Narrow-QRS complexes (≤120 ms) are due to activation of the ventricles via the His-Purkinje system, consistent with origin of the arrhythmia above or within the His bundle. However, early activation of the His bundle can also occur in high septal ventricular tachycardias (VTs), thus resulting in relatively narrow-QRS complexes (110–140 ms). In these cases the HV interval is less than 35 ms. Atrial fibrillation (AF) with rapid ventricular response may superficially resemble a regular narrow-QRS tachycardia, whereas focal or multifocal atrial tachycardia and atrial flutter may present as an irregular tachycardia as a result of varying atrioventricular (AV) conduction. Arrhythmias to be considered are presented in Box 10.1 and Fig. 10.1 .
Narrow-QRS (≤120 ms) tachycardias
Physiologic sinus tachycardia
Inappropriate sinus tachycardia
Sinus nodal reentrant tachycardia
Atrial flutter with fixed AV conduction
AV nodal reentrant tachycardia
Junctional ectopic tachycardia (or other nonreentrant variants)
Orthodromic AV reentrant tachycardia
Idiopathic VT (especially high septal VT)
Focal atrial tachycardia or atrial flutter with varying AV block
Junctional ectopic tachycardia (rare)
Regular narrow-QRS (≤120 ms) tachycardias
Several clinical characteristics are useful for the appropriate diagnosis of a narrow-QRS tachycardia. Atrial fibrillation (AF) is the most commonly treated substrate, followed by atrioventricular nodal reentrant tachycardia (AVNRT), atrial flutter, and atrioventricular reentrant tachycardia (AVRT), in patients referred for catheter ablation. Thus AVNRT is the most common diagnosis in the presence of a regular narrow-QRS tachycardia. Women are more likely to be affected by AVNRT than men, whereas the converse is true for AVRT. A relationship to the menstrual cycle has been suggested, and episodes are more frequent during pregnancy in women with preexisting supraventricular tachycardia (SVT).
A sudden onset more likely points to AVNRT or AVRT, although an atrial tachycardia (AT) may also present in this way. Reentrant tachycardias tend to last longer than AT episodes, which may occur in a series of repetitive runs. Clear descriptions of pounding in the neck (the so-called frog sign) or “shirt flapping ” would point to the possible competing influences of atrial and ventricular contraction on the tricuspid valve and to AVNRT as a likely cause. , ,
Electrocardiographic differential diagnosis
In the absence of an electrocardiogram (ECG) recorded during the tachycardia, a 12-lead ECG in sinus rhythm may provide clues for the diagnosis of SVT. The presence of preexcitation in a patient with a history of regular paroxysmal palpitations is suggestive of AVRT. The absence of apparent preexcitation does not rule out the diagnosis of AVRT because it may be due to a concealed accessory pathway (AP) that conducts only retrogradely or to an atriofascicular or nodofascicular/nodoventricular bypass tract that is not apparent during sinus rhythm. An ECG taken during tachycardia is very useful in the efficient diagnosis of SVT, although it may fail to lead to a specific diagnosis.
Initiation and termination of the tachycardia
Sudden prolongation of the PR interval occurs in typical AVNRT after an atrial ectopic beat. An AT may also be initiated by an atrial ectopic beat but is not dependent on marked PR prolongation. Automatic, focal ATs are characterized by gradual acceleration (warm-up phenomenon) followed by deceleration (cool-down phenomenon) and may also be incessant with short interruption by sinus beats. Premature atrial or ventricular beats may trigger AVRT. Premature ventricular complexes are a common trigger of atypical AVNRT but rarely induce typical AVNRT and or AT.
According to their P/QRS relationships, SVTs are classified as having short or long RP intervals. Short-RP SVTs are those with RP intervals shorter than half the tachycardia RR interval, whereas long-RP SVTs display RP greater than or equal to PR ( Fig. 10.2 ). Rarely, recording of U waves during typical AVNRT may simulate a long-RP tachycardia.
