Supraventricular Tachycardia: AVNRT, AVRT
Zachary T. Hollis
Kurt S. Hoffmayer
Melvin M. Scheinman
Supraventricular tachycardia (SVT) is an umbrella term used to describe tachycardia (atrial and/or ventricular rates in excess of 100 bpm at rest), the mechanism of which involves tissue from the His bundle or above.
Paroxysmal supraventricular tachycardia (PSVT) denotes a clinical syndrome characterized by a rapid tachycardia with an abrupt onset and termination. These arrhythmias are frequently encountered in otherwise healthy patients without structural heart disease. Recognition, identification, and differentiation of the various SVTs are of great importance in formulating an optimal treatment strategy.
While much of the early knowledge of SVTs was derived from surface electrocardiogram/electrocardiographic (ECG) recordings, it was the monumental works of Coumel, Durrer, Josephson, Jackman, Scherlag, and Wellens that yielded important mechanistic and therapeutic insights into these rhythm disturbances. Some of the seminal developments in this field include the introduction of reliable intracardiac His bundle recording and programmed electrical stimulation in the 1960s, the first successful surgical ablation of an accessory pathway (AP) in a patient in 1968, the first catheter-based ablation of an arrhythmia in a human being in 1981, and the development of radiofrequency catheter ablation (RFCA) in 1986.
The mechanism responsible for the majority of arrhythmias including SVT is reentry, while a small proportion is due to triggered activity or abnormal automaticity. Reentry requires two distinct pathways that have different speeds of conduction (slow and fast) and varying recovery times (refractoriness). Extra, early beats, such as premature atrial or ventricular contractions (PACs or PVCs), may fail to conduct down the normal (fast conducting but slow to recover) pathway but can travel down the fast recovering but slow conducting pathway. At the distal junction of the two pathways, the arriving slow impulse then returns in a retrograde fashion up the now recovered fast normal pathway. This completes the circuit with activation of the myocardial tissue at each end of the pathway. RFCA successfully eliminates the extra pathway by the application of thermal energy typically leaving only normal conduction.
EPIDEMIOLOGY
The prevalence of SVT is estimated to be 570,000 in the US population with about 89,000 new cases diagnosed annually, or 2.25 per 1,000 persons in the general population. Based on data from the Marshfield Epidemiologic Study Area (MESA) study, the average age of onset of SVT is 57 years (range: infancy to 90 years old). The three most common causes of PSVT include atrioventricular nodal reentrant tachycardia (AVNRT) (56%), followed by atrioventricular reentrant tachycardia (AVRT) (27%) and atrial tachycardia (AT) (17%).
Mechanism of SVT also appears to be influenced by age and gender. SVT using APs (73%) are most common in the pediatric population. SVT symptom onset often begins in adulthood; in one study in adults, the mean age of symptom onset was 32 ± 18 years of age for AVNRT, versus 23 ± 14 years of age for AVRT. Among pediatric populations, the mean ages of symptom onset of AVRT and AVNRT were 8 and 11 years, respectively. In comparison with AVRT, patients with AVNRT are more likely to be female, with an age of onset >30 years. Studies have shown that the incidence and prevalence of SVTs increases with advancing age, patients ≥65 years old are five times more likely to develop symptomatic SVT than those less than 65 years old. For all age groups, women are twice more likely to develop SVT than men.
Wolff-Parkinson-White (WPW) syndrome tends to be more frequent in males than females, although the difference is reduced with increasing age due to the loss of preexcitation. The incidence of manifest preexcitation or WPW pattern on ECG tracings in the general population is 0.1% to 0.3%. Furthermore, not all patients with manifest ventricular preexcitation develop PSVT. It is also known that patients with WPW who have concomitant atrial and ventricular fibrillation were more likely to be male. In contrast, both AVNRT and AT are more frequent in females than males.
CLINICAL PRESENTATION
SVT is usually regular with a heart rate of 160 to 200 bpm, but the rate can range from 100 to 240 bpm. However, they are responsible for a wide spectrum of symptoms including palpitations, dyspnea, chest pain, anxiety, and syncope. When AVNRT and AVRT are compared, symptoms appear to significantly differ. Individuals with AVNRT more frequently describe sensations of “neck pounding” that may be related to pulsatile reversed flow when the atria contract against a closed tricuspid valve.
