dual atrioventricular nodal pathways physiology

8/19/2019 Dual Atrioventricular Nodal Pathways Physiology

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Dual Atrioventricular Nodal Pathways Physiology: A Review of RelevantAnatomy, Electrophysiology, and Electrocardiographic Manifestations

Bhalaghuru Chokkalingam Mani, MD and Behzad B Pavri, MD

Author information ► Copyright and License information ►

his article has !een cited !y other articles in PMC"

Abstract

The term "dual AV nodal pathways" is loosely used by many clinicians when analyzing

electrocardiograms and telemetry strips. This term, to the novice physician, might suggest two,

distinct anatomic structures related to the atrioventricular (AV) node, but often the true

understanding of this entity is either missing or incomplete. The purpose of this manuscript is to

review the anatomy, physiology, and electrophysiologic functional characteristics of the human

AV node, and demonstrate the variety of electrocardiographic manifestations of what should

correctly be described as "dual AV nodal pathways physiology". This review may be most

helpful to physiciansintraining interns, residents, and cardiology or pulmonary fellows!

practicing internists with special interest in electrocardiography may also find this of value.

#o to$

Anatomy of the A node

The AV node is part of the AV conduction ais. #y virtue of its uni$ue property of decremental

conduction, the AV node delays the impulse arriving from the atria, thereby allowing theventricles to stay in diastole, providing sufficient ventricular filling time. This property of

decremental conduction also allows for protection of the ventricles from very rapid rates during

atrial fibrillation. Though there were numerous researchers who identified the presence of an

electrical connection between the atria and the ventricles, the physical eistence of the AV node

was definitively proven by Tawara. %&,'

The compact AV node is located at the base of the atrial septum in the triangle of och %*

(+igure &). The triangle is visualized on the right side of the endocardial surface of the interatrial

septum, and is formed anteriorly by the insertion of the septal leaflet of the tricuspid valve and

posteriorly by the fibrous tendon of Todaro %. The ape of the triangle is formed by the -unctionof these two boundaries and the base is formed by the superior lip of the orifice of the coronary

sinus %. The AV node can be considered to be made up of two zones, transitional and compact.

The transitional zone consists of "transitional cells", so called because they are intermediate in

morphology and function between the compact nodal cells and the atrial myocytes. This zone of

transitional cells envelops the compact AV node, serving as the connection between the

surrounding atrial myocardium and the compact node %/.

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+igure &

0chematic representation of the interior of the right atrium, as viewed in the right anterior

obli$ue pro-ection. The transmission of impulse from the sinoatrial node over the "fast pathway"

(green arrow) and over the "slow pathway" (red dashed arrow) ...

The compact zone measures 1 mm in length and * mm in width and is located in the triangle

of och. The compact AV node gives rise to three posterior etensions2 one in the direction of

the coronary sinus along the tricuspid annulus (the putative "slow pathway"), a second in the

anterior portion of the triangle of och near the compact portion of the AV node (the putative

"fast pathway"), and the third in the direction of the mitral annulus (the left atrial etension) %1.

The anatomic separation of about & mm %3 between the anterior (fast) and posterior (slow)approaches is what allows safe ablation of the putative "slow pathway" for the treatment of AV

nodal reentrant tachycardia without the creation of complete heart bloc4.

#o to$

Electrophysiology of the A node

The mechanism underlying the uni$ue property of decremental conduction is not fully

understood, although two hypotheses have been put forth. The first is referred to as the

decremental driving force hypothesis and suggests that conduction along the AV node may

change in such a way that the propagating "action potential becomes progressively less effectiveas a stimulus to the unecited portion of the fiber ahead of it" %5. The second hypothesis is

referred to as the electrotonic transmission hypothesis,%&6 and states that the driving voltage is

constant, but that inecitable microscopic segments cause "stagnation" between different zones

of the AV node. 7ecent studies assessing epression of gap -unction proteins, specifically

connein * (8*), shows concordance of 8* distribution along anatomically defined AV

nodal structures %&&.

