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Flashcards in Toxicology Emergencies Deck (59):

EM: Toxicology
Initial Evaluation

1. ABC’s
2. Obtain ABGs as soon as practical
3. Obtain IV access
4. Treat coma promptly


How should we treat coma promptly? 3

1. Give Glucose 50ml of 50% solution IV
2. Give naloxone (Narcan) 0.4-2.0 mg IV
3. If ETOHism is suspected, give 100mg Thiamine IM or IV


COMA TX for narcotic overdose
1. Give____ mg IV STAT,
2. if there is mild response or you know a narcotic is involved; give what how many minutes later?

1. 0.8
2. 1.6mg IV 3 minutes later (Max of Narcan is 10mg)


EM: Toxicology
Initial Evaluation
1. Maintain circulation
-If 20-30ml/kg of crystalloid does not stabilize BP, you must do what?

2. Very real risk of what? 2

Treat seizures
3. First line?
4. Failure of this?
5. Who do we put on all pts? 2

1. get a Swan in and check PCWP

-over-hydration and
-pulmonary edema

3. Diazepam 0.1-0.2 mg/kg IV over 1-2 minutes

4. Failure of diazepam, give phenobarbital 15mg/kg not faster than 50mg/min

-Cardiac monitoring
-pulse oximeter on ALL


EM: Toxicology
1. Emesis only in who?
2. Emesis may have limited efficacy if how long since ingestion?
3. Most useful when?
4. Emesis is indicated in the ED for what kind of drugs?
5. When should you not induce emesis? 2
6. How should you induce it?

1. only in patients with intact gag reflex

2. > 1 hour
3. Most useful if initiated at home within a few minutes of ingestion (home ipecac during your well baby visits)
4. Emesis is indicated in the ED for drugs not adsorbed by charcoal (eg, iron, lithium)

-Do NOT induce emesis if caustics or low-viscosity hydrocarbons have been ingested
-Do NOT induce emesis if rapid-acting convulsants have been ingested (amphetamine, cocaine, cyclic antidepressants, strychnine)

6. Ipecac syrup 30ml (adults) or 15ml (children) followed by 1-2 liters of water (water until they vomit)


EM: Toxicology

1. Gastric Lavage
Indications: 4

2. Ideally place pt in what position?

3. Must use what equipment?

4. Use tap water or saline at body temperature in 250ml increments and continue until when?

-Suspected serious ingestions when emesis has failed
-When patients are lethargic or otherwise uncooperative
-When the gag-reflex is markedly depressed
-When patients have ingested rapid-acting convulsants

2. Ideally, place patient in left lateral decubitus position with head down (if gag is depressed, protect airway)

3. Must use a large bore nasogastric or orogastric tube at least 36Fr (Cannot remove pill fragments with standard NG tube)

4. fluid returns clear and free of pill fragments


EM: Toxicology

Activated Charcoal
1. Following what give 50-100g of charcoal as slurry by mixing with equal amounts of water? 2

2. Can give before or after lavage/emesis; however need residual charcoal left in gut (when in doubt – ?)

3. Mixing charcoal with what of 70% improves taste of charcoal and provides cathartic action?

4. Charcoal has great adsorptive properties and binds most poisons (EXCEPT: ??? 4)

5. If the ingested dose of the poison is known, give at least ____ times that weight in activated charcoal

Whole Bowel Irrigation
6. Useful with what?
7. What until rectal effluent is clear?

1. emesis or lavage

2. do BOTH)

3. sorbitol 1ml/kg


5. 10

-sustained release and
-enteric coated tabs

7. Golytely 1-2L/h


EM: Toxicology
Initial Laboratory Studies
1. ______ as soon as practical
2. Draw blood for what? 3
3. Obtain ECG and monitor for what? 2
4. CXR looking for evidence of what?
5. Flat plate of abdomen looking for what?
-disadvantage with this?

6.What for toxicology screen besides blood?

7. Draw and HOLD serum tox screens; order only what?

1. ABGs

-Chem 7 and
-calculate anion
-osmolar gap

-wide QRS or
-pronlonged QT

4. pulmonary edema

5. radiopaque pills
-High false negative rate

6. Urine

7. those levels that are indicated (ie-acetaminophen)


EM: Toxicology

1. Management of the patient requires understanding of? 3

2. Dissolution and absorption of toxin or gastric emptying time may be seriously altered so peak effect is quite what?


2. delayed (ie – anticholinergics)


EM: Toxicology

1. Management of the patient requires understanding of? 3

2. Dissolution and absorption of toxin or gastric emptying time may be seriously altered so peak effect is quite what?


2. delayed (ie – anticholinergics)


EM: Toxicology

1. What is the definition of half life?
2. What is first order kinetics?
3. Zero order?

4. All that being said: Many times in an overdose situation, the elimination pathways are saturated and a drug which normally has first-order kinetics develops what?

