This is the third part of a series of articles in EP Lab Digest outlining the five components of a basic electrophysiology study. The first article discussed baseline intervals, and the second installment discussed decremental ventricular pacing (DVP). The material is adapted from the Order and Disorder Training Program.
The next part of the electrophysiology study will provide information regarding the behavior of impulse propagation from the “antegrade” perspective, the direction an impulse travels during sinus rhythm from the sinus node through the atria en route to the AV junction. As mentioned in the previous article on DVP, the AV junction is a Y-shaped structure consisting of the anterosuperior approaches to the compact AV node (fast AV nodal pathway), the posteroinferior approaches to the compact AV node (slow AV nodal pathway), and the compact AV node itself. All three of these are atrial structures and, as the compact node transitions into the bundle of His, there is a penetrating portion of the His bundle that actually crosses the annulus entering the ventricles. Figure 1 highlights these components of the conduction system as viewed from the RAO projection and provides a diagrammatic representation of this arrangement. In the right-hand panel, the dashed line identifies the route an impulse is taking over the fast AV nodal pathway. As with DVP, this is a discussion of normal anatomy and does not involve any commentary regarding accessory pathways.
To review, a retrograde impulse, originating from a ventricular pacing source, crosses the annulus over a single pathway, penetrates the compact node and immediately must choose between the diverging fast and slow pathways before activating any ordinary atrial muscle tissue. While neither of the two pathways are enclosed in a fibrous tissue sheath like much of the His-Purkinje system, the impulse is nevertheless confined to the immediate vicinity of either pathway to enable its delivery to one of the respective discrete locations: either the anterosuperior interatrial septum or the region immediately surrounding the CS os. Which route taken is translated by our recording electrograms as having earliest atrial activation either in the His recording (retrograde fast pathway conduction) or in the catheter situated at the CS os (retrograde slow pathway conduction). Close electrode spacing (2 mm) and appropriate catheter location are necessary to properly document this unique anatomic evidence. The concept of this anatomic arrangement is supported by the excellent detailed histologic descriptions by Truex and Smythe1 in 1967 and by Racker2 in 1989. In fact, Tawara’s original drawing of the conduction system from 1907 plainly shows “specialized” fibers that would be consistent with the slow AV nodal pathway projecting into the CS os from the compact AV node. During that early period, the compact node was actually thought to be a part of the coronary sinus. Not a bad idea, though, since they both derive from the primitive sinus venosus.
Quite a different situation exists when considering antegrade conduction. Here, the sinus or atrial paced impulse is destined for a “final common pathway” before entering the ventricles — no matter whether it traverses the fast or slow pathway because they converge. AV nodal conduction is more rapid during impulse propagation over the fast pathway largely because of the less complicated cellular architecture and more optimal myofiber alignment when compared to what the impulse faces as it enters the compact node via the slow pathway approaches. Hence, the PR or AH intervals are shorter than those associated with slow pathway conduction. It would also be useful to point out here that the atrial electrogram (A) seen in the His tracing signals the arrival of the impulse to the “entrance” region of the compact AV node. The “exit” indicator is the His spike (H). Therefore, the AH interval describes not only the transit time “through” the compact node, it will tell the story of its routing there via either the fast or slow AV nodal pathway. One should also note that the single wavefront of activation descending toward the AV node during sinus rhythm will not arrive at the compact node over the two pathways simultaneously because preferential conduction via the fast pathway will prevent access via the slow.
Because the sinus impulse eventually reaches a final common pathway (the compact AV node and bundle of His), there is no recordable “site of earliest activation” unique to either pathway as one readily sees in the case of retrograde conduction. Instead, an “inference” is made enabling identification of which pathway the impulse is traversing as it enters the His bundle. The inference resides in the AH interval value. Since the AV junction’s anatomic arrangement favors more rapid conduction via the anterosuperior “approaches” to the AV node, the range of AH intervals reflecting this route, the fast pathway, will be shorter than those via the slow pathway’s posteroinferior approaches. Any AH interval <150 msec reflects fast pathway conduction regardless of whether you are in sinus rhythm or have atrial pacing. Any AH interval >200 msec is slow pathway conduction, again irrespective of the rhythm’s origin (sinus or atrial pacing). The rate of impulse input to the compact node during sinus rhythm is the lowest and, therefore, provides the most favorable (quickest) conduction opportunity for an impulse transiting the fast pathway. Thus, the AH interval is always shortest during sinus rhythm.
