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Cardiac Pacing and Device Therapy

David R. Ramsdale • Archana Rao

Cardiac Pacing
and Device Therapy
Authors
David R. Ramsdale, M.B., Ch.B., Archana Rao, M.B., Ch.B.,
FRCP, M.D. MRCP, M.D.
The Liverpool Heart and Chest Hospital The Liverpool Heart and Chest Hospital
Liverpool Liverpool
UK UK

ISBN 978-1-4471-2938-7 ISBN 978-1-4471-2939-4 (eBook)


DOI 10.1007/978-1-4471-2939-4
Springer London Heidelberg New York Dordrecht

Library of Congress Control Number: 2012945913

© Springer-Verlag London 2012


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To Bernie and Pran for their patience and love.
Foreword

The first 50 years of cardiac pacing have recently been celebrated. Since the
first pacemaker implant in 1958, the continuously unfolding story of cardiac
stimulation has been a dramatic and fascinating one, enhanced by the more
recent entry of the implantable defibrillator and cardiac resynchronization
therapy onto the clinical stage. That these implantable devices have had a
great impact on the management of patients with cardiac arrhythmias, saving
and improving countless lives, is beyond scientific refute.
In keeping pace with the technological wizardry and the burgeoning
scientific evidence base underpinning device medicine, it is sometimes
difficult to appreciate the daily background to providing these benefits to
individual patients. Accurately and safely the diagnosis must be made, the
optimal device chosen and implanted specifically to match the clinical need,
and both patient and device meticulously followed up. In this book, the
authors have sought to throw open the doors of their pacing clinic and operat-
ing theater to reveal, in a plethora of fine and rare images, the ‘nuts and bolts’
of daily care for patients presenting for pacing and device therapy. A formal,
classically structured textbook of device medicine this is not – there are many
such comprehensive texts available – nor is it intended to be. This book is an
invitation to join the authors, who combine long interventional experience
and modern specialism in device therapy, in their daily decision making and
practical application, sharing the many sights they have seen through the lav-
ish illustrations which illuminate their own experience, and which they now
share both to inform and enthrall the reader.
Physicians are only part of a network of health professionals who need
increasing amounts of information about implantable devices in order to pro-
vide top class, modern care. This book can be recommended to all who are
entering, already involved in, or just fascinated by, this absorbing and satisfy-
ing branch of cardiology – especially those who would like to lighten their
learning through turning pages which are so easy on the eye!

Liverpool, UK Richard Charles

vii
Preface

This illustrated book is intended to provide an introduction to all those who


have or who are developing an interest in cardiac pacing and device therapy.
They include senior house officers, trainees, clinical fellows, consultant car-
diologists involved in a pacemaker program, cardiac physiologists and other
allied medical professionals, medical students, and colleagues in the medical
device industry.
There are few well-illustrated publications which provide a practical intro-
duction to the indications for use, technique of implantation, recognition and
treatment of complications, and the organization of follow-up and surveillance
of paced patients. We would have valued such a book when we were training
and we hope that young doctors with an interest and passion for cardiology
might find this a useful introduction to this fantastic subspecialty. Besides the
above topics, we felt it would be remiss of us not to present chapters on tem-
porary and epicardial pacing, elective generator change, explant procedures,
pacing in children, implantable cardioverter defibrillators, cardiac resynchro-
nization therapy, troubleshooting in pacing, and training guidelines/regula-
tions for those intending to make a career in pacing/device implantation.
At a time in the UK when pacing is being devolved from specialist tertiary
cardiac centers to smaller district general hospitals and in the USA where
pacemaker implantation is no longer the responsibility of the surgeon and in
the domain of cardiologists, there is a need for a text which offers a guide to
pacing issues to be used alongside a comprehensive practical training pro-
gram in an experienced pacing center. “A picture is worth a thousand words,”
and this book is intended to be generously illustrated with black and white
and color illustrations to aid understanding in the practical aspects of pacing.
Some line diagrams are used in order to simplify the teaching of technique,
and where appropriate Tables are incorporated as useful aide-mémoires. The
text is hopefully comprehensive enough for an “introduction” to the subject,
but it is not intended to be a pacing reference book nor an exhaustive electro-
physiological guide to the theoretical reasons for pacing in its various modes,
nor a detailed guide to programming. Hopefully it will be a very practical
guide to all those involved in the day-to-day care of paced patients, and par-
ticularly to those cardiologists planning a career in this most interesting and
exciting specialty – the so-called device specialist. The products described
are not intended to be a complete list and equally good alternatives may be
available in the marketplace. However, it is hoped that the text and images

ix
x Preface

will give the reader a greater understanding of the type of technology and
equipment that is currently available from the cardiac device industry.
Perhaps cardiac pacing is one of the best examples where the develop-
ments in technology and the microchip industry have resulted in outstanding
clinical benefits to patients, and it is likely that further innovation and minia-
turization will continue to make this specialty a stimulating and exciting one –
if you will pardon the pun!

Liverpool, UK David R. Ramsdale


Archana Rao
Acknowledgments

We would like to thank many colleagues for their help and cooperation with
the production of illustrations for this book. These include Sue Hughes, Sandra
Belchambers, Barbra Bishop, Tony Bennett, Julie Henderson, Drs. Lindsay
Morrison, Johan Waktare, Derick Todd, Julian Hobbs, Mr. Andy Robinson,
and Mr. Ian Kemp – all from The Liverpool Heart and Chest Hospital. We also
appreciate the assistance of Ian Culshaw, Jill Jenc, Becky Sumner, Elizabeth
McDermott and colleagues from Boston Scientific Ltd.; Carl Hughes, Angela
Reed, David Farrington, Tim Palmer and associates from Medtronic Ltd.;
Jayne Saul, Carmel Breen, and Andrew Rapson from Sorin Group UK; Emma
Hampson-Taylor, Paul Doherty, Tim Montgomery, and Bart Verwer from
Biotronik GmbH & Co.; Danny McGuinness, Denise Coley, and Amy Jo
Meyer from St. Jude Medical Inc.; Philip Needham of Cardionetics Ltd.,
David Grey of Novacor, UK, Patty Muratori from Cameron Health Inc. CA,
USA, Mathias Rosenfeld from Spectranetics Co., CO, USA and Zaida Torres
from Oscor Inc., FL, USA for help in providing technical and device data for
the Tables and some of the illustrations. We thank Dr. Joseph DeRose Jr.,
Professor of Cardiothoracic Surgery, Montefiore-Einstein Heart Center, Albert
Einstein College of Medicine Yeshiva University, New York, USA, for con-
tributing images from DaVinci Robotic surgery for epicardial lead placement
and to Intuitive Surgical®, Inc. for allowing us to publish images of the device
itself. We are grateful to the HRUK Audit Group (formerly the Network
Device Survey Group) for allowing us to use illustrations from the 2010 sur-
vey report. Our special thanks also go to Drs. Victor Grech and Oscar Aqualina
from the Mater Dei Hospital, Malta, for permission to use their images from
the Journal Images in Paediatric Cardiology, to Elizabeth Ihrig, Librarian of
The Bakken for making available to us images from The Collections of The
Bakken Library and Museum and permission to use them in Chapter 1 and to
James E. Fogerty and Ryan Barland from The Minnesota Historical Society
for providing the image of Dr. C. Walton Lillehei. Our thanks also go to The
Heart Rhythm Society and to Dan Zika of eMedicine.com for their permission
to reproduce interesting images in Chapters 15 and 21 respectively.
In particular, we are grateful to Dr. Mark Hall for contributing Chapter 15
and Dr. Adam Fitzpatrick, Dr. Jasveer Mangat, and Dr. Ian Peart for supply-
ing many of the images used in this chapter. We thank Dr. Jay Wright for
Chapter 16, Dr. Khalid Albouaini for his contributions to Chapter 17, Mr.
Aung Oo for providing images for use in Chapter 20, and our good friend, the
Jedi Dr. Simon Modi for help in writing Chapter 21.

xi
xii Acknowledgments

We truly appreciate the help and the expertise of our chapter reviewers
Mrs. Sue Hughes, Mr. Paul Wright, Drs. Richard Charles, Derick Todd,
Johan Waktare, David Bennett, Derek Connelly, and Mr. Aung Oo and repre-
sentatives from the device manufacturers for confirming that the data in the
device Tables were accurate at the time of going to press.
We also thank Mr. Grant Weston, Commissioning Editor, Wendy Vetter,
and all the production staff at Springer for their help and support in producing
this book with so many images.
Contents

1 History and Developments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1


2 Permanent Pacing: Current Overview . . . . . . . . . . . . . . . . . . . . 43
3 Pathology Associated with Need for Pacing . . . . . . . . . . . . . . . . 51
4 Permanent Pacemaker Implantation for Bradycardias:
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
5 Investigations Prior to Pacing . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
6 Permanent Pacemakers and Leads . . . . . . . . . . . . . . . . . . . . . . . 87
7 Implantation Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137
8 Predischarge Pacemaker Checks and Advice . . . . . . . . . . . . . . . 183
9 Programmable Functions and Terminology . . . . . . . . . . . . . . . . 193
10 Precautions After Permanent Pacemaker Implantation . . . . . . 215
11 Follow-up After Pacemaker Implantation . . . . . . . . . . . . . . . . . 223
12 Complications of Pacemaker Implantation . . . . . . . . . . . . . . . . 249
13 Temporary Pacing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283
14 Pacing in Patients with Structural Cardiac Abnormalities . . . . 315
15 Pacemaker and ICD Implantation in Children . . . . . . . . . . . . . 331
16 Cardiac Resynchronization Therapy. . . . . . . . . . . . . . . . . . . . . . 357
17 Implantable Cardioverter Defibrillators . . . . . . . . . . . . . . . . . . . 403
18 Elective Generator Change. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 441
19 Explant Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 455
20 Epicardial/Epimyocardial Pacing . . . . . . . . . . . . . . . . . . . . . . . . 483
21 Troubleshooting After Device Implantation . . . . . . . . . . . . . . . . 501
22 Training in Pacing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 543
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 561

xiii
History and Developments
1

Early Developments right atrium through a bipolar electrode needle


(Fig. 1.2) introduced via an intercostal space and
In 1882, von Ziemssen reported that an electrical used to stimulate the myocardium 30, 60, or
impulse could activate the exposed human heart! 120 ppm. This resuscitation therapy caused much
But it was not until almost 50 years later that two controversy at the time and Hyman experienced
doctors reported the first cardiac pacing devices. significant opposition from his peers. Siemens–
In 1928, Mark Lidwell, an anesthetist at the Royal Hulske in Germany and their American subsid-
Prince Alfred Hospital in Sydney supported by iary Adlanco produced a battery-operated version,
physicist Edgar H. Booth of the University of called the Hymanotor (Fig. 1.3). Testing was dis-
Sydney, developed a device that delivered an appointing and his attempts during World War II
alternating current via a needle inserted into the to get the US Navy to use the device for resusci-
patient’s ventricle. At the Crown Street Women’s tating dying servicemen proved unsuccessful.
Hospital in Sydney, Lidwell used intermittent Hyman abandoned his work and never published
electrical stimulation of the heart and saved the his human data. A description of Hyman’s pace-
life of a newborn child suffering cardiac arrest. maker with a photograph of Albert’s brother
He reported his work to the third Congress of the Charles “resuscitating” a young man appeared in
Australian Medical Society in 1929. the 1933 October edition of Popular Science, with
In 1932, an American physiologist, Albert S. a picture of the device in the background.
Hyman reported on his invention for reviving the At Toronto General Hospital, Canada in 1949,
“stopped heart.” Initially his therapy consisted of Wilfred Bigelow (Fig. 1.4) and John Callaghan
intracardiac injections of stimulating drugs such started using hypothermia to reduce metabolism
as epinephrine, but he soon realized that it was the and produce bradycardia and asystole to perform
needle itself that was responsible for restarting the cardiac surgery. Rewarming did not restart car-
heart by setting up an acute current of injury as it diac contraction sufficiently rapidly and so they
punctured the myocardium. His crude device was began experiments with sino-atrial node stimula-
powered by a spring-wound, hand-cranked motor, tion. In the late 1940s and early 1950s, the prin-
and consisted of a timing device and a means for ciple device available to generate electrical
controlling the duration of the pulse of the current impulses capable of stimulating the heart was a
applied. Hyman called his invention the “artificial physiological stimulator by Grass Manufacturing
pacemaker” (Fig. 1.1). The clockwork device, Company for clinical and physiology laboratory
developed in collaboration with his brother, application. It used a thyratron rectifier tube to
Charles, in the Electrophysical department of convert AC into DC suitable for stimulating bio-
New York University, drove a DC generator whose logical tissue. The stimulation rate, voltage out-
electrical impulses were directed into the patient’s put, and pulse width could be varied (Fig. 1.5).

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 1


DOI 10.1007/978-1-4471-2939-4_1, © Springer-Verlag London 2012
2 1 History and Developments

Fig. 1.1 Hyman’s “artificial G


pacemaker” (Illustration with H
permission from Aquilina [1])
B’
C B˜

E
A

D
I

L K

M’

P K
Fig. 1.2 Glass tubes (P)
holding sterile needles (L) and J
stimulating electrical R
S P
connections (Illustration with
L
permission from Aquilina [1])
Early Developments 3

Fig. 1.3 The Hymanotor


(Illustration with permission
from Aquilina [1])

With the help of electrical engineer John Hopps,


they went on to stimulate the sino-atrial node
endovenously during open-heart surgery using a
mains-powered electronic stimulating device
with vacuum tubes. This was perhaps the first
electronic device specifically built as a cardiac
pacemaker. The electrode was a bipolar intrave-
nous catheter, the predecessor of today’s elec-
trodes, stimulating the endocardium. The devices,
however, were large and only as portable as far as
the mains power cable could extend from the wall
socket!
In 1952, Paul Zoll (Fig. 1.6), a Boston cardi-
ologist, developed a tabletop external pacemaker
that could stimulate a patient with cardiac arrest
Fig. 1.4 Wilfred Bigelow (1913–2005) – cardiac sur-
transthoracically but the device produced skin
geon, Toronto General Hospital (Illustration with permis-
sion from Aquilina [1]) burns, pain, and muscular contractions over the
4 1 History and Developments

Fig. 1.5 Grass physiological cardiac


stimulator (Illustration with permission from
Aquilina [1])

whole of the chest. The “Electrodyne pace-


maker-65” comprised an electrocardiograph to
monitor the heart rhythm and an electric pulse
generator to pace the heart (Figs. 1.7 and 1.8). It
delivered electrical pulses with a 2 ms pulse
width and 50–150 V alternating current pulse
amplitude through a pair of 3 cm2 metal elec-
trodes strapped to the patient’s chest directly over
the heart. The mains-powered unit was bulky and
heavy and carried on a cart, and its portability
was also limited. Although this technique dem-
onstrated that pacing could be used to treat com-
plete heart block, it clearly was not practical for
protracted use and being a “fixed-rate” device
could cause “R-on-T” ventricular fibrillation. In
Fig. 1.6 Paul Zoll (1911–1999), seen here on the left was 1956, at St. George’s Hospital, London, Aubrey
a Boston cardiologist practicing at the Beth Israel Hospital Leatham and Geoffrey Davies produced the first
(Illustration with permission from Aquilina [1]) “demand” pacemaker which would also pace
Early Developments 5

Fig. 1.7 Transcutaneous


cardiac stimulator
(Illustration with permission
from Aquilina [1])

Fig. 1.8 Electrodyne


pacemaker-65 (Illustration
with permission from
Aquilina [1])
6 1 History and Developments

Fig. 1.10 Clarence Walton Lillehei (1918–1999) – car-


Fig. 1.9 Earl E. Bakken (1924–present) – founder of diac surgeon, University of Minnesota (Photograph cour-
Medtronic (Photograph courtesy of The Institute of tesy of The Minnesota Historical Society)
Electrical and Electronic Engineers (IEEE))

through the chest wall. A commercial version and would hang around hospital surgical suites
had several modifications, e.g., duration of asys- setting up equipment, training personnel in its
tole allowable, sensitivity controls to sense the use, and troubleshooting and repairing it as nec-
ECG, two output ranges, and a battery-operated essary. Meanwhile they forged working relation-
version. ships with physicians and their staff.
In 1957, Drs. W.L. Weirich, V. Gott, and C.W. Clarence Walton Lillehei (Fig. 1.10) was a
Lillehei (surgical investigators at the University leading cardiac surgeon at the University of
of Minnesota) and Earl Bakken of Medtronic Minnesota, Minneapolis, who by 1957 had per-
designed the first battery-powered external/wear- formed over 300 open-heart operations on young
able pacemaker and demonstrated its efficiency adults and children. This rapidly evolving field of
on 18 patients. This unit was small and made surgery was to be a major driving force toward the
independent of 110 V power by the use of the development of cardiac pacing. Despite successful
transistors. The foundation had thus been laid for repair of the congenital defect, about 10% of
the use of implanted stimulators in the long-term patients developed postoperative complete heart
treatment of atrioventricular block. The story of block due to damage to the conducting system.
the development of this first battery-powered Stimulant drugs such as adrenaline, atropine, or
pacemaker is an interesting one. isoprenaline were only helpful in the short-term
Earl E. Bakken (Fig. 1.9), was an electri- and could not prevent sudden recurrence of heart
cal engineer/TV repairman who cofounded block. It was thought that temporary pacing would
Medtronic Inc. with his brother-in-law Palmer keep the patient alive until recovery of the con-
Hermundslie on 29 April 1949, in a garage in ducting system occurred. The technology devel-
northeast Minneapolis. The company had led a oped by Zoll was clearly inappropriate as the high
precarious existence as a repair service for hos- voltage pacing stimuli delivered transthoracically
pital electrical equipment and regional distribu- would be far too traumatic for young children. The
tor for other manufacturers. They would build physiologist John Johnson proposed the utilization
new equipment to order or customize standard of the Grass stimulator that was used in the
instruments for laboratory or clinical researchers physiology labs to activate hearts. After several
Early Developments 7

Fig. 1.12 Bakken’s modified two-transistor circuit


(Illustration with permission from Aquilina [1])

regained sinus rhythm and survived. Myocardial


wires were then implanted electively, ready for
immediate use later should this become necessary.
A technique for their implantation through a hol-
low needle was also developed for nonsurgical
patients who developed Stokes–Adams attacks.
However, the stimulator was large and heavy, of
Fig. 1.11 Lillehei’s Teflon-coated multistranded,
braided, stainless steel pacing wire (Illustration with per- limited portability and scary for children.
mission from Aquilina [1]) Moreover, the system was totally dependent on its
external mains power supply and on 31 October
1957 a municipal power failure lasting 3 h resulted
experiments, Vincent Gott and William Weirich in the tragic death of a baby. The hospital had
concluded that a cardiac rhythm could be restored emergency power generation in its surgical suites
in animal hearts in which heart block had been sur- and recovery area but not in its patient rooms. The
gically created by means of a wire inserted into the next day, Lillehei asked Bakken whether Medtro-
wall of the right ventricle and connected to the nic could come up with something better.
external stimulator using low voltage pulses. Bakken recalled seeing a circuit for an elec-
Lillehei and his coworkers developed the myocar- tronic, transistorized metronome in the April 1956
dial wire: a multistranded, braided stainless steel back issue of the journal Popular Electronics.
wire in a Teflon sleeve (Fig. 1.11). One end of this The blocking oscillator circuit that was utilized
was implanted directly into the myocardium and had actually been invented at the MIT Radiation
the other end was exteriorized via a stab incision Laboratory during World War II. He simply
and connected to the stimulator. An indifferent modified the two-transistor circuit (Fig. 1.12)
electrode was buried under the skin to complete and placed it into a 4″ square and 1½″ thick alu-
the circuit. Effective pacing needed only 1.5 V as minum box with terminals and switches on the
there was direct contact with the myocardium and outside. The circuit was powered by a miniature
the wire could be pulled out once normal conduc- 9.4 V mercury battery housed within the box.
tion resumed. The first myocardial wire was There was an “on-off” switch and control knobs
implanted on the 30 January 1957 in a 3-year old for stimulus rate and amplitude (Fig. 1.13).
girl with heart block following repair of Fallot’s Bakken demonstrated that the device worked in a
tetralogy. Pacing was successful and the child soon dog in the University’s animal laboratory, but the
8 1 History and Developments

Fig. 1.13 Bakken’s “old


number one” pacemaker and
leads (Photograph courtesy
of The Bakken Museum –
The Collections of The
Bakken Library and
Museum)

Fig. 1.15 A wearable device (1958) (Illustration with


Fig. 1.14 One of the “first ten” had handles attached permission from Aquilina [1])
(Illustration with permission from Aquilina [1])

following day he was surprised to find that was made in 1958). The product literature
Lillehei had used the prototype on a child with claimed that “the pacemaker was designed for
heart block! After only 4 weeks of experimenta- internal applications with at least one wire
tion and work, the first battery-powered, transis- attached directly to the myocardium for tempo-
torized pacemaker was in clinical use. The first rary stimulation or with a bipolar patch for pro-
production run of ten or so units were more longed stimulation and that its self-contained
refined versions of the original prototype and miniature power source will operate the instru-
went into clinical use soon after at the University. ment for approximately 1,000 h” (Fig. 1.16). The
Two metal handles (borrowed from an old ECG chosen pacemaker output was a 2 ms square
machine) were added such that a strap could wave, variable in amplitude from 1 to 20 mA into
secure the pacemaker to the body (Fig. 1.14). a 1,000 W load. The blocking oscillator repetition
The Medtronic Cardiac Pacemaker was not only rate was variable from 60 to 180 ppm. Lillehei
portable but wearable (Fig. 1.15)! This pace- and Bakken published their early experience in
maker became known as the 5800 (because it JAMA in 1960 (Fig. 1.17).
Early Developments 9

Fig. 1.16 Product literature


of the “first ten” (Illustration
with permission from
Aquilina [1])

Fig. 1.17 Lillehei’s paper in


JAMA 1960

Bakken’s pacemaker was regarded as one of ascending infection via the pacing electrodes
the first successful applications of transistor tech- occurred frequently even though it could be mini-
nology to medical devices helping to launch the mized by tunneling the wire for some distance
new field of “medical electronics.” Prior to 1957, before bringing it out through the skin (Fig. 1.18).
there had never been a partly or completely Moreover although most patients with postopera-
implantable electrical device. It was however tive heart block regained sinus rhythm within a
apparent that for long-term pacing a totally few weeks, one patient required the device for
implanted device would have to be designed as 15 months. Recurrent heart block in patients who
10 1 History and Developments

Fig. 1.18 Electrodes had to exit through the skin – source of Fig. 1.19 Portability was limited by length of power
infection (Illustration with permission from Aquilina [1]) cord (Photograph courtesy of The Bakken Museum – The
Collections of The Bakken Library and Museum and The
Heart Rhythm Foundation. This picture first appeared in
Furman and Escher [2])

had recovered from their postoperative heart resumed the idioventricular bradycardia. Two
block caused several deaths. Clearly, these years later, Furman and colleagues, working
patients needed indefinite and not temporary pac- in Montefiore Medical Center in the Bronx,
ing in order to survive. In addition, the myocar- New York City, reported that they had suc-
dial wires developed exit block as scar tissue cessfully achieved endocardial unipolar ven-
grew around the site of stimulation increasing tricular pacing in ambulatory out-patients.
electrical resistance and requiring a progressive Again a Cournand catheter was used with its
increase in pacing stimulus voltage to maintain tip sited in the outflow tract of the right ven-
capture. The thoracic muscles began to twitch at tricle. A transvenous lead was inserted into
these increased voltages. A totally implantable the right ventricle via a cephalic vein cutdown
system with better designed electrodes was and the lead exteriorized through the skin and
needed. held in place with stainless steel sutures which
Meanwhile elsewhere, on the 16 July 1958, required frequent renewal. Superficial infec-
a transvenous, unipolar Cournand catheter tion was frequent. The pacing device was the
in which the electrode was at the tip of the newly available battery operated model 902M
catheter was introduced fluoroscopically by from Atronic Products, PA, USA (Fig. 1.20).
Seymour Furman, via the basilic vein into The unit was capable of sensing spontane-
the right ventricular outflow tract, in a patient ous cardiac activity and of variation in output
with fixed complete heart block who required and stimulation rate. A small meter indicated
colon resection because of a malignancy. Using emission of stimuli or sensed events. Portal
a mains-powered stimulator, pacing was con- (working with Davies and Leatham in London)
tinued for 2 h, during the operative procedure, claimed to have been using similar right ven-
and ended with slowing of the stimulation rate tricular endocardial stimulation in patients with
until an unpaced idioventricular rhythm devel- Stokes–Adams attacks from early 1960. They
oped. A 50-ft extension power cord allowed used a similar Cournand electrode catheter with
mobilization with the device being pushed on a small platinum tip and reported that right ven-
a mobile cart (Fig. 1.19). The catheter was tricular apical pacing provided the most stable
removed without complication and the patient pacing position.
Implantable Devices 11

Fig. 1.20 (Left) Atronic products Model 902M. (Right) At 67 years he had 2:1 and third degree AV block and
Mr. HN and his wife seen posing for the New York Daily syncope. The transvenous electrode was inserted via a
News outside of Montefiore Hospital in the Bronx, New cephalic vein cut-down and fastened to the skin with
York, on 23 June 1959, holding his external pacemaker. stainless steel sutures

Fig. 1.22 Rune Elmqvist (1906–1996) – engineer


Fig. 1.21 Ake Senning (1915–2000) – cardiac surgeon, (Illustration with permission from Aquilina [1])
Karolinska Hospital, Stockholm (Illustration with permis-
sion from Aquilina [1])

Implantable Devices (Fig. 1.23) at the Karolinska Institute in Solna,


near Stockholm, Sweden. Larsson was in desper-
On 8 October 1958, a major milestone in pacing ate trouble with complete heart block causing
was reached when the first pacemaker implanta- Stokes–Adams attacks 20–30 times per day
tion was performed in Sweden. The system had requiring resuscitation and his wife hounded
been developed by the surgeon Ake Senning Senning to try their invention. This first experi-
(Fig. 1.21) and the physician/engineer inventor ence with a fully implantable pacemaker system,
Rune Elmqvist (Fig. 1.22) and implanted into a the Elema 135 (Elema-Schonander), was reported
43-year old engineer called Arne Larsson at the Second International Conference on
12 1 History and Developments

Fig. 1.23 Arne Larsson (1915–2001) – first human to


receive an implanted pacemaker on 8 October 1958 Fig. 1.24 Elmqvist’s and Senning’s abstract 1960
(Illustration with permission from Aquilina [1])

Medical electronics in 1959 and published as an 60 mAh each were sealed, encapsulated, and con-
abstract in 1960 (Fig. 1.24). To avoid publicity, nected in series. Recharging was accomplished
the implantation was done in the evening when inductively. A coil antenna with a diameter of
the operating rooms were empty. Via a left-sided about 50 mm was connected to the cells via a sili-
thoracotomy two electrodes were implanted into con diode. This was inductively coupled across
the myocardium and tunneled to the pacemaker the patient’s skin to a large external flexible coil
box placed in the abdominal wall. The first pace- 25 cm in diameter attached to the patient’s abdo-
maker implanted functioned for only 8 h but the men with adhesive tape. Recharging was accom-
second one implanted in the same patient lasted plished by a 150 kHz radio-frequency current
1 week before failing possibly as a result of lead generated by an external mains-powered vacuum
fracture. The pulse generator delivered impulses tube device connected to the external coil. The
at an amplitude of 2 V and a pulse width of pacemaker required charging once a week for
1.5 ms. The pulse rate was fixed at a constant rate 12 h. The entire unit was handmade and consisted
of 70–80 bpm. The energy utilized was mini- of the nickel-cadmium batteries, the electronic
mized since Elmqvist managed to obtain a few of circuit, and the coil recharging antenna. These
the first silicon transistors imported into Sweden were encapsulated in a new epoxy resin (Araldite)
which were more efficient than the older germa- produced by Ciba-Geigy, which had excellent
nium transistors. With them Elmqvist designed a biocompatibility (Fig. 1.26). The approximate
stable and efficient blocking oscillator with a diameter and thickness became 55 mm and
small power consumption (Fig. 1.25). Several 16 mm, respectively, according to the dimensions
types of primary battery cells could have been of the Kiwi shoe polish can (Fig. 1.27). Elmquist
used in the pacemaker, but because of the poten- produced two such units using these cans as
tial for build-up of hydrogen gas at the zinc anode molds (Figs. 1.28 and 1.29). These first units had
in the zinc-mercury cells, nickel-cadmium two electrode wires, each consisting of a twinned,
rechargeable cells were chosen. Two cells of stainless steel suture wire with polyethylene
Implantable Devices 13

Fig. 1.25 Elmqvist’s circuit


(Illustration with permission
from Aquilina [1]) OA200
E4-1856 OA 200

200 K 1K
8 µF

DE 0.1 200 turns



OC OC
460 460
400 K

8µ F

300K

Fig. 1.27 The Kiwi shoe polish can was an early mold

Fig. 1.26 Pacemaker electronics were encased in Araldite


(Illustration with permission from Aquilina [1])

insulation. The distal ends of the wires were sewn


into the myocardium to act as pacing electrodes.
The proximal ends were hard-wired to the pulse
generator circuit. It was estimated that the elec-
trode had to withstand about 105 bends per day.
Elema pacemakers were implanted in Uruguay
and England in February and March 1960.
Elmqvist constructed the Elema 137 pacemaker
in 1960 using Ruben-Mallory zinc-mercury oxide Fig. 1.28 Internal electronics of pacemaker (Illustration
cells as the power source thus eliminating the with permission from Aquilina [1])
14 1 History and Developments

Fig. 1.29 Early versions


of Elmqvist’s Elema–
Schonander devices

Fig. 1.30 Elema-Schonander model 142

need for periodic recharging of the previous


nickel-cadmium cells. Arne Larsson himself
required five lead systems and 22 pulse genera-
tors of 11 different models until his death on 28
December 2001 aged 86 of a malignancy totally
unrelated to his conduction tissue disease or his
pacemaker system – surviving both the engineer Fig. 1.31 Wilson Greatbach (1919–2011) – electrical
and surgeon who saved his life. One of these engineer (Illustration with permission from Aquilina [1])
models is shown in Fig. 1.30.
The first person responsible for the introduc-
tion of an implantable pacemaker which did not a heart pacemaker required. As luck would have
require recharging was an electrical engineer it, the chief of surgery at Buffalo’s Veteran’s
teaching at the University of Buffalo where he Hospital was Dr. William Chardack who believed
was working on an oscillator to aid in the record- in the viability of an implantable pacemaker. On
ing of tachycardias. His name was Wilson 7 May 1958, Greatbatch brought what would
Greatbach (Fig. 1.31). He discovered the way to become the world’s first implantable pacemaker
make an implantable pacemaker by accidentally to the animal lab at the hospital. There, Chardack
inserting a 1 MΩ rather than a 10 kΩ resistor into and another surgeon, Dr. Andrew Gage, attached
the oscillator circuit. To his amazement the device the two pacing wires to the exposed heart of a
emitted intermittent pulses of energy – just what dog. The heart proceeded to beat in synchrony
Implantable Devices 15

Fig. 1.33 The “Bow Tie team” – Greatbach, Chardack,


and Gage (Illustration with permission from Aquilina [1])

Fig. 1.32 Greatbach’s implantable pacemaker and lead


(Top: Illustration with permission from Aquilina [1]; bot-
tom: Photograph courtesy of The Bakken Museum – The
Collections of The Bakken Library and Museum)

with the device. They were all amazed by what


they saw. Over the first 2 years, experiments were
made with animals, but in 1959, Greatbatch pat-
ented the “implantable pacemaker” (Fig. 1.32),
and William Chardack reported the first success Fig. 1.34 Patient having received Greatbach’s pace-
maker (Illustration with permission from Aquilina [1])
in a human with this unit on 15 April 1960 in a
77-year old man in complete heart block, Mr.
Henry Hennafield, at Millard Fillmore Hospital problem. This success did not go unnoticed by
in Buffalo, New York. Chardack first implanted Medtronic. On a rainy October evening in 1960,
the lead (a bipolar, Hunter-Roth myocardial lead) Hermundslie flew his own plane to Buffalo, met
and when the threshold stabilized, implanted the Chardack and Greatbach in the airport, and
pulse generator (Figs. 1.33 and 1.34). The batter- signed a contract for Medtronic to produce the
ies were powered by 10 “long-life” mercury cells, Chardack–Greatbach implantable pulse genera-
eliminating the need for frequent recharging and tor. Earl Bakken started producing the Chardack–
increasing life expectancy of the device to Greatbach pacemaker in November, and by the
1–2 years. Chardack also introduced the “early end of December 1960, Medtronic had received
warning” concept for identifying battery exhaus- orders for 50 of the $375 units. Chardack, Gage,
tion by a gradual increase in pacing rate. and Greatbatch reported a series of 15 patients
Chardack’s patient survived uneventfully for who had pacemakers implanted. Medtronic
2 years before his death from natural causes and developed ever-improving devices and pacing
the pacemaker worked for 18 months without a electrodes over the next decade. Figure 1.35
16 1 History and Developments

Fig. 1.35 Early Medtronic


bipolar electrodes (circa
1959–1962) and implantable
Pacemaker (circa 1962–
1964) in their cardboard
packaging (Photograph
courtesy of The Bakken
Museum – The Collections
of The Bakken Library and
Museum)

shows a boxed electrode set and a Model 5870 their first pacemaker in 1962 and Telectronics
pacemaker (produced 1962–1964) from the Inc. in Australia produced their first devices in
Bakken Artifact Collection. After a time with their new manufacturing facility in 1965.
Medtronic, Greatbatch founded his own com- Pacesetter Systems Inc. was founded in 1965 and
pany in 1970 (Wilson Greatbach Ltd.) and went through Dr. Robert Fischell – a physicist/inventor
on to invent the long-life corrosion-free lithium- at the Johns Hopkins University Applied Physics
iodine battery to power the device. Inventing was Laboratory – was to produce the first rechargeable
Greatbatch’s lifelong passion and he held many device in the USA which could also be
patents. He died in September 2011, aged reprogrammed by using radiowaves. Figures
92 years. Other models of pacemakers were 1.36–1.38 show a fixed-rate (VOO) device from
implanted with similar success in 1960 by Zoll Vitatron, and the battery cells, circuitry, and tran-
and colleagues, by Lillehei and colleagues in sistors are clearly visible through the transparent
1961, and in 1962 by Kantrowitz and his associ- resin. Like its competitors, the devices were large
ates. Shortly after this, other pacemaker manu- and had to be placed behind the rectus sheath in
facturers appeared. Vitatron, in Holland produced the abdomen. A Medtronic employee, Manuel
Implantable Devices 17

Bakken Museum (www.thebakken.org) presents


an amazing collection of early pacing devices
and electrodes from many of the prominent man-
ufacturers of the time.
Other investigators pursued a different line of
approach in designing self-contained implantable
pacemakers: inductive coupling. A pair of elec-
trodes were sutured to the epicardium and con-
nected to a coil antenna located subcutaneously.
Fig. 1.36 Vitatron fixed-rate (VOO) device Minimal or no circuitry was implanted and no
internal batteries were needed – getting around
the problem of unreliable pacemaker circuits and
short battery life. The coil antenna was inductively
coupled to an external coil taped to the patient’s
intact skin. This external coil was connected in
turn to a transistorized pulse generator powered
by an external battery. The electronic compo-
nents, relatively unreliable at this time, were
therefore located entirely outside the body
(Fig. 1.39). Other versions of this system included
triple-helix, silicone-insulated endocardial leads,
Fig. 1.37 Vitatron device – batteries and circuitry are and rate-control via an external knob (which the
visible through transparent casing patient himself could modify at will). Inductively-
coupled pacemakers proved to be very successful
with several hundreds being implanted and sur-
vival rates being over 10 years. These devices
were extensively used in Birmingham, UK, for a
number of years, being produced by the Lucas
factory, more commonly known for its electrical
products intended for use in cars (Fig. 1.40). One
particular disadvantage of this device was that its
removal (e.g., for bathing) could result in brady-
cardia and syncope. They continued to be used
until well into the 1970s and several patients with
Fig. 1.38 Vitatron device – lead connection point and later generation pacemakers retained the im-
device width planted coils from their original devices.
Despite these fantastic developments, faulty
batteries, body fluids leaking into the encasement
Villafana was convinced that lithium batteries through the epoxy resin, and broken leads caused
were safe to be used in pacemakers although numerous pacemaker failures that required
Medtronic were resistant to the idea because of emergency surgery. These technical problems
the potentially explosive nature of lithium. contributed to the delay in the widespread use of
Villafana left Medtronic and formed his own implanted pacemakers for several years but over
company Cardiac Pacemakers Inc. (CPI) which the next decade as pacemaker circuitry and power
became a world leader in pacing technology in its sources became more reliable and as lead design
own right. The Bakken Artifact Collection in the improved, reliability and longevity of the systems
18 1 History and Developments

Fig. 1.39 Inductively-coupled pacing. The system consists Fig. 1.40 This Abrams–Lucas inductive-coupled unit
of (a) an external pulse generator; (b) an external trans- was invented by Leon Abrams in Birmingham and made
mitting coil; (c) an internal receiving coil; and (d) myocar- by Lucas Industries. Epicardial electrodes were connected
dial electrodes. Both the transmitting and receiving coils to a coil sutured under the skin of the chest wall while
contain an iron-core strip, with which effective electromag- another coil was secured by adhesive tape onto the skin
netic coupling between the coils is achieved, thus inducing over the implanted coil. The surface coil is then connected
stimulating pulses in the receiving coil without high fre- by wires to a battery-operated pacing unit kept in a coat
quency carrier waves. These devices were implanted in the pocket and the pacing delivered with electromagnetic
University Hospital of Tokyo between 1964 and 1968 induction. The patient could easily renew the battery and
(Illustration with permission from Aquilina [1]) adjust the rate

Fig. 1.41 Hunter-Roth


electrodes (Illustration with
permission from Aquilina [1])

improved and the totally implantable system surface area including a silicone rubber base
would prove the winner and inductively-coupled plate, bearing two spike electrodes which could
systems would be abandoned forever. be pushed into the myocardium, where it was
One of the main difficulties, however, was the then sutured in place (Fig. 1.41). On the 4 April
electrode. It was soon obvious that the wire sutured 1959, they implanted such an electrode to pace a
directly to the heart was unsuitable as a long-term patient suffering from post-myocardial infarction
electrode. Stimulation threshold increased after a complete heart block. This type of electrode
few weeks until exit block developed and no improved the reliability of the pacemaker as a
more capture was possible. Moreover, the wire result of a lower chronic pacing threshold and
could not resist the enormous repetitive mechani- proved the concept of long-term cardiac pacing.
cal stresses of bending. Samuel Hunter (Professor Another lead was developed in 1959 by Elema
of surgery at St. Paul) and Norman Roth (Chief Schonander and the Telecom Company, Ericsson.
engineer at Medtronic) designed a bipolar stain- This consisted of four thin bands of stainless steel
less-steel epicardial electrode with a small defined wound around a core of polyester braid and
Implantable Devices 19

Fig. 1.42 Elema-Ericcson lead (Illustration with permis-


sion from Aquilina [1]) Fig. 1.43 Improved epicardial attachments of electrodes

insulated with soft polyethylene (Fig. 1.42). It using such an intravenously-placed electrode
was estimated to resist over 184 million flex whose tip was placed into the right ventricular
cycles, hence lasting for at least 6 years. The uni- apex. This development resulted in a broadening of
polar epicardial stimulation electrode was a plati- the indications for pacing, particularly because the
num disc, 8 mm in diameter and insulated at the lower thresholds achieved by these newer endocar-
back. Chardack also introduced spring-coil elec- dial leads also resulted in extended pacemaker life.
trodes and improvements in coil manufacturing By May 1963, the successful clinical use of a
processes which caused lead fractures to dimin- wholly implantable bipolar endocardial pacemaker
ish dramatically. Estimates were made that the system had been described by Parsonnet, Zucker
number of lead flexions without lead failure rose and colleagues and Medtronic introduced their
from 100,000 to 10,000,000 following this devel- system for clinical use in December 1963.
opment in “electrode” design. The electrodes Thus, the first decade of pacing demonstrated
would be encased within silicone rubber insula- the clinical value and feasibility of implantable
tion (Fig. 1.43). pacemakers in the revolutionary treatment of
The technique for inserting permanent trans- complete heart block and syncope induced by
venous bipolar pacing electrodes was developed in bradycardia, but there was much more work that
1962 by Victor Parsonnet and colleagues (in the was needed to be done. Cardiologists demanded
USA) and by Lagergren and coworkers (in Sweden) improvements in reliability in order to avoid
using fluoroscopic guidance and paved the way for reoperation due to exit block caused by lead frac-
the replacement of epicardial leads by transvenous ture or insufficient output energy of the generator.
leads – avoiding thoracotomy and general anesthe- Amplitude and rate programmability as well as
sia. The electrode was initially connected to an the hermetic seal of the electronics were pro-
external generator, but a few weeks later it was posed – the latter in order to avoid body fluids
then connected to a subcutaneously implanted causing short circuits and increased energy loss.
generator. Furman demonstrated that cardiac pac- Moreover, because it was soon recognized that
ing could be maintained for a prolonged period patients paced at a fixed rate exhibited diminished
20 1 History and Developments

exercise tolerance, thoughts were also turned to the rectus sheath and without fear of inevitable
developing a device that might allow the pace- generator erosion through the skin. It would also
maker’s stimulation rate to be varied according to improve the cosmetic result. For a time, the
the demands being placed on the heart by physi- devices remained large (Figs. 1.44–1.47) and
cal activity – but it would be sometime before would still be placed behind the rectus sheath
these particular dreams would be realized. requiring a general anesthetic for implantation.
In the early 1960s, the mortality of pacemaker Cordis produced the Stanicor (142 g) and the
insertion was significant (7.5%) and although this Omni Stanicor (145 g) pacemakers encased in
would soon improve, the limitations of fixed-rate epoxy resin and in 1975 the programmable
devices – the significant incidence of ventricular Stanicor g (94 g). CPI’s Microlith-A appeared
fibrillation and complaints of palpitations due to with an elliptical shape and had its circuitry/bat-
competitive pacing – remained a problem. tery coated in Parylene to protect it against mois-
ture before encasing it hermetically in the
stainless steel can. It weighed 76 g and had a
Demand Pacing

Further understanding of cardiac signals and


developments in electronics made it possible to
detect spontaneous cardiac depolarization. This
gave rise to the concept of demand pacing, where
the pacemaker would only stimulate the heart if
the intrinsic heart rate fell below a set level. This
would prevent competitive pacing on the heart’s
own QRS complexes and the risk of life-threatening
ventricular arrhythmias. At the same time a differ-
ent device emerged, using an algorithm whereby a
ventricular pacemaker was triggered by a sponta-
neous R wave, so that the stimulus fell in the abso-
lute refractory period of the ventricle (VVT mode).
However, if the R-R interval was less than a preset
limit (300 ms), the device functioned at a fixed
rate. The major application was for patients who
experienced pacemaker inhibition due to external Fig. 1.44 Telectronics 120 VVI pacemaker
stimuli such as electromagnetic interference and
repetitive mechanical or myopotential inhibition.
In May 1966, Parsonnet and colleagues were the
first to report on the clinical use of an implantable
demand generator.
The reliability of electronic circuitry was
greatly improved by packing all the components
into a hermetically sealed “can” in order to
exclude body fluids, and the use of “hybrid” tech-
nology instead of discrete components allowed a
significant reduction in size of the pacemaker.
The latter change would make the transvenous
implantation technique most attractive – allowing
the device to be placed superficially in the pecto-
ral area rather than deep in the abdomen behind Fig. 1.45 Medtronic 5945 VVI pacemaker
Demand Pacing 21

Fig. 1.46 Vitatron’s Vitalith™ VVI pacemaker

volume of 36 cc – a size more suited to prepec-


toral placement. Devices, a British company, pro- Fig. 1.47 Devices UK pacemaker
duced a pacemaker but the company proved
unable to compete with the larger US manufac-
turers whose R&D departments received heavy the conductor material. The electrode tips were
investment in the rewards that were to come. made of platinum-iridium alloy.
Other developments, such as defibrillation- Longevity of cardiac pacemakers was increa-
protection diodes would protect the detection sed from 18 to 28 months with the mercury
amplifier of demand pacemakers against strong oxide-zinc batteries to 3–6 years with the intro-
electric fields which occurred during procedures duction of lithium iodine batteries. Moreover, the
such as transthoracic defibrillation or during elec- sudden loss of output and failure to pace as the
trocautery. Patient safety was improved by mercury/zinc cells became depleted became his-
designing automatic rate-limiting circuitry for tory following the introduction of lithium batter-
single-component failure – avoiding life- ies with their more predictable and gradual power
threatening excessively high pacing rates. Most loss over time. These batteries also featured high
of these developments occurred as a result of energy densities and allowed further reduction in
close collaboration between the pacing industry pacemaker size without shortening the genera-
and the implanting cardiologists. When a prob- tor’s life. Although lithium-powered pacemakers
lem arose, the engineers incorporated a change were introduced in 1973, mercury/zinc-powered
within the device or its circuitry to fix it. devices continued to be used up until 1977 in many
Lead design also improved: “tined” and pacing centers because of the significant addi-
“flanged” tips for passive fixation (Fig. 1.48) and tional cost of the lithium pacemakers (usually 1.5
“screw-in” for active fixation (Fig. 1.49) result- times the cost). Similarly, fixed-rate devices were
ing in a fall in the displacement/malfunction rate. significantly cheaper than demand pacemakers.
The conductor material was made of corrosion- Programmability would lead to further increase
resistant nickel alloy and space-wound in a heli- in the cost of devices over nonprogrammable
cal configuration to minimize the possibility of pacemakers and initially many centers chose
wire fracture during flexion. Tips were made which device to use based on clinical criteria and
short and blunt to reduce perforation and trans- budgetary restrictions. In 1972, Medtronic/Alcatel
parent silicone rubber was used for insulation for in Paris made a radioisotope-powered pacemaker
22 1 History and Developments

Fig. 1.48 Various designs of


lead tips for passive fixation

Fig. 1.50 Medtronic/Alcatel nuclear-powered pacemaker

Fig. 1.49 Helifix electrode tip for active fixation


patients to a lifetime of old pacing technology.
In 1974, the Inter-Society Commission for Heart
which was implanted by Parsonnet and cowork- Disease Resources (ICHD) recommended a
ers (Fig. 1.50). These nuclear pacemakers had an 3-letter coding terminology to indicate the cham-
expected life of >20 years but went out of fashion ber paced, sensed, and the mode of response of
before gaining a foothold in the market mainly the pacemaker to sensing of the P wave or QRS
due to the need for extensive regulatory paper- complex. In 1987 this was developed further
work and concerns over the long-term adverse into the 5-letter NASPE/BPEG (North American
effects of radiation on the body. Perhaps of more Society of Pacing and Electrophysiology/British
concern was that such devices would confine Pacing and Electrophysiology Group) generic
Demand Pacing 23

code, which addresses the important functions pacing. The problems of pacemaker syndrome
of rate adaptive pacing and programmability, and due to loss of AV synchrony with VVI pacing
which remains in current use today. and atrial contraction against closed AV valves,
Titanium casing was developed by the resulting in venous regurgitation, atrial disten-
Telectronics pacing company in 1969 to enclose sion, impaired diastolic filling, hypotension, AV
the battery and circuitry. Cardiac Pacemakers valve incompetence, and atrial fibrillation, and
Inc. used stainless steel and Pacesetter Systems a symptoms of neck pulsation, dizziness, fatigue,
nickel alloy before moving to titanium. This light presyncope, and syncope, needed to be addressed
but very strong material replaced the epoxy resin by restoring AV synchrony. By the end of the
and silicone rubber that was previously utilized 1970s, dual-chamber pacemakers were introduced
to encase the internal components of the pace- to pace and sense in both atria and ventricles,
maker. Other innovations by Telectronics included
the introduction of integrated circuits, narrowing
the stimulating impulse to 0.5 ms, and using
microplasmic welding to join the two halves of
the pacemaker capsule and the Model 120 was
“the state of the art” in pacing in 1974 (see
Fig. 1.44). A slimline version, Model 160, fol-
lowed in 1976. Pacemakers were also made non-
invasively programmable in the mid-1970s using
hand-held and tabletop programmers (Figs. 1.51
and 1.52). Using a radio-frequency telemetry
link, a variety of pacing parameters could be
adjusted to follow the changing clinical needs of
the patient.
As the indications for pacing increased to
include sick sinus syndrome, problems of ventric-
ular sensing in the VVI mode resulting in pace-
maker inhibition required solving. Effects such as
capacitance feedback, P or T wave oversensing,
and external interference were shown to inhibit Fig. 1.51 Siemens handheld pacemaker programmer

Fig. 1.52 (Left) Spectrax™ – S Model 9700 hand- more functions than the handheld programmer and a built-
held pacemaker programmer (Medtronic). (Right) in printer for producing a permanent record for the
Spectrax™ – SX Model 9701 tabletop programmer with casenotes
24 1 History and Developments

but these remained sizeable devices (Fig. 1.53).


Synchronized timing made it possible to preserve
the atrial contribution to ventricular filling as well
as to track the intrinsic atrial rate.
During this period, the rate of pacemaker
implantation grew remarkably. In the USA in
1969, pacemakers were being implanted at the
rate of 71 per million. By 1978, the rate had
increased to 309 per million and in 1981 to 513
per million, and the rate of pacemaker generator
replacements decreased. The rate of implantation
would continue to increase.
It also became possible to transmit pacemaker
data and ECG from the patient’s home to the
ECG department within the pacing center using a
telephone receiver handset and a teletransmitter
in the patient’s home and a telereceiver in the
pacing center (Fig. 1.54).
Fig. 1.53 Medtronic 7000 dual-chamber pacemaker

Fig. 1.54 (Left) The Model 9410 TeleTrace® Receiver equipped with bracelet wrist electrodes and the 9408 used
(Medtronic®) is a telephone monitoring receiver for use finger-tip electrodes or could be used against the bare
with single and dual-chamber pacing systems and com- chest using electrodes on the back of the device. Parameters
patible with the TeleTrace® Transmitters – Models 9407 such as atrial/ventricular pulse width, pacemaker rate, and
(Upper right) and 9408 (Lower right). The 9407 was AV interval and ECG could be detected and transmitted
Flexibility, Programmability, and Physiological Pacing 25

Fig. 1.56 CMOS − 1 Intermedics Inc. programmable


pacemaker

Fig. 1.55 (Right) External ventricular demand pace-


maker (Model 5375) and (left) external AV sequential
demand pacemaker (Model 5330) from Medtronic® had
numerous features including output, rate, and sensitivity
settings, indicator lights showing pace and sense func-
tions, a battery test feature, and a safety-lock On-Off
switch to prevent inadvertent turn-off

In the area of temporary pacing, Medtronic


produced compact but versatile, battery-powered,
external demand ventricular and AV sequential Fig. 1.57 Medtronic MINIX™ SSI pacemaker showing
pacemakers for use in a wide variety of clinical the reduction in size of pacemakers as a result of advanc-
situations such as pre-, intra-, and postoperative ing technology
management of cardiac surgical patients, short-
term treatment of arrhythmias and heart block
and emergency cardiac pacing. Wide rate ranges, sively smaller (Fig. 1.57). In 1978, Intermedics
adjustable output control, and calibrated sensitiv- had the Quantum VVI pacemaker in a titanium
ity dial contributed to the versatility of the device can weighing only 42 g, and in 1980, Cordis
(Fig. 1.55). introduced Omni Stanicor g (VVI), also at 42 g
– a similar dramatic reduction in size – suitable
for a pre-pectoral pocket.
Flexibility, Programmability, Telemetry (the use of wireless communica-
and Physiological Pacing tion between devices) made the multi-program-
mable pacemaker possible, thereby offering the
With the development of CMOS (Complemen- increased flexibility needed to adapt the pace-
tary Metal-Oxide-Semiconductor) technology maker to the patient’s condition whenever
and the low-power digital integrated circuit on required. In 1977, ventricular demand pace-
microprocessors, it became possible to provide makers were introduced with limited program-
pacemakers with more functions without mability and in 1978 dual-chamber devices
significantly compromising size or service-life were implanted for the first time (Fig. 1.58).
(Fig. 1.56). Indeed, the devices became progres- Siemens-Elema produced the Vario 659 which
26 1 History and Developments

Fig. 1.59 Siemens-Elema 659 pacemaker

Fig. 1.58 Telectronics Autima® dual-chamber pacemaker

Threshold at
Start Vario test 6 Vario stens

The Vario test reveals that 6 pulses are not accompanied by


any depolarization. This indicates a sufficient threshold mar-
gin as the pacer stimulates whit 5 V and the acute voltage threshold
obviously is only 6 x 0.3 or 1.8 V. Paper speed 25 mm/s.

Fig. 1.60 Vario® (noninvasive) measurement of threshold

enabled noninvasive voltage threshold determi- also be dealt with by reprogramming. Such
nation by application of a magnet (Figs. 1.59 maneuvers avoided the need to change the pace-
and 1.60). maker in the event of these not uncommon prob-
Figure 1.61 shows the progressive reduction lems, and were both cost-saving and a more
in size of pacemakers over two decades. acceptable alternative for the patient. The pro-
Programmability had major benefits to offer gramming of hysteresis, to allow patients with
patients and cardiologists. Reprogramming the intermittent heart block or sinus bradycardia to
pacemaker’s basic rate made it possible to maintain sinus rhythm and only pace at a higher,
increase a patient’s effort tolerance if necessary, determined base rate if the native rate fell below
competitive pacing could be suppressed by repro- a set rate, became a useful programmable tool.
gramming the sensitivity setting and exit block Specific programmers were available from indi-
eliminated by increasing stimulation energy by vidual manufacturers, and these too would
either increasing the amplitude or pulse width. become more sophisticated as the technology
Undersensing and oversensing problems could developed (Figs. 1.62–1.65).
Flexibility, Programmability, and Physiological Pacing 27

Maintaining atrioventricular (AV) synchrony for electrode introduction simpler for operators
with or without variable-rate pacing based on and the use of the cephalic vein “cut-down” pro-
sino-atrial node information required a stable cedure (which was difficult if two high-profile
atrial electrode. Progress in lead technology gave electrodes were necessary) became much less
rise to multifilar and coaxial coils plus new common. These improvements resulted in an
insulating materials which made it possible to expansion of pacing modes, including atrial
produce thin, flexible leads – less prone to lead or demand pacing (AAI), ventricular pacing with
insulation breaks. The introduction of tines and atrial and ventricular sensing (VDD), and
the “screw-in” electrodes reduced lead displace- atrioventricular sequential pacing (DVI, DDI,
ment and the need for reintervention for lead DDD). In August 1982, the first QT-driven rate-
repositioning. The arrival of plastic introducer responsive pacemaker (invented by Dr. Anthony
kits (Fig. 1.66) made the subclavian vein approach Rickards) was implanted, based on the fact that

Fig. 1.61 Progressive reduction in size of pacemakers


Fig. 1.62 Vitatron handheld programmer

Fig. 1.63 The 2035 portable


programmer from CPI®
28 1 History and Developments

Fig. 1.64 Pacesetter® Systems Inc. desk-top/semi-


portable programmer

Fig. 1.66 Peel-away plastic introducer kits

Fig. 1.65 Cordis handheld “sophisticated” programmer

the QT-interval changed with both exercise and


emotion due to the influence of circulating cate- Fig. 1.67 Vitatron’s Quintech® TX rate-responsive
cholamines. This investigational device, the pacemaker
TX 1, was a multiprogrammable VVI pacemaker
which was able to sense and measure the duration
of the evoked endocardial T-wave via a conven- model with its special parameters (upper and
tional pacing electrode. The pacemaker was lower rate limit, slope, detection window, and
therefore able to continuously monitor variations T-wave sensitivity) was fully programmable.
in stimulus-T interval and adapt the pacing rate Other rate-responsive devices such as the RS4
accordingly. The Rhythmx and Quintech® TX (CPI) and Activitrax™ pacemakers (Medtronic)
911, 915, and 919 models (Vitatron) (Figs. 1.67 were subsequently designed, developed, and
and 1.68) were introduced into an extensive clini- released for clinical use in 1982–1985 (Fig. 1.69).
cal program in the early 1980s and in the mid-late The RS4-SRT pacing system used a single tripo-
1980s became commercially available. The TX lar (orthogonal) lead for bipolar sensing of the
Flexibility, Programmability, and Physiological Pacing 29

Fig. 1.69 Medtronic’s Activitrax™, activity-sensing


rate-responsive pacemaker

treating and preventing tachycardia respectively.


Fig. 1.68 Quintech® TX 911 rate-adaptive, multipro-
These devices were rarely 100% successful with-
grammable device
out additional drug therapy and although they
gained brief popularity among electrophysiolo-
gists, radiofrequency ablation would see the
“floating” atrial electrogram and ventricular pac- demise of this technology for the treatment of
ing (Fig. 1.70). The RS4 pacemaker algorithm patients with re-entrant SVT.
was designed to vary the ventricular rate to a Other changes took place rapidly during this
maximum of 110 bpm according to the average period of pacemaker/electrode development. The
sensed P-wave rate. In the Activitrax™ system, a development of the “In-line” connector concept
piezoelectric crystal within the pacemaker can reduced the size of the pacemaker connector/
detected body movement and used this as a sur- header and made systems sleeker and thinner.
rogate measure of activity. Signals from the sen- New electrode tip materials and configurations
sor were filtered and applied to an algorithm to such as the ring, porous, and carbon tips resulted
alter the pacing rate up or down. Thus, pacing in reduced atrial and ventricular thresholds and
rate would change according to the patient’s improved sensing and new conductor materials
activity level (VVIR, AAIR, and DDDR).The such as platinum/iridium and better insulating
RS4-SRT device provided an unreliable rate- materials, e.g., improved polyurethane and high-
response because of the variable atrial sensing performance silicone rubber all resulted in better
ability of the lead, but the activity-sensing device pacing performance. Consequently, the early rise
would mature into a capable and sophisticated of capture threshold was blunted and safety was
rate-responsive pacing system (Fig. 1.71) which enhanced. As a result, bipolar leads were pro-
would last. duced which were of the same size as previous
Anti-tachycardia pacemakers, e.g., PASAR- unipolar leads and this led to increased usage and
Model 4151 (Programmable Automatic Scanning a reduction in muscle/interference inhibition of
Arrhythmia Reversion), arrived in 1981 from the pacing stimulus. In the early 1980s, steroid-
Telectronics for terminating supraventricular eluting leads were also developed. These slowly
tachycardia (SVT) (Fig. 1.72). Such a fully released steroid from their tip and hence decreased
implantable automatic scanning pacemaker rec- the inflammatory response evoked by the pres-
ognized tachycardia and delivered one or more ence of the lead tip, abolishing the early thresh-
extrastimuli which automatically scanned inward old rise and providing generally lower chronic
if tachycardia continued. Other devices such as pacing thresholds. Lead and connector problems
the Orthocor II Model 284A and the Gemini II became uncommon. The “slippery” polyurethane
Model 415R from Cordis were introduced for coating made it easier to deliver two leads via the
30 1 History and Developments

c Case 1

120
Paced ventricular rate (bpm)

110
100

90
80

70

60

10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 01 02 03 04 05 06 07 08 09
Twenty four hour clock

Fig. 1.70 CPI’s RS4-SRT rate-responsive pacemaker. and frequency. (b) SRT (segmented ring tripolar) lead.
(a) PA and lateral chest X-rays show the lead and device White arrow shows the atrial sensing electrodes. (c) A
in situ. The white arrow shows the bipolar pair of orthogo- 24 h ECG tape recording was used to show the frequency
nally oriented, nonendocardial contacting atrial sensors of rate-response during daily activities
designed to optimize intra-atrial electrogram amplitude
Flexibility, Programmability, and Physiological Pacing 31

same vein without one moving the other during and Command P5® (57 g) devices. The latter had
positioning. a slimline shape, programmable rate and pulse
Bi-directional telemetry links between the width, and were available as uni- or bipolar
pacemaker and programmer developed dramati- models. These stainless steel devices followed on
cally and interrogation of the pacemaker’s from the Microlith-P® (75 g), Microlith-A® (75 g),
function and its reprogramming became an essen- and Microthin® (50 g) models. Telectronics pro-
tial part of troubleshooting pacing problems in duced the titanium-encased Optima®, Optima-MP®
clinical practice. In addition, a low energy-con- and Autima II® devices and Cordis – the Omnicor®,
suming memory made it possible for the pace- Multicor g®, and Stanicor® series (Fig. 1.74). The
maker to store the intervals between successive Multicor g® was light (42 g) and 10 mm thin. It
cardiac events for the subsequent production of had 5 programmable features, 4 output currents,
histograms for analysis. During the 1980s, CPI 14 rates, 8 sensitivities, 3 pacing modes (VVI/
produced the Microthin-P1® (50 g) (Fig. 1.73) VVT/VOO) and was the first to offer uni-/bipolar
programmability. Pacesetter Systems Inc. had the
nonprogrammable Vivalith™ 5 and 10 series –
reflecting 5 and 10 years projected longevity
(Fig. 1.75), and Programalith™ which utilized
large-scale integrated circuitry and telemetry and
offered rate, pulse amplitude, pulse width, sensi-
tivity, refractory period and hysteresis program-
mability and was available in uni- and bipolar
models. Projected life expectancy of these gen-
erators varied between 8 and 10 years and end-
of-life was signified by a reduction of pacing rate
Fig. 1.71 The Legend™ rate responsive activity-sensing or magnet rate by 6 bpm, e.g., Microthin® D2,
pacemaker was introduced in 1989

Fig. 1.72 The multipro-


grammable PASAR
antitachycardia device, its
handheld programmer, and
the external analyzer/
stimulator
32 1 History and Developments

a reduction in magnet rate by 10% below pacing enhancements while maintaining a high efficacy
rate, e.g., Programalith™, or a magnet rate of of 98% survival from sudden cardiac death at
85 bpm, e.g., Microlith-P/Command P5® (begin- 1 year. The VENTAK® 1550 combined enhanced
ning of life magnet rate was 100 bpm). longevity with energy and detection criteria pro-
The early dual-chamber devices (DDD) grammability, but these devices remained large
included Versatrax® (Medtronic 7000), Sequicor® until the mid-1990s (Fig. 1.77). A handheld pro-
(Cordis 233D), Diplos® (Biotronik), and Autima® grammer enabled communication with the device
(Telectronics) and initially were relatively large (using radiofrequency telemetry) in order to
devices. interrogate the device’s activity, e.g., arrhythmias
An even larger device, the automatic implant- detected, total patient shocks, etc., as well as
able defibrillator – the AID® from Intec Systems – enabling adjustments in shock energy levels, rate
was implanted in 1980 for the treatment of life- “cut-offs,” and morphology sensing. The prog-
threatening ventricular arrhythmias (Fig. 1.76). ress in the developments of this technology would
Although this initially required a thoracotomy to continue apace over the ensuing 20 years such
insert the electrodes (patch electrodes on the left that more sophisticated, smaller, longer-lasting
ventricle and a spring electrode into the superior devices can now be implanted transvenously/sub-
vena cava), this technology would also develop cutaneously in the pectoral region rather than by
rapidly. The AID-B, the hybridized VENTAK® thoracotomy and burial of the device in the abdo-
and the VENTAK® 1550 (CPI), the latter released men. In 2010, an implantable but entirely lead-
in 1988, would provide significant product less implantable cardioverter-defibrillator (ICD)

Fig. 1.74 Telectronics Autima II® dual-chamber and


®
Fig. 1.73 CPI’s Microthin P1 0522 unipolar device Cordis’ Stanicor single-Chamber device

Fig. 1.75 Pacesetter® Systems


Inc. Vivalith™ 10 unipolar and
bipolar devices
Sophistication, Multifunctionality, and Multiprogrammability (1990–Present) 33

Fig. 1.76 AID-B – first automatic implantable


defibrillator from INTEC

was released for clinical use (Cameron Health


Medical). Moreover, randomized clinical trials
would be performed to confirm the survival
benefits of ICD therapy.

Sophistication, Multifunctionality,
Fig. 1.77 (Top) The Ventak® PRx II was one of a series
and Multiprogrammability of AICDs from CPI in the early 1990s. It was a large
(1990–Present) device which could be used with epicardial or endocardial
electrodes. (Bottom) The Photon™ DR, dual-chamber
Over the last 15 years or more, microprocessor- AICD from St. Jude was the thinnest AICD available
when it was first implanted in December 1999
driven pacemakers have resulted in further dra-
matic change in the pacing specialty. For
example, by 1992 the dual-chamber Minuet™ briefer and pacemakers can also upload data tele-
from Medtronic weighed only 24 g, was only phonically to a central server via the internet.
6 mm thick, had a longevity of 11 years at 2.5 V Moreover, much effort has been placed into
output, boasted 11 pacing modes and full further understanding the advantages and disad-
programmability, AV interval flexibility, and vantages of correctly selecting the pacing mode
enhanced diagnostics. These included Real-Time for patients with sick sinus syndrome or AV block
and Marker Channel™ telemetry and electro- and that the mode should be prescribed for indi-
grams (EGMs) for patient monitoring. Moreover vidual patients. For example, AAI or DDD pac-
the device was compatible with both 5 mm uni- ing has been shown to reduce the incidence of
polar and IS-1 bipolar leads. chronic atrial fibrillation over VVI pacing in
Devices have become very complex systems patients with sinus node disease, while algo-
capable of detecting and storing events utilizing rithms to minimize ventricular pacing by allow-
several algorithms such that they can now deliver ing normal conduction whenever possible will
therapy and modify their internal pacing param- help to preserve ventricular function.
eters according to the changing needs of the However, a disadvantage of dual-chamber pac-
patient in an automatic manner. The rate-response ing, endless-loop pacemaker-mediated tachycar-
pattern can also adjust itself automatically to the dia, when pacemakers track atrial activity (VAT,
patient’s activity level. With the increase in auto- VDD, DDD) resulting from retrograde atrial acti-
maticity, follow-up visits have become easier and vation following a paced ventricular event was a
34 1 History and Developments

potentially serious adverse effect. This latter bipolar atrial sensing. Other sensors of movement
problem was shown to be treatable by program- and acceleration were investigated thoroughly
ming pacing modes such as DVI or DDI (such during the 1980s and the possible advantages of
that the atrium is either not sensed or not tracked). accelerometer-based sensors over vibration-based
A variety of algorithms that increase the post- sensors demonstrated during exercise and pos-
ventricular atrial refractory period (PVARP), drop tural changes. Biotec International produced the
ventricular paced events after periods of pacing at multiBIOrate® MB1 (following extensive experi-
the upper rate limit, or shorten the AV interval ence with the RDP-3 device introduced in 1982)
were also introduced to deal with this problem. which detected respiration based on the imped-
The hemodynamic importance of AV synchrony ance principle. A small auxiliary lead was
and of the AV interval also became appreciated and implanted subcutaneously in the thorax, and a
more recently pacemakers have been introduced train of low voltage constant current impulses
that have the facility for programming a rate- sent between the tip of the auxiliary electrode and
adaptive AV interval function to offer hemody- the pacing can. Variation of electrical impedance
namic benefit and enable a shorter total atrial occurred during respiration and was proportional
refractory period (TARP) with higher maximal to tidal volume (Fig. 1.78). The output of the
tracking rates during exercise. In rate-adaptive pac- impedance detector device produced a waveform
ing (available in single-chamber pacemakers since from which the rate and volume of respiratory
1986 and dual-chamber pacemakers since 1988), activity could be detected, and programming used
this has been shown to be advantageous for patients to optimize sensing. Other sensors of minute-
with chronotropic incompetence for improving ventilation, e.g., META MV® (Telectronics/
exercise tolerance and has become the program of Cordis), of the rate-of-rise of ventricular pressure
choice for such cases although programming and (dP/dt), pre-ejection interval, of autonomic ner-
follow-up are inevitably more complex. vous system activity derived from filtered intrac-
For optimal pacing in patients with atrial tach- ardiac impedance measurements (so-called VIP
yarrhythmias, which are not uncommon in pace- or ventricular inotropic parameter), of QT-interval,
maker patients, several options have been e.g., Rhythmyx® (Vitatron), central venous tem-
developed to deal with the potential disadvantage perature, O2 saturation, and of depolarization gra-
of a DDD pacemaker from the tendency to track dient were also extensively investigated. Some of
the arrhythmia. Automatic mode switching is one these have become incorporated within modern
such mechanism available in DDDR pacemakers. systems. Dual-sensor technology was pursued to
When criteria are met that the pacemaker identifies get around the problem that no single sensor
as a nonphysiologic atrial rhythm, the pacemaker offers a perfect physiologic response to all exer-
automatically switches from DDDR to VVIR pac- cise and non-exercise requirements, by providing
ing mode until a physiologic atrial rhythm is “cross-checking” of appropriate sensor response.
restored when the device switches back to DDDR – The classic development was of the combined
ensuring maintenance of rate adaptation. activity- and QT-sensor which was designed to
In a different approach to rate responsive pac- combine the fast response of activity-sensing
ing, attempts were made to use a single lead with the more proportional response to exercise
atrial-sensing, ventricular pacing pacemaker. and non-exercise requirements of the QT-sensor
Although the floating, unipolar, atrial-sensing and to prevent inappropriate response of the activ-
electrode could sometimes be effective in pro- ity pacemaker to environmental vibrations by
ducing a good rate response with exercise from cross checking. Others have included activity/
CPI’s RS4 pacemaker, atrial sensing was often minute ventilation, accelerometer/minute ventila-
suboptimal and the rate response unpredictable. tion, and even combinations of a fast acting activ-
The disadvantage of unipolar sensing (myopoten- ity sensor with a more proportional and specific
tial and other far-field signal oversensing) led to metabolic sensor. Present systems allow for the
the development of a VDD lead incorporating automated tailoring of rate response, via self
Sophistication, Multifunctionality, and Multiprogrammability (1990–Present) 35

Fig. 1.78 The MultiBIOrate® MB1 respiratory rate train of pulses sent between the tip of the lead and the can
detector. (Bottom panel) Impedance lead and trochar sys- (---). (Top left panel) chest x-ray showing the sensing
tem for tunneling the wire across the chest wall subcuta- lead, the pacemaker, and the pacing electrode
neously. (Top right panel) System in place showing the

learning rate-response algorithms, or program- been corrected. Nevertheless, future research


ming of a target rate histogram on the basis of the will define the optimum pacing parameters/set-
patient’s activity level and frequency of exercise. tings for these sophisticated systems in patients
Systems can facilitate storage of patients’ details with various cardiac pathologies. Pacing to ter-
and diagnose rhythm disturbances using sophisti- minate ventricular tachyarrhythmias requires a
cated algorithms. back-up defibrillation facility via an ICD but pac-
The indications for pacing have also expanded ing to prevent ventricular tachyarrhythmias may
beyond symptomatic bradycardia and now use continuous or intermittent (rate-smoothing
include neurocardiogenic syncope, hypertrophic or stabilization) pacing (with ventricular cap-
obstructive cardiomyopathy, and cardiac resyn- ture) to suppress triggering of ectopic beats,
chronization therapy (CRT, biventricular pac- prevent re-entry, decrease dispersion of refrac-
ing) for congestive heart failure. There has also toriness, and eliminate pauses that might induce
been progressive refinement of antibradycardia- tachyarrhythmia.
pacing function in implantable cardioverter Alongside these remarkable developments in
defibrillators (ICDs). Recent ICDs capable of dual- pacemaker technology and programmability, the
chamber and triple-chamber, rate-responsive pac- value of pacing at alternative sites to the right
ing provide state-of-the-art treatment (Fig. 1.79). atrial appendage and right ventricular apex has
Shortcomings in early-generation devices have become appreciated. For example, pacing of the
36 1 History and Developments

interatrial septum and pacing in the right ventric- amplitude safety margin and minimum voltage.
ular outflow tract using active-fixation leads may The Identity™ ADxDR pacemaker from St. Jude
prevent atrial arrhythmias and improve cardiac has a suite of diagnostic and therapeutic capa-
output respectively. In addition, left ventricular bilities aimed at managing patients with inter-
pacing via the coronary sinus has been shown to mittent atrial fibrillation besides being recently
be beneficial in patients with severe left ventric- claimed to be the world’s smallest dual-chamber
ular dysfunction and major left-sided intraven- pacemaker at 18 g and 8 cc (Fig. 1.82).
tricular conduction disorders such as left bundle Techniques for removing infected or redun-
branch block. This Cardiac Resynchronization dant pacing leads have also developed using spe-
Therapy (CRT), by resynchronizing contrac- cial sheaths to provide counterpressure and
tion of the right ventricle, left ventricular sep- countertraction as an extractor applies traction to
tum, and left ventricular lateral walls has been remove the lead from the myocardium. Locking
shown to improve LV contractility resulting in
improved morbidity and mortality (Figs. 1.79–
1.81). Moreover, programmable features such as
Managed Ventricular Pacing (MVP), AV Search
Hysteresis, and AAI-DDD safe modes may help
to reduce the amount of right ventricular pacing
and also reduce the incidence of atrial fibrillation.
Ventricular Capture Management (VCM) and
Atrial Capture Management (ACM) are achieved
by the device being designed to periodically test
ventricular/atrial thresholds, and reprogram ven-
tricular/atrial outputs based on a programmable

Fig. 1.80 Medtronic’s InSync® CRT device and leads


(Reproduced with permission of Medtronic, Inc.)