The wave front of atrial activation engages the AV node at multiple locations. The dual AV nodal

system involves two separate approaches to the compact AV node, the socalled fast and slow

"pathways". As is true for most ecitable tissue, the (anteriorly located) "fast pathway"

demonstrates the greater conduction velocity, but ta4es longer to recover from ecitation! i.e., the

fast pathway has the longer refractory period . The (posteriorly located) "slow pathway" has the

slower conduction velocity, but recovers faster from prior depolarization, i.e., the slow pathway

has the shorter refractory period . 9legant studies have shown that the posterior etension of the

AV node provides the anatomic basis for all the electrophysiologic properties ascribed to the

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"slow pathway" %&'. Although not discretely identifiable as separate anatomic structures, these

inputs result in a highly heterogeneous engagement of the AV node as shown by optical mapping

studies %&*. These approaches form the basis for "dual AV nodal pathways" physiology.

The electrophysiologic definition of dual pathways physiology in the electrophysiology

laboratory depends on the demonstration of discontinuous antegrade AV nodal conduction in

response to atrial programmed electrical premature stimulation. This involves delivery of a train

of eight impulses (A&) at a fied cycle length, followed by a single premature impulse (A'). The

conduction time of this premature impulse (A') through the AV node (the A: interval) is

measured, as the degree of prematurity is gradually increased in &6 ms decrements. ;ecremental

conduction of A' through the AV node results in progressive and gradual prolongation of nodal

conduction time with increasing prematurity. An abrupt increase in AV nodal conduction time of


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0ympathetic stimulation shortens conduction time and refractoriness, whereas vagal stimulation

provides the opposite effect. These observations have been used to control ventricular rate in

atrial fibrillation by stimulation of postganglionic vagal fibers near the ostium of the coronary

sinus in animal %& and human %&,&/, models. At rest, increasing atrial rates (as during atrial

pacing) result in decremental AV nodal conduction, as discussed above. :owever, duringeercise, increasing sinus rates are accompanied by shortening of AV nodal conduction times, as

manifested by @7 interval shortening.

Antiarrhythmic drugs may preferentially affect slow or fast pathway conduction, but these effects

are not consistent, and are influenced by the presence of underlying conduction system disease.

#loc4ade of the sympathetic and vagal influences by administration of propranolol and atropine,

respectively, renders the ma-ority of AV7T noninducible %&1! this observation supports the

"functional" $uality of dual AV nodal pathways physiology.

#o to$

Modulation of dual A nodal pathways physiology

Effect of Adenosine on dual pathways physiology

Bow doses of adenosine administered in sinus rhythm or during atrial pacing preferentially slow

conduction in the fast pathway (mean dose re$uired for fast pathway bloc4 was '.1C*.6 mg),

resulting in manifest engagement of the slow AV nodal approach! bloc4 in the slow pathway

re$uired a higher dose (mean 1.'C.1 mg) %&3. Bowdose adenosine can serve as a noninvasive

diagnostic test of dual AV nodal physiology. :igher doses bloc4 conduction in both slow and fast

approaches, and adenosine is clinically used to terminate reentrant arrhythmias that involve theAV node. #edside administration of adenosine can help ma4e the diagnosis of dual AV nodal

pathways physiology.%&5,'6

Effect of agus nerve stimulation on dual pathways physiology

+isch et al proposed that the changes in autonomic influence could be the potential trigger in

shifting conduction from the fast to the slow pathway, resulting in sudden changes in @7 interval.

8hiou et al showed that that increase in vagal tone preferentially prolonged the effective

refractory period of the fast pathway as compared to slow pathway %''. :owever, carotid

massage will often stop typical AV7T in the anterograde slow pathway (see +igure *).

+igure *

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Typical AV7T terminated by carotid sinus massage. The 7@ interval is short (less than &66ms)

favoring typical slowfast AV7T as the 0VT mechanism. The retrograde @ wave is inscribed

immediately following the D70 comple (creates the appearance of a ...

Effect of parasympathetic bloc!ade vs" adrenergic stimulation on dual pathways physiology

0tellbrin4 et al tested the comparative efficacy of parasympathetic bloc4ade vs. adrenergic

stimulation on inducibility of AV7T at the time of 9@ testing %'*. Atropine (6.6& mg?4g) was

compared to isoproterenol (6.&.6 mcg?4g?min infusion) prior to ablation. Atropine reduced

inducibility, whereas isoproterenol increased inducibility of AV7T, mainly by accelerating slow

pathway conduction velocity.

Effect of beta#adrenergic receptor bloc!ade on dual pathways physiology

9smolol was shown to have $uantitatively greater effect on antegrade refractoriness of the fast

pathway as compared to the slow pathway %'.

