Tricyclic antidepressant overdose: Clinical presentation and plasma levels

Spiker, Duane G.; Weiss, Alan N.; Chang, Sun‐Yran; Ruwitch, Joseph F.; Biggs, John T.

doi:10.1002/cpt1975185part1539

Cited by 168 publications

(28 citation statements)

References 6 publications

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“…Tricyclic drugs have now replaced barbiturates as the agent most frequently taken in overdose with suicidal intent, and tricyclic overdose has rapidly evolved into a major public health problem. Even in patients with no heart disease, overdose of tricyclic antidepressant drugs can produce severe electrophysiological abnormalities, including heart block and dangerous ventricular arrhythmias (Bigger et al, 1978;Spiker et al, 1975;Vohra et al, 1975). There is concern that even therapeutic doses of tricyclic antidepressants may cause adverse cardiovascular effects in older patients or those who have known heart disease (Goodman and Gilman, 1975).…”

mentioning

confidence: 99%

Electrophysiological effects of imipramine on ovine cardiac Purkinje and ventricular muscle fibers.

Weld¹,

Bigger²

1980

Circulation Research

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mentioning

confidence: 99%

Electrophysiological effects of imipramine on ovine cardiac Purkinje and ventricular muscle fibers.

Weld¹,

Bigger²

1980

Circulation Research

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“…The selected plasma levels, ranging from 0.035 to 6,g/ml, comprised both therapeutic plasma levels (25 to 700 ng/ml according to Yates, Todrick & Tait, 1963;Asberg, Cronholm, Sij6qvist & Tuck, 1971;Asberg, 1974;Garattini & Morselli, 1975) and those found after an accidental overdose (600 to 2190 ng/ml: Spiker, Weiss, Chang, Ruwitch & Biggs, 1975).…”

Section: Resultsmentioning

confidence: 99%

“…Impaired atrioventricular conduction was observed in man only following drug overdosage by Vohra (1974), Thorstrand (1974) and by Spiker et al (1975).…”

Section: Resultsmentioning

confidence: 99%

Plasma Concentrations and Cardiotoxic Effects of Desipramine and Protriptyline in the Rat

Bianchetti

Bonaccorsi

Chiodaroli

et al. 1977

British J Pharmacology

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Desipramine and protriptyline were administered to anaesthetized rats by two consecutive intravenous infusions in order to obtain a peak level (first infusion) followed by lower steady state concentrations (second infusion) (Wagner, 1974). Theoretical plasma level time courses were confirmed experimentally. Desipramine and protriptyline were measured in atria and ventricles. Increasing infusion rates led to proportional increases in plasma and atrial concentrations. The tissue/medium ratio ranged from 57 to 21 for desipramine and from 43 to 11 for protriptyline according to the time of determination during infusions. Heart rate changes, deviation of the electrical axis of the heart and prolongation of atrioventricular conduction were recorded at fixed times during infusion. Positive chronotropic effects were noted at plasma concentrations ranging from 0.035 to 0.1 μg/ml for desipramine and from 0.04 to 1.2 μg/ml for protriptyline. At higher plasma concentrations the positive chronotropic effect decreased and bradycardia developed. Both drugs induced right rotation of the electrical axis of the heart. Threshold plasma levels giving 40° rotation were 1.35 μg/ml (desipramine) and 1.75 μg/ml (protriptyline). Atrioventricular conduction was prolonged at threshold plasma concentrations of 2.2 μg/ml for desipramine and 3.6 μg/ml for protriptyline. Desipramine is more cardiotoxic than protriptyline. This difference is discussed in relation to the plasma and heart concentration of the two drugs.

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“…Literature in the 1970s and early 1980s suggested that the serum concentration could be useful in determining clinical toxicity [19][20][21]. This hypothesis was challenged by Boenhert and Lovejoy's landmark study which has subsequently changed the focus of determining toxicity [22].…”

Section: History Of Sodium Bicarbonate Therapymentioning

confidence: 99%

A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening

Bruccoleri

Burns

2015

J. Med. Toxicol.

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Sodium bicarbonate is a well-known antidote for tricyclic antidepressant (TCA) poisoning. It has been used for over half a century to treat toxin-induced sodium channel blockade as evidenced by QRS widening on the electrocardiogram (ECG). The purpose of this review is to describe the literature regarding electrophysiological mechanisms and clinical use of this antidote after poisoning by tricyclic antidepressants and other agents. This article will also address the literature supporting an increased serum sodium concentration, alkalemia, or the combination of both as the responsible mechanism(s) for sodium bicarbonate's antidotal properties. While sodium bicarbonate has been used as a treatment for cardiac sodium channel blockade for multiple other agents including citalopram, cocaine, flecainide, diphenhydramine, propoxyphene, and lamotrigine, it has uncertain efficacy with bupropion, propranolol, and taxine-containing plants.

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Tricyclic antidepressant overdose: Clinical presentation and plasma levels

Cited by 168 publications

References 6 publications

Electrophysiological effects of imipramine on ovine cardiac Purkinje and ventricular muscle fibers.

Electrophysiological effects of imipramine on ovine cardiac Purkinje and ventricular muscle fibers.

Plasma Concentrations and Cardiotoxic Effects of Desipramine and Protriptyline in the Rat

A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening

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