General Medicine > TCA Overdose > Flashcards

TCA Overdose Flashcards

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1
Q

What type of toxicity do tricyclic antidepressants (TCAs) cause?

A

Sodium channel blocker toxicity

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2
Q

Why is TCA toxicity particularly dangerous?

A

It can cause life-threatening arrhythmias, seizures, and coma.

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3
Q

Which other drugs can present similarly to TCA toxicity?

A

Class I antiarrhythmics

Local anaesthetics

Antimalarials

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4
Q

Why do these drugs have overlapping clinical features?

A

They all cause sodium channel blockade.

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5
Q

What is the mainstay of treatment in TCA toxicity?

A

Sodium bicarbonate (NaHCO₃).

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6
Q

Why is sodium bicarbonate effective in TCA overdose?

A

It overcomes sodium channel blockade and narrows the QRS, reducing arrhythmias.

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7
Q

Besides NaHCO₃, what other supportive treatments are important?

A

Treatment of dysrhythmias

Ventilatory support if needed

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8
Q

Is sodium channel blockade the only mechanism of TCA toxicity?

A

No — it is only one of four primary mechanisms.

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9
Q

Why is it important to remember that TCAs have multiple mechanisms of toxicity?

A

Because toxicity is multisystem and explains anticholinergic effects, CNS toxicity, and hypotension, not just arrhythmias.

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10
Q

Name common tricyclic antidepressants (TCAs).

A

Amitriptyline, Imipramine, Clomipramine, Nortriptyline.

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11
Q

What is the first major mechanism of TCA toxicity?

A

Inhibition of norepinephrine and serotonin reuptake at nerve terminals.

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12
Q

What clinical effect results from excess norepinephrine and serotonin?

A

CNS excitation → seizures

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13
Q

What is the second major mechanism of TCA toxicity?

A

Anticholinergic action.

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14
Q

What CNS effects are caused by anticholinergic toxicity?

A

Disorientation, agitation, euphoria or dysphoria, and hallucinations.

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15
Q

What is the third major mechanism of TCA toxicity?

A

Direct alpha-adrenergic blockade.

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16
Q

What clinical consequence results from alpha-blockade?

A

Profound hypotension

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17
Q

What is the fourth (and most dangerous) mechanism of TCA toxicity?

A

Membrane-stabilising effect on the myocardium via fast sodium channel blockade.

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18
Q

How does sodium channel blockade affect cardiac conduction?

A

Decreases sodium influx → reduces slope of phase 0 depolarisation.

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19
Q

What ECG change results from this effect?

A

Widened QRS complex.

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20
Q

Why is a widened QRS dangerous in TCA toxicity?

A

It predisposes to ventricular dysrhythmias and sudden death.

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21
Q

One-line pathophysiology summary for exams?

A

TCAs cause seizures (↑NE/5-HT), delirium (anticholinergic), hypotension (α-blockade), and arrhythmias (Na⁺ channel blockade).

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22
Q

Which TCA is most frequently ingested in overdose in South Africa?

A

Amitriptyline.

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23
Q

What proportion of TCA suicide attempts result in death before reaching a healthcare facility?

A

Over 50% die before arrival.

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24
Q

Historically, how did TCAs rank among causes of fatal drug ingestion?

A

They were the number one cause until the last decade.

