Anatomy and Physiology of the Atrioventricular Node

The atrioventricular (AV) junction is a complex structure, located within an area called the triangle of Koch (Fig. 17-1).¹ The triangle of Koch is bounded by the coronary sinus ostium (CS os) posteriorly, the tricuspid annulus (the attachment of the septal leaflet of the tricuspid valve) inferiorly, and the tendon of Todaro anteriorly and superiorly. The triangle of Koch is septal in location and constitutes the right atrial (RA) endocardial surface of the muscular AV septum. The compact AV node (AVN) lies just beneath the RA endocardium, at the apex of the triangle of Koch, anterior to the CS os, and directly above the insertion of the septal leaflet of the tricuspid valve, where the tendon of Todaro merges with the central fibrous body. Slightly more anteriorly and superiorly is where the His bundle (HB) lies. The mean distances from the HB electrogram recording site to the upper and lower lips of the CS os are 10 mm (range, 0 to 23 mm), and 20 to 25 mm (range, 9 to 46 mm), respectively. However, the contour of the Koch triangle may be small or even horizontal in some patients.^2–4

FIGURE 17-1 Right lateral view of the right atrium (RA). Ao = aorta; AV = atrioventricular node; BB = bundle of His, branching portion; C = coronary sinus; CFB = central fibrous body; IVC = inferior vena cava; L = limbus of the fossa ovalis; M = medial (septal) leaflet of the tricuspid valve; PA = pulmonary artery; PB = bundle of His, penetrating portion; PV = pulmonic valve; RBB = right bundle branch; RV = right ventricle; S = septal band of the crista supraventricularis; SA = sinoatrial node; SVC = superior vena cava.

(From Saffitz J, Zimmerman F, Lindsay B: In Braunwald E, McManus BM, editors: Atlas of cardiovascular pathology for the clinician, Philadelphia, 2000, Wiley-Blackwell, p 21.)

Functionally, based on activation times during anterograde or retrograde propagation, or both, and on the action potential characteristics from microelectrode recordings in the rabbit AV junction, the cells of the AVN region are frequently described as AN (atrionodal), N (nodal), and NH (nodal-His). The transition from one cell area to the other is gradual, with intermediate cells exhibiting intermediate action potentials with great changes related to the autonomic tone.^2–6

The AN region corresponds to the cells in the transitional zone, which are activated shortly after the atrial cells. The transitional cell zone represents the inferior, more open portion of the AVN into which atrial bands gradually merge (i.e., the approaches from the working atrial myocardium to the AVN). Transitional cells are histologically distinct from both the cells of the compact AVN and the working atrial myocytes. Transitional cells are not insulated from the surrounding myocardium but tend to be separated from one another by thin fibrous strands. The connections between atrial and transitional cells are so gradual that no clear anatomical demarcations can be detected.⁷ Transitional cells do not represent conducting tracts, but rather a bridge funneling of atrial depolarization into the compact AVN through discrete AVN inputs (approaches). In humans and animals, two such inputs are commonly recognized in the right septal region: the anterior (superior) approaches, which travel from the anterior limbus of the fossa ovalis and merge with the AVN closer to the apex of the triangle of Koch, and the posterior (inferior) approaches, located in the inferoseptal RA and which serve as a bridge with the atrial myocardium at the CS os. Although both inputs have traditionally been assumed to be RA structures, growing evidence supports the AV conduction apparatus as a transseptal structure that reaches both atria. A third, middle group of transitional cells has also been identified to account for the nodal connections with the septum and left atrium (LA).^2,5,8–12

The N region corresponds to the compact AVN, the region where transitional cells merge with midnodal cells. The N cells represent the most typical of the nodal cells because they are characterized by a less negative resting membrane potential and low action potential amplitude (mediated by the L-type calcium [Ca⁺²] current), slow rates of depolarization and repolarization, few intercellular connections such as gap junctions, and reduced excitability compared with surrounding cells. The N cells in the compact AVN appear to be responsible for the major part of AV conduction delay. Sodium channel density is lower in the midnodal zone of the AVN than in the AN and NH cell zones, and the inward L-type Ca²⁺ current is the basis of the upstroke of the N cell action potential. Therefore, conduction is slower through the compact AVN than through the AN and NH cell zones.^1,6 Fast pathway conduction through the AVN apparently bypasses many of the N cells by transitional cells, whereas slow pathway conduction traverses the entire compact AVN. Importantly, the recovery of excitability after conduction of an impulse is faster for the slow pathway than for the fast pathway for reasons that are unclear.^5,6,13

The NH region corresponds to the lower nodal cells, typically distal to the site of Wenckebach block, connecting to the insulated penetrating portion of the HB. The action potentials of the NH cells are closer in appearance to the fast-rising and long action potentials of the HB.

