Diagnosing SVT What each finding in the lab tells you.

1

The question being asked

AVNRT

The fast and slow “pathways” are separate atrial inputs to the compact AV node, and much of the circuit lies in the right atrium. In typical AVNRT the impulse goes down the slow pathway and returns by the fast pathway, so the earliest atrial activation is in the anterior septum, recorded on the His catheter. M sections 4 and 4.5A

Orthodromic AVRT

The impulse goes down the AV node and His–Purkinje system and returns to the atria over an accessory pathway. It is by far the most common form of AVRT. M section 5.4 “Orthodromic” and “antidromic” describe whether the His bundle is used in the normal (atria to ventricles) or reverse direction. M section 6.8

Atrial tachycardia

Independent of AV nodal conduction, so it can carry on when AV block is induced. M section 6.4

Every finding below answers one of three questions: is the AV node part of the circuit, does the ventricle take part (which means an accessory pathway), and are the atria part of it. Some manoeuvres separate the parallel activation of atria and ventricles in AVNRT from the serial activation needed in AVRT; others test whether there is more than one route between atria and ventricles. Abedin supraventricular tachycardia chapter, p. 172

The four catheters you place for the study (HRA, His, CS, RV) are what the findings below are recorded on. Show them in the explorer.

2

Baseline: is there a forward-conducting accessory pathway?

• In sinus rhythm the ventricle is activated over both the AV node and the pathway. How much of it the pathway activates depends on the relative timing of the two routes. M section 5.1
• Slowing the AV node increases pre-excitation. Adenosine or verapamil do it, and so does an atrial premature beat or extrastimulus delayed in the node by its decremental conduction. M section 5.1
• A beat that starts at the AV junction (a His extrasystole) conducts only over the His–Purkinje system and shows no pre-excitation. If the abnormal QRS normalises with a His extrasystole, that is taken as proof it was due to pre-excitation. M section 5.1
• Where you pace the atrium matters. Pacing close to the pathway makes pre-excitation obvious: for a left-sided pathway, pacing in the CS greatly increases it, while HRA pacing may show little or none because the impulse reaches the node long before the pathway. Right-sided and septal pathways are usually overt with HRA pacing. M section 5.5
• This is also how pacing helps to localise the pathway. With a left-sided pathway the stimulus-to-delta interval is shorter with CS pacing than with HRA pacing. M section 5.5B

3

Baseline: is there a backward-conducting pathway?

Concentric and eccentric atrial activation

• Concentric (conduction over the AV node): the earliest atrial signal is on the His catheter, the CS atrial signals run from proximal to distal, and the HRA signal is at least 30 ms after the His atrial signal. M section 2.4A
• The retrograde exit from the node can lie nearer the CS ostium than the His, which puts the earliest atrial signal in the proximal CS. A normal decremental pattern of conduction is still seen, so it is not by itself abnormal. M section 2.4A
• Eccentric: any retrograde atrial activation other than over the AV node. M section 5.2B
• Many patients show no ventricle-to-atrium conduction at any cycle length, even with drugs. That is also a normal finding. M section 2.4A

Watch for a change in pattern

• With a slow drive train the impulse reaches the AV node first and activation is concentric. With faster pacing or an early extrastimulus the node delays, and the pathway can now activate the atria first: the pattern changes from concentric to eccentric. M section 5.2
• The change can go the other way. An extrastimulus that reaches the pathway while it is refractory is blocked there and may still reach the atrium slowly over the node. M section 5.2
• To make eccentric activation clearer: slow the node with a drug such as adenosine, pace the ventricle close to the pathway, or look at orthodromic tachycardia, where retrograde conduction is entirely over the pathway. M section 5.2

Differential ventricular pacing

• A stimulus at the RV base (or outflow tract) must reach the apex before it enters the His–Purkinje system, so it takes longer to reach the atrium. With a right-sided pathway the basal stimulus reaches the atrium as fast as or faster than an apical one. A shorter stimulus-to-atrium interval from the base than from the apex points to a right-sided pathway. M section 5.6
• It also helps to tell a posterior exit of the AV node from a posteroseptal pathway when the earliest atrial signal is at the CS ostium. M section 5.6

4

Para-Hisian pacing

Retrograde activation over a mid- or anteroseptal pathway looks concentric, so it can be hard to tell from conduction over the AV node. Para-Hisian pacing is the technique for this situation. M section 5.7