Fig. 1.79 Boston Scientific’s Cognis® CRT-D provides


enhanced CRT therapy, atrial arrhythmia management,
SmartDelay AV optimization, and high-energy defibril- Fig. 1.81 Boston Scientific’s Contak Renewal® TR2
lation in a 9 mm thin, 35 cc can (Used with permission of (CRT) device (Used with permission of Boston Scientific
Boston Scientific Corporation, ©2010 Boston Scientific Corporation, ©2010 Boston Scientific Corporation/
Corporation/affiliates. All rights reserved) affiliates. All rights reserved)
Sophistication, Multifunctionality, and Multiprogrammability (1990–Present) 37

Fig. 1.82 St. Jude’s Identity® ADxDR device features


atrial fibrillation management, a suite of therapeutic and
diagnostic capabilities designed to help manage pacemaker
patients suffering from AF, e.g., AF suppression algorithm,
Auto-Mode Switch Log, and Physician Commanded Atrial
Therapy (NIPS – Non-Invasive Programmed Stimulation)
(Image provided courtesy of St. Jude Medical, ©2008
St. Jude Medical, Inc.)

stylets, telescoping sheaths, and excimer laser


sheaths are also now available to aid removal of
chronically adherent leads when mechanical
removal has failed (Fig. 1.83) and have been
found to be advantageous. These percutaneous
lead extraction techniques should be restricted to
experienced centers with cardiac surgical Fig. 1.83 Spectranetics® Laser extraction sheath for lead
back-up. removal
Another major development has been the
introduction of digital technology by Vitatron in
their C and T series (Fig. 1.84). They were able to
adapt Digital Signal Processing (DSP) for use in
a pacemaker platform with minimal energy con-
sumption. DSP switches the analogue signal into
a digital signal, allowing more accurate signal
analysis. This results in a high-quality intracar-
diac electrogram (IEGM) which enables the heart
rhythm to be identified more readily. Moreover,
this technology allows data storage within the
pacemaker and has made interrogation and pro-
gramming of the device rapid – using sophisti-
cated external devices (Fig. 1.85). It is also now
possible to interrogate pacing devices wirelessly
in pacing clinics as well as in the patient’s own
home using the World Wide Web. Traditionally, a
“wand” attached by a wire to the programmer is
positioned on the body’s surface over the device
implantation site in order to receive the telemetry
signal. However, the distance for radiofrequency Fig. 1.84 Vitatron’s C- and T-series of pacemakers were
communication has increased from 2–5 in. the world’s first to use digital technology
38 1 History and Developments

Fig. 1.85 Sorin’s desk-top


programmer/data analyzer –
Orchestra™

(5–12 cm) to 10–20 ft (3–6 m) and some devices


communicate without a wand. The longer dis-
tance telemetry is device-specific and employs
either the Industrial, Scientific and Medical (ISM)
band from 902 to 928 MHz or a subsection of the
Medical Implant and Communications (MICS)
band from 402 to 405 MHz. Use of telemetry in
these frequency spectra has allowed the telemet-
ric signal to be reliably and securely sent to and
from the programmer and device up to a distance
of 10 ft (3 m) distant. This has proved useful dur-
ing implantation, in the device clinic (using a
programmer), and also in the patient’s home as
part of remote monitoring (remote telemetry
device) (Fig. 1.86). Programmers now have inte-
grated printers to document the device settings,
but home monitor/communicators and program- Fig. 1.86 Merlin@Home is the home monitoring device/
mers can also communicate the interrogated data transmitter from St. Jude Medical (Image provided cour-
tesy of St. Jude Medical, ©2008 St. Jude Medical, Inc.)
to a remote printer for a hard copy presentation or
be transferred to a cardiac device database or
Electronic Medical Record (EMR). dependent on the ingenuity, vision, and drive of
Many of these innovative developments will be cardiologists and the engineers in the industry
described further in the chapters that are to follow. who remain focused on producing devices which
Suffice to say, as with all the developments and have the potential to improve patient survival and
improvements in the technology and practice of quality of life. Many of the important “Milestones
pacing described here, future advances will remain in pacing” are shown in Table 1.1.
Sophistication, Multifunctionality, and Multiprogrammability (1990–Present) 39

Table 1.1 Milestones in pacing


1928 Lidwell reports successful electrical restarting of the heart in a newborn
1932 Hyman presents the “artificial pacemaker” – a mechanical device for producing a DC current to stimulate
the right atrium directly using a bipolar needle
1949 Earl Bakken founds Medtronic Inc.
1949 Bigelow, Callaghan, and Hopps use endovenous electrode to stimulate the sino-atrial node during open
heart surgery
1952 Zoll demonstrates a transthoracic external pacemaker
1957 Transthoracic pacing performed using a pacing wire placed directly into the heart via a needle placed
through the chest wall
1958 Furman uses endovenous electrode to pace the right ventricle using a mains-powered electrical stimulator
1958 Weirich, Lillehei, and Bakken use battery powered stimulator to pace the heart via an endovenous electrode
1958 Ake Senning implants first pacemaker invented by Rune Elmqvist at Elema-Schonander in Stockholm,
Sweden, using a device powered by nickel-cadmium batteries/inductive recharging unit
Davies, Leatham, and Robinson reported “effective ventricular stimulation” in a patient with second
degree heart block in October 1958
1959 Hunter and Roth produce a stainless steel epicardial electrode with a small surface area and spikes that
could be pushed into myocardium/sutured in place
1960 Greatbatch and Chardack produce Medtronic’s first pacemaker powered by mercury batteries – recharging
unnecessary. Used clinically for first time in June 1960
Zoll implants permanent pacemaker in October 1960
1961 Noel Gray, New South Wales, Australia, founds Telectronics Company – becoming Telectronics Inc. in 1963
Lillehei et al. and Kantrowitz et al. implant permanent pacemakers in January and May 1961 respectively
1962 First Vitatron pacemaker
Lagergren and Johansson first used a unipolar endocardial electrode in the RV apex as a permanent lead.
Initially connected to an external generator for a few weeks, it was then connected to a subcutaneously
implanted generator
Wilson Greatbach patents implantable pacemaker in Buffalo, NY
1963 Zucker, Parsonnet and colleagues report the use of a wholly implantable bipolar endocardial pacemaker;
Siddons and Davies also reported use of endocardial ventricular pacing with a St. George’s generator
implanted in the axilla
First Biotronik pacemaker
1964 Telectronics facility for permanent pacemaker production established; first device, P1 (4 mercury-zinc
batteries) implanted
1965 Alfred E. Mann founds Pacesetter Systems Inc.; produce first rechargeable long-life pacemaker battery
developed by Robert Fischell at the Johns Hopkins University.
First Biotronik endocardial lead
1966 Ellis Epstein, Norman Coulshed, Charles McKendrick and colleagues in Liverpool report the use of
temporary RV pacing for the treatment of AV block complicating acute MI
1968 Vitatron demonstrate first noninvasive threshold measurement
1969 In USA, number of new pacemaker implants was 71 per million of population
1970 First nuclear-powered (Plutonium-238) Medtronic pacemaker implanted in Paris
1972 First lithium-iodine battery-powered pacemaker implanted
1972 Cardiac Pacemakers Inc. (CPI) of St. Paul, Minnesota, was formed
1973 Albert Beutel II creates Intermedics
1974 Elema-Schonander becomes Siemens-Elema
1976 Intermedics produce first small, lithium battery-operated pacemaker which tripled the life of currently
available generators
First Biotronik pacemaker with a lithium battery, a hybrid circuit, and an hermetic MP35N housing (Protasul)
1978 CPI acquired by Eli Lilly and rename the company Guidant
1979 Pacesetter Systems Inc. introduce first pacemaker to use bidirectional telemetry
1979 Anthony Rickards showed that at fixed pacing rates, the QT-interval changed on exercise and during
emotional stress due to catecholamines and that this phenomenon could be used to develop a
rate-responsive pacemaker
40 1 History and Developments

Table 1.1 (continued )


1980 First ICD, developed by Michel Mirowski and Morton Mower – the AID® from Intec Systems – implanted
in a patient by Dr. Levi Watkins, Jr (February 1980). Marlin Heilman, the founder of MedRad (a medical
device company) and Alois Langer, his chief biomedical engineer have been recognized for their pivotal
roles in developing a prototype automatic ICD alongside Mirowski and Mower from 1973 onward
1981 In USA, number of new pacemaker implants was 513 per million of population
1981 Vitatron produce world’s first microprocessor, software-driven pacemaker (DPG1), introduce “Flywheel”
mode for rate smoothing and first pacemaker diagnostics – long/short-term rate histograms
1982 Vitatron produce first rate responsive pacemaker – TX 1, a QT-sensing device which increased ventricular
pacing rate as the paced evoked-QT-interval changed with physiological demand. Devices implanted in
Europe
1983 Biotronik introduce Neos, the world’s smallest single-chamber pacemaker with bi-directional telemetry
1984 Vitatron introduce features such as “Conditional Wenckebach response,” night rate drop, rate-adaptive A-V
delay, automatic upper rate response (first mode switching), reduced ventricular tracking limit (during
paroxysmal AF). Quintech TX was introduced which improved T-wave sensing by altering the filter
characteristics (bandwidth) to favor the T-wave rather than R-wave frequencies
1985 Activitrax™ – a vibration-sensing, rate responsive pacemaker introduced by Medtronic
1985 Eli Lilly purchase Intec Systems defibrillator technology on behalf of its subsidiary CPI; Siemens,
AG purchase Pacesetter Systems Inc.
1986 CPI release VENTAK® ICD
1986 Telectronics becomes subsidiary of Nucleus Ltd., – Australian high technology health products
1986 Vitatron acquired by Medtronic
Biotronik introduce thermosol, a rate-adaptive pacemaker with a central venous temperature measurement
sensor
1988 Daily learn algorithm in Rhythmyx® introduced by Vitatron
1990 Biotronik introduce NEOS-PEP, a rate-adaptive pacemaker with a pre-ejection phase measurement sensor
1992 Vitatron produce world’s first dual-sensor rate responsive pacemaker; Sensor Cross-Checking™
1993 Vitatron produce dual sensor/dual-chamber pacemaker plus other features such as Automatic Scanning for
spontaneous AV conduction; AV delay hysteresis; Beat-to-beat mode switching; P-wave histograms
1994 St. Jude Medical purchase Siemens’ pacemaker division for $500 million
1995 ELA (a French company later acquired by Sorin) produce world’s first dual-chamber defibrillator
–DEFENDER®
1996 Pacific Dunlop sells Telectronic Pacing Systems to St. Jude Medical Inc., USA for $170 million
1997 Spectranetics introduce Excimer Laser Lead extraction device
1998 Vitatron produce 4 novel preventive pacing algorithms for preventing AF onsets
2000 Vitatron introduce new series of anti-atrial arrhythmia DDDRP pacing devices
2002 Vitatron introduce the Vitatron CRT 8000 for cardiac resynchronization therapy; Sorin Group produce
LIVING™ CHF, a CRT device with an endocardial acceleration sensor
2003 Vitatron produce world’s first digital pacemaker series – Vitatron C-series with fast and efficient digital
signal processing and a Therapy Advisor facility
Sorin introduce SafeR™ in SYMPHONY® pacemakers – the first pacing mode to limit unnecessary
ventricular pacing
2004 First Vitatron T-series released offering dual-channel electrograms
2005 Vitatron C-series models released
2006 Boston Scientific acquire Guidant for $27.2 billion
Sorin Group introduce a small ICD with the SafeR™ mode
2007 2nd Vitatron T-series released
2009 Medtronic introduce the first MRI-safe device – the Advisa MRI™
Surescan®; St. Jude Medical and Boston Scientific Ltd. introduce the first DF-4 standard leads for ICDs
2010 Quartet™ (the IS4, quadripolar LV pacing lead) is released by St. Jude Medical
2010 Biotronik launch The Evia premium pacemaker series and Biotronik ProMRI® a technology to allow MRI
scanning in their bradycardia device and leads portfolio
References 41

References 2. Furman S, Escher DJW. Principles and techniques of


cardiac pacing. New York: Harper & Row; 1970.
1. Aquilina O. A brief history of cardiac pacing. Images
Paediatr Cardiol. 2006;27:17–81.
Permanent Pacing: Current
Overview 2

Today, approximately three million people e.g., Lithuania. Pacing leads were predominantly
worldwide have a pacemaker and more than transvenous, bipolar and passive fixation elec-
600,000 pacemakers are implanted annually. trodes and active-fixation leads in the atrium are
A responsibility of the International Cardiac being used with increasing frequency. There
Pacing and Electrophysiology Society is a were marked variations from country to country.
worldwide quadrennial survey of cardiac pacing In the UK, the ratios of active- to passive-fixation
and ICD practices. Fifty countries contributed to leads in the atrium and ventricle were 16:84 and
the 2001 Worldwide Survey. Table 2.1 shows the 6:94, respectively, but in the USA the corre-
number of implanting centers per country, the sponding figures were 73:27 and 38:62, respec-
number of new and replacement pacemaker tively. The 2001 Survey showed a progressive
implants by each country, and the number of new increase in the number of ICDs worldwide with
implants per million population. The largest the largest number of implants being in the USA
implanting nation with 223,226 new implants (48,127, or 169 implants per million). Dual-
was the USA followed by Germany (69,823) and chamber and biventricular ICD devices were
France (37,250). Japan’s new implants totaled being used with increasing frequency and biven-
26,700, Canada’s 18,376, and the UK’s 17,550. tricular pacemakers themselves were being
Figure 2.1 shows the number of new implants introduced in several countries. These devices
per million. Most countries showed an increase are so expensive that few are implanted in poorly
in new implants per million compared with the developed countries. Although the next survey is
1997 survey. High degree AV block and sick likely to show a further increase in such implants
sinus syndrome were almost universally the worldwide, the contrast between developed and
major indications for pacemaker implantation, third-world countries is likely to persist. These
with <2% biventricular pacing in those countries remarkable devices have been shown to have
that implanted such devices in 2001. VVIR pac- life-saving benefits, but their expense is an
ing increased progressively in developing coun- important issue and will continue to put a
tries and values >40% were still common in financial burden on the health services of most
Europe. Most countries showed a significant countries.
increase in the use of DDDR replacing the use of In a recent report by the Heart Rhythm Society
VVIR systems. Single-lead VDD pacing systems and the European Heart Rhythm Association, it
were used throughout the world although few was estimated that in 2006 approximately
countries had greater than a 10% rate. The USA 280,000 pacemakers and 160,000 ICDs (implant-
and the UK, for example, implanted <1% of such able cardioverter defibrillators) were implanted
devices. AAIR systems were predominantly used in North America while the corresponding num-
in less socioeconomically developed countries, bers for the countries of western and central

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 43


DOI 10.1007/978-1-4471-2939-4_2, © Springer-Verlag London 2012
44 2 Permanent Pacing: Current Overview

Table 2.1 World survey 2001


New implants per
Country Population (million) No. of centers New implants million population Replacements
Germany 83 850 69,823 837 ?
USA 284 ? 223,226 786 51,616
Belgium 10 120 7,053 685 3,086
Italy 58 400 36,779 637 ?
France 59 600 37,250 628 5,871
Canada 31 125 18,376 591 1,218
Austria 8 64 4,666 583 1,232
Czech Republic 11 36 5,563 530 ?
Australia 20 105 9,498 486 1,536
Sweden 9 45 4,201 472 1,485
Denmark 5 14 2,429 467 967
Switzerland 7 65 3,014 415 846
Finland 5 24 2,128 411 ?
Spain 41 145 16,421 399 ?
Uruguay 3 12 1,160 362 496
Israel 6 18 2,009 335 663
Norway 4 29 1,472 329 301
Netherlands 16 106 5,016 314 1,891
Slovenia 2 2 621 312 142
UK 60 174 17,550 293 3,823
Lithuania 4 3 953 272 ?
Argentina 36 230 9,000 250 1,000
New Zealand 4 8 914 245 195
Croatia 4 11 1,049 238 157
Ireland 4 13 879 228 145
Slovak Republic 5 14 1,143 212 ?
Latvia 3 3 528 210 127
Japan 127 2,700 26,700 210 11,500
Hong Kong 7 16 1,004 143 92
Taiwan 22 22 2,290 102 193
Singapore 3 10 281 92 20
Brazil 170 243 15,167 89 7,182
Russia 144 97 10,950 76 100
South Africa 45 39 1,814 40 224
South Korea 45 65 1,162 26 322
Iran 60 27 1,469 24 211
Peru 25 20 550 22 80
Ecuador 12 18 180 15 15
Thailand 62 22 605 10 47
China 1,300 241 11,000 8 855
India 1,000 329 6,725 7 570
Pakistan 135 14 910 7 60
Philippines 79 10 348 4 12
Indonesia 220 21 220 1 30
Mond et al. [1]
Countries listed in order of implants per million
2 Permanent Pacing: Current Overview 45

Pacemaker implants per million worldwide − 2001 survey


1000

800

600

400

200

0
India Pakistan China Malaysia Peru S Korea S Africa Russia
Brazil Taiwan Hong Kong Japan Latvia Slovakia Ireland Croatia
Argentina Lithuania UK Slovenia Netherlands Norway Israel Spain
Finland Switzerland Denmark Sweden Australia Czech Rep Austria Canada
Italy Belgium USA Germany

Fig. 2.1 Number of new implants per million of population. Worldwide survey 2001 (Mond et al. [1])

Europe were 250,000 and 50,000 respectively. implant rates across Europe is shown in
They estimated the prevalence of these devices Figs. 2.5–2.7.
in 2007 to be 564,074 pacemakers, 234,780 ICDs, The joint American College of Cardiology/
and 148,092 CRTs (cardiac resynchroniza- American Heart Association/North American
tion therapy devices) in North America and Society of Pacing and Electrophysiology
683,472, 87,747, and 62,010, respectively, in (NASPE) Committee’s Guidelines have been
Europe. The logistics of monitoring such large updated. Generally, wherever possible, a pace-
numbers of devices is an ever increasing chal- maker device with atrial contribution, i.e., a
lenge for the cardiovascular community and the single-chamber atrial or dual-chamber device
group estimated that the number of follow-up should be used. It is justified by the additional
encounters annually for pacemakers (with or benefit expected from these devices, e.g.,
without CRT) in North America and Europe was improved hemodynamics and a better quality
3.2 million and for ICDs (with or without CRT) of life and reduced morbidity and mortality.
2.5 million. Recently the HRUK Audit Group However, several controlled, randomized trials
(formerly the Network Device Survey Group) on these issues revealed somewhat disappointing
published its sixth annual report for 2010 in the results. Only the first trial, in Denmark, studying
UK. For England, this suggested a new pace- 255 patients with sinus node disease, showed a
maker implant rate of 528 per million, an ICD significant reduction in mortality and morbidity
implant rate of 72 per million and a total CRT such as the incidence of atrial fibrillation, stroke,
implant rate of 114 per million as against targets and congestive heart failure with single-chamber
of 700, 100, and 130 per million, respectively atrial pacing versus single-chamber ventricular
(Figs. 2.2–2.4). There was considerable regional pacing. Other studies aimed at demonstrating the
variation within the UK. A comparison with survival benefits of dual-chamber pacing over
46 2 Permanent Pacing: Current Overview

600
England
Wales
500 Scotland
N Ireland

400
Per million population

300

200

100

0
2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010
Year

Fig. 2.2 Trends of new pacemaker implant rates in the UK 2010 (HRUK Audit Group)

single-chamber ventricular pacing failed to do so. RV apex results in an increased incidence of


These included the Pacemaker Selection in the atrial fibrillation, hospitalization for heart fail-
Elderly trial (407 patients), the Canadian Trial ure, and possibly death even when AV synchrony
of Physiological Pacing (2,568 patients), and the is maintained. If these results are corroborated
Mode Selection Trial (2,010 patients). However, by others, then RV apical pacing would have to
the incidences of atrial fibrillation were less fre- be avoided and sites elsewhere in the RV such as
quently observed in the dual-chamber group in the RV outflow tract (RVOT) or interventricular
all three trials. Mattioli and colleagues showed septum using an active-fixation lead might prove
similar results in their study, but the Pacemaker to be the best option. Thus, in patients with sinus
Atrial Tachycardia trial failed to do so despite node disease, single-chamber atrial pacing or
showing a survival benefit with dual-chamber dual-chamber pacing with sophisticated algo-
pacing. Two large databases such as the Danish rithms which reduce RV pacing might be the
and German pacemaker registries allayed fears answer, and for those with AV block, RV pacing
that complication rates were higher with dual- from the RVOT might prove more beneficial. In
chamber pacing compared to single-chamber the past, in patients with sinus node disease but
pacing and it is now accepted that an atrial lead without evidence of AV block, it was common
should be implanted where there is no contrain- practice to check Wenckebach rate by pacing the
dication, e.g., atrial fibrillation. atrium at high rates to assess AV conduction in
An issue that has important practical implica- order to decide whether or not to implant a ven-
tions is the question as to whether ventricular tricular lead (especially in young patients with
pacing from the RV apex may be detrimental. sinus node disease) – unfortunately this appears
Studies have shown that permanently pacing the to have poor predictive value.
2 Permanent Pacing: Current Overview 47

140
England
120 Wales
Scotland
N Ireland
100
Per million population

80

60

40

20

0
2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010
Year

Fig. 2.3 Trends of new ICD implant rates in the UK 2010 (HRUK Audit Group)

During the last decade, many attempts were cardiac failure appears to hold much promise.
made to apply pacing technology to the treatment Trials such as Pacing Therapy in Congestive
of problems other than symptomatic bradycardia Heart Failure trial, Multisite Stimulation In
– mainly to prevent atrial tachyarrhythmias and Cardiomyopathies, and Multicenter InSync
to improve the symptoms, the hemodynamics, Randomised Clinical Evaluation all demonstrate
and possibly the survival of patients with con- that CRT can improve the symptoms, exer-
gestive cardiac failure. The initial interest in the cise capacity, and the functional status of such
prevention and treatment of atrial tachyarrhyth- patients. CARE-HF showed a survival benefit for
mias with implantable devices fell as algorithms CRT pacing therapy (CRT-P). The Comparison
designed to prevent paroxysmal arrhythmias of Medical Therapy, Pacing and Defibrillation in
proved unsuccessful and then substantially Chronic Heart Failure trial showed a reduction
after publication of the results of the Atrial in mortality when CRT therapy was combined
Fibrillation Follow-up Investigation of Rhythm with an ICD (CRT-D) and MADIT-CRT showed
Management Trial. This showed no survival a reduction in progression of mild (Class I and II)
benefit for patients with vigorous rhythm control to more severe heart failure (Class III and IV) as
(i.e., attempts to retain or restore sinus rhythm) well as a 34% reduction in the risk of all-cause
compared to simple rate control in sinus rhythm mortality or heart failure in patients treated with
or atrial fibrillation. Other studies supported CRT-D compared with ICD implantation alone.
these findings, resulting in an uncertain future Besides these and other newer indications for
for pacing to prevent atrial fibrillation. More pacing, developments in pacemaker program-
optimistically, pacing to deliver cardiac resyn- mability and novel diagnostic and monitoring
chronization therapy in patients with congestive features of pacemakers and ICDs continue to
48 2 Permanent Pacing: Current Overview

140

England
120 Wales
Scotland
N Ireland
100
Per million population

80

60

40

20

0
2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010
Year

Fig. 2.4 Trends of new total CRT implant rates in the UK 2010 (HRUK Audit Group)

make this subspecialty of cardiology exciting and and their subsequent programming and trouble-
rewarding for those technicians and doctors shooting in order to optimize their function, is
intending to develop an expertise and indeed a essential and should be of a high standard.
career in this field. Opportunities for both clinical Similarly training of technical staff (cardiac
research and device development and evaluation physiologists) that are essential for running a
alongside pacemaker manufacturers and their comprehensive and high quality service both in
engineers are numerous and limited only by the the pacing theater and in the out-patient clinic is
imagination and enthusiasm of the individual. no less important. Training programs, examina-
Training of physicians in the techniques of tions, and qualifications as a testament to the
implantation of devices, their indication for use, individual’s expertise are discussed in Chap. 22.
2 Permanent Pacing: Current Overview 49

Ireland
Norway
UK
Greece
Netherlands
Switzerland
Spain
Denmark
Portugal
Czech Republic
Finland
Austria
Sweden
France
Italy
Belgium
Germany
0 200 400 600 800 1000 1200 1400

Fig. 2.5 Comparison of all pacemaker implants in the UK versus rest of Europe in 2010 (HRUK Audit Group) (Sources:
Eucomed (2010))

Portugal
Spain
UK
Greece
France
Sweden
Norway
Finland
Switzerland
Ireland
Belgium
Austria
Czech Republic
Italy
Denmark
Netherlands
Germany
0 50 100 150 200 250 300 350

Fig. 2.6 Comparison of all ICD implants in the UK versus rest of Europe in 2010 (HRUK Audit Group) (Sources:
Eucomed (2010))
50 2 Permanent Pacing: Current Overview

Greece
Spain
Ireland
Portugal
Finland
Norway
Switzerland
Sweden
France
Austria
UK
Belgium
Denmark
Netherlands
Czech Republic
Germany
Italy

0 50 100 150 200 250

Fig. 2.7 Comparison of all CRT implants in the UK versus rest of Europe in 2010 (HRUK Audit Group) (Sources:
Eucomed (2010))

Reference
1. Mond HG, et al. The world survey of cardiac pacing
and cardioverter defibrillators: calendar year 2001.
Pacing Clin Electrophysiol. 2004;27:955–64.
Pathology Associated with Need
for Pacing 3

Cardiac pacing is indicated for the treatment of omyopathy, neuromuscular dystrophies, coronary
both bradyarrhythmias and tachyarrhythmias. artery disease, cardiac surgery, and congenital
However, the major indication for pacing is heart block (Figs. 3.1–3.5). Radiofrequency (RF)
the treatment of bradyarrhythmias due either to ablation of the AV node to treat patients with
sick sinus syndrome, atrioventricular block, or a difficult supraventricular arrhythmias (e.g., atrial
combination of both, which result in symptoms fibrillation) that are unresponsive to drugs and
such as dizziness, near syncope or syncope. other RF ablative techniques may necessitate per-
Prophylactic pacing is also indicated in asymp- manent pacing (Fig. 3.6) as may alcohol-septal
tomatic individuals who have ECG evidence of a ablation in patients with hypertrophic obstruc-
significant intracardiac conduction defect which tive cardiomyopathy (Figs. 3.7 and 3.8). Sick
may result in similar symptoms or death due to sinus syndrome, a disorder of impulse formation,
asystole. is most commonly due to idiopathic fibrosis. It
The commonest causes for cardiac conduct- also occurs after cardiac surgery, especially in
ing system disease are shown in Table 3.1 and children undergoing corrective surgery for con-
include idiopathic conducting tissue fibrosis, genital abnormalities and rarely with myocardial
myocardial infarction, myocardial infiltrative dis- infiltrative disorders such as sarcoidosis, amyloi-
orders, myocarditis, infective endocarditis, cardi- dosis, Chagas’ disease, and cardiomyopathies.

Table 3.1 Causes of cardiac conducting system disease that may necessitate pacing
Idiopathic conducting tissue fibrosis
Sick sinus syndrome/tachycardia–bradycardia syndrome
Coronary artery disease
Myocardial infarction
Myocardial infiltrative disorders/cardiomyopathy
Cardiac surgery, e.g., aortic valve surgery, repair of ventricular septal defect, surgery for correcting structural cardiac
defects in children
Radiofrequency ablation of the AV node
Infective endocarditis
Myocarditis
Congenital heart block
Alcohol septal ablation for hypertrophic obstructive cardiomyopathy
Percutaneous coronary rotational atherectomy – temporary pacing
Neuromuscular diseases, e.g., dystrophia myotonica, Kearns–Sayre syndrome
Drug toxicity

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 51


DOI 10.1007/978-1-4471-2939-4_3, © Springer-Verlag London 2012
52 3 Pathology Associated with Need for Pacing

I II III aVR aVL aVF

V1 V2 V3 V4 V5 V6

Fig. 3.1 Acute inferior myocardial infarction is sometimes hypotension, or symptoms of dizziness or syncope, tempo-
complicated by second or third degree heart block. When rary pacing is indicated. This 12-lead ECG and rhythm strip
associated with marked bradycardia, a fall in cardiac output, show inferior ST-elevation and Mobitz Type II AV block

Fig. 3.2 Muscular dystrophies such as dystrophia myo- conduction disturbances such as complete heart block
tonica (evidenced by frontal balding, bilateral ptosis, and when permanent pacing is indicated
a long, haggard facial expression) may be associated with
3 Pathology Associated with Need for Pacing 53

Fig. 3.3 Infective endocarditis, particularly involving the echocardiogram shows a large vegetation on the aortic
aortic valve, may result in spread of infection and abscess valve which resulted in severe aortic regurgitation.
formation into the interventricular septum and result in (Bottom right) 2D echocardiogram showing large inter-
serious conduction disturbance, including complete heart ventricular septal abscess (AB) which was associated with
block and asystole. Patients with infective endocarditis a progressively increasing PR interval and sudden onset
and septal abscess should have a temporary pacemaker of complete heart block. Fortunately, a temporary pace-
inserted especially if a conduction disturbance develops maker was inserted when the PR interval was first noticed
on the ECG. (Top) Destructive infective endocarditis of to increase from 200 to 280 ms. VEG vegetation, AO aor-
this bioprosthetic valve due to Staphylococcus aureus tic valve, RA right atrium, RV right ventricle, LV left
caused severe aortic regurgitation. (Bottom left) 2D ventricle
54 3 Pathology Associated with Need for Pacing

Fig. 3.6 AV Node ablation either requires temporary


pacemaker implantation prior to ablation and permanent
pacing thereafter or more commonly is done 8 weeks after
permanent pacemaker implantation

Fig. 3.4 Aortic valve surgery may be complicated by


heart block and require temporary and/or permanent pac-
ing. An artificial aortic valve is shown being deployed

Fig. 3.7 Patients with hypertrophic obstructive cardio-


myopathy may be helped by dual chamber pacemaker
implantation with an RV apical lead. The echocardio-
graphic features of asymmetric LV hypertrophy and LV
outflow tract obstruction are shown here

Fig. 3.5 Aortic valve bio-prosthesis in situ


3 Pathology Associated with Need for Pacing 55

Fig. 3.8 Alcohol septal ablation for hypertrophic obstruc-


tive cardiomyopathy (shown here by the small balloon
catheter inflated in the septal artery (green arrow)) is asso-
ciated with complete heart block in 8–10% of cases and
patients will require dual chamber permanent pacemaker
implantation. The procedure is covered by temporary pac-
ing with a pacing catheter placed in the right ventricular
apex (black arrow)

Some patients will require temporary pacing


only – when the conduction defect is considered
to be a temporary phenomenon, such as after
acute myocardial infarction (see Fig. 3.1) or to
protect them against the effects of higher degrees
of heart block if this should develop during gen-
eral anesthesia, surgery, or percutaneous coro-
nary intervention, such as rotational atherectomy
in the right coronary artery (Fig. 3.9), or as a
result of drug toxicity. Combined temporary atrial
and ventricular pacing (dual chamber pacing)
may help improve cardiac output in low output
states associated with AV block or severe sinus
bradycardia when single chamber right ventricu-
lar pacing fails to improve the hemodynamic
state (Fig. 3.10).
For tachyarrhythmias such as ventricular
tachycardia, right ventricular overdrive pacing
may be used as an interim measure to terminate
the arrhythmia if pharmacological treatment has
failed or is contraindicated (Fig. 3.11). Temporary
pacing is used in intracardiac electrophysiologi-
cal studies during the investigation of supraven- Fig. 3.9 Rotational atherectomy of calcified lesions in a
large, dominant right coronary artery should be covered by
tricular or ventricular arrhythmias and in the temporary pacing as plaque ablation with the high speed
identification of accessory pathways such as in Rotablator may result in severe bradycardia or heart block
56 3 Pathology Associated with Need for Pacing

the Wolff–Parkinson–White syndrome (Figs. 3.12


and 3.13).
For patients with severe heart failure due to
impaired cardiac function, biventricular perma-
nent pacing (cardiac resynchronization therapy)
may be indicated in order to re-establish synchro-
nous RV and LV contractility (Fig. 3.14) and the
indications, technique, and benefits of this are
discussed in Chap. 16.

Fig. 3.10 Patients with cardiogenic shock and AV


dissociation after severe myocardial infarction may favor-
ably respond hemodynamically to AV sequential pac-
ing using temporary atrial and ventricular electrodes.
Unfortunately, temporary atrial leads are unstable and
frequently displace and lose capture. In this situation,
permanent pacing using actively fixed atrial and ventricu-
lar electrodes may be extremely useful in stabilizing the
hemodynamics. The arrow points to the tip of a straight
atrial electrode actively fixed into the low right atrium
where sensing and pacing thresholds were acceptable

Fig. 3.11 RV overdrive pacing can terminate ventricular confirming AV dissociation and that the rhythm is ven-
tachycardia. The top ECG is a surface lead II. The second tricular tachycardia. The bottom two ECGs (lead II) show
recording is an intracardiac recording from a temporary that the VT is overdriven by rapid RV pacing and then
electrode within the RA. The arrow shows the P-waves, terminated
3 Pathology Associated with Need for Pacing 57

Fig. 3.12 Temporary pacing electrodes are used in


intracardiac electrophysiological studies during investiga-
tion and treatment of arrhythmias such as the Wolff–
Parkinson–White syndrome (see Fig. 3.13). Here catheters
are shown in the coronary sinus, in the left atrium, and
against the Bundle of His

Fig. 3.13 ECG showing Wolff-Parkinson-White syndrome Type B


58 3 Pathology Associated with Need for Pacing

Fig. 3.14 Cardiac resynchronization therapy (CRT) has (left) alongside a chest X-ray showing leads in the RA, RV
proved useful for treatment of patients with impaired car- septum, and in a branch vein of the coronary sinus (Image
diac function. Medtronic’s InSync® III CRT device is shown reproduced with permission of Medtronic, Inc.)
Permanent Pacemaker Implantation
for Bradycardias: Indications 4

Permanent pacemaker implantation is indicated to a high vagal tone, perhaps as a result of physical
relieve symptoms of syncope, near syncope, dizzi- training such as athletes and professional sports-
ness, or dyspnea in patients with severe bradycar- men/women.
dia and to improve prognosis in asymptomatic
patients with impaired intracardiac conduction tis- Table 4.1 Indications for permanent pacemaker implantation
sue. Indications for permanent pacemaker implan- Second-degree AV block
tation are shown in Table 4.1. The ECG is the most Idiopathic/ischemic/persistent post MI/infiltrative/
post-surgery/traumaa
important guide to whether pacing is indicated.
Complete AV block
Idiopathic/ischemic/persistent post MI/infiltrative/
post surgery/traumaa
First-Degree AV Block Bifascicular blockb
RBBB + LAFB and normal PR interval
First-degree AV block alone is not usually an RBBB + LPFB and normal PR interval
indication for cardiac pacing (Figs. 4.1 and 4.2). Trifascicular block
However, if associated with syncope or near-syn- RBBB + LAFB and prolonged PR interval
cope, co-existent 2° or 3° AV block may be sus- RBBB + LPFB and prolonged PR interval
pected and investigations including continuous LBBB + long PR interval (especially if progressive
ambulatory ECG monitoring or loop event record- lengthening of PR)
ing should be performed. A prolonged PR inter- Alternating RBBB/LBBB
Junctional bradycardiab
val (>200 ms) (especially lengthening of the PR
Severe sinus bradycardiab
interval over time) in association with RBBB,
Sick sinus syndromeb
LBBB, or alternating BBB should be considered
Sinus arrest (>3 s pauses)
an indication for permanent pacing (Fig. 4.3). Carotid sinus hypersensitivityb
Malignant vasovagal syndromesb
Hypertrophic obstructive cardiomyopathy – if septal
Second-Degree AV Block ablation is complicated by 2° or 3° AV block or slow
junctional rhythm; or in drug-refractory patients
Mobitz Type I AV block (Wenckebach) in young unsuitable for septal ablation
Cardiac resynchronization therapy
people, especially if transient or nocturnal, is
Post-cardiac transplantationa
probably due to increased vagal tone and pacing
Pediatrics and congenital heart diseasea
is not indicated. In older people, the incidence of a
See text
symptoms and the prognosis is not dissimilar to b
In symptomatic patients or where considered that there is
Mobitz Type II AV block and pacing is indicated a high likelihood of progression to 2°, 3° AV block, slow
(Fig. 4.4). An exception may be adults who have junctional escape rhythm, or asystole

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 59


DOI 10.1007/978-1-4471-2939-4_4, © Springer-Verlag London 2012
60 4 Permanent Pacemaker Implantation for Bradycardias: Indications

Fig. 4.1 First-degree AV


block in a patient with
previous inferior MI

Fig. 4.2 First-degree AV


block in an asymptomatic
sportsman
Second-Degree AV Block 61

Fig. 4.3 Alternating LBBB


(left upper panel) and RBBB
(right upper panel), followed
by complete heart block
(central lower panel)

Fig. 4.4 Wenckebach Mobitz


Type I second-degree AV
block
62 4 Permanent Pacemaker Implantation for Bradycardias: Indications

Fig. 4.5 Mobitz Type II AV


block

Fig. 4.6 Third-degree AV


block or complete heart block

Mobitz Type II AV block is associated with a AV block resolves, the prognosis for future AV
high incidence of complete AV block and patients block or ventricular asystole is even less certain
with this arrhythmia should be paced permanently – but those having had anterior MI and transient
(Fig. 4.5). Perhaps the only exception is follow- second-/third-degree infranodal AV block but
ing an acute inferior MI, when second- and third- new onset BBB should probably also be paced.
degree AV block may resolve within the next
2 weeks. However, after an acute anterior MI,
these bradyarrhythmias reflect interventricular Third-Degree AV Block
septal infarction/necrosis and carry a high risk of
asystole, and those patients with persistent Mobitz This is usually due to conducting tissue fibrosis
Type II AV block should be permanently paced. (Fig. 4.6). Frequently the QRS complex is wide.
For those patients in whom second-/third-degree Other causes are shown in Table 4.1. Patients
Sick Sinus Syndrome 63

Fig. 4.7 Bifascicular block –


RBBB + LAFB with a normal
PR interval

should be paced whether they are symptomatic or Evidence of bifascicular block includes
not. Prognosis has been shown to be improved by RBBB + left anterior fascicular block (LAFB)
pacing (1-year mortality: 35–50% unpaced vs. (Fig. 4.7) and RBBB + left posterior fascicular
5% paced), and a first Stokes–Adams attack may block (LPFB) or complete LBBB alone
be fatal. (Fig. 4.8).
Complete AV block may be congenital. Here, Trifascicular disease means impaired conduc-
the level of block is higher in the His bundle or tion in all three branches at the same time, although
AV node and the QRS is narrow. Any idioven- it has been used to describe bifascicular block
tricular rhythm is usually faster than in the together with first-degree AV block (Figs. 4.9
acquired form, and it responds more to exercise and 4.10). Alternating RBBB + LBBB, RBBB +
and other autonomic stimuli. Pacing is usually alternating LAFB/LPFB, or LBBB +long PR in-
only considered necessary if associated with a terval on the same or successive ECGs are prob-
wide QRS complex, the development of brady- ably evidence of trifascicular disease.
cardia-related symptoms, if the rate fails to rise
on exercise, or if the resting junctional rate is
<50 bpm. Sick Sinus Syndrome
Second-degree or complete AV block associ-
ated with myotonic muscular dystrophy, Kearns– Sinoatrial disease may result in sick sinus
Sayre syndrome, etc., and when occurring after syndrome or “tachy–brady” syndrome. Sick
catheter ablation of the AV node or after valve sinus syndrome may be manifest as prolonged
surgery when block is not expected to resolve are sinus arrest (Fig. 4.11) or sino-atrial block
all indications for pacing. separately or combined with paroxysmal atrial
tachycardia, flutter or fibrillation (Fig. 4.12)
in the “tachy–brady” syndrome. It may also
Bundle-Branch Block coexist with AV block perhaps as a manifesta-
tion of generalized conducting tissue fibrosis
Patients with bradycardia-related symptoms (Fig. 4.13) and even ventricular arrhythmias
and evidence of bifascicular or trifascicular (Fig. 4.14). Pacing is indicated for symptoms
block should be paced. Asymptomatic patients associated with a bradycardia. Although prog-
should be treated conservatively unless evi- nosis is probably not improved by pacing,
dence of progressive AV conduction block, such the incidence of stroke and the onset of atrial
as progressive lengthening of the PR interval, is fibrillation may be diminished by atrial-based
evident. pacing.
64 4 Permanent Pacemaker Implantation for Bradycardias: Indications

Fig. 4.8 Left bundle branch


block (LBBB)

Fig. 4.9 Tri-fascicular block


(RBBB + LAFB) with a
prolonged PR interval

Carotid Sinus Hypersensitivity charge as a result of stimulation of the carotid


and Malignant Vasovagal sinus causes unusually profound sinus brady-
Syndrome (MVS) cardia/sinus arrest and in MVS profound
peripheral vasodilatation resulting in severe
These two conditions, members of a group of hypotension (Fig. 4.15). Syncope after turning
conditions known as neurocardiogenic syncope, the neck or on looking vertically upward should
are relatively uncommon. Intense vagal dis- alert one to the diagnosis. A ventricular pause
Carotid Sinus Hypersensitivity and Malignant Vasovagal Syndrome (MVS) 65

Fig. 4.10 Tri-fascicular


block (RBBB + LPFB) with a
prolonged PR interval

Fig. 4.11 Sick sinus


syndrome manifested by
prolonged sinus arrest.
First-degree and possible
Mobitz Type I (Wenckebach)
AV block indicate additional
AV nodal disease

lasting 3s or more and a fall in systolic blood Measures such as support stockings and avoid-
pressure of 50 mmHg or more is considered ance of dehydration are essential in MVS. Patients
abnormal and defines carotid sinus hypersensi- with MVS also require reassurance and education
tivity. Dual-chamber pacing may be indicated regarding the benign nature of the condition, but
for those with recurrent vasovagal syncope and based on the medical history they should also be
prolonged asystole during Holter recording informed of the likelihood of syncope recurrence.
and/or tilt testing and might improve the symp- Recognition of any associated premonitory symp-
toms. Loop recorders might help identify those toms which allows them to recognize an impend-
most likely to benefit from pacing by docu- ing episode might prompt them to sit or lie down
menting evidence of severe bradycardia/asys- or use isometric maneuvers to avert or limit the
tole coinciding with the patient’s symptoms. consequence of a loss of consciousness.
66 4 Permanent Pacemaker Implantation for Bradycardias: Indications

Fig. 4.12 Sick sinus syndrome manifesting with sinus arrest and paroxysmal atrial flutter and fibrillation

Hypertrophic Obstructive apex alters septal motion significantly (Figs. 3.7


Cardiomyopathy and 4.16). This has been shown to reduce symp-
toms. However, recent randomized trial data
In symptomatic patients, AV synchronous pacing (M-PATHY) have suggested that pacing alone
with a short AV delay may help to reduce the sub- may not benefit all patients with HOCM.
aortic gradient in hypertrophic obstructive cardi- Although alcohol-induced septal ablation
omyopathy (HOCM) since pacing from the RV may be very effective treatment for HOCM,
Hypertrophic Obstructive Cardiomyopathy 67

Fig. 4.13 Sick sinus


syndrome may be associated
with AV block as well. These
ECG strips show progressive
increase of PR interval and
sinus arrest (top) and
complete heart block
(bottom)

Fig. 4.14 The “tachy–brady” syndrome may manifest as atrial fibrillation with markedly variable ventricular rates and
ventricular arrhythmias

temporary pacemaker insertion is usually nec- fascicular block as a result of the septal
essary during the procedure because of an inci- infarction and necrosis.
dence of AV block of 10%. In 7–10% of DDD pacing may also be considered in
patients, permanent DDD pacing will be patients with contraindications for septal ablation
required for persistent 2° or 3° AV block or fol- or myectomy or in those requiring pacing for bra-
lowing the development of new bi- or tri- dycardia or with an indication for ICD implanta-
68 4 Permanent Pacemaker Implantation for Bradycardias: Indications

Fig. 4.15 Hypersensitive


carotid sinus syndrome.
Carotid sinus massage
produces sinus bradycardia
and then prolonged asystole
and near syncope

patient’s hemodynamic state. In such a situation,


insertion of actively fixed atrial and ventricular
electrodes and implantation of a permanent DDD
pacemaker may be lifesaving (see Fig. 3.10).

Post-Cardiac Transplantation

Symptomatic bradyarrhythmias due to sinus node


dysfunction or AV block 3 weeks after cardiac
transplantation or chronotropic incompetence
impeding quality of life are indications for pacing.

Fig. 4.16 Position of permanent right atrial and right Pediatrics and Congenital
ventricular lead in a patient with HOCM Heart Disease

Class I indications for pacing include congenital


tion. It may also be indicated in elderly patients 3° AV block associated with any of the following
with drug-refractory HOCM. conditions: symptoms, ventricular rates <50–55/
min, ventricular rates <70/min in congenital heart
disease, ventricular dysfunction, wide QRS escape
Cardiogenic Shock and AV Block rhythm, complex ventricular ectopy, abrupt ven-
Post Myocardial Infarction tricular pauses >2–3× basic cycle length, prolonged
QTc, or presence of maternal antibodies-mediated
Occasionally in patients with 2º or 3º AV block post block. Other indications include 2° or 3° AV block
myocardial infarction who are in cardiogenic shock, with symptomatic bradycardia or ventricular dys-
only restoration of AV synchrony will lead to an function, postoperative Mobitz type II 2° or 3° AV
improvement in cardiac output and survival may be block which persists at least 7 days after cardiac
dependent on maintaining it. Temporary atrial elec- surgery, and symptomatic sinus node dysfunction.
trodes are liable to displacement, and this may lead Class IIa indications include asymptomatic
to a sudden catastrophic deterioration in the sinus bradycardia in the child with complex
European Society of Cardiology and European Heart Rhythm Association Guidelines 69

congenital heart disease and resting heart rate <40/ block, in chronic bifascicular and trifascicular
min or pauses >3 s; bradycardia–tachycardia syn- block, after myocardial infarction, in carotid
drome requiring antiarrhythmic drugs; long-QT sinus syndrome, in vasovagal syncope, in pedi-
syndrome with 2° or 3° AV block, symptomatic atrics and congenital heart disease, after cardiac
bradycardia, or pause-dependent VT; congenital transplantation, and in hypertrophic cardio-
heart disease and impaired hemodynamics due to myopathy. They also present their recommen-
sinus bradycardia or loss of AV synchrony. Class dations for the use of biventricular pacemakers
IIb indications include congenital 3° AV block (with and without ICD) for patients with heart
without a Class I indication; transient postopera- failure.
tive 3° AV block with residual bifascicular block; The ESC/EHRA present the Class of
asymptomatic sinus bradycardia in the adolescent Recommendation and the Level of Evidence for
with congenital heart disease and resting heart each clinical indication, and these are available
rate <40/min or pauses >3 s; and neuromuscu- on the ESC website: www.escardio.org. More
lar diseases with any degree of AV block without recently, the AHA/ACC 2008 guidelines were
symptoms. similarly published on the HRS website: www.
hrsonline.org.

European Society of Cardiology


and European Heart Rhythm
Association Guidelines

The ESC/EHRA and the ACC/AHA have issued


guidelines for the appropriate use of pacemaker
devices in sinus node disease, in acquired AV
Investigations Prior to Pacing
5

A classification of syncope is shown in Table 5.1 Table 5.1 (continued)


and guidelines on the diagnosis and management Micturition
of syncope have been produced by the ESC in Post-exercise
2009 and are available on the website www. Post-prandial
escardio.org. Others (laughing, playing brass instruments,
A clinical history of sudden unprovoked diz- weightlifting)
ziness, faintness, or syncope should alert the Carotid sinus syncope
physician to the possibility of significant bra- Atypical forms (without apparent triggers and/or
atypical presentation)
dyarrhythmias or tachyarrhythmias. The history
Syncope due to orthostatic hypotension
might suggest a reflex/neurally mediated cause, Primary autonomic failure
syncope due to orthostatic hypotension, or true Pure autonomic failure, multiple system atrophy,
cardiac syncope. A witnessed event should be Parkinson’s disease with autonomic failure
researched carefully by talking to the patient Secondary autonomic failure
and to the witness, if at all possible. The report Diabetes, amyloidosis, uremia, spinal cord injuries
of “a very slow pulse” might suggest a need for Drug-induced orthostatic hypotension
permanent pacemaker implantation although Alcohol, vasodilators, diuretics, antidepressants
a vaso-vagal episode might also explain the Volume depletion
event and pacing would then be inappropriate. Hemorrhage, diarrhea, vomiting, dehydration, etc.
Carotid sinus massage producing prolonged Cardiac syncope (cardiovascular)
sinus arrest, ventricular asystole or 2° or 3° AV Arrhythmia as primary cause
block in a patient with symptoms suggestive Bradycardia
Sinus node dysfunction
of cardiac presyncope or syncope may well be
AV conduction tissue disease
Implanted device malfunction
Tachycardia
Table 5.1 Classification of syncope
Supraventricular
Reflex (neurally-mediated) syncope Ventricular (idiopathic, secondary to structural
Vasovagal heart disease or to channelopathies)
Mediated by fear, pain, emotional distress, instru- Drug-induced bradycardia or tachyarrhythmias
mentation, blood phobia Structural disease
Mediated by orthostatic stress Cardiac: valvular disease, acute MI/ischemia,
Situational HOCM, cardiac tumors, pericardial disease/
Cough, sneeze tamponade, prosthetic valve dysfunction
Gastrointestinal stimulation (swallowing, defecation, Others: pulmonary embolus, acute aortic
visceral pain) dissection, pulmonary arterial hypertension

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 71


DOI 10.1007/978-1-4471-2939-4_5, © Springer-Verlag London 2012
72 5 Investigations Prior to Pacing

CSM

Fig. 5.1 ECG during carotid sinus massage (CSM) shows inducible prolonged sinus arrest

evidence sufficient to justify pacing (Fig. 5.1). in the assessment of patients with unexplained
However, generally speaking, unmonitored syncope.
patients with such symptoms and a negative
response to carotid sinus massage will require
further investigations to support the need for Electrocardiogram
permanent pacing. These investigations include
a 12-lead electrocardiogram, continuous Holter A 12-lead ECG may demonstrate evidence of 2°
ECG monitoring, event ECG recorders, exter- or 3° AV block or junctional rhythm which would
nal ECG loop recorders and implantable ECG be sufficient to indicate the need for pacing in a
loop recorders (Table 5.2). Tilt table testing is symptomatic patient. Evidence of bi- or trifas-
indicated in the case of an unexplained single cicular block or progressive lengthening of the
syncopal episode in high risk settings, e.g., PR interval in a patient with LBBB (on serial
risk of injury, pilots, or recurrent episodes in ECGs) should raise suspicion of the need for pac-
the absence of organic heart disease, or in the ing (Fig. 5.2).
presence of organic heart disease after cardiac
causes of syncope have been excluded. It is also
indicated for discriminating between reflex and Holter Monitoring
orthostatic hypotension induced syncope and
Continuous ECG monitoring may be useful in
Table 5.2 Types of investigations available for detecting
patients with fairly frequent symptoms but a
bradyarrhythmias or tachyarrhythmias responsible for normal 12-lead ECG or abnormalities sugges-
dizziness or syncope tive of significant AV conduction abnormality,
12-lead ECG e.g. RBBB, LAD, and long PR interval or evi-
Continuous ECG “Holter” monitoring dence of sick sinus syndrome, e.g., sinus arrest
Event recorders or sino-atrial block. Mechanical tape recorders
External event recorder still exist which magnetically record the ECG
Post-symptom onset as an analog signal on cassette tape (C60/C90)
External loop recorders (Fig. 5.3), but these have virtually been replaced
Pre/post-symptom onset by “solid-state” devices which record the ECG
Implantable loop recorders digitally on memory cards within the recorder.
Pre/post-symptom Direct digital recordings avoid the artifacts that
Tilt table test may be produced by mechanical recorders and
Event Recorders 73

Fig. 5.2 12-lead ECG


showing bifascicular block

can record 1–3 channel ECG for 8–11 days. This


device measures 8.6 × 5.4 × 1.9 cm, weighs 100 g,
and can be worn around the neck attached to the
patient by the special 5-lead cable (Fig. 5.10).
The HOLTERSOFT ULTIMA Windows™-
based software platform has fast analysis mod-
ules based on powerful technologies (Wavelets
Transform, Fractal Analysis) for providing
analysis of arrhythmias, heart rate variability,
ST, QT, and QT variability, pacemaker rhythms,
Fig. 5.3 Analog 24 h Holter ECG recorder using and automatic detection of AF episodes and sleep
cassette tape apnea. The Vista Plus also has a microphone to
allow patients to record voice messages during
the limitations of data recorded in analog for- the recording.
mat. Some can record continuous ECG from
between 24 h and 11 days. Some devices have
an “event-marker” button which the patient can Event Recorders
use to identify the onset of symptoms such as
dizziness. These devices are useful for patients with less
The Vision™ 5L (Burdick®) weighs 112 g and frequent symptoms of dizziness or presyncope.
can record high quality 3-channel ECG for up to
48 h on a compact flash card. Data can be down-
loaded and analyzed rapidly using Vision Premier External “Post-symptom” Event
software on a Windows-based PC (Figs. 5.4 and Recorders
5.5). Figures 5.6–5.9 show four examples of
downloaded ECG traces showing prolonged sinus These small portable devices are kept in the
arrest, Mobitz Type I and Mobitz Type II second continual possession of the patient during the
degree AV block, and severe nodal bradycardia, prolonged monitoring period. During symptoms,
respectively. The Vista Plus device (Novacor) the patient places the device on the chest and
74 5 Investigations Prior to Pacing

Fig. 5.5 Vision™ 5L recorder and its card reader


(Burdick®)

starts the recorder by pressing an activation but-


ton. After a 10 s or so sample of ECG (usually a
single lead rhythm strip) has been recorded, this
can be transmitted to the monitoring station as
per instructions. The patient keeps the device
until several recordings have been made or for an
agreed period (maybe 2–6 weeks). These devices
only allow capture of data once the activation
button has been pressed and studies have shown
that short-lived arrhythmias may frequently be
missed by these “post-symptom onset”
recorders.
The CorDigital® Micro ER® (Instromedix®)
recorder/transmitter weighs only 42 g and
fits into a patient’s pocket, purse or handbag
(Fig. 5.11). At the onset of symptoms, the
patient simply holds the device on the chest and
presses the “record” button, which records and
stores 32s of real-time ECG in solid-state mem-
Fig. 5.4 Vision™ 5L Holter ECG recorder (Burdick®) ory. Six events can be stored before it is neces-
uses digital technology to store ECG signals on a memory
sary to transmit the information to the receiving
card (single arrow) which can be inserted in a card reader
(twin arrow) and displayed on a Windows-based PC center. The Cardiocall VS20 device
(SPACELABS Healthcare) can be used as a
Event Recorders 75

Fig. 5.6 3-channel ECG showing sinus arrest

Fig. 5.7 3-channel ECG showing Mobitz Type I second degree AV block

Fig. 5.8 3-channel ECG showing Mobitz Type II second degree AV block
76 5 Investigations Prior to Pacing

Fig. 5.9 3-channel ECG showing a slow ventricular escape rhythm. P-waves are probably visible with a rate similar or
slightly slower rate than the QRS complexes, but the P-waves and QRS complexes are independent of each other

Fig. 5.10 Vista plus device (Novacor)

simple event recorder. For “post-symptom” and pressing a “send” button on the recorder.
event recorders, transmission of the ECG The Cardiobeeper shown in Fig. 5.12 is a simi-
rhythm is usually done by dialing up the receiv- lar, earlier Event Recorder. The ECG recording
ing center, holding the recorder over the mouth- is received and printed out at the receiving cen-
piece of the patient’s own telephone handset ter (Fig. 5.13).
Event Recorders 77

Fig. 5.13 The saved ECG strip is then played to a record-


ing center over a standard telephone line

lead ECG. When an arrhythmia is felt, he/she is


Fig. 5.11 The CorDigital MicroER ®
event recorder able to activate a record feature that has been pro-
(Instromedix®) grammed for that particular individual. For
example, this might enable capture of the ECG
for any set period up to and including the event
and after the event as a loop of ECG. If no event
is detected, the loop is continually renewed and
erased. Later, when a telephone is accessible, the
patient can transmit the captured information
from the memory to the monitoring station. These
devices are useful for patients with syncope,
since the record button can be pressed once con-
sciousness has been regained, which will capture
the ECG prior to, during, and after the symptoms.
Some devices can also be programmed to auto-
matically record one or more specific
arrhythmias.
The CorDigital Micro LR™ (Instromedix®)
(Fig. 5.14) can store up to 6 events totaling 524 s
and has a battery life of 62 days or 150 record-
Fig. 5.12 The Cardiobeeper event ECG recorder is held
on the chest and activated by pressing a button ings. The King of Hearts Express™ (Instromedix®)
(Fig. 5.14) is a small and easy to use, program-
mable device and can be worn on the waist, in the
External “Pre-/Post-symptom” Event shirt pocket, or on a cord around the neck. To
Loop Recorders record an event, the patient presses the RECORD
button and to transmit the event simply dials up
These devices are useful for intermittent symp- the receiving center by telephone and places the
toms which are short-lived, when other recorders device over the telephone’s mouthpiece to trans-
have proved unsuccessful in capturing an event. mit the stored ECG for analysis. The R Test
The patient wears the digital recorder and elec- Evolution 3 (Novacor) weighs 45 g and is fully
trodes over a period of a few days to several programmable to automatically capture a variety
weeks (2–4 weeks), constantly recording a 1–3 of cardiac arrhythmias, ST shifts, and pacemaker
78 5 Investigations Prior to Pacing

Fig. 5.14 (Top left) The Genesis™ (Lechnologies Research Inc.), (top right) CorDigital Micro LR™, (bottom left)
King of Hearts Express, and (bottom right) Express II external ECG loop recorders (Instromedix®)

spikes with programmable pre- and post-event It has three times more programmable memory –
times (Figs. 5.15 and 5.16). It features transmis- up to 60 min available for detected ECG strips
sion by transtelephonic modulation, either real- and the new R.TSoft software platform. The
time transmission of the ECG or transmission of recorders cost approximately £2,000, although
recorded strips using NovaDrive – a freeware the monitor/analysis system is extra.
which allows R Test programming and reading. The Recollect™ mini Holter ECG recorder
The program can be installed on any PC and can provide continuous looping ECG recordings
transmission enabled by direct connection to for a week or more or for patient-activated
modem or by e-mail. The R Test Evolution 4 application for longer. This device allows the car-
(Novacor) offers additional advantages, includ- diologist to collect automatic recordings at
ing improved signal resolution of 200 Hz, specified times in addition to patient-activated
Advanced Wavelet Technology for improved recordings. Single- or dual-channel ECGs can
accuracy, greater loop memory from 4 to 5 min, help in clarifying the nature of any arrhythmia.
improved battery life allowing continuous moni- The data is stored on a memory card which can
toring, and automatic arrhythmia detection up to then be plugged into a Windows-based PC for
16–32 days with a change of batteries (Fig. 5.17). generation of a report.
Implantable Loop Recorders 79

Implantable Loop Recorders

The Reveal® loop recorder (Medtronic Inc.)


(Fig. 5.18) is an implantable, patient-activated
monitoring device which continually records sub-
cutaneous ECG and is indicated for patients who
experience transient symptoms that may suggest
an arrhythmia and for those with clinical syn-
dromes or situations that put them at risk of car-

Fig. 5.15 The R Test 3 Evolution external ECG loop


recorder can be worn around the neck (Novacor)

Fig. 5.16 The R Test 3 Evolution device (Novacor)

Fig. 5.17 The R Test 4 Evolution device (Novacor)


80 5 Investigations Prior to Pacing

Fig. 5.18 The Reveal® Plus implantable loop recorder Fig. 5.19 Implantation of a Reveal® device under local
(Medtronic Inc.) anesthesia and asepsis

Fig. 5.20 Chest X-ray shows a Reveal® device placed


parasternally

diac arrhythmias. The device is 6.2 × 1.9 × 0.8 cm,


9 cc in volume, weighs 15 g, and has two bipo-
lar sensing leads 3.7 cm apart within the shell of Fig. 5.21 Activator applied over Reveal® device can put
the recorded rhythm strip into a “memory loop” store
the device. Under local anesthesia, the device
is placed vertically pre-pectorally in the left
parasternal region (Fig. 5.19). Often the position There are two models currently available from
of the device is marked before implantation by Medtronic Inc. – Reveal® DX and Reveal® XT
analyzing the R-wave to ensure relevant data cap- (Fig. 5.22). Both have a patient activation (using the
ture. Figure 5.20 shows a chest X-ray in a patient Patient Assistant) and an autoactivation mode, when
with an implanted Reveal® device. When symp- rhythms may be automatically recorded when the
toms occur, the patient can place a hand-held heart rate exceeds or falls below a certain preset
activator over the device to activate storage of a limit (see Fig. 5.22). Both possess 42 min of mem-
memory loop of the cardiac rhythm (Fig. 5.21). ory for standard ECG, have a high (60–88%) diag-
The pre-activation and post-activation periods nostic yield, and are cost-effective compared to
are programmable. conventional testing-based treatments. The device
Implantable Loop Recorders 81

a b c d

Fig. 5.22 Reveal® DX (top left) and Reveal® XT (top are shown here (bottom). The recording is continuous
middle) are the latest implantable loop recorders from from a-d and resulted in permanent pacemaker implanta-
Medtronic. The Patient Assistant (top right) is the new tion in this patient with infrequent syncope. It was detected
patient-held activating device. Automatic recording of on routine interrogation prior to removal
periods of asystole from an implanted Reveal® XT device

can be programmed and data is retrieved using the Trends offers 14 months of rhythm data including
portable Medtronic 9790 Programmer. Up to 3 years daily AF burden, ventricular rate during AT/AF,
of monitoring is possible. The Reveal® devices are heart rate variability, and average day and night
MR-conditional safe, i.e., safe in standard MRI con- rates. Moreover, these devices can be remotely
ditions. Ideally, however, patients should avoid monitored using the Medtronic Carelink® Network.
sources of diathermy, high energy sources of radia- The devices should be removed under local anes-
tion, electrosurgical cautery, defibrillation, litho- thesia once the relevant diagnostic information has
tripsy, and radiofrequency ablation to avoid damage been revealed or when the battery is depleted.
to the device and/or inappropriate sensing. Their cost is approximately £1,450.
The Reveal® DX can be set up to autoclassify St. Jude Medical have the SJM Confirm™
episodes as bradycardia, asystole, ventricular tach- (Model DM2100) implantable cardiac monitor
yarrhythmia, or fast ventricular tachyarrhythmia. which is slightly smaller (Fig. 5.23). It measures
The Reveal® XT has an exclusive AF detection 5.6 × 1.8 × 0.8 cm, has a volume of 6.5 cc, and
algorithm for detecting episodes of atrial tachycar- weighs 12 g, and has an excellent longevity of
dia and atrial fibrillation. It can assess the AF bur- 3 years. It boasts Proven SenseAbility™ for
den and the ventricular rates during episodes in increased sensitivity, a number of data storage
order to guide treatment. Cardiac Compass® options for flexibility as well as automatic and
82 5 Investigations Prior to Pacing

Fig. 5.23 The Confirm® device (St. Jude Medical)

patient-activated options for electrogram cap-


ture and storage. The patient-activated option
requires a “Patient Activator” which has to be
held over the device and activated by pressing a
button. It has additional programming options
for tachycardias, bradycardias, and asystole.
The Merlin™ Patient Care System provides
communication, data retrieval, and programming
capabilities (Fig. 5.24).

