Supraventricular tachycardia

Classical SVT history is characterised by an abrupt onset of rapid palpitations. This strongly suggests SVT, and diagnosis can usually be made without electrocardiographic documentation. Gradual onset of palpitations suggests sinus tachycardia,11 and irregular palpitations often indicate atrial fibrillation.

Defining the frequency and duration of palpitations and associated symptoms enables an assessment of clinical severity. Episodes of SVT may be triggered by factors including caffeine and alcohol intake (which can increase the frequency with which ectopic beats are triggered), bending over, sudden movements, stress, physical exertion and fatigue. Patients will have a clear idea of whether any of these are common triggers in their own case. When triggers are present they should be avoided if possible, but there is no a priori reason to restrict caffeine or alcohol intake or limit exercise in patients for whom these are not triggers.

Results of cardiovascular examination are usually normal for patients with SVT, but signs of structural heart disease should be sought.

In many cases, results of a baseline electrocardiogram (ECG) in patients with SVT are normal. However, the results should be carefully evaluated for evidence of pre-excitation, defined by a short PR interval (< 120 ms) and a delta wave (slurred upstroke at the onset of the QRS complex) (Box 2). This is the classical ECG appearance of Wolff–Parkinson–White (WPW) syndrome.12

If the arrhythmia is captured on an ECG it is usually a narrow-complex tachycardia (QRS duration, < 120 ms) (Box 3), but may have a prolonged QRS interval (> 120 ms) when associated with pre-existing or rate-related bundle branch block. In wide-complex tachycardia, however, it is safest to assume that the tachycardia is ventricular in origin until proven otherwise. A normal Holter monitor reading is seen in most patients with SVT because of the intermittent nature of episodes; thus a normal reading does not exclude the diagnosis of SVT. Often, prolonged and multiple unnecessary attempts at rhythm documentation are made when the diagnosis is evident from clinical history. Occasionally, in patients with infrequent palpitations and a less definite clinical history, cardiac event recorders or implantable monitors may be necessary to capture the underlying rhythm disturbance.

An echocardiogram can be used to evaluate cardiac structure and function, but results are usually normal for patients with SVT.

Exercise testing is less useful for diagnosis of SVT unless the arrhythmia is typically triggered by exertion. Patients may complain of chest discomfort or pain during SVT episodes. These symptoms do not mandate an exercise stress test or angiography; decisions on further testing should be based on history and presence of vascular risk factors.

The most common type of SVT is AVNRT.13 The mechanism involves a re-entrant circuit that includes the posterior inputs to the compact atrioventricular node, anterior inputs to the node, and probably perinodal atrial tissue. The tachycardia is often triggered by an appropriately timed atrial ectopic beat (Box 4).

AVRT is the second most common type of SVT, and uses an accessory pathway to complete the re-entrant circuit. Accessory pathways are muscular connections composed of functional myocardial fibres that directly connect the atria and ventricles, bypassing the atrioventricular node. Many accessory pathways do not produce pre-excitation on the ECG during sinus rhythm, owing to an inability to conduct in an antegrade direction. When the pathway conducts from ventricle to atrium (retrograde conduction), with no evidence of antegrade conduction on the sinus rhythm ECG, the pathway is termed “concealed”. In this situation, the tachycardia circuit involves antegrade conduction over the atrioventricular node and retrograde conduction over the accessory pathway.

When the accessory pathway also conducts in the antegrade direction during sinus rhythm, the ventricular myocardium is activated earlier than if conduction occurred only through the atrioventricular node, resulting in ventricular pre-excitation (WPW syndrome, Box 2).12 In patients with WPW syndrome, episodes of SVT can trigger atrial fibrillation leading to rapid conduction of the atrial activity to the ventricle via the accessory pathway. Unlike the atrioventricular node, which acts as a filter between the atria and ventricles, an accessory pathway can transmit atrial rates of up to 300 beats/min directly to the ventricles (Box 5). This can lead to ventricular fibrillation and sudden death.14

Focal atrial tachycardia: This accounts for about 10% of cases of SVT, and originates from a single localised focus of atrial tissue.15-17 The atrial rate can vary widely, from 120 beats/min to 300 beats/min. Depending on the atrial rate, and on atrioventricular node conduction, the atria may conduct 1:1 to the ventricles, or with varying degrees of atrioventricular block. Focal atrial tachycardia has characteristic anatomical sites of origin. The most common site in the right atrium is along the crista terminalis, and in the left atrium common sites are the ostia of the pulmonary veins.16,18