Patients with an SVT rate ≥170 bpm were more likely to have presyncope and syncope, though true syncope is infrequent-Elderly individuals with AVNRT are more prone to syncope or near-syncope than are younger patients, but the tachycardia rate is generally slower in the elderly. In a study on the relationship of SVT with driving, 57% of patients with SVT experienced an episode while driving, and 24% of these considered it to be an obstacle to driving. This sentiment was most common in patients who had experienced syncope or near-syncope. For people with WPW syndrome, syncope should be taken seriously but is not necessarily associated with increased risk of sudden cardiac death (SCD).
Although most SVTs occur in patients without organic heart disease, they may also occur in patients with ischemic heart disease, valvular stenosis, or reduced left ventricular function. In these instances, the tachycardia episode can precipitate myocardial ischemia and heart failure. In rare instances, paroxysmal SVT may result in cardiac arrest in which the culprit tachyarrhythmia (usually atrial fibrillation or atrial flutter) conducts
rapidly over an AP. When incessant, SVT may cause cardiomyopathy, although the cardiomyopathy may be reversible when the tachyarrhythmia is treated expeditiously. Paroxysmal SVT symptoms may at times be triggered by physical or psychological stress. In premenopausal women, attacks may be related to menses. Physical findings during paroxysmal SVT usually include a rapid, regular pulse. During AVNRT, cannon A-waves may be present. In fact witnessed neck pulsations are specific and have the highest positive predictive value for AVNRT among those with SVT.
rapidly over an AP. When incessant, SVT may cause cardiomyopathy, although the cardiomyopathy may be reversible when the tachyarrhythmia is treated expeditiously. Paroxysmal SVT symptoms may at times be triggered by physical or psychological stress. In premenopausal women, attacks may be related to menses. Physical findings during paroxysmal SVT usually include a rapid, regular pulse. During AVNRT, cannon A-waves may be present. In fact witnessed neck pulsations are specific and have the highest positive predictive value for AVNRT among those with SVT.
Resting 12-lead ECG should be examined for rhythm disturbances, P-wave morphologies, premature supraventricular complexes, PR interval abnormalities (e.g., very short, or a sudden prolongation in the presence of a premature supraventricular complex), delta waves, ST-segment/T-wave abnormalities, and any evidence of structural heart disease. The presence of overt preexcitation implicates AVRT as the culprit tachycardia. The 12-lead ECG during SVT provides important diagnostic information and should be obtained as long as hemodynamic stability is not compromised. If the ECG is not available, a rhythm strip can be helpful. While most SVTs present as a narrow-complex (QRS ≤ 120 ms) tachycardia, they can also present as a wide-complex (QRS > 120 ms) tachycardia as a result of (i) functional or preexisting bundle branch block or (ii) preexcitation, either from a bystander pathway or as part of the circuit in the case of an antidromic tachycardia. Both the regularity of the QRS complexes and the relationship of the P waves to the onset of QRS complexes during the tachycardia provide important diagnostic information. Figure 2-1 illustrates the relationship of the visible P waves to the QRS complexes as a SVT discriminator (long vs. short RP). Table 2-1 provides a categorization of SVTs based on the regularity of the tachycardia and the RP versus PR relationship.
The medical history, physical examination, and ECG provide a diagnosis in only 50% of patients with symptoms such as palpitations, presyncope, and syncope. If exercise consistently triggers the arrhythmia, exercise stress testing may be needed
to elicit the rhythm abnormality. Ambulatory ECG recordings and cardiac electrophysiologic (EP) studies may be needed to obtain additional diagnostic information. Depending on the frequency of symptoms, specific ambulatory and implantable ECG recording devices can be used for arrhythmia detection. Patients with frequent symptoms (approx. three to four times per week) can be monitored with a 24- or 48-h Holter recording. Those with less frequent symptoms (approximately three to four times per month) can be monitored with a continuous loop event recorder. Finally, patients with rare (a few times per year) or unpredictable symptoms, or those with potential hemodynamic instability during an episode, can be monitored with a subcutaneously implantable loop recorder.
