Supraventricular tachycardia: AVNRT and AVRT

Overview and definitions

Start with the words the 2019 ESC guideline uses. SVT literally indicates tachycardia (atrial rates above 100 b.p.m. at rest) whose mechanism involves tissue from the His bundle or above.^[1] Traditionally the term covered all tachycardias apart from VT and AF, so it has included AV re-entry over an accessory connection, which is not, in essence, a supraventricular rhythm.^[1]

A narrow QRS tachycardia has a QRS duration of 120 ms or less; a wide QRS tachycardia has a QRS duration above 120 ms.^[1] SVT may present as either, and most, although not invariably, are regular rhythms.^[1] The SVT guideline does not cover AF, which has its own guidelines.^[1]

Classification

ESC Table 5 sorts SVT into three groups; the table below is abridged.^[1]

^{[1] [1]}

Focal AT is an organised atrial rhythm of 100 b.p.m. or more, initiated from a discrete origin and spreading over both atria in a centrifugal pattern.^[1] Multifocal AT is a rapid, irregular rhythm with at least three distinct P-wave morphologies on the surface ECG.^[1]

Epidemiology and risk factors

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Persons aged 65 years or more have more than five times the risk of developing SVT than younger individuals.^[1] Compared with patients who have cardiovascular disease, those with lone paroxysmal SVT are younger, have a faster SVT rate and an earlier onset of symptoms, and are more likely to have their condition first documented in the emergency department.^[1]

Among patients referred for catheter ablation in specialised centres, AVNRT is the most frequently treated substrate after AF, followed by atrial flutter and AVRT.^[1] Women are more likely than men to be affected by AVNRT (ratio about 70:30), while the converse is true for AVRT (ratio 45:55).^[1] The proportion of patients with AVRT decreases with age, whereas the proportions with AVNRT and AT increase with age.^[1]

The prevalence of the WPW pattern rises to 0.55% among first-degree relatives of affected patients.^[1] Not all of these people develop SVT, and intermittent pre-excitation is not rare.^[1] Compared with the rest of the population, people with pre-excitation are generally younger, predominantly male and have less comorbidity.^[1]

In a paediatric cohort of 1 967 911 live births between 2000 and 2008, 2021 patients (51.6% male, overall incidence 1.03/1000) had SVT, and WPW syndrome accounted for 16.2%. By the age of 15 years, the annual risk of sudden death was 0.01% per patient-year.^[1] A relationship with the monthly cycle has been suggested, and episodes are more frequent during pregnancy in women with pre-existing SVT.^[1]

Pathophysiology

Re-entry over an accessory pathway: AVRT

AVRT uses an anatomically defined circuit with two limbs: the AV node–His–Purkinje system and an AP, also called the bypass tract.^[1] The two limbs differ in refractoriness and conduction time, and critically timed premature atrial or ventricular beats initiate re-entry.^[1]

APs are single or multiple strands of myocardial cells that bypass the normal conduction system and directly connect atrial and ventricular myocardium. They result from incomplete embryological development of the AV annuli, without complete separation of the atria and ventricles.^[1] About 60% lie along the mitral valve (left free wall APs), 25% insert along the septal aspect of the mitral or tricuspid annulus, and about 15% insert along the right free wall.^[1] APs that conduct only antegradely are uncommon (10% or less), whereas those that conduct only retrogradely are more frequent (up to 50%).^[1] Multiple APs occur in up to 12% of patients with pre-excitation and in up to 50% of patients with Ebstein’s anomaly.^[1]

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An AP can also be a bystander: with focal AT, atrial flutter, AF or AVNRT, the QRS complexes can be pre-excited even though the AP is not a critical part of the circuit.^[1]

Re-entry in the AV node: AVNRT

AVNRT is re-entry in the area of the AV node, but the exact circuit remains elusive; the ESC lists it as a gap in the evidence.^[1] There is considerable histological and electrophysiological evidence that the right and left inferior extensions of the human AV node, and the atrionodal inputs they facilitate, may provide the anatomical substrate for the slow pathway.^[1] Onset of AVNRT seems to be bimodal: many patients have attacks early in life, but in a substantial proportion AVNRT starts later, for example in the fourth or fifth decade.^[1]

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Why vagal manoeuvres and adenosine work

Vagal manoeuvres include different techniques that stimulate the receptors in the internal carotid arteries. The stimulation causes reflex vagal stimulation and acetylcholine release, which may in turn slow conduction through the AV node and slow the heart rate.^[1] Adenosine acts through cardiac adenosine A1 receptors. Electrophysiology studies show progressive dose-related prolongation of AV conduction (an effect on the AH interval, none on the HV interval), culminating in transient AV block that terminates the tachycardia.^[1]

Vagal manoeuvres and adenosine may help in clinical diagnosis, particularly when the ECG during tachycardia is unclear.^[1] ESC 2019 lists four possible responses of a narrow QRS tachycardia to vagal manoeuvres and adenosine:^[1]

1. Slowing of AV nodal conduction with intermittent AV block, which can unmask dissociated P waves (focal AT, atrial flutter or AF waves).^[1]
2. A temporary decrease in the atrial rate of automatic tachycardias (focal AT, sinus tachycardia and JET).^[1]
3. Termination can occur in AVNRT and AVRT by acting on the AV node that is part of the circuit; more rarely, sinus nodal re-entry and ATs due to triggered activity can slow down and terminate.^[1]
4. No effect in some cases.^[1]

