Understanding Intracardiac EGMs: A Patient Centered Guide

Table of Contents

Cover

Dedication

Title Page

Copyright

Preface

Glossary

Chapter 1: Basic electrophysiology

Mechanistic tachycardia classification

Anatomic tachycardia classification

Electophysiology basics

Chapter 2: Supraventricular tachycardia case 1

Evaluation of baseline electrograms

Pacing protocols

Initiation of tachycardia and evaluation

Ablation of typical AVNRT

Chapter 3: Supraventricular tachycardia case 2

Chapter 4: Supraventricular tachycardia case 3

Chapter 5: Supraventricular tachycardia case 4

Chapter 6: Supraventricular tachycardia case 5

Chapter 7: Supraventricular tachycardia case 6: baseline preexcitation

Chapter 8: Supraventricular tachycardia case 7: baseline preexcitation

Chapter 9: Supraventricular tachycardia case 8

Chapter 10: Supraventricular tachycardia case 9

Chapter 11: Supraventricular tachycardia cases 10 and 11

Chapter 12: Supraventricular tachycardia case 12

Chapter 13: Supraventricular tachycardia case 13

Chapter 14: Supraventricular tachycardia case 14: atrial fibrillation

Chapter 15: Supraventricular tachycardia case 15: atrial tachycardia after atrial fibrillation ablation

Chapter 16: Supraventricular tachycardia case 16: atrial tachycardia after atrial fibrillation ablation

Chapter 17: Supraventricular tachycardia case 17: atrial tachycardia after atrial fibrillation ablation

Chapter 18: Supraventricular tachycardia case 18: atrial tachycardia after atrial fibrillation ablation

Chapter 19: Supraventricular tachycardia case 19: atrial tachycardia after atrial fibrillation ablation

Chapter 20: Wide complex tachycardia case 1

Chapter 21: Wide complex tachycardia case 2

Chapter 22: Wide complex tachycardia case 3: premature ventricular contractions

Chapter 23: Wide complex tachycardia case 4

Chapter 24: Wide complex tachycardia case 5

Chapter 25: Wide complex tachycardia case 6

Chapter 26: Syncope

Bradycardia

Tachycardia

CHAPTER 27: Multiple choice questions and answers

Appendix

Index

End User License Agreement

List of Illustrations

Chapter 1: Basic electrophysiology

Figure 1.1 For most types of reentry, two separate pathways have different electrophysiologic properties, and with a carefully timed impulse, depolarization can occur in one pathway and turn around to depolarize the parallel pathway. The most well-described and the best clinical example of this is a patient with an accessory pathway (a). Normally, the AV node forms the only electrical connection between the atria and the ventricles, but in patients with an accessory pathway, the second electrical connection between the atria and ventricles can allow a reentrant circuit to develop. Another common scenario for reentrant arrhythmias is ventricular tachycardia in the setting of a prior myocardial infarction (b). In this case, a patchy myocardial scar forms an alternate pathway along with normal myocardium to activate one side of a scar to the other side of the scar.

Figure 1.2 Initiation of typical atrial flutter. (a): In sinus rhythm (*), atrial depolarization proceeds down the lateral wall of the right atrium (RA) and superiorly toward the septum. (b): With a premature atrial contraction from the left atrium (*), inferior atrial depolarization blocks in the cavotricuspid isthmus (CTI), but the wave of depolarization travels superiorly to activate the superior and lateral portions of the right atrium and enters the CTI from the other direction. (c): Slow conduction through the CTI initiates atrial flutter.

Figure 1.3 Anatomic classification of tachycardias

Figure 1.4 Patient with an automatic tachycardia from the AV node region observed in the first few hours after aortic valve surgery. This arrhythmia, called nonparoxysmal junctional tachycardia (NPJT), usually resolves after 1 or 2 days. Intermittent intrinsic AV conduction can sometimes be observed when a properly timed P wave results in an early QRS complex or a subtle change in the QRS morphology (*).

Figure 1.5 Basic catheter positions for electrophysiology study in the right anterior oblique (RAO) and the left anterior oblique (LAO) projections. Quadripolar catheters are located in the right atrium (RA), His bundle region (His) straddling the tricuspid valve, and the right ventricle (RV). A decapolar catheter is placed in the coronary sinus (CS). For orientation, the approximate locations of the mitral valve (MV), tricuspid valve (TV), inferior vena cava (IVC), and superior vena cava (SVC) are shown (

Figure 1.6 Flow sheet for the evaluation of electrograms during a typical electrophysiology study.