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25
Which drug class has surpassed TCAs as the leading cause of fatal drug ingestion?
Analgesics.
26
What is the mortality rate among TCA overdose patients who reach a healthcare facility?
Approximately 2–3%.
27
Does TCA toxicity affect one sex more than the other?
It occurs in both men and women.
28
Which sex predominates in TCA toxicity presentations in the Western Cape?
Women, accounting for ~75% of cases.
29
Which age group has the highest incidence of TCA toxicity?
20–29 years
30
What key epidemiological contrast is important for exams?
High pre-hospital fatality, but low in-hospital mortality with prompt care.
31
What cardiovascular symptoms may occur in TCA toxicity?
Palpitations, chest pain, hypotension.
32
Why is hypotension common in TCA overdose?
Due to alpha-adrenergic blockade and myocardial depression.
33
What CNS manifestations are seen in TCA toxicity?
Convulsions, decreased mental status, drowsiness, coma.
34
Why do seizures occur in TCA overdose?
From excess norepinephrine and serotonin causing CNS excitation.
35
How does TCA toxicity affect respiration?
Causes respiratory depression, especially with reduced consciousness.
36
What peripheral autonomic features suggest anticholinergic toxicity?
Dry mouth, dry skin, urinary retention, blurred vision.
37
What classic toxidrome do these peripheral features represent?
Anticholinergic toxidrome.
38
What triad should make you strongly suspect TCA toxicity?
Altered mental state + seizures + cardiovascular instability.
39
Which system involvement predicts severe toxicity?
Cardiovascular and CNS involvement.
40
Are serum tricyclic antidepressant (TCA) levels useful in acute management?
No — they are slow to result and do not correlate well with toxicity.
41
Should management wait for serum TCA levels?
No — life-saving treatment must not be delayed.
42
What is the cornerstone of diagnosing TCA toxicity?
A combination of history, physical examination, blood gas, and ECG findings.
43
Why is history important in suspected TCA overdose?
It helps identify drug class, intent, timing, and risk of severe toxicity.
44
What examination findings support TCA toxicity?
Altered mental status, seizures, hypotension, and anticholinergic features.
45
Why is ECG essential in TCA toxicity?
It detects sodium channel blockade, seen as QRS widening, which predicts life-threatening arrhythmias.
46
Which ECG finding is most important prognostically?
Widened QRS complex.
47
What role does blood gas analysis play?
Identifies acidosis, which worsens sodium channel blockade and toxicity.
48
Why are simple bedside investigations emphasized?
Because early, rapid assessments save lives in TCA toxicity.
49
What is the single most important investigation in TCA toxicity?
ECG
50
Why is ECG crucial in TCA overdose?
It detects sodium channel blockade → widened QRS, predicting life-threatening arrhythmias.
51
What does an arterial blood gas (ABG) help identify?
Acidosis, which worsens sodium channel blockade and toxicity.
52
Are serum TCA concentrations useful acutely?
No — slow and poor correlation with severity.
53
Why should paracetamol levels be checked?
To exclude common co-ingestion in overdose presentations.
54
What is the cornerstone treatment for TCA cardiotoxicity?
Sodium bicarbonate (NaHCO₃).
55
What is the sodium bicarbonate dose?
0.5–2 mEq/kg IV bolus, followed by infusion if needed.
56
What is the target pH during bicarbonate therapy?
pH 7.45–7.55.
57
Why does alkalinisation help in TCA toxicity
It reduces sodium channel blockade and narrows the QRS.
58
Which electrolytes must be closely monitored?
Sodium and potassium.
59
First-line treatment for seizures in TCA toxicity?
Diazepam (benzodiazepines).
60
What if seizures persist despite benzodiazepines?
Phenobarbital.
61
Which anticonvulsant must be avoided and why?
Phenytoin — it is also a sodium channel blocker and worsens toxicity.
62
When is sodium bicarbonate indicated in TCA toxicity?
QRS ≥ 100 ms Ventricular dysrhythmias Hypotension Metabolic acidosis Seizures associated with ECG changes
63
Why is QRS duration important?
QRS ≥ 100 ms predicts seizures, and ≥160 ms predicts ventricular arrhythmias.
64
How does sodium bicarbonate work in TCA toxicity?
Alkalinises serum → reduces TCA binding to sodium channels Increases sodium load → overcomes sodium channel blockade
65
Why is alkalinisation beneficial?
TCAs bind sodium channels more strongly in acidic environments.
66
Is the benefit from alkalinisation or sodium load?
Both, but sodium load is critical.
67
What cardiovascular risks exist with over-treatment?
Arrhythmias due to hypokalaemia.
68
Should phenytoin be used for seizures?
No — it worsens sodium channel blockade.
69
Who should be admitted after TCA overdose?
All symptomatic patients.
70
What determines the level of admission (ward vs ICU)?
Clinical condition and severity of toxicity.
71
Which patients require ICU admission?
Patients with: Ventilatory support needs Recurrent seizures Significant arrhythmias or hypotension
72
Can asymptomatic TCA overdose patients be discharged?
Yes, but only after careful assessment.
73
What must be screened for in all overdose patients?
Paracetamol co-ingestion Social circumstances Risk of recurrence / suicidality
74
What observation period is required before considering discharge?
12 hours of stability
75
What conditions must be met before discharge?
Asymptomatic throughout observation Normal investigations (ECG, labs) Low suicide risk
76
Who should facilitate discharge planning?
Social Worker, with appropriate psychosocial support
77
What is the most important treatment pitfall to avoid?
Do not delay sodium bicarbonate therapy in suspected significant TCA overdose.
78
Why should sodium bicarbonate not be delayed?
Because early treatment prevents fatal arrhythmias.
79
What is a common diagnostic pitfall in TCA overdose?
Assuming single-substance ingestion.
80
What co-ingestions must always be considered?
Paracetamol and other cardiotoxic or CNS-depressant substances
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