Cardiac Pacing and ICDs E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 1069

Veröffentlichungsjahr: 2020

Beschreibung

The consummate guide to cardiac pacing and defibrillator therapy in a clinical setting

Designed to provide clinicians and fellows with a complete, up-to-date breakdown of current device therapies for pacing and defibrillation, Cardiac Pacing and ICDs reflects the latest developments in the device treatment of heart rhythm abnormalities. Topics ranging from essential principals to new and innovative techniques are explored in focused chapters, illustrated with full-color images, charts, and diagrams. Addressing every aspect of permanent and temporary pacing and defibrillation therapy, this invaluable resource covers patient indications, pacing mode selection, implantation and removal techniques, troubleshooting, and much more.

The seventh edition has been expanded and revised to enable clear and practical understanding of the field as it exists today. Drawing upon real-world experience and cutting-edge research, it offers accessible, systematic guidance with a clinical focus, as well as a wealth of bitesize tips and tricks. Access to a new companion website provides insightful supplementary material, complete with downloadable images and video clips of key techniques. This essential book:

• Provides an intuitive, easy-to-navigate guide to cardiac pacing techniques and devices
• Explains pacing hemodynamics in practical, clinically relevant terms
• Features simple algorithms for mode selection and device programming
• Offers details of novel pacing systems and techniques, such as leadless pacemaker and His bundle pacing.
• Covers pacemaker timing cycles, special features, and evaluation and management of pacing system malfunctions
• Summarizes indications and details implantation techniques of ICDs, including transvenous and subcutaneous systems
• Includes best practices in MRI safety, patient consultation, and remote patient follow-up

Cardiac Pacing and ICDs is an ideal resource for clinicians and fellows in cardiology and electrophysiology, those preparing for the IHRBE Examination in Devices, and any nurses, technicians, and other professionals caring for patients with implantable cardiac devices.

Leseprobe

Table of Contents

Cover

List of Contributors

Preface

Acknowledgments

CHAPTER 1: Indications for permanent cardiac pacing

Introduction

Anatomy and physiology of the conduction system

Indications for permanent pacemakers

Sinus node dysfunction

Acquired atrioventricular block

Reflex syncope

Spinal cord injury

Ictal bradycardia

Specific conditions associated with cardiac conduction disease

Genetic cardiomyopathies

Pacing for systolic heart failure

Pacing to prevent or terminate tachycardias

Pacing for children and adolescents (including all patients with congenital heart block)

Pacing after cardiac surgery and transcatheter aortic valve implantation

Drug‐induced bradycardia

Sleep‐disordered breathing and bradycardia

Summary

Acknowledgment

References

CHAPTER 2: Basics of cardiac pacing: components of pacing, defibrillation, and resynchronization therapy systems

Introduction

Basics of pacing

Types of cardiac implantable electronic devices

Components of the CIED system

Lead design

Special situations

References

CHAPTER 3: Hemodynamics of cardiac pacing and pacing mode selection

Introduction

Correction of bradycardia

Chronotropic incompetence and rate modulation

Atrioventricular synchrony

Pacemaker syndrome

Detrimental effects of right ventricular pacing

Left ventricular pacing and cardiac resynchronization therapy

Pacing in hypertrophic obstructive cardiomyopathy

Pacemaker mode selection

References

CHAPTER 4: Temporary cardiac pacing

Introduction

Cardiopulmonary resuscitation

Reversible causes of severe bradycardia

Other indications

Temporary pacing options

Complications

Clinical application

Conclusion

References

CHAPTER 5: Techniques of pacemaker and ICD implantation and removal

Introduction

Physician qualifications

Logistical requirements

Assessment of the patient

Special issues

Cost‐effectiveness

Informed consent

Preimplantation orders

Patient preparation

Implant procedure

Postprocedure management

Complications of implantation

Lead extraction

Medicolegal aspects of implantation and extraction

References

CHAPTER 6: Pacemaker timing cycles and special features

Introduction

Pacing nomenclature

Pacing modes

Timing cycles

Rate‐modulated pacing

Base‐rate behavior

Upper rate behavior

Rate enhancements

Mode switch

Algorithms for atrial arrhythmia detection and atrial pace/sense competition

Algorithms to prevent atrial fibrillation

Algorithms to minimize right ventricular pacing

Pacemaker‐mediated tachycardia

Biventricular pacing

Noise reversion

Magnet response

Summary

References

CHAPTER 7: Evaluation, troubleshooting, and management of pacing system malfunctions

Introduction

General considerations: approach to evaluation of pacemaker function and malfunction

Differential diagnosis of device malfunction

Radiographic imaging of pacer systems

Electrocardiographic manifestations of pacer malfunction

Problems with sensing

Analysis of stored device data

Pacemaker programming

References

CHAPTER 8: The implantable cardioverter–defibrillator

Introduction

Indications

Device selection

Function

ICD programming

Summary

References

CHAPTER 9: Cardiac resynchronization therapy

Heart failure and mechanisms of cardiac resynchronization therapy

Indications and patient selection

CRT implantation

Management of difficulties in placing left ventricular leads (Table 9.3)

Clinical outcomes

Approach to CRT non‐responders

Algorithm to approach non‐responders

Summary

References

CHAPTER 10: ICD follow‐up and troubleshooting

Introduction

ICD follow‐up

Troubleshooting

Conclusion

References

CHAPTER 11: Follow‐up of the patient with a CIED

Introduction

Acute CIED implant follow‐up

Long‐term CIED clinic follow‐up

Remote monitoring

Frequency and mode of follow‐up

Advisories

Special situations encountered by the CIED patient

Improving the experience of patients with CIEDs

Acknowledgments

References

Index

End User License Agreement

List of Tables

Chapter 1

Table 1.1 Classes of guideline recommendations

Table 1.2 Manifestations of sinus node dysfunction and their diagnosis

Table 1.3 Responses to maneuvers to identify level of block in patients with ...

Table 1.4 Types of neurally mediated syncope

Chapter 2

Table 2.1 Factors affecting pacing threshold

Table 2.2 Diagnostic considerations with changes in pacing, defibrillation or...

Table 2.3 Comparison of components of the Micra and Nanostim leadless pacemak...

Table 2.4 Summary of battery chemistries

Table 2.5 Mechanism, advantages, and disadvantages of accelerometer and minut...

Table 2.6 Components used in modern pacing and defibrillation leads

Table 2.7 Potential adverse effects of MRI in patients with a pacemaker

Table 2.8 Confirmation of MRI safety with MRI‐conditional devices

Table 2.9 Summary of management before, during, and after radiation therapy

Chapter 3

Table 3.1 Determination of optimal atrioventricular (AV) delays using the atr...

Table 3.2 Randomized controlled trials of pacemaker mode selection

Chapter 4

Table 4.1 Examples of potentially reversible causes of symptomatic bradycardi...

Table 4.2 Common causes of failure to capture with transcutaneous pacemaker

Table 4.3 Complications encountered during placement of a transvenous tempora...

Table 4.4 Loss of pacing or loss of capture during transvenous temporary paci...

Table 4.5 Comparison of temporary pacing technologies

Table 4.6 Recommendations for temporary pacing in patients with symptomatic s...

Chapter 5

Table 5.1 Special issues in the assessment of the patient who requires cardia...

