Managing Pacemaker-Related
Complications And Malfunctions
In The Emergency Department
September 2014
Volume 16, Number 9
Authors
Jennifer Martindale, MD
Assistant Professor, Department of Emergency Medicine, Kings
County Hospital/SUNY Downstate Medical Center, Brooklyn, NY
Ian S. deSouza, MD
Assistant Professor, Department of Emergency Medicine, Kings
County Hospital/SUNY Downstate Medical Center, Brooklyn, NY
Abstract
The use of implanted pacemaker devices is increasing worldwide,
owing to technological advances, new indications, and an aging
population. Despite greater experience in implantation and improved device sophistication, patients continue to face complications associated with hardware implantation and device malfunction. This review summarizes current indications for permanent
pacing, reviews epidemiologic data relevant to implant complications, and describes a clinical approach to the patient with potential pacing malfunction. The electrocardiographic diagnosis of
hyperkalemia and acute myocardial infarction in paced rhythms
is also discussed. Potential sources of electromagnetic interference
and special considerations pertaining to the cardiac resuscitation
of patients with implanted cardiac devices are reviewed. Finally,
a basic approach to implanted cardioverter-defibrillator devices
(which often accompany pacemaker devices) is presented.
Peer Reviewers
William J. Brady, MD
Professor of Emergency Medicine and Medicine, Chair,
Medical Emergency Response Committee, Medical Director,
Emergency Management, University of Virginia Medical Center,
Charlottesville, VA
Joshua M. Kosowsky, MD, FACEP
Vice Chair for Clinical Affairs, Brigham and Women’s Hospital,
Boston, MA; Assistant Professor, Harvard Medical School,
Boston, MA
CME Objectives
After reading this article, participants should be able to:
1. State the indications for pacemaker placement and cardiac
resynchronization therapy.
2. Anticipate the major complications of pacemaker
implantation.
3. Develop a differential diagnosis for pacemaker
malfunction.
4. Develop an approach to patients who are shocked by their
implanted cardiac devices.
Prior to beginning this activity, see “Physician CME Information”
on the back page.
Editor-In-Chief
Andy Jagoda, MD, FACEP
Professor and Chair, Department of
Emergency Medicine, Icahn School
of Medicine at Mount Sinai, Medical
Director, Mount Sinai Hospital, New
York, NY
Associate Editor-In-Chief
Kaushal Shah, MD, FACEP
Associate Professor, Department of
Emergency Medicine, Icahn School
of Medicine at Mount Sinai, New
York, NY
Editorial Board
William J. Brady, MD
Professor of Emergency Medicine
and Medicine, Chair, Medical
Emergency Response Committee,
Medical Director, Emergency
Management, University of Virginia
Medical Center, Charlottesville, VA
Mark Clark, MD
Assistant Professor of Emergency
Medicine, Program Director,
Emergency Medicine Residency,
Mount Sinai Saint Luke's, Mount
Sinai Roosevelt, New York, NY
Peter DeBlieux, MD Professor of Clinical Medicine,
Interim Public Hospital Director
of Emergency Medicine Services,
Louisiana State University Health
Science Center, New Orleans, LA
Nicholas Genes, MD, PhD
Assistant Professor, Department of
Emergency Medicine, Icahn School
of Medicine at Mount Sinai, New
York, NY
Michael A. Gibbs, MD, FACEP
Professor and Chair, Department
of Emergency Medicine, Carolinas
Medical Center, University of North
Carolina School of Medicine, Chapel
Hill, NC
Steven A. Godwin, MD, FACEP
Professor and Chair, Department
of Emergency Medicine, Assistant
Dean, Simulation Education,
University of Florida COMJacksonville, Jacksonville, FL
Gregory L. Henry, MD, FACEP
Clinical Professor, Department of
Emergency Medicine, University
of Michigan Medical School; CEO,
Medical Practice Risk Assessment,
Inc., Ann Arbor, MI
John M. Howell, MD, FACEP
Clinical Professor of Emergency
Medicine, George Washington
University, Washington, DC; Director
of Academic Affairs, Best Practices,
Inc, Inova Fairfax Hospital, Falls
Church, VA
Charles V. Pollack, Jr., MA, MD,
Scott Silvers, MD, FACEP
Chair, Department of Emergency
FACEP
Medicine, Mayo Clinic, Jacksonville, FL
Professor and Chair, Department of
Emergency Medicine, Pennsylvania
Corey
M. Slovis, MD, FACP, FACEP
Hospital, Perelman School of
Professor and Chair, Department
Medicine, University of Pennsylvania,
of Emergency Medicine, Vanderbilt
Philadelphia, PA
University Medical Center, Nashville,
Michael S. Radeos, MD, MPH
TN
Assistant Professor of Emergency
Stephen H. Thomas, MD, MPH
Medicine, Weill Medical College
George Kaiser Family Foundation
of Cornell University, New York;
Professor & Chair, Department of
Research Director, Department of
Emergency Medicine, University of
Emergency Medicine, New York
Oklahoma School of Community
Hospital Queens, Flushing, NY
Medicine, Tulsa, OK
Ali S. Raja, MD, MBA, MPH
Ron M. Walls, MD
Director of Network Operations and
Professor and Chair, Department of
Business Development, Department
Emergency Medicine, Brigham and
of Emergency Medicine, Brigham
Women’s Hospital, Harvard Medical
and Women’s Hospital; Assistant
School, Boston, MA
Professor, Harvard Medical School,
Boston, MA
Scott D. Weingart, MD, FCCM
Associate Professor of Emergency
Robert L. Rogers, MD, FACEP,
Medicine, Director, Division of
FAAEM, FACP
ED Critical Care, Icahn School of
Assistant Professor of Emergency
Medicine at Mount Sinai, New Medicine, The University of
York, NY
Maryland School of Medicine,
Baltimore, MD
Shkelzen Hoxhaj, MD, MPH, MBA
Chief of Emergency Medicine, Baylor
College of Medicine, Houston, TX
Alfred Sacchetti, MD, FACEP
Assistant Clinical Professor,
Eric Legome, MD
Department of Emergency Medicine,
Chief of Emergency Medicine,
Thomas Jefferson University,
King’s County Hospital; Professor of
Philadelphia, PA
Clinical Emergency Medicine, SUNY
Downstate College of Medicine,
Robert Schiller, MD
Brooklyn, NY
Chair, Department of Family
Medicine, Beth Israel Medical
Keith A. Marill, MD
Center; Senior Faculty, Family
Research Faculty, Department of
Medicine and Community Health,
Emergency Medicine, University of
Icahn School of Medicine at Mount
Pittsburgh Medical Center, Pittsburgh,
Sinai, New York, NY
PA
Senior Research Editors
James Damilini, PharmD, BCPS
Clinical Pharmacist, Emergency
Room, St. Joseph’s Hospital and
Medical Center, Phoenix, AZ
Research Editor
Michael Guthrie, MD
Emergency Medicine Residency,
Icahn School of Medicine at Mount
Sinai, New York, NY
Federica Stella, MD
Emergency Medicine Residency,
Giovani e Paolo Hospital in Venice,
University of Padua, Italy
International Editors
Peter Cameron, MD
Academic Director, The Alfred
Emergency and Trauma Centre,
Monash University, Melbourne,
Australia
Giorgio Carbone, MD
Chief, Department of Emergency
Medicine Ospedale Gradenigo,
Torino, Italy
Amin Antoine Kazzi, MD, FAAEM
Associate Professor and Vice Chair,
Department of Emergency Medicine,
University of California, Irvine;
American University, Beirut, Lebanon
Hugo Peralta, MD
Chair of Emergency Services,
Hospital Italiano, Buenos Aires,
Argentina
Dhanadol Rojanasarntikul, MD
Attending Physician, Emergency
Joseph D. Toscano, MD
Medicine, King Chulalongkorn
Chairman, Department of Emergency
Memorial Hospital, Thai Red Cross,
Medicine, San Ramon Regional
Thailand; Faculty of Medicine,
Medical Center, San Ramon, CA
Chulalongkorn University, Thailand
Suzanne Y.G. Peeters, MD
Emergency Medicine Residency
Director, Haga Teaching Hospital,
The Hague, The Netherlands
failure have translated into an increasing number
of biventricular pacing systems with integrated
ICD technology. While pacemakers have become
more complex and sophisticated, patients continue
to present to the emergency department (ED) with
symptoms related to device malfunctions. In addition, special considerations with regard to implanted
pacemakers are relevant to the diagnostic workup of
comorbid illnesses.
