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Tricyclic Overdose

Cardiovascular Complications. Thorstrand has recently reported clinical variables with special reference to the electrocardiogram in 153 cases (64 men and 89 women) of poisonings by tricyclic antidepressants. The mean age of the patients was 34 years. Amitriptyline poisoning accounted for 112 (73%) of the cases and the mean dose ingested was about 1,000 mg. Coma occurred in 87 patients (57%) and on admission 40 (26%) had a systolic blood pressure below 100 mm/Hg. The systolic BP on admission was significantly lower (p<0.001) and the heart rate (HR) higher (p<0.001) than when the patients left the ward. Increased HR (≥ 90 beats/min.) was present in 73% of the cases. The most characteristic ECG change was a QRS prolongation (≥0.11 sec), found in 42% of the cases. About the same proportion displayed a QT prolongation and 28% had prolonged PR interval. Statistical analysis of the material for clinical variables (dose of TCA, BP, coma duration, etc.) showed that the QRS duration was closely related to the severity of poisoning. Five patients (three percent) died with complications such as arrhythmias, aspiration or acidosis. All of these on admission demonstrated advanced ECG changes with arrhythmias and a mean QRS duration of 0.19 sec. Excluding dibenzepine poisoning (four cases; all fatal), the mortality rate was 0.7%.

Plasma Levels. Among individuals on the same dose of tricyclic antidepressants, there can be great variability of plasma concentration, hence monitoring of TCA plasma level is very valuable especially during overdose. Spiker et al have studied 24 patients hospitalized for overdose of tricyclic antidepressants. They were monitored clinically, and serial plasma drug measurements were taken for up to 144 hours. Six of 24 patients had maximum anti-depressant plasma levels ≥1,000 ng/ml, and their plasma levels at 96 hours were 170-1,280 ng/ml. The only reliable and valid clinical correlate of the severity of a TCA overdose was the QRS duration in the ECG. Patients with a plasma TCA level of ≥1,000 ng/ml had a QRS interval ≥100 mSec.

Sustained drug levels may play a role in the unexpected cardiac deaths in some patients three to six days post-overdose.

His Bundle Electrocardiographic (HBE) Studies. Fourteen patients admitted after tricyclic drug overdose were studied with His bundle electrocardiography (HBE). The interval between the atrium and the His bundle (AH interval) was normal in all 14 patients. The interval between the His bundle and the ventricle (HV interval) and the QRS complex widened in seven of the eight patients with overdoses of nortriptyline, imipramine or amitriptyline (the mean amount taken was 1.4 g per patient). All six patients with overdoses of doxepin had normal HV intervals (the mean amount taken was 1.3 g per patient).

Treatment of TCA Cardiotoxicity. Symptoms of acute poisoning by overdose of the tricyclic drugs include coma, choreoathetoid movements and myclonus in addition to the usual evidence of atropine-like toxicity (urinary retention, pupillary abnormalities, tachycardia and hypotension).

Attention must be paid to minimizing drug absorption, either by induced emesis in conscious patients or gastric lavage in those with depressed consciousness. In either case the addition of activated charcoal is useful to prevent further absorption of the drug. Evidence shows that forced diuresis does not appreciably increase the amount of drug excreted by the kidneys. Both peritoneal and hemodialysis have been tried and found ineffective in noticeably hastening removal of the drug from the body. Several studies have shown that the toxicity of tricyclics are exaggerated by increased cardiac work. Thus efforts should be made to minimize fluid overload, seizures, agitation and blood pressure extremes.

Use of digitalis depends on accurate and timely evaluation of the clinical assessment. Digitalis glycosides have been used in treating congestive heart failure associated with tricyclic antidepressants overdose.

The anticholinergic cardiac toxicity caused by tricyclic antidepressants has been effectively treated with physostigmine. It crosses the blood brain barrier and is therefore also effective against the central anticholinergic effects of the tricyclics. It can be given IV in a dose of one to three mg and repeated as clinically indicated.

In view of the effect of tricyclics on the adrenergic neuron, the beta adrenergic blocking drug propranolol has been used successfully in treating a variety of TCA-induced arrhythmias in man.

Diphenylhydantoin has been recommended as a means of preventing both cardiac and cerebral dysrhythmias.

Brown et al have treated over 150 children with tricyclic antidepressant overdoses in their intensive care unit, and of these 50 had serious manifestations of overdose arrhythmias, convulsions, unconsciousness or a combination of these. Sodium bicarbonate was given as a bolus of one to three mEq/Kg IV. Out of 20 patients, 19 reverted rapidly to sinus rhythm and the other patient reverted 30 minutes after diphenylhydantoin and sodium bicarbonate had been given. They have also used Practolol in treating experimentally induced arrhythmias after infusion of amitriptyline. Practolol (a cardioselective beta adrenergic blocker) was effective in terminating arrhythmias but marked hypotension was observed.

Cardioversion and transvenous cardiac pacing have also been used in treating tricyclic toxicity.

Children are at increased risk of TCA cardiotoxicity because of important pharmacokinetic differences between children and adults. The currently recommended pediatric dose of imipramine hydrochloride in treating enuresis is 2.5 mg/kg/day.

Conclusion

In summary, there is growing evidence that tricyclics, even at therapeutic levels, can be cardiotoxic. Unfortunately plasma tricyclic antidepressants levels are too variable from patient to patient to be of value in defining a safe therapeutic range. However, in adults the therapeutic range of plasma level for nortriptyline hydrochloride is generally considered to be 50-175 ng/ml.

Although it is not yet recommended that each patient placed on tricyclic antidepressants have an electrocardiogram, any patient demonstrating cardiovascular side effects should have an ECG before continuing medication. From the clinical studies to date, it appears that T-wave changes commonly occur at therapeutic dosage of tricyclic antidepressants and, less commonly, abnormally prolonged PR and QRS intervals are observed. In some cases, these ECG effects might herald a subsequent conduction disturbance or arrhythmia of clinical importance, even in patients without a history of cardiac disease and even at relatively low tricyclic antidepressants dosage. Tetracyclics should be considered in the depressed patient who is particularly predisposed to the cardiotoxic properties of tricyclic antidepressants.