This site is intended for health professionals only

At the heart of general practice since 1960

Read the latest issue online

CAMHS won't see you now

June 2008: Diagnosing patients with supraventricular tachycardia

What investigations should be carried out?

What are the treatment options?

Which patients should be referred?

What investigations should be carried out?

What are the treatment options?

Which patients should be referred?

The mechanisms of cardiac arrhythmias are complex and recognising these conditions can be difficult. When an arrhythmia is suspected, prompt recording of an ECG is vital, even if symptoms have subsided, as this may be useful for future reference, diagnosis and therapy.

Supraventricular tachycardias (SVTs) occur in 1% of the population.1 They often develop in childhood but tend to have clinical presentations in early adulthood. Atrioventricular nodal re-entry tachycardia (AVNRT) is the most common type of SVT, followed by atrioventricular re-entrant tachycardia (AVRT).

Extensive research and improved understanding of the basic mechanisms of these conditions has led to improvements in diagnosis and management.


AVNRT accounts for 60% of patients presenting with a narrow complex tachycardia.2 It occurs mainly in young adults, particularly women. Most of these patients have structurally normal hearts. However, some patients with AVNRT may have associated mitral valve disease, pericarditis, myocardial ischaemia or congenital heart anomalies.3

An appreciation of the electrophysiology of the AV nodal tissue is fundamental to understanding the mechanisms of AVNRT. See figure 1,attached.


AVRT is an accessory pathway-mediated tachycardia. The incidence of AVRT in the general population is 0.1-0.3% and it accounts for 30% of all SVTs.5 AVRT is twice as common in men than women and tends to present at a younger age than AVNRT.

Most patients with AVRT do not have structural heart disease. However, it is associated with Ebstein's anomaly and a higher prevalence of 0.55% has been reported in first-degree relatives of patients with accessory pathways. See figure 2, attached.5

Wolff-Parkinson-White syndrome

The most commonly described accessory pathway is that of Wolff-Parkinson-White syndrome (WPW). WPW should only be diagnosed in patients with evidence of pre-excitation and tachycardias. AVRT is the most common arrhythmia in patients with WPW and accounts for 95% of re-entry tachycardias.

Atrial fibrillation

About one-third of patients with bypass tracts such as in WPW havea propensity to develop dangerous atrial arrhythmias, including paroxysmal atrial flutter and fibrillation. Unlike the AV node, the accessory pathways have rapid nondecremental conduction and result in very rapid rates, which can degenerate into ventricular fibrillation and sudden cardiac death.4 As a result, patients with known pre-excitation syndromes who develop atrial fibrillation should not be administered AV nodal-blocking agents, as these may accelerate conduction down the accessory pathway and result in dangerous ventricular arrhythmias, see figure 3.6

Patients with WPW have around a 0.1% risk of sudden arrhythmic death.7


The unpredictable nature of SVTs can present a diagnostic challenge. It is difficult to determine when an attack will occur, how long it will persist and when it will terminate. These problems can lead to some arrhythmias going undetected or undiagnosed, particularly if symptoms have abated before an examination is performed or an ECG can be recorded.

AVNRT and AVRT are characterised by abrupt onset and termination. In the majority of cases they are well tolerated in the absence of structural heart disease. However, the possibility of a bypass tract must be considered as a mechanism of SVT as, paradoxically, treatment with AV nodal-blocking agents or digoxin can cause haemodynamic instability and potentially fatal ventricular arrhythmias.

Symptoms of AVNRT and AVRT may be indistinguishable (see table 1, attached). They include palpitations, lightheadedness and shortness of breath. Syncope occurs more commonly in patients with accessory pathways as rapid ventricular rates may cause inadequate cerebral perfusion.

The diagnosis and management of these arrhythmias is by review of 12-lead ECG and ambulatory recordings with correlation to the clinical setting. Continuous ECG recordings with Holter monitors, event recorders or implantable loop recorders can be carried out in the outpatient setting.

It often takes several episodes before the arrhythmia can be documented and, rarely, the arrhythmia may be elusive enough to escape recording.

Usually, SVTs are documented by an ECG showing the presence of a regular narrow complex tachycardia, with a heart rate of about 150-250bpm (see figure 4).

Distinguishing AVNRT from AVRT is not straightforward, although the surface ECG may provide some useful clues as to the diagnosis. Antegrade conduction in typical AVNRT is relatively slow and retrograde conduction is faster. Therefore the atria are often depolarised at the same time as the ventricles, causing the

P-wave to be partially or completely hidden in the QRS complex (see figure 4). This is a reliable sign of typical AVNRT.8

Furthermore, the arrhythmia may terminate with a retrograde P-wave, which suggests the site of termination is within the AV node. Following termination, a very brief period of asystole may occur, as the sinus node has been suppressed for the duration of the tachycardia and may take a few seconds to recover as the dominant pacemaker.

In the atypical form of AVNRT, the P-wave may be clearly visible before the QRS complex. In such cases, the usual functional circuit is reversed, with antegrade conduction down the fast pathway and retrograde conduction over the slow pathway, resulting in delayed atrial activation in relation to the QRS complex. These are often referred to as ‘fast-slow' AVNRTs (see figure 5).9

In cases of AVRT with accessory pathways, the ECG may reveal delta waves of pre-excitation or a short PR interval. However, many bypass tracts are concealed and only conduct from ventricle to atrium and evidence of pre-excitation on the surface ECG will be absent. The relationship of the P-wave to the QRS complex may aid diagnosis.