1. Pace the high RV septum just beyond the usual His recording site, next to the His bundle and proximal right bundle branch. M section 5.7
2. Vary the output, not the position. A high output captures the His–Purkinje system as well as the septum and gives a narrow QRS. A low output captures only the septal muscle and gives a wide QRS with a left bundle branch block shape. M section 5.7
3. Compare the stimulus-to-atrium (or VA) time between the two. No pathway: without His capture the impulse must travel to the apex and enter the His–Purkinje system retrogradely, so the VA time lengthens by at least 50 ms. Septal pathway: the atrium is activated quickly from the septum either way, with little change. M section 5.7

• A worked example takes the other route to the same answer. The interval between atrial activations stayed almost equal to the pacing interval in both beats, although the interval between His activations differed. That shows atrial activation did not depend on the His bundle and AV node, so an accessory pathway was carrying it. EHRA case 5

5

Is there dual AV node physiology?

• The fast pathway has the longer effective refractory period. An early atrial extrastimulus can block in the fast pathway yet conduct down the slow one, which takes longer, so the AH interval jumps. M section 4.1
• A jump is classically an AH increase of at least 50 ms for a 10 ms shorter coupling interval. The criterion is a convention. Dual pathways can exist with little or no discrete jump, and a break in the conduction curve with two clear sections is enough to infer them. M section 4.1 ELD 4 atrial extrastimulus testing
• With dual pathways, one atrial impulse can occasionally cause two His–ventricular depolarisations (the “two-for-one” response). M section 4.1
• An atrial extrastimulus that blocks in the fast pathway and conducts over the slow one, with an obvious AH prolongation, is how AVNRT is typically started. M section 6.1

6

During tachycardia: what to look at

Onset

• The way a tachycardia starts is often the most important clue. AVNRT needs a critical AH prolongation as the fast pathway blocks and the slow pathway takes over. M section 6.1
• Orthodromic AVRT typically starts when an early beat blocks in the accessory pathway and conducts down the AV node, then returns up the pathway once it has recovered. M section 5.4
• On the surface ECG, typical AVNRT starts with a sudden PR prolongation after an atrial ectopic beat. An atrial tachycardia can also start with an atrial ectopic beat, but it does not depend on marked PR prolongation. ESC SVT 2019 section 9.1.1.1
• AVNRT and AVRT are almost always accompanied by an obvious AH prolongation at onset. If an atrial tachycardia starts with only a trivial AH change, and the P-wave shape and atrial sequence change slightly from sinus rhythm, both are very unlikely. M section 6.1

The VA interval and atrial sequence

• At EP study the guideline’s cut-off is 70 ms: a very short VA interval (70 ms or less) usually indicates typical AVNRT, less commonly a focal atrial tachycardia, and has also been reported in AVRT. ESC SVT 2019 section 9.1.1.3
• The textbook puts it more categorically. The VA interval matches the RP interval on the surface ECG; a septal VA under 70 ms is highly predictive of typical AVNRT, and it is generally longer than 70 ms in orthodromic AVRT, atrial tachycardia and atypical AVNRT. Glover chapter 2, p. 83
• Central (concentric) activation can occur with any SVT. Eccentric activation is more common with AVRT or atrial tachycardia but can also be seen in AVNRT, depending on where the retrograde slow pathway exits. That is why pacing manoeuvres are needed. Glover chapter 2, p. 84
• Compare the P-wave shape in tachycardia with sinus rhythm. Narrower P waves suggest a septal origin for an atrial tachycardia. Glover chapter 2, p. 84

Termination

• AV node–dependent tachycardias (AVNRT and AVRT) most often end with block in the AV node, spontaneously or with drugs or vagal manoeuvres. M section 6.2
• Typical AVNRT usually ends with block in the slow pathway, so the last visible event is an atrial electrogram. AVRT that ends with block in the AV node also leaves an atrial electrogram last. M section 6.2
• When an atrial tachycardia with 1:1 conduction stops, the last beat is usually conducted, so a ventricular electrogram is last. Block exactly on the last beat is a rare coincidence, so if the last event is consistently an atrial electrogram, atrial tachycardia can be virtually ruled out. M section 6.2
• A ventricular electrogram last is less common in AVRT (block in the pathway) and AVNRT (block in the retrograde nodal pathway). M section 6.2
• The guideline says the same of the surface ECG. Termination with a P wave after the last QRS is very unlikely in atrial tachycardia and most common in AVRT and typical AVNRT. Termination with a QRS is often seen in atrial tachycardia and possibly in atypical AVNRT. ESC SVT 2019 section 9.1.2

