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Supraventricular tachycardia (SVT) refers to tachyarrhythmias that utilise atrial or atrioventricular (AV) nodal tissue as part of their mechanism. In the absence of aberrant ventricular activation, the electrocardiogram (ECG) will have normal QRS duration during tachycardia. Patients with SVT almost always present to doctors without a specialist training in cardiology, who are required to diagnose and initiate appropriate management. SVTs are usually of abrupt onset and termination and frequently occur in people without other cardiac abnormalities who have a good prognosis. Despite this reassuring aspect, supraventricular rhythm disturbance is not always benign and can compromise cardiac output enough to cause syncope, angina or a tachycardia related cardiomyopathy. Competent assessment is important because many patients do not require ongoing inpatient management. However, such arrhythmias can sometimes be life threatening-for example, atrial fibrillation in the presence of an accessory pathway.
Presentation and diagnosis
The incidence of SVT is approximately 35/100000 per year 1 (excluding atrial fibrillation, atrial flutter and multifocal atrial tachycardia). Atrial fibrillation is around 10 times as common with an incidence of between 1-3/1000 patients per year. 2 Symptoms include palpitation, light headedness, chest tightness and shortness of breath. Syncope is unusual but can occur. If an ECG during tachycardia has not been obtained, it is important to ascertain features that make "malignant" tachycardias more likely-for example, syncope, previous ischaemic heart disease or a family history of sudden cardiac death. Usually, symptoms of SVT have an abrupt onset and termination, and patients may have identified precipitants (for example, stimulants, emotion and exercise) as well as vagal manoeuvres associated with termination.
Accurate diagnosis relies upon interpretation of ECGs and sometimes invasive electrophysiology studies. The ECG in sinus rhythm should be assessed carefully for any evidence of QT prolongation, Brugada phenotype ( fig 1 ), ischaemic heart disease, pre-excitation ( fig 2 ) or an underlying cardiomyopathy; all of these features increase the probability of life threatening arrhythmias. Activation from pre-excitation will result in an abnormal pattern of depolarisation as well as repolarisation, the latter causing a change in T wave morphology. The ECG during the tachycardia may enable the differential diagnosis to be refined. It should be inspected for evidence of P waves, although these may be within the QRS complex in typical atrioventricular nodal re-entry...