NREMT Prep · Signs & Symptoms

Toxicology & Environmental

6 high-yield toxicological and environmental emergencies. Toxidrome recognition (knowing which drug causes which pattern) and CO poisoning awareness are heavily tested on the NREMT.

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6 conditions  ·  Nancy Caroline 9th Ed. + NREMT blueprint

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Toxicology · Opioid

Opioid Overdose

  • Pinpoint pupils (bilateral miosis) — most pathognomonic sign
  • Respiratory depression: slow, shallow, or absent respirations
  • Decreased level of consciousness or unresponsiveness
  • Bradycardia; hypotension
  • Cyanosis; gurgling or snoring respirations
  • Needle track marks; drug paraphernalia at scene

vs. Benzodiazepine overdose: BZD alone rarely produces the severe respiratory depression or pinpoint pupils seen with opioids. Pinpoint pupils + respiratory depression = opioid toxidrome. BZD may produce similar sedation but pupils are typically normal or slightly small, not pinpoint. Both may co-ingest — treat respiratory failure regardless.

Fentanyl and carfentanil are far more potent than heroin — multiple naloxone doses (2–4 mg or more) may be required. Respiratory arrest occurs before cardiac arrest in opioid OD — ventilate first, then administer naloxone. Watch for re-narcotization as naloxone wears off (30–60 min half-life).

Toxicology · Stimulant

Sympathomimetic Overdose — Cocaine, Meth, Amphetamines

  • Tachycardia; hypertension (significantly elevated)
  • Hyperthermia (elevated core temperature)
  • Dilated pupils (bilateral mydriasis)
  • Diaphoresis (wet/sweaty skin)
  • Agitation, paranoia, psychosis, combativeness
  • Chest pain (cocaine-induced coronary vasospasm); seizures

vs. Anticholinergic toxidrome: Both have mydriasis (dilated pupils) and tachycardia. The key differentiator is the SKIN — sympathomimetic patients are WET (diaphoretic). Anticholinergic patients are DRY ("dry as a bone, red as a beet, hot as a hare, blind as a bat, mad as a hatter"). Skin moisture = the deciding sign.

Hyperthermia + seizures + cocaine = a lethal triad. Active cooling and benzodiazepines (not antipsychotics) are the priority. Avoid physical restraint that causes isometric muscle contraction — it raises core temperature further and worsens acidosis.

Toxicology · Organophosphate

Cholinergic Poisoning — Organophosphates / Nerve Agents

  • SLUDGE: Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis
  • Bilateral miosis (pinpoint pupils) — acetylcholine excess at muscarinic receptors
  • Bronchospasm and excessive bronchial secretions
  • Bradycardia; hypotension
  • Muscle fasciculations; weakness; paralysis (nicotinic effects)
  • Seizures; loss of consciousness (CNS effects)

vs. Opioid overdose: Both produce miosis and respiratory depression, but cholinergic poisoning additionally causes SLUDGE symptoms — excessive secretions, diarrhea, urination — and fasciculations. Opioids do not cause muscular fasciculations or bronchospasm. Agricultural exposure history or mass casualty incident context is critical.

Bronchospasm combined with massive secretion production causes rapid airway obstruction. Atropine (large doses — 2–4 mg IV repeated) dries secretions and reduces bronchospasm. Pralidoxime (2-PAM) given within the first hours can reactivate acetylcholinesterase. Scene safety first — rescuers can be contaminated by contact or vapor.

Environmental · Toxic Inhalation

Carbon Monoxide Poisoning

  • Headache (most common presenting symptom)
  • Nausea, vomiting, dizziness
  • Confusion, altered mental status; syncope
  • Chest pain and tachycardia (myocardial hypoxia)
  • SpO2 falsely normal on standard pulse oximetry (COHb reads as OxyHb)
  • Cherry-red skin: late, unreliable, and rarely seen in living patients

vs. Viral illness/flu: CO poisoning clusters — multiple family members or occupants presenting simultaneously with similar symptoms. Symptoms improve when patients leave the environment. Flu does not cluster by household exposure within hours and does not improve with fresh air alone. Suspect CO in "everyone is sick" calls.

Pulse oximetry is UNRELIABLE in CO poisoning — it gives falsely normal or near-normal readings because it cannot distinguish COHb from OxyHb. A patient can have 30% CO saturation with SpO2 reading 98%. Clinical suspicion must drive treatment. High-flow 100% O2 is the field antidote.

Environmental · Heat

Heat Stroke vs. Heat Exhaustion

  • Heat Exhaustion: heavy sweating, weakness, cool/pale/moist skin, nausea, headache, normal or mildly elevated temperature, NORMAL mental status
  • Heat Stroke (Classic): HOT, DRY skin; hyperthermia >104°F (40°C); ALTERED mental status
  • Heat Stroke (Exertional): may still be sweating; occurs in young, active patients; hyperthermia + AMS
  • Both: tachycardia, weakness, nausea
  • Heat Stroke: confusion, combativeness, seizure, coma
  • Heat Stroke: hot environment exposure, outdoor work, athletic event

Altered mental status is the dividing line. Heat exhaustion = alert. Heat stroke = altered. A hot patient who is confused, combative, or unconscious = heat stroke. Temperature alone is not the sole criterion — some exertional heat stroke patients may still be sweating. AMS + hyperthermia = treat as heat stroke.

Heat stroke is a medical emergency — core temperature >106°F (41°C) causes organ failure. Aggressive cooling is the priority: ice water immersion if available, ice packs to neck/groin/axillae, wet sheets with fanning. Cooling takes precedence over IV fluid placement — start cooling immediately on contact.

Environmental · Cold

Hypothermia — Mild, Moderate, Severe

  • Mild (32–35°C / 90–95°F): shivering, confusion, ataxia, tachycardia
  • Moderate (28–32°C / 82–90°F): shivering STOPS (muscle glycogen depleted), bradycardia, hypotension, progressive AMS
  • Severe (<28°C / <82°F): apparent death — no detectable pulse, no respiratory effort, rigidity
  • Severe: J waves (Osborn waves) on ECG — positive deflection at the J point
  • Paradoxical undressing: severe confusion causes patients to remove clothing
  • VF is a significant risk below 28°C

vs. Death: Severe hypothermia can present as clinical death — no detectable pulse, apnea, fixed pupils, rigidity. The core rule: "not dead until warm and dead." Resuscitation should be continued until the patient is rewarmed (in the hospital). VF may not respond to defibrillation until the core temperature rises above 30°C.

"Not dead until warm and dead." Severe hypothermia patients in VF should be transported to an ECMO-capable facility when available — extracorporeal rewarming can salvage patients who appear lifeless. Per current AHA guidance, attempt defibrillation and consider standard ACLS medications even while hypothermic, concurrent with active rewarming — do not withhold resuscitation; response may be blunted until the core warms, so prioritize rewarming alongside standard care. Handle gently — rough handling can trigger VF.

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