Cycle length variation

• In AVRT and typical AVNRT, variation in cycle length is usually due to the antegrade AV node, which depends on rate and autonomic tone. The His–Purkinje system and the pathway or fast pathway back to the atria stay stable. M section 6.3
• The rule: changes in the HH interval that come before and predict changes in the next AA interval prove that the AV node is part of the circuit. In atrial tachycardia the variation is in the atrium and the HH intervals do not predict the AA intervals. M section 6.3

AV block and AV dissociation

• AV block can be produced with vagal manoeuvres, adenosine or verapamil, or by making the node refractory with atrial or ventricular premature beats. M section 6.4
• Atrial tachycardia and flutter continue through AV block. Adenosine usually causes AV block first, which settles the diagnosis, even when it then terminates the tachycardia. The circuits of AVNRT and AVRT include the node and end with AV block. M section 6.4
• If the atria can be dissociated from the tachycardia, the diagnosis is neither AVNRT nor AVRT. The rare exception is AVNRT with 2:1 block below the node, which gives more P waves than QRS complexes. M section 6.4
• The guideline’s version: AV block or dissociation during a narrow-QRS tachycardia is not often seen, but it rules out AVRT, because both atria and ventricles are parts of that circuit. ESC SVT 2019 section 9.1.1.3
• If the ventricle can be paced faster than the tachycardia without interrupting it, the paced impulses collide with the tachycardia below the node. This rules out the ventricle as part of the circuit (so not AVRT) but fits atrial tachycardia or AVNRT. M section 6.4

Vagal manoeuvres and adenosine

• Both slow AV nodal conduction. The possible responses are: intermittent AV block that unmasks dissociated atrial activity (focal atrial tachycardia, flutter or AF waves); a temporary fall in the rate of an automatic tachycardia (focal atrial tachycardia, sinus tachycardia, JET); termination; or no effect. ESC SVT 2019 section 9.1.2, Table 8
• Termination is by interrupting the re-entrant circuit through the AV node, so it happens in AVNRT and AVRT. Sinus node re-entry and triggered atrial tachycardias can more rarely slow and terminate. ESC SVT 2019 section 9.1.2, Table 8
• Adenosine does not interrupt macro-re-entrant atrial tachycardias. No response at an adequate dose in a tachycardia that looks supraventricular should make you think of high septal VT; fascicular VTs are verapamil-sensitive but not adenosine-sensitive. ESC SVT 2019 section 9.1.2

Bundle branch block

• If the tachycardia cycle length (TCL) lengthens when a bundle branch block appears, the diagnosis is AVRT with the pathway on the same side as the block. This is Coumel’s sign. Bundle branch block does not affect AVNRT or atrial tachycardia, and block on the opposite side has no effect. Glover chapter 2, p. 84
• With a free-wall pathway, same-side block can lengthen the VA interval by 50 ms or more. M section 6.5 A longer VA does not always lengthen the cycle length, because antegrade conduction may switch from the slow to the fast AV nodal pathway. ESC SVT 2019 section 9.1.1.3
• Measure VA from the very earliest ventricular activation, usually the start of the surface QRS. In LBBB the local ventricular signal in the CS is late, so the local VA looks short even though the true VA is long. M section 6.5

7

Pacing manoeuvres during tachycardia

The His-synchronous PVC

• A premature ventricular contraction (PVC) timed to the His deflection cannot reach the atrium over the AV node, because the His is refractory. If it still advances the next atrial electrogram, there is another route to the atria: a retrogradely conducting accessory pathway. It does not prove that the pathway is part of the circuit, since a bystander pathway can exist alongside AVNRT. M section 6.6
• The statement probably extends to RV apical PVCs within 50 ms either side of the expected His. M section 6.6
• If such a PVC terminates the tachycardia without reaching the atria, the ventricle, and so an accessory pathway, is a necessary part of the circuit. M section 6.6
• A PVC delivered far from the circuit may fail to pre-excite the atrium, so it may need to be nearer or earlier. The pre-excitation index (PEI) is the TCL minus the coupling interval of the latest RV apical PVC that advances the atrium. With RV pacing, a PEI above 75 ms suggests a left free-wall pathway, below 45 ms a septal pathway and values in between a right free-wall pathway. Very early PVCs (PEI above 120 ms) can advance the atrium even in AVNRT. M section 6.6