Table 5.2 Lead characteristics

Table 5.3 Acceptable electrical parameters for new lead placement

Table 5.4 Advantages and disadvantages of His bundle pacing

Table 5.5 Advantages and disadvantages of leadless cardiac pacing

Table 5.6 Advantages and disadvantages of S‐ICD vs. transvenous ICD

Table 5.7 Acute complications of pacemaker implantation

Table 5.8 Delayed complications of pacemaker therapy

Table 5.9 Avoidance of air embolism

Table 5.10 Causes of arrhythmia during pacer implantation

Table 5.11 HRS consensus indications for transvenous lead extraction

Table 5.12 Microbiology of pacemaker/ICD infections

Table 5.13 Risks of lead extraction

Table 5.14 Pre‐explant information

Table 5.15 Recommended personnel for lead extraction procedures

Table 5.16 Lead extraction checklist

Table 5.17 Tools and equipment for lead extraction

Table 5.18 Responsibilities of an implanting physician

Chapter 6

Table 6.1 Revised N

A

SPE/

B

PEG generic code for bradycardia, adaptive‐rate, and...

Table 6.2 Indications, advantages, and disadvantages of commonly used pacing ...

Table 6.3

A

cronyms and description of cardiac events and timing cycles in a singl...

Table 6.4 Features that may affect device behavior

a

Table 6.5 Rate smoothing/stabilization and fallback algorithms

Table 6.6 Algorithms to allow intrinsic sinus rate (SR)

Table 6.7

A

lgorithms for cardioinhibitory neurogenic syncope

Table 6.8

A

trial arrhythmia detection and atrial pace/sense competition algorithm...

Table 6.9

A

lgorithms to prevent atrial fibrillation

Table 6.10 Algorithms to minimize ventricular pacing

Table 6.11 Different algorithms for pacemaker‐mediated tachycardia (PMT)

Table 6.12 Predisposing factors and programming to avoid repetitive non‐reent...

Table 6.13 Main differences between pacemaker‐mediated tachycardia (PMT) and ...

Chapter 7

Table 7.1 Baseline data needed for pacemaker troubleshooting

Table 7.2 Symptoms suggestive of pacemaker abnormality

Table 7.3 Causes and management of sensing and pacing abnormalities

Table 7.4 Pacemaker functions that may be interpreted as malfunction (pseudo‐...

Table 7.5 Pacemaker mode selection.

Table 7.6 Basic pacemaker programming

Table 7.7 Programming considerations in special clinical situations

Chapter 8

Table 8.1 Summary of indications for ICD therapy in patients with ischemic an...

Table 8.2 Selected ICD trials for primary prevention of sudden cardiac death

Table 8.3 Summary of indications for ICD therapy in patients with rare condit...

Table 8.4 Guideline recommendation for the use of wearable cardioverter–defib...

Table 8.5 Factors involved in considering appropriate candidates for S‐ICD

Table 8.6 S‐ICD trial comparison of patient demographics

Table 8.7 Rapid oversensing with normal pacing impedance: differential diagno...

Table 8.8 Discriminator building blocks for SVT–VT discrimination algorithms

Table 8.9 Failure modes of the electrogram morphology discriminator

Table 8.10 ICD programming recommendations from 2015 Heart Rhythm Society con...

Table 8.11 Manufacturer‐specific ICD programming recommendations from 2015 He...

Table 8.12 Causes and corrections for high defibrillation thresholds (DFTs) a...

Table 8.13 Scenarios where DFT testing is useful or might be considered

Table 8.14 Considerations for ICD programming

Chapter 9

Table 9.1 Recommendations for cardiac resynchronization therapy (CRT) in pati...

Table 9.2 Assessment of optimal left ventricular (LV) lead position

Table 9.3 Management of difficulties when placing a left ventricular (LV) lea...

Table 9.4 Complications related to coronary sinus in recipients of a non‐thor...

Table 9.5 Outcomes of randomized trials in cardiac rehabilitation therapy

Table 9.6 Pooled mortality and heart failure (HF) events/hospitalizations wit...

Table 9.7 Key features of clinical outcomes

Table 9.8 Factors affecting the outcomes of cardiac resynchronization therapy

Table 9.9 Options for hemodynamic optimization in CRT devices

Table 9.10 Key features to consider in the management of non‐responders: the ...

Chapter 10

Table 10.1 Content of ICD follow‐up (every 3–6 months)

Table 10.2 Causes of ventricular oversensing

Table 10.3 Perioperative management of ICDs

Table 10.4 Multiple ICD shocks

Table 10.5 Failure to detect or treat ventricular arrhythmia

Chapter 11

Table 11.1 Example same‐day discharge (SDD) protocol for patients with cardio...

Table 11.2 Spectrum of CIED patient knowledge areas

Table 11.3 CIED clinic visit

Table 11.4 Approach to CIED interrogation

Table 11.5 Available remote interrogation information

Table 11.6 Follow‐up recommendations for CIEDs (pacemakers, ICDs, CRT devices...

Table 11.7 Electromagnetic interference and CIEDs

Table 11.8 Selected non‐medical sources of electromagnetic interference and r...

Table 11.9 Suggested considerations for institutional protocol for MRI in pat...

Table 11.10 Recommendations for management of patients with a CIED undergoing...

Table 11.11 Selected medical sources of electromagnetic interference (EMI) an...

List of Illustrations

Chapter 1

Figure 1.1 Summary of factors contributing to sinus node (SN) dysfunction. T...

Figure 1.2 Schematic of the conduction system with arterial supply shown. LA...

Figure 1.3 Rate of escape rhythm from various areas of the atrioventricular ...

Figure 1.4 Tachy–brady syndrome due to sinus arrest at termination of atrial...

Figure 1.5 A 69‐year‐old male had been started on atenolol 75 mg/day for tre...

Figure 1.6 Type I second‐degree AV block associated with Lyme disease. This ...

Figure 1.7 High‐grade AV block. This 60‐year‐old female with hypertension an...

Figure 1.8 Third‐degree AV block and junctional escape during atrial flutter...

Figure 1.9 Complete heart block with narrow QRS escape rhythm. This 70‐year‐...

Figure 1.10 Complete AV block with wide QRS escape rhythm. This 77‐year‐old ...

Figure 1.11 Exercise‐induced AV block. This 68‐year‐old male presented with ...

Figure 1.12 Bifascicular block due to right bundle branch block and left ant...

Figure 1.13 Intra‐ and infra‐His AV block induced with atrial pacing. A 68‐y...

Figure 1.14 Marked cardioinhibitory response to neurally mediated syncope. T...

Figure 1.15 Response to gentle carotid massage in carotid hypersensitivity s...

Figure 1.16 Atrial overdrive pacing to terminate atrial tachycardia. This 75...

Figure 1.17 Bradycardia‐related torsades de pointes ventricular tachycardia ...

Figure 1.18 Acute anterior myocardial infarction complicated by complete AV ...

Figure 1.19 AV block associated with acute inferior myocardial infarction. R...

Chapter 2

Figure 2.1 (a) Transmembrane potential. The cell membrane is composed of a p...

Figure 2.2 (a) Current of injury recorded during placement of a ventricular ...

Figure 2.3 Various manufacturer‐specific sensing vectors are available with ...

Figure 2.4 Signal processing in implantable cardioverter–defibrillators. The...

Figure 2.5 The strength–duration relationship (red curve) is a plot of the s...

