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Figures

Fig. 1

Electrocardiogram of one of the patients. The prominent S wave in lead I and R wave in aVR demonstrate the T40-ms rightward axis shift (255°) [16] . The ECG also shows an incomplete RBBB.

Abstract

Aim

The aims of this study are to determine the electrocardiographic (ECG) manifestations of the symptomatic patients with isolated tramadol toxicity and to predict seizures based on ECG parameters.

Methods

Medical charts of a total of 479 patients with isolated tramadol toxicity were retrospectively evaluated. Their clinical manifestations were recorded, and their ECG parameters including rate, PR interval, QRS duration, corrected QT interval, terminal 40-millisecond frontal plane QRS axis, and the height of R wave and R/S ratio in the lead aVR were measured. The data were analyzed using Kolmogorov-Smirnov test, Mann-Whitney U test, Pearson χ2, Pearson correlation coefficient (r), and the Student t test.

Results

Electrocardiographic heart rate more than 100 beats per minute in 30.6%, QRS 120 milliseconds or more in 7.5%, corrected QT interval more than 440 milliseconds in 24.6%, height of R wave more than 1 mm in lead aVR in 22.1%, R/S ratio more than 0 in lead aVR in 23.5%, terminal 40-millisecond frontal plane QRS axis greater than 120° in 31.7%, and complete or incomplete right bundle-branch block in 4.6% of the patients were detected. There were no statistically significant differences between the patients who had not convulsed and those who had convulsed after admission regarding age, sex, vital signs, and ECG findings at presentation (all P values were >.05).

Conclusions

Tramadol toxicity shows ECG changes consistent with sodium channel blockade and potassium channel blockage effects. The risk of development of seizures cannot be predicted based on the changes of ECG parameters at presentation.

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Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.

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