Hands-On Ablation: The Experts' Approach, Second Edition
Clinically useful approaches for the effective diagnosis and ablation of arrhythmias.

This updated and expanded Hands-On Ablation, The Experts' Approach, Second Edition is a comprehensive and unique book that gives an inside look at leading electrophysiology labs throughout the world and provides the reader with useful information and tips for ablation procedures directly from the experts themselves.

  • Each chapter highlights the practical knowledge of the expert author with a specific procedure.
  • “Hands-on” detail that helps translate new ideas and innovations into practice for the most state-of-the-art patient care.
  • In-depth “how-to” approaches are described for over 50 procedures, including ablations for supraventricular tachycardia, atrial fibrillation, and ventricular tachycardia. 
  • A valuable reference for every electrophysiology lab to help differentiate diagnostic challenges.
  • Fully illustrated with over 170 videos and 550 figures.
New in the Second Edition:
  • Chapters detailing the latest complex approaches to ablation of both atrial and ventricular arrhythmias.
  • A section on approaches to left atrial appendage closure.
  • An update of new technologies used for arrhythmia treatment.
  • 14 new chapters (59 total), 34 new videos (170 total), and 210 new figures (550 total).
1114005789
Hands-On Ablation: The Experts' Approach, Second Edition
Clinically useful approaches for the effective diagnosis and ablation of arrhythmias.

This updated and expanded Hands-On Ablation, The Experts' Approach, Second Edition is a comprehensive and unique book that gives an inside look at leading electrophysiology labs throughout the world and provides the reader with useful information and tips for ablation procedures directly from the experts themselves.

  • Each chapter highlights the practical knowledge of the expert author with a specific procedure.
  • “Hands-on” detail that helps translate new ideas and innovations into practice for the most state-of-the-art patient care.
  • In-depth “how-to” approaches are described for over 50 procedures, including ablations for supraventricular tachycardia, atrial fibrillation, and ventricular tachycardia. 
  • A valuable reference for every electrophysiology lab to help differentiate diagnostic challenges.
  • Fully illustrated with over 170 videos and 550 figures.
New in the Second Edition:
  • Chapters detailing the latest complex approaches to ablation of both atrial and ventricular arrhythmias.
  • A section on approaches to left atrial appendage closure.
  • An update of new technologies used for arrhythmia treatment.
  • 14 new chapters (59 total), 34 new videos (170 total), and 210 new figures (550 total).
199.0 In Stock
Hands-On Ablation: The Experts' Approach, Second Edition

Hands-On Ablation: The Experts' Approach, Second Edition

Hands-On Ablation: The Experts' Approach, Second Edition

Hands-On Ablation: The Experts' Approach, Second Edition

eBook

$199.00 

Available on Compatible NOOK devices, the free NOOK App and in My Digital Library.
WANT A NOOK?  Explore Now

Related collections and offers


Overview

Clinically useful approaches for the effective diagnosis and ablation of arrhythmias.

This updated and expanded Hands-On Ablation, The Experts' Approach, Second Edition is a comprehensive and unique book that gives an inside look at leading electrophysiology labs throughout the world and provides the reader with useful information and tips for ablation procedures directly from the experts themselves.

  • Each chapter highlights the practical knowledge of the expert author with a specific procedure.
  • “Hands-on” detail that helps translate new ideas and innovations into practice for the most state-of-the-art patient care.
  • In-depth “how-to” approaches are described for over 50 procedures, including ablations for supraventricular tachycardia, atrial fibrillation, and ventricular tachycardia. 
  • A valuable reference for every electrophysiology lab to help differentiate diagnostic challenges.
  • Fully illustrated with over 170 videos and 550 figures.
New in the Second Edition:
  • Chapters detailing the latest complex approaches to ablation of both atrial and ventricular arrhythmias.
  • A section on approaches to left atrial appendage closure.
  • An update of new technologies used for arrhythmia treatment.
  • 14 new chapters (59 total), 34 new videos (170 total), and 210 new figures (550 total).

Product Details

ISBN-13: 9781942909194
Publisher: Cardiotext Publishing
Publication date: 05/01/2017
Sold by: Barnes & Noble
Format: eBook
File size: 56 MB
Note: This product may take a few minutes to download.