Cardionetics C.Net5000

The Cardionetics C.Net5000 is a 24-h ambula-


tory ECG monitor with instant automated anal- Fig. 5.24 The Merlin™ Patient Care System (Image pro-
ysis, designed specifically for use in general vided courtesy of St. Jude Medical, © 2008 St. Jude
practice to assist in the early detection of cardiac Medical, Inc.)
arrhythmias. The three electrode configuration
is easy to fit (Fig. 5.25). A test is started with a
single button press. The C.Net5000 features fully mia detected. Using the included Cardionetics
automatic ECG analysis. The C.Net5000 is able Connect software, the report can be downloaded
to automatically detect significant arrhythmias to a PC for printing, review, and attaching to the
such as atrial fibrillation (AF), ventricular ecto- patient record.
pic beats, pauses and arrests, and wide-complex
tachycardias (including VT). The ECG trace is
shown in real time on the LCD screen, allow- Tilt Table Testing
ing cardiac events to be observed as they occur
(Fig. 5.26). The C.Net5000 analyses the sig- Tilt testing enables the reproduction of a neu-
nal and automatically records examples of any rally-mediated reflex in a laboratory setting.
arrhythmia detected. The keypad and LCD screen Blood pooling and decrease in venous return
can be locked to prevent the patient from view- due to orthostatic stress and immobilization
ing the ECG trace or interfering with the monitor trigger the reflex. The final effect, hypotension
during the test. The patient can press the symp- and usually concomitant heart rate slowing, is
tom button when they experience symptoms, and related to impaired vasoconstrictor capability
the C.Net5000 will record an ECG trace. At the followed by sympathetic withdrawal and vagal
end of the test, the analysis results can be viewed overactivity. The clinical situation correspond-
on the LCD screen, without requiring connection ing to tilt testing is reflex syncope triggered by
to a computer. The on-screen report shows prolonged standing. However, this test can also
example traces of the most significant arrhyth- be positive in patients with other forms of reflex
Tilt Table Testing 83

Fig. 5.26 Cardionetics C.Net5000 ECG recorder

Fig. 5.25 Cardionetics C.Net5000 Holter ECG recorder


attached to a patient using three electrodes cannulation a further period of 20 min supine is
recommended. The tilt table is then tilted to
between 60–80° (Fig. 5.28) for 45 min during
syncope and in patients with sick sinus careful ECG and BP monitoring (Fig. 5.29). The
syndrome. induction of reflex hypotension/bradycardia with
A modern tilt table will have a foot plate sup- reproduction of syncope or progressive orthos-
port and be electrically powered to allow rapid tatic hypotension (with or without symptoms)
achievement of upright and supine posture as are diagnostic of reflex syncope and orthostatic
well as calibrated tilt angles of between 60–80° hypotension, respectively. Isoproteronol or
(Fig. 5.27). ECG and blood pressure monitoring glyceryl trinitrate can be given to further test
should be continuous. A supine pre-tilt phase of patients whose test remains normal after
at least 5 min is recommended and after venous 40 min.
84 5 Investigations Prior to Pacing

Fig. 5.27 (Left) This electric tilt table is comfortably (CNSystems) is ideal for tilt table testing offering a
upholstered, has a foot rest, restraining straps, and an arm 6-channel display including a high resolution 3-channel
rest. The table can be tilted electrically from the horizon- ECG and CNAP™ or continuous noninvasive arterial
tal to the vertical position and also into –15° head-down pressure monitoring. A high-fidelity BP waveform is dis-
tilt. The table is usually positioned between 70 and 85° for played alongside real-time SBP, DBP, and mean BP
the tilt phase of the test. (Right) The Task Force® Monitor
Tilt Table Testing 85

Fig. 5.28 (Left) Patient secured in horizontal position on tilt table has pulse and BP measuring device on right arm/
hand. (Right) Patient is tilted to 70° while ECG and hemodynamics are monitored by two cardiac physiologists

Fig. 5.29 Task Force® monitor displays 2-channel ECG, arterial pressure waveform, and continuous SBP, DBP, and
mean BP – graphically and numerically
Permanent Pacemakers and Leads
6

Permanent Pacemaker Code (NBG) The third position denotes the response of the
pacemaker to the sensed information. This posi-
A 5-Position NBG (NASPE/ BPEG Generic) tion is directly tied into position 2. Without sens-
Code is used internationally to describe the vari- ing, there can be no mode of response to
ous pacemaker functions (Table 6.1). sensing.
The first position identifies the chamber(s) I = that the pacemaker output is inhibited by a
that is paced. sensed event. Thus, in a VVI pacemaker, the
A = atrium; V = ventricle; D = Dual, when both pacemaker senses a ventricular event and with-
atrium and ventricle can be paced. O = None. holds the ventricular output. In DDI mode, the
A device used to pace in only one chamber pacemaker simply inhibits the output of the
will be represented by either the letter A (atrium) device in the chamber where any signal is sensed.
or V (ventricle), whereas devices that are capable In the presence of a fast atrial rate and heart block,
of pacing in both chambers are represented by the the DDI pacemaker rhythm will resemble a VVI
letter D (dual). Some pacemakers allow pacing to device.
be turned OFF for diagnostic purposes, and, T = that pacing is triggered by a sensed event.
while turned off, the position 1 coding is O. This is rarely used now, but it can be useful for
There is a code letter S that identifies the pace- observing the location of sensing of intrinsic
maker as a single chamber device, which can be events. Thus if a sensing problem is suspected,
used to pace either the atrium or ventricle. This is programming to a triggered mode may show
only used as the manufacturer’s designation and exactly where in the timing of the device the
is not valid once the pacemaker is connected to a sensing abnormality is occurring. Triggered pac-
pacing lead. ing will produce pacemaker spikes concurrently
The second position indicates the chamber(s) with intrinsic sensed events (pseudo-fusion
whose intrinsic activity is sensed. A = atrium; beats).
V = ventricle; D = both atrium and ventricle; D = that ventricular sensed events inhibit pace-
O = the pacemaker is incapable of sensing. For maker output while atrial sensed events trigger
example, VDD represents a pacemaker in which ventricular stimulation. Thus, D indicates that the
the ventricle is the chamber paced, but that the device will respond to the sensed signal by inhib-
device is capable of sensing in both atrium and iting the pacemaker response, tracking the sensed
ventricle. As for position 1, S identifies the device event, or inhibiting the output on the sensed chan-
as a single chamber device, which can be used in nel and triggering an output to maintain AV syn-
either atrium or ventricle but is only used as the chrony. For example, in a DDD pacemaker, a
manufacturer’s designation and is not used once sensed atrial signal will cause the device to inhibit
the pacemaker and lead are attached. the atrial output, a timer then starts that will cause

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 87


DOI 10.1007/978-1-4471-2939-4_6, © Springer-Verlag London 2012
88 6 Permanent Pacemakers and Leads

Table 6.1 The NASPE/BPEG generic (NBG) code


Position I II III IV V
Mode Programmable Antitachycardia
Category Chamber paced Chamber sensed of response functions functions
NBG code V = Ventricle V = Ventricle T = Triggered R = Rate Modulated O = None
A = Atrium A = Atrium I = Inhibited C = Communicating P = Paced
D = Dual (A&V) D = Dual (A&V) D = Dual (T&I) M = Multiprogrammable S = Shocks
O = None O = None O = None P = Simple programmable D = Dual (P&S)
O = None
Manufacturer S = Single (A or V) S = Single (A or V)
designation
only
NASPE was the North American Society of Pacing and Electrophysiology – now Heart Rhythm Society (HRS)
BPEG was the British Pacing and Electrophysiology Group – now Heart Rhythm UK (HRUK)

a triggered ventricular output after a certain inter- ters available. P = simple programmable, usually
val unless an intrinsic ventricular complex arises. indicates that the pacemaker is limited to three or
If the patient has an intrinsic R wave during the fewer programmable parameters. This letter in
triggering period, the pacemaker will inhibit the the fourth position is limited to single chamber
ventricular output. devices. Typical simple programmable parame-
O = that there is no response to sensed events. ters include: rate, output, and sensing. O = none,
During magnet application to most pacemakers, is rarely encountered now, and indicates that the
the sensing function is temporarily switched device has no programmable features.
OFF and the device operates in an asynchronous It should be appreciated that the fourth posi-
or fixed rate mode. AOO, VOO, and DOO are tion is hierarchical in nature. For example, a VVIR
examples of fixed rate modes. Clearly the sec- pacemaker can be assumed to be, in addition to
ond and third positions are “tied together,” since rate-responsive, communicating (the sensor needs
if there is no sensing, there is no mode of to be programmable) and multiprogrammable
response. (there are usually several things to be programmed
The fourth position indicates something about on sensor-driven devices). Similarly, a DDD pace-
the programmable parameters of the pacemaker, maker can be assumed to be communicating and
whether it has a sensor to regulate the rate during multiprogrammable since many parameters need
periods of physical activity, whether and how it to be programmed. Obviously, any device that is
can be programmed, and whether it is possible to labeled with a P or M in the fourth position must
communicate with. R = a rate responsive facility also be communicating.
whereby the pacing rate is adjusted by a sensor The fifth position indicates whether the device
that detects a physiological variable such as has any anti-tachycardia features. Most bradycar-
physical activity or respiration. C = communicat- dia devices do not and are automatically assumed
ing and indicates that the pacemaker is capable of to be O devices. Some “brady-devices” do have
transmitting and/or receiving data for informa- limited anti-tachycardia capability and this posi-
tional or programming purposes. Most, if not all, tion allows this to be identified. In the pacemaker-
devices currently manufactured have a communi- only patient, the fifth position can only be
cating ability. M = multiprogrammable, indicates represented by O or P. The pacemaker either has
that the device can be programmed in more than no anti-tachycardia feature or it can attempt to
three parameters. All DDD pacemakers are pro- pace the patient out of a tachycardia episode. The
grammable. Typical programmable parameters fifth position is used fully by ICDs and their abil-
include: rate, sensing, output, refractory periods, ity to pace or shock patients out of tachyarrhyth-
mode, and hysteresis. Dual chamber pacemakers mias. Most current ICDs will be represented by
usually have many more programmable parame- D (dual – shocks and paces) in this position.
Types of Permanent Pacemakers 89

Types of Permanent Pacemakers line battery self-discharge, current drain for


device housekeeping functions, current used to
A pacemaker or pulse generator consists of a pace the heart, and current to sense the underly-
power source connected to microcircuitry which ing heart rhythm. An average pacemaker battery
controls the characteristics and timing of the gen- has about 0.5–2 Ah of battery life. Esprit™ S
erated impulse. The whole is encased in a her- (Sorin) is estimated to have a life expectancy of
metically-sealed titanium “can.” Pacemakers 10.5 years in SSI mode, set at 70 bpm, 2.5 V out-
weigh between 13 and 31 g. Their physical put, 0.5 ms pulse duration, 500 Ω with the Holter
dimensions are shown in Tables 6.2–6.6, but gen- monitor turned “on” whereas the Esprit™ DR
erally have a diameter of <50 mm and a thickness (Sorin) accelerometer-driven, rate responsive
of 6–8 mm. They are considerably smaller and dual chamber device has an estimated life expec-
lighter than the original pacemakers from the tancy of 9 years at the same settings. The power
early 1970s and 1980s (Fig. 6.1). Almost exclu- sources have a predictable, progressive discharge
sively lithium-iodine cells are the power source rate and the residual battery life and the end-of-
for pacemakers and they provide a lifespan of life (EOL) can be accurately estimated and
between 5 and 15 years depending on the com- accessed by the external programmer in the fol-
plexity and versatility of the system, the pro- low-up clinic. Unlike the earlier nickel-cadmium
grammed output, what features are programmed and mercury-zinc batteries, sudden cessation of
“on” and how much the generator is being used. pacing output does not occur with lithium-iodine
For example, modern pacemakers use current not power sources.
only for pacing but also for other functions such The cost of pacemakers varies enormously
as obtaining measurements of diagnostic data, and relates to the complexity and versatility of
measurements made by rate response sensors, the device, its programmability, its additional
and implementation of algorithms, such as for monitoring and diagnostic facility, and the size of
mode switching. Pacemaker battery life therefore the generator. Costs may vary from £800 to
depends on a variety of variables, including base- £5,000 depending on the features offered by the

Table 6.2 Single chamber pacemakers


Pacemaker manufacturer Dimensions
Series/model Weight (g) H × W × D (mm) Volume (cc) Connector (mm)
Biotronik
Talos S 24 51 × 39 × 6 9 IS-1
Effecta S 25 53 × 39 × 6.5 10 IS-1
Boston Scientific
Altrua 20 S206 SSIC 23.6 42 × 42 × 8 10.1 3.2/IS-1
Altrua 50 S508 SSI 21.5 39 × 42 × 8 9.2 IS-1
*Insignia™ devices are only currently available in Germany, Italy, China, Mexico, Indonesia, Taiwan, Peru, and
Ecuador
*Discovery™, Jade™ series no longer available
Medtronic
Sensia SES01 21.5 40 × 43 × 7.5 9.7 IS-1
Vitatron E10 S 21.5 40 × 43 × 7.5 9.7 IS-1
*Sigma™ 100/300, Thera™, and Vitatron C series no longer available
Sorin
Esprit S 19 37 × 41 × 6 7.5 IS-1
St. Jude Medical
Verity XL SC 5056 23 42 × 52 × 6 10.5 IS-1
*Regency SC+ 2402L – limited availability outside of UK
90 6 Permanent Pacemakers and Leads

Table 6.3 Dual chamber pacemakers: atrial synchronized ventricular pacemakers (VDD)
Pacemaker manufacturer Dimensions
Series/model Weight (g) H × W × D (mm) Volume (cc) Connector (mm)
Biotronik
None available
Boston Scientific
Altrua™ 50 S504a 23.5 41 × 42 × 8 10 IS-1
*Insignia devices are only currently available in Germany, Italy, China, Mexico, Indonesia, Taiwan, Peru, and Ecuador
Medtronic
Adapta® AD VDD01 23.6 45 × 43 × 7.5 11.1 IS-1
*Sigma 300 SVDD 301; Kappa 700 KVDD 701; Kappa 900 KVDD 901; and EnPulse E2 VDD01 and Thera VDD
(i-series) series no longer available
Sorin
None available
St. Jude Medical
None available
a
Model with 400 ms AV delay

Table 6.4 Dual chamber pacemakers (DDD)


Pacemaker manufacturer Dimensions
Series/model Weight (g) H × W × D (mm) Volume (cc) Connector (mm)
Biotronik
Talos D 26 51 × 42 × 6 10 IS-1
Effecta D 26 53 × 43 × 6.5 11 IS-1
Boston Scientific
Altrua™ 20 S209 (EL) 29.6 49 × 43 × 8 12.1 IS-1
Altrua™ 50 S503a 25.4 44 × 42 × 8 10.8 IS-1
*Insignia™ devices are only currently available in Germany, Italy, China, Mexico, Indonesia, Taiwan, Peru, and
Ecuador; Discovery™ II DDD no longer available
Medtronic
Sensia® Midsize SED01 27.1 45 × 48 × 7.5 12.1 IS-1
Adapta® Midsize ADD01 27.1 45 × 48 × 7.5 12.1 IS-1
Vitatron E50D 27.1 45 × 48 × 7.5 12.1 IS-1
*Thera D (i-series); Sigma D 300 Series; Kappa 700 DDD Series; Kappa 900 DDD Series; EnPulse and Ruby 3
DDD Series; and Vitatron C50 no longer available
Sorin
Esprit™ D 20 41 × 41 × 6 8 IS-1
Reply™ D 20 41 × 41 × 6 8 IS-1
St. Jude Medical
Identity® ADx XL DC5286 23.5 44 × 52 × 6 11 IS-1
Verity™ ADx XL DC5256 23.5 44 × 52 × 6 11 IS-1
*Affinity™ series no longer available
EL extended life
a
Model with 400 ms AV delay
Table 6.5 Single chamber rate adaptive pacemakers
Pacemaker manufacturer Dimensions
Series Weight (g) H × W × D (mm) Volume (cc) Sensor Connector (mm)
Biotronik
Talos SR 24 51 × 39 × 6 9 Accelerometer IS-1
Effecta SRa 25 53 × 39 × 6.5 10 Accelerometer IS-1
Estella SR/SR-Ta,b 25 53 × 39 × 6.5 10 Accelerometer IS-1
Evia SR-Ta,b 24 53 × 39 × 6.5 11 Accelerometer + CLS IS-1
Axios SLR, Philos II SLR, Protos VR, and Talos SLR no longer available
Types of Permanent Pacemakers

Boston Scientific
Altrua™ 20 S201 23.6 42 × 42 × 8 10.1 Accelerometer 3.2/IS-1
Altrua™ 20 S204 24.9 44 × 47 × 8 11.0 Accelerometer 5/6
Altrua™ 40 S401 23.4 42 × 42 × 8 10 Acc + MV IS-1
Altrua™ 50 S501 23.4 42 × 42 × 8 10 Accelerometer IS-1
Altrua™ 60 S601 23.4 42 × 42 × 8 10 Acc + MV IS-1
*Insignia devices are only currently available in Germany, Italy, China, Mexico, Indonesia, Taiwan, Peru, and Ecuador. Pulsar Max™ II and Discovery™ II SR series no
longer available
Medtronic
Sensia® Midsize SSIR SESR01 21.5 40 × 43 × 7.5 9.7 Accelerometer IS-1
Adapta® Midsize ADSR01 21.5 40 × 43 × 7.5 9.7 Accelerometer IS-1
Adapta® Midsize ADSR06 22.5 43 × 43 × 7.5 11.0 Accelerometer 5/6
Adapta® Midsize ADSR03 22.5 43 × 43 × 7.5 10.5 Accelerometer 3.2
*Sigma300 SSIR Series; Kappa400/700/900 SSIR Series; Thera i-series; EnPulse SSIR Series no longer available
Vitatron G20 SR 21.5 40 × 43 × 7.5 9.7 Accelerometer IS-1
*Clarity SSIR, Topaz 3 SSIR, Vitatron T20SR, and Vitatron C20SR devices no longer available. Clarity SSIR used QT-interval and Accelerometer for providing rate
response
Sorin
Esprit™ SR 19 37 × 41 × 6 7.5 Accelerometer IS-1
Reply™ SR 19 37 × 41 × 6 7.5 MV + accelerometer IS-1
St. Jude Medical
Accent™ SR PM1110 18 42 × 52 × 6 9.5 Accelerometer IS-1
Accent™ SR RF PM1210 23 52 × 52 × 6 12.8 Accelerometer IS-1
Identity® ADx SR5180 17 41 × 44 × 6 8 Accelerometer IS-1
*Identity SR 5172, Integrity ADx SR5160, Integrity SR 5142, Integrity mSR 5136 no longer available
91

(continued)
92
Table 6.5 (continued)
Pacemaker manufacturer Dimensions
Series Weight (g) H × W × D (mm) Volume (cc) Sensor Connector (mm)
Microny IISR+ 2525T 12.8 33 × 33 × 6 5.9 Magnetic ball IS-1
Microny K 2535Kc 12.8 33 × 33 × 6 5.9 Magnetic ball IS-1
*Microny SR + 2425T no longer available ; Regency SR models have limited availability outside of UK; Affinity™ SR models no longer available
Verity™ ADx XL SR5156 23 42 × 52 × 6 10.5 Accelerometer IS-1
Verity™ ADx XL SRM/S5157 23 42 × 52 × 6 11 Accelerometer 5/6 mm
Victory® SR 5610 17 41 × 44 × 6 8 Accelerometer IS-1
Zephyr™ SR 5620 17 41 × 44 × 6 8 Accelerometer IS-1
Zephyr™ XL SR 5626 23 42 × 52 × 6 10.4 Accelerometer IS-1
a
Remote monitoring possible
b
Estella and Evia devices are MRI conditional safe
c
For high base rates in small subjects – requires special order
6
Permanent Pacemakers and Leads
Table 6.6 Dual chamber rate adaptive pacemakers (DDDR)
Pacemaker manufacturer Dimensions
Series Weight (g) H × W × D (mm) Volume (cc) Sensor Connector
Biotronik
Talos DR 26 51 × 42 × 6 10 Accelerometer IS-1
Effecta DR/DR-Ta 26 53 × 43 × 6.5 11 Accelerometer IS-1
Estella DR/DR-Ta 25 53 × 44.5 × 6.5 12 Accelerometer IS-1
EviaDR-Ta,b 25 53 × 44.5 × 6.5 12 Accelerometer + CLS IS-1
Axios™ DR, Philos II DR, Cylos DR, and Protos™ DR/CLS are no longer available
Types of Permanent Pacemakers

Boston Scientific
Altrua™ 20 S203 25.4 44 × 42 × 8 10.8 Accelerometer IS-1
Altrua™ 20 S205 EL 32.3 54 × 49 × 8 14.9 Accelerometer 5/6 mm
Altrua™ 20 S208 EL 29.6 49 × 43 × 8 12.6 Accelerometer IS-1
Altrua™ 40 S403 25.4 44 × 42 × 8 10.8 Acc + MV IS-1
Altrua™ 404 EL 29.6 49 × 43 × 8 12.6 Acc + MV IS-1
Altrua™ 50 S502c 25.4 44 × 42 × 8 10.8 Accelerometer IS-1
Altrua™ 60 S603c 25.4 44 × 42 × 8 10.8 Acc + MV IS-1
Altrua™ 60 S602c EL 29.6 49 × 43 × 8 12.6 Acc + MV IS-1/3.2
Altrua™ 606 EL 29.6 49 × 43 × 8 12.1 Acc + MV IS-1
*Insignia devices are only currently available in Germany, Italy, China, Mexico, Indonesia, Taiwan, Peru, and Ecuador
Medtronic
Sensia® DDDR SEDR01 27.1 45 × 48 × 7.5 12.1 Accelerometer IS-1
Adapta® Midsize ADDR01 27.1 45 × 48 × 7.5 12.1 Accelerometer IS-1
Adapta® Small size ADDRS1 23.6 45 × 43 × 7.5 11.1 Accelerometer IS-1
Adapta® Midsize ADDR06 28.5 50 × 48 × 7.5 14.2 Accelerometer 5/6 mm
Adapta® Midsize ADDR03 28.1 47 × 48 × 7.5 13.0 Accelerometer 3.2 mm
Adapta® Oversize ADDRL1 31.3 45 × 52 × 7.5 13.1 Accelerometer IS-1
Versa® DDDR VEDR01 27.1 45 × 48 × 7.5 12.1 Accelerometer IS-1
Ensura DR MRI Surescan™d 22 45 × 51 × 8 12.7 Accelerometer IS-1
Advisa DR MRI™ SureScan™d,e 22 45 × 51 × 8 12.7 Accelerometer IS-1
*AT500™; Prevent AF series; Prevent AF 920; Selection 9000 AF3.0; and Diagnose AF 910 are no longer available
*Sigma DDDR series; Kappa 400/700/900 DDDR series; EnPulse DDDR series; Thera DR i-series; and EnRhythm DDDR are no longer available
(continued)
93
Table 6.6 (continued)
94

Pacemaker manufacturer Dimensions


Series Weight (g) H × W × D (mm) Volume (cc) Sensor Connector
Vitatron E60 DR 27.1 45 × 48 × 7.5 12.1 Accelerometer IS-1
Vitatron G70 DR 27.1 45 × 48 × 7.5 12.1 Accelerometer IS-1
*Vitatron C60 DR, Vitatron T60 DR, and Vitatron T70 DR are no longer available
*Clarity DDDR series and Diamond DDDR series are no longer available
Sorin
Esprit™ D 20 41 × 41 × 6 8 MV IS-1
Esprit™ DR 20 41 × 41 × 6 8 Accelerometer IS-1
Reply™ D 20 41 × 41 × 6 8 MV IS-1
Reply™ DR 20 41 × 41 × 6 8 MV/Accelerometer IS-1
* The Rhapsody DR, Symphony DR, Newliving DR, Neway DR models are no longer available
St. Jude Medical
Accent® DR PM2112 19 46 × 52 × 6 10.5 Accelerometer IS-1
Accent® DR RF PM2212 23 52 × 52 × 6 12.8 Accelerometer IS-1
Zephyr™ DR 5820 18 43 × 44 × 6 8.5 Accelerometer IS-1
Zephyr™ XLDR 5826 23.5 44 × 52 × 6 11 Accelerometer IS-1
Identity® ADx DR 5380 18 43 × 44 × 6 8 Accelerometer IS-1
Identity® ADx XLDR5386 23.5 44 × 52 × 6 11 Accelerometer 3.2 mm
Verity™ ADx XL DR5356 23.5 44 × 52 × 6 11 Accelerometer 3.2 mm (IS-1/VS 1)
Verity ADx XL DRM/S5357 23 45 × 52 × 6 11 Accelerometer 5/6 mm M/S
Victory® DR 5810 18 43 × 44 × 6 8.5 Accelerometer IS-1
6

Victory® XLDR 5816 23.5 44 × 52 × 6 11 Accelerometer IS-1


*Entity DR, Affinity DR, Identity DR 5370, Identity XL 5376, Integrity ADx DR5360, Integrity ADx XLDR5366, and Verity™ ADx XL DC5256 models are no longer
available
EL extended life
a
Transfers Home Monitoring data including trend messages and event and patient reports to the Biotronik Service Centre
b
Myocardial contraction Dynamics (CLS)
c
Model with 400 ms AV delay
d
MRI compatible; Managed Ventricular Pacing; Optivol
e
Atrial therapies, e.g., reactive ATP; Atrial arrhythmia preventive therapies; High VTR up to 210 ppm
Permanent Pacemakers and Leads
Types of Permanent Pacemakers 95

device, but CRT and ICD devices are consider-


ably more expensive (CRT-P – £3,000–£4,000;
CRT-D – £18,000–£25,000).

Storage

In most specialist pacing centers, a whole range


of permanent pacemakers, pacing electrodes, and
pacing accessories are kept in a dedicated pace-
maker store close to the pacing theater (Fig. 6.2).
For ease of use, devices should be kept in some
sort of order, e.g., type of device – single or dual
chamber device ± rate response programmability
(Fig. 6.3), and those devices with special features,
e.g., mode-switching, Managed Ventricular
Pacing, or Atrial Capture Management should be
readily identifiable (Fig. 6.4). Bi-ventricular
Fig. 6.1 Pacemakers reduced in size progressively from
1970s to 1990s. The bottom picture shows the Microny
devices (see Chap. 16) and ICDs (see Chap. 17)
SR+ pacemaker compared to a postage stamp (Courtesy and their accessories should be separated from
of Pacesetter/St. Jude Medical, Inc.) the other pacing devices (Fig. 6.5).

Fig. 6.2 Pacemakers should be kept in a store close to the pacemaker theater. Devices should be arranged in some sort
of logical order
96 6 Permanent Pacemakers and Leads

Fig. 6.3 The Vitatron C60 DDDR, Vitatron C20 SSIR, and the St. Jude Medical Verity™ ADx SSIR devices kept in
separate stacks

All devices are presented inside sealed boxes ers and they are constantly being updated and
(Fig. 6.5) and within a sterile package accompa- improved (Figs. 6.12 and 6.13). Permanent pace-
nied by the appropriate screwdriver (Fig. 6.6). makers are generally available as single or dual
Pacing leads should be kept separate from the chamber pacemakers. Single chamber devices
devices and with some semblance of order, e.g., will have one lead port to accommodate an atrial
active-fixation versus passive-fixation electrodes, or a ventricular lead, whereas a dual chamber
steroid-eluting leads, straight versus fixed-J- device will have two ports to accommodate sepa-
shaped electrodes, and atrial versus ventricular rate atrial and ventricular leads. It should be noted
leads (Figs. 6.7–6.9). Electrodes are also pre- that VDD devices (see below) will have two ports
sented in a sterile, transparent package along with to accommodate the atrial sensing electrode and
a selection of stylets, a “vein lifter” (Fig. 6.10), the ventricular sensing/pacing electrodes present
and when appropriate a tool for active-fixation of on the special single VDD lead required. Most
screw-in leads. manufacturers have now stopped production of
Pacing technicians should regularly check the these latter devices in favor of other rate-adaptive
expiry dates on devices, leads, and accessories so pacemakers (see below).
as to avoid wastage of devices that are soon to Different modes of function are available in
pass their sterilization dates. The Omnicell® cabi- today’s sophisticated multiprogrammable devices.
net system offers a slightly more secure but more For example, VVIR, DVI, AAI, AAIR, DDD, and
expensive method for “intelligent stock manage- VDD and other modes can be programmed in most
ment” (Fig. 6.11). DDDR devices and this allows great flexibility to
A whole range of multiprogrammable pace- the cardiologist for use in changing clinical situa-
makers are available from the major manufactur- tions in individual pacemaker patients.
Single Chamber Pacing (Table 6.2) 97

Fig. 6.5 Devices are presented in sealed boxes, with the


relevant warranty, patient information booklet, and
Fig. 6.4 Devices with special functions should be kept in physician’s technical information booklet
their own sections for practical purposes, e.g., the
ADAPTA™ ADDR should be stacked separately

pace in a single chamber, but the code becomes


Single Chamber Pacing (Table 6.2) redundant once the device is connected to the
electrode and implanted.
Fixed rate pacing devices (AOO, VOO, and
DOO) are very rarely used now as there is a risk
of pacing on a native “P” or “R” wave and there- Ventricular Demand Pacing (VVI, VVT)
fore initiating atrial or ventricular arrhythmias
(Fig. 6.14). When a magnet is applied to most In the absence of spontaneous ventricular beats, a
pacemakers, VOO or DOO mode is produced ventricular-inhibited pacemaker (VVI) delivers a
until the magnet is removed (Fig. 6.15). stimulus to the ventricles (usually via the RV) at
Single chamber pacemakers are now gener- a regular rate, set by the programmer (Fig. 6.17).
ally either atrial or ventricular demand devices, If spontaneous activity is sensed via the ventricu-
most are multiprogrammable, many have a rate lar electrode, the current stimulation cycle is ter-
response feature, and others more sophisticated minated, pacing inhibited, and competition avoided.
monitoring facilities. An example of a single The pacemaker then starts a new cycle and will
chamber, demand pacemaker that may be used pace again after the set interval from the last
for either atrial or ventricular pacing is the sensed ventricular beat (Fig. 6.18).
Altrua™ 20 S201 (Boston Scientific) (Fig. 6.16). In the less commonly used ventricular-trig-
The manufacturer labels the pacemaker with the gered pacing mode (VVT), a sensed event trig-
code SSI to signify that the device will sense and gers delivery of a pacing stimulus which will
98 6 Permanent Pacemakers and Leads

Fig. 6.6 A device is sealed


inside a transparent sterile
packet with its own
screwdriver

Fig. 6.7 Pacing electrodes and accessories should be organized on a separate shelf from the devices

consequently fall during the myocardial refrac- activation and recovery in order to prevent sens-
tory period and thus be ineffective (Fig. 6.19). ing the ventricular electrogram which is produced
The next cycle will then start from delivery of the by the event. This interval is referred to as the
triggered impulse. refractory period and measures between 250 and
Immediately after a paced or sensed event, the 300 ms.
pacemaker is rendered insensitive for an interval Ventricular demand pacing is indicated for
which approximates the duration of myocardial bradycardia associated with atrial fibrillation, in
Single Chamber Pacing (Table 6.2) 99

Fig. 6.8 Like all electrodes, the tined, steroid-eluting Fig. 6.9 This Tendril™ ST electrode has an active-
atrial electrode from Medtronic comes sterile in its own fixation mechanism, is bipolar, steroid-eluting at its tip,
box. The type of lead fixation, polarity, and length are and is 58 cm long – suitable for placement anywhere in
indicated on the label. A selection of straight and the right ventricle, interventricular septum, or RV
J-shaped stylets, a fixation tool, and “vein picker” are outflow-tract
available within each electrode packet

Fig. 6.10 Electrodes are


presented in a molded,
transparent packet with
several stylets and a
“vein-picker.” Active-
fixation leads also have a
“fixing-tool”
100 6 Permanent Pacemakers and Leads

Fig. 6.12 Some currently available pacemakers (with per-


mission): (Top left) Altrua™ 20 DR (Boston Scientific); (Top
right) Microny K SR (St. Jude Medical); (Middle left) Reply™
DR (Sorin Group); (Middle right) Talos DR (Biotronik);
(Bottom left) Advisa DR MRI™ (Medtronic Ltd.)

second and third degree AV block in patients


who are physically limited for other reasons such
as fraility, stroke, or other musculoskeletal
abnormalities and for those with very infrequent
bradycardia who simply require a “back-up” or
Fig. 6.11 The Omnicell® cabinets provide secure stor- “stand-by” device.
age and the OptiFlex™ CL software system can help
track equipment and device usage to the physician and
patient on each case. The system provides an opportunity
to improve the restocking process, reduce inventory costs, Atrial Demand Pacing (AAI, AAT)
and improve charge capture. However, it is an expensive
luxury that requires time and training to use effectively
and its cost-effectiveness is unproven. (Top) Cabinets in The timing cycles of AAI and AAT pacing are as
store room next to pacing theater. (Bottom) Keyboard and described above for VVI and VVT pacing
screen for inputting a code to access the equipment and to (Fig. 6.20).
record what equipment has been removed from the cabi- The atrial refractory period is usually longer
net and for which patient. (Middle left) Close-up of
devices inside the cabinet. (Middle right) Pacemaker than the ventricular refractory period in order to
accessories including suture materials, guidewires, glue, avoid inappropriate inhibition of the pacemaker
etc., can also be stored in the Omnicell® cabinets to aid by sensing the ventricular electrogram via the
inventory and cost-per case assessments atrial lead.
Dual Chamber Pacing 101

Fig. 6.13 (Left) The earlier Sigma™ series from pre-shaped, bipolar, active-fixation “J” lead, and the
Medtronic had a range of models offering different pac- bipolar, active-fixation ventricular lead are shown
ing modes – VDD, SSIR, DDD, SSI, VVI, and DDDR. attached to the pacemaker. This device has also been
In recent times, manufacturers have reduced the number superceeded by the Sensia™ and Versa™ models from
of available models which can each offer a range of Medtronic Ltd. (Images reproduced with permission of
mode programmability. (Right) The Kappa DDDR 900 Medtronic, Inc.)
series pacemaker and its programmer. The CapsureFix®

Fig. 6.14 Fixed rate VOO pacing is illustrated here. A ventricular ectopic beat does not delay the next paced beat as it
would in a ventricular demand system

Atrial pacing is indicated in symptomatic sick atrial fibrillation, stroke, and heart failure in
sinus syndrome (SSS) unless AV conduction is patients with SSS compared to those undergoing
impaired. This may be evidenced by the presence VVI pacing.
of bifascicular block, bundle branch block, or if
atrial pacing at a rate of 120 bpm causes second
degree AV block (Wenckebach rate). In these Dual Chamber Pacing
situations, a dual chamber pacemaker should be
implanted. By stimulating the atria rather than Dual chamber pacing improves cardiac output
the ventricles, the normal sequence of cardiac over VVI pacing as a result of the addition of atrial
chamber activation and cardiac output is main- transport with consequent increase in stroke vol-
tained. Atrial pacing may reduce the incidence of ume, the prevention of deleterious hemodynamic
102 6 Permanent Pacemakers and Leads

Fig. 6.15 Fixed rate DOO pacing occurs when a magnet is applied externally to a dual chamber pacemaker (arrow)

influence due to ventriculoatrial conduction,


and the provision of a chronotropic response to
exercise. It results in improved survival in patients
with symptoms of heart failure compared to VVI
pacing. Moreover, although a comparable car-
diac output during exercise can be achieved with
single chamber rate-responsive pacemakers (see
below), dual chamber pacing can spare cardiac
reserve especially at low work load.

Atrial Synchronized Ventricular


Pacing (VDD) (Table 6.3)

In VDD, ventricular pacing is triggered by


a sensed atrial event after an interval simi-

Fig. 6.16 Altrua™ 20 (S201) is an SSIR device which


can be used as an AAI or VVI, AAIR, or VVIR device
Dual Chamber Pacing 103

Fig. 6.17 VVI pacing

Fig. 6.18 VVI pacing showing resetting of pacing cycle by intrinsic cardiac rhythm

lar to the normal PR interval (Fig. 6.21) and normal. Atrial tachyarrhythmias and SSS are
the normal sequence of cardiac activation is contraindications.
maintained. With normal sinus node func- If an atrial event is not sensed, ventricular
tion, a normal chronotropic response to exer- pacing continues at a set rate – otherwise atrial
cise should occur (Fig. 6.22). The upper rate asystole would lead to ventricular asystole. In order
at which atrial activity will trigger ventricular to avoid rapid ventricular pacing should atrial
pacing (URL) is determined by the total atrial tachycardia, flutter, or fibrillation occur, an atrial
refractory period (TARP), which consists of refractory interval renders the atrial channel insen-
the AV delay plus the post-ventricular atrial sitive. This interval consists of the AV delay and a
refractory period (PVARP). Thus, if the AV period after ventricular stimulation, such that any
delay is 120 ms and the PVARP is 230 ms, sensed atrial activity at a cycle length shorter than
the TARP will be 350 ms and the URL will be this period will not trigger ventricular pacing.
60,000/350 = 171 bpm. Ventricular ectopic beats or ventricular
VDD pacing is indicated in second or third rhythms faster than the sinus rate will inhibit the
degree AV block when sinus node function is pacemaker unlike the earlier VAT systems.
104 6 Permanent Pacemakers and Leads

Fig. 6.19 VVT pacing

Specific VDD devices are being phased out. In DDI pacing, sensing occurs in both atrium
and ventricle and competitive atrial pacing is
avoided.
AV Sequential Pacing (DVI and DDI)

In DVI pacing, the atria are stimulated first AV Universal Pacing (DDD) (Table 6.4)
and after a short delay (approximately the
duration of the PR interval), the ventricles are In DDD pacing, both sensing and pacing takes
paced (Fig. 6.23). There is no atrial sensing place in the atrium and ventricle. Thus depending
but ventricular pacing is inhibited by sponta- on the heart rhythm, the pacemaker can function
neous ventricular activity. Although the pace- in atrial demand (AAI), AV sequential (DVI,
maker is inhibited by an event sensed in the DDI), or atrial synchronized (VDD) modes
ventricle, the first chamber to be stimulated is (Figs. 6.23 and 6.24).
the atrium. Pacemaker output may therefore Therefore, in sinus bradycardia, a DDD pace-
occur at the same time as spontaneous atrial maker will function as an atrial demand pacemaker.
activation because its ventricular depolariza- If AV conduction is impaired, ventricular pacing is
tion has not yet occurred. Hence, fusion beats triggered by either spontaneous atrial activity or a
are common during DVI pacing. They should paced atrial beat. When sinus node function is nor-
be recognized as such and not misinterpreted mal, the pacemaker functions in atrial synchro-
as a malfunction. nized mode and a chronotropic response to exercise
Atrial Synchronized Ventricular Pacing (VDD, DDD) 105

Fig. 6.20 AAI pacing

follows. Pacemaker output will be inhibited by tion as the sinus node rate changes and/or by the
atrial and ventricular ectopic beats. use of one or more non-atrial sensors (rate-
DDD is indicated in second or third degree AV adaptive pacing).
block. It is relatively contraindicated if atrial
tachyarrhythmias are present unless “mode-
switching” is available, otherwise the fast atrial Atrial Synchronized Ventricular
rate will trigger a fast ventricular rate. Pacing (VDD, DDD)

As indicated above, both VDD and DDD pacing


Physiological Pacing will maintain AV synchronization and allow a
chronotropic response to exercise in patients with
Physiological pacing is a generic term for sys- normal sinus node function (Fig. 6.22). Compared
tems which allow a chronotropic response to to VVI pacing, cardiac output increases with
exercise by either maintaining AV synchroniza- physiological pacing both at rest and during exer-
106 6 Permanent Pacemakers and Leads

Fig. 6.21 VDD pacing is demonstrated by the first 8 beats on this ECG strip

cise. Exertional dyspnea, dizziness, and palpita- some parameter that alters with exercise. These
tions are less than with VVI or VOO pacing. parameters include body vibrations, QT interval,
respiration, blood temperature, oxygen saturation,
RV pressure, and a number of these sensors have
Atrial Synchronized, Rate-Adaptive now been incorporated into pacemakers, either
Pacing (VDDR) individually e.g., Vitatron C and T series (acceler-
ometer) or in combination, e.g., Reply™ DR
The Verity™ ADx XL VDR pacemaker (St. Jude (Sorin Group) uses an accelerometer and a respi-
Medical) (Fig. 6.25) is a multiprogrammable, ratory minute volume sensor in order to allow an
mode-switching, rate-adaptive pacemaker designed appropriate chronotropic response to exercise.
to operate with the AV Plus DX Model 1368 sin- Such rate-adaptive ventricular pacemakers can
gle-pass bifurcated lead. Other manufacturers have achieve an enhanced exercise tolerance without
phased out these single lead devices. having to implant an atrial electrode. Ventricular
demand and dual chamber rate response pacemak-
ers are given the codes VVIR and DDDR respec-
Rate-Adaptive (or Rate-Responsive) tively, e.g., Victory™ SR and Victory™ XL DR
Pacing (VVIR, DDDR) (Tables 6.5–6.7) (St. Jude Medical) (Fig. 6.26). Some devices, e.g.,
Kappa series (Medtronic Ltd.) (Fig. 6.27) have a
The ability to increase heart rate with exercise is Sensor Cross Check feature which verifies exer-
as important as maintaining AV synchrony. tion before allowing high sensor-driven pacing
Exercise tolerance has been shown to be as good rates. The Sensia™ pacing system (Medtronic
in rate-adaptive ventricular pacing as with AV Ltd.) (Fig. 6.28) combines physiologic pacing
synchronized pacing. Pacing systems are now with automaticity. Moreover, using Search AV +,
available that can produce a rate-response to exer- the device automatically and continuously
cise which is independent of atrial activity. An searches for natural intrinsic conduction and
increase in pacing rate is usually in response to reduces unnecessary RV pacing to <20%.
Rate-Adaptive (or Rate-Responsive) Pacing (VVIR, DDDR) (Tables 6.5–6.7) 107

Fig. 6.22 VDD pacing


showing rate response with
exercise

Fig. 6.23 AV sequential


pacing
108 6 Permanent Pacemakers and Leads

Fig. 6.24 DDD pacing showing a rate response. (Bottom) plex). (Top) As the sinus rate increases to 79 bpm, the
As the sinus rate falls below 60 bpm, atrial pacing occurs ventricular pacing rate increases appropriately with nor-
at the base rate (60 bpm) which is followed by ventricular mal AV conduction (VDD)
pacing spike (fused with a normally conducted QRS com-
Rate-Adaptive (or Rate-Responsive) Pacing (VVIR, DDDR) (Tables 6.5–6.7) 109

Body Motion Sensors

These are the most widely used sensors. A piezo-


electric crystal attached to the inside of the pace-
maker unit (so-called Activity Sensor) or an
accelerometer bonded to the circuitry within the
pacemaker (but not to the can itself) senses body
vibrations as a result of physical activity and via a
specific algorithm increases the pacing rate in line
with the level of sensed activity. The sensitivity of
the response can be adjusted by programming
Fig. 6.25 Verity™ ADx VDR pacemaker (Image pro-
vided courtesy of St. Jude Medical, ©2008 St. Jude several parameters using an external programmer.
Medical, Inc.) These include the reaction time, the time to the

Table 6.7 Dual chamber A-V sequential rate responsive pacemakers


Pacemaker
manufacturer Dimensions
Series Weight (g) H × W × D (mm) Volume (cc) Sensor Connector
Biotronik
Talos SLR VDDR 26 51 × 42 × 6 10 Accelerometer IS-1
Boston Scientific
None available
Medtronic
Clarity VDDR/660 and Saphir 3/640 are no longer available
Sorin
None available
St. Jude Medical
Identity ADx 18 43 × 44 × 6 8 Accelerometer IS-1
VDR 5480 DC sensing/SC
pacing
Verity ADx XL 23.5 44 × 52 × 6 11 Accelerometer 3.2 mm (IS-1
VDR5456a or VS 1)
*Affinity VDR 5430 model is no longer available
a
Multiprogrammable, mode-switching, rate-responsive pacemaker for use with the AV Plus DX model 1368 single-pass
bifurcated lead. It has extended life

Fig. 6.26 Victory™ SR and


Victory™ DR rate respon-
sive pacemakers (Image
provided courtesy of St. Jude
Medical, ©2008 St. Jude
Medical, Inc.)
110 6 Permanent Pacemakers and Leads

Fig. 6.28 The Sensia™ DR device (Image reproduced


Fig. 6.27 The Kappa® DR 700 series pacemaker (Image with permission of Medtronic, Inc.)
reproduced with permission of Medtronic, Inc.)

Fig. 6.29 Rate response seen soon after start of exercise

initial increase in sensor-driven pacing; the slope, (see Fig. 1.67). Moreover, it shortens with increased
which determines the rate at which the pacing rate sympathetic activity and during exercise activity
increases following the onset of detection of when VOO pacing. This pacemaker senses, via the
increased body activity; and the recovery time, ventricular electrode, the interval between the pac-
the time taken to return to standby rate after activ- ing spike and the apex of the evoked T wave.
ity has ceased. It is possible also to program the A decrease in the interval leads to an increase in
sensitivity of the pacemaker’s sensor to body the pacing rate. Unlike the activity-sensor rate
activity. The Kappa 700 series DDDR pacemaker responsive devices described above, the QT-sensing
is an example of a system that used an accelerom- pacemakers will allow a rate response to emotion
eter as its sensor (Fig. 6.27). Although many of as well as exercise. The Vitatron T20 SR pace-
these devices have been implanted worldwide, the maker is an example of a current QT-sensing rate
models are being replaced by the Versa™ series. responsive pacemaker. Figure 6.29 shows the
beginning of heart rate response from a VVIR
device in a patient climbing stairs.
Evoked QT Response

This sensor was the first to be used by Vitatron in Respiration


their TX/Rhythmx and subsequently Quintech TX
pacemaker when it was discovered that the An estimate of respiratory minute volume (MV) –
QT-interval shortened with increasing heart rate change in intravascular impedance – is monitored
Multisensor Pacing 111

by a conventional bipolar pacing electrode. As tional activity. Select Biotronik pacemakers such
respiratory rate increases with effort, the pace- as the Evia DR–T device have this facility.
maker’s algorithm allows the pacing discharge
rate to increase proportionately and decrease again
as the respiratory rate falls after exercise. Unlike Alternative Sensors
some other sensors, MV sensors also respond to
stress and emotion. However, pacemakers using Other direct and indirect metabolic parameters
this sensor alone are used infrequently. Minute such as body temperature, right ventricular pres-
volume sensors have been combined with sure, oxygen saturation, and blood pH have been
accelerometers in multisensor pacing devices, e.g., investigated as sensors for rate responsive pacing
Altrua™ series (Boston Scientific) (Fig. 6.30). systems. These have not been established to be of
any additional value to activity, QT-interval, and
respiration and have not become commercially
Closed Loop Stimulation (CLS) available. The use of an additional lead with a
special sensor is disadvantageous.
CLS uses myocardial contraction dynamics to
evaluate the patient’s specific pacing demand.
The sensor converts this value to an optimal pac- Multisensor Pacing
ing rate. The device determines the impedance
waveform at the onset of each ventricular con- Over the last few years, single chamber pacemak-
traction and compares it with the reference curve ers have used combinations of sensors in order to
measured at rest. Differentiation between imped- enhance and optimize the rate response to exer-
ance waveforms at rest and while the patient is cise. The Clarity™ SSIR (Vitatron) uses a combi-
engaged in physical activities delivers a specific nation of an accelerometer to provide a prompt
parameter for individual metabolic needs. Studies response to physical activity and a QT-interval
have already demonstrated CLS’s clinical perfor- sensor to ensure that the rate response is propor-
mances. The CLS rate is thought to be much tional to the exercise load. The Reply™ DR (Sorin
closer to the sinus rate of a healthy heart in every Group) (Fig. 6.31) uses an accelerometer and a
tested situation, adapting to the hemodynamic respiratory minute volume sensor and the
need on a beat-to-beat basis. It is another technol- Clarity™ DDDR (Vitatron) again combines an
ogy that adapts the heart rate in response to emo- accelerometer with a QT-interval sensor in order
to provide an appropriate rate response to exercise
(Fig. 6.32). These are ideal for patients with chro-

Fig. 6.30 The Altrua™ 40 DR device uses a respiratory


minute volume sensor to perform as a rate-responsive
pacemaker (©2010 Boston Scientific Corporation/ Fig. 6.31 The Reply™ DR uses multisensor blending
affiliates. All rights reserved. Used with permission of accelerometer and minute ventilation to optimize rate
Boston Scientific Corporation) response to exercise (Courtesy of Sorin Group)
112 6 Permanent Pacemakers and Leads

Rest

Post
Exercise

Fig. 6.32 Rate response seen with the Clarity™ activity-sensing pacemaker

notropic incompetence due to sinus node disease, Insignia® Entra Single Sensor System (SSI)–
who will have AV synchrony at rest from sensed Model 484 having the fewest pacing and diag-
atrial activity via the atrial lead and an appropriate nostic features, and the Insignia® Ultra Blended
sensor-adjusted rate response during exercise. Sensor System (DDDR)–Model 1290/1291 hav-
ing the most. Although still available in some
countries, these devices are being replaced by the
Advanced Programmability Altrua™ series (Table 6.6).

Pacemaker manufacturers continue to produce


series and models of pacemakers with increasing Special Functionality
degrees of sophistication in pacing, sensing,
diagnostics, and other functionality. For example, Device manufacturers continue to develop and
Guidant’s series of Insignia® – Entra, Plus, AVT, produce for clinical use pacemakers with special
and Ultra – had various capabilities with the functions. When these functions are proven to be
Special Functionality 113

rithms for atrial tachyarrhythmias offer more


opportunity to restore and maintain sinus
rhythm.
EnPulse™ (Medtronic) was labeled an “auto-
matic” pacemaker (Fig. 6.35). In this device,
Atrial Capture Management (ACM) automati-
cally and regularly adapted atrial threshold levels
and Search AV™+ continuously searched for
intrinsic conduction and automatically adapted
programmed AV delays to minimize chronic RV
pacing. Cardiac Compass™ Trends also auto-
matically monitored for arrhythmias and helped
in diagnosis and assessing the effects of
therapies.
Diagnose AF (Vitatron) was a full featured
dual chamber pacemaker, specially adapted to
function as a very sensitive, accurate detection
device for gathering and analyzing valuable car-
diac data. It managed the ventricular rate during
atrial arrhythmias with beat-to-beat mode
switching and provided dual sensor rate response.
Prevent AF (Vitatron) was another revolution-
ary pacing device which not only offered brady-
cardia pacing but which had novel sensing and
pacing capabilities and a series of sophisticated
new preventive pacing algorithms aimed at sup-
Fig. 6.33 The EnRhythm™ and Adapta™ pacemakers pressing the onset of AF. These features have
(Image reproduced with permission of Medtronic, Inc.)
been incorporated into newer models.
Selection 9000 AF 3.0 offered a series of AF
useful and worthwhile, they may become incor- monitoring diagnostics, new AF prevention pac-
porated as standard features in the next genera- ing therapy and new rate control therapies. It
tion of devices produced by the company. Thus included four algorithms for triggered overdrive
many of these “new” devices are soon replaced pacing which react to onset triggers of AF – PAC
by subsequent “improved” versions with greater suppression, PAC response, post-AF response,
versatility and programmability. Some examples and post-exercise response. In addition, there
of recently produced “novel” devices are given were two more algorithms for continuous over-
here only soon to become obsolete with their drive pacing which aimed to condition the atrial
“special” features subsequently becoming “stan- activation pattern by dynamically overdriving the
dard” in the companies’ next models. atrial rate: Pace Conditioning and Rate Smoothing.
EnRhythm™ and Adapta™ (Medtronic) use This combination of continuous AF monitoring
Managed Ventricular Pacing (MVP) to promote and six preventive pacing therapies enabled fine-
intrinsic conduction and minimize unnecessary tuning. AF preventing pacing therapies are aimed
right ventricular pacing (Fig. 6.33). They operate at promoting and maintaining normal sinus
in AAI(R) pacing mode while providing the rhythm, improving hemodynamics, and reducing
safety of DDDR back-up pacing support if risk of stroke.
necessary (Fig. 6.34). Minimizing RV pacing The Symphony® DR (Sorin) introduced an
may result in reduced risks of heart failure and AAIsafeR™ mode which offered a unique and
AF. Moreover, Reactive atrial Antitachycardia comprehensive means of achieving optimal phys-
Pacing (ATP) therapies and intervention algo- iological pacing in all types of AV conduction
114 6 Permanent Pacemakers and Leads

b Single Backup Pace

c AAI(R) to DDD(R)

d
DDD(R) to AAI(R)

Fig. 6.34 AAI safe mode: (a) AAI(R) mode – atrial- the presence of transient loss of conduction. (c) DDD(R)
based pacing allowing intrinsic AV conduction. (b) switch – ventricular support if loss of AV conduction is
Ventricular backup – ventricular pacing only as needed in persistent. (d) Switching from DDD(R) to AAI(R)

disorders, including permanent first degree AV functions, including 7 min of intracardiac ECG
block, thus contributing to a reduced risk for heart recordings and expeditious follow-up tools, such
failure, AF, and death (Fig. 6.36). AAIsafeR™ is as AIDA (Automatic Interpretation for Diagnosis
a unique pacing mode suitable for the manage- Assistance).
ment of AV conduction disorders. Like AAI, Most devices cannot be exposed to MRI for
AAIsafeR™ preserves AV conduction while con- fear of damage and malfunction of device and
stantly monitoring ventricular activity, and pro- lead. However, the Advisa DR MRI™ SureScan®
vides critically needed dual chamber pacing in pacing system (Medtronic) is an MRI condi-
case of advanced AV block. In addition to the tional safe pacemaker that offers MVP®, com-
suppression of unnecessary ventricular pacing, plete automaticity including VCM and ACM,
Symphony® DR offered advanced diagnostic and automatic sensing (Fig. 6.36). Its sophisti-
Special Functionality 115

cated therapies include ATP and diagnostics ponents, changes to the internal circuitry, and
include Cardiac Compass Report™ and tachyar- device design to minimize the gradient field
rhythmia management tools to assist in the early energy coupled to the lead tip, as well as changes
detection and termination of atrial fibrillation. It to the lead body geometry to prevent lead tip
also offers Remote Follow-up via the Medtronic heating. Conditional usually means that certain
CareLink® Network and OptiVol® Fluid Status conditions should also exist before MRI scan-
Monitoring which reports fluid changes using ning takes place even with these devices. These
intrathoracic impedance measurements, Rate are outlined in Chap. 10. The Accent MRI™
Drop Response which identifies abrupt brady- pacemaker and Tendril MRI™ lead from St.
cardia and responds by pacing at an elevated rate Jude Medical, Inc. have recently been approved
– especially useful for those with cardioinhibi- as MR-Conditional in Europe and been released
tory vasovagal syncope and high upper tracking for use in India. This system features an MRI
rates (up to 210 bpm). This may be useful for Activator™ device that provides a simple alter-
pediatric patients and older active patients. The native option for programming the device to the
EnRhythm MRI™ SureScan® and the Model appropriate MRI mode for use during the scan.
5086 CapSureFix MRI™ lead are similarly Since it does not require a programmer, this
“MRI safe” or “MR conditional” because of the increases both clinical and personnel efficiency.
use of significantly reduced ferromagnetic com- The pacing parameters are preselected by the
patient’s physician and stored in the Accent MRI
pacemaker. The MRI Activator can then be used
to program the device back to its original set-
tings after the scan has been completed.
Boston Scientific Corporation have recently
released the Ingenio™ MRI and Advantio™
MRI rate-responsive pacemakers (employing
RightRate™ MV sensor and ImageReady™
technology). When used in conjunction with
Fineline II leads, they are safe for use in patients
requiring MRI scanning by programming the
device into MRI Protection Mode.
With the advent of radiofrequency ablation for
Fig. 6.35 The EnPulse™ pacemaker (Image reproduced
the treatment of re-entrant supraventricular
with permission of Medtronic, Inc.) arrhythmias, specific antitachycardia pacemakers

Fig. 6.36 (Left) The


Symphony® DR pacemaker
(with permission of Sorin
Group). (Right) The Advisa
DR MRI™ SureScan®
pacemaker (with permission
of Medtronic, Inc.)
116 6 Permanent Pacemakers and Leads

are now rarely used. The Stratos® LA (Biotronik) Atrial Tachy Response
is currently the only device available for specific
bi-atrial pacing (using RA/LA and RV leads) The percent of time mode-switched, maximum
which can be used for preventive overdrive and average mode-switch time, and number of
pacing. mode-switches can be retrieved from the memory.

Advanced Diagnostic Features Battery Status

In recent years, devices have become equipped Some pacemakers automatically evaluate battery
with advanced diagnostic features which can be status every 12 h or so. It may be displayed in the
interrogated easily at follow-up. Many of these form of a gauge (showing BOL, ERT, and EOL)
features prove invaluable during troubleshoot- and longevity remaining (>5 year to <6 months
ing of suspected pacemaker malfunction (see in 6 month increments) at 100% pacing.
Chap. 21).

Remote Monitoring
Automatic Daily Measurements
The CareLink® Network (Medtronic) using
Approximately every 24 h, intrinsic P- and Conexus® Wireless Telemetry is available for
R-wave amplitudes and atrial and ventricular patients with EnPulse™, Kappa™ 900/700
lead impedances are measured. Data for the last series, and Versa™ pacemakers (Fig. 6.38). This
52 weeks can be saved in the device memory. Internet-based remote monitoring service – com-
parable to a pacing clinic check, enables patients
who are housebound or infirm to connect to a
Arrhythmia Detection center for over-the-wire pacemaker checking.
The Medtronic CareLink® Monitor (weighs about
The frequency, type, and rate of arrhythmias can 1 lb) connects to a standard phone line, gathers
be detected by some devices, such as the the information from the device by placing an
Kappa™ 900 and Versa™ devices (Medtronic) antenna over it, and sends the data to a secure site
(Fig. 6.37). for access by technician or physician (Fig. 6.38).
Physicians can quickly access device data any-
time from any Web-capable PC.
The Evia™ and Estella™ pacemakers from
Biotronik (Fig. 6.39) transfer Home Monitoring
data automatically as trend messages, event
reports, and patient reports to the Biotronik
Service Centre using the Cardio-Messenger II®
device. The cardiologist then receives the detailed
report via the cellular telephone network. Similar
systems such as LATITUDE® (Boston Scientific)
and Merlin@home™ (St Jude Medical) are also
available and all are described in Chap. 11.

Fig. 6.37 The Versa™ DR pacemaker is a sophisticated,


multiprogrammable pacemaker which is suitable for use Intracardiac EGMs and Markers
with Medtronic’s CareLink™ home monitoring service.
The Versa™ is the successor to the Kappa™ series from
Medtronic (Image reproduced with permission of Continuous atrial and ventricular intracardiac
Medtronic, Inc.) EGMs and annotated event markers available
Digital Pacemaker Technology 117

Fig. 6.38 CareLink™


(Image reproduced with
permission of Medtronic,
Inc.) enables secure data
transfer from patient to clinic
in minutes. The medtronic
programmer/analyzer is
shown (top right)

The Medtronic Care Link Monitor and Antenna

Fig. 6.39 The Evia™ SR-T


and Estella™ DR-T pacemak-
ers allow transfer of Home
Monitoring data using the
CardioMessenger II® system
(Images courtesy of
Biotronik)

during testing and follow-up simplify evaluation sensing and analysis of the cardiac signal. DSP is
(Fig. 6.40). much faster, it allows for more storage capacity
and all diagnostics are available during initial
interrogation. The Vitatron C-series were an
Trending Evaluation example of the efficient use of digital technology
within pacemakers. Using the programmer,
Rate and sensor trending available with graphic Therapy Advisor can analyze the pacemaker data
display allows replay of rate based on new param- and translate it into therapy by giving suggestions
eter settings while sensitivity trending shows to optimize programming settings. A complete
measured intrinsic events and sensitivity levels. technical follow-up can take as little as 3 or 4 min.
The pacemakers store useful information such as
EGM digitally – up to 12 min of digital EGM in
Digital Pacemaker Technology single chamber mode and 3 min with atrial and
ventricular monitoring. The high quality digital
Recently introduced pacemakers use Digital EGM shows the actual signal that the pacemaker
Signal Processing (DSP) to convert analogue sig- uses as input signal which aids interpretation of
nals into a digital signal which provides precise ECGs, diagnosis of the heart rhythm, and appro-
118 6 Permanent Pacemakers and Leads

01-DEC-2008 Lead-II (10 mm/mV) Boston 25 mm/s 01-DEC-2008 Lead-II (10 mm/mV) Boston 25 mm/s
12:28 Atrial Scientific Filter On 12:28 Atrial Boston Scientific Filter On
Vent Vent Scientific

(AS) (AS) (AS) (AS) (AS) (AS)


(AS) (AS) (AS) (AS) (AS) (AS)
VP VP VP VP
VP VP VP VP
VP VP VP VP

Fig. 6.40 Dual chamber pacemaker showing atrial sensing and ventricular pacing – confirmed by the atrial and ven-
tricular electrograms and the annotated event markers AS (atrial sense) and VP (ventricular pace)

priate adjustment of sensitivity according to the materials used for the conductor, the electrode
signal amplitude of the EGM. tip, and the lead insulation.
Moreover, the technology is energy-efficient A lead is presented in its individual box
and allows for the EGM storage to be turned on whose labels indicate the model number, the
throughout the entire lifetime of the pacemaker lead’s length and tip shape, the type of fixation
without affecting its longevity. mechanism and polarity, and whether the tip is
steroid-eluting. The sterile package containing
the lead is transparent and also contains various
Permanent Pacemaker Leads (Table 6.8) stylets, a “vein lifter,” and a fixation tool in
leads with an active-fixation mechanism
A permanent pacemaker lead consists of an (Fig. 6.43).
insulated wire or conductor with an electrode Atrial and ventricular pacing electrodes cost
at its distal tip which attaches to the myocar- between £300 and £600 but left ventricular leads
dium. Its function is to deliver the pacing stim- for CRT and defibrillation leads for ICD devices
uli produced by the generator as well as to are significantly more expensive (£2,000 and
sense underlying myocardial activity and to £3,000).
send this information back to the pacemaker
(Fig. 6.41). At the proximal end of the lead is
the connector pin which is fixed by a screw Electrode Insulation and Tip Structures
mechanism to the pacemaker generator at the
time of implantation (Fig. 6.42). The screw is Electrodes have basically similar anatomy. They
reached through a silicone cover which self- usually consist of a multifilar, helically-coiled
seals on removing the screwdriver. All leads wire (the conductor) that is insulated by a material
have a suture collar (Fig. 6.42) for anchoring that does not cause tissue reaction or thrombosis.
the lead to the pectoral fascia and preventing The conductor is normally made of a nickel alloy
the suture from cutting through the lead’s or platinum-iridium, and the two commonest
insulation. insulating materials are silicone rubber and poly-
The last 25 years have seen much progress in urethane which are covered in a lubricious coat-
the development of permanent pacemaker leads, ing. For example, modern leads such as the
in terms of their profile, flexibility, durability, Flextend®2 (Boston Scientific) has a conductor
conductivity, shapes, fixation options, lengths, material of tri- and quad-wound helical coils of
and choice of tip types, besides the improved MP35N, a non-magnetic, superalloy, or multiphase
Table 6.8 Permanent pacemaker endocardial leads
Pacemaker manufacturer Length (cm) Steroid Elec. tip
Electrode Polarity Placement Fixtn Tip shape Diameter Insulation Elution Connector SA mm2
Biotronik
Setrox S 45/53/60 Bi A/V Active Helix/straight 6.7F 45/53/60 Yes IS-1 4.5
Selox ST 53/60 Bi V Passive Straight/tines 6.5F 53/60 Yes IS-1 1.3
Selox JT 45/53 Bi A Passive J-shaped/tines 6.5F 45/53 Yes IS-1 1.3
Siello S 45,53,60 Bi A/V Active Straight/helix 5.6F 45/53/60 Yes IS-1 4.5
Siello JT 45,53 Bi A Passive J-shaped/tines 5.6F 45/53 Yes IS-1 2.1
Digital Pacemaker Technology

Siello T 53,60 Bi A/V Passive Straight/tines 5.6F 53/60 Yes IS-1 2.1
Safio S ProMRIa,b Bi A/V Active Screw 6.7F 53/60 Yes IS-1 4.5
Solia ProMRIa,c Bi A/V Active Screw/straight 5.6F 45/53/60 Yes IS-1 4.5
(Solia S)
Solia ProMRIa,c Bi A/V Passive Tines (Solia T) 5.6F 53/60 Yes IS-1 4.5
Solox Bi VDD Passive Straight/tines 9F 58/65 Si Yes IS-1
Boston Scientific
Dextrus®
4135/4136/4137 Bi A/V Active Helix/screw 6.7F 45/52/59 Si Yes IS-1 4.5
Flextend®2
4095/4096/4097 Bi A/V Active Helix/screw 7.2F 45/52/59 Si Yes IS-1 5.7
Fineline™ II Sterox
4456/4457 Bi A/V Passive Straight 5.4F 52/58 PU Yes IS-1 5
4458/4459 Bi A/V Passive Straight 6F 52/58 Si Yes IS-1 5
4479/4480 Bi A Passive Helix/screw 5.4F 45/52 PU Yes IS-1 5
Fineline™ II Sterox EZ
4469/4470/4471 Bi A/V Active Helix/screw 5.4F 45/52/58 PU Yes IS-1 5
4472/4473/4474 Bi A/V Active Helix/screw 6F 45/52/58 Si Yes IS-1 5
Medtronic
CapSure® SP Novusd
4092-52/58 Bi V Passive Straight/tines 5.3F 52/58 PU Yes IS-1 5.8
4592-45/53 Bi A Passive J-shape/tines 5.3F 45/53 PU Yes IS-1 5.8
5092-52/58 Bi V Passive Straight/tines 6F 52/58 Si Yes IS-1 5.8
5594-45/53 Bi A Passive J-shape/tines 6F 45/53 Si Yes IS-1 5.8
(continued)
119
Table 6.8 (continued)
120

Pacemaker manufacturer Length (cm) Steroid Elec. tip


Electrode Polarity Placement Fixtn Tip shape Diameter Insulation Elution Connector SA mm2
CapSure®Z Novus (High Efficiency)d
5054-52/58 Bi V Passive Straight/tines 6F 52/58 Si Yes IS-1 1.2
5554-45/53 Bi A Passive J-shape/tines 6F 45/53 Si Yes IS-1
*CapSure®SP-4023/4; 4523/4; 5024M; and 5524M leads are no longer available
CapSureFix® Novus (small-bodied, steroid-eluting, active-fixation lead)d
4076-45/52/58/65/85 Bi A or V Active Helix/screw 5.7F 45/52/58/65/85 PU Yes IS-1 4.2
5076-45/52/58/65/85 Bi A or V Active Helix/screw 6.1F 45/52/58/65/85 Si Yes IS-1 4.2
CapSureFix® MRI
5086MRI-45/52/58 Bi A or V Active Helix/screw 6.9F 45/52/58 Si Yes IS-1 4.2
CapSureFix®
5568-45/53 Bi A preformed J Active Helix/screw 7.2F 45/53 Si Yes IS-1 6.3
SureFix® (steroid-eluting, non-retractable fixation)
5072-45/52/58 Bi V/A straight Fixed screw 7.2F 45/52/58 Si Yes IS-1 6.3
CapSure Sense®
4073-45/52/58 Uni V/A Passive Straight/tines 3.6F 45/52/58 PU Yes IS-1 2.5
4074-45/52/58 Bi V Passive Straight/tines 5.3F 45/52/58 PU Yes IS-1 2.5
4574-45/53 Bi A Passive J-shape/tines 5.3F 45/53 PU Yes IS-1 2.5
Other active fixation leads
4058M-85 Bi A/V Active 85 PU No IS-1
4557M-53 Uni A preformed J Active 53 No IS-1
6

4558M-53 Bi A preformed J Active 53 No IS-1


Select Secure®
3830-59/69/74 Bi A/V Active Fixed helix 4.1F 59/69Si/ETFE Yes IS-1 3.6
Sorin
Stelid II
BTF25/26D Bi A or V Passive Tines 8F 52/59 Si Yes IS-1 2vc
UTF25/26D Uni A or V Passive Tines 8F 52/59 Yes IS-1 2vc
BJF24D Bi Atrial J Passive Tines 8F 45 Yes IS-1 2
BJF25D Bi Atrial J Passive Tines 8F 52 Yes IS-1 2
Stelix Bi A or V Active Helix/screw 9F Yes IS-1 2vc
Stelix II
BRF25/26D Bi A or V Active Helix/screw 8F 52/59 Si Yes IS-1 2vc
Permanent Pacemakers and Leads
X-Fine™TX25D/26D Bi V Passive Tines 4.8F 52/58PU Yes IS-1 2
Beflex RF44D/45D/46D Bi A Active Screw/straight 6F 45/52/58Si Yes IS-1 4
Tilda JT Bi Atrial J Passive Tines 6.5F 45/53Si Yes IS-1 1.3
Tilda T Bi A or V Passive Tines 6.5F 53/60Si Yes IS-1 1.3
Tilda R Bi A or V Active Retract screw 6.7F 45/53/60Si Yes IS-1 4.5
Digital Pacemaker Technology

St. Jude Medical


Tendril® ST 1788TCe Bi A/V Active Helix/screw 6F 40/46/52/58/65 Yes IS-1
Tendril® ST 1782TCe Bi Atrial J Active Helix/screw 7F 40/46/52 Yes IS-1
Tendril® ST Optimf Bi A/V Active Helix/screw 6F 46/52/58 Yes IS-1
1888TC
Tendril® ST Optimf Bi Atrial J Active Helix/screw 7F 40/46/52 Yes IS-1
1882TC
Tendril™ STS 2088TCf Bi A/V Active Helix/screw 6F 46/52/58 Yes IS-1
OptiSense™ Optim™ Bi Atrial Active Helix/screw 7F 40/46/52 Yes IS-1
1999f
Isoflex Optim™ 1944f Bi Atrial J Passive Tines 7F 46/52 Yes IS-1
Isoflex Optim™ 1948f Bi A/V Passive Tines 7F 46/52/58 Yes IS-1
Isoflex 1646Tg Bi A/V Passive Tines 7F 34/40/46/52/58/85 Yes IS-1
Isoflex 1642Tg Bi Atrial J Passive Tines 7F 40/46/52 Yes IS-1
Isoflex 1644Th Bi Atrial J Passive Tines 7F 34/40/46/52 Yes IS-1
Isoflex 1648Th Bi A/V Passive Tines 7F 34/40/46/52/58/85 Yes IS-1
AV Plus DX VDD 1368g Bi VDD Single Pass/ Tines 9F 52/58/65 Yes IS-1
bifurcated
a
ProMRI – MRI conditional safe lead
b
Silicone insulation
c
Silicone/polyurethane insulation
d
Length of lead in cm is indicated after hyphen. Custom lengths of some leads are available at a surcharge
e
Silicone-insulation, endocardial, steroid-eluting, active-fixation leads
f
Optim insulation
g
Silicone insulation
h
Polyurethane insulation
121
122 6 Permanent Pacemakers and Leads

Fig. 6.41 “Tined”


passive-fixation and
“screw-in” active-fixation
leads

Fig. 6.42 (Top) IS-1 Bipolar connector pin with arrow the electrode and is usually fixed as close to the lead’s
on suture collar. (Bottom) The suture collar (arrow) for venous entry point as possible
anchoring the lead to the pectoral fascia can be slid along

alloy of nickel/cobalt/chromium/molybdenum At the lead tip is the cathode which is composed


giving it ultra high strength, toughness, ductility, of an inert meterial such as platinum-iridum, stain-
and corrosion-resistance. The anode is made of less steel, Elgiloy or vitreous carbon. The tips have
IROX (Iridium oxide-coated titanium) and the a variety of designs and are sometimes “porous”
cathode of platinum-iridium. aimed at improving the surface area of contact with
The advantages and disadvantages of silcone the endocardium and minimizing the development
and polyurethane as lead insulating materials of inflammation and fibrous tissue which may
are shown in Table 6.9. The smaller the lead increase the pacing threshold. “Porous tips” increase
profile, the smaller the introducer can be. A contact with the electrolytes, reduce polarization
small profile enables easier insertion into smaller voltage, promote rapid tissue in-growth (Fig. 6.44),
veins and allows two leads to be inserted via one secure fixation and lower thresholds. This results in
introducer–which may be useful in certain reduced current drain and increased longevity of the
situations. pacemaker.
Digital Pacemaker Technology 123

Fig. 6.43 Electrodes are presented in a sterile, sealed transparent package (upper left) inside a sealed box which is
labeled in detail on the front and side (right and bottom left)

Table 6.9 Comparative advantages and disadvantages of exposure to body fluids, the steroid elutes from
silicone and polyurethane insulation on pacing leads the collar into the cardiac tissue, lowering acute
Silicone Polyurethane and chronic pacing thresholds and maximizing
Advantages Advantages sensing potentials. The CapSure® family of
Inert Biocompatible leads (Medtronic) employ similar steroid-elut-
Biocompatible High tear strength ing and platinization technology to provide sta-
Biostable Low friction coefficient ble, low pacing thresholds and a thin lead body
Less fibrotic while Stelix II (Sorin Group) has a vitreous car-
Small lead diameters bon tip and a steroid-eluting collar and the
Disadvantages Disadvantages Fineline II Sterox series (Guidant/Boston
High friction Environmental stress Scientific) have electrode tips coated with irid-
coefficient (sticky) Cracking
Handling damage Metal ion oxidation ium oxide (IROX™) to help reduce acute and
Size (for some types) Oxidative degeneration chronic pacing thresholds.
of the polyurethane The amount of energy required to pace the
insulation heart is related to the surface area of the cathode
tip. The lower the surface area, the higher the cur-
Activated carbon, sintered platinum-iridium, rent density at the tip/myocardium interface, the
and sputtered titanium-nitride are examples of higher the impedance and the lower the current
materials used to make porous tips. Many leads drain on the pacemaker batteries. This allows low
elute steroid, e.g., dexamethasone, from their output programming and increases longevity of
tips to minimize tissue reaction and a rise in the generator. Low surface area electrodes range
stimulation threshold. For example, the from 1.2 to 5 mm2.
Flextend® active fixation leads (Guidant/Boston Leads are available in various diameters (5.3–
Scientific) have a collar at the base of the helix 9.0 Fr), which enable smaller introducer sheaths
that contains dexamethasone acetate. Upon to be used. Their distal ends may be straight for
124 6 Permanent Pacemakers and Leads

Fig. 6.45 “Tined” passive-fixation lead

Fig. 6.44 Porous tip of pacing electrode promotes tissue


ingrowth

placement in the right ventricular apex or pre-


shaped into a “J” for attachment into the right
atrial appendage and may be passively or
actively-fixed to the endocardium. MRI-safe
leads are 6–7F diameter and ICD leads are 7–9F
diameter.