Case Presentations
An ill-appearing 74-year-old woman is brought in on a
stretcher by EMS personnel who broke down her door
to find her slumped on her couch. Her temperature is
normal, her blood pressure is 86/40 mm Hg, and her heart
rate is 42 beats/min. On the cardiac monitor, you see
extremely wide QRS complexes following pacer artifacts
and intermittent pauses where pacing artifacts appear
alone. A prior ECG shows a paced rhythm and narrower
QRS complexes. What are your critical actions?
A 38-year-old woman who fainted in the grocery
store is wheeled into the last unoccupied room in your ED
with a cardiac monitor. She has cardiac sarcoidosis and
has a DDD pacemaker that was implanted 6 months ago.
She tells you that this is the third time she has fainted in
the past 24 hours. She is normotensive and her heart rate
is 48 beats/min. The cardiac monitor shows pacing artifacts that are completely dissociated from QRS complexes.
What steps will you take to diagnose the underlying cause
of this patient’s recurrent syncopal episodes?
Epidemiology
Implanted pacemakers are increasingly prevalent in
the United States.1 Approximately 370,000 pacemakers are placed annually,2 the most common indication
for which is sinus node disease.3 Regardless of the
indication for pacing, dual-chamber pacemakers have
been adopted as the technology of choice. However,
since United States Food and Drug Administration
(FDA) approval in 2001, CRT devices are being implanted more frequently.4 Most of these are combined
with defibrillation technology, and CRT-defibrillator
(CRT-D) devices have come to comprise approximately 40% of all pacemakers in the United States.5
Compared with the general population, patients
receiving implanted devices are older (mean age of
implantation of 75.6 years) and carry a higher burden
of age-adjusted comorbid illness.1,6
Introduction
Cardiac pacemakers have evolved from singlechamber devices that deliver a fixed pacing rate to
multichamber systems with programmable features
that preserve and more closely mimic normal cardiac electrophysiology. Preservation of atrioventricular synchrony, physiologic heart rate, and interventricular synchrony are significant improvements
that have been made possible with dual-chamber,
rate-adaptive, and biventricular pacing systems. For
patients, improved quality of life, increased exercise
tolerance, and decreased disease progression are
among the clinical outcomes driving new indications
for pacemaker implantation and cardiac resynchronization therapy (CRT). At the same time, mortality
benefits associated with implanted cardioverterdefibrillator devices (ICDs) in patients with heart
Critical Appraisal Of The Literature
PubMed and the Cochrane Database of Systematic Reviews were searched for English-language
articles pertaining to the management of patients
with implanted pacemakers and cardiac devices
published between January 1, 1990 and February
21, 2014. Search terms included permanent pacemakers and the thematic topics of pacemaker complications, cardiac resynchronization therapy, pacemaker
malfunction, and electromagnetic pacemaker interfer-
Table 1. American College of Cardiology/American Heart Association Classification Of
Recommendations And Level Of Evidence
Certainty of Treatment Effect
A
Recommendations derived from multiple randomized clinical trials or meta-analyses
B
Data derived from a single randomized clinical trial or nonrandomized studies
C
Only consensus opinion of experts, cases studies, or standard of care
Size of Treatment Effect
Class I
Conditions for which there is evidence and/or general agreement that the test is useful and effective
Class II
Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness or efficacy of performing the
test
Class IIa
Weight of evidence/opinion is in favor of usefulness or efficacy
Class IIb
Usefulness or efficacy is less well established by evidence/opinion
Class III
Conditions for which there is evidence and/or general agreement that the test is not useful or effective and in some cases may be
harmful
Copyright © 2014 EB Medicine. All rights reserved.
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www.ebmedicine.net • September 2014
ence. The bibliographies of review articles were
hand-searched and the level of evidence graded according to the guidelines from the American Heart
Association Task Force on Practice Guidelines.
(See Table 1, page 2.) Guidelines published by
the American College of Cardiology Foundation/
American Heart Association (ACCF/AHA), the
Heart Rhythm Society (HRS), the European Heart
Rhythm Association (EHRA), and the European
Society of Cardiology (ESC) were also reviewed.7-11
the left ventricular lead depends on cardiac venous
anatomy, avoidance of phrenic nerve stimulation,
and location of myocardial scar.
Pacemaker Modes
A 5-letter code has been adopted to identify different types of pacemakers. (See Table 2.) The first
letter corresponds to the lead location. The second
letter corresponds to the chamber (or chambers)
being sensed by the pacemaker. The third letter indicates the response of the pacemaker to a
sensed impulse. The fourth letter indicates the
pacemaker’s programmability and capacity for rate
modulation. A pacemaker capable of rate modulation (R) is also capable of communicating with
external telemetry (C) and multiprogrammability
(M), in which 3 or more variables can be modified.
Pacemakers capable of rate modulation mimic the
rate response of a normal sinus mode when physiological changes are detected by sensors for minute
ventilation, QT interval, or stroke volume. In 2002,
the code was revised to include a fifth letter indicating whether multisite pacing is present in the
atrium, the ventricle, or both.16 Emergency clinicians are most likely to encounter pacers that are
AAIR, VVIR, DDD, and DDDR.17
Review Of Normal Pacemaker Function
Components And Lead Placement
The basic components of a pacemaker are the pulse
generator and the lead. The pulse generator consists of hardware, programmable software, and a
battery with a 5- to 10-year lifespan. The longevity
of any battery depends on the proportion of paced
and sensed events, stimulation impedance, and
programmed output. Lead components include a
conductor, electrode, fixation mechanism, terminal
connector pin, and insulation. The connector pin
connects the lead to the generator and must be well
seated in the connector block of the generator for the
device to function.
Atrial leads are most commonly positioned
in the right atrial appendage. Selective site pacing
in the right atrial septum may be chosen to suppress atrial fibrillation. Right ventricular leads are
traditionally placed in the right ventricular apex;
however, pacing from this site has been shown to
result in ventricular dyssynchrony and subsequent
impairment in left ventricular function.12-15 Right
ventricular leads may be placed in the right ventricular outflow tract (RVOT) or interventricular septum
to minimize these effects, but evidence to support
improved outcomes from selective site pacing in
the RVOT is contested. The left ventricular lead of
a biventricular pacing system is placed through
the coronary sinus into one of its tributaries, in an
epicardial location along the posterior or lateral
free wall of the left ventricle. The final position of
Pacemaker Indications
The indications for permanent pacing are continually amended and are categorized by type of underlying conduction disorder or disease process. The
ACC/AHA/HRS guidelines for the use of cardiac
pacemakers, ICDs, and CRT were most recently
published in 2008,8 with a focused revision on the
indications for CRT published in 2013.7 In general,
class I recommendations apply in cases of symptomatic impaired conduction. With regard to asymptomatic conduction abnormalities, class I recommendations apply in disorders or diseases that are likely
to progress. For more information about the classes
and levels of evidence for the indications for permanent pacing, see Figure 1, page 4 for the URL and
QR code to access the PDF of the full guidelines.
