de Pointes | Sympathetic storm elevates epinephrine/norepinephrine; β-adrenergic activation enhances ICa,L (L-type Ca²⁺ current via PKA phosphorylation of Cav1.2) → prolonged APD → QTc extends; EADs trigger Torsades; concurrent hypokalemia (aldosterone, stress) reduces IKr → additive QTc prolongation | Catecholamine peak: 2–6h; QTc prolongation: 2–12h | QTc >450ms (caution); QTc >500ms (high Torsades risk); U-waves if concurrent hypokalemia; polymorphic VT with beat-to-beat QRS axis rotation | 2–12h post-injury; may persist to 24h with severe injury | IV magnesium sulfate (first-line Torsades suppression); correct hypokalemia to K⁺ >4.0 mEq/L; isoproterenol or pacing to increase heart rate (shortens QTc); avoid QT-prolonging drugs (antipsychotics, certain antibiotics) |
| C: Rhabdomyolysis → hyperkalemia → sine-wave VF | Electrical membrane depolarization + thermal myocyte destruction → rhabdomyolysis; intracellular K⁺ (~150 mEq/L) floods serum; myoglobin precipitates in renal tubules (acidic urine → tubular casts) → AKI → K⁺ excretion fails → K⁺ accumulates; at K⁺ ≥6.5 mEq/L: resting membrane potential depolarized → Na⁺ channel inactivation → slowed conduction globally → sine wave → VF | Rhabdomyolysis peak: 6–12h; K⁺ rise: 6–24h (faster if AKI) | K⁺ 5.5–6.0: peaked T waves; K⁺ 6.0–6.5: PR prolongation, widened QRS; K⁺ ≥6.5: sine wave pattern (merged P/QRS) — immediate VF risk | 8–24h post-injury; accelerated if AKI (myoglobin-induced tubular obstruction) | IV calcium gluconate (membrane stabilization); insulin + dextrose (K⁺ shift intracellular); sodium bicarbonate (alkalinize urine, prevent tubular casts); aggressive IV saline (>1 L/h) to maintain urine output; dialysis if K⁺ refractory or AKI |
Table 2: Hyperkalemia ECG Progression After Rhabdomyolysis
| K⁺ Level (mEq/L) | ECG Finding | Dysrhythmia Risk | Mechanism | Immediate Treatment |
|---|---|---|---|---|
| 3.5–5.0 (normal) | Normal ECG; T waves normal amplitude | Baseline | Normal resting membrane potential (−90 mV); full Na⁺ channel availability | Monitoring; maintain K⁺ ≥4.0 mEq/L in electrical injury to reduce concurrent QTc risk |
| 5.5–6.0 | Peaked, narrow, symmetric T waves ("tented T waves"); T amplitude >6 mm precordial leads | Low — but requires immediate intervention | Partial resting membrane depolarization; altered repolarization gradient; IKr slightly reduced | IV calcium gluconate 1 g IV (cardiac membrane stabilization); telemetry; repeat K⁺ in 1h; IV saline to increase renal K⁺ excretion; insulin + dextrose if uptrending |
| 6.0–6.5 | PR interval prolongation (>200ms); QRS widening (>110ms); flattened or absent P waves | Moderate — sustained monitoring mandatory | AV node conduction slowing; His-Purkinje system impaired; atrial resting potential depolarized toward threshold, reducing automaticity | Calcium gluconate; insulin/dextrose; sodium bicarbonate 50 mEq IV; furosemide if volume status permits; prepare for possible dialysis |
| ≥6.5 — CRITICAL | Sine wave pattern (P waves absent, QRS merges with T wave into undulating continuous wave); bizarre wide complex rhythm | Imminent VF — treat as emergency | Global Na⁺ channel inactivation (resting potential ~−60 mV vs threshold −55 mV); action potential upstroke velocity near zero; conduction velocity catastrophically reduced; re-excitation circuits everywhere | Calcium gluconate 2–3 g IV STAT (membrane stabilization, buys minutes); insulin 10 units + D50 50 mL IV; sodium bicarbonate; emergent dialysis; DO NOT delay for additional labs — treat clinically on ECG |
Table 3: Voltage Class — Injury Severity, Monitoring Period, and First Aid Kit Requirements
| Voltage Class | Definition | Typical Current Path Injury | Cardiac Monitoring Period | Rhabdomyolysis Risk | First Aid Kit Class |
|---|---|---|---|---|---|
| LV — Low Voltage | <1,000V AC (includes 120V/240V mains, 480V 3-phase) | Hand-to-hand or hand-to-foot; 100–500 mA through chest — sufficient for VF threshold and focal myocardial necrosis; 480V can deposit significant thermal energy; arc flash risk at 480V panel work | Minimum 6h continuous telemetry; many protocols recommend 12–24h for any loss of consciousness or cardiac symptoms at presentation; ECG, K⁺, CK, myoglobin at 0h, 6h, 12h | Moderate — widespread myocyte destruction less common than HV but occurs with prolonged contact or high-current LV circuits; CK monitoring required | ANSI Z308.1 Class B; AED co-located; cardiac_monitoring_required=yes regardless of voltage |