Under normal circumstances (no drugs or structural heart disease) and during sinus rhythm, antegrade conduction is present in virtually 100% of us, and it happens thanks to your fast AV nodal pathway. This evolutionary trait, designed to provide a certain atrioventricular timing relationship, allows for an optimal end-diastolic ventricular volume under a wide range of sinus rates. Note that because antegrade fast pathway conduction is preferential to slow, impulse conduction over the slow will only take place once fast pathway conduction fails. Thus, the slow pathway is always the “last man standing.” Very few of us do not have a slow pathway available for antegrade conduction. The slow AV nodal pathway is part of normal anatomy. You are born with it.
What is the slow AV nodal pathway’s claim to fame? While it is most notorious for the crimes of common and uncommon AV nodal reentry, its existence begs the question: why is it there in the first place? This is an unanswered question on evolution, but speculation might suggest it is the distal remnant of the long-lost posterior internodal tract (Thorel’s bundle — one of the three purported “tracts” connecting sinus to AV node and not proven to exist).
The following section will describe how to perform decremental atrial pacing (DAP) and what to expect to see on the tracings. DAP closely resembles what you already read about DVP. DAP — just like DVP — is a means of assessing AV nodal function as much as it is a method of determining which route an impulse accesses on the way to the ventricles. Since no “earliest site of antegrade ventricular activation” exists, the only way to tell which pathway you are on at any given time is by looking at the AH interval value.
At the outset of DAP, pacing is begun at a cycle length slightly shorter than sinus cycle length. Only then will the atrial rhythm become a paced rhythm. Unlike DVP, wherein absent VA conduction or “slow only” are possible, there will always be antegrade ventricular “capture” via the fast AV nodal pathway and 1:1 conduction will be guaranteed. The sequence of electrograms in the His bundle tracing (A, H, and V) will be identical to sinus rhythm except for the interval between the A1 and H1, which will progressively widen as PCL shortens. During basic pacing, the electrograms are labeled A1, H1, and V1 (Figure 2).
The pacing cycle length (PCL) is decremented by 10-20 msec about every 8-10 beats. You can program your stimulator to automatically do this, so sit back and enjoy. Each time the PCL is shortened, it takes a few beats for the AV node to accommodate to the new cycle length. During this adjustment to a faster rate of impulses inputting to the AV node, the A1-H1 interval will lengthen by 5- to 15-msec amounts until stabilized. Once stabilized, confirm that each A1-A1 interval is identical to its accompanying H1-H1 and V1-V1 intervals. Always measure the A1-H1 interval belonging to one of the last beats during any given PCL.
Transit time through the compact AV node increases because of “decremental conduction,” which will get progressively worse until either a shift to the slow pathway or the development of second-degree AV block. Unlike DVP, wherein the shift from fast to slow pathway conduction is obviously signaled by a change in the site of earliest retrograde atrial activation (in addition to a large change in V1-A1 interval), during DAP that change to slow pathway will only be signaled by an A1-H1 interval having exceeded 200 msec. While most of the time, the magnitude of change in the A1-H1 interval at the time of that shift is ≥35 msec, it can be so gradual that it could be missed. Typically, as long as an impulse is maintaining travel over a given pathway, whether fast or slow, the magnitude of the A1-H1 interval change from one PCL to the next will be small (5-15 msec). Only when the impulse is teetering on the limit of fast pathway conduction does the A1-H1 interval begin to change substantially (i.e., ≥35 msec), as it is about to shift to the slow. Similarly, only when an impulse is teetering on the limit of slow pathway conduction does the A1-H1 interval lengthen substantially, as AV block is imminent. As long as the PCL doesn’t change, the A1-H1 interval won’t change. The exception to this is when you are in the Wenckebach cycle length, wherein it constantly changes.
As PCL decrementing continues, you must keep your eyes on the RA recording (the A) and the QRS in V1 (the V), looking for the moment when there is a loss of V (i.e., development of block). Because these two channels are adjacent to each other, it offers the ability to quickly detect when block occurs so that you can stop pacing. Here’s how: as you progress through DAP, the A1-H1 interval lengthening creates the appearance that the RA electrogram is moving progressively to the left, farther away from the QRS it produces. However, what is easier to see is that RA electrogram getting progressively closer to the previous QRS. As the RA electrogram begins to coincide with the previous QRS, AV block is imminent and there will be a sudden lengthening of the RR interval, signaling the loss of antegrade 1:1 conduction (a missing V) that one may refer to as “the GAP in DAP” (Figure 3). Once this is reached, pacing can be stopped. Sometimes, in patients with very stable conduction over a slow pathway, the RA electrogram can move in front of the previous QRS so much that you may begin to get confused as to which A makes which V.