Table 2. The North American Society For Pacing And Electrophysiology/British Pacing And
Electrophysiology Group Generic Pacemaker Code
I
II
III
IV
V
Chamber(s) paced
Chamber(s) sensed
Response to sensing
Programmability, rate modulation
Multisite pacing
A = Atrium
V = Ventricle
D = Dual (A + V)
O = None
A = Atrium
V = Ventricle
D = Dual (A + V)
O = None
T = Triggered
I = Inhibited
D = Dual (triggered + inhibited)
O = None
P = Simple programmable
M = Multiprogrammable
C = Communicating
R = Rate modulation
O = None
A = Atrium
V = Ventricle
D = Dual (A + V)
O = None
Reprinted from Emergency Medicine Clinics Of North America. Volume 24, Issue 1. Theodore C. Chan, Taylor Y. Cardall. Electronic Pacemakers.
Pages 179-194, Copyright 2006, with permission from Elsevier.
September 2014 • www.ebmedicine.net
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Reprints: www.ebmedicine.net/empissues
of the infarcted area. Patients with atrioventricular
block and impaired intraventricular conduction after
myocardial infarction (MI) have a high likelihood of
mortality that most likely relates to extensive myocardial necrosis rather than impaired conduction.
Patients with anterior infarction and impaired systolic
dysfunction should be considered for CRT.
Sinus Node Dysfunction
Pacemakers are placed in patients with symptomatic sinus node dysfunction in order to reduce the
frequency of syncopal episodes and the risk of
stroke and atrial fibrillation. Sinus node dysfunction
includes sinus bradycardia, sinus arrest, sinoatrial
block, chronotropic incompetence, atrial tachycardia, and atrial fibrillation. The preferred pacemaker
mode in patients with sinus node dysfunction is
DDDR. Dual-chamber pacing in patients with sick
sinus dysfunction has been associated with reduced
pacemaker syndrome symptoms, reduced atrial
fibrillation, and improved exercise capacity compared with single-chamber pacing.18,19 Pacemaker
syndrome manifests as intolerance to ventricular
pacing in the absence of atrioventricular synchrony
and will be discussed in more detail on page 9. In
patients with preserved atrioventricular conduction,
AAIR pacing may be a cost-effective choice to minimize unnecessary ventricular pacing. Subsequent
atrioventricular block is a concern factored into the
choice of device and develops at an annual rate of
1.4% after atrial pacemaker implantation.20
Cardiac Resynchronization Therapy
Systolic heart failure is accompanied by prolonged
intraventricular conduction in approximately 30% of
patients.23 Delayed conduction results in further reduction of systolic function, ventricular remodeling,
and functional mitral regurgitation. Ventricular dyssynchrony, defined by a prolonged QRS duration, is
associated with increased mortality in patients with
heart failure.24 CRT improves ventricular dyssynchrony by pacing from leads in both right and left
ventricles. In patients with heart failure, improved
electromechanical synchrony has been shown to induce reverse ventricular remodeling, decrease mitral
regurgitation, decrease neurohormonal activation,
and improve peak oxygen consumption.
Results from several landmark studies have led
to the established role of resynchronization therapy
in treating heart failure. Initial randomized studies
were designed to focus on functional outcomes of
CRT. They demonstrated improved quality of life,
New York Heart Association (NYHA) functional
classifications for heart failure, exercise tolerance,
and left ventricular ejection fraction.5,25,26 Later
studies demonstrated improved morbidity (unplanned hospitalizations) and mortality outcomes in
CRT patients with NYHA Class II,27-29 III, or IV30,31
heart failure. However, improved outcomes are not
universal; approximately 10% to 40% of patients
are nonresponders, depending on how response is
defined functionally.32 Research aimed at defining
the subgroups most likely to benefit from CRT has
been incorporated into the most recent indications
for CRT.7 (See Table 3, page 5.) According to a
meta-analysis, the morbidity and mortality benefits
of CRT are limited to patients with QRS duration
≥ 150 msec.33 Moreover, patients with left bundle
branch block (LBBB) morphology have also been
Acquired Atrioventricular Block
Pacing is recommended for patients with thirddegree block and type II second-degree atrioventricular block to reduce syncope and improve survival.
The indication for pacemaker placement in type I
second-degree atrioventricular block is more controversial. Guidelines are based on whether the patient is
symptomatic and on the exact location of the block as
it relates to the likelihood that the disease will progress
to complete heart block. (See Figure 1.) Dual-chamber
pacing is recommended over ventricular pacing to
reduce the incidence of pacemaker syndrome.
Chronic Bifascicular Or Trifascicular Block
Syncope is common in patients with bifascicular
and trifascicular block, but the risk of progression to
complete heart block and death varies based on the
presence of atrioventricular block. In the absence of
atrioventricular block, the indication for pacemaker
placement depends on the presence of prolonged
His-ventricular (H-V) intervals during electrophysiologic study.
Figure 1. Indications For Permanent Pacing
After Acute Myocardial Infarction
New-onset atrioventricular block in the acute
setting of ST-segment elevation myocardial infarction (STEMI) usually resolves spontaneously within
days.21 Temporary pacing is recommended in the
setting of acute STEMI for patients with symptomatic
bradycardia that is unresponsive to medical treatment (class I, level of evidence [LOE] C).22 In the
acute phase of inferior STEMI, atrioventricular block
is more often mediated by increased vagal tone; in
anterior STEMI, the development of atrioventricular or intraventricular block is related to the extent
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shown to have greater benefit than those with nonLBBB conduction abnormalities, including right
bundle branch block (RBBB) and nonspecific intraventricular conduction delay.34
rogation can be performed. Patients should be asked
for dates of implantation and revision; if and when
programming changes were made; and about a history
of exposure to any electromagnetic interference, blunt
trauma, or environmental extremes. A complete list
of medications should be obtained, as some drugs can
alter pacing thresholds.
Pacemaker-related symptoms should be reviewed with the patient. These include light-headedness, palpitations, syncope, sense of slowed or
racing heart, and extracardiac muscle twitching.
Neurocardiogenic Syncope And Carotid Sinus
Syndrome
The role of pacemaker therapy in neurocardiogenic
syncope is controversial, as the evidence supporting its use is mixed. Open-label trials have demonstrated a decrease in syncopal events,35-37 while 2
double-blinded placebo-controlled trials (total of 129
patients) have failed to demonstrate any benefit.38,39
The alleged benefit of pacemaker therapy in
carotid sinus syncope is based solely upon observational studies40-42 and open-label randomized
trials.43,44 In a double-blind, placebo-controlled
crossover trial that included 34 patients, there was
no statistically significant difference in unexplained
falls between those with the pacemaker turned on
and those with it turned off.45 However, this study
was considered underpowered because of the
study’s high attrition rate.
Physical Examination
In addition to a standard thorough cardiac examination, the implantation site itself should be examined
for erythema, bruising, swelling, and tenderness.
Signs of swelling in the neck or ipsilateral arm
should raise suspicion for venous thrombosis. Moving the patient’s ipsilateral arm or having the patient
perform isometric exercise may help to identify
intermittent dysfunction.
Diagnostic Studies
Emergency Department Evaluation
Electrocardiogram
The 12-lead ECG is important for determining
whether depolarization is intrinsic or paced. Bipolar
leads produce smaller pacing artifacts that may be
imperceptible in some leads and easily recognized
in others. The absence of a pacer artifact before P
waves or QRS waves indicates that depolarization is
intrinsic. Pacing artifacts preceding depolarizations
indicate successful pacing and capture.
