What is the difference between sinus tachycardia and supraventricular tachycardia

Diagnosis

The diagnosis of SVT relies principally on the 12-lead ECG. Every patient suspected of having an episode of SVT should have a 12-lead ECG done immediately. Typically, patients with SVT will present with a narrow complex QRS tachycardia with a ventricular rate faster than 100 beats per minute (bpm) and typically faster than 130 to 150 bpm.

P wave morphology can be useful in discriminating rhythms. P waves with a similar axis to the sinus node can be atrial tachycardias and sinus tachycardias. P waves with retrograde depolarization of the atria (seen as inverted in the inferior leads) can be seen in AVNRT, AVRT, and atrial tachycardia. Sawtooth P waves are indicative of classical counterclockwise typical type I flutter, and an absence of P waves with irregular R-R intervals points to atrial fibrillation. Variable (>3) morphologies of P wave are suggestive of multifocal atrial tachycardia. Wide QRS complex (>0.12 sec) with initial slurring (delta wave) during sinus rhythm and short PR (<0.12 sec) is characteristic of Wolff-Parkinson-White syndrome.

In typical AVNRT, due to the small size of the circuit within the AV node and the fast retrograde conduction, there is simultaneous depolarization of the ventricles and atria, thus making the P wave “buried” in the QRS and therefore not visible or inscribed very close to the QRS at the final part of the QRS complex, and sometimes creating a “pseudo terminal S wave” usually seen in leads II, III, and aVF and “pseudo terminal R waves” at the end of the QRS in V1 and avR (Fig. 1).

In orthodromic AVRT, the P wave is usually visible close after the QRS due to the rapid conduction properties of the accessory pathway (short RP tachycardia). In AT, the P wave is usually noticed farther away after the QRS (long RP tachycardia) (Fig. 1). A unique form of orthodromic AVRT termedparoxysmal junctional reentrant tachycardia (PJRT) involves a concealed accessory pathway, usually located in the posteroseptal region, and typically presents with deeply inverted retrograde P waves in leads II, III, and aVF, with a long RP interval.

Other diagnostic maneuvers that may assist in the differential diagnosis are vagal maneuvers (such as carotid sinus massage) or giving intravenous AV nodal blocking agents (such as adenosine or verapamil) to produce AV nodal conduction block. This will terminate reentrant arrhythmia dependent on the AV node—AVNRT and AVRT—but not AT, which will continue, albeit with nonconducted P waves.

Other arrhythmias that present with narrow complex tachycardia like PSVT are:

Fascicular VT

Junctional tachycardias

Artifact such as with Parkinson disease

SVT can conduct with bundle branch block (BBB) and wide QRS either due to preexisting BBB on the baseline ECG or due to aberrant conduction (rapid rate–dependent BBB). When a patient presents with wide QRS tachycardia, VT must be excluded first. Features to distinguish SVT from ventricular tachycardia are outlined inTable 1.

Sinus Node Reentrant Tachycardia

Atrial tachycardias arising from this region are presumed to be due to microreentry in tissue near the sinus node or perinodal region (superior crista terminalis). The P-wave morphology during tachycardia should be identical to that seen during sinus rhythm. Focal atrial tachycardias may also arise from the superior vena cava.2324 Atrial tachycardia arising from the area of the superior vena cava may conduct to the right atrium. There are also reports of fibrillatory conduction in the superior vena cava with exit block to the right atrium masquerading as a focal right atrial tachycardia. In one occurrence, use of a basket catheter demonstrated a conduction delay in the superior vena cava-right atrial junction, contributing to tachycardia initiation.24

Overview/Significance: Anatomy and Physiology of Supraventricular Tachycardia

Normally, the human heart beats at approximately 80 beats/min (± 20 beats/min). If the HR exceeds 100 beats/min, it is called tachycardia. If it drops below 60 beats/min, it is called bradycardia. The heart's ability to increase the rate of a normal sinus rhythm is primarily related to age: the maximum HR possible with a sinus tachycardia is approximately 220 beats/min minus age, with normal variations as high as 10 to 20 beats/min. As an example, a 60-year-old man cannot usually mount a sinus tachycardia higher than 160 beats/min in response to sepsis, exercise, fever, anxiety, or adrenergic stimulation. Faster rates would indicate a pathologic cardiac rhythm, not a physiologic response.

