Cardiac Electrophysiology 2: An Advanced Visual Guide for Nurses, Techs, and Fellows

by Paul D. Purves, George J. Klein, Lorne J. Gula

Overview

Following the bestselling Cardiac Electrophysiology: A Visual Guide for Nurses, Techs, and Fellows, this book builds upon the basic concepts of electrophysiology introduced in the first volume and guides the reader to a more in-depth understanding of cardiac electrophysiology by working through commonly encountered scenarios in the EP lab.

Product Details

ISBN-13:	9781935395973
Publisher:	Cardiotext Publishing
Publication date:	05/01/2014
Edition description:	1
Pages:	292
Product dimensions:	8.40(w) x 10.90(h) x 0.70(d)

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Cardiac Electrophysiology 2

An Advanced Visual Guide for Nurses, Techs, and Fellows

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By Paul D. Purves, George J. Klein, Peter Leong-Sit, Raymond Yee, Allan C. Skanes, Lorne J. Gula, Jaimie Manlucu

Cardiotext Publishing, LLC

Copyright © 2014 Paul D. Purves
All rights reserved.
ISBN: 978-1-935395-97-3

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CHAPTER 1

Cardiac Electrophysiology 2

PHYSIOLOGY

OUTLINE

1.1 Common Pitfalls 2
1.2 Heart Block 6
1.3 Proximal Delay 10
1.4 Aberrancy 18
1.5 Normalization 22
1.6 Bundle Reset 30
1.7 Differentiation 34
1.8 Concealment 40
1.9 Concealment 2 46
1.10 Escape Rhythm 50
1.11 Nodal Function 54

1.1 Common Pitfalls

This figure nicely illustrates the importance of proper catheter positioning required for accurate baseline measurements. Identify the unexpected potential in the displayed channels.

Discussion

In this example, the RV apical (RVA) catheter is positioned at the basal septum, where it can often record a right bundle potential. This should not be confused with a His potential.

Mistaking the right bundle potential for a His electrogram would underestimate the true H-V interval, leading to the erroneous conclusion that an accessory pathway (AP) is present. A normal H-V interval is approximately 35 to 45 ms.

In this particular case, mistaking the right bundle potential for a His electrogram would lead to an H-V of 10 ms, falsely suggesting that the patient is preexcited. This is clearly not the ca se since there is no manifest preexcitation on the surface E CG .

In this tracing, when the H-V is properly measured using the His catheter electrograms, it is within the normal range.

1.2 Heart Block

To review, there are 3 levels of heart block (or AV nodal block). Each level represents progressively more distal conduction system disease.

First-degree AV block represents AV nodal disease and manifests as a long P-R interval (greater than 200 ms) on an ECG.

Second-degree Mobitz Type I AV block (also known as "Wenkebach") represents slightly more advanced AV nodal disease, and manifests as a progressive prolonging of the P-R interval until a P wave does not conduct.

Second-degree Mobitz Type II AV block represents conduction system disease that is distal to the AV node. This manifests as a constant P-R interval with intermittent unexpected nonconducted sinus P waves.

Third-degree AV block (also known as "complete heart block") represents severe distal conduction system disease. This manifests as sinus P waves at a rate faster than the ventricular rate, A-V dissociation, and a regular ventricular response. The ventricular escape rhythm can originate anywhere from the junction to the ventricles.

Where is the level of block in this example?

Discussion

This figure demonstrates the presence of Mobitz Type II second-degree heart block. A s mentioned, this is usually indicative of distal conduction system disease.

The intracardiac electrograms show regular atrial pacing with intermittent block to the ventricles while displaying a His electrogram (white arrow). Lack of conduction below the His is indicative of the presence of conduction disease below the AV node.

This makes A-V conduct ion unreliable and of ten progresses unpredictably to complete hear t block. Therefore, these patients are usually referred for pacemaker implantation.