1. The time required to eliminate one-half of the toxin
2. FIRST-ORDER KINETICS – a fixed percentage of the toxin is removed per unit of time (Example- Barbs)
3. ZERO-ORDER KINETICS – a fixed amount of toxin is removed per unit of time (Example- Alcohol)

4. zero-order kinetics


EM: Toxicology

1. What is clearance?
2. Includes what components? 2
3. Important to understand this process: A drug that is normally 95% metabolized and 5% renally cleared; forced diuresis will have what kind of effect on clearance?

4. Toxins with large volumes of distribution (tissue bound rather than plasma bound) are not efficiently removed by what?

1. Volume of plasma that can be cleared of toxin per unit time
2. Includes both renal and metabolic components

3. minimal effect on clearance
4. dialysis or diuresis


EM: Toxicology
Enhanced Elimination

1. The toxin must be relatively _______ soluble and ______ protein bound

2. Toxin is removed from blood into what?

3. Drugs need to have a what? 2

4. Indicated for: (MELS) 4

1. water, not highly

2. dialysate solution across a semipermeable mebrane

-small volume of distribution
-slow rate of intrinsic clearance

-Ethylene glycol,


EM: Toxicology
Enhanced Elimination

1. Advantage over hemodilaysis?

2. Drugs need to have a ______ volume of distribution and _____ rate of intrinsic clearance

3. What are not limiting factors? 3

4. Commonly associated with what and will not correct electrolyte imbalances or adjust pH?

5. Useful for: (TRI PEP-TD) what? 6

1. Drug or toxin is in direct contact with adsorbent material

2. small, slow

-High molecular weight,
-poor water solubility, and
-plasma binding proteins

4. thrombocytopenia

-Tricyclic antidepressants,


1. Acetaminophen?
2. Anticholinergics?
3. Benzos?
4. Cyanide?
5. Methanol/Polyeth. glycol?
6. Narcotics?

1. Acetaminophen: Acetylcysteine
2. Anticholinergics: Physostigmine
3. Benzodiazepines: Flumazenil (DANGER)
4. Cyanide: Na nitrite and Na thiosulfate
5. Methanol/Polyeth. glycol: Ethanol
6. Narcotics: Naloxone


EM: Toxicology
Laboratory Clues
1. Calculation of osmolar gap may be helpful in determining what?
2. Osmolar gap (Δ osm) is determined by what?

3. Equation?

4. Serum osmolality can be increased by what?

1. “intoxicant” a patient has used

2. subtracting the calculated osmolality from the measured osmolality

-Calculated: 2(Na) + Glu/18 + BUN/2.8
-Measured (from lab) – Calculated = Δ osm (Normal is


EM: Toxicology
Laboratory Clues

1. Serum concentration of an alcohol can be calculated?

2. The following are the molecular weights, lethal concentrations, and corresponding Δ osm:

3. The most common cause of Δ osm?

1. Serum concentration (mg/dl) = Δosm x Mol weight/10

2. The following are the molecular weights, lethal concentrations, and corresponding Δ osm:
-Ethanol: 46 (MW); 350 (LC); 75 (Δ osm)
-Methanol: 32 (MW); 80 (LC); 25 (Δ osm)
-Ethylene Glycol: 62 (MW); 200 (LC); 35 (Δ osm)
-Isopropanol: 60 (MW); 350 (LC); 60 (Δ osm)

3. The most common cause of Δ osm is Ethanol
Example: Δ osm = 30; 30 x (46/10) = 138 mg/dl BA


EM: Toxicology
Acetaminophen (Tylenol)

1. One of the metabolites is very toxic how?

2. Saturates the _______ detoxification system

3. Accumulates in liver and causes what?
- When?

4. Toxic dose of acetaminophen is > _____mg/kg
-LOWER in patient with what? 2

5. Dx?

1. hepatotoxic

2. glutathione

3. delayed hepatotoxicity
-24-72 hours post ingestion

4. 140
-chronic liver disease or

5. Draw levels


EM: Toxicology
Acetaminophen (Tylenol)
Tx? 3

1. Decontaminate and give activated charcoal
2. Estimate severity:
3. Acetylcysteine therapy can be life-saving!


EM: Toxicology
Acetaminophen (Tylenol)

1. Estimate severity by? 3

Acetylcysteine therapy can be life-saving!
2. MOA?
3. Dose?
4. Follow up with what doses in what time period?
5. What is the key to treatment here?