Figure 1.7 Electrograms recorded from catheter positions in Figure 1.5. The AV relationship is 1:1 with atrial activation (both P waves and atrial EGMs) preceding or driving ventricular activation (both QRS complexes and ventricular EGMs). Atrial activation is seen first in the high right atrium (HRA), followed by the His bundle, and last in the coronary sinus (vertical arrows). A His bundle deflection (H) and a right bundle (RB) potential can be seen during the isoelectric period of the PR interval. AV conduction is usually divided into two parts: the AH interval (first septal atrial activation to the His deflection) that represents conduction through the AV node and the HV interval (His deflection to first ventricular depolarization) that represents His bundle, bundle branch, and Purkinje fiber depolarization. Ventricular (V) activation is seen first in catheters located in the septum (His and RV) and later in the coronary sinus.

Figure 1.8 Initiation of atrial pacing at a cycle length of 500 ms. The first atrial pacing stimulus does not capture the atria, because depolarization via the sinus node has just occurred. However, the second and third atrial stimuli capture the atrium (the atrial stimuli are followed by atrial electrograms). The AH interval of the third stimulus is prolonged (from 82 to 97 ms) because of decremental conduction in the AV node.

Figure 1.9 More rapid atrial pacing leads to AV Wenckebach behavior. Pacing associated with gradual prolongation of the AH interval is observed until a dropped H and QRS complex. This response is characteristic of block within the AV node.

Figure 1.10 After a basic cycle length of 600 ms, a premature atrial stimulus at a coupling interval of 300 ms, the AH interval prolongs to 200 ms because of delayed conduction in the AV node.

Figure 1.11 Continuation of Figure 1.10. When the coupling interval is shortened to 250 ms, the atrial electrogram is not followed by a His bundle signal and QRS complex due to block in the AV node. The coupling interval of the two atrial electrograms recorded on the His catheter (270 ms) defines the AV node effective refractory period (AVNERP).

Figure 1.12 Baseline ventricular pacing is not associated with VA conduction. Notice the pattern of atrial depolarization remains high-low with first atrial depolarization noted in the HRA.

Figure 1.13 Continuation of Figure 1.12. Infusion of isoproterenol and sympathetic activation facilitates development of VA conduction. Notice that in response to the pacing stimulus, the pattern of atrial depolarization switches from high-low to low-high due to retrograde VA conduction via the AV node. The atrial rate now increases to the ventricular paced rate. Notice the subtle changes in the timing of atrial depolarization as activation progressively switches from being sinus node driven (S) to AV node driven (R). Although one could quibble about whether atrial activation recorded in the His bundle region (S*) for the first paced beat is actually from retrograde activation, it is likely from the sinus node, as the coronary sinus depolarization remains relatively late. Similarly, one could argue whether coronary sinus depolarization from the third paced beat is actually due to depolarization from the sinus node, but it is likely due to retrograde depolarization because of the shortened interval between atrial depolarization recorded in the His bundle and the proximal coronary sinus. It is instructive to note that as a separate but important point, the pattern of coronary sinus depolarization (from proximal to distal) is the same in this case regardless of whether atrial depolarization is sinus node driven or AV node driven.

Figure 1.14 Normal retrograde AV node response to ventricular extrastimulation. A ventricular extrastimulus at a coupling interval of 220 ms is associated with prolongation of the stimulus to atrium interval from 106 to 170 ms. Earliest atrial activation is still observed in the His bundle catheter. This response is consistent with delayed retrograde conduction in the AV node.

Figure 1.15 Flowchart for evaluation of supraventricular tachycardia. A: Atrial electrogram; V: ventricular electrogram.

Figure 1.17 Determining the direction of atrial activation during supraventricular tachycardia. The focus of investigation should be whether High to Low or Low to High and whether Left to Right, Right to Left, or Septal Outward.

Figure 1.16 Usual relationship between atrial and ventricular depolarization in patients with supraventricular tachycardia and 1:1 atrial and ventricular relationships. However, many exceptions exist and will be explored throughout the first portion of the book.

Figure 1.18 Schematic of the likelihood of a ventricular stimulus interacting with different types of supraventricular tachycardias. Because AV reentrant tachycardia (AVRT) using an AV accessory pathway encompasses such a large circuit, it is relatively easy for a ventricular stimulation to get into the circuit or interact with the tachycardia. At the other end of the spectrum, in atrial tachycardia, the reentrant circuit or focus is guarded by the bundle branches, His bundle, and AV node.

