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Broad complex tachycardias present a diagnostic and therapeutic challenge to the emergency physician. The majority of cases are ventricular tachycardias (VT) resulting from underlying ischaemic heart disease.1,2 Broad complex tachycardias may also occur as a result of a supraventricular tachycardia (SVT) in the presence of aberrant conduction. Differentiation has important implications in terms of management and prognosis. If VT is mistakenly diagnosed as SVT with aberrant conduction and treated with calcium channel blockers, the patient is likely to become haemodynamically unstable.3 Some clinicians therefore advocate assumption that all cases of broad complex tachycardia are VT.4
Fascicular tachycardia is a distinct subgroup of idiopathic VT that may be confused with either typical VT or SVT.5,6 Although well recognised by cardiologists, there is only a single report in the emergency medicine literature.7 It is characterised by the absence of structural heart disease and classic electrocardiographic and electrophysiological features.5,8,9 Vagal manoeuvres and adenosine are ineffective in suppressing fascicular tachycardia.5,8,10 It is also unresponsive to the standard pharmacological treatments, such as lignocaine (lidocaine), used for VT associated with coronary artery disease.5,8 In contrast, it is terminated or suppressed by calcium antagonists.5,6,8,9,11
A 29 year old man presented to the emergency department for evaluation of rapid palpitations and pre-syncope. This had started two hours before presentation. He had experienced one similar episode 18 months previously that had responded to medical treatment. No old notes were available and he could not recall which drugs he had been given. He had no other medical history and was on no regular medication. He was a non-smoker, drank less than 10 units of alcohol per week, and denied illicit drug use. Consumption of tea, coffee, or caffeinated drinks was minimal.
On examination he was apyrexial, heart rate 140 bpm, blood pressure 110/80 mm Hg. The remaining physical examination was unremarkable.
A lead II rhythm strip showed a broad complex tachycardia with a QRS duration of 140 ms. A lead III rhythm strip showed an apparent narrow complex tachycardia with a QRS duration of 90 ms. A 12 lead ECG revealed a wide QRS complex tachycardia with a right bundle branch block morphology and left axis deviation (fig 1). Capture beats were present. Immediate cardiology consultation was sought and a diagnosis of fascicular tachycardia was made. Intravenous verapamil 5 mg was administered with slowing and then cessation of the tachycardia. A 12 lead ECG performed immediately after cessation of the tachycardia showed reversion to a normal pattern.
Transthoracic echocardiography revealed no structural abnormality and good ventricular function. Subsequent review of the patient’s old notes, showed that on his previous admission he had been treated with adenosine and lignocaine prior to the correct diagnosis being made. The patient was discharged from the emergency department with cardiology follow up.
The diagnosis of fascicular tachycardia is difficult in the setting of the emergency department. Patients are generally young with no evidence of structural heart disease. The arrhythmia may mimic both SVT and VT. Capture beats and fusion beats may be present on the 12 lead ECG suggesting the diagnosis of VT rather than SVT. In this patient, the lead III rhythm strip was consistent with SVT while the lead II rhythm strip pointed towards VT. The width of the QRS complex should be determined by examining the lead where it appears broadest on the 12 lead ECG. The correct diagnosis was suggested by the presence of a broad complex tachycardia with a right bundle branch block morphology and left axis deviation.5,6,8,9 The QRS duration in fascicular tachycardia can vary from 100 to 140 ms.6,9 The RS interval is uniformly <80 ms in contrast with VT associated with structural heart disease where the RS interval is generally >100 ms.9 After reversion to sinus rhythm, non-specific ST segment and T wave changes may be seen, most commonly in the inferior or lateral chest leads.5,6
The tachycardia is thought to originate as a re-entrant mechanism located in the posterior fascicle of the left bundle branch.5,6,9–11 This theory is supported by the ease with which the tachycardia can be initiated and terminated by pacing.6 In some patients a false tendon has been found extending from the posterior-inferior free wall of the left ventricle to the left ventricular septum.12 Conduction via the free tendon or stretching of the Purkinje fibres in the inter-ventricular septum may induce the tachycardia in these patients.
The pharmacological treatment of choice for fascicular tachycardia is intravenous verapamil.5,6,8,9,11,13 The dramatic response to calcium channel block can again lead to misdiagnosis of SVT.6 Sotalol and amiodarone have also been reported to be effective.14 Vagal manoeuvres, adenosine, lignocaine, and propanolol have no effect.5,8,10 Recurrences may be prevented by long term, oral verapamil.8,11 Radiofrequency ablation has been reported to be successful in selected patients.15
In the emergency department, a broad complex tachycardia should be presumed to be VT in association with ischaemic or structural heart disease. If standard methods fail to convert the arrhythmia and the 12 lead ECG shows a right bundle branch block picture with left axis deviation, a diagnosis of fascicular tachycardia should be considered. If the diagnosis is confirmed, intravenous verapamil is the treatment of choice.
All three authors saw the patient and contributed to his management in the emergency department. Laura Howe and Soroosh Firoozan collected related material and edited the paper. Andrew Eynon wrote the paper and will act as guarantor.
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