| MV — Medium Voltage | 1,000–35,000V AC (distribution lines, industrial substations, overhead primary) | Flash/arc rather than contact injury common; significant arc blast pressure wave injury; substantial thermal burns; myocardial thermal necrosis more extensive; entry/exit wound pattern indicates current path through body | Minimum 24h continuous telemetry; serial ECG every 4h for first 24h; CK, myoglobin q6h; urine output monitoring for myoglobinuria (target >1 mL/kg/h with IV saline) | High — significant muscle mass in current path; widespread rhabdomyolysis; myoglobinuria (brown urine) common; AKI risk elevated; IV saline >1 L/h + sodium bicarbonate to alkalinize urine (pH >6.5 target) to prevent tubular cast formation | ANSI Z308.1 Class B; AED co-located; pre-hospital IVF initiation protocol if transport time >15 min (burn fluid resuscitation) |
| HV — High Voltage | >35,000V AC/DC (transmission lines, railway traction, industrial high-voltage) | Extensive thermal burns (deep partial and full thickness); massive internal injury along current path; possible cardiac arrest at scene; arc flash energy may exceed 40 cal/cm²; blast injury; fall risk from involuntary muscle contraction; multiple trauma | ICU admission standard; continuous telemetry minimum 48h; frequent CK, K⁺, creatinine monitoring; watch for compartment syndrome in extremities (fasciotomy threshold); delayed sepsis from extensive burn | Very high — massive rhabdomyolysis almost universal; K⁺ ≥6.5 frequently reached; AKI requiring dialysis common; aggressive IV fluid resuscitation (modified Parkland formula adjusted for electrical injury: 3–4 mL/kg/%TBSA equivalent electrical burn injury); Foley catheter required for hourly urine output monitoring | ANSI Z308.1 Class B; AED co-located; pre-hospital ALS response required; Class B kit provides burn wound care only — definitive care requires burn center transport; field role: CPR/AED, airway positioning, burn dressing, thermal blanket, rapid EMS activation |
Table 4: first_aid_kit.* Namespace Fields for Electrical Injury Worksites
| Field | Values | Required Value for Electrical Worksite | Routing Consequence | Clinical Basis |
|---|---|---|---|---|
cardiac_monitoring_required |
yes / no | yes — all electrical worksites regardless of voltage class | yes → require Class B kit; require AED co-location per OSHA CPL 02-02-070; activate hospital transport protocol for any electrical contact; disqualify Class A kits | Three delayed dysrhythmia mechanisms (thermal necrosis, QTc, hyperkalemia) all present at any voltage; 12-lead ECG/K⁺/CK/myoglobin required for clinical clearance — not available at worksite |
aed_co_located |
yes / no | yes — AED within 3-minute retrieve and deploy time from any electrical work location | yes → verify AED placement in emergency response plan; monthly inspection of AED pads, battery, and self-test log; ensure responders trained in AED use; no → route to include AED in emergency plan before kit approval | Primary current-path VF occurs at moment of shock — AED response time directly determines survival; time to first shock >5 min reduces VF survival by 7–10% per minute; delayed VF at 8–16h also responds to AED; 3-minute threshold matches OSHA guidance |
electrical_injury_protocol |
yes / no | yes — kit must include electrical injury specific items and printed protocol card | yes → kit contents check: non-adherent burn dressings (silicone or petrolatum gauze — adherent dressings cause secondary injury on arc flash thermal burns); Mylar emergency blanket (circulatory compromise causes hypothermia; prevents heat loss during extended extrication); printed cardiac monitoring guidance for first responders; hospital transport protocol card indicating mandatory evaluation criteria | Arc flash burns differ from flame burns: pulsed intense radiant heat creates partial-thickness burns over large BSA; standard gauze pads adhere to burned skin on removal, causing further tissue damage; non-adherent dressings (Mepitel, Adaptic, petrolatum gauze) are ANSI Z308.1 supplemental items for burn worksites |