History
Even with the availability of advanced device-monitoring capabilities, obtaining the history from a patient
with an implanted device remains important. This
includes cardiac history as well as noncardiac medical
history and, perhaps most importantly, the original
indication for pacemaker placement. The type of pacemaker should be identified so that appropriate inter-
Table 3. Indications For Cardiac Resynchronization Therapy7
Class
Indication
LOE
I
LVEF ≤ 35%; sinus rhythm; LBBB with a QRS duration ≥ 150 msec; and NYHA class II, III, or ambulatory class IV symptoms on
goal-GDMT
B
LVEF ≤ 35%; sinus rhythm; LBBB with a QRS duration 120-149 msec; and NYHA class II, III, or ambulatory class IV symptoms
on GDMT
B
LVEF ≤ 35%; sinus rhythm; a non-LBBB pattern with a QRS duration ≥ 150 msec; and NYHA class III/ambulatory class IV
symptoms on GDMT
A
Atrial fibrillation and LVEF ≤ 35% on GDMT if: (a) patient requires ventricular pacing or otherwise meets CRT criteria, and (b) AV
nodal ablation or pharmacologic rate control will allow near-100% ventricular pacing with CRT
B
LVEF ≤ 35%, undergoing new placement or replacement of a device with anticipated requirement for significant (> 40%) ventricular pacing
C
LVEF ≤ 30%, ischemic etiology of heart failure, sinus rhythm, LBBB with QRS duration ≥ 150 msec, and NYHA class I symptoms
on GDMT
C
LVEF ≤ 35%, sinus rhythm, a non-LBBB pattern with QRS duration 120-149 msec, and NYHA class III/ambulatory class IV on
GDMT
B
LVEF ≤ 35%, sinus rhythm, a non-LBBB pattern with a QRS duration ≥ 150 msec, and NYHA class II symptoms on GDMT
B
NYHA class I or II symptoms and non-LBBB pattern with QRS duration < 150 msec
B
Patients whose comorbidities and/or frailty limit survival and good functional capacity to less than 1 year
C
IIa
IIb
III
Abbreviations: AV, atrioventricular; CRT, cardiac resynchronization therapy; GDMT, goal-directed medical therapy; LBBB, left bundle branch block; LOE,
level of evidence; LVEF, left ventricular ejection fraction; NYHA, New York Heart Association.
September 2014 • www.ebmedicine.net
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The 12-lead ECG is also essential for evaluating
the morphology of paced QRS complexes. Leads
positioned in the right ventricular apex produce a
LBBB pattern with appropriate discordance in the ST
segments and T waves. A change in this morphology may indicate lead dislodgement. Specifically,
the presence of a new RBBB pattern may indicate
inadvertent placement of the right ventricular lead
into the left ventricle or septal perforation. A RBBB
pattern may also appear in a minority of correctly
positioned right ventricle leads.46 Simultaneous
depolarization of the left and right ventricles from
a biventricular pacing system typically produces a
dominant R wave in lead V1.47
Hyperkalemia
Delayed intraventricular conduction causes paced
QRS complexes in the hyperkalemic patient to widen. Severe hyperkalemia may result in a sine wave
following each pacing artifact. (See Figure 2.)
Severe hyperkalemia may cause ECG changes to
be mistaken for pacemaker malfunction. The pacing threshold is elevated in hyperkalemia, leading
to increased latency, intermittent capture (including Wenckebach phenomenon), or continuous loss
of capture,48,49 as well as loss of sensing.50 Latency
or failure to capture may be temporarily overcome
by programming pacemaker outputs to maximum
voltage, but definitive treatment for hyperkalemia
should be instituted without delay.
from the GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for
Occluded Coronary Arteries) trial population, that
concordant ST elevation, concordant ST depression
in leads V1 through V3, and > 5 mm of discordance
in leads with predominantly negative QRS complexes were insensitive but specific findings for
acute MI.51 (See Figure 3.) In a retrospective review
of 57 ECGs of ventricular-paced patients diagnosed
with acute MI, discordant ST elevation > 5 mm
was the most specific finding (99% specificity; 95%
confidence interval [CI], 93%-99%).52 However, discordant ST elevation can be > 5 mm in ventricularpaced rhythms in the absence of MI when negative
QRS amplitudes in leads V1 through V3 are large.53
As with application of the Sgarbossa rule to LBBB,
an elevated ratio of ST-segment elevation to S-wave
depth may be more specific for MI than the absolute measurement of 5 mm.54 Acute anterior MI in a
patient with biventricular pacing with a dominant R
wave in leads V1 and V2 presents with standard ST
elevations across the precordium.55
Radiology
A basic knowledge of the normal and abnormal
radiographic appearances of cardiac conduction
devices and their components can be important
in diagnosing complications associated with
implantation and device integrity. (See Table 4.)
Both posterior-anterior and lateral views should
Acute Myocardial Infarction
The pattern of depolarization and repolarization
in ventricular-paced rhythms may obfuscate the
electrocardiographic diagnosis of acute myocardial
infarction (MI). Sgarbossa found in a retrospective
review of 17 ventricular-paced patients selected
Figure 3. Electrocardiogram Tracing Of
Myocardial Infarction, Paced Rhythm
Figure 2. Electrocardiogram Tracing Of
Paced Rhythms In The Setting Of Severe
Hyperkalemia
Arrows point to examples of exaggerated discordance.
Table 4. Radiographic Assessment Of
The Permanent Pacemaker/Implantable
Cardioverter-Defibrillator
•
•
•
•
•
•
Arrows point out pacing artifacts.
From Jennifer Martindale, David F. M. Brown. Rapid Interpretation of
ECGs in Emergency Medicine: A Visual Guide. Reprinted with permission from Lippincott Williams & Wilkins/Wolters Kluwer, 2012.
Copyright © 2014 EB Medicine. All rights reserved.
6
Obtain posterior-anterior and lateral views.
Locate pulse generator and compare with previous chest x-ray.
Identify manufacturer, if needed.
Ensure connector pin is seated deep within header.
Identify number of leads and lead location.
Confirm integrity of each lead.
www.ebmedicine.net • September 2014
leads. ICD leads may contain a single high-voltage
coil in the right ventricle or may have an additional
coil in the superior vena cava.
Complications of implantation that can be diagnosed on plain radiographs include pneumothorax,
hemopneumothorax, myocardial perforation, and
improper seating of a connector pin. Winding of a
lead around the pulse generator may be indicative of
twiddler syndrome. (See page 8.)
be obtained to confirm correct lead position, and
radiographs should be compared with any prior
studies. In addition, the manufacturer and model
on the pulse generator can often be identified from
the chest radiograph.
Lead location and integrity should be confirmed systematically. On a lateral view, the right
atrial lead has a J-shaped appearance as it enters
the right atrium and curves upward and anteriorly
into the right atrial appendage. The J portion of the
lead is medial on the posteror-anterior projection
and anterior on the lateral projection. Atrial leads
may also be placed in the interatrial septum. Right
ventricular leads should point downward, with the
tip between the left of the vertebral column and the
cardiac apex on a posterior-anterior radiograph. The
lateral radiograph is required to confirm the anterior
and caudal course of a correctly positioned right
ventricular lead. Leads placed in the left ventricle or
coronary sinus should course posteriorly on a lateral
radiograph.
Magnification may be required to appreciate
small defects in leads. A common site of lead fracture is between the first rib and clavicle (subclavian
crush syndrome).56 Extraneous wires present on
chest radiographs may represent abandoned leads.
Malfunctioning leads are disconnected from the
generator, capped, and left in place to avoid the risks
associated with their extraction.
The key to differentiating a permanent pacemaker from an ICD is the presence of shock coils
(see Figure 4), which appear as thick bands on the
Device Interrogation
Noninvasive testing allows acquisition of measured data, interrogation of programmed parameters, and analysis of stored arrhythmias. Basic
parameters include pacing mode, and lower and
upper tracking rates can be shown during device
interrogation. Measurements of the battery’s voltage can help to determine whether battery failure
might be the cause of pacemaker malfunction.