Figure 2.6 Typical bipolar pacing circuit composed of a galvanic cell/batter...

Figure 2.7 Multiple pacing vectors in an ICD lead. (

Top

) Bipolar pacing betw...

Figure 2.8 (a) Typical cathodal pacing pulse with constant voltage and fixed...

Figure 2.9 (a) Non‐Faradic current and formation for a double layer or bilay...

Figure 2.10 Dual‐chamber pacemaker with a right atrial lead (blue) and a rig...

Figure 2.11 (a) Right anterior oblique (RAO) view of placement of a lumen‐le...

Figure 2.12 (a) ICD with shock coils in the right ventricular and the superi...

Figure 2.13 High‐voltage (HV) charging circuit converts the low‐voltage outp...

Figure 2.14 (a) Right and (b) left anterior oblique views of balloon occlusi...

Figure 2.15 Placement of a quadripolar lead in (a) right and (b) left anteri...

Figure 2.16 Components of the subcutaneous ICD system. The pulse generator i...

Figure 2.17 The three available sensing vectors of the subcutaneous ICD. The...

Figure 2.18 Manual screening tool for subcutaneous ICD. An acceptable wavefo...

Figure 2.19 (a) Micra TPS has a centrally located cathode between the passiv...

Figure 2.20 Components of the wireless cardiac resynchronization system.

Figure 2.21 Basic pacemaker circuits and function.

Figure 2.22 Surface electrocardiography obtained during active conductive te...

Figure 2.23 (a) Open loop sensor, where induced rate change does not procedu...

Figure 2.24 (a) Coaxial lead design. In this lead design the conductor cable...

Figure 2.25 (a) Durata (Abbott Laboratories, Abbott Park, IL) lead. The cent...

Figure 2.26 (a) DF4 connector pin. The tip of the pin is narrower in diamete...

Figure 2.27 Two types of surgical epicardial leads available for pacing. Bip...

Figure 2.28 (a) Anteroposterior chest X‐ray of a patient with high defibrill...

Figure 2.29 (a) DF4 adapter available on the market. Additional coils are ad...

Figure 2.30 Select features of an MRI‐conditional pacemaker system. (a) The ...

Figure 2.31 (a) Monopolar electrosurgery above the umbilicus where the curre...

Chapter 3

Figure 3.1 Effects of ventricular pacing rate on cardiac index, stroke volum...

Figure 3.2 Heart rate response at onset and termination of exercise in eight...

Figure 3.3 Work rate versus oxygen uptake at anaerobic threshold in nine pat...

Figure 3.4 Pulmonary capillary wedge (PCW) pressure recordings from a single...

Figure 3.5 Right atrial (RA) and pulmonary capillary wedge (PCW) pressure re...

Figure 3.6 Right atrial (RA) and pulmonary capillary wedge (PCW) pressure re...

Figure 3.7 Left ventricular (LV) and pulmonary capillary wedge (PCW) pressur...

Figure 3.8 Left ventricular (LV) and pulmonary capillary wedge (PCW) pressur...

Figure 3.9 Left ventricular (LV) and pulmonary capillary wedge (PCW) pressur...

Figure 3.10 Ventricular pacing with 1 : 1 retrograde conduction. In this tra...

Figure 3.11 Ventricular pacing without retrograde conduction. Transesophagea...

Figure 3.12 Representative Doppler tracings of left pulmonary vein flow in a...

Figure 3.13 Representative Doppler tracings of left pulmonary vein flow toge...

Figure 3.14 (a) Transesophageal Doppler flow image showing mitral regurgitan...

Figure 3.15 Mitral valve (a) and tricuspid valve (b) continuous‐wave Doppler...

Figure 3.16 Femoral artery pressure recordings from one patient. (

Left to ri

...

Figure 3.17 Radial artery pressure recording from a patient during right ven...

Figure 3.18 Doppler echocardiographic evaluation of the velocity time integr...

Figure 3.19 Effect of pacing site and mode on cardiac index. Measurements du...

Figure 3.20 Hypothetical ventricular function curves comparing (1) stroke vo...

Figure 3.21 Ventricular function curves comparing cardiac index (CI) and lef...

Figure 3.22 Doppler aortic flow velocity integrals (FVI) recorded at varying...

Figure 3.23 Atrial transport delay (ATD) is prolonged during atrial pacing c...

Figure 3.24 Right ventricular (RV) pacing delays left ventricular activation...

Figure 3.25 ECG tracings from a 74‐year‐old male with complaints of fatigue ...

Figure 3.26 Continuous‐wave Doppler recordings show mitral regurgitation (MR...

Figure 3.27 Doppler technique for optimizing the atrioventricular (AV) inter...

Figure 3.28 Determination of optimal paced atrioventricular (AV) delay (AVD

o

...

Figure 3.29 Hypothetical relationship of appropriate atrioventricular interv...

Figure 3.30 Normal stroke volume (SV) and heart rate (HR) response to exerci...

Figure 3.31 Hypothetical general relationship between atrioventricular (AV) ...

Figure 3.32 Schematic of the multiple reflex pathways involved in pacemaker ...

Figure 3.33 Changes in total peripheral vascular resistance (TPR) during nor...

Figure 3.34 Minimal ventricular pacing strategy to promote intrinsic atriove...

Figure 3.35 Comparison of acute changes in maximum positive rate of rise of ...

Figure 3.36 In this long‐term follow‐up study of 192 patients undergoing eit...

Figure 3.37 Raw data tracings before, immediately on initiation of left vent...

Figure 3.38 Pressure–volume loops from a patient with baseline left bundle b...

Figure 3.39 Tracings showing the impact of atrioventricular (AV) sequential ...

Figure 3.40 Pacemaker mode selection algorithm for sinus node dysfunction. A...

Figure 3.41 Pacemaker mode selection algorithm for atrioventricular block. A...

Chapter 4

Figure 4.1 Sinus rhythm with complete heart block. (

Top

) There are coupled p...

Figure 4.2 An algorithm to consider in the treatment of a patient with sever...

Figure 4.3 Components required for transcutaneous pacing. (a) Automated exte...

Figure 4.4 Transcutaneous pacing in an intubated 180‐kg patient with recurre...

Figure 4.5 Delivery of a 5‐Fr transvenous passive fixation pacing electrode ...

Figure 4.6 Delivery of a 3‐Fr transvenous passive fixation pacing electrode ...

Figure 4.7 (

Left

) Simulation of the balloon‐based positioning of the Tempo™ ...

Figure 4.8 (a) X‐ray image of a permanent bipolar pacemaker lead placed in t...

Figure 4.9 An epicardial pacing system placed during cardiac surgery. (a) Ep...

Figure 4.10 Placement of 3‐Fr active fixation electrode catheters in the rig...

Chapter 5

Figure 5.1 Venography may be helpful in documenting the patency of venous st...

Figure 5.2 Flow chart for decision process surrounding a new device implant....

Figure 5.3 Anteroposterior chest radiograph of a patient with a dual‐chamber...

Figure 5.4 Surface landmarks from the implanter’s perspective in a patient w...

Figure 5.5 Lead fracture from “subclavian crush” seen on fluoroscopy during ...

Figure 5.6 Micropuncture technique for vascular access. (a) 18‐G micropunctu...

Figure 5.7 (a) Anatomy of the subclavian venous system and skeletal landmark...

