It is easy to be confused by the variable terminology used for tachycardias arising above the ventricles: the term Supraventricular Tachycardias (SVT) could be applied to all such arrhythmias, including atrial fibrillation and flutter. It is often used as an overall label for patients with narrow complex tachycardias who have not yet been fully assessed. In common parlance in the UK though, the term includes all Atrial and Junctional Tachycardias but excludes Atrial Fibrillation.

Atrial Flutter is a specific type of re-entry tachycardia closely linked to Atrial Fibrillation but will be covered here with other re-entry tachycardias.

A narrow complex tachycardia is always supraventricular, as a normal QRS width reflects that conduction has passed down the Bundle of His in the normal antegrade manner. Sometimes SVT can present as a broad complex tachycardia, either due to an accessory pathway (ventricular depolarisation is triggered by antegrade conduction via the accessory pathway), or in the presence of a pre-existing bundle branch block.

With only limited experience of emergency medicine, one could be forgiven for thinking that SVT is a no brainer a harmless condition of the young simply requiring a bolus of adenosine then discharge home. This is untrue and several pitfalls await those doctors who combine inexperience with overconfidence.

Learning Bite

Narrow complex tachycardias are always supraventricular but not all supraventricular tachycardias are narrow complex

SVT can occur at all ages and is usually, but not always, well tolerated by the patient. In younger patients SVT may cause only a nuisance palpitation and anxiety, however rates above 150, and pre-existing cardiac disease or other co-morbidity greatly increase the likelihood of symptoms such as ischaemic chest pain, dizziness, syncope or breathlessness.

Classification

Supraventricular Tachycardias can be divided into three

Supraventricular Tachycardias

Distinct conditions (see Figure 1):

1. Atrial Tachycardias: from an ectopic focus or foci in the atria
2. Junctional Tachycardias: Re-entry which can be subdivided further into nodal or non-nodal.
3. Atrial Flutter: a specific atrial re-entry tachycardia

Paroxysmal is often used as a prefix and means recurrent episodes

The clinical presentation of patients with SVT is variable and depends on confounding factors such as age and pre-existing cardiovascular state: how much cardiovascular reserve the patient has determines how well it is tolerated.

Typically, patients present with palpitations, cardiac chest pain or tightness, pre-syncopal symptoms such as dizziness, or shortness of breath. Often the onset is abrupt, may terminate spontaneously and episodes are recurrent (paroxysmal). Patients sometimes do not seek medical help, particularly younger patients.

Each of the three main types of SVT will be discussed in turn.

Atrial tachycardia

This is a tachycardia (rate over 100, usually 150-250) arising from atrial tissue other than the sinoatrial node an ectopic pacemaker (also termed focal atrial tachycardia), or rarely, multiple pacemaker sites (multifocal atrial tachycardia). Atrial flutter is technically a form of atrial tachycardia but will be described separately below.

P waves are present on the ECG but their shape is abnormal, depending on the site of origin of the ectopic pacemaker. Most commonly, this is a benign and short-lived paroxysmal condition of the elderly. A more prolonged form may occur in children and young adults called Incessant Ectopic Atrial Tachycardia: undiagnosed, it may progress to a dilated cardiomyopathy.

Figure 2: Ectopic focus in left atrium leading to atrial tachycardia

Cardinal ECG Features:

• Rate over 100
• P waves present, before QRS (antegrade) but shape may be abnormal (distinguishes from sinus tachycardia)
• In focal atrial tachycardia there will be a consistent abnormal P wave, whilst multifocal atrial tachycardia will have multiple different P wave morphologies
• R-P baseline isoelectric (distinguishes from AF)

Atrial tachycardia may be seen with AV block in digoxin toxicity (see Figure 3).

Figure 3: Atrial Tachycardia with AV Block. Note the second P wave at the end of the ST/T wave, easily mistaken for an upright T wave.

 

Figure 4.⁵ Focal atrial tachycardia (FAT): Consistent, abnormal P wave morphology indicating an ectopic focus.

Atrial Tachycardia Treatment:

DC cardioversion is likely to terminate the tachycardia, but some rhythms may recur.

Evidence for specific drug therapy is poor, with beta-blockers, calcium channel blockers and most anti-arrhythmic drugs having potential roles. Adenosine may diagnose the rhythm but is unlikely to terminate it.
Beta-blockers & calcium channel blockers may be used first-line for chronic therapy of recurrent episodes, with catheter ablation the definitive treatment of choice.