#o to$

E$% manifestations of dual A nodal pathways physiology

;ual pathway physiology can be electrocardiographically "silent" with no manifestations

whatsoever. The prevalence of dual pathways physiology is variably reported as being

demonstrable in &6 to *E of normal people %''3 including children %'5, but may become

less common with aging %*6. A multitude of electrocardiographic manifestations %&5,*&,*' may

be eplained by dual pathways physiology (see Table &).

Table &

98F =anifestations of ;ual AV odal @athways @hysiology

Rapid ventricular rates during atrial fibrillation

#ased on its shorter refractory period (see above), it is believed that the shortest 77 intervals

(the fastest rates) during atrial fibrillation represent conduction over the "slow pathway" of the

AV node! ablation of the slow pathway region in patients with atrial fibrillation results in

significant slowing of the ventricular rates %**. This is reflected in a bimodal distribution of 77

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intervals on preablation :olter recordings, which is replaced by a unimodal pattern after

ablation of the slow pathway %*, as shown in +igure .

+igure

:istogram A 0hows #imodal 77 interval distribution in a patient with atrial fibrillation before

AV node modification. :istogram # shows unimodal 77 interval distribution after AV node

modification due to slow pathway ablation which has eliminated the ...

Gn fact, the presence of a bimodal 77 interval plot prior to ablation predicts a better outcome

after ablation of the slow pathway region, as compared to patients with a unimodal 77 interval

distribution %*.

Atrioventricular Nodal Reentrant &achycardia 'ANR&(

AV7T is the commonest form of regular supraventricular tachycardia in humans, and presents

as regular narrow comple tachycardia on the 98F. AV7T can be typical (also referred to as

the common form) or atypical (the uncommon form) depending on the location of the atrial

deflection between consecutive D70 complees. This is thought to reflect direction of reentrant

ecitation with the AV nodal circuit %*/.

Typical AV7T or the "slowfast" type is the commonest (H36E) form of AV7T. The earliest

site of retrograde atrial activation in this type is seen in the region of the fast pathway near theape of the triangle of och. Gt is usually initiated by an atrial premature depolarization which,

by virtue of prematurity, finds the fast pathway refractory and conducts to the ventricles via the

slow pathway (see +igure ), middle panel)! the surface 98F records a prolonged @7 interval. Gf

sufficient time has lapsed to allow recovery of the fast pathway, the impulse can conduct rapidly

up the fast pathway, resulting in a typical AV nodal "echo" beat! the surface 98F records a short

7@ interval. Gf this pattern perpetuates, AV7T is initiated. Typical AV7T can be initiated by

single or multiple atrial premature complees.

+igure

=odel of dual AV nodal pathways physiology in sinus rhythm, with an atrial premature beat

(A@;) which initiates typical "slowfast" AV7T, and with a ventricular premature beat (V@;)

which initiates atypical "fastslow" AV7T. 0ee tet for details.

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Atypical or the "fastslow" type of AV7T is relatively uncommon (about E). The earliest site

of retrograde atrial activation in this type is seen in the region of the slow pathway near the

ostium of the coronary sinus. Atypical AV7T (see +igure /) is often initiated by a premature

ventricular comple that conducts retrogradely through the slow pathway to the atrium, having

found the fast pathway inecitable (see+igure , right panel)! the surface 98F records a long 7@interval (see +igure ). Gf retrograde conduction is sufficiently slow, the fast pathway may

recover sufficiently to carry the ecitation bac4 to the ventricles, resulting in an atypical AV

nodal "echo" beat! the surface 98F records a short @7 interval. The earliest site of atrial

activation is near the ostium of the coronary sinus. Bess often, this form of AV7T can also be

initiated by an atrial premature comple which conducts to the ventricles over the fast pathway,

and conducts bac4 to the atrium over the slow pathway.

+igure /

Atypical AV7T! the 7@ interval is long (about *&6 milliseconds) favoring atypical fastslow

AV7T as the 0VT mechanism. The retrograde @ wave is inscribed immediately before the D70

comple and is superimposed on the T wave.

Ither atypical variants of AV7T (J&E) %*' are also described, including slowslow, fast

intermediate and slowintermediate forms which use functionally and or anatomically distinct

fast, slow or intermediate pathways to induce tachycardia. :owever, the site of earliest

retrograde atrial activation in these forms is more variable %*1. +urther studies are re$uired tounderstand why certain tissues within the AV node comple demonstrate different conduction

velocities, but one potential eplanation is the heterogeneous distribution of 8onneins within

the AV node %*3.