Assessment of Antegrade AV Nodal Function
Exactly like DVP, two pieces of information about AV nodal function are revealed during DAP: the limits of impulse input to the node, and AV nodal transit time. In determining the limits of impulse input to the AV node, one is assessing how rapidly an impulse can be delivered to the compact node and still make it through the node (i.e., 1:1 conduction must be maintained during the assessment). Once AV block occurs, it’s over. This limit can be referred to as the “shortest A1-A1 interval maintaining 1:1 conduction” or the “longest A1-A1 interval associated with block (the Wenckebach cycle length).” The two expressions are equivalent. Since most people have both antegrade fast and slow pathway conduction, different input limits can be identified for each pathway. As mentioned above, since the fast pathway is preferential, the input limit to it will always be reached first, and then, as more rapid 1:1 AV nodal conduction continues over the slow pathway, the limit over this route is finally reached.
Transit time refers to the amount of time (in milliseconds) for an impulse to travel through the compact AV node, and is directly measured by the AH interval. Unlike retrograde conduction, in which the impulse confronts a diverging pathway anatomy, it confronts converging pathways. As long as impulse transit proceeds through the node via the fast pathway, the AH interval will be <150 msec. Once it shifts to the slow, the AH interval will be >200 msec. Because of the converging anatomy between the two pathways, transitioning isn’t always so distinct: values between 150-200 msec could represent either pathway.
As during DVP, there are predictable patterns of AV nodal conduction preceding the development of second-degree AV block. Three are possible. The first involves antegrade conduction limited to the fast AV nodal pathway up to and including the Wenckebach cycle. This pattern is illustrated in Figures 4 and 5. It is the least common pattern found in about 13% patients. When AV block occurs, it usually persists with a 2:1 pattern, although a Wenckebach pattern is possible. To verify that the patient has nothing but a fast AV nodal pathway available for antegrade conduction, one needs only to look at the last conducted atrial paced beat: its A1-H1 interval will be <200 msec.
The second is seen when antegrade conduction shifts from the fast to the slow AV nodal pathway, with the shift occurring immediately before the point of AV block and reflects relatively unstable slow AV nodal pathway conduction. This pattern is illustrated in Figures 6 and 7. When block occurs, the pattern is always Wenckebach. This is found in about 36% patients, and is the second most common finding during DAP. In other words, only during the Wenckebach cycle does the slow pathway show its colors. The A1-H1 interval of the last conducted beat will always have a value of >200 msec.
The third also involves dual pathways, but the shift from fast to slow occurs well before the Wenckebach cycle (Figures 8 and 9). This patient has stable slow pathway conduction: antegrade conduction shifts to the slow pathway and remains on it, as PCL continues to decrease for at least one complete PCL. Autonomic balance is important, just as in the case of retrograde conduction: too much adrenergic tone (isoproterenol or atropine) will minimize impulse conduction lingering on the slow pathway. Too much vagal tone (sedation) may promote slow pathway conduction. This third pattern is more likely to be associated with AV nodal reentrant tachycardia, because in order to have sustained common AV node reentry, one’s slow pathway needs to have the ability to maintain stable, 1:1 antegrade conduction and at the cycle lengths typifying their tachycardia. A slow pathway that cannot show up for work is not dependable and won’t support tachycardia. When block does occur, the pattern is almost always Wenckebach, involving both pathways but may be confined to the slow pathway. The A1-H1 interval of the last conducted beat will always have a value >200 msec. This pattern accounts for 55% of all patients.
Antegrade conduction occurring exclusively over the slow AV nodal pathway is not a normal finding. Very rare and usually iatrogenic, it can be caused by large doses of drugs that result in impaired AV nodal conduction (negatively dromotropic), or an inadvertently damaged fast pathway during aortic valve replacement or TAVR. Occasionally, exaggerated vagal tone in a young, athletic individual will allow periods of sustained antegrade slow pathway conduction during sinus rhythm, but intermittent switching back to the fast in conjunction with autonomic tone changes is inevitable.