Junctional tachycardia

Junctional tachycardias are those arising from the junction between the atria and ventricles, including the AV node, and are due to re-entry circuits.

A re-entry circuit occurs when they are two separate conducting pathways:

1. The normal fast conducting pathway
2. The slow pathway- another area of conducting tissue allowing impulses to pass, only at a slower rate.

Typically, the slow pathway has a shorter refractory period meaning impulses from the atria travel down both pathways, but those from the slower pathway meet refractory tissue within the fast pathway and stop.

In some circumstances, such as a well-timed atrial premature beat, antegrade transmission travels down the slow pathway, which has already recovered first, and then can pass back up the fast pathway as it is no longer refractory. It will then pass again down the slow pathway to form a loop, which will now continue in the same direction. This circular ‘re-entry’ pathway causes increased depolarisation of the ventricles, resulting in a tachycardia.

Re-entry circuits are found:

1. entirely within the AV Node (nodal re-entry tachycardias)
2. in the presence of an accessory (slow) pathway in junctional tissue (AV re-entry tachycardias), where the fast pathway is the normal AV node, e.g. Wolff-Parkinson-White Syndrome

(i) AV Nodal Re-entrant Tachycardia (AVNRT)

The fast and slow pathways are anatomically distinct within the AV node, but re-join to create the Bundle of His for onward transmission to the ventricles. As ventricular depolarisation is always via the Bundle of His, the QRS will be narrow unless pre-existing bundle branch block is present.

Figure 4: AV nodal re-entrant tachycardia

In nodal re-entry tachycardias, transmission is usually antegrade in the slow pathway and retrograde in the fast pathway, as described under re-entry circuits, and is known as slow-fast (see Figure 5). Atrial & ventricular depolarisation are simultaneous, so retrograde P waves are often hidden within the QRS complex, or occur at the end of the QRS as a pseudo r’ or S wave. This is the ‘classical’ ECG of SVT, with a pattern of absent P waves & tachycardia.

Fig. 5 AV nodal ‘slow-fast’ re-entry circuit

10% of patients have fast-slow circuits, with P waves clearly visible before the QRS and a long RP interval.

Fig 6: AV nodal re-entrant tachycardia

Cardinal ECG Features:

• Always narrow complex (unless pre-existing bundle branch block)
• P wave simultaneous with QRS

Learning Bite

In nodal re-entry tachycardia ventricular and atrial (retrograde) depolarisation is simultaneous so the p waves are buried in the QRS complex

(ii) AV re-entrant tachycardias

These are due to an aberrant pathway (rarely multiple pathways) linking atrium and ventricle, bypassing the normal conducting system. The best-known clinical syndrome is Wolff-Parkinson-White Syndrome (WPW) where the aberrant pathway is known as the Bundle of Kent.

Figure 7: AV Re-entrant Tachycardia;
Wolff-Parkinson White syndrome: early depolarisation of ventricular tissue via an aberrant pathway (Bundle of Kent)

WPW: ECG abnormalities in sinus Rhythm:

In sinus rhythm conduction is usually via both pathways, with rapid transmission through the accessory pathway causing ventricular pre-excitation, but most ventricular depolarisation occurring normally via the Bundle of His.

This is represented on the resting ECG (see Figure 8) with:

• Short PR interval (≤120ms)
• Slurred upstroke of the R wave known as a delta wave (from ventricular pre-excitation via accessory pathway, bypassing the slower AV node)
• Wide QRS complex (>120ms)
• Discordance (in the opposite direction to the QRS) of the ST-segment & T-wave is also common, due to the abnormal direction of depolarisation & repolarisation

Sometimes the accessory pathway can only conduct retrogradely, in which case normal AV conduction occurs through the AV node and the ECG is normal in sinus rhythm (a ‘concealed’ accessory pathway).

Figure 8: The ECG Complex in WPW when in sinus rhythm

AV Re-entry Tachycardias:

There are two patterns, orthodromic and antidromic, referring to the direction of flow in the accessory pathway. Antidromic is much less common, in under 10% of WPW.

Figure 9:
Left: Orthodromic re-entrant tachycardia
Right: Antidromic re-entrant tachycardia

(i) Orthodromic Re-Entry Tachycardia

Occurs when a premature atrial impulse is transmitted via the AV node antegradely to the ventricles, then retrogradely back up the accessory pathway, depolarising the atria then passing back via the AV node and down the Bundle of His.

P waves will therefore be present, but inverted and will follow the QRS, and the delta wave disappears. (see figure 10).