Figure 5.8 Surgical access to the left cephalic vein at pacemaker implant. (...

Figure 5.9 (a–f) Placement of the ventricular lead in right anterior oblique...

Figure 5.10 (a) Posteroanterior and (b) lateral chest radiographs of active ...

Figure 5.11 (a) Right anterior oblique (RAO) and (b) left anterior oblique (...

Figure 5.12 Current of injury recorded by a pacing system analyzer after ext...

Figure 5.13 Posteroanterior radiographic views illustrating different patter...

Figure 5.14 (a–d) Motion of an atrial lead placed in the right atrial append...

Figure 5.15 Series of epicardial pacing systems in a 34‐year‐old man who und...

Figure 5.16 MDT 3830 lead used for permanent His bundle pacing. (a) Photogra...

Figure 5.17 MDT C315His guiding catheter used for placing the 3830 lead in t...

Figure 5.18 Stages of permanent His bundle pacing lead implantation I. (a) C...

Figure 5.19 Surface lead and unipolar recording from the helix of the 3830 p...

Figure 5.20 Surface ECG leads and His bundle recordings after lead fixation ...

Figure 5.21 Stages of permanent His bundle pacing lead implantation II. (a) ...

Figure 5.22 Stages of permanent His bundle pacing lead implantation III. Fin...

Figure 5.23 Continuous rhythm strip of a patient with a dual‐chamber pacemak...

Figure 5.24 Preoperative X‐ray (a) and photograph (b) obtained at the time o...

Figure 5.25 (a) Posteroanterior and (b) lateral chest X‐ray of a 38‐year‐old...

Figure 5.26 Flow chart for decisions surrounding revision of a previously im...

Figure 5.27 Micra

®

transcatheter pacing system (TPS). (a) The 27‐Fr int...

Figure 5.28 Leadless cardiac pacemaker implantation I: initial positioning. ...

Figure 5.29 Leadless cardiac pacemaker implantation II: contrast ventriculog...

Figure 5.30 Leadless cardiac pacemaker implantation III: tug test and final ...

Figure 5.31 S‐ICD system hardware (a) S‐ICD generator and lead. (b) Design o...

Figure 5.32 Fluoroscopy showing (a) posteroanterior and (b) steep left anter...

Figure 5.33 Steps in S‐ICD system implantation I. (a) Anatomical landmarks a...

Figure 5.34 Steps in S‐ICD system implantation II. (a) The S‐ICD lead is tie...

Figure 5.35 Posteroanterior (a) and lateral (b) chest X‐rays after S‐ICD lea...

Figure 5.36 Right pneumothorax after left‐sided pacemaker implantation in an...

Figure 5.37 Reconstructed computed tomographic image in right anterior obliq...

Figure 5.38 Chest radiographs of a patient after implantation of a dual‐cham...

Figure 5.39 Deep venous thrombosis (DVT) during pacemaker implantation. (a) ...

Figure 5.40 Examples of device pocket abnormalities. (a) Severe skin reactio...

Figure 5.41 Pacemaker lead infection in transesophageal echocardiographic im...

Figure 5.42 A newly extracted active fixation atrial (RA) and two ventricula...

Figure 5.43 Locking stylets for lead extraction. (a) Spectranetics LLD locki...

Figure 5.44 Tying to the “cables” of defibrillator leads. A modified sheet b...

Figure 5.45 Cook Medical One‐Tie compression device. This is a circular loop...

Figure 5.46 Different types of sheath used in lead extraction. (a) Simple te...

Figure 5.47 Basic techniques of lead extraction. (a) Lead extraction from th...

Figure 5.48 (a) Cook Medical EvolutionRL hand‐powered mechanical sheath with...

Figure 5.49 Fluoroscopic images of ventricular lead extraction by the femora...

Chapter 6

Figure 6.1 (a) VOO, (

B

)

AA

I, and (c) VVI pacing modes. Event markers represe...

Figure 6.2 (a) DDD, (b) DDI, (c) DVI, and (d) VDD pacing modes. Event marker...

Figure 6.3

B

lanking and refractory periods. Inappropriate

A

V sequential paci...

Figure 6.4 Timing cycles found on (a)

AA

I, (b) VVI, and (c) DDD pacing modes...

Figure 6.5

AA

I pacing mode. (a)

A

trial pacing (

A

P) occurs at the end of the ...

Figure 6.6 Ventricular refractory period (VRP) in VVI pacing mode.

A

prematu...

Figure 6.7 Representation of atrioventricular interval (

A

VI). (a)

A

VI corres...

Figure 6.8 Far‐field R‐wave oversensing. The R wave is inappropriately sense...

Figure 6.9 ECG demonstration of safety pacing due to atrial undersensing in ...

Figure 6.10 ECG tracing demonstrates differential atrioventricular interval ...

Figure 6.11 Schematic of automatic calculation of differential atrioventricu...

Figure 6.12 Dynamic atrioventricular (

A

V) delay.

A

s heart rate increases,

A

V...

Figure 6.13 Upper rate limit (URL) limited by total atrial refractory period...

Figure 6.14 Dynamic post‐ventricular atrial refractory period (PV

A

RP) in DDD...

Figure 6.15 The VVIR timing cycle consists of a lower rate limit (LRL), an u...

Figure 6.16 DDDR pacing mode.

A

device functioning with heart rates above th...

Figure 6.17 Rate response of the DDDR pacemaker and its behavior at both max...

Figure 6.18 (a) Ventricular‐based timing: fixed ventriculoatrial interval (V

Figure 6.19 Different responses to premature ventricular contraction (PVC) d...

Figure 6.20 Schematic representations of 2 : 1

A

V block during different bas...

Figure 6.21 Effect of different base‐rate behavior systems on rate‐modulated...

Figure 6.22 Hybrid base‐rate behavior. (a) Timing changes from atrial‐ to ve...

Figure 6.23 Modified atrial‐based timing in managed ventricular pacing (MVP,...

Figure 6.24 Upper rate behavior during non‐sustained atrial tachycardia/flut...

Figure 6.25 Wenckebach‐like and 2 : 1 pacemaker behavior.

A

pacemaker is pro...

Figure 6.26 Fallback mode and ventricular rate regularization features. (a) ...

Figure 6.27 Rate smoothing. (a) ECG demonstrates a Wenckebach‐like behavior ...

Figure 6.28 Ventricular rate stabilization.

A

short coupled premature ventri...

Figure 6.29 Rate modulation (DDDR pacing mode) acting as rate smoothing. (a)...

Figure 6.30

A

lgorithms to allow intrinsic sinus rate. (a) Rate hysteresis, (...

Figure 6.31

A

dvanced rate hysteresis. DDD pacing mode at 100 bpm (interventi...

Figure 6.32 (a) Rate drop response.

A

lgorithm detects a heart rate drop base...

Figure 6.33 Mode switch. (a) Pacing mode changes from DDDR to DDIR after the...

Figure 6.34 Diagram illustrates switching from atrial tracking to a non‐trac...

Figure 6.35 Inappropriate or false mode switch. Summed (

A

tip–Vtip) electrogr...

Figure 6.36 2 : 1 Lock‐in protection algorithm. Initial tracking of an atria...

Figure 6.37

A

trial flutter response (

A

FR).

A

trial detection inside the post‐...

Figure 6.38 Non‐competitive atrial pacing (NC

A

P). (a)

A

300‐ms NC

A

P window i...