Passive Fixation
Fig. 6.46 Fixed “J-shaped” tined electrode for passive-
Passive fixation is achieved in the RV apex by fixation in the RA appendage
wedging the tip of the lead within the trabeculae
with the tip in direct contact with the endocar-
dium. This may be helped by a wedge-shape end Active Fixation
to the lead tip or by the use of “tines,” “flanges,”
or “fins” close to the lead tip (Figs. 6.45 and Active fixation is achieved in the RV apex, RV
6.46). Passive fixation of atrial leads in the RA free wall, RV septum/outflow tract, RA append-
appendage is best achieved by a pre-shaped “J” age, or anywhere else within the RA by the
and tined lead (Figs. 6.46 and 6.47) which can deployment of an extendable/retractable helix/
usually be positioned in the appendage by remov- coil from the distal end of the lead (Fig. 6.49).
ing the straight stylet within the lead. The tines The helix is extended and screwed into the endo/
on the atrial “J” cling onto the trabeculae within myocardium using a fixation tool (Fig. 6.50). The
the appendage (Fig. 6.48). Straight leads bearing tool is attached to the terminal pin and rotated
tines can also be placed in the atrial appendage clockwise (the number of turns depends on the
using the “J-shaped” stylet, and there is surpris- manufacturer) which protrudes the helix and
ingly little tendency for the lead to detach itself fixes it to the endocardium (Fig. 6.51). The tip
from the endocardium during removal of the sty- is electrically active which allows the implanter
let. The CapSure® SP Novus 4092 is an example to find an optimal placement site before fixing
of a straight, tined lead that can be placed by pas- the lead to the chamber wall. Fluoroscopy mark-
sive fixation into the RV apex and the CapSure® ers provide visible confirmation of helix posi-
SP Novus 4592 is a pre-shaped, tined atrial “J” tion and whether it is fully extended (Fig. 6.52).
lead that can be passively fixed in the RA The Fineline™ II Sterox EZ active fixation leads
appendage. (Boston Scientific) have a capsule of mannitol
Digital Pacemaker Technology 125

Fig. 6.47 (Upper) The “J”


electrode is straightened by
inserting a straight stylet
down the electrode’s fine
inner lumen. (Lower) Pulling
back the stylet once the tip is
in the RA appendage allows
the fixed “J” to take up its
shape and allow its tines to
fix on the trabeculated
muscle there

Fig. 6.48 Close-up view of this bipolar, passive fixation “J”-shape of this atrial electrode is shown, with its distal ste-
lead. (a) Proximal end of lead showing the two poles, with roid-eluting tip, its tines for passive-fixation and the two
the most proximal, cathode pole being covered by a remov- poles of the electrode being easily seen. (c) The distal portion
able plastic funnel. The latter makes it easier to introduce a of the same electrode after inserting a straight stylet within
stylet into the electrode’s fine inner lumen. (b) Distal it
126 6 Permanent Pacemakers and Leads

which covers the distal helix but which dissolves Atrial Leads
within 4 min of introduction into the heart. It has
no moving parts. Atrial leads may be actively fixed using an
extendable helix from a pre-shaped “J” lead or
from a straight lead with an extendable helix
using a “J” stylet to aid screwing the tip into the
endocardium of the RA appendage (Fig. 6.53).
Alternatively, a straight active-fixation lead can
be placed elsewhere within the RA and screwed
into position using the fixation tool. The
CapSureFix 4568 and 5568 (Medtronic) are
examples of a pre-shaped “J” actively-fixed lead
which is ideal for reducing the incidence of atrial
lead displacement (see Fig. 6.53). The Stelix II
(Sorin) and the CapSureFix 4076 and 5076 are
straight leads which can be actively fixed to the
RA using a “J” stylet and the fixation tool.

Polarity
Fig. 6.49 Active-fixation mechanism showing the
“screw” within and extended from the distal tip of this Both unipolar and bipolar leads are available,
active-fixation lead although bipolar leads are most commonly used.

Fig. 6.50 Fixation tool on connector pin


Digital Pacemaker Technology 127

Fig. 6.51 Mechanism of deployment of active-fixation helix in Medtronic’s 5078/5079 electrodes (Image reproduced
with permission of Medtronic, Inc.)

Unipolar leads have a single pacing conductor


and the pacemaker “can” acts as the sensing
electrode (anode). Bipolar leads have one pac-
ing conductor and one sensing conductor. The
anode and cathode are within the cardiac cham-
ber to be paced – the cathode being at the lead
tip and the anode just proximal to it. The charac-
teristics of each type of lead are shown in
Table 6.10.

Terminal Pin Sizes


Fig. 6.52 X-ray showing fixation of helical coil into RV
Before the implant procedure, it is important to myocardium
be certain that the terminal pin on the proximal
end of the lead(s) will fit into the header port of Special Leads
the pacemaker (Fig. 6.54). These may be IS-1
(3.2 mm, short pin with sealing rings), 5 or 6 mm A single VDD lead is available which is bipolar
in size, and pacing leads that are compatible with and has an atrial sensing electrode 13–15 cm
the pacemaker should be chosen for the proximal to the distal tip to enable sensing of
implantation procedure. Adaptors are available atrial activity without the need for a second lead
to enable upsizing or downsizing of the connec- (Fig. 6.56). The Solox® from Biotronik is 9F
tor pins to fit into a particular generator at the compatible and has a fractal electrically active
time of generator change, although most manu- surface of iridium. The CapSure® VDD2 Steroid-
facturers have made the IS-1 connector pin and eluting, single-pass lead (Models 5038, 5038S
port on the header unit standard features to leads and 5038L) from Medtronic provides a similar
and generators, respectively (Fig. 6.55). function. It allows for atrial tracking and main-
128 6 Permanent Pacemakers and Leads

tains AV synchrony using a single, steroid-eluting


lead. This special lead is available as uni- and
bipolar configuration for the ventricular lead but
the atrial sensing electrode is bipolar (Fig. 6.57).
An MRI-conditional safe lead – the 5086
CapSureFix® MRI™ Lead – is available from
Medtronic for use with the EnRhythm DR MRI™
SureScan® and Advisa DR MRI™ Surescan®
pacing systems which are MRI safe. The lead and
pacemaker are identifiable on X-ray as being
MRI-conditional safe (see Chap. 10). The bipo-
lar, active-fixation lead has an helix/ring elec-
trode of titanium nitride coated platinum alloy, a
conductor of MP35N nickel alloy, and insulation

Table 6.10 Characteristics of unipolar and bipolar leads


Unipolar Bipolar
1 pacing conductor 1 pacing + 1 sensing
conductor
Sensing from pacemaker Arranged coaxially,
“can” co-radially, or as parallel
coils within lead body
Large pacing spike on Small pacing spikes
surface ECG
Small diameter lead body Larger diameter lead body
Less rigid lead body Stiffer lead
More susceptible to Less susceptible to
Fig. 6.53 (a) Fixed “J,” unipolar, active-fixation atrial oversensing oversensing
electrode showing the extended “screw” (b) (Medtronic May produce muscle/ Less likely to cause muscle/
Model 4557) nerve stimulation nerve stimulation

Fig. 6.54 Connector pins


inside header unit of
generator
Pacemaker Lead Accessories 129

Fig. 6.55 IS-1 connector pin

Fig. 6.56 CapSure VDD


lead (Image reproduced with
permission of Medtronic,
Inc.)

Fig. 6.57 Close-up view of the atrial sensing and ventricular sense/pacing electrodes of the Capsure® VDD lead. The
atrial electrode is bipolar but the ventricular electrode is available as a unipolar (bottom) or bipolar (top) connector

made of treated silicone rubber. It is available in range of “upsizing” and “downsizing” unipolar
three lengths: 45, 52, and 58 cm. and bipolar adaptors and lead extensions to
enable physicians to exchange pacemaker pins
to connect to different size header ports during
Pacemaker Lead Accessories generator-exchange procedures (Fig. 6.58).
Others such as the “iLink-BLV-10” bifurcated
A variety of useful accessories are available implantable lead adaptor enable the adaption of
from both pacemaker manufacturers and other one bipolar LV-1 connector and one bipolar IS-1
sources (e.g., Oscor® Inc.). These include a connector to one bipolar IS-1 header unit, and
130 6 Permanent Pacemakers and Leads

Fig. 6.58 Four of the many useful accessories from Oscor® lengths are 15 and 20 cm. (c) BIS/BIS implantable lead
Inc. (a) The VKU/V lead extender extends an implanted extension consists of one IS-1 receptacle and one IS-1 con-
unipolar lead (whose connector is removed) to a pacemaker nector – 10 and 40 cm lengths are available. (d) M/IS
with an IS-1 port – available in 10, 20, and 40 cm lengths. implantable lead adaptor consists of one 5 mm receptacle
(b) B/IS implantable lead adaptor consists of two unipolar and one IS-1 connector – 10 and 40 cm lengths are available
5 mm receptacles and one bipolar IS-1 connector. Standard (Courtesy of Oscor Inc., Palm Harbor, Fl, USA)

Fig. 6.59 (Upper) iLink-BLV-10 bifurcated implantable able lead adaptor enables the adaption of one unipolar
lead adaptor enables the adaption of one bipolar LV-1 LV-1 (1.8 mm) connector and one bipolar IS-1 connector
connector and one bipolar IS-1 connector to one bipolar to one bipolar IS-1 pacemaker header unit (Courtesy of
IS-1 header unit. (Lower) the Dyad-LV bifurcated implant- Oscor Inc., Palm Harbor, Fl, USA)

the Dyad-LV bifurcated implantable lead adap- have been in-situ for many years and where a
tor enables the adaption of one unipolar LV-1 difficult or challenging lead extraction procedure
(1.8 mm) connector and one bipolar IS-1 con- is anticipated. Figure 6.58 shows examples of the
nector to one bipolar IS-1 pacemaker header sort of adaptors and lead extensions that are
unit (Fig. 6.59). available.
In certain circumstances, they also allow oper- Silicone “end-caps,” for insulating and sealing
ators to repair fractured electrodes or leads with redundant 5 or 3.3 mm connector pins; adaptor
broken insulation without having to explant the sleeves, for adapting a 5 mm connector to a 6 mm
entire lead – particularly important in leads that connector; ligature sleeves (of various lengths)
Pacemaker Prescription 131

Fig. 6.60 Accessories include lead end-cap kits, screwdrivers, and pin-plug kits

Fig. 6.61 All the accessories are presented in well-labeled sterile packaging. Screwdriver kit, pin-plug kit, and stylet-
kit are shown

for protecting lead insulation from their anchor- Pacemaker Prescription


ing sutures; “VV-plugs” for plugging up an empty
header cavity; spare PY fixation tools, straight The type of pacemaker required for each indi-
and “J” stylets, screwdrivers and repositioning vidual patient depends on the type of conduction
kits containing stylets and fixation tool are avail- disturbance that is present, e.g., sinus node dis-
able and worth having in a busy pacing center ease, AV block etc., the basic rhythm that is pres-
(Figs. 6.60 and 6.61). ent, whether atrial tachyarrhythmias are present
132 6 Permanent Pacemakers and Leads

and whether chronotropic incompetence is pres- mittent AV block, dual chamber pacemakers with
ent or absent. It is accepted that unnecessary RV algorithms to minimize RV pacing are indicated
pacing may adversely affect heart failure morbid- and rate adaptation should not be used unless
ity and overall mortality and so it is important to there is evidence of symptomatic chronotropic
try and reduce RV pacing as much as possible incompetence. For those with complete AV block
without compromising hemodynamics. Ideally, and normal systolic ventricular function, alterna-
RV pacing should be reduced to below 40% and tive RV pacing sites may be chosen over the RV
as close to 10% as possible in order to maximize apex. In patients with symptomatic LV dysfunc-
the beneficial effects on reducing heart failure tion and AV block, CRT should be considered
morbidity. Algorithms in devices, such as MVP® (see Chap. 16). Whether this should be CRT-P or
(Medtronic) and SafeR™ (Sorin Group), are CRT -D depends on a variety of clinical factors,
designed to minimize RV pacing. Unfortunately, the etiology of the LV dysfunction, the risk of
several factors may hamper achieving the 10% sudden cardiac death, and other comorbidities
target. These include the presence of complete that influence survival.
heart block, progression of AV node disease, and Simply leaving a device set at the nominal
episodes of atrial fibrillation with a slow ventric- parameters at the time of implant is unaccept-
ular response. Closed loop stimulation pacing able. An attempt must be made to preserve
(see above) may offer some advantages in this spontaneous atrial activity and to promote
regard. The Biotronik Evia device may be useful intrinsic conduction. Thus rate adaptation
in higher risk groups. should only be used when clinically indicated
Guides to prescription for patients with sinus and the device must be programmed to promote
node disease and for those with acquired AV intrinsic conduction.
block, chronic bifascicular block, and trifascicu-
lar block are shown in Figs. 6.62 and 6.63. Correct
pacemaker prescription must now be recognized Pacemaker Analyzers/Programmers
as an issue for Clinical Governance committees
and physicians and pacing centers should be Device specialists and technicians must be famil-
shown to be practicing to recommended national/ iar with current pacemaker programmers which
international standards. are computer-based, complex devices them-
In general, every effort should be made to selves. Currently available devices are listed
minimize ventricular pacing. AAIR pacing should in (Table 6.11). Programmers enable both pro-
be used in patients with SND, a normal PR inter- grammability and telemetry of data including
val, and an intraventricular conduction delay of programming commands, administrative data,
<120 ms, where the progression to AV block is measured data, diagnostic data, and programmed
approximately 0.6% per year. In patients without data (Fig. 6.64).
chronotropic incompetence, back-up VVI pacing Data can be input using a keyboard, light pen
(40–50 bpm) may be appropriate as most cases and/or “touch-screen” facility (Fig. 6.65). The
will require pacing <1% of the time. Alternatively, telemetry interface between pacemaker and pro-
as indicated above, one could consider a device grammer/analyzer may be a “wand” placed
with an algorithm that adapts the AV delay to directly over the pacemaker and connected
promote intrinsic conduction or that mode directly to the programmer (Fig. 6.66) or more
switches from AAI to DDD pacing. commonly by wireless telemetry. Radiofrequency
In patients with AV block, the choice of pac- energy allows for rapid transmission of large
ing device depends on whether the block is per- volumes of data through high frequency waves
manent or intermittent and whether the ventricular emitted by the programmer’s antenna and
function is normal or not. For example, for inter- received by the pacemaker’s antenna.
Pacemaker Analyzers/Programmers 133

Sinus node disease

Sinus bradycardia

Atrioventricular block

No Yes

Chronotropic Chronotropic Chronotropic


Incompetence: Incompetence: Incompetence:
absent present/absent present/absent

Atrial Atrial Atrial


tachyarrhythmias: tachyarrhythmias: tachyarrhythmias:
present absent absent

DDDR + MPV AAIR DDDR + MPV


Class IIa Class I Class I
Level of evidence C Level of evidence C Level of evidence C

DDDR + MPV DDDR + MPV


+ ANTITACHY Class IIa
Class IIb Level of evidence C
Level of evidence C

ANTITACHY = antitachycardia algorithms in pacemaker; MPV = Minimization of Pacing in the Ventricles.


Note: In sinus node disease WIR and VDDR modes are considered unsuitable and are not recommended.
Where Atrioventricular block exists AAIR is considered inappropriate.

Fig. 6.62 Guide for prescription of pacemaker in sinus node disease (Courtesy of European Society of Cardiology)
134 6 Permanent Pacemakers and Leads

Atrioventricular
block, chronic bifascicular
and trifascicular block

Sinus rhythm

NO YES

Chronotropic Chronotropic
Incompetence Incompetence

No Yes No Yes

VDD/DDD* DDDR*
WI WIR Class IIa Class IIa
Class I Class I Level of Level of
Level of Level of evidence A evidence A
evidence C evidence C
WI WIR
Class IIb Class IIb
Level of Level of
evidence C evidence C

When atrioventricular block is not permanent, pacemakers with algorithms for preservation of native
atrioventricular conduction should be selected.
* WIR could be an alternative, especially in patients who have a low level of physical activity and in those
with a short expected lifespan.

Fig. 6.63 Guide for prescription of pacemaker in atrioventricular block, chronic bifascicular block, and trifascicular
block (Courtesy of European Society of Cardiology)
Pacemaker Analyzers/Programmers 135

Table 6.11 Pacemaker programmers/analyzers


Programmer Manufacturer Features
Orchestra Sorin SmartView – user-friendly; automatic recognition; color coded
interrogation and programming; easy retrieval of follow-up data;
one-touch/one screen – promotes easy navigation through
follow-up session
Merlin St. Jude Medical Three channel PSA; beat-to-beat analysis; allows bi-ventricular
testing at implantation
Zoom® Boston Scientific/Guidant Quick start-up, rapid device interrogation, touch screen, high
quality ECG
CareLink® 2290 Medtronic/Vitatron Automatic measurement of P- and R-wave amplitudes and slew
rates and lead impedance
Real-time display of atrial and ventricular EGM, rapid atrial
stimulation to 800 ppm
Antegrade and retrograde conduction tests, pulse width versus
amplitude threshold analysis; measurement reports
Renamic Biotronik Wireless antenna, fast follow-up, bluetooth file transfer, bluetooth
printing, automatic R and P wave measurement, auto-threshold,
retrograde conduction measurement, NIPS, overdrive pacing,
internal data archiving, GSM connectivity, PSA module

Fig. 6.64 Programmers/analyzers from the various manufacturers


136 6 Permanent Pacemakers and Leads

Fig. 6.65 Light-pen,


touch-screen programming
facility of the Medtronic
programmer/analyzer

Fig. 6.66 Wand placed


directly over the patient’s
pacemaker during interroga-
tion and reprogramming
Implantation Technique
7

Permanent pacemaker implantation is most com- devices are usually buried behind the rectus abdo-
monly performed via the left or right subclavian or minis muscle. In patients with an occluded superior
axillary vein. A cephalic vein may be used, and vena cava, pacing electrodes can be inserted via a
although it has advantages this approach has limita- femoral vein and the generator buried subcutane-
tions. If the leads are inserted by either of these ously in the lower abdominal wall.
routes then the generator is placed between the sub-
cutaneous fat and the surface of pectoralis major
muscle in a prepectoral pocket. In very thin or ema- Operating Theater/Pacing Room
ciated patients or in those who wish the generator to
be hidden completely from view, the generator may Pacemaker implantation should be performed
be placed behind the pectoralis muscle. An alterna- in a sterile operating theater with appropriate
tive site is the axilla, but this is rarely used. Epicardial ventilation and lighting (Figs. 7.1–7.3). A “clean”

Fig. 7.1 Sterile operating theater should be appropriately ventilated and fully equipped

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 137


DOI 10.1007/978-1-4471-2939-4_7, © Springer-Verlag London 2012
138 7 Implantation Technique

Fig. 7.2 An operating table suitable for X-ray screening, Fig. 7.3 An operating light whose angle is easy to adjust
anesthetic equipment, piped gases, and oxygen and physi- is particularly helpful
ological monitoring equipment are essential

catheter laboratory is a poor substitute for a dedi- tion for visualization of fine guidewires and have
cated pacing theater and a poor use of the dose-saving features (Fig. 7.5). It should have a
resource. The room should have the recom- 9 inch field size with three magnification fields,
mended 20 air changes per hour with positive 14, 17, and 23 cm available and a foot pedal is
pressure relative to adjoining space. The room ideal to allow the operator to screen the chest
should be adequately protected for radiation with during lead positioning. The system should be
2 mm lead-equivalent lining for walls and easy to maneuver. The angles of rotation of the
doors. C-arm should range from 45° left anterior
oblique (LAO) to lateral, with cranial and caudal
angulations of 20° as a minimum standard.
Ideally it should have a low-dose program for
Equipment and Personnel extended screening procedures, a rotating anode,
pulsed fluoroscopy and digital acquisition. A
The room should be fully equipped with a high facility for archiving images acquired during
quality fluoroscope, such as a mobile C-arm implantation and a split-screen facility for road-
fluoroscope or image intensifier, e.g., Philips BV mapping is useful (especially for CRT implants)
Pulsera (Fig. 7.4), and ideally operated by a fully but not essential. The archiving for the system
trained radiographer. The intensifier should have could be onto CD ROM or networked via a PACS
excellent image quality with good image resolu- (Picture Archiving and Communications System)
Equipment and Personnel 139

Fig. 7.4 A mobile C-arm fluoroscope or image intensifier, e.g., Philips BV Pulsera

and image transfer for static and dynamic images


should be available.
ECG monitoring is essential as is a trained
physiological measurement technician/clinical
physiologist experienced in pacing whose task
will be to perform and record the stimulation
and sensing threshold tests and lead impedance
measurements from atrial and/or ventricular
leads once they have been positioned by the car-
diologist (Fig. 7.6). Facilities for defibrillation
and external transthoracic pacing must be present
and readily available during pacemaker implan-
tation (Fig. 7.7).
An experienced theater nurse familiar with
pacing procedures is an essential member of the
pacing team. He or she will be responsible for
providing the equipment necessary for the
implantation and will be fully familiar with the
type of procedures being performed in the center.
A “scrub-nurse” or “runner” is sadly now a lux-
ury. Access to an anesthetist should be readily
available.
Staff should be trained and validated to deliver
Fig. 7.5 Excellent image quality with good image reso-
advanced life support.
lution, the facility for archiving images acquired during
implantation and a split-screen facility for road-mapping An operating table specifically designed to
is available from Philips allow X-ray screening is necessary for temporary
140 7 Implantation Technique

Fig. 7.6 Physiological measurement technician/clinical physiologist, pacemaker analyzer and ECG monitor/defibrillator

and permanent pacemaker implantation


procedures (Fig. 7.8). It should be constructed
of radiolucent carbon fiber, have a floating top,
have the facility for Trendelenburg/reverse tilt-
ing the patient into a “head-up” or “head-down”
position (±25°), be height-adjustable, and have
the pivot support of the table offset to allow
free movement and easy positioning of the
fluoroscope around the patient. The Stille
ImagiQ™ Imaging Table is a good example. A
lead shield hangs from the operator’s side of the
table to reduce radiation scatter to the operator
(Fig. 7.9).

Instrument Pack

A typical pack containing instruments that are


useful for implantation of pacemakers is shown
in Figs. 7.10–7.12. A list of the contents is
shown in Table 7.1. Included in the pack or
available as a separate item is a large specially
designed pacemaker drape with adhesive back-
ing surrounding a window through which the
Fig. 7.7 Medtronic’s pacemaker analyzer and Lifepak 12 skin incision is made (see below). This is usu-
ECG monitor/defibrillator ally large enough to drape the whole of the
Instrument Pack 141

Fig. 7.8 The Stille ImagiQ™ imaging table, specifically designed to allow X-ray screening is ideal for temporary and
permanent pacemaker implantation procedures

Fig. 7.9 A lead screen hangs from the side of the table to protect the operator against X-ray scatter
142 7 Implantation Technique

patient and create a sterile field for the operator. Preprocedure


The head of the fluoroscope is covered with a
sterile plastic cover – with asepsis in mind If not already obtained, consent for the procedure
(Figs. 7.13 and 7.14). should be obtained from the patient after due
explanation of the benefits and risks of the proce-
dure. The risks and their approximate incidence
are shown in Table 7.2. The patient should be
fasted from food for at least 6 h before an elective
procedure. Patients are generally allowed to drink
water up until 2 h prior to the procedure – as per
local sedation policy. The practice of giving anti-
biotics prophylactically pre- and postprocedure
in an attempt to prevent pacemaker wound infec-
tion is widespread, but the published literature on
its efficacy is somewhat contradictory. However,
antibiotics are no substitute for a sterile operating
theater and meticulous aseptic technique before
and during implantation.
If antibiotics are to be given, anti-staphylococcal
agents should be the treatment of choice, e.g., 1 G
flucloxacillin IV at or ½ h before implantation and
500 mg qds orally for 2 days afterward. 1.5 G cefu-
roxime given IV just prior to the procedure may be
just as effective. For those allergic to penicillin, 1 G
of vancomycin IV in 500 ml of normal saline over
2 h followed by erythromycin 500 mg qds for
2 days is reasonable, although 800 mg teicoplanin
IV 30–60 min preprocedure and again 4 h postpro-
Fig. 7.10 Sterile Instrument pack cedure is perhaps more convenient.

Fig. 7.11 The number and


type of instruments in the
tray is usually chosen by the
device specialists responsible
for implantation
Preprocedure 143

Fig. 7.12 The ShortStop®


(Merit Medical) is a useful
safety device into which all
needles and scalpel blades
can be inserted after use

Table 7.1 Equipment provided within a typical pacemaker


pack
Instruments
2 sponge-holding forceps
2 towel clips
2 Halsted Mosquito artery forceps curved 12.5 cm
1 straight scissor 13 cm
1 Kilner needleholder 16.5 cm
1 McIndoe dressing forcep 15 cm
1 Gillies toothed dissecting forcep 15 cm
1 self-retaining retractor blunt
2 Gallipot polypropylene 60 ml
Two 6″ polypropylene bowls
Scalpel
18 gauge needle
10 ml syringe
20 ml syringe
Dressings/swabs
2 towel dressing crepe fld 2 ply 45 × 50 cm N/ST Fig. 7.13 An elasticated sterile plastic cover (arrow) is
2 swab XRD gauze 32 ply 10 × 7.5 cm T5 N/ST used to cover the head of the fluoroscope
Covers/drapes
1 large disposable drape – 205 cm wide × 262 cm long –
e.g., Guardian BDF ltd., Girvan, Ayrshire, Scotland
1 plastic elasticated cover for head of fluoroscope
57 cm diameter
144 7 Implantation Technique

Fig. 7.14 Sterile plastic cover on fluoroscope head (arrow)

Table 7.2 Approximate incidence of complications during


permanent pacemaker implantation as quoted to patients
during consent procedure
Arrhythmias 1%
Pneumothorax 1%
Hematoma 1%
Lead displacement 1–2%
Infection 1%
RV perforation – hemopericardium/ £1%
tamponade

Fig. 7.15 “Scrub-up” room is adjacent to the pacing theater


It is our practice to wash the upper chest/pro-
posed pacemaker implantation site with chlor-
hexidine or povidone-iodine solution on the ward
prior to the procedure.

Procedure

After thorough hand washing in a scrub-up room


(Fig. 7.15), the operator should wear hat, gown,
gloves, and mask and use strict aseptic technique
in order to minimize the chance of infection
(Fig. 7.16).
The patient should lie comfortably on the
operating table and a pillow is provided for head
support. The skin is again washed with 0.5–2%
chlorhexidine solution, povidone-iodine solution,
or both and the area allowed to dry (Figs. 7.17–
7.19). A sterile drape should then be placed
underneath the patient’s head before covering the
patient with the large drape designed specially
for the procedure, e.g., Guardian pacemaker
drape (Guardian Ltd., Ayrshire) (Figs. 7.20– Fig. 7.16 Operator is gowned and gloved and wears hat
7.25). Some operators like to cover the “window” and mask
Procedure 145

Fig. 7.17 Antiseptic solution can be colored with a red


dye (arrow) to help ensure that the appropriate area of
Fig. 7.19 The axilla, neck, and supraclavicular region
skin is painted
should be included in the area being cleaned

Fig. 7.20 Sterile drape from Guardian showing the adhe-


sive section and the “cut-out” window to be placed over
the operation site

Fig. 7.18 Left pectoral region is cleaned with antiseptic


146 7 Implantation Technique

Fig. 7.21 Covering the patient with the sterile drape


Fig. 7.23 The drape covers the patient’s feet and creates
a large sterile field

Fig. 7.24 The patient’s face is covered with a clear plastic


section of the drape, with the latter elevated off the face

in the drape with Ioban™ (3M Health Care) for


added protection (Fig. 7.26).
Between 20 and 40 ml of 1% lignocaine (3 mg/
kg) is then infiltrated in and around the skin and
Fig. 7.22 The top of the drape is made of clear plastic subcutaneous tissue over the pectoralis major as
which is elevated above the patient’s face by a horizontal well as around and under the clavicle where the
pole fixed to the table (see Fig. 7.24) subclavian vein is to be punctured (Fig. 7.27).
Procedure 147

Fig. 7.27 1% lignocaine is infiltrated into the operation site


Fig. 7.25 Positioning the window over the site of incision

than one lead is to be inserted. Leads are inserted


via an infraclavicular subclavian vein puncture,
anchored with sutures and then connected to the
generator which is then placed in a subcutaneous
pocket fashioned by blunt dissection over pecto-
ralis major.
The left subclavian vein is usually preferred to
the right because of the straight course it takes to
the superior vena cava. There are exceptions, for
example, when a left-sided SVC is encountered
(see below). An incision is made 2 cm below the
Fig. 7.26 Ioban™ (3M Health Care) may be placed over junction of the middle and inner thirds of the
the drape and skin at the operating site clavicle and the incision extended in a lateral and
inferior direction for approximately 4–6 cm
Within 5 min, the area should be anesthetized (Fig. 7.28). A prepectoral pocket large enough to
sufficiently to proceed with implantation. accommodate the generator and attached elec-
trodes is created by blunt dissection (Figs. 7.29–
7.31). The pocket should be deep enough to take
Subclavian Approach the generator and attached leads away from the
skin edges. Any bleeding should be stopped by
This approach is widely used and the route of tying-off significant vessels by direct ligature with
choice for most cases and especially when more a suitable suture or by the use of diathermy. The
148 7 Implantation Technique

Fig. 7.28 Skin incision Fig. 7.29 A retractor may be used to help dissection
(identify the cephalic vein if necessary) and make a pocket

Fig. 7.30 The fingers are used effectively for blunt Fig. 7.31 Making the pacemaker pocket
dissection

pocket may be packed with a wet gauze swab until An 18 (1.2 mm) gauge 7 cm long needle that
the leads are ready to be attached to the generator. comes with the introducer pack is inserted into
Entry into the subclavian vein (SCV) is made the SCV just below the inferior border of the
easier if the vein is distended. Dehydration, which clavicle at the junction of its middle and inner
reduces venous pressure should be corrected. thirds and the tip aimed at the sternoclavicular
Tilting the table into a head-down position will joint, so that it passes behind and close to the pos-
help to achieve distension of the SCV (Fig. 7.32). terior surface of the clavicle (Fig. 7.33). When
Procedure 149

Fig. 7.32 Top: Head-down tilt is useful to distend the Trendelenberg position to help distend the subclavian
left subclavian vein prior to needle puncture. Bottom: vein prior to needle puncture
Table is clearly seen to be in a “feet-up”/“head-down”

the needle punctures the vein, venous blood is guidewire with a “J-shaped” tip through the nee-
aspirated easily. In patients with bowed chest dle (Seldinger technique) (Figs. 7.34 and 7.35)
walls, or where the clavicle bows anteriorly, the and into the SVC. No resistance to guidewire
SCV puncture should be performed slightly more passage should be felt; resistance usually means
laterally and aimed slightly more posteriorly than that the guidewire is not in the vein. Fluoroscopy
described above. Cannulation of the vein is then can be used to check that the tip of the J-wire is in
done by introducing a flexible 0.035″ (0.97 mm) the SVC/RA. The needle is then removed
150 7 Implantation Technique

Fig. 7.34 Inserting “J” guidewire into needle

Fig. 7.35 Guidewire inside needle within subclavian vein

Fig. 7.33 Puncture of the subclavian vein. Top:


Landmarks: The subclavian vein passes between the junc-
Fig. 7.36 Needle removed and guidewire left within the
tion of the medial and middle thirds of the clavicle and
subclavian vein
the suprasternal notch/sternoclavicular joint. Bottom: The
needle is kept parallel to the frontal plane and close to the
deep surface of the clavicle/sternum in order to avoid below the diaphragm in order to ensure that the
puncture of the pleura and subclavian artery
guidewire has not been inadvertently placed into
the subclavian artery – before advancing the
(Fig. 7.36). If a second lead is being inserted, a introducer sheath. This may be particularly help-
second SCV puncture is made and a second ful in patients with low systemic pressures.
guidewire inserted as just described (Figs. 7.37 A 20 cm long vessel dilator/sheath combina-
and 7.38). Some operators screen the wire to tion is then placed over each guidewire in turn
Procedure 151

Fig. 7.37 A second needle puncture is performed if a Fig. 7.38 Two guidewires within the subclavian vein
second lead is to be inserted

Fig. 7.39 Top: Vessel


dilator and peel-away
sheath (St. Jude Medical).
Bottom: Vessel dilator
and peel-away sheath
being advanced over a
guidewire

and pushed through the subcutaneous tissue slightly head-down position so that air embo-
and fascia and into the SCV and on into the lism is avoided. Getting the patient to stop talk-
SVC (Figs. 7.39–7.42). The wire and vessel ing and breathing during this maneuver also
dilator are then removed (Fig. 7.43) and the helps. Once the lead tip is in the upper SVC,
lead is inserted into the remaining “splittable” the sheath can be withdrawn and “peeled away”
sheath (Figs. 7.44– 7.46). This is best done in a from the lead (see below) leaving the electrode
152 7 Implantation Technique

Fig. 7.40 Vessel dilator and sheath being advanced over Fig. 7.43 Vessel dilator (blue) and guidewire being
the guidewire and through the clavipectoral fascia under removed from sheath (white)
the clavicle into the subclavian vein

Fig. 7.41 Firm pressure is necessary to advance the Fig. 7.44 The ventricular lead is inserted into the intro-
introducer into the subclavian vein ducer sheath

Fig. 7.42 Introducer fully inserted over one of the Fig. 7.45 Lead is advanced through the sheath and into
guidewires the right atrium
Procedure 153

Fig. 7.46 Lead fully inserted into sheath Fig. 7.48 Second vessel dilator and sheath being intro-
duced over the guidewire

Fig. 7.47 The ventricular lead within the subclavian vein Fig. 7.49 Introducer fully inserted
and the “peel-away” sheath removed

within the circulation (Fig. 7.47). If a second The right SCV is accessible in a similar way
lead is to be introduced into the left SCV, a sec- to the left SCV described above. However, the
ond sheath/vessel dilator is then placed along SCV may make an almost 90° descent into the
the second guidewire into the SVC and the sec- SVC.
ond lead inserted as described above A range of “peel-away” introducer sheaths
(Figs. 7.48–7.52). The sheath can then be which are available from Medtronic is shown in
“peeled away” (Fig. 7.53). Table 7.3. Some have a hemostatic valve and a
Alternatively, a guidewire can be left in the side-port for drug infusion.
first sheath and a second vessel dilator/sheath
combination placed over the wire next to the first
electrode and then the outer sheath “peeled-away” Cephalic Vein Approach
as described. The only drawback to this technique
is that the two leads tend to move each other dur- This approach was commonly used before plastic
ing positioning of the electrodes, unlike when introducer sheaths were available and is still used
two separate punctures are made – but it does routinely by some operators. After administration
reduce the number of SCV punctures. of local anesthetic to the pectoral region, it involves
154 7 Implantation Technique

Fig. 7.50 Vessel dilator being removed


Fig. 7.53 “Peel-away” sheath being removed

Table 7.3 “Peelable/splittable sheath” pacemaker lead


introducers (Medtronic)
Model no. Size
Single chamber introducersa
6207/6208/6209/6210-S1 7F/8F/9F/10F
6211/6212/6214-S1 11F/12F/14F
Dual chamber introducers (2 sheaths per kit)b
6208/6209/6210/6211-D1 8F/9F/10.5F/11F
Hemostatic, “tear-away” percutaneous lead introducer
with infusion side port (Medtronic)c
HLS 1007/1008/1009/ 7F/8F/9F/10.5F/11F
Fig. 7.51 Atrial lead being introduced into sheath
10105/1011M × 13 cm tear-away
valved sheath w/side
port
a
Cost approximately £27
b
Cost approximately £40
c
Cost approximately £45

border extending over the deltopectoral groove.


The vein is then dissected free from the fat and
sutures should be placed proximally and distally
(Figs. 7.55, and 7.56) and a cut down performed.
This should enable a guidewire and 7 Fr dilator to
be placed within the vein and then an electrode can
be introduced to the right atrium/ventricle
Fig. 7.52 Atrial lead within the sheath
(Figs. 7.57–7.62). If there is difficulty in advancing
the guidewire, venography can be done via the dila-
cutting down onto the cephalic vein (using an tor in order to demonstrate the anatomy. Unfor-
oblique incision) in the deltopectoral groove, which tunately the vein is sometimes too small to be used
can sometimes be identified by the presence of fatty or only large enough to accommodate one elec-
tissue between pectoralis major and deltoid mus- trode. This technique eliminates the risk of pneu-
cles (Fig. 7.54). Alternatively, a horizontal incision mothorax during lead implantation and reduces
2 cm below the clavicle can be made with its lateral the subsequent risk of “subclavicular crush.”
Procedure 155

Fig. 7.54 Self-retaining retractor can be used to help Fig. 7.57 A “vein-picker” (yellow) is used to help inser-
identify and anchor the cephalic vein tion of a guidewire into the cephalic vein and beyond

Fig. 7.58 “Vein-picker” or “vein-lifter”

Fig. 7.55 Suture is placed around the distal end of the


cephalic vein

Fig. 7.59 Guidewire being advanced

Fig. 7.56 A second suture is placed around the proximal


end of the cephalic vein

Fig. 7.60 Guidewire further advanced


156 7 Implantation Technique

IJV IJV
EJV EJV
RIV LS-CV

RS-CV
LIV
AxV SVC

BV
CV

MBV

Fig. 7.61 Vessel dilator and sheath being inserted into MCV
the cephalic vein over the guidewire

Fig. 7.63 Venous anatomy of the upper limb/upper medi-


astinum relevant to pacing. MCV median cephalic vein,
Fig. 7.62 Lead being inserted into the cephalic vein MBV median basilic vein, BV basilic vein, CV cephalic
vein, AxV axillary vein, RS-CV right subclavian vein, RIV
right innominate vein, LIV left innominate vein, LS-CV
left subclavian vein, EJV external jugular vein, IJV inter-
Axillary Vein Approach nal jugular vein, SVC superior vena cava

The axillary vein is an alternative conduit for the


placement of pacing and defibrillation leads for the axillary system. The axillary vein begins at
several reasons. Unlike the cephalic vein, the the lower margin of the teres major muscle as a
axillary vein is almost always large enough to continuation of the brachial vein. It continues its
accommodate multiple pacing leads. When com- course proximally until it terminates at the lateral
pared to the subclavian vein, the axillary vein margin of the first rib to become the subclavian
affords a less acute course. This potentially vein. Along its course, it receives tributaries from
decreases mechanical stress on the implanted the cephalic and basilic veins (Fig. 7.63). The
leads or catheters and results in a lower incidence vein is accompanied, along its course, by the
of mechanical lead failure. Additionally, subcla- axillary artery, which lies slightly superior and
vian access is associated with the risk of inadver- posterior to the vein. Overlying the vein are the
tently accessing the noncompressible subclavian pectoralis minor and clavipectoral fascia, fol-
artery and the potential for increased mechanical lowed more superficially by the pectoralis major.
stress on the lead from crossing the subclavius A clinician can thus accurately and reliably can-
muscle and the clavipectoral fascia. Finally, use nulate the target vessel while minimizing the
of the axillary system does not require tunneling chance of injury to adjacent structures. Techniques
of the leads over or under the clavicle. for accessing the axillary and subclavian system
A thorough understanding of the regional with the aid of ultrasonographic imaging have
anatomy is essential to successful cannulation of also been used. However, because fluoroscopy is
Electrode Positioning 157

Fig. 7.65 Steel stylet

Fig. 7.64 Fluoroscopic-guided axillary vein puncture.


The arrow shows the tip of the needle just lateral to the
medial border of the first rib

an essential component of pacemaker and ICD


insertion, ultrasonography is rarely, if ever, used
for gaining access to the axillary system for these
procedures. In essence, this is a modified subcla-
vian approach and involves a fluoroscopically-
guided infraclavicular puncture, lateral to the
medial border of the first rib (Fig. 7.64). This
ensures an extra-thoracic puncture of the vein, Fig. 7.66 The stylet has a straight tip
thus eliminating the risk of pneumothorax. All of
the above precautions and tips for subclavian
vein puncture apply to the technique of axillary
vein lead placement.

Unusual Anatomy

Implanters of pacemakers and ICDs should be


fully familiar with the anatomy of the great veins
and the possible existence of congenital anoma-
lies (see Chap. 14).

Fig. 7.67 The tip is curved by gently curving the distal


Electrode Positioning stylet with the thumb and forefinger of the right hand

Ventricular Leads
maneuverability (Figs. 7.66–7.68) before placing
Pacing leads are very soft and flexible and can it within the hollow central lumen of the pacing
only be positioned in the RV by use of a stiffen- lead (Figs. 7.69 and 7.70). Stylets are available in
ing steel stylet (Fig. 7.65). A gentle curve should different lengths and variable degrees of stiffness
be shaped on the distal end of the stylet to help (Fig. 7.71).
158 7 Implantation Technique

Fig. 7.68 This curve on the distal end of the stylet will Fig. 7.69 Steel stylet being introduced into the lumen of
help the operator to get the pacing lead across the tricus- the lead via the plastic “funnel”
pid valve and the lead’s tip into the RV apex. A bigger
curve can be made on the stylet to help in positioning the
tip of an active-fixation lead onto the interventricular sep-
tum or RV outflow tract

Fig. 7.70 Gray knob on the proximal end of the stylet


which is inside this bipolar lead. Note the plastic “funnel”
which helps to place the stylet into the lead’s lumen

Fig. 7.71 Stylets of various lengths and tip-stiffness are available


Electrode Positioning 159

Fig. 7.72 Positioning the lead under fluoroscopy I Fig. 7.74 Retracting the stylet while advancing the lead
across the tricuspid valve en route toward the RV apex

trabeculae. Once satisfactory measurements are


confirmed (see below), the stylet is withdrawn
further into the brachiocephalic vein and atten-
tion is paid to examining the shape of the lead in
the RV and RA for the amount of slack in the lead
during inspiration and expiration. An example is
shown in Fig. 7.76.
More often the lead does not fall straight into
the RV apex. A loop or curve of distal lead should
be formed by withdrawing the stylet slightly and
impinging the lead tip on the lateral wall of the
Fig. 7.73 Positioning the lead under fluoroscopy II
RA, advancing the lead a little further and then
rotating the lead in order to flick the tip across the
tricuspid valve and into the RV. Ventricular ecto-
After entering the RA, using fluoroscopy the pic beats usually occur on entering the RV. If the
lead can usually be advanced across the tricuspid tip points upward, the lead may be in the pulmo-
valve into the RV by advancing the whole lead nary artery or in the coronary sinus. If in the PA,
with the stylet slightly withdrawn making the the lead can then be withdrawn and turned down
distal segment of the lead flexible (Figs. 7.72– into the RV apex. Again, the lead tip is negotiated
7.74). A diagrammatic representation of the tech- into the RV apex by a process of lead rotation,
nique of ventricular lead placement is shown in advancement and withdrawal. A satisfactory,
Fig. 7.75. Sometimes the tip can be directly stable position should be confirmed by checking
placed into the RV apex. The stylet can then be for continuous pacing at 1 V during coughing,
fully introduced into the lead and the latter pushed deep inspiration, and expiration. The lead shape
gently into the apex. The stylet can then be half and movement within the RA and RV should be
withdrawn and the lead observed by fluoroscopy observed during these respiratory movements.
to confirm a good anatomical stable position, The right anterior oblique (RAO) view is optimal
with the tip pointing slightly downward and ante- for visualization of the full length of the lead, as
riorly (especially for passive-fixation leads) the PA view foreshortens the lead. Ideally, the
(Fig. 7.76). The latter position can be confirmed lead should straighten slightly in the RA/RV dur-
by lateral fluoroscopy if necessary (Figs. 7.77 ing inspiration but not appear to pull on the api-
and 7.78). Tines or a conical shape on the lead’s cal segment, and should form a gentle curve
tip usually ensure passive fixation among the RV through the tricuspid valve during expiration but
160 7 Implantation Technique

LIV LIV

RIV RIV
SVC SVC

PA PA

RA RA
TV TV

RV
RV

IVC IVC

a b

LIV LIV

RIV RIV
SVC SVC

PA PA

RA
RA
TV TV

RV

IVC IVC RV

c
d

Fig. 7.75 Technique for placing a permanent ventricular Once the lead tip has been shown to enter the RVOT, there
lead into the right ventricular apex. (a) The lead and its sty- is no doubt that the lead is not in the coronary sinus or in the
let are inserted via the axillary or subclavian vein, innomi- low RA. (f) The lead/stylet can then be withdrawn slightly.
nate vein, and SVC into the Right atrium. Notice the position (g) The curved stylet may then be advanced to the tip of the
of the tip of the stylet (---) within the lead. (b) With the lead and the two advanced forward into the RV apex with
stylet withdrawn further into the lead, the lead is pushed gentle pressure. (h) With the stylet withdrawn slightly, the
against the wall of the RA in order to form a generous curve lead can be further advanced gently in order to try and
which (c) with further advancement can be advanced across wedge the tip between trabeculae and against the RV endo-
the tricuspid valve and into the RV cavity. (d) Rotation of cardium RIV Right Innominate Vein; LIV Left Innominate
the lead and advancement of the curved stylet will flick the Vein; SVC Superior Vena Cava; RA Right Atrium; RV
distal part of the electrode toward the right ventricular Right Ventricle; IVC Inferior Vena Cava; TV Tricuspid
outflow tract (RVOT)/pulmonary artery (see Fig. 7.75e). (e) Valve; PA Pulmonary Artery
Electrode Positioning 161

LIV LIV

RIV RIV
SVC SVC

PA PA

RA
TV RA TV

RV RV

IVC IVC
e f

LIV LIV

RIV RIV
SVC SVC

PA PA

RA RA
TV TV

RV RV

IVC IVC
h
g

Fig. 7.75 (continued)


162 7 Implantation Technique

Fig. 7.76 PA chest X-ray showing satisfactory “down-


ward-pointing” position of this passively-fixed ventricular
lead (arrow). The chest X-ray also shows appropriate
amounts of “slack” in the atrial and ventricular leads – best
assessed by screening during inspiration and expiration
Fig. 7.78 Lateral screening shows the lead tip to be posi-
tioned anteriorly in the RV apex (arrow)

Fig. 7.77 This active-fixation lead points downward into Fig. 7.79 A “downward-pointing” lead tip is not always
the RV apex (arrow) essential to obtain, as in this case with excellent electrical
and positional stability

not produce a redundant amount of lead in the


RA. Pacing at 5 V is advisable to rule out dia- anchored by placing the short sleeve around the
phragmatic stimulation. An LAO view will lead near its entry point into the SCV and sutur-
ensure that the lead is in the RV and not in the ing it to the fascia over the underlying muscle
coronary sinus. Once the operator is happy with with two nonabsorbable sutures, e.g., Ethilon®.
the lead position (Figs. 7.79 and 7.80), measure- Fixing the lead at this point should protect against
ments, and stability, the lead should then be displacement.
Electrode Positioning 163

Fig. 7.82 Rotating the tool during active-fixation

Fig. 7.80 The lateral X-ray again shows the lead point-
ing anteriorly toward the apex of the RV

Fig. 7.83 Fixation tool on the distal connector pin after


fixing the distal tip of the lead to the myocardium and
removal of the stylet

stylet are then removed from the lead and


fluoroscopy used to ensure a stable position of
Fig. 7.81 Actively-fixing the lead tip using the “lead-
fixing” tool attached to the distal connector pin the lead’s tip and that there is the right amount of
slack in the RV and RA during inspiration and
expiration (see Fig. 7.76).
If active fixation leads are to be used, the Recently, pacing the RV outflow tract (and in
anchoring maneuver with the fixing-tool is per- particular the RV septal portion of the RVOT)
formed once the electrode tip appears to be in an rather than the RV apex is becoming more
anatomically satisfactory position. With the sty- popular on the basis that this creates more
let still within the lead, the fixing tool is attached physiological conduction and some hemody-
to the lead’s connector pin and rotated 12–15 namic advantage. In particular, it is thought that
times in a clockwise direction (Figs. 7.81–7.83). long-term ventricular remodeling and dysfunc-
This maneuver extends the helical/spiked distal tion, cardiac failure, and atrial fibrillation are
lead tip which becomes “screwed” into the adja- less likely to occur with RV outflow tract pac-
cent myocardium (see Fig. 6.51). This may be ing compared to RV apical pacing. This may be
checked by fluoroscopy when a characteristic more important in children and younger adults
feature is evident (see Fig. 6.52). The tool and the than in the elderly. Clearly, an active-fixation
164 7 Implantation Technique

function that can reduce RV pacing by tran-


siently increasing the AV delay in an attempt to
search for intrinsic conduction. An advantage is
the return to the programmed AV delay if the
device does not verify intrinsic conduction and
activates RV pacing. RV pacing, if necessary, is
performed in conjunction with a more physio-
logic AV delay. More recently, manufacturers
have introduced algorithms consisting of
modified AAI pacing modes that can be switched
from an atrial-based mode (AAI or AAIR) to a
dual chamber mode when a device detects AV
block. This results in a dramatic reduction in
RV pacing, e.g., SafeR™ (Sorin Group) and
MVP™ (Medtronic). In patients with a high
degree of AV block, reducing the percentage of
RV pacing is not really feasible, and in this pop-
Fig. 7.84 Chest X-ray showing active-fixation of atrial ulation, alternative pacing sites from the RV
lead into the RA appendage and of the RV lead into the
apex may provide a more physiological situa-
interventricular septum
tion e.g., from RVOT.
There is little evidence that dual-site RV pac-
lead is required for RV outflow tract pacing. A ing offers any significant advantage. Biventricular
typical appearance is shown in Fig. 7.84. pacing is advantageous in patients with poor LV
However, there is little data to support the theo- function (see Chap. 16).
retical advantages of RV septal pacing over RV
apical pacing and indeed it is often not possible
to know for certain whether the lead is fixed to Atrial Leads
the septum or to the anterior or free walls.
Moreover, some patients, for example, those The usual site for atrial pacing is the RA append-
with patch repairs of ventricular septal defects, age, and active and passive fixation leads may be
are not suitable for alternative-site pacing. A used in this site. Elsewhere in the atrium, such as
left bundle branch block pattern QRS morphol- the atrial free wall or the interatrial septum,
ogy confirms RV apical pacing. Occasionally, a active fixation leads must be used. A lead with a
right bundle branch block morphology may be J-shaped distal portion is usually used. Cases in
seen with pacing from the RV septum. If RV which inter-atrial septal pacing should be pre-
apical pacing is accepted, then the pacemaker ferred include those with atrial arrhythmias and
should be programmed to minimize ventricular those requiring atrial-based bi-ventricular pac-
pacing if at all possible. Clinicians frequently ing with inter-atrial conduction delay, thus syn-
attempt to minimize RV pacing while maintain- chronizing the right and left AV delay. Passive
ing a dual chamber mode by programming the fixation leads usually have tines to hold the tip
device to very long paced and sensed AV delays. against the atrial myocardium, whereas active
However, this practice has potential problems. fixation leads must be screwed into the myocar-
First, very long AV delays, even when followed dium using a helix within its tip, as described
by intrinsic ventricular conduction or fusion, above.
may compromise atrial transport function. With passive-fixation leads with a pre-shaped
Second, RV pacing may not be significantly “J,” a straight stylet is first placed within the hol-
reduced especially at high pacing rates associ- low lead which straightens the distal portion of the
ated with rate responsive pacing. Many modern lead for advancement through the introducer
dual chamber devices contain an AV hysteresis sheath to the mid-RA. The straight stylet is then
Electrode Positioning 165

Fig. 7.88 “J” stylet fully inserted into atrial lead

Fig. 7.85 “J” stylet for use in deploying a lead into the
RA appendage

Fig. 7.89 Positioning the tip of the atrial lead into the RA
appendage requires careful maneuvering of the lead and
rotation of the stylet/lead combination

Fig. 7.86 Inserting “J” stylet into the atrial lead down the center of the lead which will help the
lead tip to be pulled up into the appendage
(Figs. 7.86–7.89). Several “J” stylets are usually
provided with each atrial lead. These have differ-
ent degrees of stiffness and curve to allow for the
variation in shape/size of a patient’s atrium/
appendage (Fig. 7.90). A diagrammatic represen-
tation of atrial lead placement is shown in Figs. 7.91
and 7.92. The use of the “J-shaped” stylet is always
necessary in straight leads being actively-fixed in
the RA. Correct positioning in the RA appendage
is usually evident by the lead tip moving from
side-to-side (“windscreen-wiper motion”) during
each atrial systole. Lateral screening shows the
Fig. 7.87 Advancing the “J” stylet into the atrial lead
lead tip pointing anteriorly. A good position is usu-
ally associated with a tall P-wave amplitude – ide-
withdrawn allowing the lead to assume its J-shape. ally >2 mV, recorded directly from the distal pole
Slight withdrawal of the lead may enable the lead of the electrode. The pacing threshold should be
tip to enter the RA appendage. If this is unsuccess- low (ideally <1 mV but 1–2 mV is acceptable). For
ful, a J-shaped stylet (Fig. 7.85) may be introduced active fixation leads, this is the appropriate time to
166 7 Implantation Technique

Fig. 7.90 Top left: Three “J” stylets accompanying the Gray knob a stylet with a longer curve forming almost a
Capsurefix® Novus 5076 lead (Medtronic) are presented “U”-shape to the stylet and lead once it is placed within.
within a plastic guard. Top right: They have different These alternative stylets are useful for lead positioning in
characteristics identifiable by the color of the knob on the the right atrium of different sizes and shapes. The “J”
proximal end of the stylet. Bottom left: The Blue knob shape itself enables the lead to be maneuvered within the
signifies a thin stylet which provides a “J”- shape to the RA when searching for the optimal position for sensing/
lead for positioning in the RA. The White knob signifies a pacing. Bottom right: Left to right – Blue stylet, white
slightly thicker/stiffer stylet for a “J”–“U”-shape, and the stylet, and gray stylet

LIV LIV
RIV RIV
SVC SVC

PA PA

RA
TV TV
RA

RV RV

IVC IVC

a b

Fig. 7.91 Technique for placing a permanent, “active- lead/“J” stylet combination pulled up against the atrial myo-
fixation,” atrial lead into the RA appendage. (a) A straight or cardium, the “U-bend” will open slightly. The tip of the lead
pre-shaped “J” lead is inserted into the RA via the subclavian/ can then be actively-fixed to the myocardium using the tool
axillary vein, innominate vein, and superior vena cava (SVC) provided and the stylet can then be removed (e) RIV Right
using a straight stylet (---) within the lead. (b) The straight Innominate Vein; LIV Left Innominate Vein; SVC Superior
stylet is replaced by a “J” stylet which will allow the lead tip Vena Cava; RA Right Atrium; RV Right Ventricle; IVC Inferior
to be rotated toward the RA appendage (c). (d) With the Vena Cava; TV Tricuspid Valve; PA Pulmonary Artery
Electrode Positioning 167

LIV LIV

RIV RIV

SVC SVC

PA PA

RA TV RA TV

RV RV

IVC IVC

c d

LIV

RIV

SVC

PA

RA TV

RV

IVC

Fig. 7.91 (continued)

screw the lead’s helical tip into the myocardium Formal testing of the electrode (see below) should
using the fixation tool – with the “J-shaped” stylet now take place, and if satisfactory, stability testing of
still within the atrial lead (Figs. 7.93 and 7.94). the lead should follow. Lead stability is tested by
Protrusion of the helix can be seen on fluoroscopy. asking the patient to cough or perform deep inspira-
The J-stylet has then to be removed from the lead tion/expiration while pacing the atrium. Failure to
and this is a good test of successful fixation of the capture probably means that the lead is not fixed to
lead to the myocardium. or held against the myocardium and the lead should
168 7 Implantation Technique

LIV LIV
RIV RIV
SVC SVC

PA PA

RA
TV RA TV

RV
RV

IVC IVC

a b

Fig. 7.92 Technique for placing a permanent, “passive- passively-fixed to the trabeculated myocardium with the
fixation,” atrial lead into the RA appendage. (a) As in aid of tines at the lead’s tip RIV Right Innominate Vein;
Fig. 7.91a, the pre-shaped atrial “J” lead is inserted into LIV Left Innominate Vein; SVC Superior Vena Cava; RA
the RA using a straight stylet (---) within the lead. (b) As Right Atrium; RV Right Ventricle; IVC Inferior Vena
the straight stylet is removed, the pre-formed “J” lead will Cava; TV Tricuspid Valve; PA Pulmonary Artery
take up its “J” shape in the RA appendage and becomes

Fig. 7.93 With the stylet in situ, the active-fixation tool Fig. 7.94 The lead is actively fixed to the RA appendage
is attached to the distal connector pin by rotating the tool clockwise

be repositioned and the above tests repeated. During possible away from the skin. Before attaching the
inspiration the J-shape should straighten slightly and generator to the electrode pins, the stimulating and
take up its J-shape on expiration. It is possible at this sensing thresholds and lead impedance measure-
stage to check that an appropriate amount of slack is ments should be made.
present on the lead when the lead (at its point of If another site in the atrium is to be paced, a
appearance in the pacemaker incision) can then be straight active fixation lead should be chosen
fixed to the fascia overlying pectoralis major using and a straight stylet should be shaped by the
the suture-collar and two nonabsorbable sutures as operator to enable the site of choice to be
described above for the ventricular lead. Ideally, the reached and then the lead actively fixed using
collars should lay side-by-side and be as deep as the fixation tool.
Lead Measurements at Implantation 169

Fig. 7.95 Disposable wire connections for lead parame-


ter testing during implantation. The black/red connec-
tions in the left hand are inserted into the pacemaker
analyzer while the other black/red connections (arrow)
are attached to the distal and proximal electrodes on the
pacemaker lead

Fig. 7.97 Close-up of the connecting wire and its terminals

Lead Measurements at Implantation

For satisfactory long-term pacing, low stimula-


tion and sensing thresholds should be present at
implantation. High thresholds or poor R- or
P-wave amplitudes suggest that the cathode tip is
not abutting excitable myocardium. If this is the
case, the leads should be repositioned.
Thresholds rise after pacemaker implantation,
and usually peak 1–3 months after lead fixation.
Thresholds are measured using a commercially
available pacing systems analyzer (PSA) – ideally
matched to the generator to be implanted. This
should ensure that they both have similar sensing
and generating circuits. It is important that the unipo-
lar or bipolar electrode configuration should be the
same as that being used in the implanted system.
Fig. 7.96 Connection wire stretched across the operating A sterile bipolar lead is used to connect the
drape
uni/bipolar electrodes on the pacing leads to the
PSA (Figs. 7.95 and 7.96). For a bipolar lead, the
It is recommended to check lead locations by positive (red) lead (anode) is connected to the
fluoroscopy in the RAO and left lateral views positive electrode on the pacemaker lead and the
before anchoring the leads. negative (black) lead (cathode) is connected to
170 7 Implantation Technique

Fig. 7.98 Close-up view of the analyzer’s lead being Fig. 7.99 The black and red “crocodile clips” are seen
attached to the distal (black) and more proximal (red) attached to the distal and more proximal electrodes on the
electrodes of this bipolar lead pacemaker lead during lead assessment

Fig. 7.100 Technician


performing lead sensing,
pacing and impedance
checks

the distal tip negative electrode on the lead paced must be of sufficient amplitude if
(Figs. 7.97–7.99). The technician then begins the satisfactory sensing is to be ensured. The PSA
sensing and pacing measurements using the PSA should record an atrial and/or ventricular electro-
(Fig. 7.100). For unipolar leads the negative gram of >2 and >4 mV, respectively. ST-segment
(black) PSA lead is connected to the single distal shift due to current of injury indicates good endo-
electrode on the pacemaker lead and the positive cardial contact of RV and can be recorded as a
PSA lead (red) is connected to a metal instrument unipolar electrogram from the electrode tip
which is placed inside the pacemaker pocket. (Figs. 7.101 and 7.104). It should ensure a low
Measurements are first made on the ventricu- pacing threshold.
lar lead (Fig. 7.101) and then on the atrial lead
(Figs. 7.102–7.105).
Pacing or Stimulation Threshold

Sensing Threshold The pacing threshold is the smallest electrical


impulse delivered by the cathode of the lead
The intracardiac electrogram resulting from that consistently activates or “captures” the
spontaneous activity of the cardiac chamber to be myocardium.
Lead Measurements at Implantation 171

0.3V

Fig. 7.101 Left: Fluoroscopy shows satisfactory lead tive of good endocardial contact; Lower right: Pacing
position; Upper right: Ventricular electrogram shows threshold test: ventricular capture is lost at 0.3 V (blue
acute injury current (green arrow) and tall R-wave indica- arrow)

Fig. 7.102 Atrial lead


measurements: Pacemaker
analyzer’s crocodile clips
are attached to the two
electrodes of the atrial lead
during sensing, pacing, and
impedance measurements

To measure the pacing threshold, the PSA is output until “failure to capture” occurs (Fig. 7.101).
set to deliver impulses at 70 bpm or 10–15 bpm Care must be taken to then promptly increase the
above the patient’s own atrial or ventricular rate if output if the patient has no or little underlying
there is no bradycardia at the time. The impulse rhythm to avoid the consequences of asystole. A
duration or pulse width should be similar to that phenomenon known as the Wedensky phenome-
which the pacemaker will likely deliver (usually non refers to the fact that the pacing threshold is
0.5 ms) and a voltage output of 5 V. The threshold substantially greater when increasing from a sub-
is then measured by steadily reducing the threshold level and the technician should promptly
172 7 Implantation Technique

increase output by at least 2 V once there is failure


to capture.
With a pulse duration of 0.5 ms, a voltage
threshold of <1 V is considered acceptable in the
RV and <1.5 V in the RA. It will often be <0.5 V
in the RV if the lead is well positioned. With
active fixation leads, the pacing threshold may be
high, e.g.,1.5 V in the RV or even 3 V in the RA,
but it should fall within 5 min of fixation.
When testing bipolar leads, it is important to
ensure that the distal and proximal poles of the
electrode are connected to the PSA’s cathode (−ve)
and anode (+ve), respectively. If the poles are
reversed, the pacing threshold will be higher. With
a longer duration of pacing impulse, the more
energy is delivered per pulse and hence the pacing
threshold will be lower. The relationship is not lin-
ear, however, and 0.25–1.0 ms is usually the range
of efficient impulse duration or “pulse width.”
When testing unipolar leads, the distal pole of
the lead should be connected to the PSA’s cathode
(−ve) and the proximal electrode (+ve) connected to
a metal object such as a retractor placed within the
wound. In this situation, the surface area of the
anode should be similar to that of the pacemaker can
otherwise falsely high thresholds will be obtained.
Pacing the RV apex will lead to a ventricular
Fig. 7.103 Technician doing atrial lead tests using the complex with LBBB and left axis deviation and
pacemaker analyzer/programmer pacing the RV outflow tract, LBBB and right axis
deviation.

1.0V

Fig. 7.104 Top: Atrial electrogram shows some injury current and tall “P” wave (red arrows) suggestive of good endo-
cardial contact. Bottom: Atrial pacing threshold test shows lack of atrial capture at 1.0 V (blue arrow)
Lead Measurements at Implantation 173

1.0V

0.3V

Fig. 7.105 Top: Atrial threshold measurement. Bottom: Ventricular threshold measurement

Fig. 7.106 Anchoring the ventricular lead by inserting Fig. 7.107 Nonabsorbable 2:0 Mersilk is suitable for anchor-
two silk sutures around the lead collar ing the lead/collar although a nonbraided, nonabsorbable
suture such as “Ethilon” or “Ethibond” may be preferred

Lead Impedance ventricular leads anchored using the protective


sleeves (Figs. 7.106–7.110), the leads should
PSA will measure the resistance to current flow be inserted into the generator’s respective ports
down the lead – lead impedance. Although it in the header unit. The generator has a screw-
varies with each lead type, lead impedance should driver within the sterile packet (Fig. 7.111).
be between 400 and 1,000 Ω at 5 V and 0.5 ms. A The leads fit snugly into the ports (Figs. 7.112
very high impedance would suggest lead fracture and 7.113) and are fixed in place by tightly
and a very low impedance a break in insulation screwing the respective retaining screws using
and leakage of current. the screwdiver provided with the pacemaker.
The operator should visualize that the end of
each pin has passed the screw (Fig. 7.114)
After the Lead Measurements before tightening it with the screwdriver
(Fig. 7.115). The self-sealing silicone cover
Once satisfactory measurements from the leads which covers the screws are shown in Fig. 7.116.
have been confirmed and the atrial and/or A small tug on each lead should confirm a
174 7 Implantation Technique

Fig. 7.108 Suturing the


ventricular lead to the fascia
over pectoralis major

Fig. 7.109 Suturing the


ventricular lead

Fig. 7.110 Anchoring the atrial


lead
Lead Measurements at Implantation 175

Fig. 7.111 The pacemaker


is usually accompanied by its
relevant screwdriver inside a
sterile package

Fig. 7.112 Once the leads have been anchored, the con- Fig. 7.114 The atrial lead is inserted into its relevant port
nector pins are inserted into the ports on the header of the and particular notice has to be taken to ensure that the
pacemaker distal pin has passed beyond the second securing screw

Fig. 7.113 Ventricular lead is inserted into its appropri- Fig. 7.115 The screwdriver is used to secure the leads
ate port inside the header

secure fix inside the pacemaker (Fig. 7.117). that the atrial and ventricular leads are inserted
Some operators check the serial numbers on into the correct respective ports in the pace-
each lead with the pacing technician to ensure maker header.
176 7 Implantation Technique

Fig. 7.118 The pacemaker and leads are ready to be


implanted

Fig. 7.116 The Altrua™ 50 has white self-sealing


covers over the screws (arrow). “A” and “V” indicate that
the atrial and ventricular leads are to be inserted into the
upper and lower ports respectively (©2010 Boston
Scientific Corporation/affiliates. All rights reserved. Used
with permission of Boston Scientific Corporation)

Fig. 7.119 The generator and lead(s) are then wound


into a gentle circle before insertion into the pocket

tor and attached leads away from the skin edges


and ideally take the generator well down over
pectoralis major. In very thin or emaciated
patients, the generator may be placed under the
muscle. The generator should not be placed high
up, under the clavicle since erosion is then more
likely to occur. Any bleeding in the pocket should
be stopped by tying-off significant vessels by
Fig. 7.117 Once the leads are secured, a tug on the lead is direct ligature with a suitable suture or with
made to confirm that they are firmly fixed inside the header diathermy. The pocket may be packed with a wet
gauze swab until the leads are ready to be attached
to the generator. Once the leads are attached to
Making the Pacemaker Pocket the generator and the pocket is dry, the leads
and Inserting the Pacemaker should be gently wound in a circle and placed
behind the generator as it is placed deep in the
Most operators make the pocket before placing pocket (Figs. 7.118–7.121) – preferably with the
the leads in the RA and RV. A pre-pectoral pocket header unit placed inferiorly. Placing the leads
large enough to accommodate the generator and behind the generator in this way makes it easier
attached leads is created by blunt dissection. The to avoid cutting through the electrodes at the time
pocket should be deep enough to take the genera- of generator replacement. The subcutaneous
Lead Measurements at Implantation 177

Fig. 7.120 The pacemaker is inserted into the pocket Fig. 7.123 Braided, absorbable Vicryl suture is suitable
ensuring that the header is placed inferiorly away from the for closure of this subcutaneous layer
skin edges

Fig. 7.121 The leads are placed behind the generator Fig. 7.124 The subcutaneous fatty tissue and pocket are
closed with interrupted absorbable sutures II

Fig. 7.122 The subcutaneous fatty tissue and pocket are Fig. 7.125 The subcutaneous fatty tissue is closed with
closed with interrupted absorbable sutures I interrupted sutures III

tissue is then brought together with interrupted absorbable Dexon® (Figs. 7.127–7.131). The
absorbable suture material (Vicryl®) (Figs. 7.122– wound should be cleaned with iodine or chlor-
7.126) and the wound edges either brought hexidine solution and dried with a sterile towel.
together with a neat subcuticular suture using The edges may then be glued together with
178 7 Implantation Technique

Fig. 7.126 The skin edges are now easy to approximate Fig. 7.129 Subcuticular suture being inserted

Fig. 7.127 Absorbable 3:0 Dexon II on a straight cutting Fig. 7.130 A pleasing end result is obtained by placing
needle is ideal for the subcuticular layer each subcuticular “bite” in close proximity to each other

Fig. 7.128 A continuous subcuticular suture is used to Fig. 7.131 The suture is completed by applying tension
bring the skin edges together to both ends of the subcuticular suture and the ends are
then removed

Dermabond® topical skin adhesive (Ethicon, Inc.) edges should preclude the need for plastic spray
or Nobecutane® plastic spray may be sprayed dressing (Figs. 7.132–7.134). It is ideal if ECG
over the wound to protect it from invading skin strips showing normal sensing/pacing are
microorganisms. Satisfactory gluing of the skin recorded and placed in the casenotes next to the
Lead Measurements at Implantation 179

Fig. 7.133 Dermabond® glue being applied to the skin


edges

Fig. 7.132 Dermabond® topical skin adhesive has a high


viscosity and an easy-to-use applicator

Fig. 7.134 Finished result


with glue applied

cardiologist’s notes on the procedure that has just satisfactory right ventricular, atrial, and left
been performed (Fig. 7.135). ventricular lead positions prior to the patient’s
The procedure should take between 20 and discharge.
60 min depending on the type of pacemaker being A variety of accessories should be available in
implanted and the ease/difficulty of entering the a properly equipped pacing theater and these are
central venous system and obtaining satisfactory shown in Table 7.4.
stable lead placement with favorable electrical The best defense against litigation is full doc-
parameters. umentation in the patient’s medical records of
A PA and lateral chest X-ray should be per- every aspect of the implantation (or extraction)
formed to exclude pneumothorax and to check procedure. This should include the indication for
180 7 Implantation Technique

Fig. 7.135 ECG strips showing DDD (upper) and VDD (lower) pacing after dual chamber pacemaker implantation.
This confirms atrial and ventricular pacing and satisfactory atrial sensing

Table 7.4 Accessories that should be available in the the procedure, the informed consent form, a
pacing theater/lab during new pacemaker implants and complete procedure note to include pacing
generator change procedures parameters achieved at implantation, and any
Stylets for 52, 58, 65, 85, and 110 cm leads difficulties that were encountered. There should
J-Stylets for 45, 53, and 58 cm atrial leads be some evidence of what was done postopera-
Lead anchoring sleeve tively, such as the programmed settings at dis-
Lead end pin caps for 5, 3.2 mm, and IS-1 lead ends charge, an ECG strip confirming satisfactory
“Pinch-on” tools for active-fixation leads pacing, and a note to indicate that the chest X-ray
Screwdrivers for pacemaker generators
excluded a pneumothorax. The arrangements for
Medical adhesive
follow-up should be clearly documented.
Adaptor kits:
For extraction procedures, it is wise to docu-
Unipolar lead splice kit with IS-1 connector adaptor kit
for old generators (5866-9M) ment what exactly was removed and why.
Upsizing sleeve for 3.2 mm LP bipolar lead to 5 mm
bifurcated bipolar pacemaker (5866–22)
For changing a 5 mm unipolar to IS-1 unipolar lead Pacemaker Programming
(5866-37M)
For changing two IS-1 unipolar leads to fit a IS-1 Immediately after pacemaker implantation, the
bipolar generator (5866-38M)
device should be programmed in the pacemaker
For changing a 3.2 mm LP bipolar lead to a IS-1
bipolar generator (5866-40M) theater by the technician. Usually the pacemaker
Sleeve for upsizing a IS-1 lead to 5/6 mm unipolar prescription will have been decided beforehand
single chamber pacemaker (5866–45) and the “factory settings” may even be repro-
For downsizing 6–5 mm (5866–21) grammed with the device still within the sterile
Lead extensions: package. However, after implantation, the atrial
Unipolar, IS-1 and/or ventricular sensitivity settings and outputs
Bipolar, IS-1 can be changed according to the implant mea-
3.2 mm LP to IS-1, Bipolar surements. A reduction in output will prolong
Pacemaker Programming 181

battery life. Upper and lower rate limits should be will allow sinus rhythm to be maintained for lon-
set appropriately as should the AV delay/refrac- ger periods. For those with angina pectoris, a
tory periods if necessary. Pacing mode should be reduction in the pacing rate (and limitation of the
set and rate response turned on and set appropri- upper rate) may be important and a slightly faster
ately for each individual if necessary. Mode- rate may be helpful in patients with cardiac fail-
switching and Search AV facilities and diagnostic ure or certain arrhythmias. For those patients
tools can be turned on if appropriate but it should with paroxysmal atrial fibrillation, mode switch-
be remembered that battery-life will be shortened ing should be activated. The current device set-
slightly in proportion to the number of diagnostic tings should be noted in the case notes and entered
and therapeutic programs in use. into the pacemaker database.
For example, for patients who are predomi-
nantly in sinus rhythm, reduction of the base rate
Predischarge Pacemaker Checks
and Advice 8

Predischarge Pacemaker Checks isfactory pacing and sensing, if necessary by


adjusting the pulse width (0.4–1.0 ms), output
The day after permanent pacemaker implantation (2.5–7.5 V), and sensitivity (0.25–8 mV) settings
(or just prior to discharge if “day-case” pacing is (Figs. 8.1–8.3). The pacemaker’s upper (100–
in operation), lead position should be checked by 180 bpm) and lower rate (30–100 bpm) limit,
performing a PA and lateral chest X-ray (see pacing mode (e.g., AAI, VVI, DVI, DDD), rate
Chap. 7). Pneumothorax and early lead displace- response, polarity (uni- or bipolar), refractory
ment should be excluded. A 12-lead ECG should period (200–500 ms), and AVD delay (0–300 ms),
confirm satisfactory pacing in atrium, ventricle, etc., should also be confirmed by the clinical
or both depending on the type of pacemaker physiologist using the programmer and the set-
implanted, usually by application of the program- tings documented in the case notes. For day cases,
mer head over the device to produce a “magnet these checks will be made by the technician
ECG strip.” The pacing threshold should ideally before the patient leaves the pacing theater.
be checked and the pacing parameters set appro- Prior to discharge, the wound should be inspected
priately by the clinical physiologist to ensure sat- for signs of hematoma formation and integrity of

Fig. 8.1 Patient has device


interrogated/programmed before
discharge. Programming head is
placed over device

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 183


DOI 10.1007/978-1-4471-2939-4_8, © Springer-Verlag London 2012
184 8 Predischarge Pacemaker Checks and Advice

Fig. 8.2 Clinical physiologist uses


ECG machine and device programmer/
analyzer

Fig. 8.3 Company-specific programmer/analyzer from Medtronic (left) and Biotronik (right)
ID/Registration Card 185

Fig. 8.4 Pacemaker identification (ID) card

the wound incision and a follow-up appointment for condition, fitness, and activity level. The upper
4–6 weeks should be given to the patient. This rate limit should be set with these factors also in
should allow for early wound inspection and a fur- mind. Adjustments to the pacemaker program set-
ther assessment of pacing/sensing thresholds to tings can be made at the first pacemaker clinic
enable possible adjustments of the device settings. visit at 4–6 weeks post-implantation.