When traced inferiorly, toward the base of the triangle of Koch, the compact AVN area separates into two extensions, usually with the artery supplying the AVN running between them. The prongs bifurcate toward the CS os and tricuspid annulus (right posterior extension) and toward the mitral annulus (left posterior extension). The right posterior nodal extension has been implicated as the anatomical substrate for the so-called slow pathway in the AVN reentrant tachycardia (AVNRT) circuit. The tachycardia circuit may seldom involve the left posterior nodal extension (see later). The fast pathway is less well defined from an anatomical and structural standpoint. The probable anatomical substrate of this pathway consists of the transitional cell layers located around the compact AVN at the interface between the compact node and transitional cells.^3,4,12,14 The HB connects with the distal part of the compact AVN and passes through the fibrous core of the central fibrous body in a leftward direction (away from the RA endocardium and toward the ventricular septum). The HB then continues through the annulus fibrosis, where it is called the nonbranching portion as it penetrates the membranous septum, along the crest of the left side of the interventricular septum, for 1 to 2 cm and then divides into the right bundle branch (RB) and left bundle branch (LB). The HB is insulated from the atrial myocardium by the membranous septum and from the ventricular myocardium by connective tissue of the central fibrous body.¹ Viewed from the left ventricle (LV), the HB is marked by the area of fibrous continuity between the aortic and mitral valves adjacent to the membranous septum. Viewed from the aorta, the HB passes beneath the part of the membranous septum that adjoins the interleaflet fibrous triangle between the right and noncoronary sinuses.¹²

Tachycardia Circuit

The concept of AVN reentry is related, but not identical, to the so-called dual pathway electrophysiology. It is well established that dual AVN physiology is the underlying substrate for AVNRT; however, it is important to recognize that dual AVN physiology characterizes the normal AVN electrophysiology, and the presence of dual (or multiple) AVN pathways is not necessarily indicative of the existence of functional reentry, although it is required to maintain the reentry circuit. Nevertheless, the presence of dual AVN physiology provides the natural substrate for the occurrence of AVN reentry. In the absence of an animal model, however, the exact pathophysiological substrate for AVNRT remains uncertain.⁴

The AVNRT circuit does not involve the ventricles, but whether the circuit is confined to the compact AVN (subatrial) or involves a component of perinodal atrial myocardium is controversial. There is good evidence that the distal junction of the slow and fast pathways is located in the AVN, with the existence of a region of AVN tissue extending between the distal junction of the two pathways and the HB (called the lower common pathway), at least in a subset of patients (Table 17-1). However, the nature of the proximal link between these pathways is unclear, and the existence of an upper common pathway is still a matter of controversy (Tables 17-2 and 17-3). Based on rare cases of dissociation of atrial activation from the tachycardia (e.g., persistence of AVNRT during different patterns of VA block) and on similarities between fast-slow AV conduction and longitudinal-transverse conduction in nonuniform anisotropy, early studies proposed that AVNRT results from reentry within the compact AVN because of functional longitudinal dissociation within the AVN into fast and slow pathways and suggested the presence of an upper common pathway, at least in a subset of patients.^13,15

TABLE 17-1 Evidence against the Necessity of Ventricle in Reentrant Circuit^*

AES = atrial extrastimulation; AV = atrioventricular; AVNRT = atrioventricular nodal reentrant tachycardia; CL = cycle length; HA = His bundle–atrial; HB = His bundle; VA = ventriculoatrial; VES = ventricular extrastimulation.

* Supporting the presence of a lower common pathway.

From Josephson ME: Supraventricular tachycardias. In Josephson ME, editor: Clinical cardiac electrophysiology, ed 3, Philadelphia, 2002, Lippincott Williams & Wilkins, pp 168-271.

TABLE 17-2 Evidence for the Necessity of Atrium in Reentrant Circuit^*

AES = atrial extrastimulation; AVN = atrioventricular node; AVNRT = atrioventricular nodal reentrant tachycardia; CS os = coronary sinus ostium; SVT = supraventricular tachycardia.

* That is, against the presence of an upper common pathway.