In the same section on vagal manoeuvres and adenosine, ESC 2019 notes that termination with a P wave after the last QRS complex is very unlikely in AT and most common in AVRT and typical AVNRT.^[1] Termination with a QRS complex is often seen in AT, and possibly in atypical AVNRT.^[1] Adenosine does not interrupt macro-re-entrant ATs, and fascicular VTs are verapamil-sensitive but not adenosine-sensitive.^[1]

Clinical presentation

SVT may cause palpitations, fatigue, light-headedness, chest discomfort, dyspnoea and altered consciousness.^[1] Rapid rhythms are more likely than less-rapid ones to present acutely with a clear history, but SVT usually produces symptoms.^[1]

The story carries diagnostic weight. A sudden onset more likely points to AVNRT or AVRT, although AT may also present this way.^[1] Re-entrant tachycardias tend to last longer than AT episodes, which may occur as a series of repetitive runs.^[1] Onset in the teenage years or younger makes AT or AF continuing into adulthood less likely, and such a long history points towards a re-entrant mechanism.^[1] Clear descriptions of pounding in the neck (the frog sign) or shirt flapping point to the possible competing influences of atrial and ventricular contraction on the tricuspid valve, and to AVNRT as a likely cause.^[1]

Presyncope and syncope are less common and tend to be associated with presentation in older individuals.^[1] In older patients symptoms may be more extreme, with dizziness, presyncope and syncope, in view of the less-accommodating circulation; drops in blood pressure are usually immediate and tend to recover.^[1] Dyspnoea, or other symptoms and signs of heart failure, can occur when the patient has developed tachycardiomyopathy (TCM).^[1] A description of polyuria, possibly from atrial stretch-induced atrial natriuretic peptide activity, can be elicited in some patients, although this is infrequent.^[1]

Direct risks from SVT are unusual, but in specific situations, for example WPW syndrome with AF or after an atrial switch operation, it may lead to sudden cardiac death.^[1]

Clinical assessment and investigations

Initial evaluation points to a re-entrant arrhythmia when onset and termination are sudden, often associated with a change of position, and the tachycardia is perceived as regular.^[1] Ask what stops it: standard vagal manoeuvres, abortive measures such as drinking a glass of iced water, and responses to drugs such as adenosine or verapamil, where termination was observed but ECGs are missing, may all help the diagnosis.^[1]

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• An ECG recorded during tachycardia is ideal, and patients should be encouraged to seek medical help and an ECG during episodes.^[1]
• A 12-lead resting ECG and a baseline echocardiogram are necessary.^[1]
• 24 h ECG recordings may be useful, but episodes are usually sporadic and may not be frequent enough to record on ambulatory monitoring; transtelephonic monitoring, mobile recording devices or, very rarely, an implantable loop recorder may be required.^[1]
• Wrist-worn, optically based heart rate monitors are user-friendly, but validation of the device used is imperative.^[1]
• An exercise test may also be useful in apparent pre-excitation and in catecholamine-dependent arrhythmias.^[1]
• An EPS is usually necessary to establish the diagnosis, particularly when catheter ablation is anticipated.^[1]

Reading the narrow QRS tachycardia ECG

Narrow QRS complexes are due to rapid ventricular activation through the His–Purkinje system, which suggests that the origin is above or within the His bundle. High septal VT can, however, also give relatively narrow QRS complexes (110–140 ms).^[1]

• Sinus rhythm ECG. In a patient with a history of regular paroxysmal palpitations, pre-excitation is generally suggestive of AVRT. Its absence does not rule AVRT out: the AP may be concealed (retrograde conduction only) or an atypical (Mahaim) pathway that is latent in sinus rhythm.^[1]
• Onset. Sudden PR prolongation after an atrial ectopic beat occurs in typical AVNRT. Automatic focal ATs show gradual acceleration (warm-up) and deceleration (cool-down).^[1]
• Regularity. Re-entrant tachycardias are usually regular. Cycle-length alternans can be seen in AVNRT but stays under 15% of the cycle length; irregularity beyond 15% makes a focal arrhythmia much more likely.^[1]
• VA interval. A fixed ventriculoatrial (VA) interval with variable RR intervals excludes AT.^[1]
• RP interval. Short-RP SVTs have an RP shorter than half the tachycardia RR interval; long-RP SVTs show RP equal to or longer than PR.^[1]
• Cut-offs. At EPS a very short VA interval (70 ms or less) usually indicates typical AVNRT, or less commonly focal AT, and has been reported in AVRT. On the surface ECG a 90 ms cut-off can be used if P waves are visible, but data on actual RP measurements are scarce.^[1]
• P-wave shape. P waves like those in sinus rhythm suggest sinus tachycardia (appropriate or inappropriate), sinus nodal re-entry or focal AT close to the sinus node. P waves different from sinus rhythm, conducted with a PR interval equal to or longer than in sinus rhythm, are typically seen in focal AT.^[1]
• Rate about 150 b.p.m. Consider atrial flutter with 2:1 conduction, because atrial activity in flutter is usually 250–330 b.p.m.^[1]
• Pseudo r and pseudo S. When delayed retrograde conduction lets you identify retrograde P waves, a pseudo r deflection in V1 and a pseudo S wave in the inferior leads are more common in typical AVNRT than in AVRT or AT. They are specific (91–100%) but modestly sensitive (58% and 14%). However, in all the referenced studies, cases of AT or atypical AVNRT were limited or entirely absent.^[1]
• Other AVNRT pointers. An RP difference between V1 and III above 20 ms favours AVNRT over AVRT due to a posteroseptal pathway; a QRS notch in aVL suggests AVNRT; and a pseudo r in aVR is more sensitive and specific than a pseudo r in V1 for typical AVNRT. The same limitation applies: cases of AT or atypical AVNRT were limited or entirely absent in all the referenced studies.^[1]
• AV block or dissociation. It is not often seen during narrow QRS tachycardia, but it rules out AVRT, because both atria and ventricles are parts of that circuit.^[1]
• Bundle branch block. BBB developing during SVT may also help diagnose AVRT: BBB on the same side as the AP can prolong the cycle length through VA prolongation.^[1]