Figure 6.39

A

trial fibrillation (

A

F) suppression algorithm. The intrinsic he...

Figure 6.40

A

lgorithms to promote intrinsic atrioventricular (

A

V) conduction...

Figure 6.41

A

lgorithms to promote intrinsic atrioventricular (

A

V) conduction...

Figure 6.42 Pacemaker‐mediated tachycardia (PMT) initiated during an atrial ...

Figure 6.43 (a) Paradoxical mechanism of pacemaker‐mediated tachycardia (PMT...

Figure 6.44 Pacemaker‐mediated tachycardia (PMT) algorithm in a cardiac resy...

Figure 6.45 Role of right ventricular (RV) sensing for cardiac resynchroniza...

Figure 6.46

B

lanking (red) and refractory (blue) periods in a biventricular ...

Figure 6.47 Left ventricular (LV) offset affecting atrioventricular interval...

Figure 6.48

B

iventricular trigger feature.

A

trial fibrillation with a rapid ...

Figure 6.49 Noise reversion response.

A

fter a ventricular‐sensed (VS) event ...

Chapter 7

Figure 7.1 Examples of radiographic device identifiers. (a) EnRhythm device ...

Figure 7.2 Posteroanterior radiographic image of a unipolar pacemaker system...

Figure 7.3 Pacemaker transtelephonic transmission (TTM) summaries: (a) St. J...

Figure 7.4 Pacemaker battery depletion. The rhythm strip (lead V1) from a pa...

Figure 7.5 A patient with sinus node dysfunction presented with shortness of...

Figure 7.6 Biventricular ICD generator switched to non‐programmable safety m...

Figure 7.7 (a) Atrial and right ventricular (RV) electrogram recording from ...

Figure 7.8 Example of lead abnormality due to insulation failure. (a) Long‐t...

Figure 7.9 Chronic low impedance trend of a bipolar atrial lead. Note long‐t...

Figure 7.10 Polarity change from bipolar to unipolar pacing due to sudden ma...

Figure 7.11 (a) Posteroanterior and (b) lateral chest X‐ray 24 hours after a...

Figure 7.12 Chest X‐ray and ECG features of a typical dual‐chamber pacing sy...

Figure 7.13 Examples of pacing system abnormalities on chest X‐ray. (a) Loos...

Figure 7.14 While pacer spikes are very well seen, assessment of proper capt...

Figure 7.15 Example of how to analyze a paced ECG. The underlying rhythm is ...

Figure 7.16 ECG recorded from a patient who received a gastric stimulator fo...

Figure 7.17 Left ventricular (LV) threshold assessment in a biventricular pa...

Figure 7.18 Interpretation of intracardiac electrograms. (a) Real‐time atria...

Figure 7.19 Tracing showing atrial undersensing during atrial flutter due to...

Figure 7.20 Noise on the right ventricular (RV) lead due to myopotential sig...

Figure 7.21 (a) An episode of atrial fibrillation (AF) with atrioventricular...

Figure 7.22 A method for testing far‐field R‐wave oversensing in order to as...

Figure 7.23 (a) An electrogram from a patient who complained of intermittent...

Figure 7.24 Rhythm strip from a patient with a dual‐chamber pacemaker who de...

Figure 7.25 Repetitive non‐reentrant ventriculoatrial synchronous rhythm. Th...

Figure 7.26 Ventricular high‐rate episode recorded in a single‐chamber Medtr...

Figure 7.27 Atrioventricular (AV) sequential pacing with noise (arrow) due t...

Figure 7.28 This patient with a dual‐chamber unipolar system presented to ro...

Figure 7.29 (a) Telemetry strip in a pacemaker‐dependent patient following u...

Figure 7.30 (a) Premature ventricular contraction (PVC) and simultaneous tim...

Figure 7.31 (a) Oversensing of far‐field P wave on the left ventricular (LV)...

Figure 7.32 A pacemaker‐dependent patient with biventricular pacing presente...

Figure 7.33 (a) Sinus rhythm at a rate close to the lower rate limit. Occasi...

Figure 7.34 (a) Noise, recorded as mode switch episode, appearing in the rig...

Figure 7.35 Example of atrial fibrillation in a patient with a pacemaker. Th...

Figure 7.36 The relationship between time since device implantation and comm...

Figure 7.37 Simplified schematic for pacemaker troubleshooting. EMI, electro...

Figure 7.38 This tracing was recorded during severe hyperkalemia. Atrioventr...

Figure 7.39 Print‐out of calculated strength–duration curve in a Medtronic p...

Figure 7.40 (a) Operation of an algorithm to allow intrinsic activation and ...

Figure 7.41 Rate drop response in a patient with carotid sinus hypersensitiv...

Figure 7.42 Continuous tracing retrieved from a dual‐chamber ICD memory. Atr...

Figure 7.43 Treatment of pacemaker‐mediated tachycardia (PMT) in a St. Jude ...

Figure 7.44 (

Top

) A recorded event that resulted in inappropriate mode switc...

Figure 7.45 (a, b) Basic device data and programming parameters from a print...

Figure 7.46 Summary page of counters and histogram information from a Boston...

Figure 7.47 High ventricular rate recorded in a pacemaker memory. The ventri...

Chapter 8

Figure 8.1 Flow chart summarizing indications for ICD implant. CHF, congesti...

Figure 8.2 Schematic of automatic adjustment of sensitivity during sinus rhy...

Figure 8.3 ICD electrograms. Near‐field electrograms are true bipolar record...

Figure 8.4 Stored electrograms from a dual‐chamber ICD with a fracture of th...

Figure 8.5 Dual‐chamber electrograms from a cardiac resynchronization ICD sh...

Figure 8.6 Detection of ventricular fibrillation (VF) with undersensing. Nea...

Figure 8.7 Aborted shock for ventricular tachycardia (VT) that terminates af...

Figure 8.8 Structure of morphology algorithm. (a) The stored template repres...

Figure 8.9 A morphology discrimination algorithm. (a) The algorithm works by...

Figure 8.10 Failure modes of morphology algorithms. (a) Alignment error. (b)...

Figure 8.11 Inappropriate detection of supraventricular tachycardia (SVT) as...

Figure 8.12 Far‐field R‐wave oversensing in a dual‐chamber ICD. The close pr...

Figure 8.13 Correct classification of abrupt‐onset supraventricular tachycar...

Figure 8.14 Interaction of single‐chamber and dual‐chamber algorithms. Right...

Figure 8.15 Inappropriate detection of abrupt‐onset supraventricular tachyca...

Figure 8.16 Subcutaneous‐ICD (S‐ICD) placement and sensing vectors. (a) The ...

Figure 8.17 Examples of appropriate and inappropriate S‐ICD shocks. (a) Elec...

Figure 8.18 S‐ICD algorithms during therapy decision phase: conditional zone...

Figure 8.19 S‐ICD system: detection profiles. As heart rate increases, the S...

Figure 8.20 Graphical representation of the relationship between probability...

Figure 8.21 Suggested algorithm for management of the patient with an elevat...

Figure 8.22 Schematic of burst and ramp antitachycardia pacing (ATP). (a) Fo...

Figure 8.23 Example of successful antitachycardia pacing (ATP) for fast vent...

Chapter 9

Figure 9.1 Image integration of functional (mechanical dyssynchrony) and ana...