On electrophysiologic study, a very short VA interval (≤70 ms) from the onset of the QRS to the atrial depolarization in the His bundle electrogram usually indicates typical AVNRT, or less commonly focal AT, but has also been reported in AVRT. For surface ECG measurements, a cutoff interval of 90 ms has been shown to be useful and can be used if P waves are visible, but data on actual RP measurement during various types of SVT are scarce.
P wave morphology
P waves similar to those in normal sinus rhythm suggest appropriate or inappropriate sinus nodal tachycardia, sinus nodal reentrant tachycardia, or focal AT arising close to the sinus node. P waves different from those in sinus rhythm and conducted with a PR interval equal to or longer than the PR in sinus rhythm are typically seen in focal AT but can also be seen in atypical AVNRT ( Fig. 10.2 ). In AT the conduction to the ventricles may be fast (1:1) or slow (2:1 or more). The possibility of atrial flutter with 2:1 conduction should also be considered if the ventricular rate during SVT is approximately 150 beats per minute (bpm) because the atrial activity is usually 250 to 330 bpm. In the presence of antiarrhythmic medication in this setting, lowering the atrial rate may result in a higher ventricular rate in the absence of AV nodal blockade.
In the case of relatively delayed retrograde conduction that allows the identification of retrograde P waves, a pseudo r deflection in lead V1 and a pseudo S wave in the inferior leads are more common in typical AVNRT than in AVRT or AT. , These criteria are specific (91% to 100%) but modestly sensitive (58% and 14%, respectively). A difference in RP intervals in leads V1 and III greater than 20 ms is also indicative of AVNRT rather than AVRT caused by a posteroseptal pathway. The presence of a QRS notch in lead aVL has also been found as a reliable criterion suggesting AVNRT, whereas a pseudo r in aVR was shown to have higher sensitivity and specificity than a pseudo r in V1 for the diagnosis of typical AVNRT. However, in all referenced studies, cases of AT or atypical AVNRT were limited or entirely absent.
AV block during a narrow-QRS-complex tachycardia is most common with atrial tachycardias, sometimes occurs with AVNRT, and rules out AVRT because the atria and ventricles are requisite parts of the reentry circuit ( Fig. 10.3 ).
Bundle branch block
The development of bundle branch block (BBB) during SVT may also be helpful in the diagnosis of AVRT. BBB ipsilateral to the AP results ventriculoatrial (VA) prolongation of the VA interval as a result of lengthening of the reentry circuit attributable to transseptal conduction after conduction down the contralateral bundle. Lengthening of the VA interval may or may not result in cycle length (CL) prolongation, depending on the behavior of the AH interval. An increase in the VA interval often is accompanied by a reciprocal shortening of the AH interval that minimizes an increase in CL.
Regularity of tachycardia cycle length
The regularity of the RR interval should be assessed ( Fig. 10.4 ). Irregular tachycardias may represent focal or multifocal AT, focal AF, and atrial flutter with varying AV conduction. Patterns of irregularity can sometimes be found, such as in atrial flutter conducted with Wenckebach periodicity. Irregular arrhythmias, such as multifocal AT, typically display variable P-wave morphologies and varying PP, RR, and PR intervals. Atrial flutter can have fixed AV conduction and present as a regular tachycardia, and even AF may appear almost regular when very fast. Reentrant tachycardias, whether micro- or macroreentry, are usually regular. Incessant tachycardias may be the so-called permanent junctional reciprocating tachycardia (PJRT), focal AT, and, rarely, atypical AVNRT. CL alternans (also called RR alternans) may be seen in AVNRT, but these changes are less than 15% of the tachycardia CL. If the irregularity exceeds 15% of the CL, a focal arrhythmia is much more likely. QRS alternans initially was described to be an indicator of AVRT. , Subsequent studies have shown QRS alternans to be a rate-related phenomenon that is not specific to AVRT.
