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TCA TOXICITY
Ehsan hasanpour
10/27/2018
Tricyclic antidepressant :
They have been employed in drug therapy since the
late 1950s.
Largest group of drug agents used for the treatment
of depression.
Referred as “ tri cyclic ” compounds –three rings.
Third most common cause of drug related death in
US throughout 1980s
TCA Drugs :
 Secondary amines: -Amoxapine ,
Nortriptyline , Desipramine , Protriptyline.
 Tertiary amines:- Amitriptyline ,
Imipramine,Doxepin,Trimipramine.
 Tetra cyclic:- Maprotiline.
 Triazolopyridine :-Trazodone.
Mechanism :
 Decreases the action of acetylcholine centrally and
peripherally.
 Enhances dopamine levels.
 Reduced serotonin and norepinephrine uptake resultant
increase within the synapse.
 Respiratory dysfunction and disturbances in body temp-
respiratory center ,thermoregulatory site.
 Membrane-stabilizing effect on the myocardium by blocking
the cardiac myocyte fast sodium channels
Bioavailability :
 slowly absorbed secondary to ionization in
 the stomach and slowing of peristalsis
 Can remain in gut for 12 hours or more
 Dissolve slowly
 85-98% plasma bound
Cardiovascular manifestations of TCA Toxicity :
• Palpitation
• Chest pain
• Hypotension
• Ecg abnormality
CNS manifestations of TCA Toxicity :
• Convulsion
• Decrease mental status
• Respiratory depression
• Drowsiness
• Coma
Peripheral autonomic system manifestations :
• Dry mouth
• Dry skin
• Urinary retention
• constipation
• Blurred vision
Physical exam findings :
• Tachycardia
• Hypotension and orthostasis
• Fever
• Altered mental status
• Ileus
• Absent bowel sounds
• Rigidity
• Dry skin and mucous membranes
• Mydriasis
• Electrolyte (Na,K,Cl ,Ca)
• blood urea nitrogen (BUN), and creatinine levels
• Arterial blood gases (ABGs) for evaluation of acidosis
or hypoxia
• Anion gap Complete blood cell count (CBC)
• Blood alcohol level
Laboratory Studies :
Imaging Studies:
Chest X Ray
ECG:
Brugada Pattern :
Treatment :
 25% of cases, patients were alert and awake
 at first prehospital contact
 Immediately evaluate the patient and administer oxygen.
 Monitor vital signs.
 Stabilization : Insert an intravenous line and cardiac
monitoring.
 Altered mental status :naloxone, glucose and if indicated
thiamine.
 Adequate ventilation ,prolonged cardiac massage.
 NO IPECAC (CNS depression can be
 rapid)
 Activated charcoal
SUPPORT VITAL FUNCTIONS:
• Respiratory depression : intubation and
hyperventilation
• Hypotension :Nor epinephrine , Phenyl epinephrine,
Sodium bicarbonate , Glucagon(10mg bolus followed
by an infusion of 10 mg over 6 hours) .
• Dysrhythmias: sodium chloride, Sodium bicarbonate
• Convulsion : Diazepam(0.1 mg/kg iv). Phenytoin
infusion (15 mg/kg iv) over 30 min . Benzodiazepines
,Phenobarbital (15-20 mg/kg).
Tca toxicity

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Tca toxicity

  • 2. Tricyclic antidepressant : They have been employed in drug therapy since the late 1950s. Largest group of drug agents used for the treatment of depression. Referred as “ tri cyclic ” compounds –three rings. Third most common cause of drug related death in US throughout 1980s
  • 3. TCA Drugs :  Secondary amines: -Amoxapine , Nortriptyline , Desipramine , Protriptyline.  Tertiary amines:- Amitriptyline , Imipramine,Doxepin,Trimipramine.  Tetra cyclic:- Maprotiline.  Triazolopyridine :-Trazodone.
  • 4. Mechanism :  Decreases the action of acetylcholine centrally and peripherally.  Enhances dopamine levels.  Reduced serotonin and norepinephrine uptake resultant increase within the synapse.  Respiratory dysfunction and disturbances in body temp- respiratory center ,thermoregulatory site.  Membrane-stabilizing effect on the myocardium by blocking the cardiac myocyte fast sodium channels
  • 5. Bioavailability :  slowly absorbed secondary to ionization in  the stomach and slowing of peristalsis  Can remain in gut for 12 hours or more  Dissolve slowly  85-98% plasma bound
  • 6. Cardiovascular manifestations of TCA Toxicity : • Palpitation • Chest pain • Hypotension • Ecg abnormality
  • 7. CNS manifestations of TCA Toxicity : • Convulsion • Decrease mental status • Respiratory depression • Drowsiness • Coma
  • 8. Peripheral autonomic system manifestations : • Dry mouth • Dry skin • Urinary retention • constipation • Blurred vision
  • 9. Physical exam findings : • Tachycardia • Hypotension and orthostasis • Fever • Altered mental status • Ileus • Absent bowel sounds • Rigidity • Dry skin and mucous membranes • Mydriasis
  • 10. • Electrolyte (Na,K,Cl ,Ca) • blood urea nitrogen (BUN), and creatinine levels • Arterial blood gases (ABGs) for evaluation of acidosis or hypoxia • Anion gap Complete blood cell count (CBC) • Blood alcohol level Laboratory Studies :
  • 13. Treatment :  25% of cases, patients were alert and awake  at first prehospital contact  Immediately evaluate the patient and administer oxygen.  Monitor vital signs.  Stabilization : Insert an intravenous line and cardiac monitoring.  Altered mental status :naloxone, glucose and if indicated thiamine.  Adequate ventilation ,prolonged cardiac massage.  NO IPECAC (CNS depression can be  rapid)  Activated charcoal
  • 14. SUPPORT VITAL FUNCTIONS: • Respiratory depression : intubation and hyperventilation • Hypotension :Nor epinephrine , Phenyl epinephrine, Sodium bicarbonate , Glucagon(10mg bolus followed by an infusion of 10 mg over 6 hours) . • Dysrhythmias: sodium chloride, Sodium bicarbonate • Convulsion : Diazepam(0.1 mg/kg iv). Phenytoin infusion (15 mg/kg iv) over 30 min . Benzodiazepines ,Phenobarbital (15-20 mg/kg).