-ANY acetaminophen level is helpful
-The BEST level is 4 hours post-ingestion
-Trends are as important as initial value

2. Substitutes for glutathione and binds the metabolite
3. 140mg/kg orally of a 10%-20% solution
4. Follow-up with a 70mg/kg dose every 4 hours for 18 doses or until the Tylenol level is O (zero)
5. Key is it must be given EARLY: Do not wait for initial level; MUST be given within 12-16 hours and preferably within 8-10 hours


EM: Toxicology
1. All are CNS stimulants and cause what?

2. Some may produce significant vasoconstriction and cause what? 2

3. Hypertension may be accompanied by what kind of arrhythmias?

4. Seizure and hyperthermia may produce what? 2

5. All significant cocaine overdoses will have symptoms: such as? 9

1. sympathetic hyperactivity


3. ventricular

- rhabdomyolysis
- myoglobinuria

-toxic psychosis,
-possible MI


EM: Toxicology

1. Dx?
2. Short half- lives and peaks effects occur within?

3. Treatment: _____ decontamination as indicated?

4. Severe agitation or psychosis?

5. -Treat seizures with?

6. If DBP > 120 or HTN encephalopathy?

7. Tachycardia/Vent Arrhythmias?

8. Monitor what? 3


1. Significant toxicity will always have symptoms
2. Short half-lives and peak effects occur within 1-2 hours

3. GI
4. Diazepam 0.1-0.2mg/kg IV
5. diazepam
6. Nitroprusside

7. Beta Blocker??? (are you sure???) - be careful

-May need CT of head



EM: Toxicology
1. Which drugs? 5
2. Also seen in plants like? 3
3. MOA?
4. Significant poisoning always has some symptoms. Such as?
(whats the saying?)

-many antihistamines, and
-tricyclic antidepressants

2. Also seen in plants:
-nightshade, and
-Amanita muscaria mushrooms

3. Block cholinergic receptors both centrally and peripherally

4. Significant poisoning always has some symptoms
Delerium, blurred vision, mydriasis, hallucinations, coma, dry mucous membranes, inhibition of sweating, hyperthermia, tachycardia

“Hot as a hare, red as a beet, dry as a bone, blind as a bat, and mad as a hatter”


EM: Toxicology

Treatment? 3

1. Supportive care
2. Gastrointestinal decontamination
3. Physostigmine, 0.01-0.03mg/kg slowly IV BUT should be reserved for those patients with severe symptoms


1. When you administer Physostigmine?
2. Must be placed on what?
3. Never use with what? 3
4. Peak effects may be delayed due to what?

1. Must have atropine readily available
2. Patient MUST be on cardiac monitor
3. NEVER use with
-tricyclic overdose,
-mechanical bowel or bladder obstruction

4. significantly delayed gastric emptying and slowed peristalsis through GI tract


EM: Toxicology

1. What is the primary oral anticoagulant used therapeutically?
2. What are are common rodenticides?
3. Inhibits blood clotting by blocking what? 4

1. Warfarin (Coumadin) is the primary oral anticoagulant used therapeutically
2. The super-warfarins
-brodifacoum and
-indanediones are common rodenticides
3. Inhibit blood clotting by blocking Vitamin-K dependant clotting factors: II, VII, IX, X


EM: Toxicology

Inhibit blood clotting by blocking Vitamin-K dependant clotting factors: II, VII, IX, X

1. Only the synthesis of ____clotting factors is affected?

2. Effects may be seen ____ post ingestion as Factor II only has a 6-hour half life

3. PEAK EFFECTS are not seen for how long due to the long half-life of the other clotting factors (24-60 hours)?

4. Warfarin is highly bound to albumin with half-life of ____ hours/Metabolized by liver

1. new

2. 8-12

3. 1-2 days

4. 35


EM: Toxicology

1. A single overdose of Warfarin does not usually cause any significant problems because of?

2. Extremely-potent, long-acting anticoagulants (brodifacoum, indanediones) may produce what?

3. Excessive anticoagulation may present with: ? 8

1. the half-life of Warfarin is shorter than most of the clotting factors

2. severe bleeding disturbances for several weeks to months following a single overdose.