to elicit the rhythm abnormality. Ambulatory ECG recordings and cardiac electrophysiologic (EP) studies may be needed to obtain additional diagnostic information. Depending on the frequency of symptoms, specific ambulatory and implantable ECG recording devices can be used for arrhythmia detection. Patients with frequent symptoms (approx. three to four times per week) can be monitored with a 24- or 48-h Holter recording. Those with less frequent symptoms (approximately three to four times per month) can be monitored with a continuous loop event recorder. Finally, patients with rare (a few times per year) or unpredictable symptoms, or those with potential hemodynamic instability during an episode, can be monitored with a subcutaneously implantable loop recorder.
 Figure 2-1 Illustrative lead II tracings showing categorization of supraventricular tachycardias into short RP (tracing B, RP < PR) versus long RP tachycardias (tracing C, RP > PR). Tracing A shows normal sinus rhythm. (Reprinted from Lee KW, Badhwar N, Scheinman MM. Supraventricular tachycardia-I. Curr Probl Cardiol. 2008;33(9):467-546, Copyright [2008].) |
TABLE 2-1 Categorization of Narrow-complex Supraventricular Tachycardias Based on Regularity of QRS Complexes and RP versus PR Relationship on the ECG | ||||||||||||||||||||||||||||||
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ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA
ELECTROPHYSIOLOGY
AVNRT is the most common regular, narrow-complex tachycardia. The ventricular rate is often 180 bpm to 200 bpm but ranges from 110 bpm to >250 bpm SVT guidelines 19).The compact atrioventricular (AV) node is 5 to 7 mm in length and 2 to 5 mm in
width and is located within the triangle of Koch (bounded by the tendon of Todaro, septal leaflet of the tricuspid valve, and coronary sinus [CS] ostium). At the atrial aspect of the compact node is a zone of transitional cells that are interposed between the compact node and atrial myocardium. Distal to the node are the penetrating bundle of His and bundle branches. These are composed of tracts of specialized cells encased by insulating sheaths of fibrous tissue (central fibrous body). Node-like tissue extends anterior and inferior toward the valve tricuspid (right inferior extension) as well as leftward toward the mitral annulus (left posterior extension). There is excellent evidence suggesting that the right inferior nodal extension is the slow pathway that supports AVNRT. On rare occasions, the tachycardia circuit may involve the left posterior nodal extension in which case a left-sided ablative procedure is required.
width and is located within the triangle of Koch (bounded by the tendon of Todaro, septal leaflet of the tricuspid valve, and coronary sinus [CS] ostium). At the atrial aspect of the compact node is a zone of transitional cells that are interposed between the compact node and atrial myocardium. Distal to the node are the penetrating bundle of His and bundle branches. These are composed of tracts of specialized cells encased by insulating sheaths of fibrous tissue (central fibrous body). Node-like tissue extends anterior and inferior toward the valve tricuspid (right inferior extension) as well as leftward toward the mitral annulus (left posterior extension). There is excellent evidence suggesting that the right inferior nodal extension is the slow pathway that supports AVNRT. On rare occasions, the tachycardia circuit may involve the left posterior nodal extension in which case a left-sided ablative procedure is required.
A working model used to explain the behavior of the AVNRT circuit involves two pathways: one pathway is the so-called fast pathway which conducts more rapidly (PR interval 100 to 150 ms) and has a relatively longer refractory period, while the other pathway is the “slow pathway” which conducts more slowly (PR interval > 200 ms) and has a relatively shorter refractory period. The fast pathway constitutes the normal, physiologic, AV conduction axis. In most patients, the fast pathway is located superiorly and anteriorly in the triangle of Koch, while the slow pathway is located inferiorly and posteriorly and is close to the CS ostium (right inferior nodal extension) (Figs. 2-2 and 2-3). Dual pathways can be demonstrated in the laboratory with delivery of a premature atrial complex that results in a “jump” (>50 ms increase in AH interval with a 10 ms increase in prematurity) in the AV nodal conduction curve. This “jump” is due to antegrade block in the fast pathway with conduction over the slow pathway (Fig. 2-4). On the surface ECG, this “jump” manifests as a sudden prolongation in the PR interval.