Post#P$ PR interval prolongation # concealed conduction

8oncealed conduction is a phenomenon that describes partial penetration of an impulse into a

given tissue (e.g., the AV node), but can only be inferred by the behavior of the subse$uent

impulse that conducts through the same tissue %*5. (0ee +igure 1) 8oncealed conduction can

bloc4 the dual pathways physiology from being set into motion by prolonging the refractory period of the slow pathway.%'5

+igure 1

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@ost@V8 @7 prolongation. The th and /th beats in the top tracing are premature ventricular

contractions (@V8& and @V8')! @V8' conducts retrogradely into the fast pathway of the AV

node, and renders it refractory. The net @ wave conducts anterogradely ...

&wo families of PR )nterval

I occasion, dual AV nodal physiology can present as normal sinus rhythm with subtle 98F

changes which manifest as a abrupt lengthening or shortening of the @7 interval (see +igure 3).

The shorter @7 interval represents conduction over the fast pathway (normal) and the longer @7

represents conduction over the slow pathway. The shift in conduction from fast to slow pathway

can occur spontaneously or can be provo4ed by an atrial premature comple or a ventricular

premature comple. 0imilarly the conduction through the slow pathway can be terminated by an

atrial premature comple, a ventricular premature comple or even a short run of atrial

tachycardia. Kncommonly sinus rhythm with @7 alternans can occur in which a long and short

@7 interval alternate with each other.%&1 Gt can also manifest as two families of @7 intervals thatsignify presence of underlying dual AV nodal physiology.%&5,*6

+igure 3

A spontaneous change in @7 interval during regular sinus rhythm at / beats per minute is noted.

There are two "families" of @7 intervals2 one group of @7 intervals measure about ''6 ms

(representing conduction over the "fast pathway"), and the other ...

Gnterestingly, patients with two families of @7 interval almost never show reentrant AV7T! this

is related to etensive "fast pathway" disease, which does not allow retrograde conduction.

&wo families of RP )nterval

7arely, the same physiology described above in the anterograde direction may be seen in the

retrograde direction as well. This would manifest as -unctional or ventricular rhythms with &2&

retrograde conduction, but with ' families of 7@ interval (see +igure 5).

+igure 5

This 98F shows a -unctional (narrow comple) rhythm at ' bpm with &2& -unctiontoatrium

conduction with retrograde @ waves. :owever, the 7@ interval alternates between 36 ms and &36

ms, consistent with "dual AV nodal pathways" physiology. The DTc interval ...

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Pseudo#)nterpolation

Gn fact, one of the earliest manifestations of dual pathways physiology was shown by istin in

&5/', when he noted that apparent interpolation of @V8s was in fact due to AV nodal "echo"

beats %6. Therefore, single AV nodal echo beats can mimic interpolation (see +igure &6).

+igure &6

@seudointerpolation. A premature ventricular comple conducts to the atrium through the "fast

pathway" producing a retrograde @ wave. This @ wave then conducts through the slow pathway

with a prolonged @7 interval, producing a ventricular "echo" beat, ...

Double ventricular response to a single atrial depolari*ation # +Double ire+

Ine of the rarer 98F manifestations of dual pathways physiology, a double ventricular response

to a single atrial impulse is due to the anterograde conduction of the impulse in both the fast and

the slow pathways (see +igure &&). This re$uires that slow pathway conduction must be slow

enough to allow :is@ur4in-e tissue to recover ecitability after being depolarized by the first

ecitation over the fast pathway. Gn addition, unidirectional retrograde bloc4 in the both

pathways is essential for this to occur %&. ;ouble ventricular responses arising from one atrial

impulse may result in tachycardia that does not utilize a reentrant circuit, and has been referred

to as "double fire" or nonreentrant tachycardia, first described by 8sapo F as early as &515 %'.

0ince then, double fire tachycardia and tachycardiarelated cardiomyopathy that reverses withablation of the slow pathway have been well described %*.

+igure &&

The rhythm strip is lead V& of a surface electrocardiogram. A ladder diagram demonstrated the

proposed mechanism for &2' AV conduction via dual AV nodal pathways. 8oncealed retrograde

conduction in both fast and slow pathways led to a pseudoLenc4ebach...
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dual atrioventricular nodal pathways physiology

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