Figure 1.19 A premature ventricular stimulus delivered during supraventricular tachycardia initiates a wide complex tachycardia at a more rapid rate than the underlying tachycardia (which is unaffected by the PVC). Ventricular tachycardia can be identified immediately, because there are more QRS complexes than atrial activity during the stable wide QRS tachycardia (the last four QRS complexes).

Chapter 2: Supraventricular tachycardia case 1

Figure 2.1

Figure 2.2 Baseline electrograms. Atrial depolarization is normal with first atrial signal observed in the HRA and the last atrial signal observed in the coronary sinus. The QRS width is normal (70 ms) and has a normal frontal axis with a monophasic R wave in lead II. AV conduction is normal with an AH interval of 56 ms and an HV interval of 36 ms.

Figure 2.3 Atrial pacing at a cycle length of 500 ms. Notice the interatrial delay by comparing the interval between the pacing stimulus and the distal coronary sinus electrogram (140 ms) to sinus rhythm (109 ms). This delay is not due to intrinsic atrial conduction slowing but rather is because of the position of the high right atrial catheter within the right atrial appendage. Notice that adding the sum of the interval measured from proximal to distal electrodes in the HRA catheter almost fully accounts for the interatrial conduction delay observed during pacing. As an aside, this is the reason that generally the Asense–Vpace interval is programmed to shorter intervals than the Apace–Vpace interval in dual chamber pacing. Importantly, the AV relationship remains 1:1, and the AH interval remains essentially unchanged.

Figure 2.4 With shortening of the atrial pacing cycle length, every other atrial stimulus (*) fails to depolarize the atria. Loss of atrial capture is most easily seen in the coronary sinus electrograms.

Figure 2.5 Pacing is performed at a basic cycle length of 500 ms, and a premature atrial stimulus is delivered at a coupling interval of 290 ms. In response to the premature atrial stimulus, the AH is slightly more prolonged (93 ms) when compared to sinus rhythm (58 ms) due to normal decremental conduction properties of the AV node.

Figure 2.6 Continuation of Figure 2.5. When the coupling interval is shortened by 10–280 ms, there is loss of atrial capture because of atrial refractoriness (AERP or atrial effective refractory period).

Figure 2.7 Double atrial extrastimuli. With a basic pacing cycle length of 500 ms, double premature atrial extrastimuli at coupling intervals of 390 ms and 380 ms is associated with an AH interval of 59 ms.

Figure 2.10 Double extrastimuli. Continuing from Figure 2.8, when the coupling interval of the first extrastimulus is shortened further to 270 ms, atrial capture does not occur.

Figure 2.8 Double atrial extrastimuli. Continuing from Figure 2.7, the coupling interval of the second extrastimulus is progressively shortened, and progressive AH interval prolongation is observed. When the coupling interval of the second extrastimulus has been shortened to 270 ms, the AH interval has prolonged to 157 ms. When the coupling interval is further shortened to 260 ms, loss of atrial caprure is observed (not shown).

Figure 2.9 Double extrastimuli. Continuing from Figure 2.8, the coupling interval of both the first and the second extrastimuli are shortened, and at coupling intervals of 280 and 200 ms, the AH interval is 256 ms.

Figure 2.11 Ventricular pacing at a constant cycle length of 500 ms. The astute reader will notice that there are three forms of atrial depolarization: from sinus node activation (S), from retrograde activation via the AV node (R), and a fusion beat (F) where the coronary sinus atrial electrograms are due to retrograde conduction, and the HRA electrograms from the sinus node.

Figure 2.12 With more rapid ventricular pacing at a cycle length of 350 ms, retrograde activation via the AV node initially exhibits Wenckebach behavior with gradual prolongation of the V-A interval and subsequent block and then later develops 2:1 retrograde block.

Figure 2.13 Ventricular extrastimulation is associated with progressive delay in retrograde conduction, suggesting that this pathway has decremental conduction properties and because depolarization is midline, likely represents retrograde conduction via the AV node.

Figure 2.14 Earlier ventricular stimulation again leads to VERP (a pacing stimulus without ventricular capture).