Figure 9.2 Coronary vein anatomy. The venous branches are named. LAO, left a...

Figure 9.3 Fluoroscopy showing placement of the LV lead at the left ventricu...

Figure 9.4 (a) Gross right anterior oblique heart anatomy showing the fat pa...

Figure 9.5 Engaging the coronary sinus using a long sheath and sub‐selecting...

Figure 9.6 A mapping electrophysiology catheter is used to engage the corona...

Figure 9.7 Available left ventricular lead delivery systems: outer sheath an...

Figure 9.8 Spiral EASYTRAK

®

3 left ventricular lead (Boston Scientific)...

Figure 9.9 (a) Attain

®

Performa quadripolar left ventricular (LV) lead ...

Figure 9.10 Diagram illustrating the concept of multipoint pacing (MPP) in w...

Figure 9.11 Assessment of left ventricular (LV) lead location using fluorosc...

Figure 9.12 Examples of the final left ventricular (LV) lead position at the...

Figure 9.13 Mean QRS axis in the frontal plane during ventricular pacing. In...

Figure 9.14 (a) ECG QRS morphologies during right ventricular (RV), left ven...

Figure 9.15 Three‐dimensional reconstruction of epicardial coronary venous a...

Figure 9.16 (a) “Shepherd’s crook” take‐off of the lateral marginal vein, wi...

Figure 9.17 A venoplasty procedure performed in a patient with a persistent ...

Figure 9.18 Right (solid arrow) and left (dashed arrow) phrenic nerves. LV, ...

Figure 9.19 Coronary sinus (CS) dissection. An occlusive CS venogram that re...

Figure 9.20 Cumulative enrollment in cardiac resynchronization therapy rando...

Figure 9.21 Change in left ventricular ejection fraction (LVEF) after cardia...

Figure 9.22 Changes in left ventricular end‐systolic volume (LVESV) after ca...

Figure 9.23 Changes in 6‐min walk distance after cardiac resynchronization t...

Figure 9.24 Changes in Minnesota Living With Heart Failure scores after card...

Figure 9.25 Kaplan–Meier estimates of the probability of survival free of he...

Figure 9.26 Sensitivity, specificity, and accuracy likelihoods are plotted f...

Figure 9.27 Effects of cardiac resynchronization therapy with defibrillation...

Figure 9.28 Kaplan–Meier estimates of probability of death or heart failure ...

Figure 9.29 Distribution of scar sites and left ventricular (LV) leads locat...

Figure 9.30 A 74‐year‐old male with dilated cardiomyopathy, left ventricular...

Figure 9.31 Kaplan–Meier estimates of survival among left ventricular lead p...

Figure 9.32 A patient received cardiac resynchronization therapy with defibr...

Figure 9.33 Cardiac resynchronization therapy (CRT‐D) survival by biventricu...

Figure 9.34 Meta‐analysis of studies comparing the relative risk (RR) of cli...

Figure 9.35 Correlation of premature ventricular contraction (PVC) frequency...

Figure 9.36 Algorithm used to approach cardiac resynchronization therapy (CR...

Chapter 10

Figure 10.1 Make–break connections. Recording from a biventricular ICD with ...

Figure 10.2 Sensing of diaphragmatic myopotentials. Tracing, from top to bot...

Figure 10.3 Electromagnetic interference (EMI) and ICD shock due to poorly g...

Figure 10.4 Decay delay and threshold start. Digitally rectified signals as ...

Figure 10.5 T‐wave oversensing (TWOS) rejection algorithm. (a) Device stored...

Figure 10.6 Electromagnetic interferrence due to electrocautery during surge...

Figure 10.7 Flow diagram for evaluating ICD shocks. EGM, electrogram; EMI, e...

Figure 10.8 Inappropriate ICD shock due to T‐wave oversensing. (a) Plot diag...

Figure 10.9 ICD lead dislodgement. (a) Chest X‐ray demonstrating single‐cham...

Figure 10.10 Two examples of tachycardia initiation by a premature ventricul...

Figure 10.11 (a) Rapid monomorphic ventricular tachycardia (VT) treated with...

Figure 10.12 Types of oversensing resulting in inappropriate detection of ve...

Figure 10.13 (a) Ventricular fibrillation (VF) triggered and (b) followed by...

Figure 10.14 Electrical storm due to managed ventricular pacing. (a) Patient...

Figure 10.15 Inappropriate shock in S‐ICD. The inappropriate therapy occurre...

Chapter 11

Figure 11.1 Large hematoma managed conservatively by withholding anticoagula...

Figure 11.2 Graphic display of change in battery voltage over time of a St. ...

Figure 11.3 Right ventricular pacing auto‐capture threshold test and histori...

Figure 11.4 Lead performance report of a Medtronic Sprint Fidelis ICD lead f...

Figure 11.5 Technologies for remote monitoring.

Figure 11.6 An episode of oversensing of electromagnetic interference (EMI) ...

Figure 11.7 Intracardiac electrogram from a patient with a single‐lead ICD u...

Guide

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Cardiac Pacing and ICDs

7th Edition

EDITED BY

Kenneth A. Ellenbogen, MD

Kimmerling Professor of Cardiology and Chairman of the Division of CardiologyVCU / Pauley Heart CenterDirector of Clinical Cardiac Electrophysiology and PacingMedical College of Virginia / VCU School of MedicineRichmond, VA, USA

Karoly Kaszala, MD, PhD

Associate Professor of MedicineVCU / Pauley Heart CenterMedical College of Virginia / VCU School of MedicineDirector of ElectrophysiologyHunter Holmes McGuire VA Medical CenterRichmond, VA, USA

This edition first published 2020© 2020 by John Wiley & Sons Ltd

Edition History [6e, 2014]

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions.

The rights of Kenneth A. Ellenbogen and Karoly Kaszala to be identified as the authors of this work has been asserted in accordance with law.

Registered Office(s)John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, USAJohn Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK

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Limit of Liability/Disclaimer of WarrantyThe contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting scientific method, diagnosis, or treatment by physicians for any particular patient. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. While the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials or promotional statements for this work. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.

Library of Congress Cataloging‐in‐Publication Data

Names: Ellenbogen, Kenneth A., editor. | Kaszala, Karoly, editor.Title: Cardiac pacing and ICDs / edited by Kenneth A. Ellenbogen, Karoly Kaszala.Description: Seventh edition. | Hoboken, NJ : John Wiley & Sons, 2020. | Includes bibliographical references and index.Identifiers: LCCN 2020005340 (print) | LCCN 2020005341 (ebook) | ISBN 9781119578338 (paperback) | ISBN 9781119578352 (adobe pdf) | ISBN 9781119578284 (epub)Subjects: MESH: Cardiac Pacing, Artificial | Pacemaker, Artificial | Defibrillators, ImplantableClassification: LCC RC684.P3 (print) | LCC RC684.P3 (ebook) | NLM WG 166.5.C2 | DDC 617.4/120645–dc23LC record available at https://lccn.loc.gov/2020005340LC ebook record available at https://lccn.loc.gov/2020005341

Cover Design: WileyCover Images: © toysf400/Shutterstock, © Richman Photo/Shutterstock

List of Contributors

Jeffrey A. Brinker, MDProfessor of MedicineJohns Hopkins University School of MedicineBaltimore, MD, USA