1.3 Proximal Delay

In this example, we are doing ventricular extra-stimulus pacing to evaluate the retrograde Effective Refractory Period (ERP) of the AV node. The S1 S2 coupling interval was 600/240 ms. But, what input did the AV node actually receive?

Discussion

These proximal conduction delays suggest that the ERP of the myocardium will likely be reached before the ERP of the AV node.

1.4 Aberrancy

Both of these tracings demonstrate AV nodal reentrant tachycardia (AVNRT) with aberrant conduction. Discussion of AVNRT will be covered in a subsequent chapter. These figures focus on the physiology of aberrant conduction.

Discussion

In both tracings, AVNRT is initiated with atrial extra-stimulus pacing. We see development of a typical left bundle branch block (LBBB) in Figure 1, and a typical right bundle branch block (RBBB) in Figure 2.

These bundle branch blocks develop due to a sudden shortening of the tachycardia cycle length, which catches one of the bundle branches (most commonly the right bundle) still in its refractor y period. This is commonly referred to as a "rate-related" bundle branch block or Phase III block. This is a functional block and is a normal phenomenon.

The bundle branch block usually spontaneously resolves due to a phenomenon referred to as "peeling back of refractoriness," a process by which the refractor y period of the bundle shortens and conduction velocity is enhanced in response to increased heart rate.

See Chapter 1.5 for further clarification.

1.5 Normalization

Previously in Section 4, we discussed the reasons for aberrant conduction. However, aberrant conduction may spontaneously normalize. Please consider the reasons why this may occur.

Discussion

Spontaneous normalization of the QRS occurs due to the progressive shortening of the refractory periods of the bundle branches, as well as enhanced conduction velocity in response to an increase in heart rate and/or catecholamine levels.

As mentioned previously, this is a form of functional block and is a normal physiological phenomenon. In this example, a RBBB spontaneously resolves. Note the intermediate QRS morphology just before complete normalization.

In Figure 1, the initial RBBB occurs quite proximally in the bundle. The wave of depolarization continues to conduct down the left bundle, through the interventricular septum and retrograde up the right bundle. The collision point between the antegrade and retrograde waves is quite proximal in the right bundle.

In the next beat of tachycardia (shown in Figure 2), the collision point of the 2 waves is more distal in the right bundle. With each subsequent beat, the point of collision occurs progressively more distally in the right bundle.

When the collision occurs distal to the insertion site of the right bundle, the QR S normalizes (Figure 3).

[Presented as movie in digital version.]

1.6 Bundle Reset

As in the case displayed previously in Section 4, we have ongoing AV N RT. Once again, the physiology of the bundle branch block (aberrancy) is the focus. If spontaneous normalization does not occur, can we "force" normalization?

Discussion

In this tracing, we see a QRS transition from a LBBB pattern to a normal narrow QRS morphology following a ventricular extrasystole (or premature ventricular contraction (PVC)) from the RVA catheter.

The right ventricular P VC resolves the L BBB by preexciting both bundle branches. This shortens their refractory periods and also allows them more time to recover before the next beat of t he AVNRT tachycardia arrives.

This is also known as "resetting" of the bundle branches.

1.7 Differentiation

This is a nice example of a very common observation. The question to be answered is, "How do you differentiate between 2 AV nodal echoes versus 2 junctional beats?"

Discussion

Figure 1: Following an atrial extra-stimulus (S1S2), there is a long pause followed by 2 beats with simultaneous activation of the atrium and the ventricle. Atrial activation is concentric, and the V-A time is almost zero.

There are 2 possibilities for this observation: 1. The S2 is conducted down a slow pathway and retrograde up a fast pathway resulting in 2 sequential AV nodal echoes or 2. The S2 blocks and the 2 subsequent beats are junctional.