About the Author

EDITORS

AMIN AL-AHMAD MD
Texas Cardiac Arrhythmia Institute at St. David’s Medical Center, Austin, Texas
DAVID J. CALLANS MD
University of Pennsylvania Health System, Philadelphia, Pennsylvania
HENRY H. HSIA MD
University of California, San Francisco, San Francisco, California
ANDREA NATALE MD
Texas Cardiac Arrhythmia Institute at St. David’s Medical Center, Austin, Texas
OSCAR OSEROFF MD
Bazterrica Clinic, Buenos Aires, Argentina
PAUL J. WANG MD
Stanford University, Stanford, California

Read an Excerpt

Hands-On Ablation

The Experts' Approach


By Amin Al-Ahmad, David J. Callans, Henry H. Hsia, Andrea Natale, Oscar Oseroff, Paul J. Wang

Cardiotext Publishing, LLC

Copyright © 2017 Amin Al-Ahmad, David J. Callans, Henry H. Hsia, Andrea Natale, Oscar Oseroff, Paul J. Wang
All rights reserved.
ISBN: 978-1-942909-19-4



CHAPTER 1

How to Rapidly Diagnose Supraventricular Tachycardia in the Electrophysiology Lab

Nishant Verma, MD, MPH; Luis F. Couchonnal, MD; Bradley P. Knight, MD


Introduction

The differential diagnosis of supraventricular tachycardia (SVT) includes sinus tachycardia (ST), atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia (AT), junctional ectopic tachycardia (JET), atrial flutter (AFL), atrial fibrillation (AF), and multifocal atrial tachycardia (MAT) (Figure 1.1). The term paroxysmal supraventricular tachycardia (PSVT) is used to refer to regular SVTs with abrupt onset and termination, namely AVNRT, AVRT, and AT. AVNRT is the most common, accounting for at least 60% of PSVTs that present to the electrophysiology (EP) laboratory. AVRT and AT account for 30% and 10% respectively (Figure 1.2). This chapter will focus on the diagnosis of AVNRT, AVRT, and AT in the EP laboratory. The discussion of AVRT will focus on orthodromic reciprocating tachycardia (ORT), a narrow complex tachycardia (in the absence of aberrant conduction) with antegrade conduction via the AV node and retrograde conduction via an accessory pathway. The diagnosis of PSVT depends on evaluation of 3 key elements: (1) baseline findings prior to tachycardia initiation; (2) tachycardia characteristics; (3) tachycardia response to atrial and ventricular pacing maneuvers.


Preprocedure Planning

Before performing an EP study on a patient with PSVT, a detailed history and physical should be performed. Clinical details, like the patient's age at onset of PSVT, may give insight into the underlying mechanism. More than 70% of patients with AVRT present before the age of 20 (median age 23 ± 14 years). In contrast, 60% of patients with AVNRT present after the age of 20 (median age 32 ± 18 years). Atrial tachycardia is also influenced by age, accounting for 23% of PSVTs over the age of 70. There are also differences by gender. In a study of 1700 patients presenting with PSVT, the majority of those with AVRT were men (54%). However, the majority of patients with AVNRT and AT were women (70% and 62%, respectively).

The baseline ECG should be assessed for evidence of manifest preexcitation. The ECG during PSVT with 1:1 atrioventricular (AV) conduction should be evaluated for the P-wave morphology and the R-P interval. A long R-P tachycardia (defined as an R-P interval > 50% of the R-R interval) could represent atypical AVNRT, AVRT, or AT. However, the P-wave morphology can be useful, as AVNRT should have a superiorly directed P wave. An inferior P-wave axis would be more consistent with AT or AVRT. A similar logic applies for short R-P tachycardias. When no P waves are discernable during SVT, the terminal portion of the QRS complex during SVT should be compared to the baseline ECG. A pseudo R' in lead V1 or pseudo S' in the inferior leads, representing retrograde atrial activation, may be discernable. This finding makes AVNRT very likely. In addition, if the onset or termination of tachycardia is documented, this should be examined for clues as to the tachycardia mechanism. Tachycardia initiation with a premature atrial complex (PAC) and marked P–R prolongation usually signifies an AV nodal dependent arrhythmia. Consistent termination with AV block without a premature atrial beat makes AT extremely unlikely. However, these ECG criteria should be used with caution as studies looking at their effectiveness have shown an incorrectly classified the tachycardia 20% of the time.