Multifocal atrial tachycardia: This is characterised by electrocardiographic evidence of at least three different P-wave morphologies. It usually occurs in older patients with chronic lung disease or congestive cardiac failure, and may ultimately disorganise into atrial fibrillation.19

Inappropriate sinus tachycardia: This is an unusual clinical syndrome; it is characterised by a persistently elevated resting heart rate (> 100 beats/min) that is disproportionate to the degree of physiological and/or pathological stress. It is important to eliminate secondary causes of sinus tachycardia (eg, thyrotoxicosis, anaemia) before the diagnosis is made. Enhanced automaticity of the sinus node, excess sympathetic tone and reduced parasympathetic tone are the principal proposed mechanisms.20 Most patients who are affected by inappropriate sinus tachycardia are women, and it is particularly common in health care workers — possibly because they are more likely to self-recognise tachycardia than the general population.21 The condition is poorly understood and, after secondary causes have been excluded, patients may be misdiagnosed as having anxiety or a panic disorder. Monitoring electrocardiographic function over a 24-hour period using a Holter monitor is the most useful means of identifying inappropriate sinus tachycardia; classically, it reveals a persistently elevated sinus rate (> 100 beats/min) during the day and normalisation of the heart rate during sleep.22

Postural orthostatic tachycardia syndrome: In this syndrome an inappropriate sinus tachycardia is associated with upright posture, in the absence of postural hypotension or autonomic neuropathy.23 Symptoms overlap with those of inappropriate sinus tachycardia, and additional autonomic symptoms can occur — tremor, constipation, bladder dysfunction, feeling cold, heat intolerance, marked fatigue and exercise intolerance.24 The symptoms and the accompanying sinus tachycardia can be reproduced by tilt-table testing.22

The goal of short-term management is to terminate acute episodes of tachycardia, which can often be achieved by manoeuvres that increase vagal tone, including the Valsalva manoeuvre, application of a cold stimulus to the face and carotid sinus massage. Carotid sinus massage can also provide diagnostic information by slowing atrioventricular nodal conduction and exposing the P wave; it is performed by applying gentle pressure over one carotid sinus for 5–10 seconds during held inspiration. This manoeuvre should not be performed if there is a history of carotid artery disease or if carotid bruits are detected on examination.

If vagal stimulation is unsuccessful, recommended drugs include adenosine, and calcium antagonists such as verapamil or diltiazem.25 Adenosine is advantageous as its onset is instantaneous and it has an extremely brief duration of action. However, in rare cases it can aggravate bronchospasm, cause atypical chest discomfort or cause a sensation of impending doom. Administered by intravenous injection, a 6 mg dose of adenosine is successful in reverting SVT in 75% of patients, and a 12 mg dose is successful in more than 90% of patients.26 If adenosine therapy is unsuccessful, intravenous boluses of either verapamil or diltiazem usually terminate tachycardia,27,28 but carry the risk of potentiating hypotension and bradycardia. Intravenous verapamil is more readily available in most clinical settings than intravenous diltiazem. In adults, 5–10 mg of verapamil administered by intravenous injection over 2–3 minutes is often successful in reverting SVT. Patients given verapamil must be monitored due to the risk of bradycardia. SVT resulting in haemodynamic instability is rare but necessitates urgent direct-current cardioversion.

Long-term management is individualised based on the frequency and severity of episodes and the impact of symptoms on quality of life.29 For infrequent, self-terminating and minimally symptomatic episodes, treatment is not necessarily required; however, many patients will opt for a curative approach owing to the anxiety associated with possible recurrence of symptomatic episodes.

Definitive treatment of SVT is indicated in patients who:

• have recurrent symptomatic episodes of SVT that affect their quality of life;

• experience symptoms of SVT, and have WPW syndrome detected on ECG; and

• have infrequent episodes of SVT but are engaged in a profession or sport in which an episode of SVT could put them or others at risk (eg, pilots and divers).

Radiofrequency catheter ablation is recommended for most of these patients. It has a low risk of complications, and is curative in more than 95% of patients.30 The procedure typically takes 1–1.5 hours; it can be performed under local anaesthesia with sedation, or under general anaesthesia. Patients usually stay in hospital overnight after the procedure for cardiac monitoring and observation.