Issues to Be Considered When Setting ID/Registration Card


the Initial Program
Patients should be given a pacemaker ID card
In those patients in sinus rhythm, the base rate (Fig. 8.4) and asked to carry it with them. It should
should be set to allow sinus rhythm to be main- provide important data such as: name, address,
tained for longer periods to extend battery life and date of birth, implanting center telephone number
help minimize RV pacing and its long-term disad- and hospital number, type of pacemaker, pace-
vantages. Setting a low base rate, e.g., 50–60 bpm, maker mode and parameters at last programming,
is useful for patients with angina pectoris. Bipolar and indication for implantation. The details and
sensing and pacing should help prevent oversens- coded information are filled in by the clinical
ing and help prolong battery life respectively. physiologist at the time of implantation and car-
Atrial pacemakers require a higher sensitivity bon copies are created. The white card is folded
than ventricular devices because the atrial electro- and inserted into a plastic wallet and given to the
gram is usually lower than the ventricular electro- patient (Fig. 8.5). A green copy is provided for the
gram and the atrial sensitivity setting should be patient’s hospital file, a blue copy sent to The
set appropriately. Mode-switching should be National Registration Centre, and a yellow copy
turned on if there is a history of paroxysmal AF (Manufacturer File) is given to the relevant sales
and the type, extent, and onset of rate response representative or sent to the pacemaker company
can be set depending on the patient’s age, medical and acts a warranty application (Fig. 8.6). In the
186 8 Predischarge Pacemaker Checksand Advice

Fig. 8.5 ID card is folded


and placed in a plastic wallet

Fig. 8.6 Green, blue, and yellow carbon copies of the pacemaker data are created
Advice for Patients 187

Fig. 8.7 ID card for ICD

UK, the information is sent electronically to the Advice for Patients


Central Cardiac Audit Database (CCAD) and the
blue copy is discarded. Adhesive stickers with the General Advice
serial number (SN) of the implanted device are
provided with most devices and should be attached Patients should be advised to mobilize normally
to each page of the European Patient ID card and from day 1 but to restrict vigorous arm move-
in the patient’s hospital file. Similar ID cards ments (on the pacing side) and avoid carrying
(Figs. 8.7 and 8.8) and color-coded carbon copies heavy weights over the next 2 weeks or so. They
(Fig. 8.9) are available for ICD implantations. should be asked to wash around the pacemaker
A print-out of the pacemaker’s program at the wound for the first week, and report to the
time of the patient’s discharge (Fig. 8.10) should implanting center any undue pain, tenderness,
be placed in the patient’s casenotes and also redness, swelling, gaps in the wound, or discharge
entered into the Pacing Database available within from the wound that appears so that an urgent
the Centre. inspection can be made by a member of the spe-
188 8 Predischarge Pacemaker Checksand Advice

Fig. 8.8 ID card for ICD

cialist pacing team. Except in unusual circum- oped, usually as a result of late, inadequate, or
stances, such as a patient’s residence being a large inappropriate treatment, the pacing system is
distance from the pacing center or severe frailty or probably doomed, in that it will have to be
immobility, should any other doctor be given the removed and a new system implanted.
responsibility of treating these problems. Once Patients will be given an information booklet
there is evidence of wound dehiscence or infec- about their pacemaker (Figs. 8.11 and 8.12), told
tion, the pacing center must be made aware of the about the need for regular checks in the pace-
situation. It is suboptimal practice for anyone else maker clinic, and the approximate life expectancy
to simply prescribe antibiotics, resuture, or “ster- of their pacemaker. Discussion about the possi-
istrip” the wound edges without discussion with bility and potential for home monitoring can be
the cardiologist who was responsible for the pace- left until the first visit to the pacemaker clinic
maker implant. Once pocket infection has devel- 4–6 weeks after implantation.
Advice for Patients 189

Fig. 8.9 Colored carbon copies of the ID card for ICD

Fig. 8.10 (continued)

Fig. 8.10 “Printout” of the pacemaker’s program at the


time of discharge
190 8 Predischarge Pacemaker Checksand Advice

Fig. 8.11 Patient informa-


tion booklets from
Medtronic (left) and Boston
Scientific Ltd. (right)

Implanted
Implanted
pacemaker
pacemaker

Lead in
right atrium
Lead in right
Lead in right
ventricle
ventricle
a b

Fig. 8.12 The booklets are illustrated to help patients gain an understanding of their pacing system and the implantation
procedure itself (a) single chamber right ventricular pacemaker (b) dual chamber, atrial and ventricular pacemaker

Driving Dispensation to allow pacemaker patients not to


have to wear seatbelts may be given by the DVLA
In the UK, patients must refrain from driving or in the UK, but the person must accept the poten-
riding a motor cycle for 1 week after uncompli- tially serious consequences if an accident should
cated pacemaker implantation or generator occur. For their front-seat passenger, the driver
replacement providing there is no other disquali- may be held responsible for injury or death to
fying condition. Professional drivers of HGVs, that person if they do not “belt-up.” Some patients
buses, taxis, ambulances, or emergency vehicles have found wearing a soft pad between the safety
cannot drive for 6 weeks after implantation. belt and the pacemaker of some comfort.
Although seatbelts may press on the pace- Insurance premiums should not be increased
maker of drivers or front-seat passengers, they for pacemaker patients, unless they choose not to
have not been shown to damage them. wear a seatbelt!
Advice for Patients 191

Anticoagulant Therapy Specific Advice

Anticoagulant therapy with IV heparin or LMWH Specific advice about living and working with a
should be avoided for at least 12 h after implant. pacemaker and the precautions that should be taken
If anticoagulation is deemed necessary within the in order to avoid damaging the generator, uninten-
first week of implantation, dosing should be cau- tional reprogramming, or inhibition of pacemaker
tious to avoid a hematoma developing in the function is presented in Chap. 10, but guidance to
pocket. Warfarin may be started the day after the patients is found in the patient information booklet.
procedure but it is best to increase the dose grad-
ually rather than give large loading doses in an
attempt to reach an INR >2.5 quickly – which
will increase the likelihood of pocket hematoma
necessitating drainage.
Programmable Functions
and Terminology 9

The rapid developments in technology and exercise AV delay, AV delay extension; pacing
pacemaker research have enabled pacemak- and sensing parameters – atrial and ventricular
ers and other implantable devices to become amplitude, atrial and ventricular pulse width,
more sophisticated. Devices have numerous atrial and ventricular sensitivity, atrial and ven-
programmable features and can store sub- tricular sensing and pacing polarity; SafeR™
stantial amounts of diagnostic information parameters – Pause (max), Long PR (max and
related to device function, arrhythmia detec- min), and AVB I switch (Rest + exercise vs. exer-
tion, cardiovascular hemodynamic parameters cise). Special features include: Fallback Mode
including transthoracic impedance and patient Switching (FMS), PMT protection, rate smooth-
activity. Bi-directional telemetry using encoded ing, Atrial or Ventricular Autosensing, Ventricular
and encrypted radiofrequency signals allows Autothreshold, Min. Ventricular Amplitude,
transmission of information to the implant- Post-Ventricular Atrial Blanking (PVAB); Atrial
able device from the programmer and to the arrhythmia prevention parameters – Overdriving,
programmer from the device. This process Max Overdriving rate, Pause suppression, PAC
permits review of the programmed parameters acceleration; Rate-adaptive parameters – Sensor
and stored diagnostic data and reprogramming choice (MV + G, MV or G), Rate response mode,
of device parameters to correct identified mal- physical exercise (very low, low, medium, high,
functions and/or to optimize device function very high) (Fig. 9.2). Twenty minutes after
(Fig. 9.1). implantation, the pacing mode is automatically
It has gone far beyond simply reprogramming programmed to SafeR™. The rate response
pacing rate, upper and lower rate limits, mode of mode will be programmed to Learn, and Diagno-
pacing, electrode polarity, output and sensitivity, stics will be ON. The latter includes Diagnostic
but has evolved into clever mechanisms of AIDA – Automatic Interpretation for Diagnosis
improving function and performance to optimize Assistance, offering Intracardiac ECG/annotated
the patient’s rest and exercise cardiac physiology markers, ECG triggers for mode switching, atrial/
and abolish symptoms and exercise limitations. ventricular bursts, switches in SafeRTM mode,
For example, the ReplyTM DR DDDR pacemaker Histograms and counters for A and V rate, %
(Sorin Group) which weighs 20 g and has a vol- Pacing, atrial arrhythmias (number and time
ume of only 8 cc offers the following: basic in mode switch, bursts, Premature Atrial
parameters – mode, basic rate, rest rate, maxi- Contractions (PACs), Ventricular bursts and
mum tracking rate, rate hysteresis, rest AV delay, Premature Ventricular Contractions (PVCs),

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 193


DOI 10.1007/978-1-4471-2939-4_9, © Springer-Verlag London 2012
194 9 Programmable Functions and Terminology

Fig. 9.1 Interrogation of Reply™ DR pacemaker. First screen on Orchestra™ programmer displays all essential basic
programmed data (Courtesy of Sorin Group)

Pacing threshold follow-up, amplitudes of normal that provide for the highly reliable exchange of
and abnormal P and R waves and 24-h rate curve the encrypted information and precise communi-
(Fig. 9.3). cation with the implantable device. The program-
CRT and ICD devices are also extensively mer uses bi-directional telemetry to receive the
programmable (Figs. 9.4 and 9.5). stored information from the device and to modify
The other major manufacturers offer a simi- (program) the settings of the device if desired.
larly wide range of programmability. Usually a “wand,” attached by a wire to the pro-
grammer, is positioned on the body over the
implanted device to receive the telemetry signal
Programmers (see Fig. 8.1). The distance for radiofrequency
communication has increased from several centi-
Pacing technicians or clinical physiologists use meters to several meters (10–20 ft) and some now
manufacturer-specific analyzers/programmers to communicate without a wand – wirelessly. The
adjust the pacemaker’s settings and change its longer distance telemetry is device-specific but
function (Figs. 6.64 and 9.6). Most are user- uses either the ISM (Industrial, Scientific and
friendly and individual pages display the param- Medical) band from 902 to 928 MHz or a subsec-
eter settings as well as offering the facility to tion of the MICS (Medical and Implant and
reprogram the device (Figs. 9.7 and 9.8) A Communications) band from 402 to 405 MHz
12-lead ECG machine is useful to document nor- which allows reliable and secure signals to be
mal function of the implantable device after any sent to and from the programmer and the device
reprogramming (Fig. 9.9). >10 ft away. This is useful in the out-patient clinic
The programmer is a computer with specific using a programmer, in pacing theater when pro-
software and associated hardware modifications gramming is required over a newly-implanted
Programmers 195

Fig. 9.2 Programmable parameters for the ReplyTM DR DDDR device with an estimated longevity of 9 years
DDDR pacemaker are wide-ranging and the diagnostic (Courtesy of Sorin Group)
capability impressive for a 20 g, 8 cc rate responsive
196 9 Programmable Functions and Terminology

Fig. 9.3 Automatic Interpretation for Diagnosis Assistance (AIDA) showing 7 day Holter ECG recording illustrating
frequency of rate response from this Reply™ DR system (Courtesy of Sorin Group)

device, or over an open wound or at home as part It is essential to understand the meaning of the
of remote monitoring (remote telemetry device). terminology used in pacing in order to be compe-
However, when the encrypted data has to be tent in programming and troubleshooting and in
transmitted over a distance of miles, the commu- order to provide the best possible function from
nication is done via telephone lines or cell phone today’s sophisticated devices. Figures 9.11 and 9.12
technology – typically from the home monitor/ illustrate some basic pacemaker timing intervals.
communicator to the ECG department’s pacing
clinic or data repository (see Fig. 6.38).
Programmers have integrated printers to docu- Basic Pacing Terminology
ment the device settings (Fig. 9.10), and home
monitor/communicators and programmers can Accelerometer
communicate the interrogated data to a remote
printer for a hard copy presentation or be trans- A type of activity sensor used in a rate-responsive
ferred to the device database or Electronic pacemaker that detects motion along a geometric
Medical Record (EMR). The data are saved and plane.
transferred via disc, CD ROM, USB drive,
directly by a network cable, Bluetooth, or WIFI
communication to an Internet or intranet connec- Acute-Chronic Threshold Change
tion and then downloaded to the Database or
EMR. The ISM and MICS radiofrequency com- The observed change in stimulation threshold from
munication is used only for connecting the implant to 2 months post-implant. This begins low,
implanted device to the programmer or remote trends sharply upward at 2–4 weeks, and then
telemetry device and not for connecting the decreases slightly and levels off at 8 weeks. Large
programmer to printers, saved files, the database, changes in acute-chronic thresholds are unusual in
EMR or registries. modern leads and steroid-eluting leads.
Basic Pacing Terminology
197

Fig. 9.4 Programmable parameters for the Paradym CRT 8750 biventricular device (Courtesy of Sorin Group)
198
9

Fig. 9.5 Programmable parameters for the Paradym DR 8550 ICD (Courtesy of Sorin Group)
Programmable Functions and Terminology
Basic Pacing Terminology 199

Fig. 9.6 The Medtronic programmer being used to interrogate an implantable device in the follow-up clinic and
reprogram the device to optimize function and conserve battery life

Fig. 9.7 Parameters settings and programming screen for the Reply™ DR pacemaker – taken from the Orchestra™
programmer (Courtesy of Sorin Group)
200 9 Programmable Functions and Terminology

Fig. 9.8 Parameters screen from the Medtronic program- “buttons” to allow further interrogation of patient data,
mer displaying live annotated ECG with simultaneous lead threshold testing, and trend data. From the Medtronic
intracardiac atrial and ventricular electrograms (EGM), Advisa DR MRI SureScan™ pacemaker (Image repro-
along with the current pacemaker and lead settings and duced with permission of Medtronic, Inc.)

Algorithm

A specially designed form of pacemaker behavior


intended to achieve a specific goal, e.g., the AF
Suppression algorithm is a special form of dynamic
atrial overdrive pacing designed to suppress AF.

Asynchronous Pacing

Pacing mode (AOO, VOO, DOO) in which the


pacemaker paces but does not sense. This results
in properly-timed output pulses that are delivered,
irrespective of any intrinsic activity. Rarely used
clinically. Also known as “fixed-rate” pacing.

A-V Interval or Delay

Described for dual-chamber pacemakers, it is


equivalent to a native PR interval. It represents the
Fig. 9.9 A 12-lead ECG machine is ideal to see and time (ms) between an atrial event and a paced or
confirm with a “print out” that pacing is satisfactory from sensed ventricular event. During this time, the pace-
one, two, or three chambers, and that any major program maker discerns whether or not to pace depending
changes appear to be functioning as expected
Basic Pacing Terminology 201

Fig. 9.10 Printout from Vitatron’s programmer showing data retrieved from a Clarity DDDR device
202 9 Programmable Functions and Terminology

a (i) (ii) b
LRI LRI

VP VP AP VP AP VP
VP VP
VRP

c BP
AV VA
d
AV VA AV

AP VP AP VP

AP VS AP VS

e
AV VA f
AV VA

AS VP AS VP
AS VS AS VS

Fig. 9.11 (a) (i) Lower rate interval (LRI) VP–VP is the Period (BP), the pacemaker is “blind” to any activity. It is
lowest rate at which the pacemaker will pace (base rate set- designed to prevent oversensing the pacing stimulus or “far-
ting) in the absence of intrinsic ventricular events. (ii) field” signals and crosstalk. (c) Atrial Pace (AP), Ventricular
AP–AP is the lowest rate at which the pacemaker will pace Pace (VP), Ventriculo-Atrial Interval (VA), and Atrio-
in the absence of intrinsic atrial events. (b) Ventricular Ventricular Interval (AV). (d) Atrial Pace (AP) and
Refractory Period (VRP) is initiated by a paced or sensed Ventricular Sense (VS). (e) Atrial Sense (AS) and Ventricular
event. During the first portion of the VRP, the Blanking Pace (VP). (f) Atrial Sense (AS) and Ventricular Sense (VS)

upon sensing a native R wave and allows the ven- Auto Rest Rate
tricle time to fill following an atrial contraction.
A type of pacemaker response designed to mimic
the normal physiologic rate slow-down during
AV Synchrony sleep.

The mode in which there is 1:1 correspondence


between atrial and ventricular activity. Base Rate

The lower rate (bpm) at which the clinician/tech-


Automatic (Basic) Interval nician programs the pacemaker to pace. Typical
base rates are 50–75 bpm. It is also known as the
This is the stimulus-stimulus interval during reg- “lower rate limit.”
ular pacing.
Basic Pacing Terminology 203

Fig. 9.12 (a) Atrio-Ventricular Interval a


(AVI). Paced AV Interval (PAV) and PAV SAV
Sensed AV Interval (SAV). (b) Atrial
Escape Interval (VA Interval) is the
interval from a paced or sensed ventricu-
lar event to the next atrial event.
Ventricular Pace (VP). Atrial Pace (AP). AP VP AS VP
(c) Refractory Periods. Ventricular
Refractory Period (VRP) and Post- b
Ventricular Atrial Refractory Period VA interval
(PVARP) are initiated by sensed or paced
ventricular events. VRP is intended to
prevent self-inhibition such as by T-wave
sensing. PVARP is intended to prevent
sensing of retrograde P waves and the AP VP AP VP
inadvertent initiation of Pacemaker
Mediated Tachycardia. A PVARP of c
300 ms usually protects against this but AV interval
programming a long PVARP may limit
the upper rate limit. (d) Total Atrial
Refractory Period (TARP) equals the sum
of the AV interval (SAV) and PVARP.
Atrial Sense (AS), Ventricular Pace (VP), AP VP AP VP
Upper Tracking Rate (UTR). (e) Blanking
Periods. Atrial blanking (AB) (nonpro- AVI PVARP
grammable), Post-Ventricular Atrial
Blanking (PVAB), Post-Atrial Ventricular
Blanking (PAVB), Ventricular Blanking d
(VB) (nonprogrammable), Post-
Ventricular Atrial Refractory Period
(PVARP) Cross-Talk Sensing (CTS)
window: Inhibition of pacemaker output
by crosstalk may result in asystole. To
AS VP AS VP
prevent this, if a signal is sensed in the
CTS window a pacing spike is delivered SAV PV ARP
(safety pacing) TARP
UTR

e AVI PVARP

AP VP AP VP

Atrial
channel
AB PVAB
Ventricular
channel VB
PAVB CTS VRP
204 9 Programmable Functions and Terminology

Bipolar Pacemakers of a ventricular stimulus after a programmed AV


delay.
Most temporary pacing leads are bipolar with a
proximal ring electrode at approximately 1 cm
from the tip and a distal (tip) electrode. The prox- Cross-Talk
imal electrode is the anode (positive) and the distal
electrode, the cathode (negative). Most perma- In DDD units, sensing of electronic events from
nent pacing leads are bipolar. Generally, the pac- one channel by the other channel, e.g., an atrial
ing spikes from bipolar leads are small on the stimulus sensed by the ventricular channel result-
surface ECG. ing in dangerous inhibition of the ventricular
impulse. This is avoided by programming the
blanking period.
Blanking Period

The “Blanking Period” is the time interval after Demand Pacing (Inhibited)
a pacing impulse during which the pacemaker
is insensitive to signals from the heart or from Unlike the fixed-rate mode, spontaneous car-
the other channel (avoiding so-called cross- diac activity is sensed and inhibits the pace-
talk). maker, which delivers a stimulus only after a
pre-set interval if no further impulse is
sensed.
Capture

Depolarization and resultant contraction of the DF-1


myocardium in response to a pacemaker gener-
ated electrical stimulus. High-voltage lead connection of ICD lead (defi-
brillation coil) into port on the header of the ICD.

Cardiovascular Implantable Electronic


Device (CIED) DF-4/SJ4

Includes pacemaker, ICD, CRT device, implant- New design of ICD lead which incorporates
able loop recorder (ILR), and implantable cardio- four conductors into a quadpole, in-line con-
vascular monitor (ICM). nection replacing the defibrillation coil DF-1,
and pace-sense IS-1 connections with the “DF-
4” connection. The ICD header has one port to
Coaxial Lead accommodate the dual-coil lead instead of three
and is thus smaller. The lead is 7–10 cm shorter
Type of bipolar lead in which one conductor is because no “yoke” is required to bring the IS-1
wrapped around another conductor. and DF-1 connections to a single lead body.
This development has two advantages: a more
streamlined header connection for these devices
Committed and simplification of connection to the device
reducing pin-to-port mismatch, e.g., SJ4 Durata
A dual-chamber pacing system in which the lead (St. Jude Medical), ENDOTAK RELIANCE
delivery of an atrial stimulus forces the delivery 4-SITE (Boston Scientific).
Basic Pacing Terminology 205

Entrance Block Hysteresis

Entrance block represents the failure of a pace- The takeover rate of the pacemaker is lower than
maker to sense cardiac events. This may be the pacing rate, e.g., a pacemaker with a pacing
because the sensitivity of the pacemaker is too rate of 70 bpm and hysteresis mode set at 60 bpm
low, the signals are of too low an amplitude, or will not start pacing until the patient’s heart rate
the electrode is fractured. falls below 60 bpm when the pacing rate jumps to
70 bpm.
It is also defined as an intentionally prolonged
Escape Interval pulse interval in order to allow the generation of
a spontaneous-intrinsic electrical depolarization
The escape interval is the interval between a event.
spontaneous cardiac impulse which is sensed
and the next pacing stimulus. This is usually the
same as the automatic pacing interval unless the Intracardiac Electrogram
pacemaker is programmed to hysteresis mode, in
which case the escape interval is longer than the ECG taken from an electrode placed within the
automatic interval. heart. It contrasts with a surface ECG, which
records signals from the skin’s surface. Pacemakers
deliver intracardiac electrograms to the program-
Exit Block mer. The intracardiac electrogram is what the
pacemaker “sees” and may be more useful than a
Exit block occurs when excessive tissue growth surface ECG for assessing pacing behavior.
between the tip of the lead and the endocardium
increases the threshold to pace sufficiently to cause
failure to capture without lead displacement. IS-1

Abbreviation for International Standard 1, a lead


Filar and connector standardized size that accommo-
dates leads with a 3.2 mm diameter pin. IS-1
A strand of wire used in the conductor in a lead. leads and pacemaker connectors are the most
Some leads are unifilar (one strand), while others common used today.
are multifilar (many strands).

IS-4
Fixed-Rate Pacing
International standard in-line quadripole elec-
Regular constant pacing of the heart at a fixed trode for use in low-voltage applications, e.g.,
rate which is independent and not affected by quadripole LV lead, e.g., Quartet™ LV lead (St.
spontaneous cardiac activity. Jude Medical).

Housekeeping Current Lead Impedance

The amount of energy a device consumes even The lead impedance reflects the electrical resis-
when it is not in use (including preimplantation). tance of the lead and its tip-tissue interface. The
206 9 Programmable Functions and Terminology

lead impedance is also influenced by the size of Missing


the electrode tip; the larger the tip, the lower the
impedance. The lower the impedance/resistance This term is used to describe failure of the atrial
in the lead results in greater current flow and a or ventricular lead to capture or pace the atrium or
greater drain on the battery power. Thus low- ventricle respectively. There are multiple causes
impedance leads result in early battery depletion. including lead displacement, too low an output
Average lead impedance is 550 W. Conversely, voltage setting, and exit block. With a temporary
the higher the resistance/impedance in the lead, pacemaker, simply increasing the output voltage
the lower the current flow and less of a drain and/or pulse width may help in the short-term, but
on the battery of the generator. An electrode repositioning is likely to be necessary. With a per-
whose tip has a small geometrical surface area, manent system, the cause must be sought. Lead
enables the current applied to the myocardium to displacement will require repositioning of the
be concentrated (high current density); in turn a lead. Exit block may be overcome by reprogram-
smaller current will be required to gain capture ming the pacemaker to a higher output, or if this
and hence battery drain will be minimized. Newer is not possible by the use of oral prednisolone
electrodes have smaller electrode tips 1.2–5 mm2. therapy for 2–3 weeks. A primary lead problem
such as lead fracture or insulation break necessi-
tates explantation and implantation of a new
Magnet Rate system.

Application of a magnet over pacemakers con-


verts them into fixed rate mode at a predictable Mode
rate which depends on battery life. The response
depends on the type of pacemaker. This magnet- Indicates pacemaker’s capabilities, e.g., fixed rate
testing is used to test battery life in the follow-up or demand; atrial, ventricular, or dual-chamber
clinic and to test satisfactory pacing when there is system.
competition at a slower demand rate. For exam-
ple, if a patient’s heart rate is 75 bpm and the
demand rate is 60 bpm, the pacemaker can be Mode Switching
made to pace at a set rate, e.g., 100 bpm (defined
by manufacturer) by application of a magnet over Special feature of many dual-chamber pacemak-
the generator. ers which allows the device to change modes in
the presence of rapid, intrinsic atrial activity,
e.g., AF. Mode switching “switches off” the
Maximum Tracking Rate (MTR) atrial channel of a dual-chamber pacemaker dur-
ing periods of very high, intrinsic atrial activity.
The rate over which the pacemaker will not allow Also known as Automatic Mode Switching
the ventricles to be paced in response to atrial (AMS).
activity.

Multisite Pacing
Minute Ventilation
Device-based treatment which involves pacing
A sensor system used in rate-adaptive pace- and sensing both the RA and LA (multisite atrial
makers which detects respiration rates (based on pacing), the RV and LV (biventricular pacing), or
chest movements) and adjusts the pacing rate in RV apical/RV outflow tract pacing (multisite RV
response to sensed need. pacing).
Basic Pacing Terminology 207

Myocardial Lead Oversensing

A pacing lead designed to be attached to the epi- Inhibition of the pacemaker by inappropriate
cardium, either by screwing into the heart’s exte- sensing of myopotential signals (myopotential
rior or suturing on a patch – usually requiring inhibition), by nonphysiological electromagnetic
thoracotomy. interference, or of “T” waves is often referred to
as “oversensing.” Reducing the pacemaker’s sen-
sitivity using the appropriate external program-
Myopotential Inhibition mer is the first option.

Electrical myopotentials from skeletal muscle


close to the pacemaker (usually from pectoralis Pacemaker-Mediated
major) may be sensed by the sensing circuit of Tachycardia (PMT)
unipolar pacemakers during physical activity
involving use of this ipsilateral muscle. A rapid ventricular rate facilitated by the pres-
Pacemaker output will be inhibited if the pace- ence of a pacemaker. A PMT is not caused by
maker is programmed to a demand mode. the device, but facilitated by the retrograde
Reprogramming to bipolar sensing or a fixed rate conduction of atrial activity with subsequent
or triggered pacing mode will solve the problem. ventricular pacing. Once a re-entry tachycardia
Reducing the pacemaker’s sensitivity is rarely gets started, the pacemaker acts like a re-entry
effective. path.

Non-committed Pacemaker Wenckebach

This term describes a dual-chamber pacemaker A type of upper rate response in which the AV delay
in which the sensing of ventricular activity dur- gets longer and longer until one of the P-waves falls
ing the AV interval can inhibit the delivery of a into the PVARP and is not followed by a ventricular
ventricular impulse. event. Also called pseudo-Wenckebach.

Optimal AV Delay Pacing Interval

The optimal AV delay in a dual-chamber pace- The amount of time between paced events (ms),
maker refers to the AV interval that can lead to e.g., when a pacemaker is programmed to pace at
closure of the mitral valve due to elevation of iso- 60 bpm the pacing interval is 1,000 ms (i.e.,
volumic pressure after atrial contraction and 60,000/number of ms).
resulting in maximizing the stroke volume.

Pacing System Analyzer (PSA)


Output Pulse
Small, handheld device that can be used to gather
The electrical energy generated by the pace- intra-operative measurements of the pacing system.
maker and delivered to the heart. This output These are being replaced by the device programmer/
pulse is defined by pulse amplitude (voltage) and analyzer available from the specific device manufac-
pulse duration (length of time, measured in turer which are made available in the pacing
milliseconds). theater.
208 9 Programmable Functions and Terminology

Pacing Threshold permanent pacemakers and by adjusting the


dial/knob on a temporary pacing box. The
Minimum amount of energy required to reli- broader pulse width setting may aid atrial/ven-
ably capture (cause depolarization of) the tricular capture when narrower pulse widths
heart. Also called stimulation or capture fail, but as a consequence will lead to greater
threshold. current drain and shorter battery life of the
generator.

PMT Termination Algorithm


Relative Threshold
A special feature to help prevent or interrupt
PMTs. The relative threshold is the minimum percentage
of total available voltage required to pace the
heart. Thus a relative threshold of 20% with max-
Post-Ventricular Atrial Refractory imum unit voltage of 5.0 V is 1.0 V.
Period (PVARP)

PVARP is intended primarily to prevent sensing Rate Drop Response


of retrograde P waves. Initiated by sensed or
paced ventricular events. A special feature in some dual-chamber pacemak-
ers which may be useful for patients with neurocar-
diogenic syncope. The device is programmed to a
Programmed Standby Rate high hysteresis rate, so that pacing is mainly inhib-
ited; should a syncopal episode occur and the
Heart rate at which pacing will commence if patient’s intrinsic rate fall markedly, pacing com-
native heart rate falls below this rate. mences at a higher-than-normal rate to help com-
pensate for the temporarily diminished cardiac
output.
Pulse Amplitude

A programmable pacemaker setting which Rate-Responsive Pacing


defines the output pulse of the device. It is set in (Rate Adaptive Pacing)
volts. Increasing pulse amplitude increases out-
put pulse energy. These pacemakers allow the pacing rate to
increase and decrease in response to certain phys-
iological stimuli such as vibration, respiration,
Pulse Interval and QT interval. Pacemakers may be single-
chamber (AAIR/VVIR) or dual-chamber rate
The total time of the AV and VA intervals. The responsive (DDDR) systems.
time between pulses (ms).

Rate-Responsive AV Delay (RRAVD)


Pulse Width/Duration
A timing cycle in dual-chamber pacemakers that
The duration of the pacing stimulus (0.5–1.0 ms) automatically shortens the AV delay in response to
can be altered by the external programmer for higher atrial rates. Often used with rate-responsive
Basic Pacing Terminology 209

systems, RRAVD can also be useful for patients Sequential Pacing


with high intrinsic atrial rates.
Pacing of the atrium followed at a pre-set interval by
pacing of the ventricle allows “physiological” pacing.
Reed Switch

A small reed-like metal component within the Slew Rate


pacemaker which can close to create an electrical
circuit that causes the pacemaker to revert to This represents the rate of rise of the endocardial
magnet mode. potential (dV/dt). Those with a low slew rate may
not be sensed by the pacemaker.

Refractory Period
Strength-Duration Curve
A defined period of time (ms) during which the
heart will not contract. A refractory period may A chart which plots the various voltage settings
be physiological or it may be part of a pacemaker (pulse amplitude) in relationship to pulse width
timing cycle. This is further subdivided into abso- settings (ms) that capture the heart.
lute refractory period, when a contraction is
impossible, and a relative refractory period, when
there is limited response. Synchronous Pacing

A mode of pacing in which the pacemaker times its


Safety Margin output pulses with the heart’s own intrinsic events.

An increment used to program output settings for


a pacemaker in which the pacing threshold is Threshold
increased. A safety margin ensures capture, even
with changes in pacing threshold over the course Minimum quantity, of either amplitude (milliam-
of the day or longer. Commonly used safety mar- peres, volts), pulse duration (ms), charge (mcou-
gins involve finding the pacing threshold and dou- lombs), or energy (mjoules) produced by the
bling the voltage setting or tripling the pulse pacemaker that persistently produces an action
width. potential and myocardial contraction.

Sensing Total Atrial Refractory Period (TARP)

Dependent on the amplitude, slew rate, and sig- Total atrial refractory period or the PVARP + AV delay.
nal frequency, it describes the pacemaker’s abil- TARP is not directly programmable, but can be adjusted
ity to recognize a native electrical signal. by modifying the PVARP or AV delay setting.

Sensitivity Triggered Pacing

The minimum intracardiac signaling required by Triggered pacing occurs when a sensed spontane-
the pacemaker to initiate a pacemaker response. ous R wave results in the immediate delivery of a
210 9 Programmable Functions and Terminology

pacing stimulus into the R wave. The heart is obvi- Ventricular Refractory Period
ously refractory and is not paced. Triggered pace-
makers have a built-in refractory period to protect VRP is intended to prevent self-inhibition such as
against ventricular tachycardia should fast electrical sensing of T-waves. Initiated by sensed or paced
interference be sensed. It used to be chosen to avoid ventricular events.
myopotential inhibition and when a TPM was being
used to cover a failing permanent pacemaker. In the
latter situation, stimuli from the failing unit will Voltage Threshold
trigger the external pacemaker to fire an impulse in
the absolute refractory period (assuming the inter- Minimum voltage which will pace the heart.
nal unit’s impulse depolarized the heart) or alterna-
tively pace the heart if the permanent pacemaker’s
impulse fails to depolarize the myocardium. VS-1

Voluntary Standard, an older standard for lead


Undersensing and pacemaker connectors. Two main varia-
tions on VS-1 exist: VS-1A (for leads without
A common sensing problem in pacing in which sealing rings) and VS-1B for leads with sealing
the pacemaker inappropriately fails to sense sig- rings.
nals it ought to see. This causes the pacemaker to
pace even when it should be inhibited. Under-
sensing typically leads to overpacing and shows Advanced Pacemaker Function
on the ECG in the form of intrinsic events along and Terminology
with inappropriate, paced activity.
Advanced Hysteresis Response

Unipolar Pacing Manages special rate situations including sudden


rate drop. Available in many pacemakers now,
Here, the pacemaker “can” behaves as the anode e.g., Identity ADx™ (St. Jude Medical).
and the electrode tip as the cathode. Pacing spikes
are usually large on the surface ECG.
Advanced Sensor Technology

Upper Rate Behavior Combining sensors such as accelerometer and


minute ventilation sensors adapt the pacing rate
The way in which a dual-chamber pacemaker to the patient’s changing metabolic demand. The
will perform when trying to deal with a high cardiologist can choose either one or other sensor
intrinsic atrial rate. If the intrinsic atrial rate or a unique blend of the two.
exceeds the MTR and the TARP value, then pace-
maker “multiblock” will occur. If the atrial rate
exceeds the MTR but not the TARP value, then AF Suppression Algorithm
pacemaker Wenckebach will occur. Pacemaker
Wenckebach is preferred over “multiblock.” Program in pacemaker designed to prevent onset
of AF.

Ventriculoatrial (VA) Interval


AF Suppression Histogram
Described for dual-chamber pacemakers.
Represents the time (ms) between a ventricular Allows evaluation of the success of the AF sup-
event and a paced atrial event. pression algorithm.
Advanced Pacemaker Function and Terminology 211

AIDA Diagnostics time, onset rate, maximum rate, and storage


trigger.
Automatic Interpretation for Diagnosis Assistance
is a feature of devices from the Sorin Group. The
diagnostic aids may include Automatic analysis of AT/AF Diagnostic Suite
stored data providing advice on device manage-
ment regarding basic functioning, arrhythmia AT/AF burden trend, AT/AF stored EGM
management, and AV conduction; Trending, e.g., Trigger, AT/AF Histogram, and AT/AF Episode
summary screen with 6 month trends of heart rate, Log.
percentage pacing activity, and AF burden; Sensing
monitor to provide autosensing histograms of P
and R wave amplitudes; Lead monitor for lead Auto-Initialization
impedance and continuity curves; Arrhythmia
diary provides A and V arrhythmia episode distri- A feature of Biotronik’s Effecta series. This
bution and therapy analysis per zone; AV conduc- allows automatic activation of a series of func-
tion analysis to include type of block, circadian, or tions after lead connection. A&V Capture Control,
activity distribution and progression over time; Autosensing®, Auto Lead Check, Statistics and
Arrhythmia episode documentation for multiple IEGM recordings are functions that are activated
episodes using EGM and Markers on V and A within 10 min.
arrhythmias as well as significant other events,
e.g., mode switch, AV block switch, lead imped-
ance rise, and PhD which provides monitoring of Autolifestyle/Daily Learning™
respiratory and activity status, with day-by-day
analysis over the previous 6 months. All of these This was a feature of the Insignia Ultra (Guidant)
are available among the many other programma- and now of the Altrua™ series (Boston
ble features in the Paradym DR 8550 ICD device. Scientific) and optimizes the MV blended sen-
sor. At implant, Autolifestyle automatically
programs initial response factors at a very con-
Arrhythmia Management servative level based on age. After implantation
it automatically adjusts the MV response factor
Mode switching from DDD to VVI or VVIR at based on patient exertion level over several
the onset of atrial arrhythmias such as atrial weeks – so called coarse adjustment. The fea-
fibrillation can be programmed to happen auto- ture then automatically makes minor adjust-
matically. Each atrial event is assessed individu- ments to MV and accelerometer response factors
ally, providing beat-to-beat mode switching on as needed based on patient exertion – “fine
AF and PACs to keep the ventricular rate as stable adjustment.”
as possible and minimize palpitations. When AF The Clarity™ rate-adaptive pacemakers (Vitatron)
ends, the pacemaker immediately resynchronizes combined the physiological QT-interval sensor
atrium and ventricle to prevent retrograde con- with a fast-responding activity sensor to provide a
duction and pacemaker syndrome. Some devices rate that closely resembles that of a healthy sinus
have an Atrial Flutter Response (AFR) which node. Daily learning™ of the sensors continu-
allows immediate reaction to rapid atrial rates. A ously adapts rate response to individual needs.
programmable (130–230 ppm) trigger rate pre- Children and young, more active individuals reach
vents atrial tracking above the trigger rate. higher sinus rates during exercise and their sinus
variations from one beat to the next are larger.
Clarity’s unique combination of tracking these
Arrhythmia Logbook higher sinus rates while distinguishing sinus
rhythm from atrial arrhythmia over the entire rate
Some pacemakers automatically store events in a range allows these younger patients to be normally
logbook, each with a unique event number, date/ active.
212 9 Programmable Functions and Terminology

Automatic Capture Conducted Follow-Up

This function – a feature in Boston Scientific’s Automatic interrogation of stored data, two-chan-
Altrua™ and Guidant’s Insignia Ultra™ pacing nel, real-time intracardiac (IC) ECG with markers
system – automatically adjusts pacing output to can be helpful in troubleshooting. An indication
maintain ventricular capture and maintains out- of battery life is always available at follow-up.
put voltage at 0.5 V above capture threshold. The
pacemaker confirms capture on a beat-to-beat
basis, checks threshold every 21 h when loss of Diagnostic Memory Functions
capture is detected during beat-to-beat analysis,
and provides safety backup pulses as needed to Event counters, histograms, trends, and sensor
maintain ventricular capture. simulation are available on pacemakers such as
A similar feature called Active Capture Control Biotronik’s Axios DR pacemaker. Diagnostic
(ACC) is available in the Talos SLR (Biotronik) Observations™ available in Vitatron’s Clarity™
and permits energy efficient therapy and maxi- pacemaker alerts to anomalies recorded in the
mizes the generator’s longevity. Medtronic pace- diagnostics, e.g., rhythm disturbances, and rec-
makers feature Atrial Capture Management ommends appropriate therapy adjustments. In
(ACM) and Ventricular Capture Management addition Selected Event Recording allows the
(VCM) which provides complete long-term thre- causes and details of symptom-related events to
shold management automatically and ensures be captured for analysis and diagnosis.
pacing outputs remain at safe levels by adapting
programmed outputs to maximize longevity.
(IRSplus) Intrinsic Rhythm Support

Automatic Post-Ventricular Atrial IRSplus is a featured algorithm of Biotronik’s


Refractory Period Adjustment Effecta pacemakers which automatically pro-
motes intrinsic conduction with a full hysteresis
The promotion of AV synchrony with automatic package. After 180 consecutive pacing cycles,
PVARP adjustments reduces the likelihood of the AV scan hysteresis searches for intrinsic con-
palpitations and protects against pacemaker- duction by prolonging the AV delay to 400 ms.
mediated tachycardia (PMT).

Managed Ventricular Pacing® (MVP®)


Auto Sense
Program to allow best pacing therapy available to
Auto Sense is designed to automatically adjust the minimize RV pacing – feature of Medtronic’s
pacemaker’s sensitivity to cardiac signal changes Adapta® and Ensura™ pacemakers.
without the cardiologist’s intervention. Sensitivity Other devices offer multiple programming
is adjusted based on the measured amplitude of options to provide increased flexibility to help
previously sensed events, the type of cardiac cycle minimize unnecessary RV pacing. For example,
(paced or sensed), and a measurement of the cur- the Altrua™ 60 series (Boston Scientific) offer
rent myopotential/environmental noise level. a fixed AV Delay of 10–400 ms, a Dynamic AV
Delay extendable up to 400 ms, and AV Search
Hysteresis (AVSH) extendable to 400 ms maxi-
Automatic AV Search Hysteresis mum, allowing more time for intrinsic ventric-
ular conduction to occur after an atrial event.
Designed to reduce unnecessary RV pacing with- Medtronic’s Versa™ and Sensia™ offer long
out dropping beats, e.g., Dplus (Sorin Group) programmable AVDs and “AVD extension.”
Advanced Pacemaker Function and Terminology 213

SafeR™ Support of Intrinsic Rhythm

A pacing algorithm from the Sorin Group that AV and rate hysteresis can optimize pacing
maximizes intrinsic conduction by ensuring DDD function.
pacing when needed for all types of AV block,
provides AAI pacing while continuously monitor-
ing AV conduction and switch back to AAI mode Triggered and Continuous
whenever possible. For example, if 7 long PR Overdrive Pacing
intervals are observed, DDD pacing is initiated
(AVB I criteria); for 3 blocked P waves out of 12, A broad range of preventive pacing algorithms to
DDD pacing will be initiated (AVB II criteria); and stop AF from starting by recognizing the onset
for 2 consecutive blocked P waves, again DDD mechanism in individual patients. They include
pacing will be initiated (AVB III criteria). Post-Exercise Response, PAC Suppression, Post-
Adjustments can be made to cope with normal rest PAC Response, Post-AF Response, and continu-
and exercise such as the ability to suppress the ous overdrive pacing. These features were
AVB I criteria at rest and to rapidly switch to DDD available in Vitatron’s T-series, Prevent AF, and
during exercise if required. Similarly, it is possible Selection 9000 AF 3.0, and have been incorpo-
to reduce nocturnal pacing by allowing a long PR rated into the more recent models.
and to test for AV conduction each morning if in
DDD.
Ventricular Safety Pacing

Stored Intracardiac Electrograms Ventricular safety pacing (VSP) is an algorithm


used to prevent crosstalk inhibition and ventric-
This useful feature helps in troubleshooting pace- ular capture during the vulnerable period.
maker problems, such as an insight into arrhyth- Crosstalk is the inappropriate detection of a
mia origination. Some allow patients to trigger spontaneous or pacemaker-generated event in
their own ICECG for event recording. In some one channel by the other channel, which can
pacemakers, stored electrograms are initiated by cause the inhibition of the second channel’s out-
any of the following programmable triggers: put. There are two functions designed to prevent
patient-applied magnet, Atrial Tachy Response crosstalk inhibition. One is the ventricular
(ATR) mode switch, clinician-defined ventricular, blanking period that coincides with the atrial
and/or atrial tachycardia and nonsustained tachy- stimulus and prevents the detection of the atrial
cardia (>3 PVCs), sudden bradycardia response, spike or activation that coincides with the atrial
and PMT. stimulus. The second – VSP – delivers short-
coupled ventricular stimuli after atrial pacing
when sensing any activation in the ventricular
Sudden Bradycardia Response (SBR) lead after the end of the ventricular blanking
with Minute Ventilation (MV) Offset period (see Chap. 21).

SBR is designed to respond to sudden decreases


in intrinsic atrial rates by applying dual-chamber Ventricular Rate Regulation (VRR)
pacing at an elevated rate. MV Offset provides or Ventricular Rate Stabilization (VRS)
the ability to inhibit SBR therapy to allow appli-
cation only when a patient’s minute ventilation This feature is designed to regularize the ventric-
meets or exceeds a programmed level. This fea- ular response to conducted atrial arrhythmias
ture is present in the Altrua™ 50 and Altrua™ 60 using a historic weighted average method of
series (Boston Scientific). establishing the VRR pacing rate.
Precautions After Permanent
Pacemaker Implantation 10

Patients often ask about what precautions they and perhaps inhibit a single beat, this does not
should take to avoid damaging or affecting the appear to be of practical importance.
function of their pacemaker. The commonest Bipolar sensing/pacing is essential if a patient’s
issues discussed by patients are set out below and work is likely to bring the individual into contact
are most often seen with unipolar systems. with strong sources of EMI such as internal com-
Table 10.1 lists sources of electromagnetic inter- bustion engines, radar, and arc welding. Arc
ference and the possible effects on pacemakers. welders have to take special precautions, such as
avoid working in wet areas, avoid high currents
(<400 A), and should wear nonconductive gloves.
Electromagnetic Interference (EMI) Connecting the ground clamp to the metal close
to the welding point is advisable.
External EMI can cause reprogramming or dam-
age to the pacemaker circuitry. It may also cause
inhibition or a switch to the fixed rate mode. Magnets
Pacemakers are well shielded and protected by
appropriate filters and so generally problems are Magnets held over a pacemaker may put the
an unusual occurrence. Although patients can be device into fixed-rate mode by activation of its
reassured that the risks of EMI are small, if they reed-switch. Inappropriate sensing by the pace-
feel dizzy in close proximity to electrical equip- maker due to noise artifact created by electric
ment, they should walk away from the device. cautery will be avoided by magnet application.
Possible sources of EMI include radio transmit- Removal of the magnet is all that is required to
ters, motor car engines, microwave ovens, and restore normal function.
electric motors inside some household equip- Magnets held over ICDs do not inhibit sensing
ment. Theft detection devices in shops and stores, function but do inhibit delivery of any antitachy-
metal/weapon detection devices in security set- cardia therapy, such as ATP or high-energy
tings, for example, at airports, and radar can also defibrillation. Magnet application may therefore
cause interference. be used to prevent inappropriate ICD therapies
CB and “HAM” radios, electric drills, electric during use of electrocautery that may produce
blankets and shavers, heating pads, metal detec- noise artifact sensed by the lead as VT or VF.
tors, microwave ovens, TV transmitters, and Such a patient should be monitored, so that appro-
remote TV controls have not been shown to dam- priate, programmed ICD therapy can be delivered
age pulse generators, change pacing rates, or if required by removing the magnet. In the UK,
totally inhibit pacemaker output. Although they the Medicines and Healthcare products Regulatory
have the potential to cause occasional interference Agency (MHRA) suggested that local policies

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 215


DOI 10.1007/978-1-4471-2939-4_10, © Springer-Verlag London 2012
216 10 Precautions After Permanent Pacemaker Implantation

Table 10.1 Sources of electromagnetic interference and their possible effects on pacemakers
Item Safe Precaution Avoid
Personal items Electric blankets Cell phones Body fat measuring scales
Electric toothbrushes Keep 6″ from device (handheld)
Electric razors Keep 12″ from device Magnetic mattresses or
Hair dryers if transmits >3 W chairs
Heating pads Hold phone to ear on Electrolysis (hair removal)
Pagers opposite side of body from
Patient alert devices device
Personal digital assistants Do not carry phone in breast
(PDAs unless used as cell phones) pocket within 6″ of device
Radio-controlled clocks/ Cordless phones
watches Safe if not placed directly
Tattoos over device
Thermolysis (hair removal) Handheld massagers
Safe if not placed directly
over device
Kitchen, Air purifiers
tabletop, and Blenders
household items Clothes dryers
Convection ovens
Electric can openers/knives
Electric ovens and stoves
Food processors
Gas ovens and stoves
Microwave ovens
Portable space heaters
Sewing machines
Toasters
Vacuum cleaners
Washing machines
Office, shop, Copy machines Arc welding equipment Jackhammers
and yard Electric invisible fences Keep 24″ from device
equipment Fax machines Running motors/alternators
Personal computers especially those found in
vehicles and high-power
generators
Keep 24″ from device
Avoid leaning over running
motors/
alternators of a running vehicle
For the following items, keep
12″ from device
Battery-powered cordless
power tools
Chainsaws
Corded drills/power tools
Lawn mowers/hedge
clippers
Leaf blowers
Shop tools (drills, table
saws)
Snowblowers
Magnetic Resonance Imaging (MRI) 217

Table 10.1 (continued)


Item Safe Precaution Avoid
Entertainment AM/FM radios Bingo game magnetic wands
items CD/DVD players Keep 6″ from device
Hot tubs/whirlpool baths CB and police radio antennas
Laser tag games Keep 24″ from device
Multimedia players Slot machines
e.g., iPods/MP3 players Keep 12″ from device
Remote controls (TV, garage Stereo speakers
door, stereo, camera/video Keep 12″ from device
equipment) SCUBA diving
Tanning beds
TVs and VCRs
Video games
Travel/ Amusement parks/roller Security systems (airports, jails, Stun guns
environment coasters courthouses etc.)
Walk through security
archways normally
Tell security personnel that
you have a device and show
Medical Device ID card
Security wand should not be
held over device for >30s;
ask for hand-search
Theft detection systems
(store/library entrances)
Walk through theft detection
systems at a normal pace
Do not lean against or linger
near these systems
Magnetic fields
Transformers
High voltage lines
TV/radio towers
Radiofrequency transmitters
Residential power generators
Dental/medical CT scans Radiation therapy, MRI scansa
tests and Dental drills/cleaning equipment electrocautery used in surgery, Diathermy
procedures Diagnostic X-rays TENS unit
ECG Contact doctor in charge
Mammography (tell technician so Contact pacemaker company
that the device is not compressed) for further information
Ultrasound Cardioversion
Defibrillation
Lithotripsy
© Boston Scientific; http://www.bostonscientific.com/templatedata
a
The Advisa DR MRI™ Surescan® device (Medtronic Ltd.) is MRI safe

should be put in place to allow ICDs to be deacti- Magnetic Resonance Imaging (MRI)
vated prior to routine surgery and reactivated
afterward and that “magnet deactivation” should In general, pacemaker patients should not
only be used in an emergency situation. Detailed undergo MRI scanning and only in exceptional
advice can be found on www.mhra.gov.uk. circumstances after consulting the pacemaker
218 10 Precautions After Permanent Pacemaker Implantation

manufacturer. The appropriate device’s sensor of the electrode system. MRI at 1.5 T can cause
and magnet responses should then be turned off major temperature rise at the tissue-electrode
with the external programmer in order to try interface, tachycardia, and even ventricular
and avoid inappropriate reversion to fixed-rate arrhythmias.
mode or to fast rates which may be potentially In patients who definitely need MRI, it might
dangerous. The latter may be due to the pulsing be cautiously undertaken as long as the pace-
radiofrequency field owing to the antenna effect maker is checked before and after MRI and
dependency status checked. In those who are not
dependent, the pacemaker should be turned off if
possible and a low magnetic field used (0.5 T).
Monitoring of the patient is essential.
Recently, Medtronic Ltd. released the
EnRhythm DR MRI™ SureScan® and Advisa
DR MRI™ Surescan® pacing system which are
MRI “conditional safe” (Fig. 10.1) and an MRI-
safe lead – the CapSureFix MRI™ Lead. The lat-
ter is identifiable on X-ray (Fig. 10.2). To safely
scan patients with these devices several condi-
tions must be satisfied. These include:
• The system has been implanted for >6 weeks
• The device was implanted in the pectoral
region
• No additional active implantable device(s) are
present
• Device and leads are labeled “MR Conditional”
Fig. 10.1 The MRI-conditional safe Advisa DR MRI™
Surescan® pacemaker and leads from Medtronic Ltd.
• Leads are electrically intact (impedance
(Image reproduced with permission of Medtronic, Inc.) 200–1,500 Ω)

Fig. 10.2 The MRI-conditional safe electrode is (Model 5086) identifies the lead as MRI compatible (blue
identifiable by X-ray. A radiopaque helix in the proximal arrow). The radiopaque code (green arrow) identifies the
end of the CapSureFix MRI™ SureScan™ Pacing Lead pacemaker
Radiation 219

• Abandoned or additional leads or wires are Besides inhibition, resetting/reprogramming


not present or damage of/to the pacemaker, upper-rate pacing
• No lead extenders or adaptors are present (in Minute Ventilation rate-responsive systems),
• Capture thresholds do not exceed 2 V at 0.4 ms and internal burns and scarring as a result of the
• SureScan® is programmed ON before the scan current induced in the lead may occur. The latter
and programmed OFF after the scan may lead to a higher pacing threshold or exit
Biotronik have released the Estella series of block.
pacemakers which are MR “conditional safe” The pacemaker program and function should
(Biotronik ProMRI®) and need to be used with be checked postoperatively.
MRI conditional safe leads, e.g., Safio S and
Solia.
St. Jude Medical Inc. have produced the Accent Radiofrequency Ablation (RF)
MRI™ pacemaker and Tendril MRI™ lead which
have been approved as MR-Conditional in Europe Most pacemakers are not affected by RF catheter
and released for use in India and the Sorin Group ablation of intracardiac tissue, but it is usually
are developing the Reply MR-conditional pace- worth checking the pacemaker’s function and
maker and Filtrea pacing lead. program settings after the procedure. Both sens-
Boston Scientific Corporation have recently ing and pacing failure have been reported and
released the Ingenio™ MRI and Advantio™ care should be taken to establish whether the
MRI rate-responsive pacemakers (employing patient is pacemaker dependent prior to the pro-
RightRate™ MV sensor and ImageReady™ tech- cedure and the program adjusted accordingly to
nology). When used in conjunction with Fineline allow for potential problems that may rarely
II leads, they are safe for use in patients requiring occur.
MRI scanning by programming the device into Generally, the rate response function should be
MRI Protection Mode. turned off and the RF applications should be as brief
as possible and remote from the pacing lead tip.

Diathermy
Radiation
Short-wave or microwave diathermy uses high-
frequency, high-intensity signals, and may perma- Diagnostic X-rays do not affect pacemaker func-
nently damage the generator, cause inappropriate tion but radiotherapy may damage the circuitry. It
inhibition, or cause ventricular fibrillation by trig- probably causes damage to the thin oxide layers
gering ventricular pacing due to atrial oversens- and transistors by accumulation of positive charge
ing. Surgeons should ideally use a bipolar system. inside the circuitry leading to failure of various
If a unipolar diathermy is used, the output should battery components or accelerated battery deple-
be kept low, the active electrode kept >2–3 in. tion. Changes in sensing capability, failure of
from the pacemaker, and the indifferent electrode telemetry function, runaway function, and total
kept as far away as possible so that its dipole is at shutdown may occur. Positioning the radiation
right angles to the pacing system. field at an angle oblique to the pacemaker in order
The heart rhythm should be monitored so that to minimize the amount of radiation delivered at
diathermy can be stopped if prolonged inhibition the pacemaker site is advisable. A total accumu-
occurs. Interference can be avoided during sur- lated dosage limit of 2 rad should be estimated
gery by reprogramming the generator to a fixed and additional shielding of the pacemaker with a
rate (DOO or VOO) mode at the start of the oper- 1 cm margin may be required. If it cannot be
ation and reprogrammed to a demand mode at the shielded because it is in the path of the desired
end. Bipolar pacing systems may be less suscep- beam, then the pacemaker should be resited.
tible to inhibition. Certainly, the device’s function should be checked
220 10 Precautions After Permanent Pacemaker Implantation

after each therapy session and the pacemaker stimulation threshold, erasure of the programmed
replaced if found to be faulty. settings in the pacemaker’s memory, back-up
pacing, and myocardial burns with cardiac
enzyme release. Most have a built-in protection
Cellular Phones called “Power On Reset” which automatically
reprograms the pacemaker to a safe set of values
Mobile phones should be kept at least 6 in. away (usually VVI mode). It can then be reprogrammed
from the pacemaker and the opposite ear should to its desired parameters.
be used. There is a possibility that transient inter-
ference with pacemaker function could occur
when using a mobile phone held close to the Electroconvulsive Therapy (ECT)
pacemaker. A study of 980 patients found that
ventricular tracking of signals sensed on the atrial ECT should not cause interference with pace-
channel, noise reversion, and inhibition of ven- maker function.
tricular output were the most common types of
interference – clinically significant in 6.6% of
patients. Interference is more common in dual Transcutaneous Electrical Nerve
chamber (25.3%) compared to single chamber Stimulation (TENS)
(6.6%) systems and in digital telephones (24%)
compared to analog ones (3%). The ECG should be monitored when initially
using a TENS machine. Unipolar pacemakers
may be inhibited during TENS applied close to
Electronic Article Surveillance the pacemaker.
Systems (EAS)/Metal Detectors

Such devices which use RF scanners or magnetic Lithotripsy


sensors could transiently inhibit or reprogram a
pacemaker, but this is a rare occurrence. Pacemaker- Shocks should be aimed well away from the gen-
dependent patients should be told not to linger erator, and because of the vibrations the rate-
near such systems but that merely passing through adaptive mode should be turned off. The
them should not cause a problem. Handheld metal piezoelectric crystal of activity-driven pacemak-
detectors should not be held over the pacemaker ers can be irrevocably destroyed if placed in the
and an alternative body search should be requested focal point of an extracorporeal shock wave litho-
by pacemaker-dependent individuals. tripsy. The latter should be at least 25 cm away
from the pacemaker. It is best avoided in abdomi-
nal pacemakers.
Cardioversion/Defibrillation

In order to prevent damage to the pacemaker, the SCUBA Diving


paddles should be kept >6 in. from the pacemaker.
Positioning the paddles at right angles to the pacing Many pacemakers may be affected beyond depths
system should minimize the current induced in the of 11 m as the pacemaker titanium can may be
lead and antero-posterior rather than antero-apical compressed by severe hydrostatic pressure.
paddle placement might minimize the risks.
Unipolar pacemakers are more susceptible
than bipolar devices. The pacemaker program and Vigorous Sports
function should be checked after the procedure.
Defibrillation/cardioversion may cause under- Vigorous contact sports are best avoided, to avoid
sensing due to alteration of the intracardiac sig- injury to the generator. Rugby, boxing, wrestling,
nal, failure to capture due to an increase in the judo and karate should be avoided.
Other Sources of Electromagnetic Interference 221

Cremation ECGs, or complete interruption of telemetric


communications.
All pacemakers must be explanted before crema- Some dental instruments, e.g., ultrasound
tion since they are likely to explode. scalers/cleaners and electrosurgical instruments
can cause transient inhibition of pacing output.
Some cardiac monitoring systems used for
Other Sources of Electromagnetic recording continuous ECGs in hospitalized
Interference patients can cause inappropriate rate changes in
patients in whom rate response is as a result of
Hospital pagers may disturb telemetry in the form sensing minute ventilation.
of inaccurate battery voltage, current, and imped-
ance measurements, disturbances in intracardiac
Follow-up After Pacemaker
Implantation 11

Patients who have undergone permanent pacemaker, The aims of a pacing clinic are set out in
ICD, or CRT device implantation should be Table 11.1. The reason for such attendance is to
regularly followed-up. Follow-up normally check that the pacemaker is functioning normally,
takes place in a specifically designated, out- to troubleshoot and solve any pacemaker prob-
patient pacing clinic – the pacemaker clinic – lems (see Chap. 21), to optimize the pacing sys-
although increasing numbers of patients in tem’s programmed settings and function to each
Europe and USA are being monitored at home patient’s needs, and to download information
using a variety of remote monitoring systems. stored in the pacemaker. It is useful to ensure no
According to the HRS/EHRA expert consensus, new symptoms have developed since the implant
follow-up should include the assessment of the (e.g., angina), to examine the wound and check
device and lead status, as well as the review of for any pacemaker complications, to check the
detected episodes and hemodynamic measure- battery life and maximize longevity by adjusting
ments or recordings of any other programmed the settings, and to plan the next date for atten-
parameters. The details of their joint recom- dance. It is appropriate to confirm the patient’s
mendations can be found in the journal Europace contact details in case of manufacturer-recom-
2008;10:707–725. mended pacemaker recall. Following discharge

Table 11.1 Aims of a pacemaker clinic


Optimization of the pacing system to each patient’s needs together with safe maximization of generator life.
Monitor implant site and wound status
Identification of abnormalities in the pacemaker system (generator and any lead) and any complication to permit
prompt treatment
Prediction of end-of-life of the pulse generator to permit elective change of the pulse generator
Provision of patient support and education: provide information about the device and therapies set
Keep appropriate records of follow-up
Accumulation of a database that offers information on present and past pacing systems for each patient and general
data on the function of pulse generators and leads from as wide a field as possible (including a link to the CCAD/
NPDB).
Provision of training opportunities for medical and paramedical staff.
Provision of a clinical cardiological follow-up service where this is appropriate. In some cases, this is provided by a
separate clinic or, alternatively, at another medical facility.
To liase with MHRA (Medical Health Regulatory Agency) and pacemaker manufacturer in relation to device and
lead problems when appropriate

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 223


DOI 10.1007/978-1-4471-2939-4_11, © Springer-Verlag London 2012
224 11 Follow-up After Pacemaker Implantation

Fig. 11.1 Initial steps Confirm patient identity


carried out by pacing
technician in follow-up
clinic Identify pacemaker model/manufacturer

Select appropriate programmer

Attach patient to ECG (limb leads, I, II, III & V1, V2 for CRT patients)

Record ECG and magnet strip

Review wound (especially at first visit or if any problem reported)

If wound inflamed/tender If wound OK

Arrange medical review Interrogate Device


+/– FBC, CRP using wand Telemetry/
+/–antibiotics radiofrequency

Review trends
Organise early follow-up/review
Check intrinsic amplitudes, impedances,
and need for further treatment
thresholds, events, battery life/warnings

If Battery at ERI–list for “box Measurements OK


change”
If Battery at EOL (should not
happen!)–urgent medical review
and prompt admission for “box
change”

Arrange subsequent follow-up appointment

from hospital after pacemaker implantation, the listed in Table 11.2, and the routine tasks to be
patient should be told to contact the pacing center performed in Table 11.3. Programmers compati-
if the pacemaker becomes painful or very tender, ble with the devices implanted in the center
if the wound becomes red and/or swollen, or if should be present in the clinic (see Fig. 6.64) and
they become unwell with pyrexia. If the wound the telephone numbers for technical support of
edges gape, again the patient should return to the all the relevant pacemaker manufacturers should
center without delay if serious infection is to be be available.
avoided. The cardiologist or technician should first
The clinic should be in or close to the ECG request to see the patient’s ID card and the details
department, staffed by an experienced pacing should match what data are in the casenotes or on
technician or clinical physiologist with immedi- the pacemaker database. A brief interview about
ate access to a cardiologist familiar with normal the presence of symptoms since last reviewed
and abnormal pacemaker function. Guidelines should be accompanied by inspection of the pace-
for a physiologist-led pacemaker clinic are avail- maker wound. It should then be established
able on the HRUK website. Practical algorithms whether the patient is “pacemaker-dependent”
for technicians working in pacing clinics are and to what degree. The patient’s history and case
illustrated in Figs. 11.1–11.4. The equipment and records and a 12-lead ECG should help answer
facilities necessary in a pacemaker clinic are this question. Application of a magnet to
Follow-up After Pacemaker Implantation 225

Fig. 11.2 Lead Lead measurements


amplitude sensitivity,
pacing threshold, and Impedance Amplitudes Thresholds

impedance measurement
algorithm
(400–1,500 Ω) At 4−6 weeks
Review trends R Wave > 5 mv V threshold
Allow 20% variation P Wave > 2 mv < 1 v @ 0.4 ms
between follow-ups A threshold
< 1.5−1 v @ 0.4 ms

P & R wave sensitivity should


Check in both unipolar
be approx. 1/2 of measured Switch on Automatic
and bipolar modes
P & R wave amplitude Capture Management

Outputs should be
High impedance Low impedance reduced > 6 weeks
suggestive of suggestive of 2.5 V @ 0.4 ms or 2x voltage
conductor failure insulation failure threshold – whichever is greatest
obtain PA & Lat CXR difficult to see on CXR

Oversensing = Undersensing = If acute rise in threshold


Medical review & CXR
underpacing overpacing (> 1.5 V @ 0.4 ms after 6 weeks):
Symptoms eg: syncope,
dizziness, palpitation. Exclude:
Lead displacement – CXR
Exit block – consider steroid
therapy
Decide on need for Reprogram to reduced Reprogram to increased Medication contributing to
lead replacement sensitivity sensitivity increased threshold e.g., flecainide

Histograms & EGMs


AF, SVT, VT

Rate response
VT > 6 beats Is there adequate
AF
How many episodes have Percentage V
What is the frequency chronotropic response?
there been, beats & rate? paced > 40%?
of arrhythmia? Histograms should show
Is the device set up Is this true pacing,
Is there appropriate a range of ventricular
optimally to record fusion or pseudofusion?
mode-switching? rates – not mostly
arrhythmias? base rate activity

Is there documented Is there a documented


history of AF? history of VT? Check indication
Are there symptoms
Symptoms − do they relate Symptoms − do they relate for pacing.
of fatigue or
to EGM date/time? to EGM date/time? Is AV node
exertional dyspnea?
Is the rate controlled or ? Syncope, disease present?
fast conducted AF? ? EF < 35% or CAD

Thromboprophylaxis: Is patient on Check “rate-response”


Is RV pacing
Is the patient taking antiarrhythmics? is enabled and/or
avoidable?
anti-coagulation? i.e. Beta-blockers, adjust response
i.e. Warfarin, Aspirin Amiodarone sensitivity

Rate/rhythm control Arrange for review of


Consider adjusting
Is an antiarrhythmic/ symptoms and possibly
Assess AV delay
rate-controlling drug further adjustments
LV function +/– using RV pacing
Fig. 11.3 An assessment prescribed eg: flecainide,
reduction algorithm
of rate-response
β-blocker sensitivity
is made of the occurrence
and frequency of AF,
SVT, VT, frequency of
ventricular pacing, and Medical review
frequency and appropri-
ateness of rate response
226 11 Follow-up After Pacemaker Implantation

a CRT implant b Three month follow-up


ECGs recorded
RV, LV, BiV (Lead 1) CRT device check
Leads I and V1 as above
are most useful
Full device check
including wound check > 90% True BIV paced
Pacing OK? Y/N
Sensing OK? Y/N
AVD appropriate? Y/N
Yes No

No Yes
Medical review
Clinical response
AF/AT
Medical review > 90% True BiV paced VEs
Reprogram
CXR No Yes
Yes No

Clinical response % V sensed Living advice Y/N


ECHO optimization
NYHA Class VE’s Driving advice
AV and V-V delays
HF symtoms/diagnostics/ AF/AT Remote follow-up
heart failure meds ? reprogram
prescribed
Confirm rehab referral

? CXR ICD PPM


Yes No
LV lead position 3−6/12 follow-up 6−12/12 follow-up

Driving advice Trigger HF nurse/


Remote follow-up medical review

Medical review
ICD PPM
3/12 follow-up 6/12 follow-up

Fig. 11.4 Technician’s algorithm for use with patient with a CRT device on (a) first and (b) 3 month follow-up visits

Table 11.3 Routine pacemaker follow-up – tasksa


Table 11.2 Equipment and facilities necessary for a
pacemaker/ICD follow-up clinic Patient assessment
Resuscitation equipment including defibrillator and Symptoms
external pacemaker device Skin overlying the pacemaker system
Cardiac arrest team “call button” 12 s multichannel ECG rhythm recording with and
12-Lead ECG machine without a magnet applied over the generator to:
Magnet Verify automatic interval with/without magnet
Relevant range of pacemaker/ICD programmers/ Estimate degree of pacemaker dependence
analyzers for the devices used in the center Verify appropriate depolarization sequence, capture,
Manuals/information booklet for all relevant pacemak- sensing, fusion/pseudofusion beats
ers/ICDs and programmers Lead stability testing. Respiratory tests and lead
Contact telephone numbers of all relevant manufactur- integrity by generator manipulation – when intermittent
ers or their local agencies lead problem suspected
File of technical notes and notices from manufacturers End-of-life battery check (EOL). Use of a device
specific programmer is essential
Computerized patient database
Acquisition of generator telemetry concerning lead
Access to X-ray facilities, exercise stress testing, and
functions where available
ambulatory ECG monitoring
Verification of pacing and sensing functions by
24 h telephone answering facilities manned by
threshold assessment using the programmer and/or
competent staff
magnet application
Access to temporary pacing facilities
Recording and communicating all the above as
Access to a cardiologist appropriate in casenotes/letter to GP
A robust process for listing patients for device Recording of data on database
replacement or system revision a
Each device implanting/follow-up clinic should have a
Facilities to admit patients as emergencies at any time
protocol for the procedure to be followed
Follow-up After Pacemaker Implantation 227

Fig. 11.5 Interrogating


the device by placing the
magnetic wand or
programming head of the
programmer over the
implant site

Fig. 11.6 The program


can be adjusted appropri-
ately and saved in the
pacemaker

pacemakers usually results in reversion to an wand. Interrogation includes verification of the


asynchronous pacing mode (AOO, VOO, or administrative data, a check on the programmed
DOO), which can be recorded on ECG and which data, examination of the measured or real-time
confirms that the lead(s) can pace the myocar- data on output, battery life and lead impedance
dium (see Fig. 11.13). measurements. Data collected by the pacemaker
The technician/clinical physiologist can then are sent into the programmer and can be dis-
begin to interrogate the pacemaker by placing the played (see Fig. 9.6). The program can be adjusted
magnetic wand or programming head of the pro- appropriately and saved in the pacemaker using
grammer over the pacemaker (Fig. 11.5), although the touch screen on the programmer (Fig. 11.6).
increasingly more common, pacemakers can be A printout of the program and an ECG showing
interrogated wirelessly without the need for a satisfactory pacing should be inserted in the
228 11 Follow-up After Pacemaker Implantation

Fig. 11.7 A printout of the program and an ECG showing satisfactory pacing should be inserted in the patient’s
case records

patient’s case records (Figs. 11.7–11.11). Data should be tested and the pacemaker program
should be entered into the Pacing Database and a adjusted if necessary (Figs. 11.13 and 11.14).
copy of the recent entry placed in the casenotes Modern pacemakers and their programmers allow
(Fig. 11.12). Sensing and pacing thresholds for non-invasive pacing stimulation (NIPS) test-
Follow-up After Pacemaker Implantation 229

Fig. 11.8 Satisfactory


DDD pacing

Fig. 11.9 Satisfactory VDD


pacing

Fig. 11.10 A summary of the pacemaker check is provided for the case records
230 11 Follow-up After Pacemaker Implantation

Fig. 11.11 Lead data should include amplitude, threshold, and impedance measurements

Fig. 11.12 A typical printout


following pacemaker interrogation
Follow-up After Pacemaker Implantation 231

Fig. 11.13 Application of


magnet to this dual-chamber
pacemaker results in DOO
pacing at a rate of 100 bpm
(arrow)

Fig. 11.14 Testing the


ventricular lead threshold
shows loss of capture at 0.4 V
(arrow)

ing of pacing, sensitivity, and impedance to be (Fig. 11.17). Figures 11.18 and 11.19 show the
displayed on screen (Fig. 11.15). A useful, time- pages that can demonstrate lead data over time.
saving facility available on most programmers is Changes in lead impedance are important to
the Overview Screen or “First Page,” which pres- note. Lead impedance tends to fall in the first
ents all useful indicators gathered in one screen 2 weeks after implantation, but then reaches a pla-
when no further testing may be required teau and remains relatively stable at approximately
(Fig. 11.16). “Pages” may display live annotated 15% higher than the implantation value. Fluctuations
ECG with simultaneous intracardiac atrial and of impedance by as much as 300 Ω are considered
ventricular electrograms (EGM), along with the normal. Generally, an increase in impedance by
current pacemaker and lead settings and “but- >300 Ω suggests conductor fracture, whereas a
tons” to allow further interrogation of patient decrease of >300 Ω suggests insulation break. A
data, lead threshold testing, and trend data chest X-ray should be done if either is suspected.
232 11 Follow-up After Pacemaker Implantation

Fig. 11.15 Screen on the Orchestra™ programmer for NIPS (Non-Invasive Pacing Stimulation testing of a Reply™
DR pacemaker. Courtesy of Sorin Group)

Fig. 11.16 Interrogation of Reply™ pacemaker. First impedance measurements, device statistics and battery sta-
screen provides information on pacing mode, basic rate tus at a glance. Further interrogation is obtained by enter-
and maximum rate, sensing and pacing settings, lead ing the next series of pages (Courtesy of Sorin Group)
Follow-up After Pacemaker Implantation 233

Fig. 11.17 Page from the Medtronic programmer dis- tons” to allow further interrogation of patient data, lead
playing live annotated ECG with simultaneous intracar- threshold testing and trend data (From the Medtronic
diac atrial and ventricular electrograms (EGM), along Advisa DR MRI SureScanÒ pacemaker) (Image repro-
with the current pacemaker and lead settings and “but- duced with permission of Medtronic, Inc.)