-uterine bleeding,
-gingival bleeding,
-hemoptysis or


EM: Toxicology
Tx? 4

1. Supportive therapy/GI decontamination
2. Obtain baseline prothrombin time and repeat in 24-48 hours
3. Vita K 1-2mg IV which can restore clotting factors in 6-8h
4. In bleeding emergency; give Fresh Frozen Plasma (FFP)


EM: Toxicology
1. Many what contain trivalent arsenic? 3
2. What food may contain pentavalent arsenic (less toxic) which can cause a positive urine arsenic level but is not associated with clinical toxicity?

3. Highly-toxic Arsine gas is produced by what?

4. Arsenic is well absorbed from where? 2
-and avidly binds with what and accumulates in where?

5. Lethal dose of trivalent arsenic is about ______ mg in an adult

6. Clinical syndromes are divided into what? 2

- insecticides,
-wood preservatives

2. Shellfish

3. burning arsenic containing ores and is used in the electronic industry

4. respiratory and GI tract
-tissue proteins, tissues

5. 100-200

6. Arsenic salt ingestion (acute and chronic) and Arsine gas inhalation


EM: Toxicology

1. Acute arsenic ingestion: symptoms? 6
2. What kind of order might be on the pts breath?

3. What might resent after 1-2 days?

4. Chronic arsenic ingestion: symptoms? 6

5. Arsine gas Inhalation
-Highly toxic and causes what? 2

6. Other symptoms of arsenic toxicity are usually not seen due to what?

1. Acute arsenic ingestion
-Crampy abdominal pain,
-profuse watery diarrhea,
-burning mucosa,
-tremor and seizures.

2. A garlic odor may be on patient’s breath

3. Periorbital edema after 1-2 days

-Peripheral and sensory neuropathy,

-rapid intravascular hemolysis
-renal failure

6. the speed of onset of the acute symptoms


EM: Toxicology
1. What is most useful for monitoring the response?

2. How may you give a false positive?

1. 24-hour urine arsenic levels are most useful for monitoring the response to chelation therapy;

2. false positive levels are possible from eating shellfish with non-toxic forms of arsenic


EM: Toxicology

1. Acute ingestion poisoning: Tx? 2

2. Chronic ingestion poisoning: tx?

3. Arsine gas inhalation: Tx?

4. Chelation therapy a good idea?

-GI decontamination with GI lavage and charcoal;
-Administer dimercaperaol(BAL) 3-5mg/kgdose q4h for 5 days

- penicillamine 100mg/kg/d (max 1 Gm) orally divided qid (May not reverse neurological damage)

-Transfusion may be necessary and adequate hydration to prevent renal hemaglobin deposition.

4. Chelation therapy is of no value in the acute exposure to arsine gas


EM: Toxicology
Carbon Monoxide (CO)
1. WARNING: Pulse oximetry cannot be used to access oxygenation because what?

2. Patients with minimal symptoms, no loss of consciousness, awake and cooperative require very minimal testing and therapy: tx how? 2

3. Patients with moderate to severe sx: order what? 10

4. Tx?

1. the device confuses COHgb for O2Hgb and gives falsely high values!

2. COHgb level and ECG

-Chem 7,
-Serum lactate,
-Serum CK-MB and
-urine myoglobin, and
-CXR (any pt with persistent dyspnea).

4. Treatment is primarily 100% FiO2 for 4 hours
Half-life of COHgb is 4h on room air, 60 minutes when breathing 100% FiO2, and 15 minutes with 100% FiO2 at 2.5 atmospheres (HBO)


1. CO binds with Hgb ______ times stronger than with O2
2. CO binds with myoglobin ______ times stronger than O2
3. High COHgb imposes a sudden “chemical” ______ in patient.
4. High O2 extracting organs (such as) quickly become dysfunctional from CO intoxication? 2

5. Symptoms?

6. More severe in patients with comorbidities of what? 6

1. 230-270

2. 20-25

3. anemia

4. heart/brain

CNS: Fatigue, malaise, flulike, nausea, confusion, loss of memory, emotional lability, dizziness, paresthesias, weakness, vomiting, lethargy, somnolence, stroke, coma, seizures, respiratory arrest

Cardio: Chest pain, myocardial ischemia, palpitations, dysrhythmias, poor capillary refill, hypotension, cardiac arrest

-drug ingestion,
-myocardial ischemia,
-cerebrovascular dz, or
- smoke inhalation.