With some devices, the estimated remaining life of
the battery can be determined. Measurements of
lead status can help to identify lead failures (such
as a break in insulation or conductor fracture). A
sudden drop in impedance, for example, might
indicate an insulation break.
The pacemaker is also capable of telemetry.
The relative time spent between paced and native
activity in each chamber is recorded. Heart rate
measurements are stored and a graphical representation of time spent in different heart rate intervals
can be displayed as a histogram. The date, time, and
duration of arrhythmia episodes and their associated
electrograms are also stored by implanted devices.
This capability makes implanted pacemakers valuable diagnostic tools for ruling out tachyarrhythmia
as the underlying cause for a patient with recent
symptoms. (See Table 5.)
Figure 4. Radiograph Of Dual-Chamber,
Biventricular Pacemaker/Implantable
Cardioverter-Defibrillator System
Table 5. Methods To Identify Device
Manufacturer
Abbreviations: LV, left ventricle; RA, right atrium; RV, right ventricle.
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7
Ask patient for
pocket card
This will specify the type of pacemaker, type
of leads, manufacturer, date of implantation, paced rate, as well as contact information for the patient’s primary physician.
Place magnet
over pulse
generator
This will dentify magnet-induced pacing rate
(specific to each model).
Call manufacturer hotlines
Medtronic, Inc.: 1-800-328-2518
The Boston Scientific Corporation:
1-800-CARDIAC
St. Jude Medical, Inc.: 1-800-722-3774
Obtain chest
x-ray
Look for manufacturer code on pulse
generator.
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Lead Dislodgement
Implant-Related Complications
A relatively more common lead-related issue is
lead dislodgment. Dislodgement occurs in 2.4% of
implantations, and may result in inadequate sensing or failure to capture.62 This issue usually occurs
very early post procedure but may occur as late as 3
months afterward.57,63 Dislodgement is often suspected when undersensing or failure to capture is
detected on follow-up telemetry. Subtle cases may
be detectable only upon device interrogation demonstrating changes in pacing thresholds, while more
pronounced cases can be visualized by chest radiography.63 Rarely, temporary external or transvenous
pacing may be needed until repositioning or replacement of the leads can be performed. Lead dislodgement can sometimes result in lead migration or
malposition. Migration of a lead through an occult
septal defect can result in pacing of the left ventricle
rather than the right. Malposition near the phrenic
nerve may stimulate the nerve or the diaphragm
directly and cause chronic singultus (hiccoughs).63,64
Lastly, lead dislodgement can cause myocardial
perforation in 0.3% of cases in the days to weeks
following implantation, resulting in pericardial effusion and, potentially, tamponade.62,64
See Table 6 for a list of common complications arising from the surgical implantation procedure itself
or problems with device components.
Hematoma
Postprocedural bleeding and generator pocket
hematoma are relatively common complications that
may be encountered immediately after implantation.
Bleeding may occur from within the soft tissue of the
pocket itself or it may originate from the venous insertion site. Hematomas are managed conservatively
in all but 1% to 2% of cases, in which expanding,
tense, or painful collections require surgical evacuation and hemostasis.57 Patients who are anticoagulated with clopidogrel or heparin are at greater risk
of developing a pocket hematoma.58
Infection
As with any surgical procedure, device implantation
carries a small risk of surgical site infection (0.2%
in one retrospective study).59 Examination of the
generator pocket itself may reveal signs of inflammation, dehiscence, or erosion. However, even in the
absence of such findings, infection of an implanted
device should still be considered when there is
fever without an identified source. If infection is
confirmed, device removal with lead extraction is
typically required, followed by antibiotics and reimplantation at a later date.59,60
A subset of cardiac device infections will result in
cardiac device infective endocarditis (CDIE). CDIE is
a serious infection occurring at rate of 0.4%.59 Clinical
findings, vegetations found on echocardiogram, and
positive blood and lead tip cultures are criteria used
for diagnosis.59,60 Staphylococci are the predominant
bacteria involved.61 CDIE is also treated by removal
of the device, prolonged intravenous antibiotics, and
possible reimplantation on the contralateral side at a
later date.59,60
Twiddler Syndrome
Lead dislodgement can also be caused by a patient’s own compulsive manipulation of the pacemaker generator, causing the leads to become
retracted and coiled around the manipulated pulse
generator. This is referred to as twiddler syndrome,
and the diagnosis is made by the radiographic
appearance of pacing leads coiled about the generator. Woven Dacron® pouches have been used to
prevent migration and flipping of the pulse generator, but subpectoral implantation may be required
to prevent recurrent device rotation.65,66
Table 6. Implant-Related Complications
Complication
Diagnosis Method
Management
Pocket hematoma
Examination
Conservative (rarely, surgical evacuation)
Pocket infection
Examination
Explantation, antibiotics
Endocarditis
Echocardiography, blood cultures, TEE
Explantation, antibiotics
Lead dislodgement
Chest radiography, telemetry/ECG
Repositioning or replacement
Venous thrombosis
Sonography/venography
Anticoagulation, angioplasty, or surgery
Pneumothorax, hemothorax
Chest radiography
Conservative or aspiration/thoracostomy
Tricuspid regurgitation
Echocardiography
Lead extraction and/or annuloplasty/valve
replacement
Cardiac perforation
Computed tomography, echocardiography
Pericardiocentesis, lead withdrawal and repositioning
Abbreviations: ECG, electrocardiogram; TEE, transesophageal echocardiogram.
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Venous Thrombosis
Pacemaker Syndrome
Subclavian or brachiocephalic venous thrombosis is
a relatively more common occurrence after pacemaker implantation, with reported incidental rates
of 2% to 22% from several days up to 9 years postoperatively.67,68 The range of reported rates (both in
incidence and time) is a product of how the disease
is typically discovered. Venous thrombosis is typically an incidental finding during a preoperative
venogram in an asymptomatic patient undergoing
lead revision. Thrombosis may be more common
in patients who have systemic infection.67 Signs are
often absent, but there may be typical manifestations
of acute deep venous thrombosis and even superior vena cava syndrome, with the latter occurring
in 0.2% of procedures.63 Ultrasonography may not
be diagnostic, even in symptomatic cases, and a
venogram will be required.68 If thrombosis is found,
vascular surgery consultation should be sought.
Although it is a relatively common finding, venous
thromboses associated with cardiac devices are of
questionable clinical importance, as pulmonary
embolism is a rare complication in these patients.63,68
Treatments range from heparin/warfarin to percutaneous angioplasty or even open surgery.63,68
Pacemaker syndrome is defined as intolerance to
ventricular pacing in the absence of atrioventricular synchrony.70 The Mode Selection Trial (MOST)
investigators suggest the following criteria: (1) new or
worsened dyspnea, orthopnea, rales, elevated jugular
venous pressure, and edema with ventriculoatrial
conduction during ventricular pacing; or (2) dizziness, weakness, presyncope or syncope, and a > 20
mm Hg reduction of systolic blood pressure when the
patient has VVIR pacing compared with atrial pacing
or normal sinus rhythm.70-73 It is hypothesized that
ventricular pacing leads to ventriculoatrial contraction with resultant increases in atrial pressures.64,70
Baroreceptor overload then alters vagal tone and
there is resultant reduced cardiac output. This
reduced output is further complicated by the loss of
atrial contribution to preload.64,70 Pacemaker syndrome is usually treated by the restoration of some
level of atrioventricular synchrony. This may involve
replacing a single-chamber device with a dual-chamber device or reprogramming a dual-chamber device
from VVI to DDD function.
Pacing System Malfunctions
Pneumothorax
Pacemakers and ICDs are complex medical devices and, while they are generally regarded as
safe and reliable, they are subject to electrical and
hardware malfunction. (See Table 7, page 10.)