Fig. 11.18 Quick Look II Screen from the Medtronic interrogation of this Medtronic Advisa DR MRI™
programmer showing the facility for trending lead data SureScanÒ pacemaker. It includes links to more detailed
and the amount of time atrial sensing/pacing and ventricu- status and diagnostic information stored in the device
lar sensing/pacing. This is the initial screen shown upon (Image reproduced with permission of Medtronic, Inc.)
234 11 Follow-up After Pacemaker Implantation

Fig. 11.19 Continuous atrial and ventricular lead threshold values represent the most recently measured threshold or
and impedance data can be displayed on a page of the lead impedance value for the particular lead, while the graph
Medtronic programmer. This allows an assessment of the represents measurements taken over the previous 12 months
performance and integrity of the leads. The “last measured” (Image reproduced with permission of Medtronic, Inc.)

CRT and ICD devices are interrogated in simi- Devices can show peak atrial rate histograms, %
lar fashion and the programmer used to print out AT/AF burden, and the details of each and every
details of the retrieved data (Figs. 11.20 and 11.21). episode. AF suppression diagnostics can show
Modern programmers present a series of “pages” how often this was required, what circumstances
as screenshots which can be accessed by “touch provoked it, and how well it performed.
buttons” to reveal data on program settings, lead Intracardiac EGMs are really useful diagnosti-
and battery data, arrhythmia detection settings, cally and should be downloaded at follow-up.
information on therapy delivery, etc. These may be single-channel EGM or dual-
(Figs. 11.22–11.25). channel EGM in dual-chamber systems. EGM
Specific diagnostic functions should be triggers are programmable and may include high
checked and evaluated. For example, heart rate atrial rate activity, PVCs, and mode-switch
histograms can assess rate adaptive function, events. Some devices allow patient-triggered
sleep rate, hysteresis function, and automatic EGM recordings. Most devices seen in clinical
mode switching. Event histograms include ecto- practice today also offer annotated ECG strips
pic counts as well as the percentage of time spent which allow one “to see events” exactly as the
in a particular pacing state such as AS-VP activity. device interprets them. Generally, the letter codes
AT/AF histograms can show the frequency of are AS (for atrial sensed events), AP (for atrial
high atrial rates and how the device responded. paced events), VS (for ventricular sensed events),
Follow-up After Pacemaker Implantation 235

Fig. 11.20 Interrogation of Contak Renewal CRT device – summary for case notes

and VP (for ventricular paced events) (Fig. 11.26). the programmed settings consistent with the
Intervals are stated numerically, often with hori- patient’s ECG recordings? (2) Does every pacing
zontal lines, to help identify where they belong. spike lead to capture and a depolarization? (3) Is
Where sensing problems are suspected, evidence the QRS normal or are there fusion beats? (4) Is
may be sought for crosstalk, myopotential inhibi- sensing appropriate, does sensing lead to inhibi-
tion, and retrograde VA conduction. tion of an output pulse, and does sensed atrial
At the end of the session, the technician should activity lead to sensed or paced ventricular activ-
be able to answer the following questions. (1) Are ity? (5) What is the patient’s underlying rhythm?
236 11 Follow-up After Pacemaker Implantation

Fig. 11.21 Interrogation of Contak Renewal CRT device – detailed summary of data printed from programmer

Fig. 11.22 “Therapy guide” page on the Medtronic programmer interrogating the Protecta CRT-D device (Image
reproduced with permission of Medtronic, Inc.)
Follow-up After Pacemaker Implantation 237

Fig. 11.23 Battery and lead data are available on a separate page on the Medtronic programmer when interrogating the
Protecta CRT-D device (Image reproduced with permission of Medtronic, Inc.)

Fig. 11.24 Ventricular arrhythmia detection settings for this Protecta CRT-D device are shown on this page (Image
reproduced with permission of Medtronic, Inc.)
238 11 Follow-up After Pacemaker Implantation

Fig. 11.25 The “ventricular therapies” program for this Protecta CRT-D device is shown on this page (Image repro-
duced with permission of Medtronic, Inc.)

Fig. 11.26 Pacemaker interrogation of a possible rhythm (top), the atrial electrogram (middle), and the ventricular
disturbance. Interpretation is aided by the ECG in Lead II electrogram (bottom), as well as the annotations AS and VS

(6) Would the patient benefit from having particu- lems that may require troubleshooting (e.g., sen-
lar features turned on, for example hysteresis, AF sor-driven rates that seem inappropriate for that
suppression, or sleep rate function? (7) Are the individual’s activity, much high-rate atrial activity
diagnostic data consistent with the programmed with fast ventricular response)?
settings and is there anything unusual in the Besides the device’s diagnostics, other investi-
diagnostics? (8) Are the programmed algorithms gations can be of use during follow-up in order to
functioning appropriately? (9) Are there any sug- try and identify suspected problems or optimize
gestions from the diagnostics of possible prob- function.
Frequency and Timing of Follow-up 239

Fig. 11.27 Holter ECG


monitoring confirms that this
patient’s palpitations are due
to pacemaker-mediated
tachycardia

Fig. 11.28 Checking the


pacemaker wound for
evidence of infection is an
important advantage of
“in-person” follow-up

Holter monitoring and treadmill exercise Frequency and Timing of Follow-up


testing may be useful for assessing exercise toler-
ance, chronotropic competence, exercise-induced The first follow-up appointment after pace-
arrhythmias/pacemaker-mediated tachycardia, and maker implantation should be at approximately
maximal heart rate achievable – paced or unpaced 4–6 weeks unless some specific concern
(Fig. 11.27). Although Holter monitoring may be demands an earlier review. Examination of the
arranged on the same clinic day, exercise testing is pacemaker wound is important at this stage
often best arranged on a separate occasion. (Fig. 11.28), and antibiotics should be given for
After interrogation is complete and the data saved any superficial wound infection. Pacing thresh-
and printed, the diagnostic counters should be old should be assessed and the pacemaker out-
cleared so that new follow-up data can be collected. put programmed to at least twice the stimulation
240 11 Follow-up After Pacemaker Implantation

threshold or three times pulse width. If there is Table 11.4 Factors determining frequency and type of
any suggestion of pacing or sensing loss, a chest follow-up after device implantation
X-ray should be performed to check the Patient factors
electrode(s) position. Lead impedance should Cardiovascular symptom stability
be checked. If all is well, a further appointment Rhythm stability
at 6 months should be arranged and then annu- Patient, family or physician issues, e.g., patient
distance from F/U clinic, medical/social issues
ally until any reduction in battery life appears
High/unstable pacing thresholds
when 1–3 monthly checks should then be rein-
Change in antiarrhythmic drug or heart failure
stituted. If at anytime lead, generator, or wound treatment
concerns occur, follow-up can be adjusted Frequency of ICD therapies
accordingly. Device factors
Manufacturers recommend follow-up for Reliability of the device and lead(s)
ICDs and CRT devices at 3–6 monthly intervals, Programmed parameters that are switched “on” and
and those patients with frequent arrhythmic epi- that influence battery life, e.g., frequency of shock
therapy, pacing frequency, pacing threshold
sodes, shocks, and/or heart failure may need to be
Age of device
seen more frequently.
Complexity of device
The frequency of follow-up depends on a
Drugs that may influence pacing or defibrillation
number of patient-related, device-related, and threshold
disease-related factors. These are shown in Arrhythmia/heart failure diagnostics, e.g., patient
Table 11.4. Troubleshooting in the event of car- activity, transthoracic impedance
diac-sounding symptoms or possible pacemaker Disease factors
malfunction will require experience and exper- Frequency and severity of symptoms, e.g., recurrent
tise from technicians and cardiologists. dizziness/syncope/palpitations
Troubleshooting is discussed in Chap. 21. Changes in cardiovascular therapy, e.g., b-blockade,
flecainide
Diagnosis of other serious/life-threatening conditions,
e.g., terminal cancer, stroke

Pacemaker Reprogramming
to Preserve Battery Life sensing circuits and rate adaptation if not
required will also help. Anything that reduces
A pacemaker that is programmable for rate, the % pacing will help prolong battery life.
pulse width, and output may have its battery
life prolonged by reducing these parameters
after confirming low pacing thresholds
3–4 months after implantation to allow estab- Pacemaker Alerts/Recall
lishment of the chronic threshold. If a pace-
maker with hysteresis mode is available, the Pacemaker manufacturers occasionally report that
takeover rate may be set lower than the basic a fault has been reported in one of its pacemakers
pacing rate in order to conserve battery life. or leads and that close monitoring of patients pos-
Turning off unused sophisticated monitoring/ sessing the particular model (Fig. 11.29) is nec-
Pacemaker Alerts/Recall 241

Fig. 11.29 Urgent medical


device information from
manufacturer

essary. The MHRA also send out device alerts to are not dependent, consideration of the benefits
pacing centers (Figs. 11.30 – 11.32) with infor- and risks involved in a replacement procedure
mation about which device(s) is being referred is important especially in the elderly and infirm.
to, what the problem is, what action needs to be Each center should be able to identify a list of the
taken, and the frequency of follow-up required relevant patients using its own database. The lat-
for monitoring. The failure rate is usually very ter can also be used by the center’s cardiologists
low and only if potentially serious is it recom- to assess any suspected trend in pacemaker fail-
mended that generators should be recalled and ures ahead of any alert or recall. Each advisory
replaced. For patients who are pacemaker-depen- or recall should be managed separately and an
dent, replacement is essential, but for those who action plan developed by each implanting center.
242 11 Follow-up After Pacemaker Implantation

Fig. 11.31 Medical device alert from MHRA indicates


the relevant device, the problem, and the action advised
Fig. 11.30 Medical device alert from MHRA

Battery Depletion/End-of-Life change to simpler pacing mode, for example,


Parameters DDDR to VVI, VVIR to VVI or VOO to
reduce battery current drain may be an ERI or
In the past, pacemakers were tested for battery EOL. Specific values of EOL and ERI vary
depletion by applying a magnet over the pace- between manufacturers.
maker. A reduction in the fixed pacing rate to Most pacemakers can now be extensively
the “end-of-life” (EOL) parameters set by the interrogated by telemetry using a handheld pro-
manufacturer (usually 5–10% of the implant grammer. Large reductions in battery voltage and
or beginning-of-life (BOL) rate) – measured increase in its internal resistance are indicators of
precisely by the handheld device – was the battery depletion. Recommended elective replace-
indicator to plan elective generator replace- ment time (ERT) indicates that elective replace-
ment. The free-running rate may also decrease ment should be organized over the next 3 months
according to design. Increase in pulse width or so. The EOL parameters indicate that genera-
duration in some pacemakers to compensate tor replacement should be performed without
for a lower voltage output may be an elective delay. In some systems, a pacemaker battery
replacement indicator (ERI). Some devices energy gauge can be displayed on interrogation.
Home Monitoring 243

Fig. 11.32 Medical device alert from MHRA regarding ICD

Older style remote monitoring of pacemakers


Home Monitoring used transtelephonic monitoring using modem
technology. These devices transmitted the patient’s
In addition to programmer-based interrogations in heart rhythm recording by converting the ECG
a hospital-based follow-up clinic, device follow- information into sound and sending it over the
up has been expanded with a system of remote telephone line to a decoding machine which
interrogation tools. These home monitors/com- changed the sound back into the “rhythm strip” at
municators employ telephone-based links to the other end. Heart rate, rhythm and battery sta-
extend the bidirectional telemetry links into the tus, and, to some degree, sensing and capture
patient’s home or with cellular technology unre- function can be obtained. A typical protocol to be
stricted by landlines. Remote transmissions may followed by technical staff doing transtelephonic
be completed by connecting the transmitter to any device monitoring is shown in Table 11.5.
form of telecommunication network (wired or Such remote monitoring technology reduces
wireless). These bedside or handheld communi- the need for some face-to-face clinic visits and
cation devices employ either a wand with short may facilitate, when needed, visits triggered by a
distance radiofrequency communication with the clinical event. In addition, remote monitoring and
programmer or by the long distance ISM or MICS the storing of monitoring data may facilitate the
band radiofrequency telemetry described earlier detection of device system performance issues
in Chap. 9. This home monitor/communicator is and clinical conditions that may lead to the need
then linked by telephone to a central (Internet for increased frequency of in-person or remote
based) data repository where the data are stored surveillance. However, although technically fea-
and analyzed and disseminated electronically. sible and probably reliable, remote reprogram-
244 11 Follow-up After Pacemaker Implantation

Table 11.5 Procedure protocol for technician doing the change in the device’s parameters after
transtelephonic follow-up reprogramming.
Single-chamber/single-chamber-rate-adaptive The TRUST clinical study demonstrated the
pacemakers safety and effectiveness of remote monitoring
Verify pacemaker performing according to pro- and that it reduced 43% of in-office follow-ups
grammed parameters
without any impacts on patients’ safety [1]. The
Determine the underlying rhythm – if possible
Review of programmed parameters
HRS/EHRA expert consensus on the monitoring
Mode of cardiovascular implantable electronic devices
Ratea recommends in-person follow-ups after implan-
Pulse width tation and annual follow-ups. However, during
Hysteresis (off/on) the maintenance phase of follow-ups and when
Pacing polarity configuration the patient’s medical condition is stable and no
BOL/EOL characteristics anticipated device programming is required, fol-
ECG analysis: single-chamber pacemaker low-ups could be accomplished remotely.
Verify pacemaker performing according to pro- Home monitoring is now available in the UK
grammed parameters from most of the device companies using wireless
Verify pacing spikes are present
or telephone technology and can help to reduce pac-
Verify 1:1 capture is present
ing clinic visits – especially desirable for those
Check intrinsic activity sensed appropriately
patients living remotely from the pacing clinic or
Oversensing
with poor transport links. It has been more widely
Undersensing
Verify normal/abnormal function of the pacemaker
used in the USA for several years. Transtelephonic
Monitor technician provide technical comment pacemaker data collection has been available for
Dual-chamber/ dual-chamber-rate-responsive pacemakers many years and can provide information with
Verify pacemaker performing according to pro- respect to battery status, pacing threshold, lead
grammed parameters impedance, parameters, and diagnostic data. Intra-
Determine the underlying rhythm cardiac electrograms showing events and mode
Review of programmed parameters switching data showing AF can also be transmitted,
Mode but lead testing cannot be performed via this tech-
Rate (Lower programmed rate – maximum tracking)b nology. Patients with symptoms or changes in clini-
Pulse width cal status and those requiring reprogramming and
Hysteresis (off/on)
optimization need to be seen in pacing clinic.
Pacing polarity configuration
Medtronic’s CareLink® service was launched
BOL/EOL characteristics
in Europe in 2007 and is available in 14 European
Automatic mode switch – (off/on)
countries with a few thousand patients on active
ECG analysis: dual-chamber pacemaker
Verify pacemaker performing according to pro-
follow-up. In the USA, CareLink® is well estab-
grammed parameters lished with over 150,000 patients being followed-
Check if atrial and/or ventricular spikes present up remotely (Figs. 6.38, 11.33 and 11.34). The
Verify 1:1 capture is present Medtronic CareLink® Network with Conexus™
Check intrinsic activity is sensed appropriately Wireless Telemetry offers automatic data trans-
Oversensing missions and customizable alert notifications.
Undersensing With wireless device interrogation, routine follow-
a
Check lower programmed rate and maximum sensor rate ups occur automatically while the patient sleeps,
in rate-responsive pacemakers alleviating patient compliance issues (Fig. 11.35).
b
Maximum sensor rates in rate responsive systems
Using the Medtronic CareLink® Clinician web-
site, clinic staff can preschedule up to six auto-
ming of devices is not currently permitted – mainly matic device checks for each patient, minimizing
due to the limited ability to respond to potential time spent rescheduling missed appointments and
changes in the patient’s condition as a result of the difficulties contacting patients by phone. The
Home Monitoring 245

patient’s implanted device can be programmed


to notify clinicians of programmed alerts. If the
device detects a potential problem, such as atrial
fibrillation or a lead integrity issue, it initiates a
data transmission and a Medtronic CareAlert®
notification via pager and/or voicemail/e-mail.
Physicians have flexibility and control in program-
ming both wireless and audible device alerts and
notification methods. Conexus™ Telemetry uses
the Medical Implant Communications Service
(MICS), a radio frequency band designated for
implantable medical devices. The MICS band
protects Medtronic’s wireless transmissions from
interference caused by cell phones or other com-
Fig. 11.33 Medtronic CareLink® monitor for home
mon electronic devices.
monitoring

Fig. 11.34 Inside the device


is the mains plug, the
telephone socket connection
and the “wand” which must be
placed over the implanted
device

Fig. 11.35 The Medtronic CareLink® Network with Conexus™ Wireless Telemetry offers automatic data transmis-
sions while the patient sleeps (Image reproduced with permission of Medtronic, Inc.)
246 11 Follow-up After Pacemaker Implantation

Fig. 11.36 Biotronik’s


CardioMessenger I offers a
bedside (CardioMessenger S)
and a portable version
(CardioMessenger I) for
home monitoring of devices
(Image reproduced with
permission of Biotronik)

Biotronik’s CardioMessenger was first used in


2001, and there are >60,000 Biotronik devices with
home-monitoring implanted worldwide (>50% in
the USA). The implant – pacemaker, CRT, or ICD
– transmits diagnostic, therapeutic, and technical
data to an exterior device, the CardioMessenger,
using an integrated antenna. The patient is not
required to do anything. The CardioMessenger II is
compatible with all Lumax ICD and CRT devices,
whereas the CardioMessenger I serves all other
implants. The CardioMessenger S is a bedside ver-
sion of the more portable CardioMessenger I
(Fig. 11.36). The CardioMessenger forwards the
data to the Home Monitoring Service Center via Fig. 11.37 CardioMessenger II® is also available as a
the cellular phone network. The Service Center bedside monitor (CardioMessenger II®S) and a portable
analyzes the data and edits a CardioReport. The device, CardioMessenger II® (Image reproduced with per-
mission of Biotronik)
information flow is entirely automated. The cardi-
ologist can evaluate the patient’s data at any time
using a secured website. Upon request, one can
receive customized additional information per fax,
e-mail, or SMS when selected events occur.
There are two versions of CardioMessenger
II® (Figs. 11.37). The portable CardioMessenger
II® offers patients unwavering assurance along
with complete mobility (Fig. 11.38). Its small
size, integrated Quad-band modem, and multi-
voltage transformer make it ideal for unrestricted
traveling in more than 50 countries. The
convenient belt clip and carrier strap along with
lithium ion batteries that last up to 72 h provide
increased freedom and mobility (Fig. 11.39).
With only one button and a simple LED icon dis-
play, the CardioMessenger II® is today’s small- Fig. 11.38 The CardioMessenger II® is the more porta-
ble version (Image reproduced with permission of
est, most advanced, remote monitoring system Biotronik)
available. All CardioMessenger II® devices also
contain a unique call-back function. It allows
physicians to request a patient call-back through ity of life. The CardioMessenger II®S is a
a flashing LED on the CardioMessenger, result- simplified bedside version of the CardioMessenger
ing in less patient disturbance and increased qual- II®, suitable for those patients requiring less
Home Monitoring 247

Fig. 11.40 Boston Scientific’s LATITUDE® home mon-


itoring device

CRT-D and ICD devices. It consists of a wireless


communicator that automatically collects infor-
mation from the implanted device at predeter-
mined times without any patient involvement
(Fig. 11.40). The LATITUDE® Communicator
then transmits the information via the phone line
(plugs into a standard phone jack and power out-
let) to a secure server that can be accessed by the
pacing clinic technicians or cardiologist via the
LATITUDE® website with a username and pass-
word. A “wanded Communicator” is also avail-
able but the patient must actively participate in the
data collection process. At scheduled times, a light
on the Communicator prompts the patient via the
Active Button to place the wand over their
implanted device. The Communicator will then
walk the patient through the appropriate steps that
are necessary to send the device data to the cardiac
center. Remote transmissions usually include
scheduled remote device follow-ups, where the
Fig. 11.39 The CardioMessenger II® can be clipped on a Communicator collects information similar to that
waist belt (Image reproduced with permission of Biotronik) of a hospital-based device-check (without per-
forming any threshold testing) including a real-
mobility (see Fig. 11.37). It has all the features of time electrogram. In addition, LATITUDE® can
the portable CardioMessenger II® and can also be monitor for any alerts both during and between
used when traveling worldwide. Like the follow-ups, for example, if the battery power of
CardioMessenger II® it is compatible with all the device reaches ERI status. It also allows
Lumax ICDs and CRTs and with all future patients to send device data other than during
implantable cardiac devices. scheduled follow-up or remote monitoring check.
Guidant/Boston Scientific’s LATITUDE® Patients receiving the Cognis® CRT-D device can
home-monitoring system has only recently have changes in their weight and blood pressure
become available in Europe, but >20,000 devices at home monitored using specific, dedicated
are under active follow-up in the USA. This device weighing scales and sphygmomanometer which
remotely collects data from Boston-Scientific’s communicate with the LATITUDE® home
248 11 Follow-up After Pacemaker Implantation

Management System has just been released in


Europe for use with Boston Scientific’s advanced
INGENIO™ and ADVANTIO™ pacemakers
and the INVIVE™ CRT-P device.
St. Jude Medical’s Merlin@home™ trans-
mitter allows patients to have their device
checked and monitored remotely at home (see
Fig. 1.86). The data are uploaded to Merlin.
net™ PCN a safe and secure web-based man-
agement system which can be accessed by the
technicians and cardiologist at the cardiac center
using a username and password. Connected to a
Fig. 11.41 Dedicated weighing scales and blood pres- telephone line, the device can monitor, down-
sure monitor for home monitoring of heart failure in load, and transmit the device’s data while the
patients with the Cognis® CRT-D device and the
LATITUDE® home monitoring device (Boston Scientific)
patient is asleep.

monitoring system using Bluetooth technology


(Fig. 11.41). The website www.aboutlatitude.com
Reference
provides useful information for patients and their 1. Varma N, et al. Evaluation of efficacy and safety of
families with links to technical support represen- remote monitoring for ICD follow-up: the TRUST
tatives. The LATITUDE™ NXT Remote Patient trial. Circulation. 2008;118:2316, A4078.
Complications of Pacemaker
Implantation 12

Complications associated with pacemaker implan- cavity and when positioning the electrode in the
tation are generally uncommon when temporary RV apex. They settle spontaneously and do not
and permanent pacing are performed by experi- require treatment. Sustained ventricular tachy-
enced personnel. cardia and ventricular fibrillation are unusual
Complications can be divided into early occurrences (Fig. 12.2) but may be more likely in
(intra-, peri-, or postoperative) (<30 days) and a clinical setting of myocardial infarction. DC
late (>30 days) complications (Table 12.1). Early cardioversion may be necessary, especially if
complications mainly consist of procedural com- hemodynamic compromise occurs.
plications occurring as a result of lead insertion Complete heart block and asystole may
and lead positioning which are similar for tempo- also occur during electrode insertion. Quick
rary and permanent pacing procedures. Late positioning of the pacing electrode and prompt
complications, occurring after hospital discharge, pacing is the ideal treatment but a precordial
are obviously only relevant to permanent pace- thump, cardiac massage, IV atropine or isopre-
maker implant procedures. naline, emergency transthoracic pacing, and
full cardiopulmonary resuscitation may be
required.
Early Complications
Table 12.1 Acute complications of pacemaker electrode
Arrhythmias insertion
Arrhythmias Atrial/ventricular
Atrial ectopic beats, atrial tachycardia, flutter or tachyarrhythmias
fibrillation may be produced by maneuvering the A-V block
Pneumothorax/hemothorax
electrode in the right atrium en route to the RV.
Myocardial perforation/
These arrhythmias usually settle/revert spontane- SVC perforation
ously, although atrial flutter/fibrillation may take Infection
several hours or more (Fig. 12.1). If AF fails to revert Hemorrhage
spontaneously, the arrhythmia can be addressed and Air embolus
treated by DC cardioversion. If AF develops after a Thrombophlebitis/venous
dual chamber implant, the pacemaker may be repro- thrombosis
grammed to a VVI or VVIR mode until sinus rhythm Brachial plexus injury
is restored, when DDD pacing can be reinstituted Thoracic duct injury
using the external programmer. Failure to pace Lead displacement
Ventricular ectopic beats and even couplets Lead disconnect
and triplets invariably occur on entering the RV Failure to sense

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 249


DOI 10.1007/978-1-4471-2939-4_12, © Springer-Verlag London 2012
250 12 Complications of Pacemaker Implantation

Fig. 12.1 Atrial fibrillation may occur during lead manipulation within the right atrium

Fig. 12.2 Ventricular tachycardia/ventricular fibrillation is an uncommon occurrence during pacemaker lead position-
ing and as shown above requires immediate DC cardioversion

Pneumothorax

The apical pleura may be punctured during sub-


clavian vein puncture prior to sheath/electrode
insertion (Figs. 12.3–12.5). Aspiration of air
indicates when this has happened, and a post-
procedure chest X-ray is essential. Pneumothorax
can be obvious and large (Figs. 12.6 and 12.7) or
localized if pleural adhesions happen to be pres-
ent. Percutaneous drainage using an underwater
seal drainage system is necessary if >50% of
the thoracic cavity is air-filled or if breathless-
ness or signs of tension pneumothorax develop.
Otherwise, a watchful, conservative approach Fig. 12.3 Left apical pneumothorax is visible (arrow)
after device implantation
with daily chest X-rays might suffice (Figs. 12.8
and 12.9).

rary pacing electrodes which are relatively stiff


Myocardial Perforation devices. Positioning a permanent pacing electrode
with the shaping stylette still in situ also makes it
Perforation of the RV myocardium may occur stiffer and increases the chance of perforation.
during manipulation and positioning of tempo- Screwing-in an active-fixation lead at the RV
Early Complications 251

Fig. 12.4 Underwater sealed chest drain (arrow) is


inserted
Fig. 12.6 Large pneumothorax (arrows) requires inser-
tion of chest drain

Fig. 12.5 Pneumothorax diminishing 12 h after chest


drain insertion (arrow)

apex can also result in myocardial perforation


(Fig. 12.10). Elderly patients with a thin RV Fig. 12.7 Reduction in size of pneumothorax (black
arrow) after chest drain inserted (green arrow)
muscle wall are particularly at risk (Figs. 12.11
and 12.12). Sharp chest pain during the insertion,
evidence of cardiac tamponade with breathless- requires emergency pericardiocentesis and pos-
ness, raised jugular venous pressure, falling sys- sibly cardiac surgical repair. Echocardiography
temic blood pressure, and cyanosis are likely should confirm hemopericardium (Fig. 12.13)
sequelae and suggest hemopericardium that and may even show the electrode tip in the
252 12 Complications of Pacemaker Implantation

Fig. 12.10 Transthoracic echocardiogram (subcostal


view) shows the helical coil tip (red arrow) of this active-
fixation lead protruding through the apex of the right ven-
tricle (RV). The green arrow shows the lead within the RV
cavity, and the yellow arrows the anterior, apical, and
septal portions of the RV. RV right ventricular free wall
Fig. 12.8 A smaller pneumothorax may be localized to
the apex (green arrow)

Fig. 12.11 Frail elderly patients may have extremely


thin RV myocardium and RV perforation is not difficult,
especially when positioning the lead with the stiffening
stylet in position. RV lead is shown in situ with tip close
to perforation point

Fig. 12.9 Blood or serosanguinous fluid may result in


opacification if the air is replaced with fluid (arrow) A less common cause of myocardial perforation
may occur during explant/implant procedures.
Actively fixed electrodes – especially attached to
the right atrial free wall – may be impossible to
pericardial space (see Fig. 12.10). Other signs of remove by manual traction and persistence and
perforation may be loss of pacing or symptoms additional force may result in myocardial avulsion
and signs of pericarditis – including a pericardial (Fig. 12.14) and rapid demise as a result of sud-
friction rub. den hemopericardium. This was more a concern
Early Complications 253

Fig. 12.12 Histology in this case shows a perforation track Fig. 12.14 Some active fixation leads are firmly fixed to
into the epicardial fat and an atrophic RV myocardium. It the myocardium and forceful traction may result in myo-
was not clear whether this had been caused by the emer- cardial avulsion and fatal, sudden hemopericardium unless
gency TPM (removed) which had been placed during the surgical drainage and repair is not urgently performed
resuscitation of this elderly lady brought in unconscious in
complete heart block and a ventricular rate of 10 per min
unlikely to solve the problem and surgical inter-
vention is likely to be required. If the guidewire
is still in situ, an attempt can be made to close
such a perforation with the Angioseal™ device
or similar percutaneous closure device. Early
recognition and immediate vascular repair is
paramount.
Venous oozing from the insertion site of a
temporary electrode is more likely to occur if the
central venous pressure is raised, for example, in
patients with heart failure or if the patient is anti-
coagulated. Generally the subclavian route should
be avoided if the patient is anticoagulated with
heparin or coumarin anticoagulants and the
cephalic vein used instead.
After permanent pacemaker implantation,
Fig. 12.13 Echocardiography should confirm hemoperi-
continued bleeding into the pacemaker pocket is
cardium (arrow) and be helpful in determining the success
of pericardiocentesis usually as a result of a missed bleeding arteriole
or vein within the pocket. Hematoma formation
with the old “helifix” leads than the more modern usually occurs within the first few hours and if
“screw-in” electrodes. large/tense or if associated with pain requires
drainage by opening the pocket under sterile con-
ditions in theater without delay (Fig. 12.15).
Hemorrhage Anticoagulant therapy should be stopped prior
to pacemaker implantation and the INR normal-
Serious bleeding only occurs if the subclavian ized with vitamin K or fresh frozen plasma if
artery is punctured. Swift removal of the needle necessary. Wherever possible, aspirin and clopi-
will often solve the problem. However, if the dogrel should be stopped for 1 week before in an
operator is unaware of the inadvertent arterial attempt to minimize hematoma formation which
puncture and the introducer sheath is pushed may increase the incidence of later pocket
into the artery, simply removing the sheath is infection.
254 12 Complications of Pacemaker Implantation

Fig. 12.15 Small hematoma


as a result of venous oozing
within pacemaker pocket

Hemothorax

Hemothorax may occur if the needle is inserted


through both walls of either the subclavian artery
or vein (Fig. 12.16) and especially if the intro-
ducer sheath is also pushed into the subclavian
artery and then withdrawn. A widening mediasti-
nal shadow, a new ipsilateral pleural effusion, or
total opacification of the ipsilateral thorax on the
chest X-ray might follow serious bleeding fol-
lowing subclavian artery puncture and suggests
hemothorax. A fall in hemoglobin and typical
signs on examination of the chest would support
this serious complication that demands urgent
surgical referral.
Fig. 12.16 Hemothorax is a serious complication –
usually caused by perforation of the subclavian artery.
Left-sided hemothorax is shown
Air Embolism

Air embolism is rare but may occur if the needle and when removing the vessel dilator
patient is in a head-up position and/or hypov- prior to introducing the lead.
olemic with either the needle or the introducer
sheath in the SCV without the syringe attached
or the guidewire in place. In this situation, it is Brachial Plexus Injury
more likely to occur on inspiration. It can be
avoided by having the patient in a head-down This is rare and due to the needle puncture being too
position when detaching the syringe from the posterior. Symptoms usually resolve spontaneously
Early Complications 255

Fig. 12.17 PA chest X-ray showing normal “J-shape”


position of the atrial lead (arrow)

Fig. 12.18 Lateral chest X-ray showing normal “J-shape”


after a few weeks. Rarely, infraclavicular lignocaine and anterior pointing position of the atrial lead at implan-
can cause temporary plexus nerve paralysis. tation (arrow)

Thoracic Duct Injury

This is rare. The main thoracic duct drains into


the junction of the left subclavian and left inter-
nal jugular veins. Milky aspirate should give a
clue to the needle misplacement. Conservative
treatment is usually the correct management.

Lead Displacement

Displacement of a passively fixed atrial lead is a


not infrequent occurrence. It results in failure to
sense and pace the atrium and is confirmed by a
PA/lateral chest X-ray. It is unusual with actively
fixed atrial leads which are now more commonly
used in order to reduce the problem. However, it Fig. 12.19 PA chest X-ray showing the atrial lead to
have lost its “J-shape” and to be hanging down vertically
may still occur even after using a “screw-in” lead (arrow) into the right ventricle
(Figs. 12.17–12.20).
Displacement of a ventricular lead is less
common and indeed rare when using active- of the atrial lead. In pacemaker-dependent indi-
fixation or “tined” passively fixed leads but it viduals, this may result in ventricular stand-
is potentially more serious than displacement still or severe bradycardia if there is no or only
256 12 Complications of Pacemaker Implantation

Fig. 12.21 Chest X-ray shows normal position of ven-


tricular lead in the apex of the RV

Fig. 12.20 Lateral chest X-ray showing that the atrial


lead has become displaced and fallen into the RV close to
the tip of the RV lead (arrow). The ECG shows loss of
atrial capture

an extremely slow ventricular escape rhythm.


Microdisplacement results in a rising pacing
threshold, failure to sense and intermittent cap-
ture, or complete failure to pace. A PA and lateral
chest X-ray should be obtained post-implantation
whenever lead displacement is suspected and Fig. 12.22 Chest X-ray shows that the reason for loss of
repositioning of the lead should be done imme- ventricular capture and syncope after pacemaker implan-
tation is displacement of the RV lead back into the right
diately using fluoroscopy under sterile conditions atrium (arrow)
(Figs. 12.21–12.23). Although leads fixed in the
RV outflow tract are probably no more prone to Connection Failure
displacement than those fixed in the RV apex, lead
displacement can occur (Figs. 12.24–12.26). Connections between a temporary pacemaker
Figures 12.27 and 12.28 show both atrial and box and temporary lead should be checked regu-
ventricular lead displacement in a patient with three larly since disconnection could result in cata-
leads as part of cardiac resynchronization therapy. strophic loss of pacing and cardiac output.
Early Complications 257

Fig. 12.23 Chest X-ray shows restoration of the correct Fig. 12.25 Within 24 h, the patient’s ECG showed loss
RV apex position of the ventricular lead of capture and the chest X-ray showed displacement of the
RV lead into the RV outflow tract

Fig. 12.24 Chest X-ray in a patient with a dual chamber Fig. 12.26 Chest X-ray after repeat active fixation of the
pacemaker with the RV lead actively fixed into the inter- RV lead into the interventricular septum
ventricular septum rather than the RV apex

Infection

Inadvertent failure to secure the head screws Pacing should be performed under sterile
between the permanent pacemaker and its perma- operating theater conditions with full aseptic
nent leads may result in intermittent or total fail- technique. Pyrexia, local inflammation, and dis-
ure to pace and will require the pacemaker wound charge of pus from a temporary electrode inser-
to be reopened (Fig. 12.29). tion site suggest infection which is commonly
258 12 Complications of Pacemaker Implantation

Fig. 12.27 The more leads that are inserted, the greater Fig. 12.28 However, within 12 h, both the atrial (black
the incidence of displacement! This patient underwent arrow) and ventricular leads (green arrow) had displaced –
cardiac resynchronization therapy requiring repositioning

Fig. 12.29 Failure to


secure the connector pin
with the screw in the header
unit will lead to sudden loss
of capture. X-ray of dual
chamber ICD in a patient
with intermittently high lead
impedance. Note the distal
pin of the ventricular IS-1
connector (arrow). Unlike
the atrial connector which is
seen immediately above, the
pin is not wholly engaged
within the female connector
in the header. This led to an
intermittent break in the
pacing circuit causing high
pacing impedances and
intermittent loss of capture
Early Complications 259

Fig. 12.30 Staphylococcus


aureus is usually responsible
for early pacemaker
infections. Agar plates
showing golden colonies of
Staphylococcus aureus (left)
and the white colonies of
Staphylococcus epidermidis
(right)

due to Staphylococcus aureus or Staphylococcus


epidermidis. It is best to remove the infected elec-
trode and proceed to permanent pacing as soon as
possible – if indicated – in order to avoid this
complication which can lead to septicemia. When
the temporary pacemaker is required to be left in
situ for >2 days, for example in acute MI, the
insertion site should be washed daily with chlor-
hexidine or povidone iodine solution and then
covered with a sterile, transparent dressing. When
infection is obvious or confirmed, the electrode
should be removed after inserting a new electrode
Fig. 12.31 Redness, pain, swelling, and tenderness of
via a different route. Blood cultures should be the pacemaker pocket are the usual signs of serious
taken and antibiotics administered intravenously. Staphylococcus aureus infection. Although antibiotics
Infection of a permanent pacemaker site diminish the signs of inflammation, chronic exudates/dis-
may occur in <1% of cases. Again the respon- charge from the wound forms a crust covering the wound
sible organism is nearly always staphylococcus
(Fig. 12.30). Superficial infection of the wound However, it should be avoided in patients with
edges can usually be promptly treated with anti- bacteremia and in younger/fitter individuals who
biotics. Pocket infection, however, will require will require a new pacing system, since persistent
lead and generator extraction, wound drainage bacteremia, tricuspid endocarditis, and infection
and prolonged systemic, anti-staphylococcal of the new system is likely to follow. Extraction
antibiotics (Figs. 12.31–12.33). Lead extraction procedures are discussed in Chap. 19.
may be not too difficult early after implantation,
although screw-in leads have to be unscrewed
from the myocardium before applying traction to Subclavian Vein Thrombosis/
the lead(s). Removal late after implantation can Thrombophlebitis
be very difficult and requires the use of a lock-
ing stylet, laser extraction, and even thoracotomy. This is an unusual occurrence with the relatively
Cutting the lead short, capping the proximal end, low profile temporary pacing leads used today. It
and suturing it away from the infected area some- is more likely if a temporary lead is left in situ for
times has to be the treatment of choice in patients >1 week or if it becomes infected.
who are unlikely to tolerate an explant/implant This complication is rare after permanent pac-
procedure or thoracotomy and especially if life ing, but is more common when redundant leads
expectancy is very limited for other reasons. are left in the same subclavian vein (perhaps
260 12 Complications of Pacemaker Implantation

Fig. 12.32 Opening the


wound releases bloody,
yellow pus

Fig. 12.33 Large globules


of pus (arrow) can be sent
for culture and antibiotic-
sensitivity testing. Leads and
generator have to be
removed

from an old pacing system that could not be and signs of phlebitis will disappear as recanali-
removed in entirety) (Fig. 12.34). It presents as zation of the thrombosed subclavian vein occurs
discomfort and swelling in the ipsilateral arm within the first 4–6 weeks.
and shoulder, often with distended veins in the In the rare event of persistent, progressive
upper arm and in the subclavicular and pectoral edema and pain in the arm, removal of the pacing
region and often an engorged external jugular leads and generator will be necessary and a new
vein (Figs. 12.35 and 12.36). Venography of the system will be required on the contralateral side.
axillary/subclavian vein will confirm the diagno-
sis and the exact site of occlusion (Figs. 12.37
and 12.38). Late Complications
Patients should be treated initially, at least, by
analgesia and anticoagulant therapy for Complications seen after hospital discharge are
3–6 months. Usually the swelling, discomfort, listed in Table 12.2.
Late Complications 261

Fig. 12.34 Multiple leads placed in the subclavian vein


(arrow) may lead to fibrosis and/or thrombosis and signs
of venous obstruction

Lead Displacement

Atrial and ventricular pacing leads may dislodge


from their implantation positions between dis-
charge and the first follow-up appointment. Loss
of atrial or ventricular pacing or sensing on the
ECG may be the first clue to a problem, although
a recurrence of dizziness/near syncope/syncope
may result from ventricular lead displacement if
the patient is pacemaker dependent. X-ray of the
chest in PA and lateral views should confirm the
diagnosis (see Figs. 12.21–12.23). Repositioning
of the leads will be necessary to restore the
function.
Twiddler’s syndrome can be a cause of early Fig. 12.35 Left subclavian vein thrombosis causes dis-
lead displacement. tended veins in the left pectoral region, left side of neck
(arrow) and left arm as well as discomfort and swelling of
the left arm

Failure to Sense

Most pacemakers will be programmed in a ectopic QRS complexes (Fig. 12.39). This may
demand mode, whereby the pacemaker senses be hazardous and risks causing ventricular
spontaneous atrial and ventricular activity and fibrillation, especially in patients with myocar-
only discharges a stimulus if a native beat has not dial infarction.
occurred within a pre-set period, which is pro- It may be solved by lowering the setting for
grammable. Failure to sense spontaneous activ- R-wave sensitivity, for example, from 5 to 2 mV,
ity due to microdisplacement or tissue growth thus making the pacemaker more sensitive. At
may result in pacemaker discharge on intrinsic or the 2 mV setting, the pacemaker will sense any
262 12 Complications of Pacemaker Implantation

Fig. 12.36 Distended veins


in the subclavicular/pectoral
region

Fig. 12.37 Venography of


the left axillary/left
subclavian vein identifies
subclavian/axillary vein
thrombosis (black arrow).
Distended collateral veins
are evident on venography
(white arrows)
Late Complications 263

Table 12.2 Late complications after pacemaker


implantation
Problem Consequence
Lead displacement Failure to sense, failure to pace,
diaphragmatic stimulation
Exit block Failure to pace
Inappropriate Intermittent failure to pace,
inhibition e.g., myopotential inhibition
Lead fracture Failure to pace
Insulation break Failure to sense/pace; muscle
twitching
Infection
Early Staphylococcus aureus
Late Staphylococcus epidermidis
Erosion Generator erosion
Lead erosion
Superior vena caval SVC obstruction syndrome
obstruction
Fig. 12.38 Long segment of thrombosis of the left sub-
Subclavian vein Pain, swelling of ipsilateral
clavian and axillary veins (between the black arrows).
thrombosis limb
Note the distended collateral veins which are visible clini-
cally as well as angiographically Premature generator Failure to pace
failure
Pacemaker syndrome Dyspnea, neck pulsation,
signal of 2 mV or more but not a signal of <2 mV. dizziness
At the 5 mV sensitivity setting, the pacemaker Twiddler’s syndrome Lead displacement/fracture
will sense signals of ³5 mV but not those <5 mV. “Rate-responsive” Inappropriate heart rate
system specific changes
Thus, lowering the sensitivity setting (e.g., complications
3–1.5 mV) makes the pacemaker more capable of Pacemaker-mediated Palpitations
sensing lower R-wave amplitudes, that is, 1.5 mV tachycardia
setting has a higher sensitivity than 3 mV.
Conversely, raising the sensitivity setting (e.g.,
from 1.5 to 4 mV) will make the pacemaker less If all these maneuvers fail, the lead will have to
sensitive – only sensing any signals of 4 mV or be replaced.
greater.

Inappropriate Pacemaker Inhibition


Exit Block
External inhibition of a demand pacemaker
Excessive tissue growth between the tip of the from myopotentials from the underlying
lead and the endocardium may increase the or nearby muscles or from electromagnetic
threshold to pace sufficiently causing pacing waves emitted from nearby electrical equip-
failure without lead displacement. The ECG ment can sometimes inhibit pacemaker output
will show pacing spikes but no following QRS (Fig. 12.41). The ECG will show absent pac-
complex (Fig. 12.40). This is an infrequent ing stimuli and usually the electrical poten-
problem now with modern leads with porous tials that are responsible for the inhibition.
electrodes and steroid-eluting tips. It is most It can be demonstrated by asking the patient
likely to occur during the first 3 weeks to to push their hands firmly together or push
3 months after implantation. Usually the prob- against a wall. Myopotential (EMG) inhibition
lem can be solved by reprogramming the pace- may cause syncope or severe dizziness in a
maker to an increased output and/or pulse width. pacemaker-dependent patient when using their
264 12 Complications of Pacemaker Implantation

Fig. 12.39 Failure to sense

Fig. 12.40 Failure to


capture

Fig. 12.41 Myopotentials (arrow) from upper chest wall tem – resulting in the onset of dizziness. Typical activities
muscles during arm exercises cause inhibition of pace- are shown in Figs. 12.43–12.45
maker output due to oversensing from this unipolar sys-

arms or upper body musculature such as pecto- ing or by reducing the pacemaker’s sensitivity.
ralis major muscle, which are situated close to Reprogramming the pacemaker to fixed rate
the pacemaker (Fig. 12.42). Cutting a hedge, mode (VOO) will also prevent inappropriate
hoeing the garden, carrying boxes, hanging out inhibition and in days gone by surrounding the
the washing, and even hugging a loved one are generator in an insulating boot will also make
examples of such movements (Figs. 12.43– the phenomenon unlikely to occur.
12.45)! It is most likely to occur in pacemak- False inhibition or oversensing may also occur
ers programmed to unipolar sensing and can be with spurious signals from lead fracture or be
abolished by reprogramming to bipolar sens- due to large T-wave voltage. Increasing the
Late Complications 265

Fig. 12.42 Large myopotentials (arrow) when using the left upper arm cause pacemaker inhibition of this unipolar
system, asystole and transient presyncope

pacemaker’s sensitivity setting (e.g., from 2 to


5 mV) should make the device less able to sense
such spurious signals while maintaining the abil-
ity to sense normally conducted or ectopic R
waves.

Muscle Stimulation/Twitching

This usually only occurs in unipolar pacing and


is due to the can being the anode, which leads to
stimulation of the underlying pectoral muscle.
Reprogramming to a bipolar mode (if possible)
or reducing output and/or pulse width might
help. Diaphragmatic stimulation may occur
when a thin RV overlies the diaphragm and
phrenic nerve stimulation when thin atrial mus-
cle separates it from the atrial electrode. Reducing
the output and/or pulse width might stop the
problem; otherwise, the lead will need to be Fig. 12.43 Adduction of the arms, e.g., during carrying
repositioned. heavy weights
266 12 Complications of Pacemaker Implantation

Fig. 12.44 Hoeing soil

Lead Fracture

Lead fracture is now rare with modern leads, but


may occur late after pacemaker or ICD implan-
tation. It often occurs at the point of entry of the Fig. 12.45 Hugging a loved one can result in near syn-
lead into the subclavian vein, at the site of liga- cope/syncope
ture fixation or at any point of excess angulation
of the lead (Figs. 12.46 and 12.47). It would in pacemaker “twiddlers.” Replacement of the
present as a recurrence of syncopal symptoms pacemaker system will be necessary.
in pacemaker-dependent patients and pacing Poor/loose fixation of the lead’s connector pin
stimuli will be absent on the ECG. Lead imped- into the pacemaker may present after hospital
ance will be very high (>1,000 Ω). X-ray of the discharge, similarly with loss of stimuli on the
lead in PA and lateral views may show a gap or ECG or a high pacing threshold and high lead
fracture in the lead. It may still be a problem impedance.
Late Complications 267

Fig. 12.46 The lead


insertion point is a vulnerable
site for lead fracture as in this
muscular weight lifter where
the leads lay between the left
clavicle and head of the left
first rib

Fig. 12.47 Subsequent lead


fracture (arrow)

Insulation Break leads may be more susceptible (Figs. 12.50 and


12.51). Insulation breaks will allow current leak-
This is often due to the insulation being cut age and may cause stimulation of nearby mus-
through by a tight fixation ligature applied to the cles, twitching, and early battery depletion. Lead
lead without using the protective plastic collar, impedance will be very low (<250 Ω). ECG
and it may be possible to see the defect on a chest should show pacing spikes but capture may or
X-ray (Figs. 12.48, and 12.49). Polyurethane may not be preserved.
268 12 Complications of Pacemaker Implantation

Fig. 12.48 Insulation breaks


on leads can result in local
muscle twitching, premature
battery depletion, and loss of
capture. Careful scrutiny of
the chest X-ray might suggest
the problem (arrow)

Fig. 12.49 Magnified view


of the site in question
confirms a section of lead
without its insulation (green
arrow). Loss of capture and
low lead impedance result

Fig. 12.50 Tight silk


sutures applied to the lead
directly rather than over the
protective collar can cut
through lead insulation
Late Complications 269

Infection procedures. Having to reopen the pocket because


of early lead displacement or hematoma forma-
Pacemaker pocket infection is a serious complica- tion increases the risk of infection.
tion which invariably necessitates removal of the Within the first month of implantation, the
whole system – generator and electrode(s), and commonest organism is Staphylococcus aureus.
implantation of a new pacing system. It is usually Patients will present unwell with a pyrexia and
due to poor aseptic technique, poor skin prepara- discomfort over the pacemaker pocket which
tion, and poor practical technique and prolonged may be tender and usually inflamed (Figs. 12.52
and 12.53). The wound may discharge exudate
or pus and this will usually be revealed when the
pocket is incised. Blood cultures and swab from
the wound should be collected and intravenous
antibiotics, usually IV flucloxacillin, should be
started prior to removal of the pacing system.
IV antibiotics alone, even over prolonged peri-
ods, will invariably not solve this problem but
may give rise to fungemia, which is difficult to
treat. Echocardiography should be performed
to exclude tricuspid valve (TV) endocarditis
(Fig. 12.54). Every effort should be made to
remove the leads from such patients as not infre-
quently the electrodes are infected with bacteria.
If TV endocarditis develops, a prolonged
course of antibiotics should be given after removal
of the infected system. Tricuspid regurgitation
Fig. 12.51 Magnified view showing fractured lead insu-
may develop and be demonstrated by echocar-
lation at site of “anchoring” silk suture diography (Fig. 12.55). Only if vegetations fail

Fig. 12.52 Swollen, inflamed area at site of


epicardial pacemaker implant suggests pocket
infection or even abscess formation in this case
270 12 Complications of Pacemaker Implantation

Fig. 12.53 Close-up view showing


the infected pacemaker pocket with
impending generator erosion

Fig. 12.54 Transthoracic echocar-


diogram showing large vegetation on
the tricuspid valve in this patient with
infective endocarditis as a result of an
infected pacing system

Fig. 12.55 Transthoracic echocar-


diogram showing severe tricuspid
regurgitation in this patient with
vegetations on the tricuspid valve as a
result of an infected pacing system
Late Complications 271

to resolve and appear to be increasing in size responsible for pacemaker pocket infection.
despite antibiotics should surgery be considered. This may present only as a swelling over the
Pulmonary abscesses should resolve with effec- generator, without much in the way of pain or
tive IV anti-staphylococcal agents (Fig. 12.56). signs of inflammation (Fig. 12.62). Blood cul-
If large vegetations are present on the lead(s) or tures should be checked and, if positive, IV anti-
on the TV, fungal infection should be considered biotics – perhaps Teicoplanin or flucloxacillin
and surgical removal of lead(s) should probably – should be commenced (Fig. 12.63) and plans
be preferred to removal via the subclavian vein made to remove the infected system.
(Fig. 12.57 and 12.58). Surgical removal of
the lead(s) may be required if traction or laser-
removal devices fail to free the leads from the Superior Vena Caval Obstruction
endocardium (Figs. 12.59–12.61).
Beyond 6 months after implantation, Multiple leads placed in the SVC can cause cica-
Staphylococcus epidermidis is more commonly tricial fibrosis where the leads are in contact with
the wall of the SVC. If blood flow is significantly
impaired past the obstruction, venous thrombosis
and SVC obstruction may occur. This will present
with fairly typical SVC obstruction syndrome
with engorged head and neck, suffused conjuncti-
vae, distended neck veins and prominent veins
over the upper chest (Fig. 12.64 and Fig. 12.36).
Venography of the SVC should clearly identify
the anatomical problem. Percutaneous balloon
angioplasty of the obstruction may relieve it and
the signs of SVC obstruction will disappear imme-
diately (Fig. 12.65). Anticoagulation with heparin
and then long-term warfarin should be given.
Alternatively, the pacing leads should be removed
Fig. 12.56 Chest X-ray showing a pulmonary abscess.
Note the fluid level (arrow) visible within the abscess due
and the system replaced by either an epicardial
to Staphylococcus aureus infection on the pacemaker, system or a pacing system with leads placed in the
pacing lead, and tricuspid valve RV via the IVC from the femoral vein. The gen-

Fig. 12.57 Open heart


surgery is sometimes
necessary to remove infected
pacemaker systems whose
leads are fixed to the wall of
the great veins, tricuspid
valve, right atrium, or right
ventricle
272 12 Complications of Pacemaker Implantation

Fig. 12.58 Atriotomy


showing infected tricuspid
valve with vegetations and
the pacing leads that are
about to be removed

Fig. 12.59 Infected


pacemaker and leads
removed at open heart
surgery

erator is then buried in the lower abdomen region suggest that diagnosis and anticoagulant
(Fig. 12.66). therapy should be commenced (see Fig. 12.35).

Subclavian Vein Thrombosis Pacemaker Lead or Generator Erosion

Clinical evidence of this is uncommon but This is less of a problem than it used to be
would present as a swollen arm that feels heavy with higher-profile leads and the older, larger
and tight or painful. Distended veins on the generators. Emaciated patients are most at
upper arm, chest in the sub/supra-clavicular risk (Fig. 12.67). Both lead and generator
Late Complications 273

Pacemaker Generator Failure

Unexpected recurrence of symptoms of dizziness


or syncope may be due to unexpected pacemaker
failure and loss of output (Fig. 12.72). This is
rare with modern lithium iodine batteries and
with regular follow-up of patients in a pacemaker
clinic. Regular checks on battery life in the clinic
enable safe planning for elective generator
replacement. However, for those patients who
fail to attend follow-up pacemaker checks, they
are at risk of sudden loss of pacing if the battery
reaches end-of-life (EOL) (Fig. 12.73).
Unexpected component failure is very rare. In
the event of such an occurrence anywhere in the
world, the pacemaker manufacturer will investi-
gate the case as an emergency, and if component
failure is thought to be possible they will send an
urgent warning of potential component failure to
Fig. 12.60 This infected system removed by open heart all implanting centers. Elective generator replace-
surgery shows the excess tissue that can form around the ment may be advised and usually the generators
lead and make it completely adherent to the wall of the
RV/RA and even to the tricuspid valve. Such tissue has to
will be provided free of charge.
be resected surgically in order to free the lead sufficiently Several factors may lead to premature bat-
to enable its removal tery depletion. These include low lead imped-
ance with a large electrode tip, wide pulse width
erosion through the skin may occur if the or high amplitude settings, constant pacemaker
pocket is too small and the system is too close use or fast pacing rate and complex circuitry in
to the skin. Both are usually associated with DDD units with two sensing and two pacing cir-
pocket infection. cuits or use of several monitoring facilities
Pre-erosion skin changes include a dusky pur- using sophisticated microprocessors within the
ple or red discoloration of the skin, which is often pacemaker.
thin and tethered to the lead or generator The EOL of most pacemakers used to be
(Fig. 12.68). It may be tender to pressure. This is indicated by slowing of the basic pacing rate or
an opportunity to promptly revise the pacemaker magnet rate, an increasing pulse width or a decrease
pocket and move the whole system deeper in output voltage; however, routine interrogation
beneath the subcutaneous fat and away from the of the generator in the pacemaker follow-up clinic
skin. Once the skin has eroded and the electrode will indicate the amount of battery life that remains
or generator has been exposed through the skin, it and the expected time for replacement.
may be assumed that skin organisms have entered
the pacemaker wound and removal of the whole
system is inevitable (Figs. 12.69–12.71). Once Pacemaker Syndrome
erosion is evident, merely trying to bury the lead
and/or generator rarely leads to a successful out- Pacemaker syndrome occurs when a patient in
come, although in certain situations, for example, sinus rhythm but complete AV block undergoes a
in very frail, elderly demented patients who VVI pacemaker implantation. At frequent intervals,
would have difficulty tolerating an explant/ with loss of AV synchrony, the atria will contract
implant procedure, it may be worth attempting, at against closed A-V valves resulting in cannon
least initially. waves – often visible in the internal and external
274 12 Complications of Pacemaker Implantation

Fig. 12.61 This extracted, infected lead is covered in vegetations

Fig. 12.62 Late pocket


infection may only present
as slight discomfort around
a swollen pocket and no
other signs of local
inflammation

jugular veins. It is associated with an impaired car- Twiddler’s Syndrome


diac output during exercise, the unpleasant sensation
from the cannon waves, dizziness, and even syn- Twiddler’s syndrome is characterized by rotation
cope. Hypotension is more marked on standing and of the pacemaker or ICD with subsequent coiling
most severe during the first few seconds of ventric- of the lead(s). Rotation of the pulse generator is
ular pacing. It can be corrected by implanting an made possible by the loose subcutaneous pocket
atrial electrode and restoring A-V synchrony. and the size and weight of the generator relative to
Late Complications 275

Fig. 12.63 After opening the


pocket and culturing fluid from
within it, Staphylococcus epider-
midis is the commonest cause found
at this stage. Antibiotic sensitivities
will help guide appropriate
treatment

the pocket. It may occur spontaneously or by will-


ful manipulation by the patient. Coiling of the
lead(s) may induce lead displacement or lead
fracture and may be a serious complication in a
pacemaker/ICD-dependent patient (Figs. 12.74
and 12.75). Lead displacement can produce muscle
stimulation or phrenic/brachial plexus stimulation.
Lead fracture requires lead replacement, and
lead displacement will require lead repositioning or

Fig. 12.64 Superior vena caval obstruction can occur


following fibrosis/thrombosis at the site of adherent leads.
The more leads that are present increase the likelihood of
this complication. A swollen, suffused face with engorged
veins in the neck and on the upper chest should suggest
this complication
276 12 Complications of Pacemaker Implantation

Fig. 12.65 (Upper left) Venogram showing SVC obstruc- fully inflated at higher pressure dilates the stenosis; (lower
tion by a critical stenosis at the site of pacemaker leads left) larger balloon fully dilated relieves the obstruction
which have become adherent to the wall; (upper middle) immediately; (lower right) after balloon dilatation, the
angioplasty balloon to dilate the stenosis is severely SVC obstruction is immediately relieved and long-term
indented by this fibrotic narrowing; (upper right) balloon anticoagulant therapy is commenced

removal if severe coiling/twisting of the lead has dual chamber pacemakers. The device forms the
occurred (Fig. 12.76). The opportunity should be anterograde (A → V) limb of the circuit, and the
taken to create a tighter/smaller generator pocket atrioventricular node is the retrograde limb
and to fix the lead(s) to the fascia by direct suturing. (V → A) of the circuit. The patient must have
Simply burying the generator behind the pectoralis V → A conduction with an atrial activation time
major muscle might also prevent further twiddling. that is longer than the programmed postventricu-
lar atrial refractory period (PVARP). A ventricu-
lar-paced beat or a properly timed PVC conducts
Pacemaker-Mediated Tachycardia retrograde via the AV node (or accessory path-
way) to the atrium. If the atrial depolarization
Pacemaker-mediated tachycardia (PMT) is defined occurs after the programmed PVARP, but before
as any condition in which a pacing device paces the next timed atrial-paced beat, ventricular pac-
the ventricles at rates that are “inappropriately ing will be triggered at the programmed AV inter-
fast.” This term was classically reserved for the val. PMT tends to occur at or close to the
reentrant tachycardia occurring in patients with programmed URL and depend upon the pro-
Late Complications 277

Fig. 12.66 Dual-chamber Kappa™ (Medtronic) pace-


maker is implanted in the right inguinal region (arrow)
using CapSure Fix™ active-fixation leads in the right
atrium and ventricle, avoiding traversing the SVC in this
patient recently treated by balloon angioplasty for SVC
obstruction at the site of multiple previous pacing leads –
which were also removed
Fig. 12.67 Pre-erosion of this right-sided pacemaker is evi-
dent (arrow). The area is usually painful, tender, and reddened.
grammed AV delay and the PVARP. This gener- Usually the skin is adherent to the underlying generator
ates an incessant reentrant arrhythmia (so-called
“endless-loop tachycardia”) that lasts for as long PVC or with an incessant tachycardia at the URL
as there is continuous VA conduction with atrial or prevent one atrial sensed event from being
activation outside the PVARP (Fig. 12.77). Atrial tracked.
undersensing can also result in PMT and interro- PMT may also be due to a too sensitive rate-
gation of a modern device should be able to clarify responsive setting, tracking of an atrial tachyar-
this is the mechanism. Modern devices possess rhythmia related to the upper rate settings,
specific algorithms which can terminate PMT if tracking of atrial noise (e.g., EMI) or with inap-
tracked rates persist at the URL. The device can propriate pacemaker manipulation with the rate-
be programmed to lengthen the PVARP after a response turned on.
278 12 Complications of Pacemaker Implantation

Fig. 12.69 Lead erosion in this rather superficially


placed pacemaker will necessitate the whole system to be
replaced on the opposite side. Subpectoral placement
should be considered in thin emaciated patients

Fig. 12.70 This permanent pacemaker lead could not be


extracted when an attempt was made to remove an infected
Fig. 12.68 (Top) At the site of purple discoloration, the system and so the lead was simply cut and the pacemaker
pacemaker is adherent to the skin only 14 months after wound closed. A few months later the lead/bare wire
implantation. The area is usually tender to palpation. This eroded through the skin. The patient tried initially to cover
is a typical appearance of pre-erosion and the generator it with cotton wool but it was uncovered when she attended
should be resited or removed completely without delay. for a routine pacemaker check. The lead had to be removed
(Bottom) Close-up view via an atriotomy
Late Complications 279

Fig. 12.71 Severely eroded


and infected epicardial
pacing system

Fig. 12.72 Loss of capture (pacing spike but no ensuing QRS complex) and loss of output (absence of pacing spikes
and asystole) are both evident on this ECG in this patient whose device is at EOL

Fig. 12.73 Sudden loss of pacing spikes indicates loss of output due to impending battery failure – so-called “end-of-
life” or EOL

Troubleshooting should establish the mecha- respond to pressure/vibrations applied to the device
nism and allow preventive therapy. and so the heart rate may increase without exer-
cise. Some examples include sleeping in a prone
position or turning in bed might cause inappropri-
Unwanted Symptoms Associated ate tachycardia; horseback riding or riding in a car
with Rate-Adaptive Pacemakers or on a cycle over rough terrain; using hand-held
drills, for example, pneumatic or dental drills; in
Sensors of Body Motion close proximity to very loud rock music – deep
Pacemakers with piezoelectric crystals attached to base/low frequencies. Postoperative shivering or
the inside of the can (so-called activity sensors) epileptic fits may also increase the pacing rate.
280 12 Complications of Pacemaker Implantation

Fig. 12.75 Twiddler’s syndrome. This young patient had


Fig. 12.74 Twiddler’s syndrome. This young man had a
a Maximo II DR ICD implanted 6 weeks earlier. Continual
Teligen™ ICD device (Boston Scientific) implanted
rotation of the device within its pocket caused the atrial
4 weeks earlier. By continual rotation of the device within
lead to be pulled out of the RA into the pocket itself.
its pre-pectoral pocket, he managed to place enough tension
Tension is also placed on the RV lead although it has not
on this active-fixation, Sprint Quattro, single, RV bipolar
yet been pulled off the RV myocardium. Note the coiling
lead (Medtronic) that it became detached from the RV myo-
of the leads around the ICD device. (Top) Active-fixation
cardium and retracted back into the left subclavian vein
leads placed in the RA and RV shown immediately after
implantation of this ICD. (Bottom) 6 weeks later, contin-
ual rotation of the device within the pocket has pulled the
RA lead off the RA myocardium and its tip is now in the
pocket. The RV lead has been stretched and the tip fixed to
the RV apex is also likely to soon come free from the
myocardium. Both leads had to be repositioned
Late Complications 281

Fig. 12.76 Defibrillator lead removed in a patient with the lead displaced into the left brachiocephalic vein. The
Twiddler syndrome. Constant rotation of the device within lead had to be extracted and a new lead inserted
the pocket eventually placed tension on the lead tip and

Fig. 12.77 Pacemaker-mediated tachycardia is initiated by an ectopic beat in the left-hand ECG and almost initiated
by several ventricular ectopic beats in the right lower ECG

Sensors of Minute Ventilation especially rotating shoulder actions on the side


Coughing, hyperventilation, and tachypnoea of the pacemaker may increase the pacing
can lead to an increase in pacing rate, as can an rate. Electrocautery may change transthoracic
increased ventilation rate during anesthesia. impedance and cause an increase in pacing
Vigorous movement of the ipsilateral arm and rate.
282 12 Complications of Pacemaker Implantation

Q-T Sensors
Frequent ventricular ectopics may make T wave
detection difficult and the Q-T interval may be
affected by electrolyte disturbances, drugs, and
ischemic heart disease giving an unpredictable
rate response.
Dual sensors and sensor “blending” in pace-
makers and sensor “cross-checking” reduce the
frequency of false responses.