EM: Toxicology
Carbon Monoxide (CO)
Indications for Referral to HBO


1. Altered mental status or abnormal neuro exam
2. History of LOC or near-syncope
3. History of seizure
4. Coma
5. History of hypotension during or shortly after exposure
6. Myocardial ischemia
7. History of prolonged exposure
8. Pregnant with COHgb levels > 15%
9. Persistent acidosis (Relative)
10. Concurrent thermal or chemical burns (Relative)


EM: Toxicology
1. What are sources? 6
2. All contain cardiac ________?
3. Enhance cardiac _________?
4. Slow _______ conduction?

5. Affect Automataticity how?

6. Digoxin has a ______ volume of distribution and a half-life of ______ and is excreted unchanged in the urine (It is the most commonly precribed)

7. Digitoxin has a _______ volume of distribution, is _______ protein bound, and undergoes extensive enterohepatic recirculation;

8. Half-life is how long?!

-lilly of the valley and
-some rodenticides

2. glycosides

3. contractility

4. atrioventricular

5. Enhance

6. large, 40 hours

7. small, highly

8. 7 DAYS


EM: Toxicology
1. Most patients patients will present how? 5

2. ECG shows? 4

3. Acute ingestion of an overdose is often associated with what?


1. Symptoms may include
-nausea, vomiting,
-abdominal pain,
-blurred vision, and/or color vision disturbance

2. ECG shows toxic effects of
-3rd degree AV block,
-ventricular ectopy, or
-paroxysmal atrial tachycardia with AV block

3. Acute ingestion of an overdose is often associated with HYPERkalemia (Probably a better measure of severe toxicity than serum dig levels)



EM: Toxicology
1. If hyperkalemia is severe (>7) treat BUT USE WHAT?

2. For symptomatic bradycardia, 2nd or 3rd degree AV block give what?

3. For ventricular ectopy use what?

4. Avoid D/C countershock and only if absolutely necessary, use the what?

5. Will dialysis or hemoperfusion work in this?

1. glucose + insulin therapy and NOT the NaHCO3 + CaCl therapy! (CaCl may kill the patient!)

2. give atropine 0.5mg IV q5min to max of 2mg. May need transcutaneous or transvenous pacer

3. lidocaine 1mg/kg IV followed by a 1-4mg/min drip

4. lowest dosage possible

5. Dialysis or hemoperfusion is of no use in digoxin overdose due to the large volume of distribution


EM: Toxicology
Treatment (Continued)
1. Antidote?

2. Indicated for any patient with what? 2

3. Toxicity is reversed in what timeline and the digitalis-digibind complex is excreted in urine?

4. WARNING: Most labs measure total serum digitalis with assay. The bound digitalis is NOT active drug, BUT is in the serum. Following the administration of Digibind, the serum digoxin level may change how?

5. Formula for the number of vials of Fab (Digibind):?

Treatment (Continued)
1. Digitalis-specific Fab
fragment antibodies (Digibind)

-serious arrhythmias or
-severe hyperkalemia

3. 5-10 minutes

4. increase by as much as 20X

Number of vials = Sr Dig level (ng/ml) x Pt’s wt (kg)/100


EM: Toxicology

1. CNS depressant or stimulant?
2. Metabolized by?
3. Metabolized at what rate?
4. Symptoms? 4
5. Treatment?
6. Watch what as ETOH inhibits gluconeogenesis?

7. Give thiamine to prevent?

1. Ethanol is a CNS depressant

2. Metabolized by alcohol dehydrogenase (fixed-rate, zero-order kinetics)

3. Metabolized at a rate of 7-10g/h resulting in decrease of BAT of 20-30mg/dL/h

4. Symptoms:
-depressed sensorium,

5. Treatment is supportive

6. Watch blood glucose as ETOH inhibits gluconeogenesis
7. Give thiamine 100mg IM/IV to prevent Wernicke’s


EM: Toxicology

Amatoxin (Amanita Genus)
1. Severe gastroenteritis followed by what?