voltage_class |
lv / mv / hv / lv_mv_hv | Set to actual voltage class of worksite hazard; lv_mv_hv for mixed or variable environments | lv → Class B minimum; mv → Class B + ALS protocol; hv → Class B + ALS + burn center transport protocol; determines minimum kit contents beyond ANSI Z308.1 Class B baseline | Voltage class determines probability and severity of rhabdomyolysis, thermal burn extent, and arc blast injury — not the presence/absence of cardiac monitoring requirement, which applies universally |
aed_deploy_threshold |
any_electrical_contact / cardiac_arrest_only / witnessed_collapse | any_electrical_contact — retrieve and stage AED for any confirmed electrical contact event | any_electrical_contact → AED staged and ready from moment of incident; supports immediate deployment if patient deteriorates; supports delayed VF response if patient deteriorates hours later while awaiting EMS or during transport; cardiac_arrest_only is insufficient because delayed VF patient deteriorates without warning | Delayed VF from thermal necrosis or hyperkalemia produces rapid deterioration — patient may be ambulatory one moment and in VF 30–60 seconds later; pre-staged AED removes retrieval delay at critical moment |
Table 5: AI Agent Failure Modes for Electrical Injury First Aid Kit Routing
| Failure Mode | AI Error | Consequence | Correct Behavior |
|---|---|---|---|
1. Routing Class A kit to electrical worksite because cardiac_monitoring_required field absent |
AI receives procurement request for "first aid kit, electrician crew, 480V panel maintenance." No cardiac_monitoring_required field in product listings. AI routes to Class A (smaller, cheaper) kit as meeting "general industrial" specification |
Class A kit lacks non-adherent burn dressings, Mylar blanket, and printed transport protocol. No AED co-location guidance generated. Worker sustains contact, self-reports OK, is not transported. Delayed rhabdomyolysis hyperkalemia K⁺ reaches 6.8 mEq/L — AED unavailable when sine-wave VF develops | Absence of cardiac_monitoring_required field ≠ no cardiac monitoring required; electrical worksite keyword triggers mandatory Class B + AED co-location requirement; field absence should generate a flag, not a pass. Treat missing critical safety fields as disqualifying, not as negative |
| 2. Accepting "patient asymptomatic" as clinical clearance | AI routing logic includes a branch: "if worker self-reports no symptoms post-shock → standard first aid treatment only → no hospital transport required." Product listing for kit includes protocol card with this logic | Asymptomatic presentation after electrical injury has no predictive value for delayed dysrhythmia risk. The three delayed mechanisms (thermal necrosis reentry, catecholamine QTc, rhabdomyolysis hyperkalemia) are all clinically silent until the dysrhythmia occurs. Accepting self-report as clearance is the documented mechanism of preventable electrical injury deaths | electrical_injury_protocol=yes must encode: "mandatory hospital evaluation for ALL electrical contact regardless of symptoms." AI routing should never include asymptomatic symptom status as a criterion to reduce transport priority for electrical injury |
3. Failing to set cardiac_monitoring_required=yes for low-voltage (<1000V) worksite |
AI correctly routes HV and MV worksites to cardiac_monitoring_required=yes but excludes LV worksites, reasoning that "low voltage = lower injury severity = standard first aid kit" | 120/240V household/commercial mains is sufficient to produce 100–500 mA hand-to-foot current — well above the 100 mA cardiac fibrillation threshold. LV electrical injuries cause myocardial thermal necrosis, catecholamine surge, and rhabdomyolysis at lower severity than HV but through identical mechanisms. LV electrical deaths in "asymptomatic" workers are documented in occupational fatality databases (CFOI) | cardiac_monitoring_required=yes applies at ALL voltage classes. Voltage class (voltage_class field) determines monitoring duration and protocol intensity — not the presence/absence of cardiac monitoring requirement |