T. Jared Bunch, MDProfessor of MedicineDivision of Cardiovascular MedicineUniversity of Utah School of MedicineSalt Lake City, UT, USA

Yong‐Mei Cha, MDConsultant and Professor of MedicineDepartment of Cardiovascular DiseasesDivision of Heart Rhythm ServicesMayo ClinicRochester, MN, USA

John D. Day, MDIntermountain Heart Rhythm SpecialistsIntermountain Heart InstituteIntermountain Medical CenterSalt Lake City, UT, USA

Kenneth A. Ellenbogen, MDKimmerling Professor of Cardiology and Chairman of the Division of CardiologyVCU / Pauley Heart CenterDirector of Clinical Cardiac Electrophysiology and Pacing Medical College of Virginia / VCU School of MedicineRichmond, VA, USA

Michael E. Field, MDCardiac Electrophysiologist, Professor of MedicineMedical University of South CarolinaCharleston, SC, USA

Michael R. Gold, MDMichael Assey Chair in CardiologyProfessor of MedicineMedical University of South CarolinaCharleston, SC, USA

Michael Hoosien, MDCardiac Electrophysiologist, Piedmont Heart InstitutePiedmont Atlanta HospitalAtlanta, GA, USA

Jose F. Huizar, MDDirector, Arrhythmia and Device ClinicHunter Holmes McGuire VA Medical CenterAssociate Professor of MedicineVCU School of MedicineRichmond, VA, USA

Kevin P. Jackson, MDAssociate Professor of MedicineDuke University, School of MedicineDurham, NC, USA

Roy M. John, MBBS, PhD, FRCPDirector, Center for Advanced Management of Ventricular ArrhythmiasNorthshore University HospitalManhasset, NY, USA

Karoly Kaszala, MD, PhDAssociate Professor of MedicineVCU / Pauley Heart CenterMedical College of Virginia / VCU School of MedicineDirector of ElectrophysiologyHunter Holmes McGuire VA Medical CenterRichmond, VA, USA

Ammar M. Killu, MBBSConsultant and Assistant Professor of MedicineDepartment of Cardiovascular Diseases, Division of Heart Rhythm ServicesMayo ClinicRochester, MN, USA

Justin Z. Lee, MDClinical Cardiac Electrophysiology FellowMayo ClinicRochester, MN, USA

Charles J. Love, MDProfessor of MedicineJohns Hopkins University School of MedicineBaltimore, MD, USA

Joseph E. Marine, MDVice‐Director, Division of CardiologyAssociate Professor of MedicineJohns Hopkins University School of MedicineBaltimore, MD, USA

Siva K. Mulpuru, MDConsultant, Division of Cardiovascular DiseasesAssociate Professor of MedicineMayo ClinicRochester, MN, USA

Jeffrey S. Osborn, MDIntermountain Heart Rhythm SpecialistsIntermountain Heart InstituteIntermountain Medical CenterSalt Lake City, UT, USA

Kristen K. Patton, MDProfessor of MedicineUniversity of WashingtonSeattle, WA, USA

Arun R.M. Sridhar, MD, MPHAssistant Professor of MedicineUniversity of WashingtonSeattle, WA, USA

Bruce S. Stambler, MDCardiac Electrophysiologist, Piedmont Heart InstitutePiedmont Atlanta HospitalAtlanta, GA, USA

Vaibhav Vaidya, MDClinical Cardiac Electrophysiology FellowMayo ClinicRochester, MN, USA

Niraj Varma, MD, PhDStaff PhysicianCardiac Electrophysiology and PacingHeart and Vascular InstituteCleveland ClinicCleveland, OH, USA

Preface

Management of an aging population with increasing co‐morbidities challenges each of us every day and individualizing patient treatment using an evidence‐based approach is a common goal of health care providers. Device therapy to treat cardiac arrhythmias remains relevant as device indications expand and survival in chronic disease increases. Our aim with this new edition of the book is to provide an up‐to‐date source of basic principles and a resource for device technicians, industry representatives, medical students, nurses, residents and fellows and anyone interested in the care of patients with cardiac implantable electronic devices (CIEDs) or interest in cardiac device therapy. Most sections of this book have undergone extensive revision with several key chapters being completely revised. All chapters were updated to include the most relevant clinical progress. Discussions about indications for device therapy now reflects the most current ACC/AHA clinical guidelines. We took a fresh look at different device and lead components and pacing physiology and hemodynamics. Basic pacemaker function and pacing algorithms are extensively discussed along with troubleshooting. The hemodynamic, pacemaker timing cycles, device algorithm and troubleshooting sections all are updated to summarize the most current, clinically relevant scenarios. Since the last edition, several important advances in device therapy became commonplace. Novel technologies, such as leadless pacemakers, His bundle pacing, and subcutaneous ICDs offer alternative therapies to patients and these therapies have reached mainstream application. Beyond discussing the basics of pacing and defibrillation, in the current edition there are step‐by‐step instructions for the implant procedure. Indications, best uses, and the nuts and bolts of these novel technologies are added and explained. Numerous real‐life examples are included to illustrate specific problems and troubleshooting. It is hard to believe that 8 years ago we had only limited availability and acceptance of quadripolar left ventricular pacing leads for cardiac resynchronization therapy and now this is the norm. These chapters have been updated with new information on multisite pacing. Over the last five years, patient follow‐up has been revolutionized with widespread use of remote monitoring and the final chapter provides a thorough review of current evidence and standard practice for patient follow‐up.

Of course this book would have never come to fruition without the support of Wiley and the meticulous work of the authors to whom we are greatly indebted. Their outstanding contributions are reflected through each chapter, with excellent summaries of complex topics written in a simplified yet clinically relevant manner and supported by great illustrations. We hope that this new edition will continue to be a helpful resource to all of our colleagues who are interested in learning about cardiac device therapy

Kenneth A. Ellenbogen, MD

Karoly Kaszala, MD, PhD

VCU / Pauley Heart CenterMedical College of Virginia/VCU School of MedicineRichmond, VA, USA

February 2020

Acknowledgments

To my parents, Roslyn and Leon Ellenbogen, who inspired a lifelong thirst for learning. To my wife, Phyllis, and children, Michael, Amy, and Bethany, whose patience and love made this project successful.

Kenneth A. Ellenbogen, MD

To my parents, the late Karoly and Dr Agnes Kaszala for their guidance, unconditional support and love, to my wife Gabriella, and children Julia, Dalma, and Balazs for their love, patience and understanding.

Karoly Kaszala, MD, PhD

CHAPTER 1Indications for permanent cardiac pacing

Roy M. John

Center for Advanced Management of Ventricular Arrhythmias, Northshore University Hospital, Manhasset, NY, USA

Introduction

Defects of cardiac impulse generation and conduction can occur at various levels in the cardiac conduction system. In general, intrinsic disease of the conduction system is often diffuse. For example, normal atrioventricular (AV) conduction cannot necessarily be assumed when a pacemaker is implanted for a disorder seemingly localized to the sinus node. Similarly, normal sinus node function cannot be assumed when a pacemaker is implanted in a patient with AV block. Conduction disorders that lead to important bradycardia or asystole may result from reversible or irreversible causes. Recognition of reversible causes is critical to avoid unnecessary commitment to long‐term pacemaker therapy. This chapter reviews the common disorders that warrant cardiac pacing and lists the recommended indications set out by published guidelines.