Figure 2: In this figure, an S3 is added after the same S1S2 we see in Figure 1. In this sequence, the pause following the S2 is interrupted by the S3, which appears to conduct

There are also 2 possible explanations for this response:

1. The S2 is conducted down a slow pathway and the S3 blocks. If this were the case, the S3 would not be able to penetrate the AVNRT circuit since the antegrade fast pathway would be refractory and the slow pathway is being used. Therefore, the timing between the S2 and the next QR S should be the same as we see in Figure 1.

Alternatively ...

2. The S2 blocks and the S3 conducts down the fast pathway. If this were the case, the S3 should advance the next QRS (i.e., it should occur earlier than it did in Figure 1).

Figure 3 provides the answer. In this figure, calipers mark the interval between the S2 and the first QRS seen in Figure 1. As you can see, the QR S clearly occurs earlier than it did in Figure 1, suggesting that it was advanced by the S3 .

This suggests that the S2 likely blocked, and that the last 2 beats in Figure 1 are actually junctional beats and not AV nodal echoes.

1.8 Concealment

This figure nicely demonstrates the concept of concealed conduction.

Discussion

The first beat in this tracing shows a normally conducted sinus beat, followed by a junctional beat (with the His def lection being first), and then a sinus beat conducted with a long A-H interval.

The prolonged A-H interval on the third beat is due to "concealed" retrograde conduct ion into the AV node from the preceding junctional beat. This means that the wave of depolarization generated by the junctional beat retrogradely penetrated the AV node (just as an extra-stimulus would), causing the AV node to decrement when the next sinus beat arrives. In other words, the junctional and sinus beats in sequence, produced the same response as a tightly coupled "S1S2" from either the atrium or the ventricle.

Another POSSIBLE explanation is that the junctional beat could have concealed into the AV nodal fast pathway, rendering it refractory, thus forcing the sinus beat to conduct over a slow pathway. Dual AV nodal physiology would need to be demonstrated during the EP study to make this scenario possible.

1.9 Concealment 2

This figure nicely demonstrates the concept of concealed conduction into an accessory pathway.

Discussion

Draw your attention to the last 2 beats on Figure 1 (# 6 and #7). Based on the short A-V interval and presence of a delta wave on the surface E CG , the patient is preexcited.

Now examine the first 4 beats.

Pacing from the R VA catheter demonstrates no V- A conduction, suggesting that there is block in the AV node and in the AP at this pacing rate.

After R VA pacing ceases, a sinus beat conducts with a long A-H interval and a narrow QR S (beat #5). Why is this beat not preexcited?

Although there is no V-A conduction, the AV node and AP still receive retrograde input from the RV pacing. This "concealed conduction" into the AV node causes it to decrement, making the subsequent sinus beat conduct with a longer A-H interval. Simultaneously, concealed conduction into the accessory pathway renders the AP refractory to the oncoming sinus beat, which is why the QRS #5 is narrow.

Interestingly, beats #6 and #7 demonstrate slightly different QRS morphologies due to variable degrees of preexcitation.

Concealed conduction into the AV node or the AP can change their conduction properties without electrogram or electrocardiographic manifestations.

1.10 Escape Rhythm

This example demonstrates an atrial S2 that blocks in the AV node. Following is a sinus beat and a very short A-V inter val. How do you explain beat # 3?

Discussion

The PR interval associated with this first sinus beat is physiologically too short to conduct down the AV node. Therefore, beat #3 must be a junctional beat that occurred at the same time as the sinus beat. The oncoming sinus wave of depolarization could not conduct through the AV node since the junction and ventricles have already been depolarized and are therefore refractory.

This is an example of a junctional escape beat. This occurred due to overdrive suppression of the sinus node from programmed atrial extra-stimulus pacing. Recovery of the sinoatrial (SA) node from this overdrive suppression was long enough to allow the junctional escape rhythm to take over.

1.11 Nodal Function

This tracing demonstrates atrial extra-stimulus pacing with preexcitation on the surface ECG. What is the AV node doing?