Generator malfunctions occur at a mean annual
rate of 4.6 per 1000 implanted pacemakers and
20.7 per 1000 implanted ICDs.74,75 A meta-analysis
of prospective device registries demonstrated that
rates of generator failure have improved over the
past 2 decades, and the most common cause of
device failure was battery malfunction.76
The majority of lead failures are caused by insulation defects. Typically, insulation breaks are a
late complication, occurring at a median time of 7.5
years (+/- 2.5 y) after implantation.77 Lead problems can be detected by measuring lead impedance. Very high impedance results from an open
circuit (conductor fracture), while low impedance
implies an insulation defect.
Clinical symptoms of device malfunction include syncope, palpitations, dizziness, fatigue, and
muscle twitching from extracardiac stimulation.
Overall, however, pacemaker malfunction is a rare
cause of syncope. In one retrospective study, device
malfunction was found to be the cause of syncope in
only 8 of 162 patients.78
An assessment of pacing system malfunction
should include evaluation of the pulse generator, the
leads, programmed settings, and algorithms, as well
as any patient status (eg, electrolyte disturbance)
that may affect the electrode-myocardial interface.
From an electrocardiographic standpoint, pacemaker
As in other procedures that involve subclavian
venous puncture, device implantation may result
in pneumothorax from inadvertent pleural injury.
In one study, pneumothorax was the second most
common complication overall and occurred in 1.5%
of patients.62 Hemothorax may occur due to unintentional arterial puncture or laceration, which can
be minimized by proper use of fluoroscopic guidance. Postprocedural pneumothorax and hemothorax are often asymptomatic,63 but some cases may
require needle aspiration or tube thoracostomy. Not
surprisingly, these complications are less likely with
axillary vein cannulation techniques.
Tricuspid Regurgitation
Tricuspid regurgitation may occur after pacemaker
lead placement, although the mechanism of this
occurrence is not fully understood. Commonly
postulated mechanisms include direct damage to
valve leaflets or impairment of valve closure due
to scar formation or thrombus. Ventricular asynchrony is also a possible mechanism. Many patients
are asymptomatic, but some may present with
signs of right-sided congestive heart failure and a
systolic murmur that increases with inspiration.69
Diagnosis is made by 3-dimensional transthoracic
echocardiography. Leads that are adherent to the
valve may require extraction. Unfortunately, the
lead extraction procedure itself can lead to progression of tricuspid regurgitation.69
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malfunction can be categorized as failure to capture,
failure to pace, and undersensing. (See Figure 5.)
defects. Crosstalk refers to a specific type of oversensing, in which the ventricular lead senses an atrial
pacing stimulus, thereby inhibiting ventricular
output. A programmed ventricular blanking period
following atrial pacing helps to prevent crosstalk.
Intrinsic signals that can be oversensed include
retrograde P waves, T waves, ventricular afterdepolarizations, and skeletal muscle myopotentials.
Myopotentials from the pectoralis, diaphragm,84 and
rectus abdominus muscles can all cause oversensing.85 External electromagnetic interference can also
result in inappropriate oversensing.
Blunt trauma to the pulse generator may cause
failure to pace due to output failure.86 Lead fracture,
dislodgement, or loose connections can also result in
output failure and failure to pace.
Undersized pacing artifacts may not be visible
on the ECG and can give the appearance of failure to
pace. Intrinsic events (such as a premature atrial contractions or premature ventricular contractions) that
may not be appreciated on a single telemetry lead can
give the false impression of failure to pace when, in
fact, there is appropriate inhibition of pacing.
Failure To Capture
Failure to capture is defined as the delivery of a
pacing stimulus without subsequent depolarization.
(See Figure 5, view A, page 11.) Failure of depolarization may be functional or pathologic. Functional
failure to capture occurs if a pacing impulse is delivered when the myocardium is in a refractory state.
Pathologic failure to capture may occur in the setting
of myocardial disease, electrolyte disturbance, and
antiarrhythmic drugs. The same conditions can also
result in latency, which can sometimes be mistaken
for failure to capture. Occasionally, isoelectric depolarization can give the appearance of failure to
capture, in which case multichannel recording can
confirm that depolarization is occurring.
Lead dislodgement, perforation, fracture, or an
insulation defect can increase the pacing threshold
and cause intermittent or persistent failure to capture. Increased pacing threshold can occur several
weeks after pacemaker placement due to excessive
fibrosis at the electrode-myocardial interface. Capture threshold can also be increased in the setting of
hypothyroidism79,80 and infiltrative cardiomyopathies.81 Among the medications that are most likely
to affect pacing thresholds are class IC antiarrhythmic drugs.82 Hyperkalemia is also an important
cause of failure to capture.83
Failure To Sense
A signal is sensed when a myocardial depolarization
wave passes up the lead wire and is filtered through
the pacemaker. Signals that exceed the sensingthreshold voltage are programmed to inhibit pacing. To prevent double-counting of intrinsic cardiac
depolarizations and to prevent sensing of evoked
responses as intrinsic depolarizations, pacemakers
are programmed to have blanking and refractory
periods that immediately follow pacing artifacts and
intrinsic depolarizations. Long blanking and refractory periods can cause a functional undersensing of
events that occur during these periods. (See Figure
5, view C, page 11.)
Undersensing can also occur when there is a
Failure To Pace
Failure to deliver a stimulus to the heart is referred
to as failure to pace. The clearest indication of this
is absence of pacing artifact when the intrinsic rate
is less than the set lower limit of the device. (See
Figure 5, view B, page 11.) Oversensing is the most
common cause of failure to pace. Oversensing can
occur due to partial lead fracture or insulation
Table 7. Causes Of Pacemaker Malfunction, By Category
Source of Malfunction
Failure To Capture
Failure To Sense
Failure To Pace
Functional failure
Pacing output delivered when myocardium functionally refractory
Intrinsic event delivered during
programmed blanking period or
refractory period
Appropriate inhibition
Pseudofailure
Isoelectric depolarization; recording
artifacts
Not applicable
Small bipolar pacing artifacts; ventricular avoidance algorithms
Pulse generator
Circuit failure; battery depletion
Battery depletion
Blunt trauma; battery depletion
Lead
Lead fracture; lead insulation break;
lead dislodgement
Lead fracture; lead insulation
break; lead dislodgement
Lead fracture; lead insulation break
Electrode-myocardial interface
Electrolyte abnormality (hyperkalemia); drug effect (class IC antiarrhythmic drugs); myocardial infarction; defibrillation/cardioversion
Intracardiac signals
Not applicable
Change in intrinsic complex (new
bundle branch block)
Retrograde P waves; afterdepolarizations; T waves; crosstalk; far-field
sensing
Extracardiac signals
Electromagnetic interference
Electromagnetic interference
Electromagnetic interference
Copyright © 2014 EB Medicine. All rights reserved.
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Nonmedical Sources Of Interference
change in the morphology or vector of the depolarization pattern. Premature ventricular contractions,
bundle branch block, and certain forms of ventricular
tachycardia may not exceed the sensing thresholds
applied to the previous intrinsic depolarization pattern; however, undersensing is most commonly the
result of a break in lead insulation. Undersensing that
occurs soon after implantation can be caused by lead
dislodgement or perforation. Class IC antiarrhythmic
drugs and hyperkalemia may also alter the sensing
threshold.50 Finally, undersensing can occur as the
pacemaker battery becomes depleted.