There are two general categories or types of tachycardias: SVT and VT. SVT describes a rapid HR that has its electrochemical origin either in the atria or in the upper portions of the AV node. VTs originate in the ventricular free walls or interventricular septum (or both). VTs can quickly become unstable and require special consideration (Fig. 11.1F).

SVTs can be further classified as narrow-complex (QRS duration < 0.12 second; or three small boxes on the ECG) and wide-complex tachycardias (QRS duration > 0.12 second). The rhythms of these dysrhythmias can be regular or irregular. Examples of narrow-complex SVTs are sinus tachycardia (seeFig. 11.1A); atrial fibrillation (AF) (seeFig. 11.1C); atrial flutter (seeFig. 11.1D); AV nodal reentry; atrial tachycardia (seeFig. 11.1B), both ectopic and reentrant; multifocal atrial tachycardia (MAT); junctional tachycardia; and accessory pathway-mediated tachycardia. The term wide-complex tachycardia describes rhythms such as VT (seeFig. 11.1F), SVT with aberrancy (seeFig. 11.1E), or a preexcitation tachycardia facilitated by an accessory pathway between the atria and ventricles.

Tachycardias can be benign or can have significant physical effects on the patient. When the HR is 60 beats/min, approximately one cardiac cycle of contraction (systole) and relaxation (diastole) occurs per second. The excitation for cardiac contraction typically originates in the SA node, the intrinsic pacemaker of the heart. The pacemaker impulse traverses across and depolarizes the atria, which causes atrial contraction or systole. Subsequently, the depolarization reaches the AV node. On initiating depolarization of the AV node, the conduction velocity of this depolarizing impulse transiently decreases (i.e., undergoes “decremental conduction”) so that the ventricles can fill with blood from the antecedent atrial contraction. (Remember: the duration of diastole must be roughly twice the duration of systole to allow adequate ventricular filling.) The AV node also serves as a gate or selective block to prevent an excessive number of depolarizing impulses from reaching the ventricles when the atrial rate is accelerated.

Classification

Supraventricular tachycardia is a type of tachycardia (heart rate >100 beats per minute) that originates in an area of the heart other than the ventricular area. Supraventricular tachycardias are classified as to origin. The classes include sinus tachycardia, which arises from the sinoatrial node (Fig. 1), atrial tachycardia, which arises from atrial myocardial tissue (Fig. 2), tachycardia due to impulses generated in the atrioventricular node (termed junctional tachycardia) (Fig. 3), and tachycardia due to a reentry circuit in the atrioventricular (AV) node. Tachycardia due to a reentry circuit can be further subdivided into a reentry due to two pathways of conduction (circus movement) in the AV node (Fig. 4) and reentry due to an accessory pathway between the atria and ventricles Kadish and Passman (1999) Ganz and Friedman (1995).

Tachycardia due to reentry is also called reentry tachycardia. Wolff-Parkinson-White Syndrome is a common type of reentry tachycardia associated with an accessory pathway. If the supraventricular tachycardia is intermittent, it is sometimes referred to as paroxysmal supraventricular tachycardia, a term that encompasses atrial tachycardia, AV nodal reentrant tachycardia, and atrioventricular reentrant tachycardia with an accessory pathway. Atrial tachycardias may be either unifocal or multifocal depending on the number of sites of origin of tachycardia within the atria. Sinus node reentrant tachycardia is a rare type of reentry tachycardia in which the sinus node participates in the reentry circuit. Atrial fibrillation and flutter are also types of atrial tachycardia.

SVT-VT Discrimination

The combination of ventricular rate and duration serves as an implicit SVT-VT discriminator and suffices in many patients,25,27 but patients in whom SVTs and VTs overlap in rate require an explicit discrimination process in which a sequence of sensed EGMs that satisfies rate and duration criteria for VT/VF are classified as either SVT or VT/VF.Discriminators are individual algorithm components or “building blocks” that provide a partial or complete rhythm classification for a subset of rhythms. Individual discriminators may be considered in relation to the EGMs analyzed (ventricular only or both atrial and ventricular), the rhythm that they identify (e.g., AF, sinus tachycardia, VT), or the type of EGM information analyzed (intervals versus morphology).25,27eTable 41.5 summarizes the most commonly used individual discriminators.Discrimination algorithms integrate complementary component discriminators to classify tachycardias as VT/VF or SVT (eFigs. 41.13 to 41.15).