Traditionally, AVNRT has been categorized into typical or atypical. If the retrograde limb of the circuit is the fast pathway, it is deemed typical; if it is slow, it is atypical. Typical AVNRT is much more common (90%) and involves a slowly conducting antegrade limb with a rapidly conducting retrograde limb (slow-fast variant). In contrast,
atypical AVNRT is much less common (10%) and includes the fast-slow and slow-slow variants. Typical AVNRT is usually initiated by a PAC that blocks in the fast pathway and conducts over the slow pathway. If enough time has elapsed such that the fast pathway has recovered excitability, the impulse can conduct in retrograde fashion over the fast pathway, resulting in an echo beat (Fig. 2-3). If the impulse reenters into the slow pathway, AVNRT may be initiated (Figs. 2-5 and 2-6). Since the atrium and ventricle are activated simultaneously during the tachycardia, the retrograde P wave is either hidden within the QRS or embedded in the terminal portion of the QRS resulting in RP less than PR with pseudo r’ waves in lead V1 (Fig. 2-7) and pseudo s waves in the inferior leads. In most cases, typical AVNRT can be initiated by single or multiple PACs. On rare occasions, the tachycardia can be initiated by single or multiple PVCs. It is important to note that although typical AVNRT is usually associated with earliest retrograde atrial activation in the His bundle electrogram, earliest retrograde atrial activation at the CS ostium has also been observed due to a posteriorly located fast pathway (8% of cases). Such a transposition of the anatomic locations of the slow and fast pathways has important implications in slow pathway ablation.
atypical AVNRT is much less common (10%) and includes the fast-slow and slow-slow variants. Typical AVNRT is usually initiated by a PAC that blocks in the fast pathway and conducts over the slow pathway. If enough time has elapsed such that the fast pathway has recovered excitability, the impulse can conduct in retrograde fashion over the fast pathway, resulting in an echo beat (Fig. 2-3). If the impulse reenters into the slow pathway, AVNRT may be initiated (Figs. 2-5 and 2-6). Since the atrium and ventricle are activated simultaneously during the tachycardia, the retrograde P wave is either hidden within the QRS or embedded in the terminal portion of the QRS resulting in RP less than PR with pseudo r’ waves in lead V1 (Fig. 2-7) and pseudo s waves in the inferior leads. In most cases, typical AVNRT can be initiated by single or multiple PACs. On rare occasions, the tachycardia can be initiated by single or multiple PVCs. It is important to note that although typical AVNRT is usually associated with earliest retrograde atrial activation in the His bundle electrogram, earliest retrograde atrial activation at the CS ostium has also been observed due to a posteriorly located fast pathway (8% of cases). Such a transposition of the anatomic locations of the slow and fast pathways has important implications in slow pathway ablation.