(ii) Antidromic re-entry tachycardia

Conduction is antegrade, delivering the impulses to tissue in the right ventricle not specialised for conduction. Ventricular depolarisation spreads from this point, leading to a widened and abnormal QRS (see figure 10).

Retrograde conduction through the AV node leads to atrial depolarisation, and consequently the P waves will be buried in the wide and abnormal QRS. This rhythm may be indistinguishable from ventricular tachycardia unless a previous ECG is available- one clue is that the re-entry tachycardia will be exactly regular.

Figure 10: Rhythm Strip showing typical appearances of orthodromic and antidromic re-entry tachycardia

Cardinal features of WPW:

In sinus rhythm, the ECG may be completely normal or there may be a short PR interval, slurred upstroke of the R wave known as a delta wave, and right (type A) or left (type B) bundle branch block pattern QRS abnormalities (see Figure 11).

During episodes of re-entry tachycardia:

1. Orthodromic– narrow complexes, no delta wave, inverted P waves follow QRS
2. Antidromic– wide aberrant complexes, no visible P waves

Figure 11: QRS abnormalities in WPW

Treatment of re-entry tachycardias:

Measures to increase AV block may terminate the arrhythmia by blocking the re-entry circuit:

• Synchronised DC cardioversion if haemodynamically unstable, or if failed vagal & drug therapy
• Vagal manoeuvres, e.g. Modified Valsalva Manoeuvre- asking patient to blow into 20ml syringe, followed by repositioning them supine with passive leg raise
• Adenosine potent if vagal manoeuvres fail, in orthodromic
• Diltiazem, Verapamil & Beta-Blockers may be appropriate if failure to respond to vagal manoeuvres & adenosine in orthodromic AVRT
• If distinguished from VT, treatment of antidromic AVRT may involve Class I antiarrhythmics
• Outside of the acute episode, catheter ablation is recommended for symptomatic recurrent AVRT.

Atrial Fibrillation in Wolff-Parkinson-White Syndrome

In atrial fibrillation the atrial rate is 400-600bpm, but the AV node stops the majority of these signals reaching the ventricles. In WPW, the accessory pathway allows for rapid conduction directly to the ventricles, bypassing the AV node. Recognition is essential, as administering AV-nodal blocking drugs may cause the excessive electrical impulses to preferentially pass down the accessory pathway, precipitating ventricular arrhythmias and cardiac arrest.

ECG Features (figure 12):

• Rate >200bpm (may be >300bpm, which is too rapid to be conducted via the AV node)
• Irregular rhythm
• Delta wave
• Wide QRS (abnormal ventricular depolarisation via accessory pathway)
• Stable axis (differentiates for polymorphic VT)

Management involves DC cardioversion if the patient is unstable, or type I antiarrhythmics if stable, such as procainamide.

Figure 12: ‘pre-excited’ Atrial Fibrillation in a patient with an accessory pathway

Pitfall

In patients with atrial fibrillation suspected of having an accessory pathway (e.g. WPW), all AV-nodal blocking drugs are contraindicated due to risk of precipitating ventricular arrhythmia or death. These include adenosine, beta-blockers, diltiazem, verapamil, digoxin and amiodarone.

Atrial Flutter

Atrial Flutter is a common dysrhythmia in older patients and has similar causes to Atrial Fibrillation. A rare cause is digoxin toxicity and this should always be considered before treatment.

Many patients have episodes of both flutter and fibrillation and patients with Atrial Flutter often progress to Atrial Fibrillation with advancing age or if left untreated. It is unusual for patients to remain in Atrial Flutter long term.

Prevalence:

• Aged 25-35 years: 2-3 cases per 1000 people
• Aged 55-64 years: 30-90 cases per 1000 people
• Aged 65-90 years: 50-90 cases per 1000 people

Male: Female ratio is 2:1

Pathophysiology:

Atrial Flutter is a form of re-entry tachycardia where the circuit is almost always confined to the right atrium: rare left atrial cases have been reported.

Figure 13: Atrial Flutter rhythm strip

Typical (Type 1) atrial flutter will have an atrial rate of around 300/ min (250-350/min) and most commonly produces a negative sawtooth appearance in inferior leads II, III and aVF (see Figure 14). Reverse Typical Flutter produces a positive sawtooth in the inferior leads at around the same rate, and is due to the electrical impulses passing round the re-entry circuit in the reverse direction.

Atypical (Type 2) atrial Flutter is rare, faster, 350-450/min and arises from a different pathway.