From Josephson ME: Supraventricular tachycardias. In Josephson ME, editor: Clinical cardiac electrophysiology, ed 3, Philadelphia, 2002, Lippincott Williams & Wilkins, pp 168-271.

TABLE 17-3 Evidence against the Necessity of Atrium in Reentrant Circuit^*

AF = atrial fibrillation; AH = atrial–His bundle; AV = atrioventricular; AVN = atrioventricular node; AVNRT = atrioventricular nodal reentrant tachycardia; CL = cycle length; VA = ventriculoatrial.

* Supporting the presence of an upper common pathway.

From Josephson ME: Supraventricular tachycardias. In Josephson ME, editor: Clinical cardiac electrophysiology, ed 3, Philadelphia, 2002, Lippincott Williams & Wilkins, pp 168-271.

Current evidence, derived from multielectrode recordings and optical mapping studies, supports the role of perinodal tissue and suggests that the fast and slow pathways involved in the reentrant circuit of AVNRT represent conduction over different atrionodal connections, thus making at least a small amount of atrial tissue a necessary part of the reentrant circuit (Video 19 ). As noted, the compact AVN is surrounded by transitional cells whose structure and function are intermediate between those of atrial and compact nodal cells. If one considers the compact AVN and the surrounding transitional cells as a functional AVN unit, which implies that the AVN tissue occupies the bulk of the triangle of Koch, then the AVN reentrant circuit may be considered as confined to the AVN. Therefore, much of the disagreement on the presence or absence of an upper common pathway and the role of the atrium in the genesis of the reentrant circuit may, in part, be related to the definition of the extent of the AVN.¹⁶

Nevertheless, the understanding of the AVN as having superior (anterior) and inferior (posterior) inputs that form the fast and slow pathways, respectively, is a simple conceptual framework that seems to enable the clinician to confront most cases. Reentry occurring along these pathways is the basic mechanism for the various subtypes of AVNRT. The proximal atrial insertions of the fast and slow pathways are anatomically distinct during retrograde conduction, and several important functional differences exist between the two pathways (Table 17-4).^13,14

TABLE 17-4 Functional Differences between Fast and Slow Atrioventricular Node Pathways

AH = atrial–His bundle; ERP = effective refractory period.

Multiple slow pathways (as demonstrated by multiple discontinuities in the AVN function curves; see later) are present in up to 14% of patients with AVNRT, although not all these pathways are involved in the initiation and maintenance of AVNRT. Whether these pathways represent discrete anatomically distinct circuits or are functionally present because of nonuniform anisotropy is unclear. Frequently, multiple slow pathways are in close proximity within the triangle of Koch, and elimination of multiple slow pathways with radiofrequency (RF) ablation at one site is observed in approximately 42% of cases. Slow pathways with longer conduction times have a more inferior location in the triangle of Koch when compared with locations producing a shorter atrial-HB (AH) interval.

Types of Atrioventricular Nodal Reentry

Slow-Fast (Typical, Common) Atrioventricular Nodal Reentrant Tachycardia

Typical AVNRT accounts for 90% of AVNRTs. The reentrant circuit uses the slow AVN pathway anterogradely and the fast pathway retrogradely. The earliest atrial activation during typical AVNRT is usually in the apex of the triangle of Koch; however, retrograde atrial activation over the fast pathway is heterogeneous and may be found at the CS os or on the left side of the septum in up to 9% of patients (Fig. 17-2).^8,13,17,18

FIGURE 17-2 Atrioventricular nodal reentrant tachycardia (AVNRT) with early atrial activation in the coronary sinus (CS) ostium region. Sinus rhythm is shown on the left, slow-fast AVNRT is shown in the center, and ventricular pacing during sinus rhythm appears on the right. The dashed line denotes earliest atrial activation (proximal CS, near ostium), significantly before the His bundle atrial activation (most visible during ventricular pacing). CS_dist = distal coronary sinus; CS_prox = proximal coronary sinus; His_dist = distal His bundle; His_mid = middle His bundle; His_prox = proximal His bundle; HRA = high right atrium; RV = right ventricle.

During typical AVNRT, atrial and ventricular activations occur almost simultaneously. The AH interval is relatively long (more than 200 milliseconds) and the HA interval is relatively short (less than 70 milliseconds), resulting in a short RP tachycardia.