When there is CL variability in short-RP tachycardias, if the change in atrial CL precedes that change in the ventricular CL, this strongly favors atrial tachycardia. On the other hand, when the change in ventricular CL precedes the change in atrial CL, this strongly favors AVNRT or AVRT. During long-RP tachycardias, analysis of the sequence of change in CL in the atrium and ventricle is less helpful. , A fixed VA interval in the presence of variable RR intervals excludes AT.
Vagal maneuvers and adenosine
Vagal maneuvers (such as carotid sinus massage) and adenosine injection may help in clinical diagnosis, particularly in situations in which the ECG during tachycardia is unclear. Possible responses to vagal maneuvers and adenosine are shown in Fig. 10.5.
Termination of the arrhythmia with a P wave after the last QRS complex is very unlikely in AT, and most common in AVRT and typical AVNRT. Termination with a QRS complex is often seen in AT, and possibly in atypical AVNRT. Adenosine does not interrupt macroreentrant ATs (MRATs). Fascicular VTs are verapamil sensitive but not adenosine sensitive. Most VTs, as opposed to SVTs, do not respond to carotid sinus massage, but a narrow-QRS VT originating at the left bundle branch and terminated with carotid sinus massage has been reported.
At electrophysiology study, the differential diagnosis typically is between AVNRT, AVRT caused by a concealed or manifest accessory pathway, and atrial tachycardia. Automatic junctional tachycardia is rare in adults. Nevertheless, differentiating AVNRT from junctional tachycardia is of clinical importance because ablation of the latter is associated with an increased risk of AV block. The distinction between AVNRT and a septal atrial tachycardia can be challenging, but various maneuvers should always lead to the correct diagnosis. We present the most useful and easily applicable maneuvers. A detailed discussion can be found elsewhere.
Retrograde atrial activation sequence during tachycardia
AVNRT may display eccentric atrial activation and septal pathways may have decremental conduction properties and concentric retrograde atrial activation, thus making the differential diagnosis challenging. Although the retrograde atrial activation sequence is usually concentric in AVNRT, heterogeneity of both fast and slow conduction patterns has been well described, and all forms of AVNRT may display variable retrograde activation patterns. Posterior or left septal fast pathways have been described in up to 7.6% in patients with typical AVNRT, and studies with left septal mapping indicate that left-sided retrograde fast pathways are used in a considerable proportion of patients with AVNRT ( Fig. 10.6 ). In atypical AVNRT, retrograde atrial activation can be quite eccentric and even suggestive of a left lateral accessory pathway. Spontaneous changes of the VA interval without changes in the retrograde atrial activation sequence suggest different pathways for retrograde conduction in AVNRT. Moreover, if this occurs with a stable ventricular rate, it suggests the atrium is not a necessary component of the reentry circuit and confirms the diagnosis of AVNRT.
Ventricular pacing during sinus rhythm
Ventriculoatrial conduction block, especially when it is not resolved with isoprenaline, rules out orthodromic AVRT.
Atrial and ventricular conduction starts almost simultaneously in AVNRT, and VA times during tachycardia are therefore shorter than during ventricular pacing. Consideration of the ratio between the minimum ventriculoatrial interval during tachycardia and during ventricular pacing in sinus rhythm is useful. Ratios of 0.32 to 0.27 indicate typical AVNRT, 0.91 to 1.08 indicate AVRT using a posteroseptal pathway, and 0.94 to 1.29 indicate AVRT using an anteroseptal pathway. Cases of atypical AVNRT, however, were not included in this study. A difference in the VA interval during tachycardia and right apical ventricular pacing greater than 90 ms has been reported to differentiate patients with typical or atypical AVNRT from those with AVRT. VA times obtained by apical right ventricular (RV) pacing can be misleading in the case of simultaneous nodal and accessory pathway retrograde conduction or in the presence of multiple accessory pathways.