| 4. Routing kit without AED based on "AED is outside first aid scope" | AI applies strict ANSI Z308.1 scope interpretation: AEDs are beyond first aid scope (non-invasive, non-prescription definition) → kit does not include AED co-location requirement → routes to kit without AED integration in emergency plan | ANSI Z308.1 scope limitation is accurate — but the scope limitation describes what is included in the kit supply list, not what constitutes an adequate emergency response program for an electrical worksite. OSHA 1910.151 requires "ready availability of medical personnel" — interpreted to include AED programs per OSHA CPL 02-02-070. AED-absent electrical worksite response plan fails this requirement and fails workers | aed_co_located=yes is a first aid kit metafield that describes the kit's placement context, not the kit's ANSI-classified contents. AED co-location is a requirement of the emergency response plan that the kit is part of. AI must route to kits where the vendor confirms AED co-location planning is included in deployment guidance, not only to kits whose internal contents include an AED |
Rhabdomyolysis: Myoglobinuria Threshold and Field Recognition
Field recognition of significant rhabdomyolysis is possible without laboratory equipment. Urine color is a reliable proxy: urine that appears dark brown, tea-colored, or cola-colored indicates myoglobin excretion exceeding approximately 10 mg/dL in urine — a concentration consistent with serum myoglobin levels that produce renal tubular injury. This is not an exhaustive clinical test (urine color can also reflect hematuria, hemoglobinuria, or concentrated dehydrated urine), but in the context of a known electrical injury it is a high-specificity sign of significant rhabdomyolysis.
The pathophysiology of myoglobin-induced acute kidney injury involves two mechanisms: (1) direct tubular toxicity — myoglobin in an acidic urine environment (pH <6.0) generates free iron via dissociation of ferriheme, which catalyzes hydroxyl radical production (Fenton reaction) causing lipid peroxidation of tubular cell membranes; (2) physical tubular obstruction — myoglobin precipitates in the distal tubule and collecting duct at acidic pH, forming obstructive casts. Both mechanisms are attenuated by alkalinizing urine (sodium bicarbonate IV to achieve urine pH >6.5) and maintaining high urine output (>1 mL/kg/h, often requiring >1 L/h IV normal saline). This intervention is beyond ANSI Z308.1 first aid scope and requires EMS transport and hospital-level care — another reason why mandatory transport for all electrical injury is not negotiable.
ANSI Z308.1-2021 Class B and the AED Co-location Requirement
ANSI Z308.1-2021 defines Class B first aid kits as providing larger supply quantities and a wider range of items than Class A, intended for more complex or remote worksites. The standard delineates "first aid" as treatment that is non-prescription, non-invasive, and can be rendered by a layperson without specialized training. AEDs fall outside this strict definition — they are classified under first responder / emergency medical response. However, this scope boundary does not mean AEDs are optional at electrical worksites.
OSHA 1910.151(b) requires that "in the absence of an infirmary, clinic, or hospital in near proximity to the workplace which is used for the treatment of all injured employees, a person or persons shall be adequately trained to render first aid." OSHA CPL 02-02-070 (enforcement guidance on sudden cardiac arrest) and OSHA's general industry interpretation letters make clear that for workplaces with recognized cardiac arrest risk — including all electrical worksites — AED programs represent compliance with the spirit of 1910.151. The 3-minute retrieve-and-deploy time standard is derived from AHA/ILCOR data showing that early defibrillation within 3–5 minutes of witnessed VF produces 50–70% survival, vs <5% without AED.