Figure 2.15 Rapid pacing from the coronary sinus initiates tachycardia with a cycle length of 275 ms. Notice that the tachycardia initiation is associated with a series of dramatic increases in the AH interval. Once tachycardia is initiated, the ECG and electrograms show almost simultaneous depolarization of the atria and the ventricles. This finding cannot be associated with AVRT using an accessory pathway. In addition, with the initiation of tachycardia, the HA interval remains constant despite changes in the cycle length, thus making AVNRT a much more likely diagnosis than atrial tachycardia.

Figure 2.16 Flowsheet for the clinical evaluation of SVT. HPS, His Purkinje System; AVNRT, AV node reentrant tachycardia; AT, Atrial tachycardia; AVRT, AV reentrant tachycardia.

Figure 2.17 Schematic showing the differences between HA intervals during tachycardia and VA intervals during ventricular pacing for both AVNRT and AVRT.

Figure 2.18 Schematic of possible tachycardia mechanisms. The near simultaneous ventricular and atrial depolarization rules out AVRT. As the earliest atrial signal is located in the midportion of the coronary sinus (CS), the tachycardia could represent AVNRT from a reentrant circuit within the atrial septal region, or an atrial tachycardia (*) somewhere within the left atrium (because right atrial depolarization is so late) with first-degree AV block.

Figure 2.19 Electrograms from another patient with AVNRT that continues despite AV block. The patient has left bundle branch block (see lead V1) and a long HV interval. During AVNRT, tachycardia continues despite AV block because block is occurring distal to the His bundle (H).

Figure 2.20 Electrograms from another patient with spontaneous termination of the tachycardia ending with an atrial electrogram. This termination implies the tachycardia is AV node dependent with anterograde block within the AV node and rules out atrial tachycardia.

Figure 2.21 Termination of tachycardia in this patient ends on a ventricular signal. Before termination, both the AH and HA intervals remain constant. Termination could be due to either cessation of an atrial tachycardia (with passive AV conduction) or retrograde block in an AV node pathway in AVNRT.

Figure 2.22 Scanning ventricular stimuli: a ventricular stimulus given 230 ms after the QRS does not reset the tachycardia (2 CL = 592 ms in all EGMs).

Figure 2.24 If single extrastimuli do not interact with the circuit, double ventricular stimuli can be used. In this case, two prematureventricular contractions at coupling intervals of 210 and 200 ms, the second premature ventricular stimulus shortens the intervalbetween electrograms recorded from the proximal CS from 290 to 270 ms. Despite the change in the tachycardia interval, the HAinterval remains constant (52 ms), making AVNRT the likely diagnosis.

Figure 2.25 In another patient with AVNRT, a premature ventricular stimulus given 250 ms from the prior QRS terminates thetachycardia without an atrial electrogram, thus confirming the AV node dependence of the tachycardia.

Figure 2.26 Schematic showing the electrophysiologic basis of the Morady maneuver. Ventricular pacing is performed at a rate faster than the tachycardia, and the tachycardia is entrained in the atrium when the atrial electrogram cycle length is equal to the paced cycle length. On cessation of pacing, the last atrial signal will lead to a subsequent ventricular signal (more accurately, a His bundle electrogram because there could be distal His block – but generally, a QRS complex is used, and it is referred to as a V-A-V response) in AVNRT, whereas in atrial tachycardia, the last entrained atrial electrogram will be followed by an atrial signal from the atrial tachycardia and then a ventricular signal (V-A-A-V response).

Figure 2.27 Morady maneuver from another patient with AVNRT showing a V-A-V response. Atrial capture is confirmed by shorteningof the atrial electrogram cycle length to the paced cycle length. On cessation of pacing, a V-A-V response is observed.

Figure 2.28 Morady maneuver in another patient with an atrial tachycardia near the coronary sinus os. With cessation of pacing, aV-A-A-V response diagnostic of an atrial tachycardia is observed.

Figure 2.29 A Morady maneuver terminates the tachycardia but confirms the presence of an AV-node-dependent tachycardia becausethe tachycardia terminates without an early atrial electrogram (*). If the patient had an atrial tachycardia, the only way ventricularpacing could terminate the tachycardia would be by early atrial depolarization via retrograde AV node conduction.

