Key result
Physostigmine administration did not immediately improve ECG findings in a 22-year-old woman with tricyclic antidepressant poisoning, leading the authors to doubt its efficacy for cardiac toxicity.
Why the study?
Does physostigmine improve cardiac toxicity in tricyclic antidepressant poisoning?
Does physostigmine improve cardiac toxicity in tricyclic antidepressant poisoning?
Answers are grounded in this paper and cite their sources.
This letter questions the efficacy of physostigmine for treating TCA-induced cardiac toxicity, highlighting the confounding effect of concurrent lidocaine administration.
To the Editor.— Tobis and Das (235: 1474, 1976) report, for the first time, successful use of physostigmine salicylate in the treatment of malignant ventricular arrhythmias and conduction defects caused by tricyclic antidepressant (TCA) poisoning in a 22-year-old woman admitted two hours after ingesting about 1,000 mg amitriptyline hydrochloride. Among other measures, large doses of physostigmine were given and, after 48 hours, ventricular conduction abnormalities and arrhythmias abated. Improvement in cardiac toxicity was attributed to physostigmine therapy. If this conclusion were correct, physostigmine might be an important addition to the therapy of TCA cardiotoxicity. However, we are doubtful that improvement in cardiac status was caused by this drug. Physostigmine (6 mg) was given to the patient immediately on arrival, but the ECG did not change. Shortly afterward, a rhythm interpreted as ventricular tachycardia developed, and the patient was given lidocaine hydrochloride and physostigmine. By the following morning, the QRS complex
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J. Thomas Bigger (1977) conducted a letter in Tricyclic antidepressant (TCA) poisoning (n=1). Physostigmine was evaluated on Improvement in cardiac toxicity (ventricular arrhythmias and conduction defects). Physostigmine administration did not immediately improve ECG findings in a 22-year-old woman with tricyclic antidepressant poisoning, leading the authors to doubt its efficacy for cardiac toxicity.
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