The presence of a lower common pathway in typical AVNRT remains controversial. Although some studies suggested the existence of a lower common pathway in most patients with typical AVNRT, others demonstrated that most patients with AVNRT without evidence of a substantial lower common pathway had typical AVNRT (i.e., the lower turnaround is within the proximal HB), and the presence of a lower common pathway was strongly associated with the atypical variants of AVNRT. Nevertheless, it is recognized that the lower common pathway in typical AVNRT, if present, is very short (as assessed by the degree of HB prematurity required for a ventricular extrastimulus [VES] to reset the tachycardia, and by comparing the HB-atrial (HA) interval during AVNRT with that during ventricular pacing at the tachycardia cycle length [CL]).⁸

Epidemiology

AVNRT is the most common form of paroxysmal supraventricular tachycardia (SVT). The absolute number of patients with AVNRT and its proportion of paroxysmal SVT increase with age. The reason may be related to the normal evolution of AVN physiology over the first two decades of life, as well as to age-related changes in atrial and nodal physiology observed in later decades.²⁴ AVNRT is unusual in children less than 5 years of age, and it typically initially manifests in early life (e.g., in the teens). Conversely, atrioventricular reentrant tachycardia (AVRT) manifests earlier, with an average of more than 10 years separating the time of clinical presentation of AVRT and that of AVNRT. There is also a striking 2:1 predominance of AVNRT in women, in whom symptoms start at a significantly younger age.^24,25 In fact, female sex and older age (i.e., teens versus newborns or young children) favor the diagnosis of AVNRT over AVRT.²⁶ Gender differences in the anterograde and retrograde AVN electrophysiological (EP) properties have been observed and may contribute to the pathogenesis of AVNRT.²⁵

Clinical Presentation

Patients with AVNRT typically present with the clinical syndrome of paroxysmal SVT. This is characterized as regular rapid tachycardia of abrupt onset and termination. Patients commonly describe palpitations and dizziness. Rapid ventricular rates can be associated with complaints of dyspnea, weakness, angina, or even frank syncope and can at times be disabling. Episodes can last from seconds to several hours. Patients often learn to use certain maneuvers such as carotid sinus massage or the Valsalva maneuver to terminate the arrhythmia, although many require pharmacological treatment. There is no significant association of AVNRT with other types of structural heart disease.

About half of patients with typical AVNRT report experiencing a pounding sensation in the neck during tachycardia, which is caused by simultaneous contraction of the atria and ventricles against closed mitral and tricuspid valves. The physical examination correlate of this phenomenon is continuous pulsing cannon A waves in the jugular venous waveform (described as the “frog” sign). This clinical feature has been reported to distinguish paroxysmal SVT resulting from AVNRT from that caused by orthodromic AVRT. Although atrial contraction during AVRT occurs against closed AV valves, the longer VA interval results in separate ventricular and then atrial contraction and a relatively lower RA and venous pressure; therefore, the presence of palpitations in the neck is experienced less commonly (about 17%) in patients with AVRT.²⁶

Initial Evaluation

History, physical examination, and 12-lead ECG constitute an appropriate initial evaluation. In patients with brief, self-terminating episodes, an event recorder is the most effective way to obtain ECG documentation. An echocardiographic examination should be considered in patients with documented sustained SVT to exclude the possibility of structural heart disease.²⁷ Further diagnostic studies (e.g., cardiac stress testing) are indicated only if there are signs or symptoms that suggest structural heart disease.⁸

The diagnosis of AVNRT as the mechanism of SVT can be strongly suspected based on the surface ECG but is often difficult to confirm, especially when only single-lead rhythm strips are available during the SVT. EP testing, however, is not indicated unless a decision to proceed with catheter ablation is undertaken.

Principles of Management

P Wave Morphology

In typical (slow-fast) AVNRT, the P wave is usually not visible because of the simultaneous atrial and ventricular activation. The P wave can distort the initial portion of the QRS (mimicking a q wave in the inferior leads), lie just within the QRS (inapparent), or distort the terminal portion of the QRS (mimicking an s wave in the inferior leads or an r wave in lead V₁) (Fig. 17-3).⁸ When apparent, the P wave is significantly narrower than the sinus P wave and is negative in the inferior leads, findings consistent with concentric retrograde atrial activation over the fast AVN pathway.⁸ In atypical (fast-slow) AVNRT, the P wave is relatively narrow, negative in the inferior leads, and positive in lead V₁ (see Fig. 17-3).⁸

FIGURE 17-3 Surface ECG of the different types of atrioventricular nodal reentrant tachycardia (AVNRT). Arrows mark the P waves. In slow-fast (typical) AVNRT, the P wave may lie within the QRS (invisible, first panel) or distort the terminal portion of the QRS (mimicking an r wave in V₁, second panel). In slow-slow AVNRT, the P wave lies outside the QRS in the ST-T wave, and the RP interval is longer than that in slow-fast AVNRT. In fast-slow AVNRT, the P wave lies before the QRS with a long RP interval. In all varieties of AVNRT, the P wave is relatively narrow, negative in the inferior leads, and positive in V₁.

