Most SVTs are associated with a regular ventricular rate. If the rhythm is irregular, the ECG should be scrutinized for discrete atrial activity and for any evidence of a pattern to the irregularity (e.g., grouped beating typical of Wenckebach periodicity). If the rhythm is irregularly irregular (i.e., no pattern can be detected), the mechanism of the arrhythmia is either multifocal AT or AF (Fig. 20-2). Multifocal AT is an irregularly irregular atrial rhythm characterized by more than three different P wave morphologies, with the P waves separated by isoelectric intervals and associated with varying P-P, R-R, and PR intervals (see Fig. 11-1). On the other hand, AF is characterized by rapid and irregular atrial fibrillatory activity and, in the presence of normal AVN conduction, by an irregularly irregular ventricular response. P waves cannot be detected in AF, although coarse fibrillatory waves and prominent U waves can sometimes give the appearance of P waves. At times, the fibrillatory activity is so fine as to be undetectable.

FIGURE 20-2 Differential diagnosis of narrow QRS tachycardia. AF = atrial fibrillation; AFL = atrial flutter; AT = atrial tachycardia; AV = atrioventricular; AVNRT = atrioventricular nodal reentrant tachycardia; AVRT = atrioventricular reentrant tachycardia; PJRT = permanent junctional reciprocating tachycardia.

(From Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al: American College of Cardiology; American Heart Association Task Force on Practice Guidelines; European Society of Cardiology Committee for Practice Guidelines [Writing Committee to Develop Guidelines for the Management of Patients with Supraventricular Arrhythmias]: ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines [Writing Committee to Develop Guidelines for the Management of Patients with Supraventricular Arrhythmias], Circulation;108:1871, 2003.)

Atrial Activity

Identification

If the patient’s rhythm is regular or has a clearly discernible pattern, the ECG should next be assessed for P waves (atrial activity).⁵ The P waves may be easily discernible; however, frequently, comparison with a normal baseline ECG is needed and can reveal a slight alteration in the QRS, ST segment, or T waves, suggesting the presence of the P wave. If the P waves cannot be clearly identified, carotid sinus massage or the administration of intravenous adenosine may help clarify the diagnosis. These maneuvers may also terminate the SVT.

Carotid Sinus Massage

Carotid sinus massage can result in one of four possible effects: (1) temporary decrease in the atrial rate in patients with sinus tachycardia or automatic AT; (2) slowing of AVN conduction and AVN block, which can unmask atrial electrical activity—that is, reveal P waves or flutter waves in patients with AT or AFL by decreasing the number of QRS complexes that obscure the electrical baseline; (3) with some SVTs that require AVN conduction, especially AVNRT and AVRT, the transient slowing of AVN conduction can terminate the arrhythmia by interrupting the reentry circuit; less commonly, carotid sinus massage can cause some ATs to slow and terminate; or (4) in some cases, no effect is observed.

Adenosine Administration

Adenosine results in slowing of the sinus rate and AVN conduction. In the setting of SVT, the effects of adenosine are similar to those seen with carotid sinus massage described earlier. For intravenous adenosine administration, the patient should be supine and should have ECG and blood pressure monitoring. The drug is administered by rapid intravenous injection over 1 to 2 seconds at a peripheral site, followed by a normal saline flush. The usual initial dose is 6 mg, with a maximal single dose of 12 mg. If a central intravenous access site is used, the initial dose should not exceed 3 mg and may be as little as 1 mg. Adenosine can precipitate AF and AFL because it shortens atrial refractoriness. In patients with Wolff-Parkinson-White (WPW) syndrome and AF, adenosine can result in a rapid ventricular response that can degenerate into VF. However, this problem has not been observed frequently, and the use of adenosine for diagnosis and termination of regular SVTs, including AVRT, is appropriate as long as close patient observation and preparedness to treat potential complications, such as with immediate electrical cardioversion/defibrillation, are maintained.