Differential diagnosis

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ESC Table 6 also notes that occasionally, AF with a very fast ventricular response may resemble a regular narrow QRS tachycardia.^[1] Pre-excited AF shows irregularity, a varying QRS morphology and a rapid ventricular rate.^[1]

Management: the acute episode

The initial approach tends to be non-drug-based, with escalation to intravenous (IV) drugs or electrical cardioversion if the tachycardia is not corrected early.^[1] Immediate DC cardioversion is the first choice in haemodynamically compromised patients with narrow QRS tachycardia.^[1]

Narrow QRS tachycardia without an established diagnosis

^[1]

Table footnotes: IV beta-blockers are contraindicated in decompensated heart failure, and IV verapamil and diltiazem are contraindicated in hypotension or heart failure with reduced ejection fraction (HFrEF).^[1]

^{[1] [3]}

Vagal manoeuvres

Conventional vagal manoeuvres, when correctly performed, terminate SVT in a reported 19–54%.^[1] Many can be performed with minimal risk at the bedside or in an office setting, and they can be both diagnostic and therapeutic.^[1] The ESC calls the Valsalva manoeuvre safe and an internationally recommended first-line emergency treatment for SVT, although a Cochrane review found insufficient evidence to support or refute its utility.^[1] It has generally been most effective in adults, and in AVRT rather than AVNRT.^[1]

The modified Valsalva manoeuvre considerably improves conversion (43% vs 17%): the strain is done semi-recumbent, followed by supine repositioning and passive leg raise after the strain.^[1] Blowing into a 10 mL syringe with enough force to move the plunger may standardise the strain.^[1]

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Carotid sinus massage is done with the neck extended and the head turned away from the side of pressure. It should always be unilateral, because there is a potential risk with bilateral pressure, and limited to 5 s, with the patient monitored. It should be avoided after a previous transient ischaemic attack or stroke and in patients with carotid bruits.^[1] Other manoeuvres, such as facial immersion in cold water or forceful coughing, are rarely used now.^[1]

Adenosine

In haemodynamically stable narrow QRS tachycardia, ESC 2019 calls adenosine (6–18 mg IV bolus) the first drug of choice; its recommendation row applies if vagal manoeuvres fail.^[1] The mean dose required for termination is about 6 mg.^[1]

^[1]

Adenosine has a very short half-life: it is deaminated to inactive inosine within seconds, and end-organ effects are complete within 20–30 s, so repeat administration is safe within 1 min of the last dose.^[1] The dose range between patients may be very wide, and more than 90% success is generally expected. Dipyridamole and theophylline may on occasion affect dose requirements, but any influence of recent caffeinated drinks is disputed.^[1]

• Dyspnoea, flushing and chest pain. Transient dyspnoea is common and is more likely to result from stimulation of pulmonary vagal C fibres. Facial flushing may occur. Chest pain has been associated with increased coronary sinus blood flow, so may well be of cardiac origin.^[1]
• Sinus node. Depression of sinoatrial node function is expected, but prolonged bradycardia is unusual; approach adenosine cautiously in known sinus node disease.^[1]
• Heart transplant. Perceived bradycardia risk in denervated heart transplant recipients, in whom SVT is common, prompted a relative contraindication, but more recent substantive evidence supports adenosine use in this group with no particular cautions.^[1]
• Suspected atrial flutter with 2:1 block. Adenosine may increase the degree of AV block and reveal the flutter pattern, but it can produce a rebound increase in AV conduction to 1:1 and may also precipitate AF, so it should only be used if deemed necessary for diagnosis and with resuscitation equipment available.^[1]
• AF. AF may follow adenosine, and appears more commonly associated with AVRT than AVNRT. Adenosine may also occasionally cause or accelerate pre-excited atrial arrhythmias.^[1]
• Asthma. Clinically important bronchoconstriction after IV adenosine for SVT has rarely been reported. Isolated well-documented reports suggest care in asthma: adenosine can be used cautiously, although verapamil may be a more appropriate choice in severe asthma.^[1]

Calcium channel blockers and beta-blockers

In haemodynamically stable narrow QRS tachycardia, IV verapamil or diltiazem and IV beta-blockers (e.g. esmolol, metoprolol) are of value, particularly in patients with frequent atrial or ventricular premature beats.^[1] Verapamil and diltiazem should be avoided in patients with haemodynamic instability, HF with reduced LV ejection fraction (under 40%), a suspicion of VT, or pre-excited AF.^[1] Evidence that beta-blockers terminate SVT is limited, but they have an excellent safety profile in haemodynamically stable patients. They are contraindicated in decompensated HF, and caution is needed when IV calcium channel blockers and beta-blockers are combined, because hypotensive and bradycardic effects may be potentiated.^[1]