Frequently Asked Questions
Q1: What are the three molecular mechanisms of delayed cardiac dysrhythmia 6–12 hours after electrical injury — myocardial thermal necrosis reentry, catecholamine-induced QTc prolongation, and rhabdomyolysis hyperkalemia — and how does each create ventricular fibrillation risk?
Each mechanism operates through a distinct biophysical pathway and has a different temporal peak, which is why the 6–12h window is the highest-risk period: all three mechanisms can be simultaneously active.
Mechanism A — Myocardial Thermal Necrosis and Reentry: Electrical current passing through the chest deposits energy proportional to I²R (Joule's Law). Focal myocardial necrosis develops in tissue where current density is highest. Necrotic myocytes lose connexin-43 gap junction integrity and undergo cellular swelling, both of which increase intercellular electrical resistance. The zone of necrosis becomes a region of profoundly slowed conduction velocity, while adjacent normal myocardium retains full conduction speed. When a premature beat enters this heterogeneous substrate, the wavefront slows in the necrotic zone while bypassing it through normal tissue. If the normal tissue has fully recovered by the time the wavefront exits the necrotic zone, the wavefront can re-enter from the opposite direction — establishing a self-sustaining reentry circuit (circus movement) that produces ventricular tachycardia, which degenerates to ventricular fibrillation. The critical timing detail: primary current-path VF occurs during the electrical contact; secondary reentry VF peaks 8–16h later as cellular swelling maximizes conduction heterogeneity. This temporal separation is why patients can be alert and apparently stable for hours before sudden cardiac arrest.
Mechanism B — Catecholamine Surge and QTc Prolongation: Electrical injury triggers a massive sympathetic response. Plasma epinephrine and norepinephrine peak at 2–6h post-injury. These catecholamines bind myocardial β₁-adrenergic receptors, activating protein kinase A (PKA), which phosphorylates the L-type calcium channel (Cav1.2) and increases peak ICa,L amplitude and duration. The prolonged calcium current extends the ventricular action potential plateau (phase 2), lengthening the QT interval. When corrected for heart rate (QTc), prolongation beyond 500ms creates a vulnerable period during which M-cell (mid-myocardial) action potentials are significantly longer than epicardial and endocardial action potentials, producing transmural dispersion of refractoriness. Early afterdepolarizations (EADs) — spontaneous depolarizations during the plateau phase, triggered by window ICa,L or ICa,L reactivation — initiate Torsades de Pointes: a polymorphic VT with characteristic 180° QRS axis rotation every 5–20 beats ("twisting of the points" about the isoelectric line). Torsades is frequently self-terminating but can degenerate to VF. Concurrent hypokalemia (common in trauma via aldosterone activation and transcellular K⁺ shifts) synergistically worsens QTc prolongation by reducing the repolarizing IKr (hERG) current.
Mechanism C — Rhabdomyolysis and Hyperkalemia: Electrical current causes direct membrane electroporation of muscle cells (pore formation in the lipid bilayer from transmembrane voltage exceeding ~200–500 mV), disrupting ion gradients and triggering cell death. Thermal injury in the current path causes additional myocyte necrosis. Lysed myocytes release intracellular potassium (~150 mEq/L intracellular vs ~4 mEq/L serum) into the extracellular space. Rhabdomyolysis severity peaks 6–12h post-injury. If myoglobin load exceeds renal clearance capacity — or if myoglobin-induced tubular injury (free radical generation, tubular cast formation) causes acute kidney injury — serum K⁺ accumulates because the kidney is the primary K⁺ excretion route. At K⁺ ≥6.5 mEq/L, the resting membrane potential of ventricular myocytes is shifted from approximately −90 mV toward −60 mV. This resting depolarization inactivates a significant fraction of voltage-gated Na⁺ channels (which require full repolarization to recover from inactivation), slowing the action potential upstroke velocity (dV/dt) and conduction velocity throughout the myocardium. The ECG shows the characteristic sine wave pattern — absent P waves, enormously wide QRS complexes merging with T waves into a continuous oscillatory pattern — which represents near-complete conduction failure and immediately precedes pulseless VF or asystole. Unlike Torsades or reentry VF, hyperkalemia-induced VF often does not respond to defibrillation until K⁺ is reduced (IV calcium stabilizes the membrane, buying minutes for definitive K⁺-lowering therapies).