Termination of the Arrhythmia

Carotid sinus massage or adenosine can terminate the SVT, especially if the rhythm is AVNRT or AVRT. A continuous ECG tracing should be recorded during these maneuvers, because the response can aid in the diagnosis.⁵ Termination of the tachycardia with a P wave after the last QRS complex is most common in AVRT and typical AVNRT and is rarely seen with AT (see Fig. 18-22), whereas termination of the tachycardia with a QRS complex is more common with AT, atypical AVNRT, and permanent junctional reciprocating tachycardia (PJRT; see Fig. 18-19). If the tachycardia continues despite development of AV block, the rhythm is almost certainly AT or AFL; AVRT is excluded and AVNRT is very unlikely.

Characterization

Atrial Rate

An atrial rate greater than 250 beats/min is usually caused by AFL. However, overlap exists, and AT and AVRT can occasionally be faster than 250 beats/min. AVRT tends to be faster than AVNRT and AT; again, significant overlap exists and this criterion does not usually help in distinguishing among different SVTs.

P Wave Morphology

A P wave morphology identical to sinus P wave suggests sinus tachycardia, inappropriate sinus tachycardia, sinoatrial nodal reentrant tachycardia, or AT arising close to the region of the sinus node. An abnormal P wave morphology can be observed during AVNRT (P wave is concentric; see Fig. 17-3), AVRT (P wave can be eccentric or concentric; see Fig. 18-9), AT (P wave can be eccentric or concentric), and AFL (lack of distinct isoelectric baselines between atrial deflections is suggestive of AFL, but can also be seen occasionally in AT; see Fig. 12-2).⁵

The P waves may not be discernible on ECG, which suggests typical AVNRT or, less commonly, AVRT (especially in the presence of bundle branch block [BBB] contralateral to the BT).

Characterization of the P/Qrs Relationship

RP/PR Intervals

SVTs are classified as short or long RP interval SVTs (see Fig. 20-2). During short RP SVTs, the ECG will show P waves inscribed within the ST-T wave with an RP interval that is less than half the tachycardia R-R interval. Such SVTs include typical AVNRT (most common), orthodromic AVRT, AT with prolonged AV conduction, and slow-slow AVNRT. A very short RP interval (<70 milliseconds) excludes AVRT.^5,⁶

In typical AVNRT, the P wave is usually not visible because of the simultaneous atrial and ventricular activation. The P wave may distort the initial portion of the QRS (mimicking a q wave in inferior leads) or lie just within the QRS (inapparent) or distort the terminal portion of the QRS (mimicking an s wave in inferior leads or r′ in V₁; see Fig. 17-3).

Long RP SVTs include AT, atypical (fast-slow) AVNRT, and AVRT using a slowly conducting AV BT (e.g., PJRT). If the PR interval during the SVT is shorter than that during normal sinus rhythm (NSR), AT and AVRT are very unlikely, and atypical AVNRT, which is associated with an apparent shortening of the PR interval, is the likely diagnosis. ATs originating close to the AV junction are also a possibility.

Atrial-Ventricular Relationship

SVTs with an A/V ratio of 1 (i.e., equal number of atrial and ventricular events) include AVNRT, AVRT, and AT. On the other hand, an A/V ratio during the SVT of greater than 1 indicates the presence of AV block and that the ventricles are not required for the SVT circuit, thereby excluding AVRT and suggesting either AT (most common; see Fig. 11-2) or AVNRT (rare; see Fig. 17-4). AV dissociation (i.e., complete AV block) can be observed during AT (most common) or AVNRT (rare).

QRS Morphology

The QRS morphology during SVT is usually the same as in NSR. However, functional aberration can occur at rapid rates. Functional aberration occurs frequently in AF, AFL, and AVRT, is less common in AT, and is very uncommon in AVNRT.