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Intranasal etripamil

In the first trial of etripamil, a short-acting L-type calcium channel blocker with rapid onset after intranasal administration, conversion of SVT to sinus rhythm ranged from 65% to 95% (ESC 2019).^[1]

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Wide QRS tachycardia without an established diagnosis

^[1]

Haemodynamic instability may occur with any wide QRS tachycardia, regardless of the cause, but is more likely with VT. Synchronised cardioversion is recommended for any persistent wide QRS tachycardia causing hypotension, acutely altered mental status, chest pain, acute HF symptoms or signs of shock.^[1] In a haemodynamically stable patient with wide QRS tachycardia, SVT with aberrancy, if definitively identified, may be treated like narrow complex SVT, with vagal manoeuvres or drugs (adenosine and other AV nodal blocking agents such as beta-blockers or calcium channel blockers).^[1]

Some drugs used for SVT, such as verapamil, can cause severe haemodynamic deterioration in a patient with previously stable VT, so they should be used only when the diagnosis of SVT is fully established and secure.^[1] Adenosine may help by allowing a diagnosis or interrupting an adenosine-sensitive VT, but it must be avoided if pre-excitation on the resting ECG suggests a pre-excited tachycardia: in antidromic re-entry, adenosine may precipitate cardiac arrest if it induces AF, as may occasionally occur.^[1] In the PROCAMIO trial, in well-tolerated wide QRS tachycardia with or without reduced LV ejection fraction, procainamide was associated with fewer major cardiac adverse events and more terminations within 40 min than amiodarone.^[1] If the mechanism is not fully understood, treat the arrhythmia as VT.^[1]

Irregular tachycardia

A wide QRS irregular tachycardia is usually AF. Rarely, polymorphic VT and, very rarely, monomorphic VT may also present as irregular tachycardias. Electrical cardioversion is the acute treatment of choice for irregular pre-excited tachycardias with haemodynamic instability.^[1]

Specific types: diagnosis and treatment

AVNRT

AVNRT is typically a narrow complex tachycardia (QRS under 120 ms) unless there is aberrant conduction, usually of right bundle branch block (RBBB) type, or a previous conduction defect.^[1] AV dissociation is exceptionally uncommon but can occur, because neither the atria nor the ventricles are necessary for the circuit; coexisting AF or AV block is possible but rare.^[1]

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Specific, although modestly sensitive, ECG criteria for AVNRT rather than AT or AVRT are a pseudo R deflection in V1, a pseudo S wave in the inferior leads, a notch in aVL and a pseudo R in aVR.^[1]

^[1]

Table footnotes: IV verapamil and diltiazem are contraindicated in hypotension or HFrEF; IV beta-blockers are contraindicated in decompensated heart failure.^[1]

Most data on vagal manoeuvres and adenosine come from mixed SVT populations, but they seem less successful in AVNRT than in AVRT.^[1] A single oral dose of diltiazem 120 mg plus a beta-blocker (propranolol 80 mg) may convert up to 94% of patients, with a risk of hypotension, transient AV block or, rarely, syncope. Caution is needed in the elderly and in known sinus or AV nodal conduction disturbance.^[1] A single oral dose of flecainide (3 mg/kg) may also be effective, albeit at a lower rate, and intranasal etripamil is described as promising.^[1]

Why ablate? A randomised trial of first-line catheter ablation against antiarrhythmic drugs showed significant benefits in arrhythmia-related hospitalisations. Catheter ablation is the current treatment of choice for symptomatic patients because it substantially improves quality of life and reduces costs.^[1] Slow-pathway modification works in both typical and atypical AVNRT, usually with a combined anatomical and mapping approach and lesions at the inferior part of the triangle of Koch, from the right or the left septal side.^[1]

^[1]

• In experienced centres, typical and atypical AVNRT can be ablated with almost no risk of AV block by targeting the inferior nodal extension and avoiding the mid-septum and the roof of the coronary sinus.^[1]
• Recurrences are usually seen within 3 months in symptomatic patients with frequent episodes, but in the young (aged 18 years or under) they may appear as long as 5 years after ablation.^[1]
• Advanced age is not a contraindication. Pre-existing first-degree heart block carries a higher risk of late AV block, and avoidance of extensive slow-pathway ablation is preferable under such conditions.^[1]
• There is almost no procedure-related mortality.^[1]
• Cryoablation may carry a lower risk of AV block but a significantly higher recurrence rate; its safety profile and higher long-term success in younger patients make it especially attractive for children.^[1]
• AVNRT can cause inappropriate shocks in patients with implantable cardioverter defibrillators (ICDs); with frequent episodes, catheter ablation is clearly indicated.^[1]

Not everyone needs treatment. Patients with minimal symptoms and short-lived, infrequent episodes can be followed up without ablation or long-term drugs, and about half of them may become asymptomatic within 13 years.^[1] Chronic antiarrhythmic drugs decrease the frequency and duration of AVNRT, but have a variable success rate in abolishing episodes (13–82%), and up to 20% of patients may discontinue therapy. In view of the excellent success rate and minimal risk of ablation in symptomatic cases, the value of long-term antiarrhythmic drugs seems very limited.^[1] AVNRT may result in AF, which is usually, although not invariably, eliminated by catheter ablation of the AVNRT.^[1]

AVRT and the WPW syndrome

^[1]