QRS Morphology

QRS morphology during AVNRT is usually the same as in normal sinus rhythm (NSR). The development of prolonged functional aberration during AVNRT is uncommon, and it usually occurs following induction of AVNRT by ventricular stimulation more frequently than by atrial stimulation, or following resumption of 1:1 conduction to the ventricles after a period of block below the tachycardia circuit.⁸ At times, alternans of QRS amplitude can occur when the tachycardia rates are rapid. Occasionally, AVNRT can coexist with ventricular preexcitation over an AV bypass tract (BT), whereby the BT is an innocent bystander.⁸

P-QRS Relationship

In typical (slow-fast) AVNRT, the RP interval is very short (–40 to 75 milliseconds). Variation of the P-QRS relationship with or without block can occur during AVNRT, especially in atypical or multiple-form tachycardias.⁸ This phenomenon usually occurs when the conduction system and the reentry circuit are unstable during initiation or termination of the tachycardia, likely secondary to decremental conduction in the lower common pathway. The ECG manifestation of P-QRS variations with or without AV block during tachycardia, especially at the initiation of tachycardias or in cases of nonsustained tachycardias, should not be misdiagnosed as atrial tachycardias (ATs); these variations may represent atypical or, rarely, typical forms of AVNRT. Moreover, the variations can be of such magnitude that long RP tachycardia can masquerade for brief periods of time as short RP tachycardia.

Usually, the A/V ratio during AVNRT is equal to 1; however, 2:1 AV block can be present because of block below the reentry circuit (usually below the HB and, infrequently, in the lower common pathway). In such cases, narrow, inverted P wave morphology in the inferior leads inscribed exactly between QRS complexes strongly suggests AVNRT (Fig. 17-4). The incidence of reproducible sustained 2:1 AV block during induced episodes of AVNRT is approximately 10%. Rarely, VA block can occur because of block in an upper common pathway.⁸

FIGURE 17-4 Typical atrioventricular nodal reentrant tachycardia (AVNRT) with intermittent 2:1 AV block. His potential (H) is observed following conducted atrial impulses, but not after blocked atrial impulses, thus indicating AV block in the lower common pathway or in the portion of the His bundle proximal to the recording site. Note that intermittent AV block results in long-short cycle sequences associated with a right bundle branch block (RBBB) pattern during complexes conducted following a short cycle. RBBB is also observed intermittently during supraventricular tachycardia with 1:1 AV conduction. Note the lack of effect of RBBB on the tachycardia cycle length (A-A interval) or ventricular-atrial (VA) interval. CS_dist = distal coronary sinus; CS_prox = proximal coronary sinus; HRA = high right atrium; RVA = right ventricular apex.

In atypical (fast-slow) AVNRT, the RP interval is longer than the PR interval. In slow-slow AVNRT, the RP interval is usually shorter than, and sometimes equal to, the PR interval. Occasionally, the P wave is inscribed in the middle of the cardiac cycle, thus mimicking atrial flutter or AT with 2:1 AV conduction (Fig. 17-5).¹⁹ Slow-slow AVNRT can be associated with RP intervals and P wave morphology similar to that during orthodromic AV reentrant tachycardia (AVRT) using a posteroseptal AV BT. However, although both SVTs have the earliest atrial activation in the posteroseptal region, conduction time from that site to the HB region is significantly longer in AVNRT than in orthodromic AVRT. The results are a significantly longer RP interval in lead V₁ and a significantly larger difference in the RP interval between lead V₁ and inferior leads during AVNRT. Therefore, ΔRP interval (V₁ – III) of more than 20 milliseconds suggests slow-slow AVNRT (sensitivity, 71%; specificity, 87%).