2. Onset of symptoms is what post ingestion?

3. Treatment is what?

Muscarine (Inocybe or Clitocybe)
4. Symptoms are muscarinic: such? 4

5. Onset of symptoms is ________ post ingestion

6. Treatment is supportive and ________ for severe cholinergic symptoms

1. delayed hepatic and renal failure in 48-72 hours

2. 6-24 hours

3. supportive only and hospitalize all with baseline renal and hepatic functions


5. 30 min-1 hour

6. Atropine


EM: Toxicology
Psilocybin (Psilocybe genus)
1. Symptoms are what?
2. Onset is what post ingestion?

3. Treatment is ?

Ibotenic acid and muscimol (Amanita muscaria)
4. Symptoms are anticholinergic: ? 4

5. Onset is what post ingestion?

6. Treatment is what? 2

1. hallucinations (used by several NA tribes)

2. 15-30 minutes

3. supportive


5. 30 min to 2 hours

6. supportive and physostigmine for severe sx


MOST COMMONLY seen mushroom poisoning (intentional)?

Psilocybin (Psilocybe genus)


EM: Toxicology

Monomethylhydrazine (Gyromitra)
1. Symptoms are what? 2
2. Onset of symptoms is what post ingestion?
3. Treatment is what?

4. What may prevent the hepatic/renal failure?

-severe gastroenteritis with occasional hemolysis,
-hepatic and renal failure

2. 6-12 hours

3. supportive

4. IV pyridoxine


EM: Toxicology

1. Multiple forms from propoxyphene (Darvon) → Heroin. One form often overlooked is what?

2. Act on CNS receptors causing what? 5

3. MOST opiates have a half-life of _______

4. except what? 2

5. Opiate intoxication should be considered in any patient who is what?

1. dextromethorphan

-hypothermia, and
-respiratory depression

3. 3-6 hours

-propoxyphene (12-15 hours)
-methadone (15-20 hours)

5. unconscious from unknown cause


EM: Toxicology
1. Typically what symptoms? 3
2. Diagnosis is confirmed with what? 2

3. ________ overdose may appear identical to opiate overdoes, but they do NOT respond to naloxone?

4. Treatment is what? Dosing?

5. What overdose is particularly resistant to naloxone?

-pinpoint pupils
-Respiratory depression

-toxic levels of opiates are found in urine or
-if patient awakens with the administration of naloxone IV

3. Clonidine

4. IV naloxone 0.2-2.0 mg; repeat 3-4 times if no response and opiate OD is suspected; 10-20mg have been required

5. Propoxyphene


1. Naloxone’s half-life is only how long?

2. and effects last only how long?

3. Most opiates have much longer half-lives; therefore what will be required?

4. Acute what may be precipitated in chronic opiate abusers, but not life-threatening?

5. Admit all who respond to naloxone unless it is a what?

1. 1 hour

2. 2-3 hours
3. repeated doses of naloxone WILL be required

4. withdrawal syndrome

5. heroin overdose


Heroin overdose can safely be discharged if they are asymptomatic _______ after last naloxone dose

3 hours


EM: Toxicology

1. Cholinesterase inhibitors are found in many what?
2. What is the most lethal chemical known to man?
3. MOA?

1. insecticides (organophosphates and carbamates)

2. VX nerve gas (produced in the thousands of metric tons by both the US and the former USSR)

3. Inhibit cholinesterase, allowing accumulation of acetylcholine (ACh) at muscarinic and nicotinic receptors an neuromuscular junctions


EM: Toxicology
1. All are rapidly absorbed from where? 3
2. Farm workers constantly exposed to low levels and who else are at greater risk?

3. Symptoms include what? 7

4. Mnemonic: DUMBELS –? 7

5. May have profound what? 2

6. Death is caused by what?

-intact skin,
-GI tract, and
-respiratory tract

2. infants with underdeveloped cholinesterase levels

-excessive salivation,
-hyperactive bowel sounds,
-muscle fasiculations, and


5. bradycardia (muscarinic effect) or tachycardia (nicotinic effect)

6. respiratory arrest


EM: Toxicology

1. Initial treatment is decontamination and aggressive airway management due what?

2. _______ IV in LARGE doses: 1-2 mg initially followed by 2-4 mg q5-10 minutes (Use of up to 50mg in 24h is not unusual)

3. What competitively inhibits binding of organophosphates to ACh?

Obviously all are admitted and all are advised to avoid future exposures for an extended period

