Wide Qrs Tachycardia in a Young Woman with a Drug Overdose

Abstract

A depressed young woman attempted suicide by taking approximately 2 g of nortriptyline. She had multiple seizures, a systolic blood pressure of 50 mm Hg, and a respiratory arrest and was comatose when brought by ambulance to the emergency department, where she was immediately intubated. The electrocardiogram recorded on admission shows a minimally irregular wide-QRS tachycardia with a long QT interval (heart rate, 104 beats/minute; QRS duration, 0.20 seconds; QTc interval, 0.52 seconds) that could be ventricular tachycardia but is probably sinus tachycardia with right bundle branch block and a northwest QRS axis (Figure ​(Figure11). An electrocardiogram recorded 4.4 hours later shows a nearly identical heart rate (105 beats/minute), incomplete right bundle branch block (QRS duration, 0.115 seconds), a markedly rightward QRS axis, a long QTc interval (0.54 seconds), and a rhythm that is clearly sinus (Figure ​(Figure22). In both electrocardiograms the terminal 0.04-second QRS vector in the frontal plane is in the northwest quadrant, i.e., between 180° and 270°. Figure 1 Electrocardiogram recorded on admission. See text for explication. Figure 2 Electrocardiogram recorded 4.4 hours after that in Figure ​Figure1.1. See text for explication. Tricyclic antidepressants are used far less frequently than they were 20 years ago, when it was estimated that they accounted for some 500,000 drug overdoses in the USA per year, with a mortality rate disproportionately higher than with other drug overdoses (1). From these cases emerged recognition of a typical electrocardiographic pattern of overdose with tricyclic antidepressants: sinus tachycardia, a corrected QT interval of 0.418 seconds or longer, and a terminal 0.04-second QRS vector in the frontal plane between 130° and 270° (2). These criteria had positive and negative predictive values for tricyclic ingestion of 66% and 100%, respectively, when tested on 299 patients with drug overdose, and the efficiency of the electrocardiogram as a diagnostic test was 97% (2). Both of our patient's electrocardiograms met all three of these criteria. Tricyclic antidepressant drugs block the reuptake of serotonin and norepinephrine, and that action is thought to be the basis of their beneficial effects in patients with depression. These drugs also are competitive inhibitors of histamine receptors, both H1 and H2, have anticholinergic effects, and exert direct effects on cell membranes that are similar to those of quinidine (1). The cardiovascular manifestations of the tricyclic antidepressants are the result of various combinations of these drug effects. The more serious adverse cardiovascular sequelae of tricyclic antidepressants include hypotension, atrioventricular block below the A-V node, ventricular tachycardia and fibrillation, asystole, and intractable myocardial depression (1–3). The more serious adverse neurologic results of the drugs are seizures, respiratory depression, and coma (1). Sinus tachycardia, the result of anticholinergic effects, often occurs with therapeutic doses of tricyclic antidepressants and has been a poor marker for serious toxicity. In a small study of patients with an acute overdose of tricyclic antidepressants, QRS prolongation, probably a manifestation of the quinidine-like effects of the drugs, was a better predictor of seizures and ventricular arrhythmias than was a serum drug level (4). Thus, the electrocardiogram has demonstrated both diagnostic and prognostic power in patients suspected of taking an overdose of tricyclic antidepressants.