Table footnotes: IV verapamil and diltiazem are contraindicated in hypotension or HFrEF, and IV beta-blockers in decompensated heart failure. IV ibutilide is contraindicated with a prolonged QTc. IV procainamide prolongs the QTc, but much less than class III agents. IV flecainide and propafenone are contraindicated in ischaemic or structural heart disease and also prolong the QTc, but much less than class III agents. IV amiodarone prolongs the QTc, but torsades de pointes is rare.^[1]

Adenosine should be used with caution in AVRT because of the potential induction of fast AF, and AF with fast ventricular conduction could induce ventricular fibrillation; electrical cardioversion should always be available.^[1] During orthodromic and antidromic AVRT, drug therapy could be directed at the AV node (beta-blockers, diltiazem, verapamil or etripamil) or at the AP (ibutilide, procainamide, propafenone or flecainide).^[1] Antidromic AVRT is associated with malignant WPW syndrome due to a very fast-conducting AP, and drugs acting mainly on the AP should be preferred.^[1]

Catheter ablation is the treatment of choice for symptomatic and recurrent AVRT or pre-excited AF. For patients with asymptomatic and infrequent episodes, the risks and benefits of ablation should be balanced against long-term commitment to drug therapy.^[1] AP ablation has a high acute success rate and a low complication rate that depends on pathway location. Major complications include cardiac tamponade (0.13–1.1%) and complete AV block (0.17–2.7%) in patients in whom ablation of septal APs is attempted.^[1] With septal pathways, cryoenergy gives less AV block than radiofrequency energy, but recurrence of previously blocked pathways has been reported to be significantly higher.^[1]

When ablation is not desirable or feasible in pre-excitation with symptomatic antidromic AVRT, and structural or ischaemic heart disease has been excluded, class IC drugs act mainly on the AP and can be used.^[1] In pre-excited AF, take care not to transform AF into atrial flutter with 1:1 conduction.^[1] Apart from class IC drugs, beta-blockers, diltiazem or verapamil may also be considered for orthodromic tachycardias if no signs of pre-excitation are observed on the resting ECG.^[1]

Concealed pathways, PJRT and atypical pathways

• Concealed APs give rise only to orthodromic AVRT and are not detectable on the resting ECG. They are not associated with an increased risk of sudden cardiac death.^[1]
• PJRT is a long-RP tachycardia due to the slow conduction properties of the AP, with deeply inverted retrograde P waves in II, III and aVF. Its incessant nature may cause TCM, which usually resolves after successful radiofrequency catheter ablation, particularly in younger patients.^[1]
• Atypical APs (Mahaim fibres) connect the right atrium or AV node to the right ventricle, into or close to the right bundle branch.^[1]

Pre-excited atrial fibrillation

Paroxysmal AF has been found in 50% of patients with WPW and may be the presenting arrhythmia. These patients are typically young and have no structural heart disease.^[1] AF with a fast ventricular response over an overt AP with a short anterograde refractory period is a potentially life-threatening arrhythmia in WPW syndrome, because of potential degeneration into VF.^[1]

^[1]

Table footnotes: IV ibutilide is contraindicated with a prolonged QTc. IV procainamide prolongs the QTc, but much less than class III agents. IV flecainide and propafenone are contraindicated in ischaemic or structural heart disease and also prolong the QTc, but much less than class III agents.^[1]

Ibutilide can achieve pharmacological cardioversion of pre-excited AF or delayed AP conduction. Drugs such as procainamide, propafenone or flecainide, which affect conduction over the AP, may also be used even if they may not restore sinus rhythm, but class Ic drugs should be used with caution because they also act on the AV node.^[1]

Asymptomatic pre-excitation

Most people with an asymptomatic WPW pattern go through life without any clinical event related to the pre-excitation. About one in five will develop an AP-related arrhythmia during follow-up.^[1] In WPW syndrome the commonest arrhythmia is AVRT (80%), followed by a 20–30% incidence of AF.^[1] The most feared manifestation is sudden cardiac death from pre-excited AF conducting rapidly over the AP and degenerating into ventricular fibrillation.^[1] The risk of cardiac arrest or ventricular fibrillation has been estimated at 2.4 per 1000 person-years (95% CI 1.3–3.9), but no deaths were reported in a registry of 2169 patients over 8 years.^[1] In a Danish registry of 310 people with pre-excitation (aged 8–85 years), there was a greater risk of AF and HF, driven by a right anteroseptal AP, and a significantly higher risk of death in those aged over 65 years.^[1]

Non-invasive markers are imperfect. Abrupt and complete normalisation of the PR interval with loss of the delta wave during exercise testing, or after procainamide, propafenone or disopyramide, has been considered a marker of low risk.^[1] Catecholamine sensitivity is a major limiting factor of all tests, both invasive and non-invasive, including exercise testing.^[1] Intermittent loss of pre-excitation on a resting ECG or ambulatory monitoring has been associated with APs with longer ERPs and accepted as a credible risk-stratification tool.^[1] However, recent studies including both symptomatic and asymptomatic patients indicate that more than one-fifth of patients with intermittent pre-excitation have AP ERPs under 250 ms, so it is now recognised as an imperfect marker of a low-risk AP.^[1]

One prospective RCT randomised 37 patients with asymptomatic pre-excitation to catheter ablation and 35 to follow-up without treatment: ablation reduced arrhythmic events (7% vs 77%, P under 0.001) over 5 years, and one control patient had cardioverted ventricular fibrillation.^[1]