Vascular Access and Catheter Placement

Informed consent and labs (complete blood count, coagulation studies, and chemistries) are obtained in the cardiac surveillance unit on or before the day of the procedure. The majority of patients undergoing an electrophysiology (EP) procedure for PSVT receive intravenous sedation administered by the EP nursing staff under the direction of the attending physician. Most EP procedures for PSVT can be performed using access via a single femoral vein. Standard sheaths for an EP procedure for PSVT include 3 sheaths from the right femoral vein. After the patient is prepped and draped, access to the right femoral vein is obtained via the modified Seldinger technique. When the suspicion is high that the PSVT mechanism is AVNRT, a long guiding sheath can be placed initially, and an ablation catheter can be placed in the His bundle location and used for the diagnostic portion of the study. A standard 4-mm electrode-tip deflectable ablation catheter is typically used. A soft-tip quadripolar catheter is positioned in the RV apex. A steerable quadripolar catheter is positioned in the high right atrium (HRA). The ablation catheter or the HRA catheter can later be moved to the coronary sinus (CS) to assess for eccentric or concentric atrial activation, if needed to help with the diagnosis. After catheters are positioned, the patient receives an intravenous bolus of heparin (3000 U) followed by an additional 1000 U every hour to prevent thrombus formation. A multipolar catheter can be placed in the CS at the beginning of the procedure if there is evidence of pre-excitation suggestive of a left-sided pathway. Though not technically necessary, an advanced 3D mapping system can be helpful and is usually employed.


Baseline Observations in the EP Lab

Before initiation of SVT in the EP lab, baseline observations can be made that may help guide the differential diagnosis to a particular tachycardia mechanism. Ventricular preexcitation on the surface ECG or an HV interval less than 35 ms has a positive predictive value (PPV) of 86% and a negative predictive value (NPV) of 78% that the patient will have AVRT. Dual AV nodal physiology, defined as an increase of ≥ 50 ms in the A2-H2 interval with a 10-ms decrement in the A1-A2 interval during extrastimulus pacing has a PPV for AVNRT of 86%. Despite these numbers, 10% of patients with ventricular preexcitation will have inducible AVNRT and 15% of patients with dual AV nodal physiology will have AVRT or AT. Lack of baseline VA conduction at a ventricular pacing cycle length of ≥ 600 ms makes the presence of an accessory pathway (AP) unlikely. However, 5% of patients without evidence of VA conduction at baseline will have inducible AVRT, as retrograde AP conduction may be dependent on catecholamine stimulation. Furthermore, evidence of decremental VA conduction with ventricular extrastimulus pacing makes the presence of an AP unlikely. However, a small percentage of pathways do exhibit decremental conduction. Evidence of intra-atrial conduction delay or atrial scar, as determined by low-voltage or fractionated atrial electrograms, may suggest atrial tachycardia as the culprit mechanism. Although administration of adenosine with atrial or ventricular pacing can help determine the presence of an extranodal pathway, 38% of patients with typical AVNRT continue to have VA conduction via the fast pathway even in the presence of adenosine.


Parahisian Pacing

Parahisian pacing can be utilized at baseline to determine the presence or absence of retrograde conduction over a septal AP. To perform this maneuver, the pacing catheter is positioned at the basal RV septum. The distal pacing electrodes should record both His and ventricular electrograms. To avoid inadvertent atrial capture, atrial electrograms should be minimized at the distal pacing electrode. Pacing should initially be performed at higher outputs (5–10 mA) to ensure His bundle capture and decremented until loss of His bundle capture with QRS widening.

Parahisian pacing results in both antegrade and retrograde conduction via the His-Purkinje system (HPS). The antegrade wavefront conducts via the HPS, resulting in a relatively narrow QRS morphology. In the absence of an AP, the retrograde wavefront conducts over the His bundle, with a Stim-His (S-H) interval of 0 ms, followed by atrial activation, with a Stim-Atrial (S-A) interval equal to the His-Atrial (H-A) interval. As the pacing output is decreased, loss of His bundle capture results in widening of the QRS as a result of antegrade conduction occurring directly over slowly conducting ventricular myocardium. Retrograde His bundle capture is delayed as conduction first occurs over ventricular myocardium, followed by retrograde activation of the right bundle with resultant activation of the His bundle. This delayed His activation results in prolongation of the S-A interval, which is a sum of the S-H and H-A interval. This is typical of a nodal response to parahisian pacing (Figure 1.3A). In the setting of a septal AP, the S-A interval remains constant, with loss of His bundle capture as atrial cproperties of the AP connecting the ventricular myocardium to the atrium (Figure 1.3B).