To summarize, this is how to recognize whether an impulse is traveling over the fast or slow AV nodal pathway:
- Fast: Any AH interval <150 msec. AH intervals between 150-200 msec may represent “slowly conducting” fast pathways.
- Slow: Any AH >200 msec. Likewise, “rapidly conducting” slow pathways can also be in the range of 150-200 msec.
We talked much about the “atrial activation sequence” in our previous discussion on DVP, but have said little about it during this current discussion on DAP. Why? During DVP, the particular arrangement of atrial electrograms (the so-called retrograde atrial activation sequence) is entirely dependent on the location of the route introducing the impulse to the atria. Hence, the retrograde atrial activation sequence plainly discloses exactly what we are looking for: the location of a specific route connecting the atria to the ventricles, the choices being fast pathway, slow pathway, or accessory pathway. Not so with DAP. Because we are pacing the atria, the atrial activation sequence only reflects what we already know: the site of the RA pacing catheter where the impulse starts atrial activation. As long as we pace from this same site, the atrial activation sequence will never change regardless of how our impulse gets into the ventricles.
The purpose of DAP is to characterize the nature of antegrade AV nodal conduction: how fast can you pace the atria and still maintain 1:1 fast pathway conduction? How fast can you pace the atria and still maintain 1:1 conduction over the slow pathway? What is the longest fast AV nodal pathway A1-H1 interval? What is the longest obtainable A1-H1 interval? One of the most useful applications of the information provided in this article is the ability to know, in advance of catheters even being placed in the heart, what will be seen on the monitor as you watch DAP unfold. In any patient (without an accessory pathway), only three possibilities exist.
A point worth mentioning at this juncture is that DAP is actually more relevant than atrial extrastimulus testing (AET, the next article installment in this series) in disclosing the presence of a slow pathway. In the quest for diagnosing the mechanism of a given PSVT, our endpoint is uncovering AV nodal reentry — the most common PSVT — or coming up with an alternative explanation. The difference between DAP and AET is that DAP uniquely uncovers slow pathways having stability: those capable of conducting 1:1 over a range of PCL, particularly at cycle lengths typifying their tachycardia. AET will only give you a single beat’s worth of slow pathway disclosure, because the technique employs only a single extrastimulus rather than continuous pacing. Moreover, many patients with dual physiology won’t exhibit the >50 msec jump in consecutive A2-H2 intervals, AET’s traditional defining feature of dual physiology. The take-home message is that if a tachycardia is going to use a slow pathway as a part of its circuit, its impulse must conduct over it on a repetitive basis — and at the kind of rates at which the tachycardia exists. Thus, a “one-beat” disclosure of a slow pathway by AET may or may not be clinically meaningful unless it belongs to the beat that initiates AVNRT.
Final Thoughts: Jump or Block?
This article will end on an important comment regarding a more advanced concept not possible to cover here. It’s about an often difficult distinction between an impulse undergoing a shift to a prominent slow pathway versus one undergoing AV block where there is no slow pathway to shift to. Either can produce the visible “GAP in DAP,” and you are going to want to know which: jump or block? Here’s how: the AH interval of the beat ending the GAP should always be longer than the AH interval during sinus rhythm (Moulton’s rule) when AV block is the cause of the GAP. In Figure 9, the A1-H1 interval ending the GAP is 100 msec, longer than the patient’s sinus rhythm AH interval of 65 msec (not shown in the figure). That means that the GAP in DAP was due to AV block, not a jump to the slow pathway.
If the A1-H1 interval of the beat ending the GAP is shorter than the sinus rhythm AH interval, it’s not a real A1-H1 interval. It is a “pseudo” AH interval: having an A that will belong to the next QRS but positioned in front of the His spike that belongs to the previous beat, and representing a jump to a prominent slow pathway. These pseudo-AH intervals are always less than the AH interval measured during sinus rhythm. Given the normal behavior of progressive lengthening of the A1-H1 interval during DAP, it would be impossible to conduct more rapidly than that seen during sinus rhythm, when one is pacing at the very short cycle lengths as you reach the end of DAP. You can play the game “jump or block” during your cases.
Disclosures: The authors have no conflicts of interest to report regarding the content herein.
- Truex RC, Smythe MQ. Reconstruction of the human atrioventricular node. The Anatomical Record. 1967;158(1):11-19.
- Racker DK. Atrioventricular node and input pathways: a correlated gross anatomical and histological study of the canine atrioventricular juntional region. The Anatomical Record. 1989;224(2):163-176.