Common household appliances (such as televisions or microwave ovens) do not interfere with
pacemaker function. Potential nonmedical sources
of electromagnetic interference include cell phones,
security gates, and electronic article surveillance
devices. Pacemaker device manufacturers have developed filters that account for common frequencies
employed by cell phones. In a study of 679 patients,
interaction between cell phones and pacemakers
was found in only 0.3% of patients, and there were
no clinical manifestations.89 The consequences of the
interaction were mostly activation of asynchronous
pacing and, rarely, oversensing or inappropriate
tracking. Interactions occurred at higher rates with
unipolar lead pacemakers and only during the ringing phase when the phone was positioned within
10 cm of the pacemaker. Cell phones have not been
shown to interact with ICDs.90
Despite the low incidence of interaction with
cardiac devices, the common-sense recommendation
for patients should be to position the phone at the
ear contralateral to the device. Patients with cardiac
devices may trigger alarms at airport security gates
when they are screened, but no alteration of function should be expected. In a study of 388 patients
screened with handheld metal detectors, there were
no observed pacing or sensing abnormalities or
reprogramming.91 Interactions with article surveillance devices in retail stores are rare but may occur
during prolonged exposure, resulting mostly in
asynchronous pacing.92 It should be recommended
that patients avoid lingering near these security
gates. Additionally, digital music players can cause
some interference but do not directly affect the device.93 However, portable headphones often include
a powerful magnetic substance that can produce
electromagnetic interference and interactions when
placed within 3 cm of the cardiac device.94
Electromagnetic Interference
For simplification, recent reviews have separated
electromagnetic interference sources into nonmedical sources and medical sources.87,88
Figure 5. Electrocardiogram Appearance of
Pacemaker Failure
Failure to Capture
Failure to Pace
Failure to Sense
Electrocardiographic appearance of different types of pacemaker
malfunction. (A) The appearance of appropriately timed pacing artifacts that are not immediately followed by expected P or QRS waves
may indicate that a pacemaker's failure to capture is the cause of a
patient's symptoms. In this case of atrioventricular pacing, atrial pacing artifacts are followed by inverted P waves, whereas ventricular
pacing artifacts are not immediately followed by any QRS waves.
The asterisk identifies where QRS waves would be expected to
appear in the first 2 beats. The first beat in this strip is a native atrial
impulse (appropriately sensed) followed by ventricular pacing artifact
that fails to capture. The following beats are atrial-paced with capture
and ventricle-paced with failure to capture. (B) Failure of pacing
artifacts to appear when expected may indicate that a pacemaker is
malfunctioning by failing to pace. This is a ventricular-paced rhythm.
The absence of a fifth pacing artifact represents failure to pace,
commonly caused by oversensing. (C) The appearance of a pacing
artifact at an inappropriate location on the electrocariogram may
indicate that the pacemaker is failing to sense native conduction. The
asterisk indicates a pacing artifact appearing too soon after a native
QRS wave.
Medical Sources Of Interference
Medical sources of electromagnetic interference
include electrocautery (most common), magnetic
resonance imaging (MRI), ventricular assist devices,
extracorporeal shock wave lithotripsy, therapeutic
ionizing radiation, and external cardioversion.87
Physical movement of the cardiac device has not been
reported during MRI,88,95 but MRI may affect pacemaker function through 3 mechanisms: (1) the static
magnetic field of the MRI will typically close the reed
switch and lead to asynchronous pacing; (2) the gradient magnetic fields of the MRI may cause alteration
of function or dysrhythmia through direct current
effects on pacemaker output circuits;95,96 and (3) the
radiofrequency energy of the MRI may be captured
by pacemaker leads, which act as antennae to concentrate the energy to myocardium.95,96
In one study, 555 MRI studies were performed
From Jennifer Martindale, David F. M. Brown. Rapid Interpretation of
ECGs in Emergency Medicine: A Visual Guide. Reprinted with permission from Lippincott Williams & Wilkins/Wolters Kluwer, 2012.
September 2014 • www.ebmedicine.net
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on 438 patients with cardiac devices.97 Only 3 devices
went into a temporary back-up mode, and there
were no significant changes in function, leading the
authors to conclude that MRI can be done safely in
monitored patients with selected devices.97 The AHA
and the American College of Radiology (ACR) offer
guidelines that state that the decision to perform
an MRI on patients with cardiac devices should be
patient-specific, with assessment of risks and benefits, and coordination by both cardiology and radiology services.95,98 Therapeutic radiation can produce
electromagnetic interference that may directly damage the device circuitry. Manufacturers recommend
against radiation therapy if the device is within the
treatment field, and there are recommendations for
maximum doses.
External direct cardioversion or defibrillation
may also cause device malfunction. Pacing and sensing function may be affected as a result of associated
increases in the myocardial stimulation thresholds,
some of which may be permanent.99 Activation of
the backup function/rate or mode switch may also
occur.99 In patients with bipolar systems, anteriorposterior cardioversion with pads more than 8 cm
away from the device will rarely cause adverse
effects.100 Contemporary extracorporeal shock wave
lithotripsy can be performed safely in patients with
cardiac devices, as the rate of interaction is estimated
to be less than 1%.101
dysrhythmia.103 After a pacemaker-mediated tachycardia event is successfully treated, the device will
need to undergo adjustments to its atrial sensing
thresholds. Most modern devices include programming to prevent pacemaker-mediated tachycardia.
With such programming, the device may disregard
atrial stimuli when atrial rates exceed its own upper
limit, or it can mode-switch to discontinue atrial
tracking altogether. (See Figure 6, views B and C.)
In patients who have older devices with unipolar leads, abnormal, rapid ventricular pacing may
occur through a different mechanism. Unipolar
systems are more susceptible than bipolar devices to
sensing of myopotentials from neighboring muscle
activity, and these myopotentials can trigger a rapidly paced rhythm.104
In patients who are ventricular paced, sinus
tachycardia (whether physiologic or pathophysiologic) will result in rapid ventricular pacing up
to the preset rate limit. Some pacemakers have
rate-responsive sensors that can detect changes in
physiological parameters (ie, minute ventilation, QT
interval, and stroke volume) and permit higher heart
rates when dictated by the environment.71 It must be
noted that sensory-induced tachycardia will appear
identical to pacemaker-mediated tachycardia on an
ECG; differentiation between them may be possible
only through device interrogation.
Management
Approach To The Pacemaker Patient With
Tachycardia
Figure 6. Pacemaker-Mediated Tachycardia
Pacemaker-mediated tachycardia (also known as
pacemaker re-entrant tachycardia or endless loop
tachycardia) is observed exclusively in patients with
dual-chamber devices. Pacemaker-mediated tachycardia is similar to other re-entrant dysrhythmias
except that the pacemaker itself forms part of the
re-entry circuit. An intrinsic premature complex is
sensed by the atrial lead of the pacemaker, which
responds by generating a ventricular impulse. This
ventricular impulse is then conducted retrograde
through the atrioventricular node to the atria. The
impulse, now in the atria, is sensed by the atrial lead
to complete the loop and again trigger the pacemaker to generate a ventricular impulse. The ECG will
show a regular wide-QRS tachycardia with a pacing
artifact prior to each complex, and retrograde P
waves may be seen. (See Figure 6, view A.) This reentrant tachycardia will not exceed the pacemaker’s
programmed upper rate limit; however, tachycardia
may be significant enough to cause symptoms necessitating emergent treatment. A trial of adenosine
may or may not be effective in treating this tachycardia.102 On the other hand, placing a magnet over the
pacemaker will definitively terminate this re-entrant
Copyright © 2014 EB Medicine. All rights reserved.
A
Retrograde Ps
B
Lack of atrial capture
Lack of atrial capture
C
Atrial capture and termination of PMT
(A) First 3 asterisks indicate premature ventricular contractions with
retrograde P that triggers onset of PMT. (B) Arrow shows lack of
atrial capture; a failed attempt at termination by device. (C) Arrow
indicates successful atrial capture and termination of PMT.
Abbreviation: PMT, pacemaker-mediated tachycardia.