Figure 14: Type 1, typical atrial flutter, counterclockwise, with 4:1 block

The atrial rate can be slowed by Class 1A, 1C drugs and amiodarone. Patients already taking these drugs may present with rates of around 200, and sometimes the AV node then allows 1:1 transmission, resulting in a ventricular rate of 200 or so.

Cardinal Features:

Classic sawtooth Flutter waves may be seen best in II, III, aVF and V1 (may be made more apparent by turning the ECG upside-down). Sometimes the sawtooth morphology is absent and diagnosis depends on identifying flutter waves at a rate usually around 300 (variable, depending on factors above) or having a high index of suspicion for atrial flutter when faced with an ECG with a ventricular rate of half of this (i.e.150bpm in a 2:1 block).

The atrial rate can be slowed by Class 1A, 1C drugs and amiodarone. Patients already taking these drugs may present with rates of around 200/min, and sometimes the AV node then allows 1:1 transmission, resulting in a ventricular rate of 200 bpm or so.

Adenosine can be used diagnostically where there is doubt, in order to temporarily block the AV node and provide a few seconds of rhythm strip devoid of ventricular complexes. The presence of flutter waves is then obvious. However, use of adenosine can then cause the AV conduction to increase to 1:1 or precipitate AF.

The ventricular rate seen in patients with Flutter is dependent on the degree of AV nodal block: normally the AV node cannot transmit impulses at 300/min, so only alternate impulses reach the ventricles, giving a rate of 150/min. This is called Atrial Flutter with 2:1 block and is the most common ventricular response (see Figure 15).

Figure 15: Atrial Flutter with 2:1 block

Mortality and morbidity in Atrial Flutter are related to:

1. rate-related complications such as heart failure and ischaemia
2. thrombo-embolic events, caused by a pro-thrombotic atrial state and leading to a risk of embolic events approaching that of atrial fibrillation.

Both of these issues need to be considered when intervention for Atrial Flutter is considered.

Treatment of atrial flutter:

Treatment of Atrial Flutter is broadly the same as for Atrial Fibrillation, though the condition is more sensitive to DC shock and less so to chemical cardioversion.
The urgency and aims of treatment depend on symptoms, which are usually rate-related.

The various therapeutic options include:

(i) DC Cardioversion

The patient with recent-onset flutter and a rapid ventricular rate may be unstable, with haemodynamic compromise, ischaemic pain or overt pulmonary oedema. These patients require emergency synchronised DC cardioversion. Electrical cardioversion may also be used after failure of pharmacological management. 25J may be sufficient though 50-100J is more reliably effective. Sometimes the first shock converts the rhythm to atrial fibrillation, requiring further shocks to achieve sinus rhythm.

(ii) Rate control

For stable patients with high rates, rate control is preferred first line, but may be difficult to achieve. Drugs include amiodarone (may well also result in cardioversion), beta blockers or calcium channel blockers (eg. verapamil or diltiazem).

(iii) Chemical Cardioversion

Chemical cardioversion can be achieved best with class III anti-arrhythmic drugs. Class Ic antiarrhythmic drugs (e.g. propafenone, fleicanide) aren’t recommended due to risk of slowing atrial rate, resulting in 1:1 AV conduction.

(iv) Electrophysiological ablation therapy

Antiarrhythmic drugs maintain sinus rhythm in only 50-60% of patients. Radiofrequency catheter ablation is successful in more than 90% of cases, interrupting the re-entrant circuit in the right atrium and avoiding the long-term toxicity observed with antiarrhythmic drugs.

(v) Anticoagulation

There are no studies of the effect of anticoagulation on embolic risk in atrial flutter. There is a consensus that since the risk of embolic events seems to be similar to that of atrial fibrillation, anticoagulation should be used similarly, i.e. if the arrhythmia has been present for more than 48 hours then anticoagulate for 4 weeks prior to cardioversion. Long term anticoagulation is rarely required in Flutter as the condition is permanently cured by radio-catheter ablation, or deteriorates into atrial fibrillation.

• Narrow complex tachycardias are always supraventricular in origin.
• Broad Complex Tachycardia is occasionally supraventricular if there is antegrade (antidromic) conduction via the accessory pathway or a pre-existing bundle branch block.
• Typically young patients with a rate of 150 or below tolerate SVT well with only minor symptoms, but those with pre-existing heart disease or other comorbidity, or a rate above 150, may have circulatory compromise.
• Atrial Flutter requires different management to other SVT and should be actively sought, especially when the ventricular rate is around 150.

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