EDITOR:
The prophylactic administration of 5-HT3 antagonists has proven beneficial in the prevention of postoperative nausea and vomiting [Reference Gan1]. However, there have been case reports of the arrythmogenic effects of some of these agents [Reference Bosek, Hu and Robinson2–Reference Higgins and Bunker5]. We would like to report one such incident probably associated with the use of tropisetron.
Case report
A 14-yr-old male (72 kg) was admitted to undergo an attic-antrostomy for chronic middle ear infection. Following 4 h of stable anaesthesia induced with fentanyl, propofol and sevoflurane and maintained with desflurane in an air/oxygen mixture, tropisetron (2 mg) was administered intravenously (i.v.). Twenty minutes later, during skin closure, he developed a broad complex tachycardia with a rate of 201 bpm (previous rate 80 bpm) with no changes in saturations or capnography and maintaining his blood pressure (95/60 mmHg). This was sustained and a 70 mg bolus of lignocaine was given i.v. with no effect, followed by 300 mg of amiodarone (in two boluses) and 20 mmol of magnesium sulphate. The broad complex rhythm persisted, slowing to 186 bpm and systolic blood pressure dropped to 75 mmHg. A synchronized monophasic DC shock (200 J) was administered, which restored rhythm to normal sinus and heart rate to 80 bpm. The duration of the event was approximately 12 min and arterial blood gas analysis revealed no acidosis, hypoxia, hypercapnia or electrolyte abnormality. Anaesthesia was discontinued, the patient awoke normally and was transferred to the paediatric intensive care unit for overnight monitoring. Subsequent 12-lead electrocardiography and transthoracic echocardiography revealed no abnormalities. The patient denied prior similar episodes or family history and no further arrhythmias were noted. Following consultation with a paediatric cardiologist and cardiac electro-physiologist he was discharged home with instructions to return if any syncopal episodes or palpitations occurred.
Discussion
The arrhythmia experienced was either ventricular tachycardia (VT) or supraventricular tachycardia (SVT) with aberrant conduction. Although the clinical impression at the time was that this was VT, cardiological opinion suggested that an SVT with aberrancy was more likely. The normal electrolytes, echocardiogram and electrocardiogram have prompted reflection as to the cause of the arrhythmia. While there are many causes of tachyarrhythmias during anaesthesia, the only notable event prior to this was the administration of tropisetron [Reference Thompson and Balser6]. A previous report noted SVT accompanied by ST segment depression following i.v. tropisetron, which responded to sublingual nitroglycerin [Reference Mitterschiffthaler and Putz7]. These authors postulated that the 5-HT3 antagonists may suppress the von Bezold-Jarisch reflex (BJR), which then leads to the development of tachyarrhythmias. This has been speculated upon previously regarding similar events following administration of ondansetron and dolasetron [Reference Bosek, Hu and Robinson2,Reference Kasinath, Malak and Tetzlaff4,Reference Higgins and Bunker5]. BJR is a cardioinhibitory reflex which classically induces bradycardia, hypotension and peripheral vasodilatation [Reference Campagna and Carter8]. Blockade of 5-HT3 receptors on cardiac vagal afferents may result in cardiac stimulation leading to tachyarrythmias and sometimes ischaemia.
Tropisetron accompanying product information does mention the possibility of prolongation of QT interval but suggests that the relationship has not been established. The purpose of this report is to draw attention to a rare but noted potential complication of a very effective and useful group of agents.