In order to properly interpret the results of parahisian pacing, the retrograde atrial activation sequence (RAAS) must be closely observed. When there is evidence of loss of His bundle capture with the same S-A interval and no change in RAAS, conduction is via only an AP. However, if there is a change in the RAAS after loss of His bundle capture, conduction is likely occurring either via multiple APs, simultaneous conduction up the fast and slow AV nodal pathways, or concomitant conduction up the AV node and an AP. To differentiate among these possibilities, close attention is needed to determine if changes occur in the S-A interval or H-A interval and if there is evidence of fusion on a multipolar CS catheter. The sensitivity of the extranodal response to parahisian pacing for detecting the presence of an AP is 46%. This likely reflects the fact that an extranodal response is less likely to be elicited for pathways farther from the AV nodal (i.e., lateral pathways). The specificity of this finding is 96%.


Differential RV Pacing

Another maneuver utilized to determine the presence of a septal AP is to perform differential RV pacing. Ventricular pacing is performed at both apical and basal RV sites at the same pacing cycle length (CL) and the interval from the RV pacing stimulus to the high right atrial (HRA) electrogram (V-A interval) is measured. In the absence of an AP, the V-A interval is longer when pacing basally compared to pacing apically, because conduction from the base must proceed over the septal myocardium before entering the HPS at the RV apex. However, in the presence of a HRA AP, the V-A interval is shorter when pacing basally compared to apically, as retrograde atrial activation is dependent on conduction via the basally located AP. The V-A index can be calculated, which is the difference in the V-A intervals apically compared to basally (VAapical - VAbasal). A V-A index of > 10 ms had a sensitivity, specificity, and PPV of 100% for detecting the presence of a posteroseptal AP.


Tachycardia Characteristics

After initiation of SVT, there are several observations that can be made to determine the tachycardia mechanism. The tachycardia cycle length (TCL) gives insight into the mechanism of the tachycardia, although there is significant overlap. In general, AVNRT tends to be slower than AVRT. Slow tachycardias (CL > 500 ms) tend to be AVNRT, with a PPV of 83%. The first measurement made at the initiation of the tachycardia is the septal V-A interval, measured from the beginning of the surface QRS to the earliest septal atrial electrogram. In adults, a septal V-A interval of less than 70 ms excludes AP-mediated tachycardias and makes typical AVNRT highly likely. Less than 1% of ATs will exhibit a V-A interval of less than 70 ms.

When tachycardia is initiated, spontaneous oscillations ("wobble") in the TCL should be noted. If changes in the A-A interval precede changes in the H-H interval (the As are driving the Vs), the most likely mechanism is AT. However, if changes in the H-H interval precede changes in the A-A intervals, the most likely mechanism is AVNRT or ORT.

If the septal V-A time is greater than 70 ms, the CS catheter can be used to determine whether the RAAS during tachycardia is concentric or eccentric. During typical AVNRT, the RAAS is concentric, as the area of earliest atrial activation is near the fast pathway that inserts near the His bundle at the apex of the triangle of Koch. With atypical AVNRT, the earliest atrial activation is near the CS ostium. With the exception of paraseptal AVRT and AT, AVRT and AT will demonstrate varying degrees of eccentric atrial activation, depending on the pathway or foci locations relative to the AV node. Evidence of eccentric activation excludes most all forms of AVNRT as the tachycardia mechanism. However, a small number of patients with ANVRT have evidence of eccentric atrial activation and can only be successfully ablated from within the CS or along the mitral annulus, related to the leftward extensions of the slow pathway.