Electrophysiological Testing

Discussion in this section will focus on differential diagnosis of narrow QRS complex paroxysmal SVTs, including AT, orthodromic AVRT, and AVNRT. The goals of EP testing in these patients include the following: (1) evaluation of baseline cardiac electrophysiology; (2) induction of SVT; (3) evaluation of the mode of initiation of the SVT; (4) definition of atrial activation sequence during the SVT; (5) definition of the relationship of the P wave to the QRS at the onset and during the SVT; (6) evaluation of the effect of BBB on the tachycardia cycle length (CL) and ventriculoatrial (VA) interval; (7) evaluation of the SVT circuit and requirement for the atria, His bundle (HB), and/or ventricles in the initiation and maintenance of the SVT; (8) evaluation of the SVT response to programmed electrical stimulation and overdrive pacing from the atrium and ventricle; and (9) evaluation of the effects of drugs and physiological maneuvers on the SVT.

Baseline Observations during Normal Sinus Rhythm

The presence of preexcitation during NSR suggests AVRT as the likely diagnosis; however, it does not exclude other causes of SVT during which the AV BT is an innocent bystander. Furthermore, the absence of preexcitation during NSR does not exclude the presence of an AV BT or the diagnosis of AVRT mediated by either a concealed or a slowly conducting BT. The presence of intraatrial conduction delay suggests AT, but does not exclude other types of SVTs.

Programmed Electrical Stimulation during Normal Sinus Rhythm

The programmed stimulation protocol should include (1) ventricular burst pacing from the right ventricular (RV) apex (down to pacing CL at which VA block develops); (2) single and double ventricular extrastimuli (VESs, down to the ventricular effective refractory period, ERP) at multiple CLs (600 to 400 milliseconds) from the RV apex; (3) atrial burst pacing from the high right atrium (RA) and coronary sinus (CS; down to the pacing CL at which 2:1 atrial capture occurs); (4) single and double atrial extrastimuli (AESs, down to the atrial ERP) at multiple CLs (600 to 400 milliseconds) from the high RA and CS; and (5) administration of isoproterenol infusion (0.5 to 4 µg/min) as needed to facilitate tachycardia induction.

Atrial Extrastimulation and Atrial Pacing During Normal Sinus Rhythm

Dual Atrioventricular Nodal Physiology

Although the demonstration of dual AVN physiology during programmed atrial stimulation favors AVNRT as the mechanism of SVT, it is not an uncommon finding in patients with other types of SVTs. Furthermore, failure to demonstrate dual AVN physiology does not exclude the possibility of AVNRT, and might be related to similar fast and slow AVN pathway ERPs. Dissociation of refractoriness of the fast and slow AVN pathways can then be necessary (see Chap. 17).

Ventricular Preexcitation

Atrial stimulation can help unmask preexcitation if it is not manifest during NSR because of fast AVN conduction, slow BT conduction, or both. AES and atrial pacing from any atrial site result in slowing of AVN conduction and, consequently, unmask or increase the degree of preexcitation over the AV BT (see Fig. 18-4). Moreover, atrial stimulation close to the AV BT insertion site results in maximal preexcitation and the shortest P-delta interval because of the ability to advance the activation of the AV BT down to its ERP from pacing at this site caused by the lack of intervening atrial tissue, whose conduction time and refractoriness can otherwise limit the ability of the AES to stimulate the BT prematurely (see Fig. 18-14).

Failure of atrial stimulation to increase the amount of preexcitation can occur because of markedly enhanced AVN conduction, the presence of another AV BT, or pacing-induced block in the AV BT due to the long ERP of the BT (longer than that of the AVN). It can also occur because total preexcitation is already present in the basal state as a result of prolonged AVN/His-Purkinje system (HPS) conduction.

Atrioventricular Nodal Echo Beats

These beats occur in the presence of anterograde dual AVN physiology (see Fig. 4-23). Such beats require anterograde block of the atrial stimulus in the fast AVN pathway, anterograde conduction down the slow pathway, and then retrograde conduction up the fast pathway. AVN echo beats have several features: they appear reproducibly after a critical AH interval; the atrial activation sequence is consistent with retrograde conduction over the fast pathway, with the earliest atrial activation site in the HB; and the VA interval is very short, but it can be longer if the atrial stimulus causes anterograde concealment (and not just block) in the fast pathway.