1. to significant secretions and bronchospasms

2. Atropine

3. Pralidoxime (2-PAM Chloride)


EM: Toxicology
Phencyclidine (PCP)
1. Also known as what? 2
2. taken how? 4

3. PCP is what?

4. Rapid onset of action when done how? 2

5. Rarely a serious overdose by this route. Why?

6. Ingestion of ______ mg PCP can cause severe intoxication

1. “angel dust” or “crystal”

2. Smoked, snorted, ingested or injected

3. a sympathomimetic, hallucinogenic, dissociative agent (originally a vet anesthetic)

4. smoked or snorted

5. as they self-titrate

6. 20-25


EM: Toxicology
Phencyclidine (PCP)
1. What kind of volume of distribution with a half-life of several days?

2. Eliminated primarily by what?

3. Symptoms range from what?

4. Symptoms? 8

5. Treatment aimed at limiting seizures and violence using what? 2

6. Monitor and prevent what?

1. Very large

2. metabolism

3. severe, paranoid, bizarre violent behavior → quiet stupor

-Vertical and horizontal nystagmus,
-marked muscle rigidity,


6. rhabdomyolysis


EM: Toxicology
Tricyclic Antidepressants
1. Major tricyclics include? 4

2. Analogs of phenothiazines with complex effects

3. Absorbed and bound how?
4. Distribution?
5. Prognosis?

-amitriptyline (Elavil),
-imiparamine (Tofranil),
-doxepin (Adapin, Sinequan).
-maprotiline (Ludiomil) is a tetracyclic antidepressant with similar properties

-Alpha-adrenergic receptor blocking
-Quinidine like activity on the heart

3. Well absorbed and very-highly tissue bound

4. Huge volumes of distribution (10-40L/kg)

5. Probably the single worst OD to try to care for with the absolute worst outcomes regardless of your skill


EM: Toxicology
Tricyclic Antidepressants

1. All are eliminated primarily by metabolism where?
2. Half lives are what?
3. Average toxic dose is? Severe poisoning at?
4. Many symptoms are those of anticholinergic effect such as? 7

1. All are eliminated primarily by metabolism in the liver
2. Half-lives are 10-30 hours
3. Average toxic dose is 5mg/kg with severe poisoning at 10-20mg/kg
4. Many symptoms are those of anticholinergic effect
-dry mouth,
-Onset of coma may be rapid (even precipitous)
-Frequently totally refractory seizures


EM: Toxicology
Tricyclic Antidepressants
Cardiovascular manifestations are the most dramatic, life-threatening, and difficult to manage

Quinidine-like slowing of conduction seen by what? 5

PROFOUND HYPOtension due to what? 3

Dx is usually based on what? 4

1. widening of the QRS to > 100ms
2. prolonged QT and PR intervals
3. Varying degrees of AV block and
4. V. tach are common
5. Torsade de pointes may occur

1. decreased contractility and
2. vasodilitation occurs and is
3. often the cause of death

Diagnosis is usually based on
-relevant PE findings,
-widened QRS and
-prolonged QT


EM: Toxicology
Tricyclic Antidepressants
1. REMEMBER the “3-Cs” of tricyclic toxicity?

2. Can confirm diagnosis by what?

3. Treatment is obviously critical (but controversial)? 3

4. ALL must have what?

5. Treat seizures with diazepam of phenytoin. Do NOT use what as some recommend?

-Cardiac abnormalities,

-quantitative serum assays but there is no clear correlation between drug level and severity of toxicity

-GI decontamination (BUT- Do NOT induce emesis)
-Emesis can precipitate seizures and coma
-Gastric lavage and instill charcoal

4. continuous cardiac monitoring

5. physostigmine as some recommend (80% chance of death)


EM: Toxicology
Tricyclic Antidepressants

Treatment of cardiac abnormalities
1. Sinus tach?
2. What will worsen conduction abnormalities and should NEVER be used? 3

3. Ventricular arrhythmias and conduction defects MAY respond to what? 3

4. Hypotension treated with what? 2

5. If no response after 2L, you MUST do what?

1. Sinus tachycardia is usually benign and does not require therapy
-Physostigmine and

-NaHCO3 (50-100 mEq IV)
-Lidocaine 1-2mg/kg
-Phenytoin 15-18mg/kg may be effective
4. NaHCO3 (50-100 mEq IV) and crystalloid (0.9% NaCl)

5. place a Swan to prevent iatrogenic pulmonary edema