Figure 2.30 Schematics showing the different electrophysiologic patterns observed in AVNRT. The relationship between the atrial and ventricular electrograms will be dependent on the relative conduction velocities of anterograde and retrograde pathways. In typical AVNRT, anterograde conduction is much slower than retrograde conduction, leading to a short VA interval and near-simultaneous depolarization of the atria and ventricles. In the atypical forms of AVNRT, anterograde conduction is not as slow relative to retrograde conduction (either anterograde conduction is more rapid or retrograde conduction is slower), and the P wave will be observed later after the preceding QRS.

Figure 2.31 Schematic of the anatomy of the floor of the right and left atria. The slow pathway is generally anterior to the coronary sinus and posterior to the tricuspid valve (TV). Since the tricuspid valve is more apically displaced than the mitral valve (MV), the electrogram in this region is characterized by a larger ventricular signal and smaller atrial signal. IVC: inferior vena cava.

Figure 2.32 Anatomy of the proximal coronary sinus region. A decapolar catheter and a balloon-tipped catheter have been placed in the coronary sinus. A decapolar catheter is located on the superior septum straddling the right atrium and right ventricle. Contrast has been injected into the coronary sinus. The slow pathway is often located just anterior to the coronary sinus os in line with the most superior portion of the roof of the coronary sinus (black arrowheads). The fast pathway is generally superior (White arrowheads). RAO, right anterior oblique; LAO, left anterior oblique.

Figure 2.33 Fluoroscopic positions of catheters for slow pathway modification. Diagnostic quadripolar cathters are located at the His bundle and right ventricle, and a decapolar catheter is placed in the coronary sinus. The ablation catheter (identified by its larger distal electrode) is just anterior to the coronary sinus os. RAO, right anterior oblique; LAO, left anterior oblique.

Figure 2.34 Electrograms obtained from the ablation catheter demonstrate a smaller atrial signal and larger ventricular signal.

Figure 2.35 During ablation, junctional rhythm develops. Importantly, junctional rhythm is associated with retrograde conduction via the fast pathway suggesting that normal AV node conduction remains intact.

Figure 2.36 Premature atrial stimulation protocol. With two extrastimuli at coupling intervals of 290 and 240 ms, the AH interval is 157 ms.

Figure 2.38 Continuation of premature atrial stimulation protocol. With two extrastimuli at coupling intervals of 290 and 220 ms, AV node refractory period (AVNERP) is reached (330 ms).

Figure 2.39 In another patient, a single echo after ablation. The patient had sustained AVNRT before the ablation, but after slow pathway modification, the slow pathway cannot be repetitively activated.

Figure 2.40 Graphs showing the relationship between the coupling interval of an atrial extrastimulus and the AH interval (delay in the AV node). Left: In most patients, the AH interval will gradually prolong until block develops. Right: In patients with dual pathway physiology, a discontinuity will be observed because of sudden prolongation of AV nodal conduction as conduction switches from the fast pathway to the slow pathway. In some cases, ablation shortens the tachycardia window. The initial relationship between the coupling interval and AH prolongation (solid line) shows a jump to the slow pathway at a relatively long coupling interval. After ablation (dashed line), a jump still occurs but only at very short coupling interval near the AVNERP.

Chapter 3: Supraventricular tachycardia case 2

Figure 3.1

Figure 3.2 Baseline electrograms. The baseline cycle length is 871 ms. AV conduction is normal with an AH interval of 82 ms and an HV interval of 43 ms.

Figure 3.3 A premature atrial contraction is delivered at a coupling interval of 360 ms, and the AH interval is 330 ms as measured from the proximal coronary sinus electrodes. Notice the low-frequency, low-amplitude signals on the distal His catheter that appear to be independent of cardiac activity (*). These signals probably represent artifact. Another low-frequency, low-amplitude signal can be observed on the distal right ventricular electrograms (T). These signals are related to prior ventricular activation and represent ventricular repolarization and are the intracardiac electrogram equivalent of T waves.

Figure 3.4 Continuation of atrial extrastimulation. At a coupling interval of 350 ms, AV block occurs because of block in the AV node. Some interatrial conduction delay can be observed with a slight increase in the interval between the stimulus and the proximal sinus electrogram.

Figure 3.5 Ventricular pacing at a cycle length of 700 ms demonstrates a single retrograde atrial electrogram (*) before block.