Initiation, termination, and zones of perturbation during tachycardia can give insight into the mechanism of the arrhythmia. When tachycardia induction is reproducibly dependent on a prolongation of the A-H interval with atrial pacing, the most likely diagnosis is AVNRT, with a PPV of 91%. This prolongation is related to block in the fast pathway and "jumping" to the slow pathway, usually with a change in the A-H interval of at least 50 ms with an atrial extrastimulus. Initiation of AVRT may also demonstrate some AV delay, but delay can also occur anywhere within the circuit, including intramyocardial conduction delay. As AT is independent of the AV node, AV nodal delay is not required for tachycardia induction.

The development of LBBB is more commonly seen with ORT, with a PPV of 92%. There are several reasons for this phenomenon. The faster rate of ORT likely favors the development of aberrant conduction. The occurrence of LBBB aberration also promotes the development of ORT by allowing the AP time to recover to allow for retrograde conduction to occur. Furthermore, as induction of AVNRT is dependent on the development of AV nodal delay, resulting in a longer H1-H2 interval, the development of aberration is unlikely. In contrast, a critical A-H delay is not required for initiation of ORT. Therefore, the short A-H interval during tachycardia initiation encroaches on the refractoriness of the HPS, resulting in aberration. An increase in the V-A interval by greater than 20 ms with bundle branch block (BBB) is diagnostic of ORT using an AP that is ipsilateral to the side of block, with a PPV of 100%. This increase in the V-A interval is related to relatively slower intramyocardial conduction caused by the BBB. This increase in the V-A interval may result in a corresponding increase in the TCL. However, the increased VA time may also result in

Evidence of AV block during SVT excludes ORT, as the ventricle is obligate for continuation of the reentrant circuit. AV block can be seen in both AT and AVNRT, with block occurring infranodally in the latter.

A spontaneous termination of tachycardia should be inspected carefully for clues as to the tachycardia mechanism. Typically, spontaneous termination of AVNRT and ORT is caused by antegrade block in the AV node. As a result, AVNRT and ORT usually terminate with a P wave not followed by a QRS (Figure 1.5). Conversely, when AT with 1:1 conduction terminates, the last atrial beat typically conducts to the ventricle. The simultaneous termination of the AT with AV block would be an exceedingly rare phenomenon. Therefore, a tachycardia that reliably terminates with a P wave that is not premature excludes AT. However, a tachycardia that terminates with a QRS does not differentiate between AVNRT, AVRT, or AT.


Pacing Maneuvers During Tachycardia

Ventricular Overdrive Pacing

After evaluation of the baseline findings and the tachycardia characteristics, pacing maneuvers are performed to further define the tachycardia mechanism. The first pacing maneuver performed is ventricular overdrive pacing (VOP). To perform VOP, the ventricle is paced at a CL 10–40 ms less than the TCL, with the goal of accelerating the atrium to the pacing CL. With cessation of ventricular pacing, the tachycardia should return to its original CL. After ensuring acceleration of the atrial activation to the pacing CL, the RAAS of the tachycardia is compared to the entrained activation. If the paced atrial activation sequence differs from the tachycardia, either a bystander pathway or an atrial tachycardia is suspected. The electrogram sequence after the last paced ventricular complex is evaluated to determine whether the conduction sequence can be described as atrial-(His)-ventricular (A(H)V) or atrial-atrial-(His)-ventricular (AA(H)V). An A(H)V response is consistent with either AVNRT, or AVRT, as the last entrained atrial beat travels via the retrograde limb of the circuit (i.e., AV nodal pathway or AP) and then antegrade down the AV node (Figure 1.6A). However, an AA(H)V response is consistent with atrial tachycardia because during VOP, retrograde conduction occurs via the AV node resulting in transient overdrive suppression of the AT focus. Cessation of VOP results in resumption of AT with conduction down the AV node (Figure 1.6B).


(Continues...)

Excerpted from Hands-On Ablation by Amin Al-Ahmad, David J. Callans, Henry H. Hsia, Andrea Natale, Oscar Oseroff, Paul J. Wang. Copyright © 2017 Amin Al-Ahmad, David J. Callans, Henry H. Hsia, Andrea Natale, Oscar Oseroff, Paul J. Wang. 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.

Table of Contents

SECTION I: Ablation of Supraventricular TachycardiaSECTION II: Ablation of Atrial FibrillationSection III: Ablation of Ventricular TachycardiaSection IV: Miscellaneous Procedures
From the B&N Reads Blog

Customer Reviews