Retained Fragments
Occasionally when attempting to remove leads
from the heart and great veins, the lead may frac-
ture when under stress by forceful traction.
Fragments of the lead such as the tip may become
embedded in the wall of the right ventricle or a
vein wall and separated from the fine filaments of
Fig. 12.78 Two lead tip fragments have been retained in
the wall of the left subclavian vein, having fractured from the stretched/fractured electrode. These small
the lead’s coil/insulation during attempted removal fragments usually cannot be retrieved and are
by traction best left alone (Fig. 12.78).
Temporary Pacing
13

Indications eral anesthesia as do patients with certain drug


overdosage associated with severe bradycardia,
Patients with significant intracardiac conduction for example, digoxin toxicity, b-blocker, or vera-
defects who are symptomatic with dizziness or pamil overdosage.
syncope due to bradycardia should have a tempo- Temporary pacing is also indicated during
rary pacemaker (TPM) inserted if the defect is interventional procedures such as percutaneous
thought to be reversible, or if when deemed irre- coronary rotational atherectomy to a dominant
versible, permanent pacemaker implantation right or left circumflex coronary artery and for
cannot be done immediately. After acute myo- AV node ablation (unless a permanent pacemaker
cardial infarction (MI) (see Fig. 3.1) or cardiac is present) since both may be associated with pro-
surgery, evidence of new or extensive intracar- found bradycardia or heart block (see Fig. 3.9).
diac conduction defect, prolonged sinus arrest or A TPM is indicated for patients with hypertro-
asystole requires a TPM. Those with “at risk” phic obstructive cardiomyopathy who are under-
conduction defects require a TPM prior to gen- going alcohol septal ablation, as this procedure

Fig. 13.1 Temporary


epicardial pacing is not
infrequently required after
certain types of open heart
surgery such as aortic valve
replacement shown here

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 283


DOI 10.1007/978-1-4471-2939-4_13, © Springer-Verlag London 2012
284 13 Temporary Pacing

Fig. 13.2 Epicardial


pacing leads exit the
chest wound and are
attached to the connect-
ing cable which in turn
is connected to the
temporary pacing box

may be associated with AV block (see Fig. 3.8). Table 13.1 Clinical indications for temporary pacing
Temporary epicardial pacing may be necessary Dizziness or syncope due to chronic disease of the
after cardiac surgery, especially after surgery conducting tissue (if permanent pacing is not immedi-
close to the AV node or bundle of His (Figs. 13.1 ately possible)
and 13.2). TPMs are also used in electrophysio- Hemodynamics compromised by bradycardia
logical studies (see Fig. 3.12) and for overdrive Bradycardia-induced ventricular arrhythmias
Intracardiac conduction defects after acute myocardial
pacing in patients with ventricular tachycardia
infarction (see Table 13.2)
(see Fig. 3.11). Prior to general anesthesia in patients “at risk” of 2° or
Patients with infrequent bradycardias should 3° AV block (see Table 13.3)
not routinely receive a TPM while awaiting per- Prior to rotational coronary atherectomy in a dominant
manent pacemaker implantation. right or left circumflex coronary artery
The clinical and electrocardiographic indica- Post-cardiac surgery (see Table 13.4)
tions for TPM are shown in Tables 13.1–13.4. Termination of refractory tachyarrhythmias, e.g.,
ventricular tachycardia
During electrophysiological studies, e.g., initiation/
termination of arrhythmias
AV Block in Acute MI During AV node ablation
Drug toxicity, e.g., digoxin, B-blockers causing
Complete AV Block symptomatic, severe or life-threatening bradycardia

In anterior MI, complete AV block usually is a


result of septal infarction and requires tempo-
rary pacing. In inferior MI, complete AV block Second-Degree AV Block
most often occurs as a result of right coronary
artery occlusion with loss of the AV nodal Mobitz Type I (Wenckebach), where there is a
artery, and temporary pacing is necessary progressive increase in the PR interval eventu-
(Fig. 13.3). ally leading to complete failure of a P wave to
AV Block in Acute MI 285

conduct and produce a QRS complex is usually adverse clinically significant hemodynamic
due to decremental conduction at AV node level. effects. It may respond to IV atropine (1 mg). In
In acute inferior MI, it usually does not require anterior MI, this type of AV block may be more
temporary pacing unless the bradycardia causes sinister and patients should be temporary
paced.
Mobitz Type II AV block is evident by a fixed
Table 13.2 ECG indications for temporary pacing in PR interval with sudden failure of conduction of
acute myocardial infarction
the atrial impulse (P wave). It frequently occurs
Alternating RBBB/LBBB in the presence of a wide QRS perhaps because it
Long PR + new RBBB + LAFB is commonly associated with more distal fascicu-
New RBBB + LPFB lar disease. It requires temporary pacing in both
Long PR + LBBB
inferior and anterior MIs as complete AV block
RBBB + new LPFB
often follows (Fig. 13.4).
Wenckebach (Mobitz type I) 2° AV Block in anterior
MI (in inferior MI if bradycardia poorly tolerated)
Mobitz type II 2° AV block in anterior MI and in
inferior MI if heart rate <40 beats/min or associated First-Degree AV Block
with hypotension or ventricular tachyarrhythmia
Complete AV block Although approximately 40% of patients with
Symptomatic junctional bradycardiaa first-degree AV block may eventually develop
Symptomatic sinus arrest (>3 s or if hemodynamically higher degrees of AV block, patients with first-
affected)a
degree heart block do not require temporary
Severe symptomatic sinus bradycardiaa
Asystole
pacing.
a
If unresponsive to atropine
Table 13.4 Types of cardiac surgery which are more
likely to be associated with the need for temporary
Table 13.3 ECG indications for temporary pacing prior pacing
to general anesthesia for noncardiac surgery
Aortic valve replacement for calcific aortic stenosis
Alternating RBBB/LBBB (with calcium extending into the septum)
Long PR + new RBBB + LAFB Aortic valve surgery/interventricular septal abscess
New RBBB + LPFB drainage/repair in infective endocarditis
Long PR + LBBB Tricuspid valve surgery/Ebstein’s anomaly repair
RBBB + new LPFB Repair of AV canal defects
Wenckebach (Mobitz type I) 2° AV block Ostium primum atrial septal defect repair
Mobitz type II 2° AV block Surgical repair of corrected transposition/AV discor-
Complete AV block dance defect
Sick sinus syndrome – severe sinus bradycardia/sinus Myomectomy for hypertrophic obstructive
arrest cardiomyopathy

Fig. 13.3 Complete heart block


286 13 Temporary Pacing

Fig. 13.4 Mobitz type II AV block

Fig. 13.5 Trifascicular block manifested by 1° heart block, right bundle branch block and left axis deviation

Bundle Branch Block Nonadjacent bifascicular disease includes


RBBB + new LPFB. If LBBB + long PR develops
Patients with trifascicular disease or so-called in acute anteroseptal MI, the LBBB is assumed to
nonadjacent bifascicular disease complicating represent LAFB + LPFB, although a His-bundle
acute MI should receive temporary pacing. study would need to be done to confirm this. RBBB
Trifascicular disease (Fig. 13.5) includes + LAFB (left axis deviation) is not uncommon after
alternating RBBB/LBBB, long PR + new RBBB acute anterior MI as these two fascicles are in the
+ LAFB, long PR and new RBBB + LPFB, and anterior portion of the septum. A long PR in this
long PR + LBBB. situation should indicate the need for pacing.
Techniques 287

Fig. 13.6 Wenckebach 2° AV block in conjunction with prolonged sinus arrest

Sino-Atrial Disease the calcium extends into the interventricular sep-


tum, aortic valve replacement in infective endo-
Marked sinus bradycardia or sinus arrest may carditis especially when infection has caused septal
occur after acute MI, most commonly inferior MI. abscess formation – when permanent pacing is
Since this is likely to be vagotonically mediated, indicated (see Fig. 3.3), tricuspid valve surgery and
it usually responds to IV atropine. Only if unre- Ebstein’s anomaly, repair of AV canal defects and
sponsive to atropine or poorly tolerated should ostium primum ASD and closure of a VSD in cor-
temporary pacing be considered (Fig. 13.6). rected transposition or of the ventricular compo-
nent of a complete AV canal defect.

Prior to General Anesthesia


Techniques
ECG abnormalities as listed in Table 13.3 should
indicate the possible need for prophylactic pacing Temporary pacing may be performed transcutane-
prior to general anesthesia, especially if there is ously by the application of external pacing elec-
evidence of any recent deterioration such as a trodes to the chest wall or by insertion of pacing
lengthening PR or the development of new LAFB. electrodes transvenously. The latter may be inserted
Holter ECG monitoring should be considered using a femoral, subclavicular, supraclavicular,
prior to surgery to identify those possibly at higher internal jugular, or antecubital approach. When
risk. As a minimum, ECG monitoring, IV access, pacing is necessary in a patient who has received
and an external transcutaneous pacing facility thrombolytic therapy for acute MI, a TPM should
should be available in theater if patients are thought be placed via the femoral, brachial, or internal jug-
to be at risk of developing severe bradycardia or ular route – sites that are compressible. During car-
higher degrees of AV block during general anes- diac surgery, temporary pacing can be established
thesia. If a strong indication for permanent pacing by direct attachment of special pacing wires to the
exists and the surgery is not urgent, permanent epicardium – so-called epicardial pacing.
pacemaker should occur first and the procedure Transesophageal ventricular pacing, devel-
requiring general anesthesia postponed. oped in 1969, has been abandoned because of its
relative ineffectiveness compared to modern tran-
sthoracic, transcutaneous pacing. Transesophageal
During or After Cardiac Surgery atrial pacing is more reliable than transesopha-
geal ventricular pacing but is now rarely used and
Temporary epicardial pacing may be required in has been replaced by transvenous atrial pacing
cardiac surgery adjacent to the AV node and bundle (see below).
of His. Such surgery includes aortic valve replace- A review of temporary cardiac pacing was
ment for calcific aortic stenosis, particularly when presented by McCann in 2007. He concluded that
288 13 Temporary Pacing

Fig. 13.7 Lifepak 20 (Medtronic Inc.) is both a defibrillator and external pacemaker

cardiologists who implant TPMs have lower com- connector which is then inserted into the external
plication rates and higher success rates than non- pacing device (Fig. 13.10). One electrode pad is
specialists, that the internal jugular vein (R > L) placed on the front of the chest and a second on the
followed by the subclavian (L > R) and then femo- back over the right or left scapula (Figs. 13.11–
ral vein were the most preferred route of access, and 13.14), although anterior and lateral placement is
that antibiotics and ultrasound probes should be also effective. The arterial pulse should be moni-
contemplated for all temporary wire insertions. The tored for effective pacing as the ECG may not
commonest complications were sepsis, followed by show pacing spikes. Transthoracic pacing causes
incorrect placement of the wire causing failure to chest wall muscle twitching, which is painful and
pace, arrhythmias, myocardial and lung perforation. usually requires sedation.
Training in the skills required to insert transvenous This form of pacing should be considered only
TPMs is essential before accepting the responsibil- as an emergency or rescue treatment and a more
ity for this potentially hazardous procedure. stable and reliable transvenous pacemaker should
be placed as soon as possible

External, Transthoracic Pacing


Transvenous Pacing
Modern transcutaneous, transthoracic pacemakers
function in demand mode and have a maximum General Requirements
output in the region of 150 mA (Fig. 13.7).
Appropriate pacing electrodes (some which can Written consent from the patient should be obtained
act as defibrillator pads) are required (Figs. 13.8 after due explanation of the risks and benefits of
and 13.9), which are linked via a cable to a special the procedure – preferably in the presence of their
Transvenous Pacing 289

next of kin, although this may be impractical in a designed for the use of X-ray fluoroscopy. Cardiac
serious or life-saving situation. The procedure catheter laboratories are often used for insertion
should ideally be performed in a sterile theater but are at best clean areas rather than sterile envi-
dedicated to such procedures and specially ronments. A TPM may be inserted in a coronary
care unit when a “cath-lab” is not available on site.
However, the patient must be on a “screening bed”
and a mobile C-arm image intensifier must be
readily available (see Figs. 7.1 and 7.4).

Fig. 13.8 Quik-Combo™ (Medtronic) external pacing/


defibrillator adhesive pads Fig. 13.10 Pacing cable attached to the Lifepak 20 (arrow)

Fig. 13.9 Quik-Combo™ pads removed from sealed packet


290 13 Temporary Pacing

Fig. 13.11 One pad is placed over the precordium

Fig. 13.13 Connecting cable inserted into the fitting


attached to the disposable pads

Fig. 13.12 The second pad is placed on the back


intended puncture site should be cleaned with an
antiseptic solution of povidone iodine and/or
A specially trained coronary intensive care chlorhexidine (Fig. 13.16) and the area covered
nurse or cath-lab nurse is required, as is a radiog- with sterile drapes before administering the local
rapher who is familiar with X-ray fluoroscopy and anesthesia (Fig. 13.17).
who can set up and operate a portable fluoroscope During insertion of the TPM, the heart rhythm
or cath-lab X-ray screening equipment. The oper- must be monitored and equipment for external
ator should be trained in the technique and be able pacing and resuscitation should be available.
to operate independently, possess a certificate
confirming his/her ability to use the X-ray equip-
ment, and ideally be able to perform advanced life Methods
support procedures if necessary.
The operator must scrub carefully with anti- Temporary ventricular pacing is performed by
septic, and put on a sterile gown, face-mask, and introducing a pacing lead into a systemic vein
gloves to perform this aseptic procedure and advancing it, with the help of X-ray
(Fig. 13.15). A wide area of skin around the fluoroscopy, to the apex of the right ventricle.
Methods 291

Fig. 13.14 Cable attached to the


Lifepak 20

Fig. 13.15 The operator should


be in a sterile gown and gloves
and wear mask and hat
292 13 Temporary Pacing

Fig. 13.18 Fluoroscopic image showing a temporary


pacemaker in the right ventricular apex (arrow) from the
femoral vein. Permanent RA and RV leads are present in
this pacemaker-dependent patient undergoing a box-
change procedure

to an external pulse generator (Fig. 13.19) whose


pulse rate and energy output can be adjusted.
Several approaches are used and are described
below. Generally, access via the right internal
Fig. 13.16 The skin over the insertion site (inguinal jugular vein is least hazardous but the complica-
region for femoral vein insertion) is cleaned with chlor- tions of carotid artery puncture may be serious
hexidine antiseptic solution and the lead position is often uncomfortable for
the patient.
Temporary atrial pacing is performed by intro-
ducing a J-shaped atrial lead (Fig. 13.20) into a
systemic vein (not femoral vein) and advancing
it, with the aid of X-ray fluoroscopy, to the right
atrium. The preformed J-shaped lead is pulled up
into the right atrial appendage and then sutured
to the skin at the skin puncture site (see below).
Atrial temporary pacing leads are frequently
unstable and capture/pacing of the atrium is then
lost. However, an active fixation temporary lead
is available for placement in the atrium which
should offer more reliable atrial sensing/pacing
for as long as is necessary (see below).

Fig. 13.17 The site is covered with a sterile drape with a


purpose-designed window
Temporary Pacing Leads

Extruded polyurethane bipolar pacing catheters


Techniques for reaching the right ventricular with stainless steel electrodes are most com-
apex with the lead tip are described below, but monly used in catheter laboratories and coronary
once positioned (Fig. 13.18) the lead is connected care units for temporary pacing (Fig. 13.21). TC
Temporary Pacing Leads 293

Fig. 13.19 The bipolar temporary electrode’s pins are connected to the cable which is then attached to the temporary
pacing box

is the current bipolar temporary pacing catheter


from Biotronik. It is easily visible on fluoroscopy
due to its coaxial shaft design. Its standard 2 mm
adapter pins allow direct connection to all com-
mon external pacemakers and EP devices. High-
quality NBIH and Goetz catheters with platinum
electrodes are also available in 4–7F sizes. The
Bard temporary pacing catheter is available in
6F, 7F, and 8F sizes and the catheter is shown in
Figs. 13.22 and 13.23.
Balloon flow-assisted catheters (Fig. 13.24) are
available for use when fluoroscopy is not immedi-
ately available and more specialist designs have
specific uses. The Zucker® catheter is ideal for right
heart bipolar pacing, intracardiac ECG sampling,
and infusion. The Myler® catheter is suited for pul-
monary artery pressure monitoring and sampling
while pacing the right ventricle and the Gorlin®
catheter for coronary sinus sampling while simul-
taneously pacing the right atrium. A CVP/pacing
lumen electrode catheter is ideal for pressure moni-
Fig. 13.20 Temporary bipolar “J” lead for positioning in toring and sampling from the vena cava or right
the RA appendage atrium while simultaneously pacing the right ven-
294 13 Temporary Pacing

Fig. 13.21 Upper: Three


bipolar temporary ventricular
leads from Biotronik Ltd.
Lower: TB is a 110 cm long
bipolar temporary pacing lead
available as 4F, 5F or 6F
diameter, straight or preformed
“J” version (Courtesy of Oscor®
Inc., Palm Harbor, FL, USA)

Unshrouded
2 mm pin (non-USA)

Atraumatic tip

Shrouded 2 mm pin (USA)

Depth markings

Fig. 13.23 6F bipolar temporary pacing lead from Bard.


The distal tip is gently curved which aids placement into
Fig. 13.22 6F bipolar temporary pacing lead from Bard the RV apex from the femoral route. The proximal con-
is presented in a well-labeled sterile package nector pins are also shown
Temporary Pacing Leads 295

Quick release luer


activated valve Latex-free compliant balloon

Atraumatic
tip

Shrouded (USA)
or Unshrouded (non-USA) Depth markings

Fig. 13.24 Top: The floatation pacing lead has an pacing lead is a 5F latex-free radiopaque bipolar tempo-
inflatable distal balloon which helps delivery of the distal rary pacing lead (110 cm long) with 8 mm balloon
tip into the pulmonary artery and hence positioning of the (Courtesy of Oscor® Inc., Palm Harbor, FL, USA)
bipolar leads in the RV. bottom: The Helios™ temporary

Stylet, for better positioning


Shrouded 2 mm pin (USA)

Unshrouded 2 mm pin (non-USA)

Atraumatic tip
Depth markings

Fig. 13.25 The TAU 110 cm long bipolar electrode catheters have an inner lumen through which a stylet may
catheters (4–6F) are designed for EP studies – suitable for be inserted in order to help placement within the right
recording intracardiac signals and temporary pacing. The heart (Courtesy of Oscor Inc., Palm Harbor, FL, USA)

tricular apex. The TAU 110 cm long bipolar leads right ventricle. They are 110 cm long, are avail-
(4–6F) are designed for EP studies – suitable for able in 4–7F size, and the electrodes are 1 cm
recording intracardiac signals and temporary pac- apart. The coaxial design, incorporating stainless
ing (Oscor® Inc.). The leads have an inner lumen steel conductors along the length of the catheter,
through which a stylet may be inserted in order to ensures maximum strength and precise torque
help placement within the right heart (Fig. 13.25). control. The smooth polyurethane surface reduces
V-Pace™ (APC Cardiovascular, Ltd.) are also the risk of thrombosis and offers excellent
bipolar temporary pacing leads for use in the biocompatibility.
296 13 Temporary Pacing

Fig. 13.26 The VascoStim


Screw 2/6F screw-in
temporary pacing lead
(VascoMed®)

Fig. 13.27 Temporary pacing box from APC Medical

tracks P/R wave peak amplitudes and adjusts


atrial and ventricular sensitivities accordingly.
Most are now small enough to allow the patient
to be ambulant, although atrial lead stability
is the limiting factor in this regard. Generally,
however, patients should be confined to bed
when a temporary pacing lead is in situ. The
generator’s batteries should be checked daily
(a 9 V alkaline battery provides approximately
5 days of continuous operation in the PACE
203 H) and care should be taken to avoid drop-
The VascoStim bipolar semi-floating pacing ping the device and inadvertently pulling the
leads (VascoMed) are available in 4–6F diame- lead out of position. Some generators allow high
ters and in a straight, curved, or J-shape. A tem- rate pacing – using a “x3” key, to allow for over-
porary screw-in lead is also available (VascoStim drive pacing of ventricular tachyarrhythmias
Screw 2/6F) (Fig. 13.26). (Fig. 13.31) or up to 1,000 ppm for rapid atrial
pacing (e.g., PACE 203 H).

External Pulse Generators


for Temporary Pacing Techniques of TPM Insertion

The external pulse generator allows adjust- It is important to be familiar with the venous
ment of pacing output (voltage ± current), anatomy (Fig. 13.32).
pulse width, pacing rate, mode and sensitiv-
ity to intrinsic activity (Figs. 13.27 and 13.28). Internal Jugular Vein Puncture
Dual-chamber generators will offer adjust- The right internal jugular vein (IJV) is preferred
ment of AV delay, PVARP, and MTR depend- to the left. Injury to the thoracic duct is avoided.
ing on stimulation rate (Figs. 13.28, 13.29, and The patient is tilted 15° head down and the head
13.56) and a three-chamber temporary pacing turned toward the opposite side. The landmarks
generator for biventricular pacing is also avail- are first identified. The IJV lies lateral to the
able from Osypka (Fig. 13.30). The Oscor® carotid artery. The sternocleidomastoid muscle
PACE 203 H from Osypka provides easy mea- (SCM) overlies the IJV in the lower half of the
surement of P/R wave amplitude and optional neck. The apex of the triangle where the clavicular
AUTOSENSE function that automatically and sternal heads of the SCM meet is identified
External Pulse Generators for Temporary Pacing 297

Features

• Single-chamber pacing − 4 modes


Features
• Rapid atrial pacing − 80−800 ppm
Features
• Single-chamber pacing − 4 modes • Single and dual chamber pacing − 11 modes
• Constant voltage output up to 12 V • Rapid atrial pacing − 100−800 ppm
• Pacing and sensing led indicators • Rapid atrial pacing − 90−450 ppm
• Constant voltage output up to 12 V • Suspended output and resume function
• Low battery indicator − led and tone
• Larger faceplate and knobs − user friendly • Ten second operating time during battery change • Auto setting of atrial and ventricular refractory period
• Pacing and sensing led indicators • Auto setting of av delay and mtr
• Built-in bedrail hanger • Constant voltage output up to 10 V
• Redel® terminal for quick easy connection • Low battery indicator
• Light weight − user friendly • LCD display with backlight
• Defibrillation protected • Low battery indicator
• Collet terminals
• Keypad locking switch
• Collet terminals

Fig. 13.28 Current temporary pacing devices available pulse generator; right: MicroPace™ dual-chamber
from APC Medical. Left: Bedside™ single-chamber pulse external pulse generator
generator; center: Miniature™ single-chamber external

Fig. 13.29 Dual-chamber


temporary pacemaker
(Medtronic Inc.)

and local anesthetic should be infiltrated into this patient. As the needle is advanced, aspiration on
area. “Scouting” for the IJV with an 18 gauge the syringe should yield venous blood on enter-
needle is sometimes helpful and ultrasound-guided ing the IJV. Keeping a finger on the carotid artery
access of the IJV is to be recommended. An ensures that the puncture/needle direction is
introducer needle is then inserted at a 45° angle always lateral to the artery (Fig. 13.33). Once the
pointing toward the ipsilateral nipple of the needle is within the IJV lumen, a guidewire and
298 13 Temporary Pacing

Fig. 13.31 This temporary pacing box from APC cardio-


vascular has a key to enable X3 pacing for overdrive
pacing

IJV IJV
EJV EJV
RIV LS-CV

RS-CV
LIV
AxV SVC

BV
CV
Fig. 13.30 PACE 300 three-chamber temporary pace-
maker (Osypka) has a large range of features including MBV
AUTO SENSE for automatically tracking P/R wave peak
amplitudes and adjusting atrial and ventricular sensitivities. MCV
An optional function automatically adjusts the settings for
AV delay, PVARP and MTR depending on selected stimu-
lation rate. A wide range of pacing modes are available

introducer/sheath can be inserted over the wire


and the sheath then sutured to the skin. The pac-
ing lead can then be introduced through the
sheath and positioned in the right ventricle and/
or right atrium using fluoroscopy.

Subclavian Vein Puncture


This provides a suitable route of access to the Fig. 13.32 Venous anatomy of the upper limb/upper
venous system. It is quick, infection and lead dis- mediastinum relevant to pacing. MCV median cephalic
placement are unusual, and in experienced hands vein, MBV median basilic vein, BV basilic vein, CV
cephalic vein, AxV axillary vein, RS-CV right subclavian
complications are rare. However, if permanent
vein, RIV right innominate vein, LIV left innominate vein,
pacing is going to be required, then it is generally LS-CV left subclavian vein, EJV external jugular vein, IJV
accepted to use the internal jugular, antecubital, internal jugular vein, SVC superior vena cava
External Pulse Generators for Temporary Pacing 299

Sagittal
45°

20°

Frontal

Index

21G Head

18G

Guidewire

Fig. 13.33 Landmarks for puncture of internal jugular vein

or femoral vein so as to leave the subclavian veins The patient lies flat or in a slightly head-down
available for permanent lead placement. position. A tiltable table is preferable so that the
The subclavian vein runs behind the medial legs can be raised to improve venous return and
third of the clavicle and can be punctured using distend the subclavian vein if the patient is hypo-
either supra- or infraclavicular approaches. The volemic (Fig. 13.34). Alternatively, intravenous
left subclavian venous approach is easier than the fluid can be given prior to puncturing the vein.
right, because of the straighter run into the superior A needle is introduced through a 0.5 cm skin
vena cava (SVC). The technique of subclavian vein incision just below the inferior border of the clav-
puncture and lead insertion is shown in Chap. 7. icle and just lateral to the mid-clavicular point
300 13 Temporary Pacing

Fig. 13.34 Head-down tilt


on the pacing table may be
helpful for avoiding
air-embolism during
temporary pacemaker
insertion from the subcla-
vian/jugular veins

Fig. 13.35 Landmarks for


subclavian vein puncture

and is directed toward the suprasternal notch so it When the subclavian vein is entered, venous
passes immediately behind the posterior surface blood will be easily aspirated from this large vein.
of the clavicle (Fig. 13.35). Feeling the undersur- The syringe is removed (taking care not to move
face of the clavicle with the needle tip during the needle) and a soft-tipped J-shaped guidewire is
entry helps to keep it superficial and avoid sub- then inserted through the needle and into the sub-
clavian artery puncture and pneumothorax (see clavian vein and advanced through the left bra-
Chap. 7). chiocephalic vein into the SVC. The needle is then
External Pulse Generators for Temporary Pacing 301

Fig. 13.36 Local anesthetic being administered in region Fig. 13.37 Blood aspiration from the femoral vein
of femoral vein

removed and a sheath within which there is a


tapered vessel dilator is passed over the wire into
the vein. Care must be taken to ensure that the
guidewire always extends outside of the sheath
during its insertion in order to avoid losing the
guidewire within the venous system. The guide-
wire and dilator are then removed, leaving the
sheath in situ, and the pacing lead is then passed
through the sheath along the same route to the SVC
and right atrium. Ensuring a head-down position
during insertion and blood flow out of the needle
and sheath during insertion of the guidewire and
pacing lead, respectively, should prevent air embo-
lism from occurring. An alternative approach Fig. 13.38 Insertion of the guidewire
should be considered if the patient has received
thrombolytic therapy, is anticoagulated, or if the
contralateral subclavian vein has been used and common iliac veins and into the inferior vena cava
permanent pacing is likely to be required. and then into the right atrium using X-ray
fluoroscopy. Most leads are slightly curved and
Femoral Vein Puncture advancing the lead across the tricuspid valve into
This is perhaps the easiest and quickest venous the RV apex usually requires little manipulation
access route for establishing temporary pacing. (see Fig. 13.18). Figure 13.43 shows a diagram-
Using a similar needle/sheath technique to that matic representation of this usually simple maneu-
described above and local anesthesia, entry into ver. Unfortunately lead stability is not as good as
the femoral vein is usually easy, the femoral vein when inserted via the subclavian vein, and infec-
being located just medial to the femoral artery tion and venous thrombosis are slightly greater
pulse (Figs. 13.36–13.41). A splittable sheath can risks. It should be reserved for short-term emer-
also be used. The lead is then inserted into the gency pacing such as post-cardiac arrest/collapse
sheath (Fig. 13.42), passed up the external and complicated or caused by complete heart block,
302 13 Temporary Pacing

Fig. 13.39 Setting up the


introducer sheath

severe bradycardia, sinus arrest, or asystole. Once Antecubital Vein Puncture


established, a subclavian pacemaker can then be This route may be chosen if the patient has
inserted more leisurely and then the femorally received thrombolytic therapy or is anticoagu-
placed lead removed. Electrophysiologists use the lated. A medially placed vein should be used such
femoral route for inserting one or more temporary as the median basilic vein. Although enticing,
pacing leads during EP studies (see Fig. 3.12) and laterally placed veins do not provide easy entry
when temporary pacing cover is required during a into the SVC. Like the femorally placed leads,
generator change in a pacemaker-dependent lead stability is relatively poor and phlebitis and
patient. infection are not uncommon.
External Pulse Generators for Temporary Pacing 303

Fig. 13.40 Inserting the


introducer sheath over the
guidewire

Fig. 13.41 Introducer sheath fully inserted into the fem-


oral vein

Positioning of the Lead


Fig. 13.42 Inserting the temporary pacemaker lead into
From the Antecubital, Subclavian, the sheath
or Jugular Vein
After placing the pacing lead into the venous sys- again under fluoroscopy. Occasionally congenitally
tem, the lead is advanced into the SVC and into the abnormal anatomy may be encountered such as a
right atrium. There should be no resistance during left-sided SVC, when the course of the lead should
advancement. If obstruction is felt, the lead should raise this possibility (Fig. 13.44). Contrast injection
be withdrawn slightly, rotated and then advanced can usually show the operator unusual anatomy or
304 13 Temporary Pacing

a b

LIV LIV

RIV RIV

SVC SVC

PA PA

RA TV RA TV

RV RV

IVC IVC

Fig. 13.43 (a) From the femoral vein, a temporary pacing apex (arrow) RIV Right Innominate Vein; LIV Left
lead is simply advanced up the IVC and into the RA using Innominate Vein; SVC Superior Vena Cava; RA Right
fluoroscopy. A gentle pre-shaped curve on the lead helps Atrium; TV Tricuspid Valve; IVC Inferior Vena Cava; RV
to point the tip across the tricuspid valve. (b) The lead tip Right Ventricle; PA Pulmonary Artery
can be simply advanced across the valve and into the RV

LSVC

CS

Fig. 13.44 Unusual route taken by pacemaker lead via a Fig. 13.45 Contrast injection can identify areas of obstruc-
left-sided SVC is confirmed by injection of contrast agent tion in the great veins resulting from fibrosis associated
CS Coronary Sinus; LSVC Left Superior Vena Cava with chronically implanted permanent leads (arrow)

venous obstructions that can sometimes occur in in the subclavian vein or SVC (Figs. 13.45 and
patients who have had several pacing leads placed 13.46).
External Pulse Generators for Temporary Pacing 305

RV outflow tract when screening in the PA pro-


jection. Correct placement can be confirmed by
fluoroscopy in the left anterior oblique or left
lateral view. If in the coronary sinus, the lead will
usually point posteriorly, whereas in the RV
outflow tract or apex the lead tip will point ante-
riorly (Fig. 13.48).

From the Femoral Vein


The lead is advanced up the inferior vena cava
into the right atrium. The “C”-shaped distal sec-
tion of most temporary pacing leads makes it
quick and easy to advance across the tricuspid
valve into the RV apex. Slight rotation of the
pacing lead may be necessary to cross the tricus-
pid valve (see Fig. 13.43).
Fig. 13.46 Multiple leads in the SVC (current and redun-
dant) are more likely to result in fibrosis and obstruction
of the SVC (arrow)
Initiating Pacing

Once within the right atrium, a loop should be Once a stable pacing lead position is obtained,
formed by pushing the lead tip against the atrial the proximal and distal poles of the lead should
wall while simultaneously advancing the lead be connected to the external pacemaker
(Fig. 13.47). The lead may then cross the tricus- (Figs. 13.49–13.51). The proximal pole should
pid valve (TV) or this can be achieved by twist- be connected to the pacemaker’s anode (+ve)
ing the lead in order to rotate the loop toward and (red) and the distal pole to the cathode (−ve)
across the TV. Otherwise slight advancement or (black), respectively. If the poles are inadvertently
withdrawal should allow the lead to cross the TV reversed, the pacing threshold will be significantly
into the RV. It can then be gently advanced and higher.
slightly rotated into the RV apex. Further slight The minimum voltage necessary for pacing
withdrawal and advancement may be necessary stimuli to capture or pace the ventricle consistently,
to position the lead tip in an optimal position the pacing threshold should then be measured by
with a low pacing threshold. Alternatively if the the technician (Fig. 13.52). Starting at 3 V, the
lead is advanced up into the pulmonary artery, pacemaker amplitude or output is decreased by
which confirms entry into the RV, the lead must 0.1 V progressively until the pacing spike ceases
then be withdrawn into the body of the RV and to produce a QRS complex (Fig. 13.53). This is
then rotated and advanced into the RV apex. the pacing threshold and generally it should be less
Fluoroscopy in anteroposterior view shows the than 1 V with a pulse duration of 1 ms. Usually, the
lead tip pointing toward the RV apex with a output is set at 2 V (or double the threshold) above
gentle downwards curve (see Fig. 13.18). the pacing threshold. The stability of the pacing
Ventricular ectopic beats commonly occur on lead is tested by observing the paced ECG during
entering the RV and nonsustained ventricular deep inspiration or coughing. It is usually worth
tachycardia less commonly. looking at the lead by fluoroscopy during the deep
As indicated above, during lead positioning it inspiration to ensure the correct amount of “slack”
is often useful to cross the TV and advance the is present in the right atrium. Figures 13.54 and
lead into the right ventricular outflow tract before 13.55 respectively show the ECG before and after
withdrawing it and rotating the tip downwards right ventricular pacing.
into the RV apex. Placement of the lead into the If pacing output needs to exceed 5 V or 10 mA,
coronary sinus looks similar to placement in the repositioning should be considered.
306 13 Temporary Pacing

LIV LIV

RIV RIV

SVC SVC

PA PA

RA TV RA TV

RV RV

IVC IVC

a b
LIV LIV

RIV RIV

SVC SVC

PA PA

RA TV RA TV

RV RV

IVC IVC

c d

Fig. 13.47 Placement of a temporary pacing lead into ing toward the RVOT, the lead can then be straightened by
the RV apex from the internal jugular, subclavian or gentle withdrawal (f) and then advanced toward the RV
axillary veins (a). Once into the SVC, the lead tip should apex (g). (h) Some slack should be left in the RA to allow
be pushed gently against the RA free wall in order to form for straightening with inspiration and the tip should ide-
a “C-curve” (b). (c) Further advancement will prolapse ally point slightly downwards and anteriorly RIV Right
the lead across the tricuspid valve (TV) and into the RV. Innominate Vein; LIV Left Innominate Vein; SVC Superior
(d) Once across the TV, the lead can be rotated in order to Vena Cava; RA Right Atrium; TV Tricuspid Valve; IVC
turn the bipolar tip to point and be advanced upwards Inferior Vena Cava; RV Right Ventricle; PA Pulmonary
toward the RVOT. (e) With the tip of the electrode point- Artery
External Pulse Generators for Temporary Pacing 307

LIV LIV

RIV RIV

SVC SVC

PA PA

RA
TV RA TV

RV RV

IVC
IVC

e LIV f LIV

RIV RIV

SVC SVC

PA PA

RA RA
TV TV

RV RV

IVC IVC

g h

Fig. 13.47 (continued)


308 13 Temporary Pacing

Fig. 13.48 Left (PA view): Contrast filling of the coro- such a lead is positioned posteriorly. Note the permanent
nary sinus (CS) shows how placement of a lead into the pacemaker lead in the apex of the RV and pointing anteri-
CS may look similar to an RV outflow tract position. Right orly (arrow)
(left lateral view): contrast filling of the CS shows that

Fig. 13.49 The temporary pacing lead and sheath are sutured to the skin and extended across the drape to be connected
to the pacing cable attached to the temporary pacing generator/box

In an emergency, if the position is not ideal After cleaning the skin with povidone-iodine or
and the threshold high, repositioning the lead is chlorhexidine solution, the site should then be
necessary. However, if the patient has become covered with a sterile dressing.
pacemaker dependent, a second pacemaker lead The pacing threshold should be checked daily
should be placed from the femoral vein until the as should the battery and electrical connections.
subclavian lead is safely repositioned. Unnoticed accidental disconnection might lead to
The pacing lead is then sutured to the skin ventricular standstill and death.
with two sutures at its point of entry with separate Paced patients should be monitored on a coro-
sutures securing redundant loops to the skin. nary or intensive care unit.
External Pulse Generators for Temporary Pacing 309

Fig. 13.50 Operator gives the sterile connections to the technician who plugs them into the cable connections

Fig. 13.51 Pacing connections being made


310 13 Temporary Pacing

AV Sequential Pacing lead must be connected (Fig. 13.56). The atrial


pacing threshold tends to be higher than the ven-
For patients with a low cardiac output and sinus tricular threshold.
bradycardia or heart block, AV sequential pacing
can improve cardiac output by up to 30% more
than ventricular pacing alone. Two pacing leads – Complications
a pre-shaped J lead placed in the RA appendage
and a straight pacing lead placed into the RV Although transvenous temporary pacing is
apex – are necessary (see above). A special AV superficially a simple procedure, complications are
sequential temporary pacing generator is required not uncommon. They may be avoided by ensuring
to which the anode and cathode of each pacing that the procedure is only performed by experienced
or supervised operators and only when indicated.
Insertion and positioning of a temporary trans-
venous pacemaker lead may be associated with car-
diac arrhythmias such as atrial and ventricular
ectopic beats, atrial tachycardia, flutter or fibrillation,
ventricular tachycardia, ventricular fibrillation,
complete heart block, and asystole. Other compli-
cations include pneumothorax, hemothorax, right
ventricular perforation, hemopericardium and
cardiac tamponade and are all serious. Pericarditic
pain and a pericardial friction rub suggest RV
perforation. An “intracardiac signal” can be
recorded by connecting the TPM lead to the V lead
of an ECG machine. If the lead tip is against the
endocardium, a good endocardial potential of 1.5–
10 mV should be evident. After myocardial perfo-
ration and with the lead tip in the pericardium, the
endocardial signal is lost and ST-depression and
T-wave inversion will be recorded.
Injury to the brachial plexus and thoracic duct,
bleeding from the subclavian vein, and even
hemothorax as a result of subclavian artery punc-
ture are potential but rare complications when
pacing is performed via the infraclavicular route.
Lead displacement may result in failure to pace
and failure to sense and inappropriate pacing.
Fig. 13.52 Pacing threshold being tested using the ECG Microdisplacement (no obvious displace-
on the Lifepak 12 as the voltage output from the tempo- ment on CXR) may be overcome by increasing
rary pacing box (Medtronic Inc.) is slowly reduced the pacing output voltage and/or pulse width. If

Fig. 13.53 An example of a rhythm strip showing loss of ventricular capture at 0.27 V
Complications 311

Fig. 13.54 12-Lead ECG showing complete heart block prior to pacing

Fig. 13.55 12-Lead ECG showing VVI pacing


312 13 Temporary Pacing

Fig. 13.57 Semi-permanent pacing. Here a permanent


pacing lead is placed and actively fixed into the interven-
tricular septum via the right internal jugular vein and then
inserted into a nonsterile permanent generator attached to
Fig. 13.56 Dual-chamber temporary pacing generator the skin on the chest wall by adhesive tape
(Courtesy of Oscor® Inc., Palm Harbor, FL, USA)

Deep venous thrombosis and thromboembo-


this fails, repositioning of the lead will be neces- lism may be a complication when pacing is per-
sary – as when lead displacement is obvious formed from the femoral vein.
radiologically.
Disconnection of the lead from the pacing box
or inappropriate settings may result in pacing fail- Semi-permanent Pacing
ure as may breakage of the lead or its connections.
Once the TPM is placed in the RV, the patient Occasionally, temporary pacing is required for
may become immediately pacemaker-dependent, several weeks, for example, in patients with
making repositioning difficult. infective endocarditis affecting the tricuspid
Infection is not uncommon when temporary valve as a result of an infected pacing system and
pacing is required for several days. At the first requiring several weeks of IV antibiotics. In this
signs of infection, swabs should be taken from the situation, a permanent lead may be placed into
site and antibiotics commenced. If pyrexia occurs, the RV apex via the internal jugular vein, and
blood cultures should be taken. Staphylococcus tunneled under the skin to the pectoral region
epidermidis/aureus are the commonest organisms where it is inserted into a nonsterile permanent
responsible for infection, although coliforms may generator attached to the skin by a tape and/or a
be responsible when the femoral route has been suture (Figs. 13.57 and 13.58).
used. In the presence of pyrexia, IV antibiotics,
for example, IV flucloxacillin 1 G QDS should be
commenced once blood cultures have been sent to Temporary Epicardial Pacing
the microbiology laboratory, since staphylococ-
cal septicemia is likely. A move should be made to If temporary pacing is indicated during cardiac
remove the infected TPM and replace it with a new surgery, special myocardial pacing leads can be
TPM on the opposite side if temporary pacing is still sutured directly to the surface of the right atrium,
required. right ventricle, or left ventricle (Fig. 13.59) and
Temporary Epicardial Pacing 313

Fig. 13.58 Permanent pacemaker is fixed externally to lar septum and attached to the permanent pacemaker in
the skin above the clavicle by a clear adhesive dressing. A order to provide semi-permanent pacing
lead is actively fixed to the right side of the interventricu-

Fig. 13.59 Epicardial leads from Medtronic. Top left: coil; Bottom right: The Convenience (Model 6494) unipo-
Unipolar myocardial lead (Premium 6500); Top right: lar lead has some improved features such as smaller diam-
Bipolar coaxial (Model 6495) lead with fixation coil; eter needles and color-coded wires (Image reproduced
Bottom left: Pediatric unipolar lead (Model 6491) has fea- with permission of Medtronic, Inc.)
tures specifically useful for children, e.g., smaller fixation
314 13 Temporary Pacing

the proximal ends tunneled out through the skin


for connection to a temporary pacing box
(Fig. 13.2). The leads can be unipolar or bipolar.
Atrial epicardial leads are also available
(Fig. 13.60). The leads can be removed when no
longer required by simply applying firm traction
to the leads exiting the skin.

Fig. 13.60 Atrial epicardial unipolar lead from Medtronic


(Model 6492) is well suited for suturing to thin, delicate
atrial tissue (Image reproduced with permission of
Medtronic, Inc.)
Pacing in Patients with Structural
Cardiac Abnormalities 14

Although most adult patients requiring pacemaker or previous cardiac catheterization notes may
or ICD implantation will have normal cardiac be useful in noting anatomical abnormalities.
anatomy, occasionally significant abnormalities In recent times with the advent of biventricular
will be found only at the time of the procedure, pacing, it is relevant also to know the position of
since they had not given rise to symptoms or any the coronary sinus, for example in patients with
obvious physical signs. These include persistent Ebstein anomaly who have already undergone
left-sided superior vena cava (SVC) (with or tricuspid valve replacement.
without a right-sided SVC), dextrocardia, atrial It goes without saying that many patients who
septal defect, and patent foramen ovale. Such receive permanent pacemakers as children fol-
abnormalities may give rise to practical prob- lowing surgery for their congenital heart disease
lems during lead placement and operators should will require several further procedures in the
be aware to recognize the problem immediately years to come. These range from generator
and know how to deal with it. Patients (adults change (at EOL), lead problems requiring
or children) with congenital structural cardiac replacement of a lead, resiting or replacement of
abnormalities, such as transposition, corrected the whole system, and intervention for venous
transposition, tetralogy of Fallot, univentricular thrombosis/occlusion.
heart, or post-operative “corrected” defects, will
require special consideration before proceeding
to the pacing theater. In particular, the opera- Dextrocardia
tor will need to know whether the transvenous
approach is feasible, what problems might be This positional abnormality in which the cardiac
encountered during lead implantation, and how apex is located on the right side of the chest
to seek the best and most stable of electrode posi- should not pose a problem to pacemaker implan-
tions. Preoperative investigations, including tran- tation once the cardiologist is oriented as long as
sthoracic and transesophageal echocardiography, no other cardiac structural defects are associated
CT and MRI cardiac imaging as well as angiog- with the dextrocardia. Providing the pre-paced
raphy, for example, left arm venography, should rhythm is not complete heart block with a wide
be used to clarify the cardiac and venous anatomy QRS complex, the 12-lead ECG should give the
in order to safely embark on transvenous lead diagnosis before the patient enters the pacing
placements. Simply reviewing previous surgical theater. If not, fluoroscopy will suggest the
notes (following cardiac surgery in earlier life) abnormality (Fig. 14.1).

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 315


DOI 10.1007/978-1-4471-2939-4_14, © Springer-Verlag London 2012
316 14 Pacing in Patients with Structural Cardiac Abnormalities

Fig. 14.1 Active fixation leads are


placed in the right ventricular outflow
tract (arrow) and in the low right
atrium (twin arrows) via the left-sided
superior vena cava in this patient with
dextrocardia. A redundant right atrial
lead remains attached to the right atrial
myocardium

Persistent Left-Sided Superior


Vena Cava

0.3% of the general population has a persistent


left-sided SVC, and this anomaly may be present
in 4.3–11% of patients with congenital heart dis-
ease. In 90% of cases, the persistent left SVC
connects to the right atrium via the coronary sinus
(Fig. 14.2). In the other 10%, it connects to the
left atrium when most will have an associated
ASD or heterotaxy syndromes and a small right-
to-left shunt.
The anomaly is due to failure of regression of
the left anterior and common cardinal veins and
left sinus horn. The persistent left SVC starts at
the junction of the left subclavian vein and left
Fig. 14.2 This patient is shown to have bilateral SVCs hav-
internal jugular vein, passes lateral to the aortic ing had pacing leads introduced via the left-sided SVC and
arch, and receives the left superior intercostal coronary sinus. An active fixation lead is placed into the RA
vein. It then passes anterior to the left hilum, is appendage and a tined passive fixation lead into the RV apex
joined by the hemiazygous system, crosses the
posterior wall of the left atrium, and receives the Although it can be difficult to maneuver the
great cardiac vein to become the coronary sinus. atrial and ventricular leads into ideal positions in
In 65% of cases, the left brachiocephalic vein the RA and RV respectively as they course through
is absent or small (Fig. 14.2), and although the the coronary sinus, persistence and the use of active
majority of patients will have bilateral SVCs fixation leads usually proves successful (Fig. 14.5).
(Figs. 14.2 and 14.3), in 10–18% the right SVC is Left ventricular pacing via a cardiac venous tribu-
absent (Fig. 14.4). tary is usually not difficult to achieve but persis-
Ebstein’s Anomaly 317

LSVC

RA CS

Fig. 14.3 This patient has clear communication between


right and left-sided SVCs via the left brachiocephalic
vein. Previously placed RA and RV leads have been
placed via the right-sided SVC (green + orange arrows)
and a new RV lead (because of loss of capture of previous
RV lead) is shown to enter a left-sided SVC (blue arrow)
and coronary sinus (CS) en route to the RV apex

tence in placing a lead into the RV is often


worthwhile in pacemaker-dependent patients.
Thrombosis of a large coronary sinus following
pacemaker lead implantation has been reported.

Ebstein’s Anomaly

Ebstein’s anomaly is rare (1 in 20,000 live births;


0.5% of all congenital heart disease) and charac-
terized by downward displacement of the tricuspid
valve orifice so that the cusps originate from the
right ventricular wall rather than the tricuspid
annulus (Fig. 14.6). The displaced tricuspid valve
divides the RV into two parts – an atrialized por-

Fig. 14.4 This patient had a single chamber pacemaker


implantation inserted using the right subclavian vein for
lead insertion. However, the right-sided SVC is absent and
the lead passes across to a persistent left-sided SVC
(LSVC) which runs into the coronary sinus (CS). The RV
tined lead is manipulated into the right atrium (RA) and
across the tricuspid valve into the apex of the right ven-
tricle (RV) (black arrow)
318 14 Pacing in Patients with Structural Cardiac Abnormalities

Fig. 14.7 Chest X-ray in Ebstein’s anomaly shows


marked cardiomegaly. This patient was being investigated
for recurrent palpitations and dizzy spells using an
Fig. 14.5 It is probably preferable to use an active implantable loop recorder. Significant tricuspid regurgita-
fixation lead when placing leads via a left-sided SVC, as tion is not uncommon in Ebstein’s anomaly resulting in
in this case where a new RV lead actually enters a left- marked dilatation of the RA. Active fixation leads should
sided SVC and enters RA/RV via the coronary sinus. probably be employed if there is a clinical indication for
Clearly this patient also has a right-sided SVC down permanent pacemaker implantation
which were placed the original RA and RV leads

tion lying between the tricuspid annulus and the


displaced tricuspid orifice and the remainder of
the true RV which lies beyond the tricuspid valve.
The relevance to pacemaker implanters is that
approximately 20–25% of such patients develop
arrhythmias and conduction abnormalities and
SVC
3–4% require pacing (Fig. 14.7). The commonest
indications for pacing include persistent atrial
standstill and AV block (de novo, post-AV node
Ao PA ablation, or post-surgery). The atrialized portion
LA
of the RV varies in size, muscularity, and thick-
ness but it has the electrophysiologic characteris-
Patent tics of the RV. Hence, the RV lead can be placed
foramen above the valve rather than through it. Active
ovale, fixation leads should be used in the atrium, the
or ASD Enlarged RA LV
atrialized portion of the RV, and in the RV apex or
RV outflow tract to avoid displacement in such
patients who often have significant tricuspid
IVC regurgitation. It is worth remembering that other
congenital cardiac defects may coexist with
Small RV TV Ebstein’s anomaly, for example, ASD and VSD.
When it is impossible to insert leads in the right
Fig. 14.6 Ebstein’s anomaly is characterized by down- atrium and ventricle, one may use the cardiac veins
ward displacement of the tricuspid valve orifice so that the
via the coronary sinus to achieve left ventricular
cusps originate from the right ventricular wall rather than
the tricuspid annulus. Other congenital cardiac defects pacing. However, in pacemaker-dependent patients,
may coexist with Ebstein’s anomaly, e.g., ASD and VSD epicardial pacing may be more appropriate.
Other Structural Defects Not Requiring Corrective Surgery 319

If surgery for tricuspid valve reconstruction/


replacement takes place, a pacing lead can still be
inserted. After annuloplasty, the lead can be
placed across the valve in the usual fashion. If
valve replacement is required, a lead can be
buried behind the sewing ring. The lead can be
tunneled to the anterior abdominal wall or pecto-
ral region and connected to a generator or capped
for future use. If a mechanical prosthesis is LA
Ao
implanted, then epicardial pacing should be the PA
method of choice, although even here endocar- RA
dial pacing is not impossible if the coronary sinus
TV
is positioned on the atrial side of the prosthesis.

MV RV
Atrial Septal Defect/Persistent
Foramen Ovale
LV

Generally, isolated foramen ovale and atrial sep-


tal defect do not hinder permanent pacemaker
implantation. It is possible to enter the LA and
the LV and if positioned there may inadvertently
result in systemic embolization – including Fig. 14.8 Congenitally corrected transposition of the
stroke. They should be removed or the patient great vessels
anticoagulated.
Fluoroscopy will suggest LV placement of a
lead. The lead will arch over the atrial septum at the RV apex or within the interventricular sep-
and the ECG will confirm LV pacing, that is, tum. A regurgitant tricuspid valve and enlarged/
RBBB complexes. scarred right atrium/ventricle can result in
When an ASD has been repaired by a patch or difficulty placing leads into stable, effective posi-
a closure device, atrial septal pacing may not be tions and generally active fixation leads should
possible because of fibrosis. Moreover, if the be used from the outset.
right-sided chambers are dilated as a result of a
long-standing defect, active fixation leads should
be preferred in order to try and prevent lead Other Structural Defects
displacement. Not Requiring Corrective Surgery

Congenitally Corrected L-Transposition


Ventricular Septal Defect of the Great Vessels

Patients with small VSDs that do not warrant clo- In this condition, a morphologic RA drains into a
sure may require pacemaker implantation. Care right-sided morphologic LV which gives rise to
should be taken to be sure that the lead does not the pulmonary artery. Pulmonary venous blood
cross into the LV when systemic embolization enters the LA and then an LV with a right ven-
and stroke may be an associated risk. tricular morphology and then into the aorta
Patients who have had surgical or device clo- (Fig. 14.8). Although rare (<1% of all congenital
sure of a VSD may be difficult to pace endocardi- heart disease), 95% have associated anomalies,
ally due to scarring/fibrosis or synthetic material for example, VSD with pulmonary stenosis.
320 14 Pacing in Patients with Structural Cardiac Abnormalities

Fig. 14.9 PA (left) and lateral (right) chest X-ray from a (curved green arrows) to allow for somatic growth. Aged
26-year-old woman with corrected transposition of the 17 years, insulation break resulted in intermittent loss of
great vessels, ventricular septal defect and congenital sensing and pacing in the RV lead which was replaced. It
complete heart block who underwent permanent pace- proved impossible to enter the left subclavian vein which
maker implantation at 4 years of age at the time of pulmo- was now occluded and so the lead was inserted via the left
nary artery debanding and VSD closure. The surgeon internal jugular vein and tunneled subcutaneously over
implanted a screw-in lead to the systemic ventricle and the left clavicle (red arrow) to the pre-pectoral pocket.
sutured an epicardial lead to the surface of the RA – The tip of this active-fixation RV lead can be seen to point
implanting a dual-chamber pacemaker in the left subcos- vertically downwards (black arrow) – fairly typical of this
tal pouch. Four years later, failure to pace necessitated congenital abnormality. Seven years later, the Kappa™
implantation of a new endocardial pacing system DDD (Medtronic) was replaced by a Sensia™ DDD
(Minuet™, Medtronic) via the left subclavian vein using device (Medtronic) but within 2 years – at the age of
active fixation leads to the RA appendage (straight green 26 years – further lead problems required a new endocar-
arrow) and anatomical RV apex with redundant loops dial system from the right subclavian vein (see Chap. 15)

Congenital atrio-ventricular block (AVB) will anteriorly or posteriorly and may even point to
occur in 15–20% of patients, and AVB may be the right on AP fluoroscopy. An intracardiac ECG
precipitated by surgical repair of the VSD. When will confirm good endocardial contact but active
pacing is necessary in early childhood, multiple fixation leads should be preferred because of the
subsequent procedures that are likely to be smaller trabeculae that are usually present.
required can lead to access problems and redun-
dant leads requiring explantation.
The anatomy should be understood. The After Corrective Surgery
ventricles lie side-by-side to each other rather for Congenital Cardiac Abnormalities
than the RV being anterior to the LV in a normal
heart. The septum is thus AP rather than left to Tetralogy of Fallot
right. The atrial lead should position normally
but the ventricular lead may pass inferiorly Tetralogy of Fallot is the commonest cyanotic
through the tricuspid valve to the RV apex (ana- congenital heart defect occurring in 1 in 3,600
tomic LV) and the tip point vertically downwards live births. Usually, patients with this anomaly
(Fig. 14.9). However, the lead tip may also point who require permanent pacing or ICD implanta-
After Corrective Surgery for Congenital Cardiac Abnormalities 321

PA
Ao

LA
RA

LV Fig. 14.11 Following failure of the RV apical lead in this


RV
patient with Fallot’s tetralogy, a second RV lead is actively
fixed to the interventricular septum. The proximal end of
the redundant lead is capped and then fixed with a suture
to the fascia over pectoralis major

Fig. 14.10 Tetralogy of Fallot


large coronary sinus may coexist in 10% of
patients and the operator might consider imp-
tion will have had a previous surgical procedure. lanting on the right side to avoid this potential
This would usually have been a preliminary sys- problem.
temic-pulmonary artery anastomosis as an infant
if significantly symptomatic. Waterston (ascending
aorta-right pulmonary artery), Cooley (ascending Tricuspid Atresia/Univentricular Heart
aorta-right pulmonary artery), Potts (descending
aorta-left pulmonary artery), or Blalock-Taussig In this congenital abnormality, survival depends
(left subclavian artery-pulmonary artery) shunt on an effective atrial septal communication.
are the usual temporary procedures prior to a more Surgery to separate and redirect venous blood
definitive intracardiac repair as the individual gets flow involves the Fontan repair or one of its
older. In these situations if AVB occurs, these modifications. In the classic Fontan procedure,
procedures should not form a barrier to conven- the atrial septal defect is closed and a direct right
tional transvenous pacemaker implantation. atrial-pulmonary artery anastomosis is created
However, since the presence of a VSD and over- and the connection between PA and RV/LV is
lying aorta persists, the risk of stroke exists and closed by sutures or banding (Fig. 14.12).
epicardial pacing should probably be preferred Frequently, the ultimately elevated atrial pres-
(Fig. 14.10). Total corrective surgery usually sures result in severe atrial dilatation and an
consists of patch closure of the VSD and infundib- increase in wall thickening, sinus node dysfunc-
ular widening using a synthetic or pericardial tion, and atrial arrhythmias. Variations on the
patch up to or across the pulmonary valve annu- Fontan repair include a number of procedures
lus. Pulmonary regurgitation and a dilated RV, aimed at connecting the venous circulation to the
prosthetic material, and myocardial fibrosis not pulmonary artery either by directly connecting
only make atrioventricular block a likely compli- the venae cavae to the pulmonary artery or by
cation but also make endocardial lead placement using an extracardiac or intra-atrial tunnel/con-
difficult and active fixation leads should be pre- duit. These procedures are known as total
ferred (Fig. 14.11). A left SVC draining into a cavopulmonary connections (Fig. 14.13). As with
322 14 Pacing in Patients with Structural Cardiac Abnormalities

the bidirectional Glenn shunt, when the SVC is D-Transposition of the Great Vessels
detached from the RA and anastomosed to the
PA, conventional transvenous pacing is not pos- Complete transposition of the great vessels (TGA)
sible in these cases. accounts for 5% of all congenital heart disease
cases. Without surgery soon after birth, infants
would not survive this situation where the pulmo-
nary artery arises from the LV and the aorta from
the RV (Fig. 14.14). Usually a coexisting commu-
nication such as a patent ductus arteriosus, ASD,
or VSD allow the infant to survive (40–50% will
have an associated VSD). Many infants will have
had an ASD created or a balloon atrial septostomy
Ao to allow mixing of venous and arterial blood.
Ideally, the arterial switch operation with reim-
plantation of the coronary arteries into the neo-
LA
aortic root should be performed. Alternatively,
RA
interatrial repair procedures may be preferred
PA depending on the clinical situation. The Senning
and Mustard procedures redirect venous blood by
removal of the atrial septum followed by the inser-
tion of an intra-atrial baffle which cleverly redis-
tributes the desaturated venous blood behind the
baffle to the mitral valve, LV, and to the transposed
PA (Fig. 14.15). Saturated pulmonary venous
blood is directed in front of the baffle to the RA,

Fig. 14.12 Fontan operation for tricuspid atresia

SVC
LA
PA
Ao
RA
PA

RA LV
Extra cardiac
conduit
RV

IVC Fig. 14.14 D-transposition of the great arteries. The pul-


monary artery arises from the LV and the aorta from the
RV. Usually a coexisting communication (not shown)
such as a patent ductus arteriosus, ASD or VSD allow the
Fig. 14.13 Total cavopulmonary connection surgery infant to survive (40–50% will have an associated VSD)
After Corrective Surgery for Congenital Cardiac Abnormalities 323

tricuspid valve, RV, and aorta. The Mustard proce-


dure uses atrial pericardium or synthetic material
as the baffle. Atrial tachyarrhythmias, junctional
rhythm, and complete heart block occur in these
patients and may require pacing (Fig. 14.16). In
the Senning procedure, flaps of the atrial septum
PVA and RA free wall are used to reroute systemic and
pulmonary venous return, and sinus node damage
Ao PA and atrial arrhythmias are not uncommon, presum-
ably as a result of the extensive atrial surgery.
SVA Although pacing in patients with
D-transposition may be a daunting task, surpris-
ingly it may be straightforward. The atrial lead
is advanced via the SVC and the stump of the
RA, behind the baffle and into the LA where it
LV
should be actively fixed to the roof of the LA
(Fig. 14.17). Lateral screening should show
RV posterior positions of both LA and LV leads
(Fig. 14.18). Preferably a curved or steerable sty-
let should be used to place the lead as medial as
possible in order to avoid phrenic nerve stimula-
tion (see Fig. 14.21). Steerable catheter delivery
Fig. 14.15 Senning operation for D-transposition of the
great arteries
systems may be useful for positioning the atrial
lead in optimum position. The ventricular lead is

Fig. 14.16 In D-transposition of the great arteries treated by the Mustard procedure, junctional bradycardia and com-
plete heart block may occur and require pacemaker implantation
324 14 Pacing in Patients with Structural Cardiac Abnormalities

advanced along the same route, across the mitral venography might be helpful to show the anatomy
valve and into the LV, where it should be actively better prior to device implantation. Ventricular
fixed. The ECG should confirm satisfactory dual- leads must pass into the LA and into the LV before
chamber pacing (Figs. 14.19 and 14.20). being anchored actively. Figure 14.21 shows a
When baffles become obstructed as the patient more medial position of the atrial lead in order to
grows (>20% of patients), CT, MRI scans, or try and prevent phrenic nerve stimulation. It is
worth remembering that chronic atrial arrhythmias
are not uncommon because of the extensive atrial
surgery, and if atrial fibrillation is present, then a
rate-adaptive (VVIR) pacemaker with a single
pacing lead is appropriate (Fig. 14.22).
If a Rastelli operation has been performed for
patients with TGA/VSD/ pulmonary stenosis and
AVB subsequently develops, leads can be placed
in the RA and RV by a conventional transvenous
approach rather than opting for epicardial pacing
(Fig. 14.23). The latter may be more appropriate
if the AVB occurs at the time of VSD closure.

Structural Defects Requiring


Epicardial Pacing

Fig. 14.17 After a Mustard or Senning procedure, if Occluded superior vena cava or subclavian veins,
dual-chamber pacing is required, the atrial lead may be mechanical tricuspid valves, and no access to
passed behind the baffle into the LA and actively fixed to the venous ventricle, for example in tricuspid
the roof of the left atrium. The ventricular lead follows the atresia, make endocardial pacing impossible and
same route into the left atrium and then advanced across
the mitral valve into the LV where it is actively fixed epicardial pacing is necessary.

Fig. 14.18 This illustration shows a posterior position of both leads in the LA and LV in this patient who had under-
gone a Mustard procedure
After Corrective Surgery for Congenital Cardiac Abnormalities 325

Fig. 14.19 Complete heart block in a patient after a Mustard procedure

Fig. 14.20 ECG of same patient as in Fig. 14.19 after dual-chamber pacemaker implantation

After the Fontan procedure and its many vari- to the right atrium, an atrial lead can be sutured
ants and after patch closure of a VSD, when in the pectoral region and the epicardial ventric-
atrial bradyarrhythmias and AV block occur, ular lead (usually from the LV) tunneled to the
pacing is indicated but endocardial pacing is or pectoral pocket for pacemaker connection
may be impossible and epimyocardial pacing is (Fig. 14.25). Alternatively, the atrial lead can be
necessary (Fig. 14.24). If there is a venous route extended and tunneled to the anterior abdominal
326 14 Pacing in Patients with Structural Cardiac Abnormalities

wall and the pacemaker buried behind the rectus where the RA can be accessed via the SVC, a
sheath. subcutaneous pectoral pacing system can be
Figure 14.26 shows that a transvenous atrial used. Clearly, if a total cavopulmonary anasto-
lead can be placed and actively fixed in the RA mosis is created, then epicardial pacing will be
which is often very dilated. In this situation, necessary.

Fig. 14.21 Following a Mustard procedure at the age of (Vitatron) because of reaching the ERT. A subsequent
19 months, a dual-chamber pacemaker was implanted in procedure was required 4 years later to replace the mal-
this patient at the age of 16 years. An active fixation lead functioning ventricular lead which was not extracted. The
was placed in the LA (venous atrium) but placed more lateral view shows the atrial lead positioned posteriorly
medially to try and avoid phrenic nerve stimulation. An but pointing anteriorly and the two actively fixed ventricu-
active fixation lead was placed in the apex of the LV and lar leads posteriorly placed in the LV. The generator was
an Elite DDDR generator (Medtronic) implanted. Ten exchanged for a Sensia™ DDDR device (Medtronic) at
years later, the generator was changed to a Clarity DDDR the same procedure

Fig. 14.22 After a Mustard procedure, if atrial fibrillation


and a slow ventricular rate are present or if atrial pacing is
not possible, a single active fixation lead can be passed
into the left ventricle (venous ventricle) and attached to a
rate-responsive pacemaker. This 19-year-old man had
transposition of the great vessels, had an atrial septostomy
at day 1 and a Mustard procedure at 15 months of age. At
the age of 12 years he developed complete heart block. No
acceptable pacing threshold could be obtained in the baffle
or LA and so the proposed dual-chamber procedure was
changed to a Thera SR rate-responsive pacemaker using a
single, actively fixed LV lead. Seven years later, the gen-
erator was replaced by an Identity™ SR (St Jude Medical)
and 6 years later by a Symphony SR device (Sorin) – both
as a result of battery depletion
After Corrective Surgery for Congenital Cardiac Abnormalities 327

PA

LA

RA

VC
LV

Fig. 14.25 Following a Fontan procedure, the large and


dilated RA can be accessed to allow transvenous implantation
RV
of an atrial lead. If AV block is present, then epicardial dual-
chamber pacing may be more appropriate, although a hybrid
procedure of endocardial RA and epicardial RV pacing may
be possible. In this situation, tunneling of one or other leads to
Fig. 14.23 Rastelli operation. Here a valved conduit the pectoral or abdominal sites will be necessary
(VC) is created between the RV and PA

Fig. 14.24 After closure of a perimembranous ventricular device instead. However, it proved impossible to either
septal defect with a Dacron patch atrioventricular block is remove the adherent lead or dilate the stenosis. Surgical
not uncommon. This patient developed complete heart block treatment was performed to remove the lead and repair the
5 years later and a Legend VVIR pacemaker was implanted SVC obstruction, at which time an endocardial lead was
using a single ventricular lead. When SVC obstruction fixed in the RA and tunneled to the epigastrium. An epicar-
developed as a result of lead adhesion/fibrosis accompanied dial lead was attached to the surface of the RV and the lead
by a very low lead impedance, it was decided to remove the tunneled to the epigastrium where both leads are attached to
lead and dilate the SVC obstruction and implant a DDDR a DDDR generator and buried behind the rectus sheath
328 14 Pacing in Patients with Structural Cardiac Abnormalities

Fig. 14.26 Following a Fontan procedure, an active Fig. 14.28 An active fixation lead is placed in the RV
fixation lead is placed in this dilated RA and connected to apex across a bioprosthetic tricuspid valve in this patient
a pectorally placed generator to function as an AAI with aortic (green arrow), mitral (blue arrow) and tricus-
system pid valve prostheses (yellow arrow) undergoing dual-
chamber permanent pacemaker implantation

Fig. 14.27 When several procedures


have resulted in difficult or impossible
access to the RV transvenously (red
arrow shows remnant of old leads from
previous extractions), epicardial pacing
may be necessary. Here new epicardial
atrial and ventricular leads have been
tunneled to the abdominally placed
generator (green arrow)

Epicardial pacing may be necessary if access to use the femoral vein. After entering the femo-
to the atrium or ventricle cannot be achieved ral vein using the standard Seldinger technique, a
transvenously (Fig. 14.27). guidewire and sheath are inserted to enable deliv-
ery of a ventricular lead to the right atrium.
Usually a long pacing lead is required and this
Superior Vena Cava Obstruction/ should be actively fixed in the right ventricle. The
Occlusion lead can then be tunneled under the skin into the
lower abdominal wall where an incision can be
If the superior vena cava is severely stenosed or made and a pocket created for the generator to
occluded, an alternative to an epicardial system is which the lead can be attached (see Fig. 12.66).
After Corrective Surgery for Congenital Cardiac Abnormalities 329

An atrial lead can be similarly delivered if dual- present, epicardial RV lead placement will be
chamber pacing is desired. required if pacing is necessary. However, a perma-
nent lead can be placed across a bioprosthetic tri-
cuspid valve without too much difficulty (Fig. 14.28)
Prosthetic Valves and an active fixation lead should be chosen espe-
cially if there is dilatation of the RA or RV.
Pacing leads cannot be placed across mechanical An alternative approach is LV pacing via the
valves. Generally, if a mechanical tricuspid valve is coronary sinus.
Pacemaker and ICD Implantation in
Children 15

Introduction Normal Heart Rates in Children

The implantation and follow-up of pacemakers Resting heart rates in small children are consider-
and ICDs in children poses unique challenges. ably higher than in adults. A resting heart rate of
Less than 1% of all pacemakers and ICDs are 50 bpm, while normal in an athletic 15-year-old
implanted in children and the numbers of implants would represent profound bradycardia in an
taking place within individual centers are low. In infant (Fig. 15.1). Moreover, in the presence of
a recent US survey, the mean annual number of CHD, levels of bradycardia or loss of AV syn-
new pacemaker implants per center was less than chrony may lead to symptoms which would not
25. A significant proportion of the pediatric pop- occur in the presence of normal cardiovascular
ulation who require pacemaker and ICD implan- physiology. It is important, therefore, to correlate
tation are survivors of palliative surgical symptoms with age- and disease-specific rates of
procedures for complex congenital heart disease bradycardia rather than absolute rates.
(CHD). Physicians are thus faced with the
difficult situation of implanting few devices in
complex patients and as a result sometimes adult AV Block in Children
cardiologists may be asked to implant devices in
children. This chapter focuses on the key differ- As in adults, pacing is mandatory for children with
ences between adults and children in terms of symptomatic complete AV block. Although dra-
pacemaker and ICD indications, implantation, matic symptoms such as syncope are readily appar-
and follow-up. ent, children may find it difficult to describe more
subtle symptoms such as lethargy, breathlessness, or
dizziness and a high index of suspicion is required.
Bradycardia Pacing Indications There is increasing evidence that asymptom-
atic patients with complete AV block have a risk
There are no randomized trials of cardiac pacing of developing left ventricular dysfunction if left
in children or patients with CHD; as a result unpaced. There is also a small but definite risk of
most recommendations are consensus-based. sudden death. Permanent pacing is recommended
The current indications for bradycardia pacing in for neonates and infants (children aged less than
children are summarized in the latest ACC/AHA/ 1 year) if the ventricular rate is less than 55 and in
HRS guidelines published in 2008 and con- children over 1 year if the heart rate is less than
densed in Table 15.1. Specific issues are dis- 50. In patients with structural CHD associated
cussed next. with complete AV block, pacing is recommended

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 331


DOI 10.1007/978-1-4471-2939-4_15, © Springer-Verlag London 2012
332 15 Pacemaker and ICD Implantation in Children

Table 15.1 Indications for permanent pacing in children, adolescents, and patients with CHD
Class I: Permanent pacing is indicated in the following groups of patients
1. Symptomatic third-degree AV block or high-grade second-degree AV block
2. Following cardiac surgery for CHD, postoperative third-degree AV block or high-grade second-degree AV
block which persists for at least 7 days
3. Asymptomatic congenital third-degree AV block with a wide QRS escape rhythm, complex ventricular ectopy,
or evidence of ventricular dysfunction
4. Asymptomatic congenital third-degree AV block in infants with a ventricular rate <55 bpm in the absence of
CHD or <70 bpm in the presence of CHD.
5. Sinus node disease with correlation of symptoms with age-inappropriate bradycardia
Class IIa: Permanent pacing is reasonable in the following groups of patients
1. Asymptomatic congenital third-degree AV block over 1 year of age with an average heart rate <50 bpm or
pauses of 2–3 times the basic cycle length
2. Sinus bradycardia in the presence of complex CHD with a resting heart rate of less than 40 bpm or pauses of >3 s
3. Patients with CHD who have impaired hemodynamics as a result of sinus bradycardia or loss of AV synchrony
4. Unexplained syncope in the patient with prior surgery for CHD complicated by transient third-degree AV block
after evaluation to rule out other causes of syncope
5. CHD and sinus bradycardia for the prevention of recurrent episodes of atrial tachyarrhythmias
Class IIb: Permanent pacing can be considered in the following groups of patients
1. Patients who have undergone surgery for CHD who experienced transient postoperative third-degree AV block
and subsequently reverted to sinus rhythm with residual bifascicular block
2. Asymptomatic congenital third-degree AV block with an acceptable rate, a narrow QRS complex, and normal
ventricular function
3. Asymptomatic sinus bradycardia after biventricular repair of CHD with a resting HR of <40 bpm or pauses of >3 s
Class III: Permanent pacing is contraindicated in the following groups of patients
1. Asymptomatic Wenckebach
2. Asymptomatic sinus bradycardia with pauses of <3 s and a minimum HR of >40 bpm
3. Patients who have undergone surgery for CHD who experienced transient postoperative third-degree AV block
and subsequently reverted to sinus rhythm with normal AV conduction
4. Patients who have undergone surgery for CHD who did not experience transient postoperative third-degree AV
block but who develop asymptomatic first-degree AV block or bifascicular block
Adapted from Ref. [1]

if the resting heart rate is less than 70. Other fac- Permanent Pacing as Therapy
tors such as chronotropic competence, the pres- for Tachyarrhythmias Following
ence of pauses, and effort intolerance should be Surgery for Congenital Heart Disease
taken into consideration.
Patients who develop complete AV block as a Some children who have undergone palliative
result of surgery for CHD are at particularly high surgery for CHD develop recurrent atrial
risk of ventricular standstill, regardless of the rate arrhythmias (Fig. 15.3). Some cardiologists
of the escape rhythm. If complete AV block per- advocate the implantation of pacing systems
sists for more than 7 days after surgery, perma- which can be used to overdrive pace these
nent pacing is required. Mobitz Type II AV block arrhythmias. With advances in mapping tech-
also warrants permanent pacemaker implantation nology, radiofrequency ablation of these arrhyth-
(Fig. 15.2). Even if AV nodal function recovers, mias is often possible, removing the need for
there is still a risk of late recurrence of AV block pacing. In most centers, pacing for the treatment
years or decades after surgery. Syncope in this of atrial tachyarrhythmias is reserved for those
group of patients should be considered to be due cases in whom ablation is not possible or
to AV block until proven otherwise. unsuccessful.
Introduction 333

Fig. 15.1 A normal ECG recorded from an infant in sinus rhythm, with a resting heart rate of 137 bpm

Vent. Rate 77 bpm Ref. MD: NM abnormality


PR interval 144 ms Technician: JG
QRS duration 58 ms System Evaluation:
QT/QTC 452/511 ms *** Pediatric ECG analysis ***
P-R-T axes 70/43/56˚ Sinus bradycardia
P duration 82 ms Left axis deviation
RR/PP interval 779/775 ms Possible Left ventricular hypertrophy
Borderline Prolonged QT, may be secondary to QRS

Fig. 15.2 2:1 AV block in an infant. The ventricular rate is well preserved and the QRS complexes narrow, in keeping
with an escape rhythm originating high-up in the His-Purkinje system
334 15 Pacemaker and ICD Implantation in Children

Fig. 15.3 Incessant atrial tachycardia following surgery for congenital heart disease

Table 15.2 Indications for ICD implant specifically in


ICD Indications in Children pediatric patients and patients with CHD
Class I: ICD implant is indicated in the following
We have witnessed an evolution in ICD indica- groups of patients
tions for children. Implants were initially 1. Survivors of cardiac arrest after evaluation to
restricted to survivors of cardiac arrest. We now exclude a reversible cause
implant routinely for hemodynamically unstable 2. Symptomatic sustained VT in association with CHD
after electrophysiological and hemodynamic
VT and for primary prevention in patients per- evaluation
ceived to be a risk of sudden cardiac death (SCD). Class IIa: ICD implant is reasonable in the following
ICDs are considered to be a safe and effective groups of patients
way of preventing SCD in children as well as 1. CHD with recurrent syncope of uncertain origin
adults, but the decision to implant will continue but with ventricular dysfunction or inducible
ventricular arrhythmias at EP study
to involve balancing the risks of SCD versus
Class IIb: ICD implant can be considered in the
those inherent with long-term ICD therapy. following groups of patients
1. CHD with recurrent syncope of uncertain origin
with significant ventricular dysfunction where
Secondary Prevention ICDs thorough invasive and noninvasive investigations
have failed to determine the cause
Class III: ICD implant is contraindicated in the
The current guidelines for secondary prevention following groups of patients
ICDs (survivors of cardiac arrest and patients with 1. As per adult recommendations
documented ventricular arrhythmias) are very sim- Adapted from Ref. [1]
ilar to the adult guidelines (Table 15.2). Whereas
in the adult population the predominant cause of Primary Prevention ICDs
ventricular dysfunction is ischemic heart disease,
in the pediatric population it is CHD with a small It is easy to make the case for ICD implant for
contribution from dilated cardiomyopathy. secondary prevention in young survivors of cardiac
ICD Indications in Children 335

arrest, who have a 30% 1-year risk and a 55% lower than the risk of SCD in adults with coronary
3-year risk of recurrent arrhythmias. The decision disease and advanced left ventricular dysfunction
to implant an ICD on a primary prevention basis in who make up the majority of adult primary pre-
a child is much more difficult. Often the child will vention ICD recipients. As a result it is necessary
have a family member who has died suddenly and for the ICD to be in place for longer to obtain
there is understandable anxiety about the diagno- comparable benefit. The longer life expectancy
sis. This increases pressure on the physician to of pediatric primary prevention ICD recipients
implant a device. counterbalances their lower annual risk.
In children, there is perhaps a greater need to In contrast to the adult population, there is
weigh the potential benefits of lifelong ICD ther- little or no prospective data available to guide the
apy against the undoubted drawbacks, with the
attendant risks of lead fracture, infection, and Table 15.3 Inherited conditions associated with sudden
inappropriate shock therapy. Most children who cardiac death in children and adolescents
receive a primary prevention ICD do so because Long QT syndrome
they have an inherited cardiac condition associ- Catecholaminergic polymorphic VT (CPVT)
ated with an increased risk of arrhythmia Hypertrophic cardiomyopathy
(Table 15.3). The estimated annual risk of sud- Brugada syndrome
den cardiac death in high-risk patients with long- Arrhythmogenic right ventricular cardiomyopathy
QT syndrome (Fig. 15.4) is of the order of 2% (ARVC)
and in hypertrophic cardiomyopathy 3%. This is Dilated cardiomyopathy

Fig. 15.4 Long QT syndrome in a 3-year-old girl who was resuscitated after a cardiac arrest. The corrected QT interval
is 532 ms
336 15 Pacemaker and ICD Implantation in Children

Fig. 15.5 ECG of a patient with complex congenital heart disease. There is right bundle branch block

use of primary prevention ICDs specifically in mization in the pediatric population. This may in
children. At the moment, pediatric indications for part be because heart failure etiology in children
these conditions are identical to adult indications is so heterogeneous. We do not know which of the
(Chap. 17). Children with advanced ventricular many substrates may be amenable to CRT. For
dysfunction, often in the setting of CHD, are at this reason, CRT is often reserved for those
particularly high risk of ventricular arrhythmias. patients in whom medical treatment is failing,
The risks appear to be particularly high in patients prior to cardiopulmonary transplantation. One
with repaired tetralogy of Fallot, d-transposition encouraging study found an average improve-
of the great arteries and severe aortic stenosis. ment in left ventricular ejection fraction of 6%
and an 87% improvement in functional status in a
group of patients in whom 77% had CHD. Patients
Cardiac Resynchronization with single ventricle physiology did particularly
Indications in Children well; it may be that CRT will be used earlier in the
disease process in CHD patients in the future.
Biventricular pacing, or cardiac resynchroniza- In children with two ventricles and a systemic
tion therapy (CRT), is a well-established therapy left ventricle, established adult criteria are
in the adult population, particularly in heart fail- applied. In more complex CHD (systemic right
ure patients with left bundle branch block (LBBB) ventricle and univentricular hearts), there is no
(Chap. 16). LBBB is quite rare in pediatric popu- clear consensus.
lations. Right bundle branch block (RBBB) is The presence of multiple substrates for heart
much more common, especially in children with failure may explain the observation that echo evi-
CHD (Fig. 15.5). dence of mechanical dyssynchrony rather than
There have been no randomized trials investi- QRS duration seems to be the best predictor of
gating patient selection, lead site location or opti- response.
Issues Unique to Device Implantation in Children 337

Fig. 15.6 Redundant loops of atrial


and ventricular leads (curved arrows)
are usually left to allow for somatic
growth in children in the hope of
preventing tension on the leads and
even lead displacement

Issues Unique to Device Implantation lar challenges. Patients who have undergone a
in Children total cavopulmonary (Fontan) correction cannot
usually be paced endocardially. Up-to-date echo
Somatic Growth and pre-procedural MR imaging and the use of
contrast radiology during the procedure improve
Most children continue to grow after their pacing the chance of a successful outcome (Fig. 15.8).
systems have been implanted. Pacing leads need The small number of device procedures per-
to be implanted with large loops of redundant formed in children means that specifically
lead (Fig. 15.6) in order to prevent leads from designed pediatric pacing systems are not avail-
tightening/stretching and possibly displacing as able. Instead, adult equipment must be used. Adult
the child grows (Fig. 15.7). Epicardial leads and pacing leads are relatively large in diameter (6–9F)
defibrillation patches can “strangulate” the heart in comparison to the small vessels found in small
if insufficient slack is allowed. children. Implanting such leads can lead to loss of
the vessel altogether, with resulting symptoms of
venous obstruction (Fig. 15.9). As a result, very
Congenital Heart Disease small children (less than 10–15 kg) are usually
paced epicardially in an attempt to preserve
An increasing number of children are survivors of venous structures for later in life (Fig. 15.10).
surgery for complex CHD, which has palliated Most children receiving cardiac devices will
rather than corrected the underlying circulatory outlive not only their generators but also their
physiology. It is vital that the operator understands leads, and multiple surgeries will inevitably be
the anatomy before embarking on any procedure. required for generator changes and the need for
Univentricular hearts and the presence of atrial replacement and extraction of malfunctioning
baffles placed to redirect bloodflow pose particu- leads (Figs. 15.11 and 15.12).
338 15 Pacemaker and ICD Implantation in Children

Fig. 15.7 Chest X-ray showing a right


ventricular shock lead which has
become taut and partially dislodged
from the right ventricular apex as the
child has grown

Superior vena cava


Hemiazygous vein

Fig. 15.8 Three-dimensional


reconstruction of cardiac
anatomy in a patient being
considered for permanent
pacing. The image is Left atrium
projected in a left sagittal
view. The right atrium and
ventricle are rudimentary. A
left-sided superior vena cava,
the inferior vena cava, and a Right ventricle
hemiazygous vein empty into
Inferior vena cava
the left atrium (Image
courtesy of Dr. T. Bragadeesh
Right atrium
and Dr. D. Bardo)
Device Implantation 339

Fig. 15.9 Digital subtrac-


tion venogram in a patient
with a dual-chamber
pacemaker showing
obstruction of the innomi-
nate vein as it enters the
superior vena cava with
extensive collateralization

Anesthesia

Mobile While permanent pacing in adults is normally


performed under local anesthesia with or without
Supine
sedation, pacing all but the oldest children
requires a general anesthetic, even for simple
procedures such as generator changes and minor
wound revisions. The presence of CHD may
make safe anesthesia a challenge.