Figure 3.6 After initiation of a low dose of isoproterenol, ventricular pacing at 650 ms initiates supraventricular tachycardia at a cycle length of 570 ms. Notice that the first beat of tachycardia occurs after the first ventricular paced beat as shown by the early atrial electrograms observed in the proximal coronary sinus (*), as a shortened stimulation to intracardiac electrogram interval (arrows) would not be the normal behavior of the AV node from the second pacing stimulus. Although this behavior could be observed by retrograde conduction switching from the AV node to an accessory pathway, the very short VA interval observed on the next beat rules out AVRT using an AV accessory pathway. The astute reader will note that the third QRS complex is a fusion beat due to tachycardia and ventricular pacing.

Figure 3.7 The supraventricular tachycardia has a cycle length of 590 ms, and a short HA interval terminates spontaneously on an atrial electrogram, providing strong evidence that the tachycardia is AV node dependent and ruling out atrial tachycardia.

Figure 3.8 The tachycardia is terminated with two premature ventricular stimuli with minimal resetting of the atrial electrograms. This finding makes reentry the most likely mechanism for the tachycardia.

Figure 3.9 Morady maneuver. The tachycardia cycle length is 570 ms. Ventricular pacing at 550 ms entrains the tachycardia as evidenced by shortening of the atrial cycle length to 550 ms (dashed arrows). The last pacing stimulus does not capture the ventricles (*), but a V-A-V response is still observed, making AVNRT the likely diagnosis.

Figure 3.10 Fluoroscopic position of catheters with an ablation catheter placed inferoseptally between the coronary sinus and the tricuspid valve in the right anterior oblique (RAO) and left anterior oblique (LAO) projections.

Figure 3.11 Electrograms recorded from the fluoroscopic position shown in Figure 3.10. The ablation catheter has a multicomponent atrial signal with a discrete potential (SP) that occurs just before His depolarization (h). Pacing from the coronary sinus shows dissociation of this potential from the His bundle electrogram.

Figure 3.12 Baseline ECG of a patient complaining of chronic fatigue. The hart rate is approximately 100 bpm. The P wave is inverted in leads I and aVL and biphasic in lead aVR, suggesting that the sinus node is not initiating atrial depolarization.

Figure 3.14 ECG after ablation showing sinus rhythm and a normal-appearing P wave, now deeply negative in lead aVR and positive in lead II. (Kusumoto 2009. Reproduced with permission of Springer Science + Business Media.)

Figure 3.13 Electrograms showing an atrial tachycardia arising from the os of the pulmonary vein with prompt termination during catheter ablation. A decapolar catheter is located in the coronary sinus, and an 8 splined, 64 electrode basket catheter is located in the pulmonary vein. The ablation catheter (Abl) is located at the os of the left superior pulmonary vein and has an early atrial electrogram (*).

Chapter 4: Supraventricular tachycardia case 3

Figure 4.1 Baseline electrograms show a basic cycle length of 1022 ms with normal conduction properties and normal atrioventricular conduction (PR interval: 150 ms, AH interval: 103 ms; HV interval: 30 ms) and normal QRS morphology.

Figure 4.2 With an atrial premature beat delivered at a coupling interval of 370 ms, the AH interval is prolonged (290 ms from the earliest CS activation). As the atrial coupling interval was shortened, there was gradual prolongation of the AH interval without a jump (50 ms increase with a 10 ms decrease in the coupling interval).

Figure 4.3 With a coupling interval of 360 ms, the premature atrial stimulus results in atrial capture but no His electrogram signifying block in the AV node and defining the AVNERP.

Figure 4.4 At a drive cycle length of 600 ms, a premature ventricular stimulus at a coupling interval of 530 ms leads to a stimulation to atrial electrogram of 260 ms, which is slightly longer than the stimulation to atrial electrogram interval during basic pacing 250 ms. The pattern of atrial activation is similar to the first atrial electrogram recorded in the mid-coronary sinus.

Figure 4.5 Continuation of Figure 4.4. Shortening the coupling interval to 450 ms is associated with an increase in the stimulation to electrogram interval of 313 ms with the same pattern of atrial activation observed at the longer coupling interval. This gradual decrement suggests that this pattern of retrograde activation is produced by tissue with decremental conduction properties such as the AV node.

Figure 4.6 After initiation of an isoproterenol infusion, coronary sinus pacing at a baseline pacing cycle of 400 ms, with two premature beats (260 and 230 ms), the patient has an AV interval of 262 ms.

Figure 4.7 Continuation of Figure 4.6. Shortening the last coupling interval (s3) to 220 ms leads to sudden prolongation of the AV interval to 430 ms and initiation of tachycardia. Unfortunately, a His bundle electrogram is not available, but such a profound prolongation in the AV interval can only be mediated by delay in AV nodal conduction.