 Figure 2-2 Anatomy of the AV junction, including landmarks of the triangle of Koch (bounded by the tendon of Todaro [A], septal leaflet of the tricuspid valve [B], and CS ostium [C]). Locations of the fast and slow pathways are labeled. (Reproduced with permission from David Criley.) |
 Figure 2-3 Diagram of a sinus impulse conducting over the fast and slow pathways (A); a premature atrial complex resulting in conduction block at the fast pathway with conduction solely over the slow pathway (B); atrial echo due to retrograde conduction over the fast pathway (C). Atrial structures: CFB, central fibrous body; CSos, coronary sinus ostium; CT, crista terminalis; ER, eustachian ridge; FO, fossa ovalis; His, bundle of His; IAS, interatrial septum; IVC, inferior vena cava; N, compact AV node; PNE, posterior nodal extension; SVC, superior vena cava; TA, tricuspid ridge; TT, tendon of Todaro. (Reprinted from Lee KW, Badhwar N, Scheinman MM. Supraventricular tachycardia-I. Curr Probl Cardiol. 2008;33(9):467-546, Copyright [2008].) |
 Figure 2-3 (continued) |
 Figure 2-4 A patient with dual AV nodal pathways demonstrated by delivery of a single atrial extrastimulus from the distal high right atrium: a 10-ms increase in atrial stimulus prematurity resulted in an AH “jump” greater than 50 ms (140 to 240 ms denoted by arrows) (A, B). Surface and intracardiac recording arrangement: ECG leads I, II, III, V1, V3, and V5 on top, followed by intracardiac electrograms distal high right atrium bipole (HRAd), proximal high right atrium (HRAp), proximal His (HISp), middle His (HISm), distal His (HISd), proximal coronary sinus bipole (CSp), seven to eight bipole coronary sinus (CS7 to 8), five to six bipole coronary sinus (CS5 to 6), three to four bipole coronary sinus (CS3 to 4), distal coronary sinus (CSd), proximal right ventricular apex (RVAp), distal right ventricular apex (RVAd), stimulation channel (STIM). (Reprinted from Lee KW, Badhwar N, Scheinman MM. Supraventricular tachycardia-I. Curr Probl Cardiol. 2008;33(9):467-546, Copyright [2008].) |
Atypical AVNRT may be initiated by a PAC that blocks in the slow pathway and conducts antegrade over the fast pathway with subsequent retrograde conduction over the slow pathway (fast-slow variant, Fig. 2-5). More commonly, the fast-slow variant of atypical AVNRT is initiated by PVC that blocks in the fast pathway; the impulse then conducts to the atrium via the slow pathway, and returns to the ventricle via the fast pathway. Since the atrium is activated late relative to the ventricle, the RP interval is greater than PR. Retrograde P waves are usually discernible and are usually positive in V1 and always negative in inferior leads (Fig. 2-8). In atypical AVNRT, earliest retrograde atrial activation is usually seen in the slow pathway region (posterior septum). However, unusual cases of atypical AVNRT associated with an
earliest retrograde atrial activation recorded at the anterior and mid septum (middle type) have been reported.
earliest retrograde atrial activation recorded at the anterior and mid septum (middle type) have been reported.
 Figure 2-5 Simplified schematic diagram of the AVNRT reentrant circuit. During sinus rhythm (left panel), the impulse conducts antegrade over the fast pathway and retrogradely penetrates the slow pathway, concealing antegrade slow pathway conduction. During typical AVNRT (center panel), the impulse finds the fast pathway refractory and conducts over the slow pathway. When the fast pathway has recovered excitability, the impulse is able to rapidly conduct up the fast pathway while also traveling down to activate the ventricle; hence, the atrium and ventricle are activated simultaneously. During atypical AVNRT (right panel), the impulse conducts down the fast pathway and up the slow pathway; here, the atrium is activated after the ventricle. AVNRT, atrioventricular nodal reentrant tachycardia. (Reprinted from Lee KW, Badhwar N, Scheinman MM. Supraventricular tachycardia-I. Curr Probl Cardiol. 2008;33(9):467-546, Copyright [2008].) |
 Figure 2-6 Typical AVNRT (slow-fast) initiated with double atrial extrastimuli from the distal HRA (450-230-260 ms) resulting in antegrade conduction down the slow pathway (bold arrow) and retrograde conduction up the fast pathway (dashed arrow). During the tachycardia, the atrium and ventricle are activated simultaneously, resulting in an “A on V” tachycardia. Surface and intracardiac recording arrangement same as Fig. 2-4. (Reprinted from Lee KW, Badhwar N, Scheinman MM. Supraventricular tachycardia-I. Curr Probl Cardiol. 2008;33(9):467-546, Copyright [2008].) |
Sometimes in the electrophysiology (EP) laboratory, tachycardia may not be readily initiated with programmed stimulation alone in the baseline state and pharmacologic augmentation of autonomic tone may be needed. Drugs commonly used in this situation include isoproterenol, atropine, and phenylephrine. Isoproterenol facilitates initiation of AVNRT by shortening the refractory period of the retrograde fast pathway while prolonging antegrade slow pathway conduction at rapid pacing rates. Isoproterenol can be especially helpful in initiating tachycardia in patients without baseline inducibility.