Anatomy and physiology of the conduction system

For a complete understanding of rhythm generation and intracardiac conduction, and of their pathology, a brief review of the anatomy and physiology of the specialized conduction system is warranted.

Sinus node

The sinus node or sinoatrial (SA) node is a crescent‐shaped subepicardial structure located at the junction of the right atrium and superior vena cava along the terminal crest. It measures 10–20 mm (with larger extension in some studies) and has abundant autonomic innervation and blood supply, with the sinus node artery commonly coursing through the body of the node. Endocardially, the crista terminalis overlies the nodal tissue, although the inferior aspect of the node has a more subendocardial course. Histologically, the sinus node comprises specialized nodal cells (P cells) packed within a dense matrix of connective tissue. At the periphery, these nodal cells intermingle with transitional cells and the atrial working myocardium, with radiations extending toward the superior vena cava, the crista terminalis, and the intercaval regions [1,2]. The absence of a distinct border and the presence of distal fragmentation explain the lack of a single breakthrough of the sinus node excitatory wavefront. The radiations of the node, although histologically distinct, are not insulated from the atrial myocardium. Hence, a clear anatomical SA junction is absent. The sinus node is protected from the hyperpolarizing effect of the surrounding atria, probably by its unique structure wherein electrical coupling between cells and expression of ion channels vary from the center of the node to the periphery. The pacemaker cells at the center of the node are more loosely coupled, while those at the periphery are more tightly coupled with higher density If (funny current, a mixed sodium and potassium current carried by the HCN channels) and INa currents [2].

The SA node has the highest rate of spontaneous depolarization (automaticity) in the specialized conduction system and is responsible for the generation of the cardiac impulse under normal circumstances, although normal human pacemaker activity may be widely distributed in the atrium. The unique location of the sinus node astride the large SA nodal artery provides an ideal milieu for continuous monitoring and instantaneous adjustment of heart rate to meet the body’s changing metabolic needs.

Impulse generation in the sinus node remains incompletely understood. Sinus nodal cells have a low resting membrane potential of −50 to −60 mV. Spontaneous diastolic (phase 4) depolarizations are probably triggered by several currents, including If. The predominant inward current in the center of the node is ICaL that generates a “slow” action potential. The action potentials spread peripherally into the musculature of the terminal crest. In the periphery of the node, INa is operative and necessary for providing sufficient inward current to depolarize the larger mass of atrial tissue. Defects of a number of molecular and biophysical factors that govern the ionic channels of the sinus node can lead to sinus node dysfunction (Figure 1.1).

Differential sensitivity to adrenergic and vagal inputs exists along the nodal pacemaker cells, such that superior sites tend to dominate during adrenergic drive while the inferior sites predominate during vagal stimulation [3]. Interventions including premature stimulation, autonomic stimulation, and drugs have been shown to induce pacemaker shifts (due to multicentric origins) with variable exit locations [4].

Figure 1.1 Summary of factors contributing to sinus node (SN) dysfunction. The central node (CN) shown in red is surrounded by the peripheral nodal (PN) structure in blue. RAA, right atrial appendage; SVC, superior vena cava; IVC, inferior vena cava.

Source: modified from Monfredi O, Boyett MR. Sinus sinus syndrome and atrial fibrillation in older persons: a view from the sinoatrial nodal myocyte. J Mol Cell Cardiol 2015;83:88–100. Reproduced with permission of Elsevier.

Atrioventricular node

The compact AV node is a subendocardial structure situated within the triangle of Koch and measuring 5–7 mm in length and 2–5 mm in width [5,6]. On the atrial side, the node is an integral part of the atrial musculature, in contrast to the AV bundle which is insulated within the central fibrous body and merges with the His bundle. Based on action potential morphology in rabbit hearts, atrial (A), nodal (N), and His (H) cells have been defined. Intermediate cell types such as AN and NH define areas toward the atrial and His bundle ends of the compact node, respectively. Histologically, the mid nodal part has densely packed cells in a basket‐like structure interposed between the His bundle and the loose atrial approaches to the node. The AN cells are composed primarily of transitional cells. Distinct electrical and morphological specialization is seen only in the progressively distal His fibers. Rightward and leftward posterior extensions of the AV node were described by Inoue and Becker [7]. These extensions have clinical implications for defining reentrant circuits that act as a substrate of AV nodal reentrant tachycardia.

The AV node has extensive autonomic innervation and an abundant blood supply from the large AV nodal artery, a branch of the right coronary artery, in 90% of patients, and from the left circumflex artery in 10% (Figure 1.2). AV nodal conduction is mediated via “slow” calcium‐mediated action potential and demonstrates decremental conduction due to post‐repolarization refractoriness as a result of delayed recovery of the slow inward currents. AV nodal tissue closer to the His bundle (NH and proximal His bundle area) generates junctional escape rhythms (Figure 1.3). Escape rates are dependent on the site of dominant pacemaker activity. Isoproterenol stimulation, for example, accelerates junctional escape and shifts the dominant activity to the transitional cells in the AN region and posterior extensions of the node [8–10].

His–Purkinje system

Purkinje fibers emerging from the area of the distal AV node converge gradually to form the His bundle, a narrow tubular structure that runs through or around the membranous septum to the crest of the muscular septum, where it divides into the bundle branches. The bulk of the His bundle cells contribute to the left bundle branch with a smaller contribution to the right bundle. Longitudinal strands of Purkinje fibers, divided into separate parallel compartments by a collagenous skeleton, can be discerned by histological examination of the His bundle [11]. The collagen sheathing minimizes lateral spread of impulses from the main body of the bundle branches. The rapid conduction of electrical impulses across the His–Purkinje system is responsible for the almost simultaneous activation of the right and left ventricles. The His bundle has relatively sparse autonomic innervation, although its blood supply is quite ample, emanating from both the AV nodal artery and the septal branches of the left anterior descending artery (Figure 1.2).

The bundle branch system is a complex network of interlaced Purkinje fibers that varies greatly among individuals. It generally starts as one or more large fiber bands that split and fan out across the ventricles until they finally terminate in a Purkinje network that interfaces with the myocardium (Figure 1.2). In some cases, the bundle branches clearly conform to a tri‐ or quadri‐fascicular system. In other cases, however, detailed dissection of the conduction system has failed to delineate separate fascicles. The right bundle is usually a single discrete structure that extends down the right side of the interventricular septum to the base of the anterior papillary muscle, where it divides into three or more branches. The left bundle more commonly originates as a very broad band of interlaced fibers that spread out over the left ventricle, sometimes in two or three distinct fiber tracts. There is relatively little autonomic innervation of the bundle branch system, but the blood supply is extensive, with most areas receiving branches from both the right and left coronary systems.

Figure 1.2 Schematic of the conduction system with arterial supply shown. LAD, left anterior descending coronary artery; LBB, left bundle branch; LCX, left circumflex coronary artery; RBB, right bundle branch; RCA, right coronary artery.

Figure 1.3 Rate of escape rhythm from various areas of the atrioventricular conduction system. AVN, atrioventricular node; infra‐His, below the bundle of His; intra‐His, within the bundle of His.

His–Purkinje conduction disease may be relatively proximal in some patients and can potentially be overcome by pacing distal to the site of block. His bundle pacing is thus feasible in some patients with left bundle branch in order to normalize QRS complexes and synchronize ventricular contraction [12].

Indications for permanent pacemakers