Ventricular overdrive pacing

• Pace the ventricle slightly faster than the tachycardia until the atrial rate matches the paced rate, then stop. Look at the first beats after the last paced beat. Abedin supraventricular tachycardia chapter, p. 173
• V–A–A–V (two atrial signals after the last paced ventricular beat, before the next ventricular signal) is typical of atrial tachycardia. EHRA case 8 Abedin supraventricular tachycardia chapter, p. 173
• V–A–V with simultaneous atrial and ventricular activation points to typical AVNRT or a junctional tachycardia. Abedin supraventricular tachycardia chapter, p. 173
• In a long-RP tachycardia, check the AA timing: a “pseudo-VAAV” looks like V–A–A–V, but the second atrial beat after the last paced beat still follows the pacing rate, so it is really V–A–V. That keeps AVNRT and AVRT in play, not atrial tachycardia. EHRA case 28
• If the tachycardia is not entrained, or stops when pacing stops, try to start it with ventricular pacing instead. A V–A–V response at that point also excludes atrial tachycardia. Abedin supraventricular tachycardia chapter, p. 173
• A tachycardia interrupted by ventricular overdrive without the atrium being reset rules out atrial tachycardia. EHRA case 45

Post-pacing interval minus tachycardia cycle length (PPI − TCL)

• After entrainment, subtract the TCL from the first post-pacing interval (PPI). A value above 115 ms suggests AVNRT; a shorter interval suggests septal AVRT. The value is not 100% specific and some patients fall in a grey zone. Abedin supraventricular tachycardia chapter, p. 173
• In a long-RP tachycardia with apical pacing, a PPI − TCL above 115 ms (212 ms in the worked case) was consistent with atypical AVNRT. EHRA case 28

Atrial overdrive and VA linking

• After atrial overdrive pacing, look at the V-to-A interval of the return cycle. A difference of more than 14 ms from the interval in tachycardia suggests atrial tachycardia. In AVNRT or orthodromic AVRT the V-to-A interval is expected to stay fixed (within 10 ms), because atrial timing depends on ventricular activation (“VA linking”). EHRA case 41

8

Long RP and pre-excited tachycardias

Long RP′ tachycardia

A regular narrow-complex tachycardia in which the RP′ is longer than the PR can be an atrial tachycardia, atypical (fast–slow) AVNRT, or AVRT over a slowly conducting retrograde pathway. M section 6.7 Onset pattern and P-wave axis often help; the differential is harder when atrial activation seems to come from the low right atrium, where an ectopic focus is also common. M section 6.7

• The retrograde slow limb of atypical AVNRT exits in the low posterior septum near the CS ostium. M section 6.7
• A pathway with slow, decremental retrograde conduction, usually posteroseptal, gives permanent junctional reciprocating tachycardia (PJRT, also called Coumel’s tachycardia): the AV node is the antegrade limb, P waves are negative in II, III and aVF and the VA time is long. It is classically seen in children and adolescents and is often incessant. M section 6.7 Glover chapter 2, p. 83
• The guideline describes it as a rare form of AVRT using a concealed pathway, usually posteroseptal, with retrograde decremental conduction. Because it is incessant it can cause tachycardiomyopathy, which usually resolves after ablation. Ablation is strongly recommended in symptomatic patients or when LV function is impaired. ESC SVT 2019 section 11.3.8

Typical and atypical AVNRT

The guideline classifies AVNRT by the His–atrial (HA) and ventriculoatrial (VA) intervals and the AH/HA ratio. Here VA is measured from the onset of ventricular activation on the surface ECG to the earliest atrial deflection on the His electrogram. ESC SVT 2019 Table 12

• Atypical AVNRT has traditionally been split into fast–slow (AH/HA under 1 and AH under 200 ms) and slow–slow (AH/HA over 1 and AH over 200 ms). Intermediate, unclassified types also exist. ESC SVT 2019 Table 12