FIGURE 17-5 Surface ECG leads II and V₁ and endocardial recordings of the different types of atrioventricular nodal reentrant tachycardia (AVNRT). The dashed line marks the site with the earliest atrial activation. In slow-fast (typical) AVNRT, the initial site of atrial activation is usually recorded in the His bundle (HB) catheter. In slow-slow AVNRT, the P wave lies outside the QRS in the ST-T wave, and the RP interval is longer than that in slow-fast AVNRT. The earliest retrograde atrial activation is usually in the inferoposterior part of the triangle of Koch. Slow pathways with longer conduction times have a more inferior location in the triangle of Koch. In fast-slow AVNRT, the earliest site of retrograde atrial activation is usually recorded at the base of the triangle of Koch or coronary sinus ostium (CS os). An eccentric retrograde atrial activation sequence with the earliest retrograde activation site inside the CS can be observed in the left variant of AVNRT, more common in atypical than typical forms of AVNRT. CS_dist = distal coronary sinus; CS_prox = proximal coronary sinus; HRA = high right atrium; RVA = right ventricular apex.

Baseline Observations during Normal Sinus Rhythm

Atrial Extrastimulation and Atrial Pacing During Normal Sinus Rhythm

Anterograde Dual Atrioventricular Nodal Physiology

Demonstration of anterograde dual AVN pathway conduction curves requires a longer effective refractory period (ERP) of the fast pathway than the slow pathway ERP and atrial functional refractory period (FRP), as well as a sufficient difference in conduction times between the two pathways. Dual AVN physiology can be diagnosed by demonstrating the following: (1) a “jump” in the AH interval in response to progressively more premature AES; (2) two ventricular responses to a single atrial impulse; (3) a PR interval exceeding the R-R interval during rapid atrial pacing; and/or (4) different PR or AH intervals during NSR or fixed-rate atrial pacing.²⁸

Atrial-His Interval Jump

In contrast to the normal pattern of AVN conduction, in which the AH interval gradually lengthens in response to progressively shorter AES coupling intervals, patients with dual AVN physiology usually demonstrate a sudden increase (jump) in the AH interval at a critical AES (A₁-A₂) coupling interval (Fig. 17-6). Conduction with a short PR or AH interval reflects fast pathway conduction, whereas conduction with a long PR or AH interval reflects slow pathway conduction. The AH interval jump signals block of anterograde conduction of the progressively premature AES over the fast pathway (once the AES coupling interval becomes shorter than the fast pathway ERP) and anterograde conduction over the slow pathway (which has an ERP shorter than the AES coupling interval), with a longer conduction time (i.e., longer A₂-H₂ interval). A jump in the A₂-H₂ (or H₁-H₂) interval of 50 milliseconds or more in response to a 10-millisecond shortening of either the A₁-A₂ interval (i.e., AES coupling interval) or the A₁-A₁ interval (i.e., pacing CL) is defined as a discontinuous AVN function curve and is considered evidence of dual anterograde AVN pathways (see Fig. 4-23).⁸

FIGURE 17-6 Dual atrioventricular node (AVN) physiology. H₁-H₂ intervals (left) and A₂-H₂ intervals (right) are at various A₁-A₂ intervals, with a discontinuous AVN curve. At a critical A₁-A₂ interval, the H₁-H₂ and A₁-H₂ intervals increase markedly. At the break in the curves, atrioventricular nodal reentrant tachycardia is initiated.

(From Olgin JE, Zipes DP: Specific arrhythmias: diagnosis and treatment. In Libby P, Bonow RO, Mann DL, Zipes DP, editors: Braunwald’s heart disease: a textbook of cardiovascular medicine, ed 7, Philadelphia, 2008, Saunders, p 880.)