EFIGURE 41.14. Correct classification of rapidly conducted atrial fibrillation (AF) by ventricular EGM morphology. The atrial EGM, right ventricular sensing EGM, and dual-chamber marker channel are shown. Most intervals are classified in the ventricular fibrillation (VF) zone (FS), which is programmed to less than 320 milliseconds. The “AF” designation at right of the marker channel (red box) indicates that the rhythm is classified as AF. The basis for this classification is shown in thelower panel, which compares the morphology of shock (high-voltage) EGMs during tachycardia (solid lines) with those of a template stored during baseline sinus rhythm (dotted line). Match percentages of 70% or greater between the two EGMs are considered sufficiently close that the rhythm is classified as “supraventricular.” It is designated as AF based on the atrial rhythm.

ETABLE 41.5. SVT-VT Discriminators Used in ICDs

AEGM, atrial electrogram;AF, atrial fibrillation;AV, atrioventricular;SVT, supraventricular tachycardia;VEGM, ventricular electrogram;VF, ventricular fibrillation;VT, ventricular tachycardia.

Electrophysiological Differential Diagnosis of Focal Atrial Tachycardia

Atrial tachycardias, particularly those originating from the septal region, must be differentiated from concealed septal bypass tract–mediated tachycardia (i.e., orthodromic reciprocating tachycardia), atrioventricular node reentry tachycardia (AVNRT) and its variants, and other rare entities such as concealed nodoventricular or nodofascicular pathways. One of the most useful electrocardiographic or electrophysiological findings is AV block during tachycardia; when it occurs, a concealed bypass tract is eliminated as a diagnostic possibility.

Adenosine administration is a useful diagnostic tool in patients with supraventricular tachycardia.86 In a report from Scheinman et al., 229 patients with supraventricular tachycardia during an electrophysiology study received intravenous boluses of 6 to 18 mg of adenosine. For patients with AT (n = 53), no consistent correlation was found between the response to adenosine and the location of the atrial focus. Termination or suppression of tachycardia with adenosine was observed in 56% of patients, but was not helpful for differentiating automatic tachycardias from triggered or reentrant tachycardias. Only patients with ATs demonstrated atrial cycle length oscillations (23%) before suppression with adenosine. AV block after adenosine was observed only in patients with AT, but it occurred uncommonly, being noted in only 27% of patients. Termination of AT renders the presence of a macroreentrant AT highly unlikely.

A variety of pacing maneuvers have been reported to be useful for the differentiation of AT from other forms of supraventricular tachycardia87,88 (Tables 73-1, 73-2). Ventricular pacing can be useful for differentiating AT from AV nodal reentry tachycardia and AV reentry tachycardia. Ventricular burst pacing for at least 3 to 6 beats at a cycle length shorter than the tachycardia cycle length results in tachycardia termination, entrainment of the tachycardia, or dissociation of the ventricle from the tachycardia. If the ventricle is dissociated from the tachycardia, a bypass tract is excluded. If burst pacing reproducibly terminates tachycardia without conduction to the atrium, AT is excluded as the mechanism.

Burst pacing sometimes can be performed from the right ventricle for longer periods at a cycle length just shorter than the tachycardia cycle length. When atrial activation is accelerated to the pacing rate with 1 : 1 ventriculoatrial conduction, and if the atrial activation sequence during pacing is different from that during tachycardia, then either an AT or a bystander accessory pathway is present. When ventricular pacing is stopped and the electrogram sequence following the last paced ventricular beat demonstrates a V-A-A-V response (i.e., the last atrial complex accelerated to the pacing rate is followed by another atrial complex before the next ventricular complex), an AT is present. This finding is apparent because, following cessation of ventricular overdrive pacing during an AT, the last entrained atrial depolarization cannot conduct in an anterograde manner because the AV node is refractory after recent retrograde conduction; this results in two atrial depolarizations between ventricular depolarizations (V-A-A-V response). A “pseudo” V-A-A-V response may be seen in patients with slowly conducting septal accessory pathways or AV node reentry, particularly of the fast-slow or slow-slow types. A “V-A-H-A-V” sequence also may be seen with AV nodal reentry.

Delivering a ventricular extrastimulus during tachycardia might also provide diagnostic clues to the mechanism of an SVT. Any effect with a ventricular extrastimulus when the His bundle is refractory, including tachycardia termination without depolarizing the atrium, atrial preexcitation, or paradoxical delay of the subsequent atrial response excludes a diagnosis of AT.