^[1]

The ESC states that the proper management of asymptomatic pre-excitation and strict catheter ablation indications have not been established.^[1] Its key messages add that non-invasive screening may be used for risk stratification, but its predictive ability remains modest.^[1]

Focal atrial tachycardia

In asymptomatic young people (under 50 years), the reported prevalence of focal AT is as low as 0.34%, rising to 0.46% in symptomatic arrhythmia patients.^[1] Symptoms may include palpitations, shortness of breath, chest pain and, rarely, syncope or presyncope.^[1]

Identifying the P wave on a 12-lead ECG during tachycardia is critical; depending on AV conduction and AT rate, P waves may be hidden in the QRS or T waves.^[1] A discrete P wave with an intervening isoelectric interval suggests focal AT, and adenosine can help by slowing the ventricular rate or, less frequently, terminating focal AT.^[1]

^[1]

Table footnotes: IV verapamil and diltiazem are contraindicated in hypotension or HFrEF, and IV beta-blockers in decompensated heart failure. IV ibutilide is contraindicated with a prolonged QTc. IV flecainide and propafenone are contraindicated in ischaemic or structural heart disease and also prolong the QTc, but much less than class III agents. IV amiodarone prolongs the QTc, but torsades de pointes is rare.^[1]

Hard data to guide acute drug choice in focal AT are scarce. Acute therapy may start with beta-blockers or calcium channel blockers, which may terminate focal AT or slow the ventricular rate.^[1] IV adenosine may terminate AT (delayed after-depolarisation-triggered AT), but the tachycardia may also continue with AV block.^[1] DC cardioversion usually terminates the tachycardia acutely, but in incessant focal AT due to enhanced automaticity the arrhythmia reinitiates and repeated cardioversion is unlikely to be appropriate.^[1] Catheter ablation is the treatment of choice for recurrent focal AT, especially incessant AT causing TCM, with a reported success rate of 75–100%.^[1]

Tachycardiomyopathy

Tachycardia-induced cardiomyopathy (TCM), or more accurately arrhythmia-induced cardiomyopathy, is a reversible cause of impaired LV function due to persistent tachycardia or very frequent ventricular premature beats that can lead to HF and death.^[1]

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Complications and pitfalls

• Verapamil in a wide QRS tachycardia. It can cause severe haemodynamic deterioration in patients with previously stable VT, so it should only be used when the diagnosis of SVT is fully established and secure; in haemodynamically stable patients, it is not recommended in wide QRS tachycardia of unknown aetiology (Class III, level B).^[1]
• AV nodal blockers in pre-excited AF. In the acute setting any AV nodal modulating agent should be avoided, because it may contribute to a risk of ventricular fibrillation; the ESC AVRT recommendations (chronic therapy) also list digoxin, beta-blockers, diltiazem, verapamil and amiodarone as not recommended and potentially harmful in patients with pre-excited AF (Class III, level B).^[1]
• Adenosine and pre-excitation. Adenosine may occasionally cause or accelerate pre-excited atrial arrhythmias.^[1]
• Class IC drugs. Do not use flecainide or propafenone in patients with left bundle branch block (LBBB), or ischaemic or structural heart disease (ESC key message).^[1]
• Sotalol. The ESC key messages say: do not use sotalol in patients with SVT.^[1]
• Calcium channel blocker plus beta-blocker. Caution is needed when combining them IV, because hypotensive and bradycardic effects may be potentiated.^[1]
• Carotid sinus massage. Avoid it after a previous transient ischaemic attack or stroke and in patients with carotid bruits; it should always be unilateral, because there is a potential risk with bilateral pressure.^[1]
• Ablation complications. AVNRT ablation has been associated with a risk of AV block under 1% in previous reports. For AP ablation, major complications include cardiac tamponade (0.13–1.1%) and complete AV block (0.17–2.7%) in patients in whom ablation of septal APs is attempted.^[1]

Prognosis and disposition

Direct risks from SVT are unusual, although in specific situations it may lead to sudden cardiac death, and concealed pathways are not associated with an increased risk of sudden cardiac death.^[1] About half of patients with minimal symptoms and short-lived, infrequent AVNRT may become asymptomatic within 13 years.^[1] Patient-reported outcome measures show significant improvements in quality of life after ablation.^[1]

In all re-entrant and most focal arrhythmias, the ESC key messages say catheter ablation should be offered as an initial choice, after explaining the potential risks and benefits in detail.^[1] Women are more often prescribed antiarrhythmic drugs before ablation than men, and recurrence after AVNRT ablation is higher in young women.^[1]

Special populations

Pregnancy (2025 ESC pregnancy guideline)

Pregnancy recommendations here come from the 2025 ESC guideline for cardiovascular disease and pregnancy. New-onset narrow QRS tachycardias in pregnancy are treated according to haemodynamic stability. In all cases of haemodynamic instability caused by any SVT, including AF and atrial flutter, synchronised DC cardioversion is indicated, and the fetal heart rate should be closely monitored afterwards.^[2] Electrical cardioversion is safe and effective in all phases of pregnancy, and shock energies should be the same as in non-pregnant patients.^[2]