Initial mechanistic studies of AVNRT postulated the circuit to be within the compact AV node. Data from human and animal studies have suggested that in some patients, the circuit is bounded by an upper common pathway (between the circuit and the atrium) and a lower common pathway (between the circuit and the His bundle), both of which have AV nodal properties. These pathways are believed to gate-keep atrial and ventricular inputs into the circuit. This may explain the finding that in some cases the atrium can be disassociated from the tachycardia, and on rare occasions, neither atrial nor ventricular complexes or extra stimuli are able
to penetrate the circuit. In addition, left atrial inputs to the circuit may also play a role. For either typical or atypical form of AVNRT, antegrade conduction appears to use the right posterior nodal extension, but on rare occasions, the circuit appears to be entirely localized to the LA and can be cured only by ablation within the CS or at the mitral annulus.
to penetrate the circuit. In addition, left atrial inputs to the circuit may also play a role. For either typical or atypical form of AVNRT, antegrade conduction appears to use the right posterior nodal extension, but on rare occasions, the circuit appears to be entirely localized to the LA and can be cured only by ablation within the CS or at the mitral annulus.
 Figure 2-7 Patient with typical AVNRT. Retrograde P wave is seen as a pseudo r’ in lead V1 during tachycardia (arrow in [A]). Baseline ECG is shown in (B). |
PHARMACOLOGIC TREATMENT
Patients with hemodynamic compromise synchronized electrical cardioversion should be delivered without delay. In most cases, the tachycardia does not cause significant hemodynamic compromise. Vagal maneuvers can be used to safely and rapidly terminate the tachycardia. They transiently prolong AV nodal refractoriness and conduction resulting in a block in the antegrade slow pathway in the typical AVNRT circuit or block in either the antegrade or retrograde slow pathway in the atypical AVNRT circuit. Examples of vagal maneuvers include “gag reflex” (finger in the throat), “dive reflex” (facial immersion in cold water), “upside down positive”
(legs against the wall), Valsalva maneuver, Müller maneuver, and carotid sinus massage. These maneuvers can be taught to the patient. In the elderly and in those with suspected carotid disease, the carotid sinus massage should be used with caution or avoided altogether.
(legs against the wall), Valsalva maneuver, Müller maneuver, and carotid sinus massage. These maneuvers can be taught to the patient. In the elderly and in those with suspected carotid disease, the carotid sinus massage should be used with caution or avoided altogether.
 Figure 2-8 Patient with atypical (fast-slow) AVNRT. Retrograde P waves are seen in V1 and II, III, aVF during tachycardia (arrows in [A]). Note the P waves are positive in V1 and negative in the inferior leads. Baseline ECG is shown in (B). |
When vagal maneuvers are ineffective, medications known to prolong refractoriness in the antegrade limb of the AVNRT circuit can be used. These agents include intravenous (IV) calcium-channel blockers (verapamil, diltiazem), β-blockers (metoprolol, atenolol, propranolol, nadalol, and esmolol), and adenosine. They should be administered with continuous ECG monitoring. IV adenosine also has a rapid onset of action with an extremely short half-life (1 to 10 s) and is very effective in terminating this tachycardia. Because of its high efficacy and short duration of action, adenosine may be a good option to effect tachycardia termination in patients with impaired left ventricular function. Caution should be exercised in the use of IV verapamil and diltiazem in patients with impaired left ventricular function and in those with wide-complex tachycardia possibly due to ventricular tachycardia (VT).
Adenosine usually causes mild adverse effects that are of short duration (<30 s), although in patients with severe reactive airway disease, this drug should be used with caution. Use of digoxin in the acute management of SVT is of limited value and because of its delayed onset of action, narrow therapeutic window, due to heightened sympathetic tone in the patient with SVT.
Adenosine usually causes mild adverse effects that are of short duration (<30 s), although in patients with severe reactive airway disease, this drug should be used with caution. Use of digoxin in the acute management of SVT is of limited value and because of its delayed onset of action, narrow therapeutic window, due to heightened sympathetic tone in the patient with SVT.
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