Atrial pacing maneuvers also can be helpful to differentiate the various forms of supraventricular tachycardia. Overdrive pacing of the right atrium during tachycardia at a cycle length slightly shorter than the tachycardia cycle length can result in tachycardia termination (diagnostic maneuver not helpful) or tachycardia continuation upon cessation of pacing. If the V-A interval of the return cycle is within 10 ms of the V-A interval during the tachycardia, then the tachycardia is due to AV nodal reentry or a bypass tract. If the V-A interval is variable or different after pacing ceases, then AT is present. A second maneuver is atrial overdrive pacing during tachycardia at the longest cycle length, which results in AV block. The last paced atrial-His bundle (A-H) interval upon cessation of pacing is evaluated. If termination of the tachycardia is associated with a relatively short A-H interval compared with the A-H intervals that resulted in continuation of the tachycardia, then the tachycardia is considered to be AV node dependent and cannot be an AT. Another useful maneuver is to compare the A-H interval during tachycardia and atrial pacing from the high right atrium at or near the tachycardia cycle length. If the A-H interval during atrial pacing at the tachycardia cycle length is more than 40 ms longer than the A-H interval during tachycardia, atypical AV nodal reentry is much more likely. The A-H intervals during atrial pacing and tachycardia will be within 20 ms for ATs and concealed bypass tracts. Atrial pacing should be performed as soon as possible after tachycardia termination.

Tachycardia cycle length variability of 15 ms or more associated with a change in atrial cycle length that predicts a change in ventricular cycle length favors either AT or atypical AVNRT. A change in atrial cycle length that is preceded by the change in the preceding cycle length or H-H interval is suggestive of AVNRT or orthodromic reciprocating tachycardia.89

The postpacing interval response to atrial overdrive pacing during tachycardia also may be useful to localize the site of origin of focal AT. Mohamed et al.90 performed atrial overdrive pacing during AT at a rate slighter faster than the tachycardia rate. Measurement of the postpacing interval minus the tachycardia cycle length (PPI-TCL) from various sites in the right and left atria localized the tachycardia focus when the PPI-TCL was minimized (e.g., for the successful ablation site, 11 ± 8 ms). The investigators explained this observation by hypothesizing that the difference between the PPI and the TCL was proportional to the distance of the pacing site to the tachycardia focus and conduction time through the surrounding or perifocal tissue. In this study, overdrive suppression of the AT focus was not apparent. The PPI-TCL was never greater than 20 ms at a successful ablation site, suggesting minimal slowing by tissue near the atrial focus.

Basic Information

Conclusions

Junctional tachycardia presents in a variety of clinical settings. It can occur in a congenital form, which is poorly tolerated and causes significant morbidity and mortality if not adequately controlled. Postoperative junctional tachycardia is associated with longer recovery time and poor outcomes; therefore aggressive intervention with medical therapy and hypothermia is often warranted. The spontaneous form of JET is uncommon in children and rare in adults. Recent data suggest that this enigmatic arrhythmia can occur as the result of abnormal automaticity or triggered activity. Treatment is aimed at suppression of symptoms and prevention of tachycardia-associated cardiomyopathy and hemodynamic compromise. With the advent of cryothermal ablation and additional insights into electrophysiological targets for ablation, catheter-based ablative therapy is increasingly used for both children and adults.

1 What does the term supraventricular tachycardia (SVT) mean?

By strict definition, a supraventricular tachycardia is any tachycardia whose genesis is not in the ventricles. Thus, the term can encompass atrial fibrillation and flutter, atrial tachycardia and multifocal atrial tachycardia, and reentrant tachycardias. Others will use the terms SVT or paroxysmal SVT to more specifically refer to the reentrant tachycardias of atrioventricular (AV) nodal reentrant tachycardia (AVNRT) and AV reentrant tachycardia (AVRT), as well as atrial tachycardia and several uncommon supraventricular arrhythmias. For the purposes of this chapter, we will use the term SVT to refer to any tachycardia not caused by ventricular tachycardia and the term paroxysmal SVT to refer to tachycardias as a result of AVNRT, AVRT, and atrial tachycardia (although the reader should recognize that this is somewhat arbitrary and not universally accepted, and we will not discuss in detail other rare causes of paroxysmal SVT).