Pre-excited tachycardias

• Bystander pre-excitation accompanies another tachycardia, most often pre-excited atrial fibrillation. Atrial tachycardia, flutter and AVNRT can also be passively pre-excited. This gives a regular wide-complex tachycardia that can look like VT. Similarity to the sinus-rhythm pre-excited QRS is a clue. M section 6.8
• Only two forms need the pathway: antidromic AVRT (down the pathway, back up the His–Purkinje system and AV node) and pathway-to-pathway tachycardia. M section 6.8
• A wide-QRS tachycardia is VT, SVT with bundle branch block, or SVT over an accessory pathway in about 80, 15 and 5% of reported cases. The default diagnosis is VT until proven otherwise, because drugs used for SVT can be harmful in VT. ESC SVT 2019 section 9.2
• High-risk features of a pathway at EP study are a shortest pre-excited RR interval during atrial fibrillation of 250 ms or less, an effective refractory period of 250 ms or less, multiple pathways, and an inducible pathway-mediated tachycardia. ESC SVT 2019 section 11.3.11 The older textbook puts the RR threshold lower, at under 200 ms. M section 6.8

9

Summary: what each finding points to

Each row is a finding in tachycardia and what the cited source says it favours or rules out. No single finding is enough on its own.

10

Pitfalls

• Bystander pathways. Atrial advancement by a His-synchronous PVC shows a pathway exists, not that it is in the circuit. M section 6.6
• Not 100% specific. Cut-offs such as PPI − TCL above 115 ms leave a grey zone. Abedin supraventricular tachycardia chapter, p. 173
• Pseudo-VAAV in long-RP tachycardias: read the AA timing before calling atrial tachycardia. EHRA case 28
• Where you measure VA. With bundle branch block, the local ventricular signal can mislead; use the earliest ventricular activation. M section 6.5
• Very early PVCs. They can advance the atrium even in AVNRT (PEI above 120 ms). M section 6.6
• Junctional ectopic tachycardia (JET) is unaffected by atrial or ventricular pacing and may conduct to the atria intermittently or not at all, unlike AVNRT. M section 6.4
• A very short VA is not exclusive to AVNRT. It usually indicates typical AVNRT but is less commonly seen in focal atrial tachycardia and has been reported in AVRT. ESC SVT 2019 section 9.1.1.3
• Wide-QRS tachycardia. Treat it as VT until proven otherwise. ESC SVT 2019 section 9.2
• Eccentric does not exclude AVNRT. It depends on where the retrograde slow pathway exits. Glover chapter 2, p. 84

Test yourself on these findings in the quiz, or take module 8 of the course.

Further viewing

A longer talk on the same topic, in the same order: Cooper J. Diagnosis of SVT in the EP lab. Arrhythmia Education, YouTube, 31 January 2024 (3 h 12 min). It is a teaching resource, not a source for any statement above; every statement here is taken from the books cited.

11

From diagnosis to treatment

What the 2019 ESC guideline recommends for catheter ablation once the mechanism is known. “Class I” means recommended; “IIa” should be considered; “IIb” may be considered. The letter is the level of evidence. ESC SVT 2019 section 11

Each row is from the guideline’s recommendation tables ESC SVT 2019 recommendation tables, section 11. Several recommendations are only summarised here; the table gives the class and level exactly as printed in the guideline.

What the guideline says about success and risk

• AVNRT. Ablation is the current treatment of choice in symptomatic patients, and slow-pathway modification works in both typical and atypical forms. The usual approach targets the inferior part of the triangle of Koch. Success is reported at about 97%, recurrence at about 1.3% and AV block at under 1%. In experienced centres, targeting the inferior nodal extension and avoiding the mid-septum and the roof of the CS is described as bringing almost no risk of AV block. In adults with congenital heart disease, success is lower and heart block risk higher. ESC SVT 2019 section 11.2.1.2.2
• Accessory pathways. Ablation has a high acute success rate and a low complication rate that depends on pathway location. Major complications include tamponade (0.13–1.1%) and, for septal pathways, complete AV block (0.17–2.7%). Cryoenergy lowers the AV block risk for septal pathways but is associated with more recurrence. Left-sided pathways can be reached by a transseptal or a retrograde aortic approach; in experienced hands the transseptal approach gives less radiation and shorter procedures. ESC SVT 2019 section 11.3.10.2
• Asymptomatic low-risk pathways. Ablation can be reasonable in experienced centres by informed patient choice, but the risk of heart block with anteroseptal or mid-septal pathways may argue against it. ESC SVT 2019 section 11.3.11

The workflow page’s consent table gives the older textbook’s figures for AV block (step 1); these are the guideline’s more recent ones.