In haemodynamically stable narrow QRS tachycardia, vagal manoeuvres (modified Valsalva, carotid sinus massage) may terminate AV(N)RT; if they fail, IV adenosine (6–18 mg bolus) is recommended for termination of AV(N)RT.^[2] IV beta-1-selective blockers (preferably metoprolol) can be given for all SVTs to terminate the SVT or slow AV conduction and the ventricular rate. In the pregnancy guideline’s Figure 14 (management of narrow QRS tachycardia in pregnant women), atenolol is contraindicated, IV metoprolol is 2.5–15 mg and IV verapamil is a 2.5–10 mg bolus over 5 min.^[2]

^[2]

In women with pre-existing SVT (AVNRT, AVRT or focal AT), chronic oral prophylaxis can be achieved with beta-blockers (metoprolol) or verapamil; for drug-refractory SVT or contraindications to these drugs, flecainide or sotalol are reasonable alternatives, as is propafenone if flecainide is not available.^[2] In pregnant women with pre-existing AVRT and WPW syndrome, oral flecainide, or propafenone when flecainide is not available, can prevent episodes. When AV nodal blocking agents are used in WPW syndrome and AF occurs, the risk of rapid ventricular rates is increased; however, in women without documented AF, with known orthodromic AVRT and intermittent pre-excitation, long-term AV blockade is acceptable for prevention.^[2] When performing catheter ablation during pregnancy, the use of non-fluoroscopic mapping and navigation systems should be considered (2025 ESC pregnancy, Recommendation Table 15, Class IIa, level C).^[2]

Catheter ablation in pregnant women should preferably be performed after the first trimester in a centre with experience in non-fluoroscopic electro-anatomical mapping and catheter navigation systems.^[2] It may be considered for drug-refractory and poorly tolerated VT, or for recurrent drug-refractory AVNRT, AVRT, focal AT, cavotricuspid isthmus-dependent atrial flutter and certain benign right-sided VTs, to avoid potentially harmful antiarrhythmic drug effects during pregnancy; it has no role in AF.^[2]

Older adults

Older patients may have more extreme symptoms, including presyncope and syncope.^[1] Advanced age is not a contraindication for slow-pathway ablation, but the oral diltiazem plus propranolol single dose needs caution in the elderly.^[1]

Children and young people

In the paediatric cohort above, the annual risk of sudden death by age 15 was 0.01% per patient-year.^[1] After AVNRT ablation, recurrences in the young (18 years or under) may appear as long as 5 years later.^[1] Cryoablation may carry a lower risk of AV block but is associated with a significantly higher recurrence rate; its favourable safety profile and higher long-term success rate in younger patients make it especially attractive for children.^[1]

Adult congenital heart disease, transplant, asthma and devices

• Adult congenital heart disease. AVNRT ablation has lower success (82%) and a higher heart block risk (14%) in adult congenital heart disease. Multiple APs occur in up to 50% of patients with Ebstein’s anomaly.^[1]
• Heart transplant. More recent substantive evidence supports adenosine use in denervated heart transplant recipients with no particular cautions.^[1]
• Asthma. Adenosine can be used cautiously; verapamil may be more appropriate in severe asthma.^[1]
• ICD patients. AVNRT can cause inappropriate shocks; with frequent episodes, catheter ablation is clearly indicated.^[1]
• Athletes and high-risk occupations. EPS with isoprenaline is recommended to risk-stratify asymptomatic pre-excitation in competitive athletes and in people with high-risk occupations or hobbies (Class I, level B). Atypical AVNRT has a higher documented incidence in athletes.^[1]

Evidence, guidelines and regional differences

This page uses the 2019 ESC SVT guideline (Eur Heart J 2020) as corrected by its published corrigendum, and the 2025 ESC pregnancy guideline as corrected by its published correction. The SVT corrigendum added “preferably in the supine position with leg elevation” to the vagal manoeuvre row for wide QRS tachycardia.^[7] It also added “ischaemic or” to a row in the 2019 SVT guideline’s own pregnancy recommendations (section 14.1), which now reads: flecainide or propafenone in patients without ischaemic or structural heart disease should be considered if AV nodal blocking agents fail to prevent SVT. This page uses the 2025 pregnancy rows instead.^[1][7] The pregnancy correction changed the Figure 15 (atrial fibrillation and atrial flutter) legend to read verapamil 2.5–10 mg.^[8]

The 2015 ACC/AHA/HRS SVT guideline appears here only through the ESC text, which notes that it reported major complication rates after radiofrequency ablation of 3.0% for AVNRT and 2.8% for AVRT.^[1] The ESC says these rates are much higher than those reported by experienced electrophysiologists in the current era, but the procedure still carries a very small, non-negligible mortality risk.^[1]

The trials and the review summarised above are REVERT for the modified Valsalva manoeuvre, the Cochrane systematic review of adenosine vs calcium channel antagonists (searches in July 2017), and RAPID for etripamil.^[4][5][6] In RAPID, 184 of 692 randomly assigned patients self-administered etripamil or placebo for a confirmed AV-nodal-dependent episode between October 2020 and July 2022.^[5]

In Australia and New Zealand

The Australian and New Zealand Committee on Resuscitation (ANZCOR) Guideline 11.9, Managing Acute Dysrhythmias, part of the adult advanced life support guidelines, gives the following acute approach for adults.^[3]

• Adverse features that suggest a need for immediate treatment: systolic BP under 90 mmHg, heart rate over 150/min, chest pain, heart failure, or drowsiness or confusion.^[3]

Under its heading for regular narrow-complex tachycardia, ANZCOR gives the following.^[3]