Side and Site

Most pacemakers are implanted in the left pecto-


ral region, as this approach is easier for the opera-
tor and more comfortable for the right-handed
patient. CRT-P systems are considerably easier to
implant from the left side. Left-sided ICDs, where
Fig. 15.10 Epicardial pacing system with abdominal the can forms part of the defibrillation circuit,
generator in a child with dextrocardia and complex con- have lower defibrillation thresholds than right-
genital heart disease
sided systems, although right-sided systems do
successfully defibrillate. The choice of site is not
infrequently limited by the site of previous pac-
Device Implantation ing systems, particularly if there has been infec-
tion and the need for extraction (Fig. 15.13).
Implanting an endocardial permanent pacemaker Subpectoral implants are preferred for chil-
or ICD in a child is procedurally similar to an dren, largely for cosmetic reasons but also to
adult implant (Chaps. 7 and 17). The following protect from manipulation, trauma, and possi-
section highlights the important differences bly infection. ICD generators almost always
between adult and pediatric pacing. need to be implanted subpectorally. Subpectoral
340 15 Pacemaker and ICD Implantation in Children

Fig. 15.11 Chest X-rays from a 26-year-old woman with in the RV lead which was replaced. It proved impossible to
corrected transposition of the great vessels, ventricular sep- enter the left subclavian vein which was now occluded and
tal defect, and congenital complete heart block who initially so the lead was inserted via the left internal jugular vein (yel-
underwent permanent pacemaker implantation at 4 years of low arrow) and tunneled subcutaneously over the left clavi-
age at the time of pulmonary artery debanding and VSD clo- cle to the pre-pectoral pocket. The tip of this active-fixation
sure. Left: The surgeon implanted a screw-in lead to the sys- RV lead can be seen to point vertically downwards (green
temic ventricle and sutured an epicardial lead to the surface arrow) – fairly typical of this congenital abnormality. Seven
of the RA – implanting a dual-chamber pacemaker in the left years later, the Kappa™ DDD (Medtronic) was replaced by
subcostal pouch. Four years later, failure to pace necessi- a Sensia™ DDD device (Medtronic) but within 2 years – at
tated implantation of a new endocardial pacing system the age of 26 years – further lead problems required a new
(Minuet™, Medtronic) via the left subclavian vein using endocardial system from the right subclavian vein (right),
active fixation leads to the RA appendage (blue arrow) and using a Medtronic 5592 lead to the RA appendage (orange
anatomical RV apex (red arrow) with redundant loops (black arrow), a Tendril® ST active-fixation lead (St. Jude Medical)
arrows) to allow for somatic growth. Aged 17 years, insula- to the interventricular septum (pink arrow) and an Altrua™
tion break resulted in intermittent loss of sensing and pacing 50 DDDR pacemaker (Boston Scientific)

implants pose a greater surgical challenge at but the surgery involved is more complex and may
the time of generator change, with greater require the presence of a surgeon as well as a car-
scope to damage leads. Leads placed directly diologist. There is a propensity for pacing and
below subpectoral generators may become ICD leads to fracture as they traverse the costal
adherent to the ribs, making extraction extre- margin due to repeated abdominal flexion
mely difficult. Many operators prefer to coil (Fig. 15.15).
the leads superficial to the generator for this
reason.
Generators are implanted in the rectus sheath in Venous Access
very small children, especially if the leads have
been placed epicardially, as the access point and In older children and adolescents, the cephalic
generator are close to one another (Fig. 15.14). vein may be large enough to accept one or two
This provides good protection for the generator, pacing leads. However, it is more usual to insert
Device Implantation 341

Fig. 15.12 Multiple leads in a patient.


This patient has catecholaminergic
polymorphic VT and underwent
implantation of an epicardial system
which has been extracted, leaving
behind the tips of the epicardial pace/
sense leads and a shocking coil in the
subcutaneous tissues. A new right-sided
ICD system has been implanted with an
endocardial shocking lead (green
arrow) and a stand-alone SVC coil in
the left subclavian vein (blue arrow)

Fig. 15.13 Infected pacing system

Fig. 15.14 Abdominal generator implanted in rectus


sheath in an infant
leads using a subclavian approach. Crushing of
the lead under the medial clavicle (Fig. 15.16) is
a not infrequent cause of lead failure and can perform subclavian puncture as laterally as pos-
result in loss of pacing due to conductor fracture sible. Using the extrathoracic subclavian or axil-
(Fig. 15.17) or oversensing in bradycardia devices lary vein (Fig. 15.19) minimizes the risk of lead
and inappropriate shocks due to oversensing with crush and also eliminates the possibility of
ICDs (Fig. 15.18). Many operators try and pneumothorax.
342 15 Pacemaker and ICD Implantation in Children

Epicardial Pacing Systems

When reliable endocardial systems became


available in the 1970s and 1980s, adult pacing
moved away from epicardial systems to endo-
cardial systems. Initial enthusiasm for endocar-
dial systems in children was tempered by the
realization that vessel loss (due to implantation
of large leads in small veins with resulting
thrombosis and occlusion) had major implica-
tions in patients who had a lifetime of pacing
ahead of them. As a result, epicardial systems
are preferred if the patient weighs less than
10–15 kg in order to preserve the endocardial
approach for later in life.
Epicardial systems are also implanted in
children who require open heart surgery for
other reasons, in those in whom anatomy
prevents an endocardial approach (e.g., Fontan
circulation) and if the only ventricle which can
be paced is systemic and there is a perceived
high risk of systemic embolization despite
anticoagulation.
Fig. 15.15 Atrial lead fracture immediately below the
left costal margin in abdominal system in a child several
Epicardial lead implantation requires more
years after the Fontan procedure. This lead fracture is at invasive surgery with sternotomy, thoracotomy, or
the most common site, due to repetitive flexion movements VAT-assisted surgery. Failure rates of epicardial
(Reproduced with kind permission of Silka et al. [2] and bradycardia pacing leads are slightly higher than
the heart rhythm society)

Fig. 15.16 Subclavian “crush.” One of the pacing leads appears thinned as it passes below the clavicle due to damage
to the insulation (blue arrow)
Device Implantation 343

for endocardial leads, although steroid-eluting


epicardial leads mean that the rate of exit block is
comparable. Many surgeons will implant two
ventricular leads so that there is a redundant lead
available in the event that the first lead fails.

Fig. 15.19 Axillary vein puncture

Fig. 15.17 Pacemaker lead fracture

Jan 25, 2010 15:01:06 Jan 25, 2010 15:01:09


9979 Software Version 7.0 9979 Software Version 7.0
ICD Model: Maximo VR 7232 ICD Model: Maximo VR 7232
Copyright Medtronic, Inc. 2003 Copyright Medtronic, Inc. 2003
Serial Number: PRN619862S Serial Number: PRN619862S
VT/VF Episode #81 Report Page 1 VT/VF Episode #81 Report Page 1

ID# Date/Time Type V. Cycle Last Rx Success Duration ID# Date/Time Type V. Cycle Last Rx Success Duration
81 Jan 24 07:44:07 VF 270 ms VF Rx 6 No 4.4 min 81 Jan 24 07:44:07 VF 270 ms VF Rx 6 No 4.4 min

• V-V VF = 320 ms FVT = 260 ms VT = 370 ms


V-V Interval (ms)
2,000 35.1 J 34.8 J 35.2 J No Match 10 % Match 91 % No Match 0 % No Match 10 %
1,700 35.2 J 35.1 J 35.1 J
1,400 4 mV
1,100
800 20 ms
QRS
600 Template
400

200 No Match 7 % No Match No Match 13 % No Match

−30 −20 −10 0 10 20 30 40 50 60 70


Time (s) [0 = Detection]

Fig. 15.18 Inappropriate ICD shock due to lead fracture causing noisy electrogram. The electrogram is interpreted as
VF and a shock is delivered
344 15 Pacemaker and ICD Implantation in Children

Fig. 15.20 PA and lateral chest X-rays of a ventricular pacing lead placed in the right ventricular outflow tract

Active versus Passive stylet. This necessarily weakens the lead and also
Endocardial Leads increases the diameter. One manufacturer has
released a lumenless lead which is delivered
Active fixation leads are preferred by many oper- though a steerable outer catheter akin to an endo-
ators, especially those who also extract leads. cardial LV lead (SelectSecure®, Medtronic, Ltd.).
Unless life expectancy is shortened due to coex- The lead is only 4F and theoretically will have
isting cardiovascular or other disease, it is almost significantly better longevity than a conventional
inevitable that any implanted lead will fail within pacing lead, two factors of key importance in
the lifetime of the child. It is often very difficult children (Fig. 15.22). The lead is difficult to place
to implant new leads alongside old ones due to in patients with distorted anatomy due to the need
venous occlusion. In such situations, one must for a steerable catheter.
make a difficult choice between abandoning the
current site and moving elsewhere and extracting
the failed lead, leaving a channel for a new lead Right Ventricular Lead Placement
on the same side. Extraction of active fixation
leads is possibly easier and lower in risk than Conventionally the right ventricle is paced at
extraction of passive, tined leads. the apex as the trabeculated myocardium found
Active fixation leads also have the advantage there provides good stability for passive fixation
of being able to be placed almost anywhere within leads. Right ventricular apical pacing causes the
the heart, rather than relying on the presence of resulting paced QRS to have a broad left bundle
trabeculated myocardium as is the case with pas- branch block configuration. This leads to inter-
sive leads. This has potential advantages if one is ventricular dyssynchrony and in adults has
trying to maintain physiological ventricular acti- been shown to increase the risk of developing
vation by pacing the interventricular septum heart failure and atrial fibrillation. Pacing the
rather than the apex (Fig. 15.20) or faced with right ventricular outflow tract (RVOT) or mid-
unconventional pacing sites due to the presence interventricular septum is hemodynamically
of CHD (Fig. 15.21). superior to right ventricular apical pacing and
One factor which limits a lead’s life expec- studies are ongoing in adults to see whether this
tancy is the need for a lumen in which to pass the hemodynamic benefit translates to improvement
Device Implantation 345

Fig. 15.21 PA and lateral chest X-rays of a patient with transposition of the great arteries in whom a ventricular pacing
lead has been placed via an ASD into the left ventricle

Fig. 15.22 Left: Medtronic SelectSecure® pacing lead (4F fixed screw lumenless pacing lead). Right: Cut-away steer-
able introducer sheath (Image reproduced with permission of Medtronic, Inc.)

in clinical outcomes. There are no equivalent One Lead or Two?


studies in pediatric populations, although it has
been estimated that RV apical pacing contributes When pacing small children with high-grade AV
to the development of heart failure in approxi- block, there is a necessary compromise between
mately 7% of pacemaker recipients. As a result, keeping a system simple and preserving AV syn-
it is common practice to apply active-fixation chrony. The more leads that are present, the
ventricular leads to the mid-septum or RVOT greater potential problems exist and the higher the
(Fig. 15.20). risk of venous occlusion. However, there is clear
346 15 Pacemaker and ICD Implantation in Children

200 200
Heart rate ( 1 min Avg ) Aberrant beats per minute
HR max. = 183 bpm
180 HR mean = 123 bpm 180

160 160

140 140

120 120

100 100
HR max. = 94 bpm
80 80

60 60

40 40

20 20

0 0
11:00 17:00 23:00 +05:00 +11:00

Arrhythmia criteria :
Pause : ≥ 1.50 s Bradycardia : minimum of 4 beats at ≤ 60 bpm
Dropped beat : ≥ 180% of RR interval SVT : minimum of 5 beats at ≥ 160 bpm
VT : minimum of 5 beats at ≥ 130 bpm Premature aberrant : ≤ 90 % of RR interval
Salvo : minimum of 4 beats Premature normal : ≤ 66 % of RR interval

Fig. 15.23 Holter monitor of physiological heart rate in an 18-month-old patient. The heart rate varies between 94 and
183 bpm

evidence that preserving AV synchrony leads to ventricular arrhythmias (Fig. 15.24). The few chil-
better left ventricular function in the long term. dren with sinus node disease may only require
In the past, VDD leads with an integrated atrial atrial support pacing with a single atrial lead. The
sensing electrode have been implanted. Results function of the AV node is tested at the time of
have been variable but overall seem disappointing. implant by gradually increasing the pacing rate to
Somatic growth leads to movement of the atrial 140 bpm and looking for the presence of
electrode relative to the right atrium and frequently Wenckebach phenomenon. If this phenomenon is
leads to issues with undersensing. Few of these present, it is usual to implant a ventricular lead and
leads are implanted in current practice. Using very a dual-chamber device. In patients with CHD and
low-profile leads, for example, Medtronic sinus node disease, operators usually have a low
SelectSecure® (Fig. 15.22), allows two leads to be threshold for implanting a ventricular lead as there
placed independently. Although such leads have is an increased risk of developing AV block later in
not been available for long enough for long-term life (particularly if there has been cardiac surgery).
data to be available, it is hoped that smaller diam-
eter leads will reduce the risk of venous occlusion
compared to standard diameter leads. Children ICD Device and Lead Issues in Children
who receive ICDs often benefit from the presence
of an atrial lead. Higher sinus rates in children ICD system implantation in teenagers with struc-
mean that there is frequently overlap in the rate of turally normal cardiac anatomy is technically lit-
sinus tachycardia and ventricular arrhythmias tle different than in adults. However, in younger
(Fig. 15.23). Patients with CHD are at increased children and in those with CHD, it may be a
risk of rapid atrial arrhythmias and an atrial lead significant challenge and it is wise to have a strat-
aids discrimination between supraventricular and egy or plan of action involving customized/hybrid
ICD Device and Lead Issues in Children 347

Fig. 15.24 Atrial lead aiding discrimination


between VT and SVT. Upper panel: From top to
bottom there is an atrial intracardiac bipolar
electrogram, a ventricular intracardiac bipolar
electrogram and marker channel. There is a
regular ventricular rhythm with more ventricular
than atrial events indicating VT. Lower panel:
From top to bottom there is a surface electrogram,
atrial intracardiac bipolar electrogram, ventricular
bipolar intracardiac electrogram, and marker VF Rx 1 Defib

channel. There is a slow, slightly irregular


ventricular rhythm. The atrial rate is rapid and 3−AUG−2004
5: 41
Lead− I
Atrial EGM
Vent EGM
(10 mm/mV)
GUIDANT
25
F11

slightly irregular and subsequent electrophysi-


ological study showed it to be an atrial tachycardia
arising from a pulmonary vein

AS (AS) (AS) AS (AS) (AS) AS (AS) AS AS (AS) AS AS


195 190 185 188 193 185 190 188 168 195 185 188 19
AS) (AS) AS (AS) (AS) AS (AS) (AS) (AS) (AS) (AS) (AS) (AS)
85 183 185 188 185 188 193 183 193 200 183 183 175
VS VS VS VS
5 VS 655 VS 623 VS 473 VS 468
423 468 750 620

techniques if necessary in order to achieve the


best outcome. The problems of body size, growth,
activity, and the need for future device and lead
insertion/replacement must be considered. An
important fact to remember is that defibrillator
pace/sense/shock leads are of a more complex
structure than bradycardia pacing leads and as a
result are more prone to damage at the time of
implant and subsequently.

Epicardial Patches and Leads

As ICD leads tend to be bulky, their size lim-


its their use to children over 15 kg. Children
under this weight require the placement of epi-
cardial patches and/or subcutaneous arrays for
defibrillation (Fig. 15.25), either alone or in com-
bination with an endocardial pace/sense lead. Fig. 15.25 Subcutaneous ICD arrays in a child with long
Various ingenious alternatives to endocardial sys- QT syndrome. An epicardial pace/sense lead is in place
tems have been devised to preserve venous struc- together with subcutaneous arrays for shocking. An endo-
cardial atrial lead has been placed at a later date to enable
tures, including conventional leads placed in the atrial support pacing
pericardium for pacing and sensing (Fig. 15.26)
or epicardial pacing/sense leads placed via vid-
eoscopic techniques via a small subxiphoid inci- procedure and for this reason epicardial systems
sion. Such lead placements are likely to have are almost exclusively used in secondary preven-
lower defibrillation thresholds than subcutane- tion cases. Epicardial patches can in theory lead
ously placed leads. The placement of epicardial to pericardial constrictive physiology, although
patches requires a more prolonged, more invasive in practice this seems to be relatively rare.
348 15 Pacemaker and ICD Implantation in Children

Fig. 15.26 Pericardial ICD lead in a 3.5-year-old child Fig. 15.27 Endocardial single coil lead placed in a
with CHD and dilated cardiomyopathy using a trans- 3-year-old. The shock coil is within both right ventricle
venous design ICD lead placed in the posterior pericar- and right atrium
dium, DDD epicardial pacing leads, and subcutaneous
coil in the left lateral chest wall. The lead seen in the right
into the right atrium, this can lead to shunting of
pleural space is the pace/sense portion of the ICD lead,
which is capped because the epicardial pacing leads are current away from the ventricular myocardium
used for sensing and pacing in this configuration and an increase in defibrillation threshold.
(Reproduced with kind permission of Berul [3] and the Choosing a lead with a shorter coil and short coil/
Heart Rhythm Society)
tip spacing can alleviate these difficulties.

Subclavian Crush
Lead Diameter
It is particularly important to avoid subclavian
crush, as in addition to the risk of failure to sense Conventional ICD shock leads are 9F in diameter,
or pace, there is a risk of inappropriate shocks. which poses significant problems in smaller chil-
Partial fracture of the pace/sense portion of the dren, such as venous occlusion. Newer leads have
lead results in repeated “make/ break” potentials been developed which are smaller in diameter, for
which are detected by the device and interpreted example, 7F Durata (St Jude Medical) (Fig. 15.28).
as ventricular fibrillation (Fig. 15.16). Multiple Although initial enthusiasm has been tempered by
inappropriate shocks may lead to lasting psycho- the realization that certain smaller diameter leads
logical damage. may be more prone to early failure, for example,
Sprint Fidelis (Medtronic) and RiataTM (St. Jude
Medical), the perceived benefits of a lower profile
Coil Spacing lead mean that many implanters prefer them.

In smaller children, the shock coil portion of the


leads can extend into the right atrium, traversing T-Wave Oversensing
the tricuspid valve (Fig. 15.27). As the coil is much
stiffer than a conventional pacing lead, this can Many pediatric ICD recipients have long QT
lead to fouling of the tricuspid valve and significant syndrome. Significant QT prolongation can lead
tricuspid regurgitation. If the shock coil overrides to T-wave oversensing and double counting of
ICD Device and Lead Issues in Children 349

Fig. 15.28 St. Jude Medical


7F Durata® active-fixation
ICD shock lead (Image
provided courtesy of St. Jude
Medical, ©2008 St. Jude
Medical, Inc.)

ventricular sensed events (Fig. 15.29). It is difficult to extract, as the SVC coil becomes
important to assess for the presence of this phe- adherent to the SVC. Extraction has the potential
nomenon at implant as it is very difficult to pro- for tearing of the SVC with resulting massive
gram around. bleeding. If the defibrillation threshold is high
with a single coil lead, a stand-alone SVC coil can
be implanted.
Potential Future Extraction

Complex ICD leads are more likely to fail than Subcutaneous Defibrillators
conventional bradycardia leads. The coil tends to
become closely adherent to the myocardium Subcutaneous “leadless” ICDs have been devel-
making extraction a challenge. The Gore™ oped, where there are no endocardial or epicardial
expanded PTFE-coated leads, for example, components; instead, a lead for sensing and
Endotak Reliance G/SG (Boston Scientific Ltd.), defibrillation is placed subcutaneously and con-
prevent ingrowth of tissue into and around the nected to a generator placed in the rectus sheath or
coils and theoretically make extraction easier pectoral region. These devices have the advantage
(Fig. 15.30). that the venous system is preserved without the
need to perform sternotomy to place epicardial
patches. The energy required to defibrillate from a
Single Versus Dual Coil Leads subcutaneous array is higher than for endocardial
leads or epicardial patches. This makes the devices
Somatic growth places more strain on ICD leads larger than conventional ICDs and limits their use
than on bradycardia pacing leads, as the coil in smaller children. In addition, they cannot pro-
moves as well as the pace/sense portion of the vide permanent bradycardia pacing or antitachy-
lead. Single coil leads are usually chosen as the cardia pacing, although they can provide
spacing of the coils in adult-sized dual-coil leads temporary post-shock pacing. These factors have
means that the SVC coil is usually in the neck or limited the take-up of subcutaneous devices in
pocket. Dual-coil leads are also much more children.
350 15 Pacemaker and ICD Implantation in Children

Fig. 15.29 T wave oversensing in an ICD. The patient is rate and the ICD interpreting the rhythm as VF. The device
in slow VT (the ventricular rate is faster than the atrial begins to charge but the oversensing terminates and the
rate) which self-terminates. The T waves are oversensed shock is aborted
(arrows), leading to double counting of the ventricular

Advantages and Disadvantages


of Lead Route Options

The advantages and disadvantages of the various


routes for ICD insertion are shown in Table 15.4.

Placing Endocardial Leads in Patients


with Congenital Heart Disease Fig. 15.30 Gore™-coated shock coils in the Endotak
Reliance® lead (Boston Scientific Ltd.) (©2010 Boston
Access to the right ventricle may be hampered by Scientific Corporation/affiliates. All rights reserved. Used
with permission of Boston Scientific Corporation)
the presence of congenital heart defects, for
example, tricuspid atresia, or by interventions a Fontan circulation effectively prevents access
designed to palliate congenital lesions, for exam- to the right heart from the venous system, in other
ple, Fontan procedure and atrial baffles. Although situations it is often possible to pass a lead into a
Choice of Device 351

Table 15.4 Advantages and disadvantages of the various routes for ICD lead placement
Route Advantages Disadvantages
Transvenous Easy insertion, common use Lead fractures, venous occlusion/obstruction, lead
insertions may be difficult in CHD, lead extractions
may be difficult
Subcutaneous array Minimally invasive, no trans- Higher DFT, little long-term data
or coil venous coil, no epicardial patch
Pericardial lead Low DFT, no transvenous coil, no Surgical procedure, adhesions may make visualization
epicardial patch with VAT system difficult, little long-term data
Epicardial patch Good DFT, long-term data Surgical procedure, patch failure, possible constrictive
pericarditis may develop
Subcutaneous No transvenous or epicardial Higher DFT, no pacing or antitachycardia pacing
leadless ICD access required minimally invasive facility

chamber and secure it well enough to provide traction can be identified using echocardiography
permanent pacing. The use of active-fixation (speckle tracking) or by using the latest ventricu-
leads, steerable stylets and introducers, venogra- lar activation as a surrogate. Standard coronary
phy as well as a thorough prior understanding of sinus sites are limited by venous anatomy and for
the anatomy helps ensure a successful outcome. this reason many operators place epicardial leads
Placing a permanent pacing lead into a systemic electively, particularly if surgery is being con-
chamber (e.g., pacing the left ventricle via a septal templated for other reasons.
defect in a patient with tricuspid atresia) is often pos-
sible as an alternative to epicardial pacing. It is impor-
tant to weigh the perceived risks of thromboembolism Choice of Device
against the need for sternotomy. Lifelong anticoagu-
lation is mandatory in such situations. Size
Pacing unconventional sites increases the risk
of phrenic nerve stimulation and it is important to Most modern pacemakers are between 8 and
test for this with high output pacing during the 11 cc in volume. They provide sophisticated fea-
implant procedure. tures including automatic capture management,
Chapter 14 discusses more extensively the rate response, rate drop response, and algorithms
topic of device implantation in patients with car- to minimize ventricular pacing (see below).
diac structural abnormalities. Smaller pacemakers are available for very small
children, for example, Microny® (St Jude
Medical) (Fig. 15.31). Opting for a smaller pace-
Lead Placement in Pediatric maker usually requires some sacrifice in terms of
CRT Recipients features, for example, single chamber only.
The different ICDs that are available tend to
Placing left ventricular leads by the conventional be of a similar volume (around 30 cc) but vary in
coronary sinus route may pose a significant chal- shape, some being wide and flat, for example,
lenge in pediatric patients, especially those with Teligen® (Boston Scientific Ltd.) (see Fig. 17.7)
CHD. Smaller hearts and guide catheters with and others shorter and wider, for example,
adult-sized curves make access to the coronary Secura™ DR/VR and Maximo DR/VR
sinus difficult. A steerable electrophysiology cath- (Medtronic Ltd.) (Fig. 15.32). The choice of
eter over a straight guide catheter may be helpful. device will depend on the intended implantation
Siting the LV lead at the site of latest contrac- site. At the time of generator change it is often
tion appears to result in the best improvement in helpful to replace like with like to save having to
left ventricular function. The site of latest con- refashion the pocket.
352 15 Pacemaker and ICD Implantation in Children

Pacing Modes sensing in those with a scarred right atrium and


changing lead position as the child grows have
Pacing that restores or preserves AV synchrony is virtually confined this system to history. In con-
preferable particularly in those with ventricular trast to adults, some young patients with isolated
dysfunction. Although single-lead VDDR sys- SND (often due to cardiac surgery) do not require
tems have been widely used to provide effective dual-chamber pacing and AAI pacing can be
restoration of AV synchrony, problems of atrial used if 1:1 AV conduction is maintained at heart
rates >140/min. AAIR pacing is also preferable
to DDD pacing in patients with ventricular
dysfunction.

Pacing Modes to Avoid RV Pacing

As well as avoiding right ventricular apical pac-


ing by pacing elsewhere in the right ventricle, it is
also possible to minimize right ventricular pacing
by the use of proprietary algorithms. Most mod-
ern pacemakers include an algorithm which either
progressively extends the AV delay, for example,
Search AV® (Medtronic Ltd.), or mode switches
between AAI and DDD mode, for example,
Managed Ventricular Pacing® (Medtronic Ltd.)
(Fig. 15.33). The more sophisticated algorithms
command a significant price premium, but work
Fig. 15.31 Microny K® pacemaker weighs 12.8 g, is 6 mm
thin, and has a volume of 5.9 cc (Image provided courtesy of very well in patients who have sinus node disease
St. Jude Medical, ©2008 St. Jude Medical, Inc.) alone or only intermittent AV block. Although

Fig. 15.32 Secura™ DR and Maximo™ DR ICDs (Image reproduced with permission of Medtronic, Inc.)
Choice of Device 353

AAI(R) Mode

Back up V pace in
the event of
Wenckebach

Switch to DDDR if
AV conduction
does not recover

Fig. 15.33 Managed ventricular pacing (MVP™) algorithm. This algorithm switches between AAI(R) and DDD(R)
pacing depending on intrinsic AV conduction (Image reproduced with permission of Medtronic, Inc.)

the majority of pediatric pacemaker recipients Current ICD longevity is significantly shorter
have permanent complete AV block, many ICD than for bradycardia pacing systems (4–5 years).
recipients do not and these algorithms are now Unlike the pacing population, many ICD recipi-
found integrated into most ICDs. ents have structurally normal hearts and, apart
from their arrhythmia, should have a normal life
expectancy. However, multiple generator changes
Longevity are likely. When programming ICDs in children,
care must be taken to extend the longevity of the
There is little to choose between most modern device as much as possible, for example by mini-
pacemakers in terms of longevity. Most have pro- mizing unnecessary bradycardia pacing.
jected working life spans of 6–8 years. Epicardial
leads often have higher thresholds and this affects
device longevity. Many pacemakers automatically MR Compatibility
measure pacing threshold and adjust the pacing
output to just above this. In this way, the life span Magnetic resonance imaging is rapidly emerging as
of the device can be increased by a few months. the investigation of choice for cardiac disease and
354 15 Pacemaker and ICD Implantation in Children

CHD as well as a huge number of noncardiac con- adults. Growth may lead to tension on leads and
ditions. Although there are theoretical issues with eventual displacement.
movement, local heating, loss of pacing, and dam-
age to the generator, with appropriate precautions,
many modern pacemakers can enter an MR scanner Lead Fracture
with only a very small risk of problems. Nevertheless,
there is often profound reluctance by radiology Lead fractures are more common in the pediat-
departments to allow patients with pacemakers and ric pacing population than in the adult popula-
ICDs into the scanning room. tion (see Fig. 15.17). One series suggests that
Medtronic Ltd. has developed an MR-safe 15% of bradycardia pacing leads in pediatric
pacemaker (SureScan™ MRI) and MR-safe bra- cases failed over an average follow-up of
dycardia pacing leads. If a child is likely to need 6.2 years. Twenty-eight percent of patients will
MR scanning, one could reasonably make an experience multiple lead failures. The factors
argument for implanting such a device. At the associated with lead fracture include age
time of writing, no MR-safe ICD had been <12 years at implant, a history of CHD, and an
released. epicardial lead.
Many pediatric pacemaker recipients, particu-
larly those with complete heart block, become
Upper Rate profoundly pacemaker-dependent. Syncope may
suggest incipient lead failure and requires prompt
The upper rate (sensed and sensor driven) of most evaluation.
pacemakers is 200 bpm. This is less than the max-
imum predicted heart rate of many young chil-
dren who receive pacemakers. At high levels of Infection
exertion, upper rate behavior (pacemaker
Wenckebach) will occur. It is important to use a System infection is not uncommon in the pediat-
pacemaker with a high upper rate and program ric pacing and ICD population. Infection affects
the upper rate as high as possible in small chil- 3–5% of those receiving new implants, com-
dren, as increases in cardiac output in young chil- pared to 0.5–1% of adults. This may reflect more
dren depend on increases in heart rate rather than invasive procedures, for example, epicardial sys-
stroke volume. tems, complex anatomy with long procedure
times or low-volume operators. Infection almost
always requires complete removal of a system
Remote Follow-up Capability with reimplant at a later stage on the contralat-
eral side.
Pediatric patients often receive their device in a ter-
tiary center many miles from their home. Pacemaker
follow-up may require long journeys. Some newer Adjuncts to Standard Follow-Up
pacemakers and most ICDs can be followed up
remotely via a remote telephone/internet link, Poorly functioning or inadequately programmed
reducing the need to travel for very frequent fol- pacing systems may produce symptoms which
low-up appointments. This is important if there are children may find more difficult than adults to
concerns over lead integrity or arrhythmias. describe. Prolonged monitoring or exercise test-
ing can often be helpful. Some pacemakers have
a Holter monitor feature which can be activated
Pacemaker Follow-Up by the application of an external magnet (magnet
application triggers electrogram storage rather
Problems identified during follow-up are than fixed rate pacing) which can be useful to
significantly more frequent in children than in diagnose the cause of infrequent symptoms.
Choice of Device 355

Fig. 15.34 Self-terminating ventricular tachycardia in a child with long-QT syndrome. The device detects ventricular
tachycardia and is charging when the episode spontaneously terminates

Ventricular Arrhythmias sinus tachycardia and ventricular tachycardia


using electrogram morphology and rate of onset.
Patients with CHD, especially those who have The presence of an atrial lead also helps rhythm
undergone surgical repair for Fallot’s tetralogy, discrimination. It may be necessary to prevent
may be prone to ventricular arrhythmias. Syncope sinus tachycardia pharmacologically, for exam-
in such patients, if not due to device malfunction, ple, by beta blockade.
should prompt a thorough evaluation. Most pace- Supraventricular arrhythmias occur in 30% of
makers can be programmed to automatically patients with CHD and should ideally be antici-
store electrograms during ventricular high-rate pated before inappropriate shocks are delivered.
episodes. This feature should be programmed Drugs and ablation should be considered as well
“on” if possible. as device reprogramming.

ICD Programming and Follow-Up Detection Duration

All patients, but particularly children, find shock Monomorphic VT is a much less common indi-
therapy distressing. It is considered good practice to cation for ICD in children than in adults.
program ICDs to prevent unnecessary shocks when- Polymorphic VT, torsades de pointes VT and VF
ever possible. As in adults, programming anti- are more frequently the indication. Very often
tachycardia pacing results in a substantial reduction ventricular arrhythmias are self-terminating and
in appropriate shock therapy with no observable asymptomatic. Shock therapy in such situations
delay in shock delivery if ATP fails – even if the can and should be avoided by programming long
ventricular arrhythmia is very rapid. Most ICDs detection intervals (Fig. 15.34).
now permit the delivery of ATP during charging.

Failure Rate of ICD Leads


Detection Rate and Epicardial Patches

The default rate for the VF zone in many ICDs is Perhaps due to their more complex construction,
188 bpm. Most teenagers and all younger chil- ICD leads and patches appear to have a substan-
dren regularly achieve sinus rates of over tially higher failure rate than bradycardia pacing
190 bpm. It is usually necessary to program leads. In one study, system failure rates were 27%
higher detection zones in children than in adults. at 1 year, 45% at 2 years, and 51% at 3 years.
If this is not possible, for example if there is a Epicardial patches had three times the failure rate of
ventricular arrhythmia which occurs at physio- endocardial leads. In patients who receive such sys-
logical heart rates, ICDs can distinguish between tems, regular and frequent follow-up is required.
356 15 Pacemaker and ICD Implantation in Children

In conclusion, from a pacing and device point tion as children. Many of these patients will pose
of view, children are not “small adults.” In the a considerable challenge in terms of lead compli-
pacing population, there is a high incidence of cations and frequent surgical intervention.
congenital heart disease and there are significant
differences in cardiac physiology between chil-
dren and adults, even in normal hearts. Pacing
and ICD hardware has been designed principally References
with adults in mind and this means that frequently
1. Epstein AE et al. ACC/AHA/HRS 2008 Guidelines for
some ingenuity is required when implanting and
Device Based Therapy of Cardiac Rhythm abnormali-
following up devices. There is still an unaccept- ties. J Am Coll Cardiol 2008; 51:e l–62.
ably high failure rate for systems, particularly 2. Silka MJ et al. Pacemakers and implantable cardioverter-
ICDs. This may improve with the introduction of defibrillators in pediatric patients. Heart Rhythm.
2006;3:1360–6.
newer lead technology. It seems highly likely that
3. Berul C Defibrillator Indications and Implantation in
cardiologists will encounter increasing number young children. Heart Rhythm. 2008;5:1755–7.
of adult patients who underwent device implanta-
Cardiac Resynchronization Therapy
16

Heart failure can potentially complicate all forms III–IV), left ventricular ejection fraction (LVEF),
of heart disease. Over the last 20 years, there has etiology, and wide QRS complex. The latter is
been a significant increase in both its incidence most commonly present in the form of left bundle
and prevalence due to the advancing age of the branch block (LBBB), which occurs in one quarter
population and improved survival from coronary to one third of patients with heart failure. It is usu-
heart disease – the principal cause of heart failure. ally associated with delayed depolarization and
Despite improvements in pharmacologic manage- contraction of the left ventricular free lateral wall,
ment, many patients with heart failure have severe, whereas the interventricular septum contracts nor-
resistant symptoms and their prognosis remains mally resulting in paradoxical septal motion.
poor. Medical therapy consists of angiotensin con- Hence, patients with heart failure and altered elec-
verting enzyme inhibitors (ACEI), aldosterone trical depolarization manifest further mechanical
antagonists, and b-blockers, all of which have been cardiac pump failure with a resultant deterioration
shown to reduce morbidity and mortality. Digoxin in symptoms and prognosis. Currently, four cate-
and loop diuretics provide symptomatic benefit gories of electromechanical dyssynchrony are rec-
only. More recently, however, prospective random- ognized in heart failure. These are prolonged AV
ized clinical trials have shown that cardiac resyn- delay, interventricular delay, intraventricular delay,
chronization therapy (CRT), also known as and the most recently described intramural delay.
biventricular pacing, results in improvements in In its simplest form, the concept of CRT is to
LV function, exercise capacity, quality of life and simultaneously depolarize both right and left
mortality in selected patients with heart failure. ventricles, thereby correcting electromechanical
This chapter will describe the rationale for CRT, dyssynchrony, and in turn enhance ventricular
the features that predict a potential benefit from contraction.
CRT, the technique of implantation and the equip-
ment required for the procedure, the complications
that may occur, the follow-up that is required, and Indications for CRT
finally, the evidence that currently exists that sup-
ports its use. CRT is indicated for patients with advanced cardiac
failure (NYHA Class III–IV despite medical treat-
ment) due to systolic dysfunction (LVEF £ 35%)
Rationale for CRT with intraventricular conduction delay (generally
LBBB, QRS duration >120 ms) and mechani-
Many clinical and laboratory variables predict cal LV dyssynchrony. These have been recom-
mortality in patients with advanced heart failure mended by the ACC/AHA in their Guidelines
including severity of symptoms (NYHA class for Heart Failure Treatment (2005). The recently

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 357


DOI 10.1007/978-1-4471-2939-4_16, © Springer-Verlag London 2012
358 16 Cardiac Resynchronization Therapy

Sinus Rhythm Permanent AF Need for Pacing

NYHA III/IV(amb.) NYHA II NYHA III/IV(amb.) NYHA III/IV NYHA II

EF ≤ 35% EF ≤ 30% EF ≤ 35% EF ≤ 35% EF ≤ 35%

LBBB Non- LBBB Non- QRS ≥ 120ms any QRS any QRS
LBBB LBBB
Slow V rate or
QRS ≥ QRS ≥ QRS ≥ QRS ≥ Post AVN ablation or
120ms ≤ 60bpm at rest &
150ms 130ms 150ms ≤ 90bpm on ex.

Class Class Class Class Class Class Class


IA IIa A I A IIa A IIb C IIa C IIb C

CRT-P CRT-P Preferably Preferably CRT-P CRT-P CRT-P


CRT-D CRT-D CRT-D CRT-D CRT-D CRT-D CRT-D

Eur Heart J. 2012 All patients under Optimal Pharmacological Therapy & life expectancy > 1 year

Fig. 16.1 ESC HF Guidelines 2012: CRT Summary

released ESC Heart Failure Guidelines advocate necessitates AV node ablation but can occasion-
the use of CRT in less severe heart failure patients ally be achieved with high-dose-rate-limiting
(NYHA II) with a stress on LBBB morphology medication with drugs such as b-blockers or
rather than just QRS duration (figure 16.1). CRT digoxin. In order to achieve simultaneous ven-
has been shown to restore synchrony within the tricular depolarization, pacing leads must be
impaired LV, to equilibrate energy consumption positioned to pace both the right and left ventri-
and improve LV performance and to reduce mitral cles. Right ventricular (and atrial) pacing can be
regurgitation, which in turn result in improved achieved as previously described in Chap. 7.
long-term clinical outcomes. Although one might expect that LV pacing
In patients with sinus rhythm, simultaneous would necessitate direct arterial access or a
ventricular depolarization can be triggered by trans-septal puncture and the resultant risk of
atrial sensing and the use of a short AV delay. In severe complications, it can be achieved by plac-
such cases, CRT may correct AV, interventricu- ing the lead in the coronary sinus (CS) via the
lar, and intraventricular conduction delays. The right atrium.
resultant improvement in left ventricular systolic
contraction may then be associated with an
improvement in intramural delay. Selecting Cases for CRT
Similar benefits may be achieved in patients
with atrial fibrillation, provided that the intrinsic Currently, most device specialists use the current
heart rate can be suppressed to a slower rate than guidelines for selecting suitable patients for
that programmed in the device. This usually CRT, which include LV electrical dyssynchrony
Technique 359

based on a QRS duration of >120 ms. However, echocardiography (RT3DE). However, evidence
approximately 30% of patients fail to show a to support these claims is currently lacking.
favorable response to CRT and much work has Finally, it is useful to know the site and extent
been carried out to try and identify more specific of transmural myocardial scars in order to ensure
determinants of CRT response. Three major fac- that the LV lead is not placed at these sites and
tors appear to be important. These are the pres- that an optimum outcome from CRT can be real-
ence and severity of LV dyssynchrony, the ized. Techniques for assessing myocardial scar
position of the LV lead in relation to the area of include gadolinium contrast-enhanced MRI,
LV with the latest mechanical activation, and the echocardiographically measured regional wall
extent and location of LV scar tissue. end-diastolic wall thickness (<5 mm), integrated
Echocardiography may be useful for evaluating backscatter imaging, myocardial contrast
these three issues. Other imaging modalities echocardiography (areas of nonenhancement),
such as MRI have been used with some success and low-dose dobutamine stress echocardiogra-
in scar mapping. phy, which can all identify areas of the myocar-
In heart failure patients, cardiac dyssyn- dium to be avoided if at all possible.
chrony may be atrio-ventricular (between atria Ideally, the presence of significant LV
and ventricles), inter-ventricular (between RV mechanical dyssynchrony, an LV lead position
and LV), or intra-ventricular (within LV). It is concordant with the latest mechanically acti-
of paramount importance to obtain A-V syn- vated segment and low amount of myocardial
chrony to optimize LV filling and stroke vol- scar, provides the highest likelihood of a favor-
ume but estimates of LV filling time using able response to CRT. Studies suggest that a
pulse-wave Doppler transmitral flow record- QRS width of >150 ms seems to predict response
ings do not predict a favorable response follow- (with a heavy bias toward LBBB). More
ing CRT although may be of use for optimizing recently, the presence of RBBB or indetermi-
CRT response during follow-up. In contrast, nate bundle branch block rather than LBBB has
estimates of inter-ventricular and intra-ventric- shown to be a predictor of “nonresponse” in
ular dyssynchrony appear to be predictive of these patients. Unsurprisingly other adverse
response to CRT and likely long-term clinical predictors in CRT include atrial
outcome. fibrillation, pulmonary hypertension, renal dys-
Estimates of inter-ventricular dyssynchrony function, and diabetes mellitus. This has been
are based on the “inter-ventricular mechanical reflected in the recent ESC heart failure guide-
dyssynchrony index.” The time-intervals between lines 2012.
the onset of the QRS complex to the onset of the
pulmonary and aortic ejection periods (pulmo-
nary and aortic pre-ejection times) are measured. Technique
Significant inter-ventricular dyssynchrony is sug-
gested by a difference of >40 ms between the two Preparation of the patient for CRT pacemaker
pre-ejection times and predicts favorable out- implantation is as described in Chap. 7. However,
come after CRT. Tissue Doppler imaging (TDI) two or three leads need to be inserted. Three sub-
can provide other indices that are similarly clavian vein punctures may be used (Fig. 16.2) or
predictive. two subclavian vein punctures and a cephalic
Assessment of LV dyssynchrony may be the vein may be used (Fig. 16.3). A splittable safe-
best method for evaluating candidates who are sheath with a hemostatic valve is used for venous
likely to benefit the most. These echocardio- access to the CS to prevent excessive blood loss
graphic parameters include the septal: posterior and air embolism (see below). If the patient is in
wall motion delay (SPWMD) assessed by sinus rhythm, besides inserting leads into the RA
M-mode echocardiography, TDI techniques, 2D and RV, a third lead needs to be placed into the
speckle tracking imaging, and real-time 3D CS usually in a posterolateral branch vein where
360 16 Cardiac Resynchronization Therapy

Fig. 16.2 Two or three


leads will need to be inserted
depending on whether the
patient is in sinus rhythm or
not. If three leads are
required, three subclavian/
axillary vein punctures can
be made

the activation delay is generally most pronounced


(Fig. 16.4). This has been shown to provide the
best hemodynamic result from CRT, although not
necessarily the best clinical response. In atrial
fibrillation, only a RV and LV lead are necessary.
Given the proximity of the CS os to the right bun-
dle, the possibility of “bumping” the right bundle
during catheter manipulation may result in com-
plete heart block in a patient with underlying
LBBB. It is thus generally sensible to place the
RV (and RA lead, if necessary) lead first before
placing the LV lead into the CS and one of its
branches, so that in an emergency the RV lead
can be used to pace the ventricle.

Cannulating the Coronary Sinus/


Positioning the LV Lead

Entering the CS may be easy and straightforward,


but can be impossible. The membranous Thebesian
valve close to the CS ostium may make it difficult
to enter the CS with a catheter and Vieussen’s
valve at the ostium of the primary posterolateral
vein at the junction of the CS and great cardiac
Fig. 16.3 Alternatively, two subclavian vein punctures vein may make it difficult to advance the catheter
and a cephalic vein cut-down may be chosen within the CS.
Technique 361

Fig. 16.4 Chest X-ray shows typical lead positions in the Fig. 16.5 A specially designed sheath or catheter is used
RA, RV, and coronary sinus (LV) in a patient undergoing to enter the coronary sinus and demonstrate the coronary
CRT venous anatomy using injection of contrast agent. (Single
arrow) Great cardiac vein; (Double arrow) posterolateral
cardiac vein; (Triple arrow) middle cardiac vein
The CS is initially cannulated usually with a
specially designed sheath or catheter and the CS
and coronary venous anatomy demonstrated by of equipment for accessing the CS and then opti-
contrast injection (Figs. 16.5 and 16.6). These mal LV lead stimulation while avoiding blood
catheters are used in conjunction with a hemo- loss (Fig. 16.12). Steerable/selective catheters
static valve to facilitate safe manipulation of a are also available, for example, SafeSheath
guidewire and enable injection of contrast agent Worley Telescopic Braided lateral vein intro-
(see below). Various delivery sheaths are avail- ducer (LVI) (Fig. 16.13) and a wide variety of
able of different diameters (5F–7F) and shapes catheters and telescopic systems are available
for accessing the CS (Fig. 16.7). Some implant- from the device companies (Figs. 16.14 and
ers use a coronary angiography catheter or 16.15). Biotronik offer their Streamer, Selectra
deflectable EP catheter to cannulate the CS and and ScoutPro® series. The left ventricular lead
the sheath is then advanced into the CS body may then be inserted down the sheath and posi-
using the catheter as a railing system. Once the tioned in a suitable epicardial vein – if necessary
CS is cannulated, a standard balloon occlusion with the aid of a sub-selective catheter and con-
catheter (Fig. 16.8) may be inserted and retro- trast injection (Figs. 16.16 and 16.17). The
grade venography performed using hand-injected sheaths have different methods of removal (split-
contrast agent to define the exact anatomy ting, slitting, and over the lead removal)
(Figs. 16.9–16.11). It is preferable to perform a (Figs. 16.18 and 16.19). The ultimate lead posi-
prolonged injection for image acquisition in order tion is accepted on the basis of obtaining adequate
to fully define the anatomy as several branches pacing parameters and stability as with any other
and, in particular, the middle cardiac vein may pacing lead. Stability within the CS is best
fill late. The SafeSheath® CSG® Pressure secured by having as many points of contact with
Products™ Inc. provides a comprehensive range the endothelial lining as possible and is aided by
362 16 Cardiac Resynchronization Therapy

Fig. 16.6 The top two images show placement of the arrow) (right). The bottom two figures show contrast filling
coronary sinus sheath (left) (arrow) and delineation of the of the posterolateral (left) vein (open arrow) and placement
coronary venous anatomy by contrast injection (blue of the LV lead into a distal position (right) (arrow)

Fig. 16.7 A range of different-shaped catheters/sheaths


are available for accessing and delineating the coronary
venous anatomy and for delivering LV leads
Technique 363

Fig. 16.8 Balloon occlusion catheter for use in the coro-


nary sinus while performing retrograde venography. (Top)
Balloon catheter – deflated balloon at tip (arrow); (Bottom)
Close-up of inflated balloon

Fig. 16.9 Coronary sinus (CS) balloon catheter placed


inside ostium of CS. Balloon (arrow) is inflated to occlude
the CS and enable contrast delineation of the great cardiac
vein and its branches and aid placement of the LV lead
into a stable position (curved arrow) with good sensing
and pacing characteristics
364 16 Cardiac Resynchronization Therapy

Fig. 16.10 Coronary sinus contrast injection shows the


main body of the CS (single arrow) and the middle car-
diac vein (twin arrows)

Fig. 16.11 The top two images show delivery of the LV bility was unacceptable. The bottom two images show
lead through the coronary sinus via the great cardiac vein repositioning of the LV lead into the posterolateral vein
and into an anterolateral vein. However, the electrical sta- with acceptable sensing and pacing
Technique 365

Fig. 16.12 SafeSheath® accessories reduce blood loss


during positioning of the LV lead and facilitate LV cathe- Fig. 16.13 SafeSheath® Worley superselective/steerable
ter manipulation without risk of air embolism. The safe introducer system for accessing distal branches of the
adaptor is used at the distal end of the LV catheter to facil- coronary venous system
itate use of contrast via the side port and manipulation of
the guidewire within the catheter itself

Fig. 16.14 A variety of different shaped sheaths available left) CPS Venture™ Wire Control Catheter has a deflectable
for accessing the coronary sinus and its branches for LV lead tip for steering guidewires during left heart vein subselection.
delivery from St. Jude Medical. (Top left) CPS Aim™ Slittable (Bottom right) CPS Luminary™ Cannulator is a bideflectable
Inner Catheter Subselector enhances access to first vein catheter with a lumen for cannulation of the coronary sinus
choice through Direct-to-Target™ placement. (Top right) and subselection of target vein (Images provided courtesy of
CPS Direct ™ SL Slittable Outer Guide Catheter designed for St. Jude Medical, ©2008 St. Jude Medical, Inc.)
coronary sinus access and left heart lead delivery. (Bottom
366 16 Cardiac Resynchronization Therapy

Fig. 16.15 (Top left) Medtronic’s equipment include the vessel subselection; (bottom left) Attain Prevail™ steer-
range of Attain Command™ coronary sinus cannulation able catheter for delivery of LV leads; (bottom right)
catheters; (top middle) Attain® deflectable catheter deliv- Attain Select® II Left Heart delivery system (Image repro-
ery system for changing tip shapes of a single guide cath- duced with permission of Medtronic, Inc.)
eter; (top right) Attain Select™ guide catheters for aiding

utilizing leads with pre-shaped curves leads may be deployed using both techniques
(Fig. 16.20), spiral formations (Figs. 16.21 and applied sequentially. With the stylet in the distal
16.22), and other fixation mechanisms. tip of the lead, the lead is stiff and straight, but as
Unfortunately pre-shaped leads have reduced the stylet is withdrawn, the lead assumes its shape
tracking ability within the coronary sinus and with a curve on the end. After the lead is placed
this can make delivery to the desired target into the proximal vein segment using the stylet, it
difficult. To overcome this, the tips of CS leads is then advanced into the target branch by the
have valve-like structures permitting a guidewire OTW technique. Using a conventional 0.014″
to be placed through the central lumen of the angioplasty guidewire, the OTW technique is
lead, producing an “over the wire” lead to aid particularly useful in tortuous veins and veins
delivery in a manner akin to a coronary artery with a sharp-angled course. Leads may have
stent or angioplasty balloon (Fig. 16.23). “tines” to aid stability but the absence of trabecu-
Occasionally it is necessary for an operator to lae within the coronary venous system limits
negotiate tortuous CS anatomy or even venous their value. Although most “fixation” is achieved
stenosis (Fig. 16.24). Hence, skills and tech- by simply wedging the tip of the lead in the distal
niques acquired in the catheter laboratory can be segment of the branch vein or by anchoring the
put to good use in the pacing theater. The use of lead against the wall of the vein using a fixed
balloon venoplasty to dilate stenosed target “spiral” or “J” shape of the distal end of the lead,
branches has been described (Fig. 16.25). the StarFix® LV lead has a unique mechanism for
Leads can either be placed using the stylet or helping it to fix itself against the vein’s wall
by the “over the wire” (OTW) technique. Some which is useful for veins of larger diameter
Technique 367

Fig. 16.17 Coronary sinus venogram enables careful


Fig. 16.16 (Top left) X-ray showing the telescopic coro- placement of the LV lead (arrow) into the anterior inter-
nary sinus catheter system (green arrow) used to reach ventricular vein
and delineate the distal anterior interventricular vein (3
arrows) (middle left) and enable placement of the LV lead
(open arrows) (bottom left)
368 16 Cardiac Resynchronization Therapy

Fig. 16.18 Slitting of


LV sheath. Note
stabilization of LV lead in
order to prevent
displacement

Fig. 16.19 Slitting tool

Fig. 16.20 Medtronic’s over-the-wire LV leads. (Top)


Bipolar Model 4194; (Bottom) Unipolar Model 4193.
These have steroid-eluting tips to minimize threshold
peak, angled distal ends for steerability and stable fixation,
a tip seal for allowing guidewire reinsertion without blood
ingress, guidewire or stylet delivery and availability in
three lengths – 78, 88 and 103 cm (Image reproduced with
permission of Medtronic, Inc.)
Technique 369

Fig. 16.21 (Left) The Acuity® Spiral LV lead uses the


spiral shape to help fix the lead once it has been placed in
the desired branch coronary vein by delivering it over a
guidewire. (Right) the Acuity® Steerable IS-1 LV lead has Fig. 16.23 Fluoroscopic image showing an LV lead
a J-shaped tip to aid positioning and enhance stability. The placed in the anterior vein with leads in the RA and RV
tip is deflectable with the aid of a stylet but can be deliv- apex
ered over-the-wire (©2010 Boston Scientific Corporation/
affiliates. All rights reserved. Used with permission of
Boston Scientific Corporation)
bias fixation lead for stability in larger veins
(Easytrak®3 LV lead) (Fig. 16.27).
The caliber of the target vein relative to the
diameter of the lead is another important aspect
of lead selection. Stiff, thick leads (>1.5 mm) can
be placed safely in large straight veins with a
diameter of more than 3.5 mm, whereas thin dis-
tally pre-bent leads may not be stable in these
vessels and lead displacement with loss of cap-
ture may occur. These leads are more suited for
narrow or kinked and tortuous veins. Thick leads
might also traumatize the venous endothelium
with resulting vessel occlusion due to thrombosis
Fig. 16.22 Easytrak® LV leads from Boston Scientific or dissection.
Ltd. have an over-the-wire design, steroid-eluting tips,
The success rate of the transvenous approach
uni- or bi-polar configurations and tines to reduce lead
displacement (©2010 Boston Scientific Corporation/ has improved during the last decade from 90% to
affiliates. All rights reserved. Used with permission of 95%. This represents greater operator experience
Boston Scientific Corporation) over a steep learning curve and the availability of
superior implanting equipment. The most com-
(Fig. 16.26). Boston Scientific offers a steerable mon reasons for unsuccessful left ventricular
LV lead with a deflectable “J-shaped” tip implants include the inability to access the CS,
(Acuity®Steerable), a spiral LV lead for extra sta- acute dislodgment or unstable lead position, and
bility (Acuity®Spiral LV lead), a bipolar lead electrical issues with lead threshold and phrenic
with silicone tine fixation and over-the-wire nerve stimulation. What can be done in these sit-
delivery (Easytrak®2 LV lead), and a 3-D helical uations is discussed below.
370 16 Cardiac Resynchronization Therapy

Fig. 16.24 (Upper left) This image shows the coronary distal venous anatomy. The lateral vein is shown to have a
sinus sheath entering the small cardiac vein (arrow) in this severe stenosis (red arrow). (Lower middle) The telescopic
patient with a dual chamber ICD already in situ. (Upper inner sheath (green arrow) is used to select the branch with
middle) This shows the sheath (arrow) in the CS after con- the aid of a guidewire (arrow). (Lower right) Once the
trast injection. (Upper right and lower left) A balloon cath- branch is selected the guidewire can be removed and the LV
eter (green arrow) occludes the CS and demonstrates the lead inserted. The arrows show local dissection of the CS

Testing After Lead Positioning twitch threshold should always be measured


and Completing the Procedure during CRT implantation, and unless there is a
considerable margin over the pacing threshold in
Once the lead position is acceptable, the R wave case of lead microdisplacement, the risk of dia-
amplitude, the lead’s pacing threshold, and its phragmatic stimulation postoperatively is a real
impedance should be measured. Before anchor- possibility. Diaphragmatic stimulation should not
ing the lead using the suture collar and a nonab- occur when pacing at 10 V. When all leads have
sorbable suture, the lead’s stability should be been secured using nonabsorbable sutures (such
checked by ensuring pacing is steady at 1 V out- as Ethilon™) around the collars provided on the
put during deep breathing/coughing. Occasionally leads, the biventricular device can be attached to
higher thresholds than this have to be accepted. the leads using the screwdriver provided, and the
Moreover, because the posterolateral vein is in device and leads buried in the pre-pectoral pocket.
close proximity to the phrenic nerve, lead stimu- The wound can then be closed in layers, with
lation can result in diaphragmatic stimulation and absorbable, nonbraided sutures such as
uncomfortable twitching for the patient. The Monocryl™ to the subcutaneous tissue and
Technique 371

Fig. 16.25 (Left) A severe stenosis is found in the target to dilate the stenosis (arrow). The subselective guide
branch of the coronary sinus (arrow); (right) a 2.0 mm catheter is clearly visible in the coronary sinus (open
Sprinter balloon over a 0.014″ BMW guidewire is used arrow)

Fig. 16.26 Attain StarFix® (Medtronic) is the first active Fig. 16.27 LV leads from Boston Scientific. From left to
fixation LV lead with exclusive deployable lobes allowing right: Acuity® Steerable IS-1, Easytrak® 3 and Easytrak®
for customized lead placement in a wide variety of vein 2 and Acuity® Spiral (©2010 Boston Scientific
sizes and locations (Image reproduced with permission of Corporation/affiliates. All rights reserved. Used with per-
Medtronic, Inc.) mission of Boston Scientific Corporation)
372 16 Cardiac Resynchronization Therapy

Fig. 16.28 Chest X-ray


shows leads placed in the RA,
RV septum and an LV lead
placed in the postero-lateral
vein

Fig. 16.29 PA and lateral chest X-rays showing typical positions of actively-fixed RA and RV outflow tract leads and
a LV lead passively placed in posterior branch of the coronary sinus

subcuticular layer and Dermabond® glue to the A 12-lead ECG should be recorded and this
skin edges. shows characteristic features of biventricular
Before discharge from hospital, a PA and lateral pacing with a shortish AV delay and predomi-
chest X-ray should be performed to confirm sat- nantly positive complexes in lead V1 and/or neg-
isfactory positions for the implanted leads and no ative complexes in lead 1 (Figs. 16.31 and
evidence of pneumothorax (Figs. 16.28–16.30). 16.32).
CRT Devices and LV Leads 373

CRT Devices and LV Leads that offer both CRT pacing and defibrillation
(CRT-D) (Figs. 16.37–16.42). Some of these
CRT Devices devices are listed in Table 16.1. CRT systems
consist of a pulse generator plus two or three leads
A range of devices for CRT are now available – RV/LV or RA/RV/LV. The RV lead is typically
from several manufacturers. They are generally placed about midway on the RV septum, and the
divided into those devices which offer CRT pac- LV lead into a coronary vein via the coronary
ing only (CRT-P) (Figs. 16.33–16.36) and those sinus. The RA lead is as for a conventional pace-
maker. A CRT-D device uses a RV defibrillation
lead. The LV lead is unique to CRT systems and
does not usually have a fixation mechanism (see
below). It is anchored in place because of its dis-
tal geometry or a spiral shape of its distal end.
These modern devices have extensive and
sophisticated programmability (Fig. 16.43), for
example, independent channel programmability,
possess patient-centric diagnostics, for example,
activity log, heart rate variability monitor (Figs. 16.44
and 16.45), and have the ability to be interrogated
remotely, for example, using the Latitude® home
monitoring system (Boston Scientific Ltd.).

LV Leads

A range of LV leads for implanting into the


Fig. 16.30 Lateral chest X-ray shows the anterior place-
ment of the RA and RV leads and the posterior placement cardiac venous system via the coronary sinus
of the coronary sinus lead are available from the various pacemaker

Fig. 16.31 ECG in a patient pre CRT-P implantation shows sinus rhythm but a wide QRS complex of LBBB
374 16 Cardiac Resynchronization Therapy

Fig. 16.32 ECG after CRT-P implantation shows ventricular pacing with a narrow QRS complex

Fig. 16.33 Contak® Renewal™ TR CRT-P device


(Guidant Ltd.) (©2010 Boston Scientific Corporation/
affiliates. All rights reserved. Used with permission of
Boston Scientific Corporation)

Fig. 16.34 InSync® III CRT-P device (Image reproduced


with permission of Medtronic, Inc.)
CRT Devices and LV Leads 375

Fig. 16.35 The Frontier™ II and Anthem™ RF CRT-P


devices (Images provided courtesy of St. Jude Medical,
©2008 St. Jude Medical, Inc.)

Fig. 16.36 Stratos LV-T CRT-P device (Courtesy of


Biotronik)

Fig. 16.37 InSync Maximo™, InSync Marquis™ and


InSync II Marquis™ CRT-D devices (Image reproduced
with permission of Medtronic, Inc.)
376 16 Cardiac Resynchronization Therapy

Fig. 16.39 The Concerto™ CRT-D device (Image repro-


duced with permission of Medtronic, Inc.)

Fig. 16.38 Cognis™ 100-D CRT-D device is small and


thin and can deliver 41 J shocks. The stored data is easily
printed out on interrogation (©2010 Boston Scientific
Corporation/affiliates. All rights reserved. Used with per-
mission of Boston Scientific Corporation) Fig. 16.40 The Livian® CRT-D device (©2010 Boston
Scientific Corporation/affiliates. All rights reserved. Used
with permission of Boston Scientific Corporation)
CRT Devices and LV Leads 377

provide more pacing vectors, allowing more


options and greater control in minimizing implant
complications such as diaphragmatic stimulation
and high pacing thresholds.

Complications

The complications of biventricular pacemaker


implantation (Table 16.3) include those associ-
ated with conventional pacing (see Chap. 12) and
those specifically related to the positioning of the
LV lead. The latter include failure to deploy the
LV lead, phrenic nerve stimulation, CS dissection
or perforation, and embolic phenomena.
Fig. 16.41 The Lumax 340 HF-T CRT device (Courtesy
of Biotronik) The coronary venous anatomy precludes suc-
cessful LV lead placement in up to 15% of cases.
This may be due to absence of an appropriate
lateral branch, anomalous drainage into the left
atrium, stenosis or a vessel of insufficient caliber
obstructing passage of the lead. However, the
major technical problem encountered is the
inability to locate and enter the CS with the guid-
ing catheter. The anatomy may be distorted in
dilated hearts increasing the difficulty. Although
once the guide catheter has engaged the CS, it is
rare, with the newer technologies available, not
to be able to enter the target branch vessel.
However, occasionally it proves impossible to
advance a guidewire because of acute angulation
or stenosis. Early displacement may occur – par-
ticularly during guide catheter removal. The lead
displacement risk is dependent upon several
factors including the position and type of lead
used, the angle of the opening of the CS, and the
experience of the operator. Lead dislodgement
results in late failure of LV capture in 5–10% of
cases.
Fig. 16.42 The Promote™ + CRT-D device seen next to The more serious procedural complications
the Current™ + ICD device (Images provided courtesy relate largely to the use and manipulation of the
of St. Jude Medical, ©2008 St. Jude Medical, Inc.) guiding catheters within the heart. Serious
arrhythmias occur in up to 5% of all implanta-
manufacturers. These are listed in Table 16.2. tions. For example, guide catheter manipulation
Recently, quadripolar leads have been produced, may cause right bundle branch block, and in those
for example, Quartet™ (St. Jude Medical), with a patients