Mobitz type 1 second‐degree atrioventricular block by triazolam and brotizolam overdose

Dear Editor

We report a case of transient Mobitz type 1 second‐degree atrioventricular (AV) block after triazolam and brotizolam overdose. A 40‐year‐old woman presented to the emergency room with mild consciousness disturbance 4 h after she had taken 12 mg triazolam (0.25 mg/L tablets, therapeutic dose 0.25 mg/day) and 5 mg brotizolam (0.25 mg/L tablets, therapeutic dose 0.25 mg/day). She was depressive just before this episode, had not taken other drugs, and had no other history of disease. She had no complaint of cardiovascular symptoms. Her physical examination showed: a Glasgow Coma Scale score of E3V5M6; respiratory rate, 16 beats/min; blood pressure, 102/64 mmHg; heart rate, 50 b.p.m.; and body temperature, 36.2°C. A urine drugs screening test detected positive only for benzodiazepine. A chest X‐ray revealed no abnormal findings. Her initial electrocardiogram (ECG) indicated sinus bradycardia; subsequently, continuous monitoring presented as PR prolongation, and developed Mobitz type 1 second‐degree AV block 8–20 h after taking the drugs (Fig. 1). An ECG carried out 6 years previously had shown normal sinus rhythm (PR 0.16 ms). A follow‐up ECG taken 2 days later revealed normal sinus rhythm (PR 0.19 ms). During the course, she had no complaint of symptoms. We did not administer flumazenil.

Figure 1.

Electrocardiogram of a 40‐year‐old woman with Mobitz type 1 second‐degree atrioventricular block after 20 h from triazolam and brotizolam overdose.

Potentially life threatening arrhythmias such as AV block are not often seen after benzodiazepine overdose. Therefore, benzodiazepines have been believed to be relatively safe drugs, except for respiratory suppression. However, there are reports that AV block may occur with benzodiazepines, but we could not find any case of triazolam and brotizolam overdose in published reports. Atrioventricular block by alprazolam, olanzapine, and clonazepam have been reported.1, 2, 3 Considering that the conduction change of ECG of this patient was transient, the differential diagnosis might be focused on the transient event. There was no evidence of cardiovascular event, such as ischemic heart attack. No hypothermia (36.2°C) and no electrolyte disturbance were observed. We did not undertake procedures that transiently increase vagal tone, such as nasogastric tube insertion. Most cases of AV block are due to drugs, however, the patient did not use drugs that may cause AV block, such as β‐blockers, calcium channel blockers, or digitalis. Although we could not evaluate the interaction of triazolam and brotizolam, the theoretical background indicates that benzodiazepines generally can cause this type of arrhythmia because they alter L‐type Ca2+ channel function.1 Therefore, we emphasize the importance of a continuous monitoring of this type of patient overdose. Eizadi‐Mood et al. analyzed 267 cases of benzodiazepine overdose and reported that 96.67% of these patients had normal ECGs; PR prolongation (PR interval >0.21 ms) was observed in 1.12% of patients.4 Although they concluded that cardiovascular toxicity with benzodiazepine is not common, we see that in 1.12% of their cases PR prolongation was observed. This report gives us supportive evidence of transient arrhythmic change in our case of benzodiazepine overdose. As for the management of the case, flumazenil might have some adjunct role in the management of AV block caused by benzodiazepine, as suggested by Mullins.1

In conclusion, although arrhythmic change in overdose of benzodiazepines might be rare, it can occur in some cases. We reported the case of transient AV block in overdose with triazolam and brotizolam. This case reminds clinicians of the rare but potentially life‐threatening cardiovascular complications that may be associated with benzodiazepine overdose.

Conflict of Interest

None.