• Regular narrow-complex tachycardias include sinus tachycardia, AVNRT (the commonest type of SVT), AVRT (caused by WPW syndrome) and atrial flutter with regular AV conduction (usually 2:1).^[3]
• If the patient is unstable with adverse signs caused by the arrhythmia (other than sinus tachycardia), attempt synchronised electrical cardioversion, with sedation as required.^[3]
• It is reasonable to give adenosine to an unstable patient with a regular narrow-complex tachycardia while cardioversion is prepared, but do not delay cardioversion if adenosine fails to restore sinus rhythm.^[3]
• For a regular narrow-complex tachycardia without adverse features, start with vagal manoeuvres (for example the Valsalva manoeuvre). If the arrhythmia persists and is not atrial flutter, give adenosine 6 mg as a rapid IV bolus followed by a flush of at least 20 mL; if there is no response, give a 12 mg bolus (which may be repeated).^[3]
• If the ventricular rate slows transiently but the arrhythmia persists, look for atrial flutter or another atrial tachycardia and treat accordingly.^[3]
• If adenosine is contraindicated or fails to terminate a regular narrow-complex tachycardia without demonstrating atrial flutter, give a calcium channel blocker (for example verapamil 2.5–5 mg IV over 2 min, or diltiazem 15–20 mg over 2 min).^[3]

From other headings of the same guideline:^[3]

• Broad-complex tachycardia: in the peri-arrest setting, assume broad-complex tachycardias are ventricular in origin.^[3]
• Irregular broad-complex tachycardia: if pre-excited AF (or flutter) is suspected, avoid adenosine, digoxin, verapamil and diltiazem; electrical cardioversion is usually the safest option.^[3]

Note the differences from ESC 2019, and name the source you are quoting. ANZCOR gives verapamil 2.5–5 mg IV over 2 min, whereas ESC 2019 gives 0.075–0.15 mg/kg IV (average 5–10 mg) over 2 min.^[1][3] ANZCOR allows a 12 mg adenosine bolus that may be repeated, whereas ESC 2019 goes from 6 mg to 12 mg and then says an 18 mg dose should be considered, taking into account tolerability and side effects in the individual patient.^[1][3]

Exam pearls

• A fixed VA interval with variable RR intervals excludes AT; AV block during narrow QRS tachycardia rules out AVRT.^[1]
• When retrograde P waves can be identified, a pseudo r in V1 and a pseudo S in the inferior leads are more common in typical AVNRT than in AVRT or AT: specific (91–100%) but modestly sensitive (58% and 14%), in studies in which cases of AT or atypical AVNRT were limited or entirely absent.^[1]
• REVERT: modified vs standard Valsalva manoeuvre, sinus rhythm at 1 min 43% vs 17%.^[4]
• Adenosine in adults: 6 mg, then 12 mg, then consider 18 mg (taking into account tolerability and side effects), as a rapid bolus with an immediate saline flush (ESC 2019).^[1]
• Haemodynamically stable wide QRS tachycardia of unknown aetiology: verapamil is not recommended (Class III, level B); IV procainamide should be considered if vagal manoeuvres and adenosine fail (Class IIa, level B).^[1]
• Pre-excited AF in a stable patient: IV ibutilide or procainamide should be considered (Class IIa, level B; IV ibutilide is contraindicated with a prolonged QTc); IV amiodarone is not recommended (Class III, level B).^[1]
• Asymptomatic pre-excitation, high-risk AP at EPS: SPERRI 250 ms or less, AP ERP 250 ms or less, multiple APs, inducible AVRT.^[1]
• Asymptomatic pre-excitation: about 1 in 5 develop an AP-related arrhythmia; cardiac arrest or VF risk about 2.4 per 1000 person-years.^[1]
• Slow-pathway ablation for AVNRT: 97% success, about 1.3–4% recurrence, AV block risk under 1% in previous reports.^[1]
• Do not use amiodarone in pre-excited AF, sotalol in SVT, or flecainide or propafenone with LBBB or ischaemic or structural heart disease (ESC key messages).^[1]

References8ShowHide

1. [1]Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardiaThe Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J, 2020.PMID 31504425
2. [2]De Backer J, Haugaa KH, Hasselberg NE, et al. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy. Eur Heart J, 2025.PMID 40878294
3. [3]Australian and New Zealand Committee on Resuscitation Guideline 11.9 – Managing Acute Dysrhythmias ANZCOR, 2026.Source
4. [4]Appelboam A, Reuben A, Mann C, et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet, 2015.PMID 26314489
5. [5]Stambler BS, Camm AJ, Alings M, et al. Self-administered intranasal etripamil using a symptom-prompted, repeat-dose regimen for atrioventricular-nodal-dependent supraventricular tachycardia (RAPID): a multicentre, randomised trial. Lancet, 2023.PMID 37331368
6. [6]Alabed S, Sabouni A, Providencia R, et al. Adenosine versus intravenous calcium channel antagonists for supraventricular tachycardia. Cochrane Database Syst Rev, 2017.PMID 29025197
7. [7]European Society of Cardiology Corrigendum to: 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. Eur Heart J, 2020.PMID 31837137
8. [8]European Society of Cardiology Correction to: 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy: Developed by the task force on the management of cardiovascular disease and pregnancy of the European Society of Cardiology (ESC) Endorsed by the European Society of Gynecology (ESG). Eur Heart J, 2026.PMID 41428090