If ventriculoatrial conduction proceeds over the normal conduction system, the VA interval during right ventricular apical stimulation should be shorter than during right ventricular posterobasal stimulation because of earlier invasion of the His-Purkinje system. The opposite should happen in the presence of a septal AP. The difference between the ventriculoatrial interval obtained during apical pacing and that obtained during posterobasal pacing (the ventriculoatrial index) discriminates patients with posteroseptal pathway (>10 ms) from patients with nodal retrograde conduction (<5 ms). A ventriculoatrial index 10 to 70 ms indicates AVRT (septal AP), whereas a ventriculoatrial index –50 to 5 ms indicates AVNRT ( Fig. 10.7 ). These VA indices may not a reliable when there is coexistence of fast retrograde nodal conduction and a slow septal accessory pathway, conduction over a left lateral accessory pathway, and retrograde right BBB (RBBB) that delays atrial activation. A different activation sequence during RV pacing and SVT makes an atrial tachycardia highly likely.
During AVNRT, the HA interval represents the time interval between activation of the His bundle and activation of the atrium. Ventricular pacing during sinus rhythm in the presence of an AP may allow activation of both the AP and the His bundle in parallel in contrast to AVRT during which they are activated sequentially. The ΔHA during pacing versus tachycardia has been used for differential diagnosis ( Fig. 10.8 ). In one study the ΔHA was more than 0 ms in AVNRT and less than −27 ms in orthodromic AVRT incorporating a septal accessory pathway. An intermediate ΔHA of –10 ms had 100% sensitivity, specificity, and predictive accuracy in differentiating the two forms of tachycardia. The main limitation of this technique is the potential inability to record a retrograde His potential during ventricular pacing. Techniques that require recording of retrograde His potential are cumbersome and may not be possible in a substantial number of cases.
Para-Hisian pacing during sinus rhythm is very useful for distinguishing between AV nodal and septal AP retrograde conduction. An extranodal response through a septal accessory pathway is present when the retrograde atrial activation sequence and the stimulus to A interval during His bundle plus ventricular capture and during ventricular capture alone are the same ( Figs. 10.9 and 10.10 ). Para-Hisian pacing is a sensitive and specific maneuver to establish the presence of a septal AP. However, it requires closely spaced bipolar electrodes (2-mm interelectrode spacing) for recording of retrograde His bundle activation and this may not be possible, especially in patients with very proximal RBBB.
Ventricular pacing during tachycardia
AVNRT and AVRT can always be terminated by overdrive ventricular pacing, whereas atrial tachycardia is rarely terminated. Tachycardia termination by a ventricular extrastimulus that did not conduct to the atrium rules out an atrial tachycardia. The demonstration of AV dissociation by either atrial or ventricular pacing rules out AVRT, whereas the induction of the arrhythmia by ventricular extrastimulation makes atrial tachycardia extremely unlikely.
The development of BBB either spontaneously or after introduction of ventricular extrastimuli during AVNRT does not change the AA or HH intervals. A significant change in the VA interval with the development of BBB is diagnostic of orthodromic AVRT and localizes the pathway to the same side as the block.
Tachycardia resetting: His-synchronous ventricular extrastimulation, his bundle premature complexes, and the preexcitation index.
In the presence of septal pathways, ventricular extrastimuli introduced during His bundle refractoriness during tachycardia (i.e., delivered coincident with the His potential or up to 50 ms before the His) may advance or delay subsequent atrial activation, depending on their decrement conduction properties. In AVNRT, atrial activity is not perturbed with His-synchronous ventricular depolarizations. Failure to reset the atria suggests, but does not prove, that an accessory pathway is not present or that it is relatively far from the site of premature stimulation. Demonstration of resetting excludes AVNRT unless the extrastimulus is delivered very close to inferior nodal extensions ( Figs. 10.11–10.13 ). This is a useful and easily performed maneuver. However, it identifies the presence of a pathway when positive but cannot rule out this possibility when negative. In addition, spontaneous variability in VA interval lessens the utility of this observation.