Abstract

BackgroundAdenosine is the first-line pharmacotherapy for termination of supraventricular tachycardia through its action on the atrioventricular node. However, pro-arrhythmic effects of adenosine are also recognised, most notably in the presence of pre-excited atrial fibrillation. In this case report, we describe the induction of ventricular fibrillation in a patient with no demonstrable accessory pathway, nor any other structural heart disease. This rare, idiosyncratic reaction has never previously been reported and is of relevance given the widespread and routine use of adenosine in clinical practice.Case presentationA 26-year-old woman of Cypriot origin presented to our emergency department with a sudden onset of palpitations and chest discomfort. She was healthy, with no previous medical history and no regular medications. An electrocardiogram demonstrated a narrow complex tachycardia with a rate of 194 beats per minute. Following failure of vagal maneuvers to terminate the tachycardia, the assessing physician administered a single intravenous dose of 6 mg adenosine. Our patient instantaneously developed coarse ventricular fibrillation and circulatory collapse. Cardiopulmonary resuscitation was initiated and our patient was rapidly defibrillated to sinus rhythm with a single 150 J direct current shock. A 900-mg loading dose of intravenous amiodarone was commenced and our patient was managed in the cardiac high dependency unit. No further arrhythmias were identified on continuous cardiac monitoring.On review, her presenting electrocardiogram had demonstrated rapidly conducted atrial fibrillation with no evidence of ventricular pre-excitation. Concordantly, her resting electrocardiogram was not suggestive of any accessory pathway. This was conclusively excluded on invasive electrophysiology study, with negative programmed ventricular stimulation up to three extrastimuli. Extensive laboratory investigations were unremarkable and failed to identify an underlying cause for her episode of atrial fibrillation. Furthermore, cardiac magnetic resonance imaging demonstrated a structurally normal heart, with no edema, fibrosis or infarction as well as normal coronary artery anatomy.ConclusionsAdenosine remains a safe and highly efficacious therapy for supraventricular tachycardia. However, this unusual case demonstrates the ability of adenosine to induce circulatory collapse and reminds the clinician that prompt access to resuscitation, defibrillation, and transcutaneous pacing equipment is mandatory with every administration of this drug.

Highlights

  • Adenosine is the first-line pharmacotherapy for termination of supraventricular tachycardia through its action on the atrioventricular node

  • Adenosine remains a safe and highly efficacious therapy for supraventricular tachycardia. This unusual case demonstrates the ability of adenosine to induce circulatory collapse and reminds the clinician that prompt access to resuscitation, defibrillation, and transcutaneous pacing equipment is mandatory with every administration of this drug

  • An intravenous bolus dose of 6 mg adenosine was administered. This was followed by immediate development of coarse ventricular fibrillation (VF) (Fig. 1b) and circulatory collapse

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Summary

Conclusions

This unusual case serves as a reminder of the ability of adenosine to induce ventricular tachyarrhythmias associated with circulatory collapse. The wellrecognised adverse effects of bronchospasm, chest pain and bradycardia, combined with the potential for ventricular arrhythmias should mandate all physicians to use adenosine only where there is prompt access to resuscitation, defibrillation, and transcutaneous pacing equipment. Physicians should not be deterred from using this highly efficacious agent where an appropriate assessment of the risks incurred has been borne in mind

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