Atrioventricular Echo Beats

AV echo beats occur secondary to anterograde conduction of the atrial stimulus over the AVN-HPS and retrograde conduction over an AV BT (concealed or bidirectional BT). If preexcitation is manifest during atrial stimulation, the last atrial impulse inducing the echo beat will demonstrate loss of preexcitation because of anterograde block in the AV BT, and atrial activation sequence and P wave morphology of the echo beat will depend on the location of the BT (see Fig. 3-10). These beats have a relatively short VA interval, but always longer than 70 milliseconds. Moreover, the VA interval of the AV echo beat remains constant, regardless of the varying coupling interval of the AES triggering the echo beat (VA linking). Alternatively, AV echo beats can occur secondary to anterograde conduction of the atrial stimulus over a manifest AV BT and retrograde conduction over an AVN, in which setting the last paced beat is associated with anterograde block in the AVN and fully preexcited QRS complex.

Ventricular Extrastimulation and Ventricular Pacing During Normal Sinus Rhythm

Retrograde Dual Atrioventricular Nodal Physiology

Demonstration of retrograde dual AVN physiology during programmed ventricular stimulation suggests AVNRT (occurring most commonly during atypical AVNRT), but it can also be observed with other SVTs.⁷ Importantly, failure to demonstrate retrograde dual AVN physiology in patients with AVNRT can be the result of similar fast and slow AVN pathway ERPs, in which setting dissociation of refractoriness of the fast and slow AVN pathways is required (see Chap. 17).

VA block at a ventricular pacing CL greater than 600 milliseconds or decremental VA conduction during ventricular pacing makes the presence of a retrogradely conducting BT unlikely, except for decrementally conducting BTs and the rare catecholamine-dependent BTs. In addition, development of VA block during ventricular pacing in response to adenosine suggests the absence of BT.

Retrograde Atrial Activation Sequence

VA conduction over the AVN produces a classic concentric atrial activation sequence starting in the anteroseptal or posteroseptal region of the RA because of retrograde conduction over either the fast or the slow AVN pathways, respectively. In the presence of a retrogradely conducting AV BT, atrial activation can result from conduction over the AV BT, over the AVN, or a fusion of both (see Fig. 18-16). An eccentric atrial activation sequence in response to ventricular stimulation suggests the presence of an AV BT mediating VA conduction (see Fig. 18-16). The presence of a concentric retrograde atrial activation sequence, however, does not exclude the presence of a retrogradely conducting BT that could be septal in location or located far from the pacing site, allowing for preferential VA conduction over the AVN.

Extra Ventricular Beats

Ventricular stimulation can trigger extra ventricular beats or echo beats. These beats can be caused by different mechanisms.

Bundle Branch Reentrant Beats

During RV stimulation at close coupling intervals, progressive retrograde conduction delay and block occur in the right bundle branch (RB), so that retrograde HB activation occurs via the left bundle branch (LB). At this point, the His potential usually follows the local ventricular electrogram. Further decrease in the coupling interval produces an increase in retrograde HPS conduction delay. When a critical degree of HPS delay (S₂-H₂) is attained, the impulse can return down the initially blocked RB and result in a QRS of similar morphology to the paced QRS at the RV apex—specifically, it will look like a typical left bundle branch block (LBBB) pattern with left axis deviation because ventricular activation originates from conduction over the RB. The His bundle–ventricular (HV) interval of the bundle branch reentrant (BBR) beat is usually longer than or equal to the HV interval during NSR. Retrograde atrial activation, if present, follows the His potential (see Fig. 4-27).