In more resistant cases, stress testing may be used as an ancillary test to reproduce the suspected transient arrhythmia. Alternatively, electrophysiology studies can be used if patients have recurrent symptoms but ECG recordings have failed to document the nature of the arrhythmia. They may also be helpful in identifying the nature of the underlying pathway and its exact anatomical location to determine the best method of treatment, map the re-entrant circuit and plan for ablation.


Initial therapy for an acute episode of a narrow complex tachycardia includes vagal manoeuvres, such as carotid sinus massage and the Valsalva manoeuvre. These can be safely performed in general practice and may increase vagal tone to terminate the tachycardia. Vagal manoeuvres should not be attempted in patients with hypotension.

If these measures are unsuccessful and the patient is symptomatic but stable, drugs can be used to terminate the tachycardia. These include calcium-channel blockers (verapamil or diltiazem), beta-blockers (atenolol, metoprolol or bisoprolol) or digoxin, providing that there is no evidence of pre-excitation on the surface ECG. Indications for referral to a cardiologist are listed in table 2, below.

41195147Patients with any evidence of haemodynamic instability or severe prolonged symptoms should be referred to the emergency department for monitoring and administration of iv bolus doses of adenosine. Short-acting beta-blockers or calcium-channel blockers may also be given. Immediate termination can also be achieved with direct current cardioversion, although this is rarely required.


Preventative therapy for AVNRT may be required in patients with frequent, prolonged or highly symptomatic episodes that do not resolve spontaneously or are difficult
to terminate. Similar drugs are used for prevention of recurrence as for acute episodes.

Radiofrequency catheter ablation of the slow pathway may be considered for some patients. Indications for ablation depend on clinical judgement and patient preference. Factors that may contribute to referral for ablation include:

• The duration and frequency of tachycardia
• Tolerance of symptoms
• Efficacy and tolerance of antiarrhythmic drugs
• The need for lifelong drug therapy
• The presence of concomitant structural heart disease.

Success rates for ablation procedures approach 95%, while drug efficacy is in the range of 30-50%.6 Catheter ablation is preferred to long-term drug therapy and may be offered as an initial therapy in cases such as athletes, pilots, drivers, people who operate dangerous machinery or women planning pregnancy. However, patients undergoing radiofrequency ablation must be advised that there is a 1% risk of AV block, requiring permanent pacemaker implantation.5,10

AVRT or pre-excitation

Patients with AVRT or pre-excitation may be more difficult to treat. Accessory pathway conduction is not affected by calcium-channel blockers or beta-blockers and digoxin is contraindicated in patients with WPW.

Patients with ECG evidence of pre-excitation or a family history of bypass tracts or sudden death should be referred to a cardiologist or electrophysiologist for further evaluation. Drugs blocking conduction in accessory pathways include class Ia (procainamide) and class Ic drugs (flecainide, propafenone). These are indicated if drug therapy becomes necessary for bypass-mediated tachycardias. In patients with WPW who develop atrial fibrillation and ventricular tachycardia cannot be excluded, the drugs of choice include amiodarone or class Ia drugs such as procainamide.

Long-term medical therapy for the prevention of recurrence usually involves combination therapy with an AV nodal-blocking agent and a class Ic (flecainide) or class III (amiodarone) drug. Class Ic drugs should be avoided if structural heart disease is present.

Unfortunately, drug therapy is poorly tolerated and can be unpredictable and variable in its response. Therefore patients with bypass tracts and symptomatic tachycardias (WPW) should undergo catheter ablation as first-line therapy, which has a success rate of 85-90%. The NASPE prospective catheter ablation registry reported an overall incidence of 1% for AV block.10 This tends to occur with attempted ablation of septal pathways as these are located close to the AV junction. These data have been confirmed by others.11,12

Patients with SVT and infrequent symptoms who do not have evidence of pre-excitation can be treated with a variety of approaches based on patient preference. These arrhythmias are rarely dangerous. Catheter ablation has sufficient efficacy and low risk to be used for symptomatic patients, either as initial therapy or for patients experiencing side-effects or arrhythmia recurrence during drug therapy.


AVNRT and AVRT are common, mostly stable cardiac arrhythmias that can be clinically difficult to distinguish. Routine ECG assessment will provide clues to the diagnosis. Simple manoeuvres can terminate these arrhythmias and patients with recurrent symptoms or more complex presentations can be referred to a specialist to help elucidate the underlying mechanisms and determine appropriate treatment.

Systems are being developed for more urgent referral of patients with sustained or compromising arrhythmias. The development of rapid access multidisciplinary arrhythmia clinics will allow access to expert opinion for initial assessment and formulation of a care plan. This should improve long-term management in primary care and reduce hospital admissions.

Diagnosing patients with supraventricular tachycardia Authors

Dr Malini Govindan
research fellow

Professor A John Camm
Professor of Clinical Cardiology, St George's Hospital, London

Key points Figure 1. Mechanism of AVNRT Figure 2. Mechanism of AVRT Table 1. Summary: diagnosis and investigation of SVTs Tab 2_referral AVNRT. Narrow complex regular tachycardia.

Q waves are buried in the end of the QRS complexes, causing a short RP interval Figure 4 Atrial fibrillation in Wolff-Parkinson-White syndrome. Broad complex atrial fibrillation with 1:1 conduction via the bypass tract and a rapid ventricular rate which subsequently degenerates to ventricular fibrillation Figure 3 Atypical AVNRT. Here the P waves actually occur at the onset of the T wave Figure 5

Rate this article 

Click to rate

  • 1 star out of 5
  • 2 stars out of 5
  • 3 stars out of 5
  • 4 stars out of 5
  • 5 stars out of 5

0 out of 5 stars

Have your say