Discussion

Notice also that the intracardiac electrograms show that the His "V" electrogram occurs before the local ventricular electrogram recorded at the RVA catheter. This suggests that the ventricle is being activated at the base before the RV apex (where the His-Purkinje and right bundles activate the ventricle). This is intracardiac evidence of preexcitation.

In Figure 2, the arrow points to a His def lection that occurs after the local His "V" electrogram. Why does this happen?

Recal l that, unless the patient is in AV reentrant tachycardia (AVRT) (either orthodromic or antidromic), there is always fusion of conduction between the AV node and the AP. Therefore, as the atrial extra-stimulus pacing is delivered earlier and earlier, the AV node will progressively decrement, but the AP usually will not. Therefore, the A-V interval will remain constant, but the A-H interval will continue to prolong. The local His bundle electrogram may eventually be seen after the local His "V" electrogram.

CHAPTER 2

Cardiac Electrophysiology 2

AVNRT

OUTLINE

2.1 Signal ID 60
2.2 Pathways 64
2.3 Initiation 68
2.4 Reset 72
2.5 Cool Initiation 76
2.6 Block to A 80
2.7 Bundle Blocks 84
2.8 Echoes? 88
2.9 Atypical 92
2.10 Will S3 Help? 96
2.11 PAC Effect 100

2.1 Signal ID

The first step in analyzing any tracing involves identifying the atrial (A), ventricular (V), and His bundle (H) electrograms (E GM) where appropriate. In some tachycardias, this identification may be difficult.

Discussion

This tracing shows atrial extra-stimulus testing with the last of the S1 drive train and the S2 displayed. The S2 generated an AV nodal echo beat, as evidenced by the presence of the unstimulated "A" in the high right atrium (HR A) channel.

In typical AVNRT, the S2 propagates antegradely down the slow AV nodal pathway, through the His and on to the ventricles. Simultaneously, retrograde conduction back up the AV nodal fast pathway is occurring. The distance and conduction velocity of these competing activation wavefronts can sometimes result in the "A" preceding the "V," making correct identification of the "A" and the "V" electrograms more difficult.

When in doubt, place a caliper on the earliest onset of ventricular activation on any surface ECG lead. Most of the time (there are always exceptions), electrograms to the right of the caliper line are ventricular and electrograms to the left of the line are atrial. This is why measured V-A t imes in AVNRT are of ten zero or negative values!

2.2 Pathways

During any electrophysiology study for AVNRT, we identify the number of antegrade and retrograde AV nodal pathways by obser ving how many distinct populations of A-H and V-A intervalsoccur. How many pathways do you see in this tracing?

Discussion

In this tracing, extra-stimulus testing elicited 3 out of the 4 AV nodal pathways; 2 in the antegrade direction and 1 in the retrograde direction.

1. The S1's conduct to the His via an antegrade fast pathway with a short A-H interval.

2. The S2 conducts to the His via an antegrade slow pathway as evidenced by the much longer A-H interval.

3. Following the fourth QRS, retrograde conduction up an AV nodal slow pathway results in a retrograde "A" with a long V-A interval.

Not seen on this tracing, the patient also demonstrated a retrograde fast pathway.

Also of note in this tracing, the fifth QRS is the result of the AV nodal echo (back down the fast AV nodal pathway with a short A-H interval). The QRS morphology has a RBBB pattern due to Ashman's phenomenon.

(Continues...)

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Excerpted from Cardiac Electrophysiology 2 by Paul D. Purves, George J. Klein, Peter Leong-Sit, Raymond Yee, Allan C. Skanes, Lorne J. Gula, Jaimie Manlucu. Copyright © 2014 Paul D. Purves. Excerpted by permission of Cardiotext Publishing, LLC.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

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Table of Contents

Contents

About the Authors, vii,
Foreword, ix,
Preface, xi,
Acknowledgments, xiii,
Glossary and Abbreviations, xv,
1. Physiology, 1,
2. AVNRT, 59,
3. AVRT, 105,
4. AF, 171,
5. The Unexpected, 185,
6. Case Studies, 219,