Supraventricular tachycardia

Caroline Medi, Jonathan M Kalman and Saul B Freedman
Med J Aust 2009; 190 (5): 255-260. || doi: 10.5694/j.1326-5377.2009.tb02388.x
Published online: 2 March 2009
Clinical features

Younger patients with SVT usually have structurally normal hearts, and are more than twice as likely to be female as male.3 Most females with SVT present during their childbearing years (15–50 years),4 and this has been linked to the effect of progesterone on the myocardium.5 Women with SVT are more likely to have AVNRT than men,4 whereas there is a male predominance in AVRT.6

For the three most common types of SVT, peak incidence of presentation for ablation occurs in the middle decades of life: at 36 years for AVRT, 48 years for AVNRT, and 50 years for AT.7 The proportion of SVT caused by AVRT declines progressively with age, from 60% during the first decade of life to 9% after age 70. Correspondingly, there are steady increases in the proportions of AVNRT (from 33% to 68%) and AT (from 7% to 23%). In one study, AVNRT replaced AVRT as the dominant paroxysmal SVT mechanism at age 40 in males and at age 10 in females.7 A significant proportion of patients have symptoms for a prolonged period (> 1 year) before the diagnosis of SVT is made, and occasionally episodes are misdiagnosed as anxiety or panic disorders.8 These misdiagnoses occur more frequently in women.

Evaluating the patient with SVT

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.

Mechanisms of SVT
Atrioventricular nodal re-entrant tachycardia

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).

Atrioventricular re-entrant tachycardia

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

Atrial tachycardia

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

Sinus tachycardias

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

Management of SVT
Short-term management

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

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:

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.

Pharmacological management

Long-term pharmacotherapy is generally used in patients who decline catheter ablation, and in whom the procedure carries an unacceptably high risk of atrioventricular node injury and pacemaker dependence. The goal of long-term pharmacotherapy is to reduce the frequency of episodes of SVT. In only a small minority of patients will episodes be completely abolished by antiarrhythmic drugs. Recommended drugs include atrioventricular nodal blocking drugs and antiarrhythmic drugs of Class Ic and Class III. Beta blockers and calcium-channel blockers (Class II and IV) are suitable first-line treatments when WPW syndrome is not detected on a surface ECG. Randomised studies have not demonstrated clinical superiority of any single agent, but beta blockers and calcium-channel blockers are perceived to be superior to digoxin as they provide better atrioventricular nodal blocking action during states of high sympathetic tone, such as exercise.31 Digoxin should not be used in patients with WPW syndrome, as it may facilitate rapid conduction over the accessory pathway during atrial fibrillation — potentially leading to ventricular fibrillation.32 Combining atrioventricular nodal blocking agents increases efficacy, but also increases adverse effects.33

For patients who do not respond to these drugs, or for those with WPW syndrome, alternative drugs include flecainide (Class Ic actions) and sotalol (Class II and Class III actions). Flecainide and sotalol are more effective than atrioventricular nodal blockers in terms of preventing SVT, but are associated with a small a risk of ventricular tachycardia. This risk is small in patients without structural heart disease, but it is has been reported to occur in 1%–3% of patients taking sotalol, particularly those taking higher doses.34,35 Amiodarone has no role in long-term prevention of SVT, owing to the high incidence of serious toxicities associated with its long-term use.36

Beta blockers are first-line therapy for the management of inappropriate sinus tachycardia; the dose should be titrated to balance symptom control with prevention of hypotension and bradycardia.22 Verapamil and diltiazem are alternatives for patients in whom beta blockers are contraindicated. A new agent, ivabradine, acts by blocking the sodium current responsible for spontaneous depolarisation in the sinus node (If), which results in sinus bradycardia.37 Ivabradine has no negative inotropic effects but may produce visual disturbance that is reversible on discontinuation of the drug. It is licensed for treating angina and, although there is relatively little published data on its efficacy, it may be trialled off-label in patients with inappropriate sinus tachycardia who do not respond to beta blockers and calcium-channel blockers. In patients with postural orthostatic tachycardia syndrome, increased fluid and salt intake, resistance exercises, squatting and compressive stockings may be effective.38 When non-pharmacological strategies are ineffective, beta blockers and/or fludrocortisone may be beneficial.22

1 Types of supraventricular tachycardia and their features

Atrioventricular nodal re-entrant tachycardia

Atrioventricular re-entrant tachycardia

Atrial tachycardia

Sinus tachycardias

Physiological sinus tachycardia

Inappropriate sinus tachycardia

Postural orthostatic tachycardia syndrome

Rare forms of supraventricular tachycardia

Permanent junctional reciprocating tachycardia

Junctional ectopic tachycardia

Mahaim tachycardia

  • Caroline Medi1,2
  • Jonathan M Kalman1,2
  • Saul B Freedman3,4

  • 1 Department of Cardiology, Royal Melbourne Hospital, Melbourne, VIC.
  • 2 Department of Medicine, University of Melbourne, Melbourne, VIC.
  • 3 Department of Cardiology, Concord Clinical School, Concord Hospital, Sydney, NSW.
  • 4 Vascular Biology Laboratory, ANZAC Research Institute, University of Sydney, Sydney, NSW.


Competing interests:

None identified.

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