1:2 Response

Rapid atrial pacing or AES can result in two ventricular complexes to a single paced atrial impulse. The first ventricular complex is caused by conduction of the atrial impulse over the fast AVN pathway, and the second complex is caused by conduction over the slow AVN pathway (Fig. 17-7). This response requires unidirectional retrograde block in the slow AVN pathway. Typically, in the presence of dual AVN pathways, conduction propagates simultaneously over both fast and slow AVN pathways. However, the wavefront conducting down the fast pathway reaches the distal junction of the two pathways before the impulse conducting down the slow pathway, and, subsequently, it conducts retrogradely up the slow pathway to collide with the impulse conducting anterogradely down that pathway. Thus, the anterograde impulse conducting down the slow pathway does not have the opportunity to reach the HB and ventricle. Rarely, the slow pathway conducts anterogradely only or has a very long retrograde ERP. In this setting, the wavefront traveling anterogradely down the fast pathway blocks (but does not conceal) in the slow pathway retrogradely and fails to retard the impulse traveling anterogradely down that pathway. Consequently, the wavefront traveling down the slow pathway can reach the HB and ventricle to produce a second His potential and QRS in response to a single atrial impulse. Because retrograde block in the slow pathway is a prerequisite to a 1:2 response, when such a phenomenon is present, it indicates that the slow pathway cannot support reentrant tachycardia using the slow pathway as the retrograde limb (i.e., atypical AVNRT cannot be operative). The 1:2 response should be differentiated from pseudo–simultaneous fast and slow pathway conduction, which is a much more common phenomenon during rapid atrial pacing. In the latter case, all paced atrial impulses block anterogradely in the fast pathway and conduct exclusively down the slow pathway with prolonged AH intervals (with PR intervals longer than atrial pacing CL), so that the last paced atrial impulse falls before the His potential caused by conduction of the preceding paced atrial impulse. Thus, the last paced atrial impulse is followed by two His potentials and two ventricular complexes. The last response may then be followed by induction of AVN echo beats or AVNRT, mimicking simultaneous fast and slow pathway conduction (Fig. 17-8).^8,29

FIGURE 17-7 Rapid atrial pacing during normal sinus rhythm (NSR). Each paced atrial impulse conducts anterogradely over the fast atrioventricular node (AVN) pathway (red arrows). The last paced impulse, however, conducts anterogradely over both the fast (red arrow) and slow (blue arrow) pathways, resulting in two His bundle and ventricular responses. CS_dist = distal coronary sinus; CS_prox = proximal coronary sinus; HRA = high right atrium; RVA = right ventricular apex.

FIGURE 17-8 Induction of typical atrioventricular nodal reentrant tachycardia (AVNRT) with atrial pacing. A, Each of the atrial paced impulses (S1) conducts anterogradely over the slow AVN pathway. The last paced impulse, following anterograde conduction down the slow pathway, also conducts retrogradely up the fast AVN pathway to initiate typical AVNRT with right bundle branch block (RBBB). B, Each of the atrial paced impulses conducts anterogradely over the slow AVN pathway with a long PR interval (blue arrows); this is longer than the pacing cycle length (CL), resulting in crossing over, which can mimic a 1:2 AV response caused by anterograde conduction over both the fast and slow AVN pathways. Following anterograde conduction down the slow pathway, the last paced impulse also conducts retrogradely over the fast pathway, initiating typical AVNRT. Red arrows illustrate atrial activation sequence during atrial pacing versus AVNRT. C, Atrial pacing from the coronary sinus ostium (CS os) induces typical AVNRT. Each of the atrial paced impulses (S1) conducts over the fast AVN pathway except for the last paced impulse, which conducts over both the fast and slow AVN pathways (blue arrows), resulting in a 1:2 response (i.e., 2 ventricular responses); this is followed by induction of typical AVNRT with RBBB. The possibility of conduction of the paced atrial beats over the slow AVN pathway with a long atrial–His bundle (AH) interval (longer than the paced CL) is unlikely because the His potential preceding the first tachycardia complex (indicated by the green arrow) occurs later (i.e., at a longer AH interval) than what would be expected if that His potential was actually a result of conduction of the last atrial stimulus (as compared with the previous AH intervals). CS_dist = distal coronary sinus; CS_prox = proximal coronary sinus; HRA = high right atrium; RVA = right ventricular apex.

PR Interval Longer than Pacing Cycle Length During Atrial Pacing

The PR interval gradually prolongs as the atrial pacing rate increases. When a critical pacing rate is reached, the PR interval typically exceeds the R-R interval, with all AVN conduction over the slow AVN pathway (see Fig. 17-8). This manifests as crossing over of the pacing stimulus artifacts and QRSs; that is, the paced atrial complex is conducting not to the QRS immediately following it, but rather to the next QRS, because of a very long PR interval. There should be consistent 1:1 AV conduction that remains stable over the span of several cycles for this observation to be interpreted (i.e., without Wenckebach block). Such slow AVN conduction is seen only when conduction propagates over a slow AVN pathway, and it is not seen in the absence of dual AVN physiology. This phenomenon is diagnostic of the presence of dual AVN physiology, even in the absence of an AH interval jump and therefore is very helpful in patients with smooth AVN function curves. In fact, 96% of patients with AVNRT and smooth AVN function curves have a PR interval/RR interval ratio greater than 1 (i.e., PR interval longer than pacing CL) during atrial pacing at the maximal rate with consistent 1:1 AV conduction (versus 11% in controls).