Figure 4.8 Electrograms during tachycardia reveals a tachycardia cycle length of 390 ms, an HA interval of 105 ms, and a VA interval of 75 ms, with earliest atrial activation observed in the proximal coronary sinus.

Figure 4.9 Premature ventricular stimulus at a coupling interval of 350 ms does not reset the tachycardia.

Figure 4.10 Two extrastimuli at very short coupling intervals (230 and 220 ms) both interact with the tachycardia circuit and shorten the atrial electrogram intervals. The interesting termination suggests that the second extrastimulus retrogradely activated the atria via the slow pathway because of the significant prolongation of the stimulus to atrial electrogram interval and the subsequent anterograde activation via the fast pathway as evidenced by the short PR interval. With this interpretation, the tachycardia terminated because of retrograde block in the slow pathway.

Figure 4.11 Response of the tachycardia to ventricular pacing. Once the tachycardia is entrained, cessation of pacing leads to a V-A-V response ruling out atrial tachycardia. Of the two remaining possibilities – AVRT using a septal accessory pathway and AVNRT, comparing the VA intervals between tachycardia and ventricular pacing can be extremely useful. In a tachycardia using a septal accessory pathway, the VA interval should be similar for both tachycardia and ventricular pacing. In this case, the VA interval is dramatically longer with ventricular pacing, making AVNRT a more likely diagnosis.

Figure 4.12 Schematic showing the reason for differences in retrograde conduction times between AVNRT and AVRT during tachycardia and ventricular pacing.

Figure 4.13 Morady maneuver in another patient with a septal accessory pathway. The patient is in supraventricular tachycardia at a cycle length of 430 ms. On cessation of ventricular pacing at 400 ms, a V-A-V response is noted. The ventricular stimulus to atrial electrogram interval (116 ms) is shorter than the HA interval (134 ms).

Figure 4.14 Pacing the His bundle during supraventricular tachycardia can also be useful. In this case, His bundle capture is confirmed by the slight change in the QRS complex that remains narrow (*), but the tachycardia is not reset, providing evidence that the distal is bundle is not participating in the circuit. The His bundle electrogram can be seen just before the pacing stimulus (arrowheads).

Figure 4.15 Schematic showing the use of His bundle pacing during sinus rhythm. On the left-sided drawings, a stronger stimulus strength leads to capture of the His bundle and adjacent ventricular myocardium. On the right-sided drawings, a decrease in the stimulus strength only captures ventricular myocardium. In the presence of an accessory pathway, an extranodal response will be observed where regardless of whether the His bundle is captured, the VA interval will remain relatively constant (a). In contrast, a nodal response is characterized by a shorter VA interval with His bundle capture, as the wave of activation has a head start when compared to ventricular depolarization only (b).

Figure 4.16 Electrograms from His bundle pacing. On the left panel, the narrower QRS complex (first QRS complex) is associated with a shorter stimulus to atrial time when compared to RV only capture (second and third QRS complexes). The stimulus to right ventricular electrogram is shorter during His bundle pacing due to more activation via the His Purkinje system. On the right panel, a problem associated with His bundle pacing is shown. In this case, atrial capture occurs on the second and third paced peats. The pacing stimulus to atrial electrogram interval is the same whether (second stimulus) or not (third stimulus) ventricular capture occurs.

Figure 4.17 Coronary sinus angiography can to help define inferior septal anatomy. (a) The location and position of the coronary sinus in the left anterior oblique (LAO) view. (b) The catheter is located just outside the coronary sinus, but it is impossible to determine this from just a single image and requires corroboration from an orthogonal fluoroscopic view. The right anterior oblique (RAO) view confirms that the catheter is just between the coronary sinus and the tricuspid valve (c).

Chapter 5: Supraventricular tachycardia case 4

Figure 5.1

Figure 5.2 Baseline electrograms. The baseline cycle length is 770 ms. Atrioventricular conduction appears normal with a PR interval of 153 ms, an AH interval of 84 ms, and an HV interval of 44 ms. At first glance, the QRS appears normal with a QRS width of 101 ms.

Figure 5.3 Atrial pacing at a rate of 450 ms is associated with 1:1 atrioventricular conduction, but changes in the QRS morphology are noted. With atrial pacing, as expected the AH interval increases, but in the QRS complexes associated with