Atrioventricular Node Echo Beats

These beats are caused by reentry in the AVN in patients with retrograde dual AVN physiology (see Fig. 17-11). The last paced beat conducts retrogradely up the slow AVN pathway and then anterogradely down the fast pathway to produce the echo beat. AVN echoes appear reproducibly after a critical H₂-A₂ interval (or V₂-A₂ interval, when the His potential cannot be seen), and manifest as extra beats with a normal anterograde QRS morphology and atrial activity preceding the His potential before the echo beat. This phenomenon can occur at long or short coupling intervals and depends only on the degree of retrograde AVN conduction delay. In most cases, this delay is achieved before the appearance of a retrograde His potential beyond the local ventricular electrogram (i.e., before retrograde block in the RB).

Atrioventricular Echo Beats

These beats occur secondary to retrograde block in the HPS-AVN and VA conduction over an AV BT, followed by anterograde conduction over the AVN, or secondary to retrograde block in the AV BT and VA conduction over the AVN-HPS, followed by anterograde conduction over the AV-BT. In the latter setting, the echo beat is fully preexcited (see Fig. 18-16).

Intraventricular Reentrant Beats

This response occurs most commonly in the setting of a cardiac pathological condition, especially coronary artery disease, and usually occurs at short coupling intervals. It can have any QRS morphology, but more often right bundle branch block (RBBB) than LBBB in patients with prior myocardial infarction (MI). These responses are usually nonsustained (1 to 30 complexes) and typically polymorphic. In patients without prior clinical arrhythmias, such responses are of no clinical significance.

Catheter-Induced Ventricular Beats

Such beats usually have the earliest ventricular activation site recorded at that particular catheter tip and have the same QRS morphology as the QRS produced by pacing from that catheter.

Right Bundle Branch Block during Ventricular Extrastimulation

During the delivery of progressively premature single VESs, an abrupt increase in the VA conduction interval is often seen. This may be due to a variety of reasons including a change in activation from a BT block to the AVN or a change from fast to slow pathway conduction, or it may be the result of an abrupt change when the refractory period of the RB has been reached.

Retrograde RBBB occurs frequently during VES testing, and can be diagnosed by observing the retrograde His potential during the drive train and its abrupt displacement with the VES. Often, however, it is difficult to visualize the retrograde His potential during the pacing train; even then, the sudden appearance of an easily distinguished retrograde His potential, separate from the ventricular electrogram, may be sufficient to recognize retrograde RBBB.

The VH interval prolongation occurs because, following RBBB, conduction must traverse the interventricular septum (which requires approximately 60 to 70 milliseconds in normal hearts), enter retrogradely via the LB, and ascend to reach the HB. Although an increase in the VH interval necessarily occurs with retrograde RBBB, whether a similar increase occurs in the VA interval depends on the nature of VA conduction. Measurement of the retrograde VH and VA intervals on development of retrograde RBBB during VES can help the distinction between retrograde AVN and BT conduction.

In the absence of a BT, the AVN can be activated in a retrograde fashion only after retrograde activation of the HB; as a consequence, VA activation will necessarily be delayed with retrograde RBBB, and the increase in the VA interval will be at least as much as the increase in the VH interval. In contrast, when retrograde conduction is via a BT, there will be no expected increase in the VA interval when retrograde RBBB is induced. Thus, the increase in the VA interval is minimal and always less than the increase in the VH interval.⁸

All types of paroxysmal SVTs can be inducible with atrial stimulation (except automatic AT). SVT initiation that is reproducibly dependent on a critical AH interval is classic for typical AVNRT (see Fig. 17-8). Atypical AVNRT is usually initiated with modest prolongation of the AH interval along the fast pathway with anterograde block in the slow pathway, followed by retrograde slow conduction over the slow pathway. Therefore, a critical AH interval delay is not obvious (see Fig. 17-10). AT initiation also can be associated with AV delay, but that is not a prerequisite for initiation. Orthodromic AVRT usually requires some AV delay for initiation; however, the delay can occur anywhere along the AVN-HPS axis. In patients with baseline manifest preexcitation, initiation of orthodromic AVRT is usually associated with anterograde block in the AV BT and loss of preexcitation following the initiating atrial stimulus, which would then allow that BT to conduct retrogradely during the SVT.⁹

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