Different PR or AH Intervals During Normal Sinus Rhythm or At Identical Atrial Pacing Cycle Lengths

This phenomenon can occur when the fast pathway anterograde ERP is long relative to the sinus or paced CL (Fig. 17-9). Such a phenomenon also requires a long retrograde ERP of the fast pathway. Otherwise, AVN echo beats or AVNRT would result, because once the impulse blocks anterogradely in the fast pathway and is conducted down the slow pathway, it would subsequently conduct retrogradely up the fast pathway if the ERP of the fast pathway were shorter than the conduction time (i.e., shorter than the AH interval) over the slow pathway.⁸

FIGURE 17-9 Dual atrioventricular node (AVN) physiology manifesting as two different PR intervals during normal sinus rhythm. Note that the shift in AV conduction from the fast to the slow AVN pathway (arrow) occurs without any changes in the sinus cycle length (CL) (680 milliseconds). This phenomenon indicates that the fast pathway anterograde effective refractory period is long relative to the sinus CL.

Multiple Atrioventricular Nodal Pathways

Multiple AH interval “jumps” in response to AES, a finding suggesting the presence of multiple AVN pathways, can be observed in up to 14% of patients with AVNRT. These phenomena are characterized by multiple AH interval jumps of 50 milliseconds or more in response to an increasingly premature AES. In these patients, a single AES may initiate multiple jumps in only 68%, whereas double AESs or atrial pacing is required in 32%. Such patients can have AVNRT with longer tachycardia CLs and longer ERP and FRP of the AVN. It is uncommon for multiple AVNRTs with different tachycardia CLs and P-QRS relationships to be present in the same patient.

Prevalence of Dual Atrioventricular Nodal Physiology

The presence of dual AVN pathways can usually be demonstrated by using a single AES or atrial pacing in 85% of patients with clinical AVNRT. In 95% of patients, the presence of dual AVN pathways can be shown by using multiple AESs, multiple-drive CLs (typically 600 and 400 milliseconds), and multiple pacing sites (typically high RA and CS). Failure to demonstrate dual AVN physiology in patients with AVNRT can be caused by similar fast and slow AVN pathway ERPs. Dissociation of refractoriness of the fast and slow AVN pathways may then be required. This can be achieved by any of the following: introduction of an AES at a shorter pacing drive CL; introduction of multiple AESs; burst atrial pacing; or administration of drugs such as beta blockers, verapamil, or digoxin. In general, if fast pathway conduction is suppressed in the baseline (as evidenced by a long AH interval at all atrial pacing rates or VA block during ventricular pacing), isoproterenol infusion (and occasionally atropine) usually facilitates fast pathway conduction. In contrast, if the baseline ERP of the fast pathway is very short, conduction over the slow pathway can be difficult to document. Increasing the degree of sedation or infusion of esmolol can prolong the fast pathway ERP and allow recognition of slow pathway conduction.

Another potential reason for the inability to demonstrate dual AVN physiology is block in the fast AVN pathway at the pacing drive CL (i.e., pacing drive CL is shorter than fast pathway ERP). Additionally, atrial FRP can limit the prematurity of the AES. Consequently, AVN activation cannot be adequately advanced to produce block in the fast pathway because a more premature AES would result in more intraatrial conduction delay and less premature stimulation of the AVN. This obstacle can be overcome by the introduction of an AES following a shorter pacing drive CL, introduction of multiple AESs, burst atrial pacing, or stimulation from multiple atrial sites. A typical programmed electrical stimulation protocol used for EP testing in patients with AVNRT is outlined in Table 17-5.²⁸

TABLE 17-5 Programmed Stimulation Protocol for Electrophysiology Testing of Atrioventricular Nodal Reentrant Tachycardia

Atrial burst pacing from the RA and CS (down to AV Wenckebach CL)

Single and double AESs at multiple CLs (600-400 msec) from the high RA and CS (down to atrial ERP)

Ventricular burst pacing from the RV apex (down to VA Wenckebach CL)

Single and double VESs at multiple CLs (600-400 msec) from the RV apex (down to ventricular ERP)

Administration of isoproterenol infusion as needed to facilitate tachycardia induction (0.5-4 µg/min)

AES = atrial extrastimulus; AV = atrioventricular; CL = cycle length; CS = coronary sinus; ERP = effective refractory period; RA = right atrium; RV = right ventricle; VA = ventriculoatrial; VES = ventricular extrastimulus.

Induction of Tachycardia