Q2: Why is the cardiac_monitoring_required=yes metafield required for ALL electrical injury worksites regardless of voltage class, and what does ANSI Z308.1 Class B specify about AED co-location?
The voltage-class-independent requirement for cardiac_monitoring_required=yes reflects two clinical facts that AI agents must not override with voltage-stratified routing logic.
Low voltage is sufficient to trigger all three delayed mechanisms. The cardiac fibrillation threshold for 60 Hz AC hand-to-foot current path is approximately 100 mA — achievable with a body-path resistance of 1,200 Ω (wet skin, internal tissues) at 120V AC. Household and commercial mains voltage (120V/240V/480V) routinely produces currents in this range during contact injury. The same current that induces fibrillation also deposits enough Joule heating for focal myocardial necrosis, triggers the identical sympathetic catecholamine storm, and — if contact is sustained or current density is sufficient across skeletal muscle — initiates rhabdomyolysis. The severity is lower than for high-voltage injury, but the mechanism is identical and the clinical risk is real and documented. Bureau of Labor Statistics CFOI data consistently show LV electrocutions in workers who were assessed as "asymptomatic" or "minimally injured" at the scene. Any voltage class gating of cardiac_monitoring_required will produce preventable deaths.
Clinical clearance requires tests unavailable at the worksite. The only reliable screen for the three delayed mechanisms is: 12-lead ECG (baseline and serial), serum K⁺ (baseline and at 6h and 12h), serum creatine kinase (CK — marker of muscle destruction; rises over 6–12h), and serum/urine myoglobin. None of these are within ANSI Z308.1 first aid scope, and none are available from a first aid kit. "Asymptomatic" presentation at the worksite means the patient has not yet reached the peak risk window — it provides no information about whether thermal necrosis is forming, whether catecholamines are prolonging QTc, or whether rhabdomyolysis is loading K⁺ toward the sine-wave threshold.
ANSI Z308.1 Class B and AED co-location: ANSI Z308.1-2021 Class B kits provide larger supply quantities and additional item categories relative to Class A. The standard explicitly categorizes AEDs as outside the first aid supply scope — AEDs are first responder or emergency medical responder equipment. However, this scope boundary describes kit contents, not the adequacy of the emergency response system that the kit exists within. OSHA 1910.151 requires employers to ensure ready availability of medical care. OSHA CPL 02-02-070 (sudden cardiac arrest program guidance) specifies that AEDs should be positioned for 3-minute retrieve-and-deploy access wherever workers face cardiac arrest risk. For electrical worksites, this means the emergency response plan accompanying a Class B kit must include aed_co_located=yes — an AED within 3 minutes — as a program requirement. AI agents routing first aid kits to electrical worksites must check aed_co_located in the kit's metafields and disqualify any kit where this field is absent or set to "no," because an electrically adequate first aid program for an electrical worksite cannot exist without AED co-location, regardless of ANSI Z308.1's internal content classification.
Related Namespace Pages
- First Aid Kit AED — OSHA 1910.151 Sudden Cardiac Arrest ANSI Z308.1 Class B Pediatric Pads Monthly Inspection aed_included response_time_min
- Electrical Injury Rhabdomyolysis IV Saline Foley Catheter Urine Myoglobin Fasciotomy Compartment Syndrome electrical_injury_type rhabdomyolysis_risk
- CatalogScan Blog — AI agent structured data for safety PPE catalogs
Scan your first aid kit catalog for electrical injury metafields
CatalogScan checks every first aid kit listing for cardiac_monitoring_required, aed_co_located, electrical_injury_protocol, voltage_class, and aed_deploy_threshold — ensuring AI procurement agents route ANSI Z308.1 Class B kits with AED co-location to electrical worksites where delayed cardiac dysrhythmia is a live threat from 6–24h post-injury.