Anton Verrijcken, Wim Huybrechts, and Rik Willems. PacemakerMediated Tachycardia With Varying Cycling Length: What is the
Mechanism? Europace. 2009, Volume 11, Issue 10, page 14001402. By permission of Oxford University Press.
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www.ebmedicine.net • September 2014
Magnets turn off the antitachycardia functions
of an ICD without affecting its ability to perform
backup bradycardia pacing. As such, magnets can
be used to terminate inappropriately delivered
device shocks. Some ICDs are programmed to play
alert tones to indicate high lead impedance, pacing
impedance, battery depletion, and delivery of more
than 3 shocks. These tones can be replayed to the
clinician by applying a magnet over the ICD.106
The Magnet
Most pacemakers and ICDs have magnetic reed
switches. In pacemakers, placement of a magnet
turns off the sensing function, effectively making the
pacemaker fire asynchronously at a specified rate.
Removal of the magnet causes the pacemaker to
switch back to its programmed mode.
The magnet response is specific to the manufacturer, model, and programmed response of the device. Each pacemaker has a fixed rate programmed
to reflect different levels of battery status. For
example, in a Medtronic pacemaker (Medtronic, Inc.,
Minneapolis, MN), a rate of 85 beats/min reflects
beginning-of-life status and 65 beats/min indicates
that elective replacement is indicated. At the battery’s end of life, the response of a pacemaker to the
magnet is unpredictable.105 If there is no electrocardiographic response to a magnet, there are several
possibilities to consider. (See Table 8.) The battery
may be at the end of its life or completely depleted,
the magnet may need to be repositioned, or the
pacemaker may be distanced by adipose tissue.
More than 1 magnet may be needed to activate the
reed switch of a pulse generator placed in an obese
patient. Rarely, a device may also be programmed to
ignore magnet application (magnet “OFF” mode).
There are several clinical applications for placing a magnet on a pacemaker, one of which is to
terminate pacemaker-mediated tachycardia, as
the ventriculoatrial limb of the re-entrant circuit is
broken when atrial sensing is disabled by a magnet. (See Table 9.) Inappropriate sensing (whether
from electromagnetic interference or another cause)
will be inhibited by placement of a magnet. Absent
pacing artifacts on an ECG can distinguish output
failure or lead disruption from oversensing.
Some devices are programmed to initiate ECG
storage (electrogram mode) under the influence of
a magnet. By applying a magnet, the patient can
trigger the pacemaker to store ECG data during
episodes of palpitations or light-headedness.
Advanced Cardiovascular Life Support In
Patients With Pacemakers Or Implantable
Cardioverter-Defibrillators
With few exceptions, Advanced Cardiovascular Life
Support (ACLS) procedures should be performed in
patients with pacemakers or ICDs in the same manner as in those without the devices. Shocks delivered
by an implanted device during a cardiac arrest do not
pose a risk to ACLS providers or other equipment.107
External defibrillation is ordinarily not necessary in a
patient with a device that has antitachycardia function;
however, it should be noted that a dysrhythmia may
persist after a normally functioning pacemaker or ICD
has completed its programmed sequence of therapy. To
conserve battery life, typical sequences are limited to 5
successive shocks. In some cases, the implanted device
Table 9. Clinical Applications Of Magnet On
Implanted Cardiac Device
Permanent Pacemaker
• Break pacemaker-mediated tachycardia
• Prevent pacing inhibition from electromagnetic interference
• Demonstrate ability to pace
• Electrocardiograph storage (electrogram mode)
Implantable Cardioverter-Defibrillator
• Cessation of inappropriate shocks
• Inhibit antitachycardia therapy during procedures with electromagnetic interference
Table 8. Expected Response To Magnet Placement Over Pacemaker/Implantable CardioverterDefibrillator And Clinical Implications Of Different Magnet Responses
Implantable Cardioverter-Defibrillator
Permanent Pacemaker
Tachyarrhythmia therapy
Suspended
Not applicable
Effect on pacing
Not applicable
• Asynchronous pacing (DOO, AOO, VOO)
l
l
l
Upon magnet removal
Tachyarrhythmia therapy restored
At 85 beats/min*: Functioning battery at beginning of life
At 65 beats/min*: Elective replacement interval
No pacing response: Depleted battery; battery at end of life; pacemaker is programmed to ignore magnet for safety (electrogram mode);
magnetic field doesn’t reach device (deep placement or obese patient);
poorly positioned magnet
Sensing function restored
*Rates specific for Medtronic pacemaker (Medtronic, Inc., Minneapolis, MN, USA).
For an explanation of pacemaker codes, see Table 2, page 3.
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Clinical
Pathway
For Emergency
Department
Management
Of Multiple
Clinical
Pathway
For Suspected
Pacemaker
Malfunction
Shocks
Obtain device history
Obtain 12-lead ECG
Pacemaker malfunction
apparent on ECG?
YES
YES
NO
Patient asymptomatic
during ECG but reports
recent symptomatic
episodes
Electrolyte abnormality?
NO
Correct electrolyte
abnormality (Class II)
Change in ST segments or
positive cardiac markers?
NO
Interrogate device
YES
• Antithrombotic therapy
• Revascularization
(Class II)
• Check battery status
• Check lead status
• Check event record
(Class II)
Replace battery,
if necessary
If abnormal lead impedance, obtain chest x-ray
(Class II)
Abbreviation: ECG, electrocardiogram.
Class Of Evidence Definitions
Each action in the clinical pathways section of Emergency Medicine Practice receives a score based on the following definitions.
Class I
Class II
• Always acceptable, safe
• Safe, acceptable
• Definitely useful
• Probably useful
• Proven in both efficacy and effectiveness
Level of Evidence:
Level of Evidence:
• Generally higher levels of evidence
• One or more large prospective studies
• Nonrandomized or retrospective studies:
are present (with rare exceptions)
historic, cohort, or case control studies
• High-quality meta-analyses
• Less robust randomized controlled trials
• Study results consistently positive and
• Results consistently positive
compelling
Class III
• May be acceptable
• Possibly useful
• Considered optional or alternative treatments
Level of Evidence:
• Generally lower or intermediate levels
of evidence
• Case series, animal studies, consensus panels
• Occasionally positive results
Indeterminate
• Continuing area of research
• No recommendations until further
research
Level of Evidence:
• Evidence not available
• Higher studies in progress
• Results inconsistent, contradictory
• Results not compelling
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright © 2014 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.
Copyright © 2014 EB Medicine. All rights reserved.
14
www.ebmedicine.net • September 2014
Risk Management Pitfalls For Implantable Devices
1. “The ventricular-paced rhythm makes the ECG
uninterpretable for diagnosing MI. I’ll call cardiology if the troponin comes back positive.”
While concordant ST-segment changes and
exaggerated discordance are insensitive findings
for diagnosing acute MI in paced rhythms, they
are diagnostically useful, when present.
6. “I didn’t think to compare the chest x-ray with
a previous one or consider lead dislodgement
as a complication that could occur so far out
from implantation.”
Lead migration more commonly occurs
shortly after implantation, but it can be a late
complication. Comparison with previous
x-rays is helpful in detecting macro lead
dislodgements.
2. “Pacing artifacts appear stranded among widened and regular QRS complexes at a ventricular rate of 42. There must be a problem with the
pacemaker.”
Hyperkalemia can cause QRS widening,
bradycardia, and failure to capture. Obtain a
serum potassium level quickly and consider
immediate administration of calcium. Always
consider hyperkalemia before attributing
failure to capture to a hardware problem or
programming error.
7. “The 12-lead ECG appeared normal. I didn’t
think the patient needed device interrogation.”
Pacemaker interrogation is critical in evaluating
the possibility of pacemaker dysfunction that
might not be apparent on a 12-lead ECG.
8. “The patient experienced syncope and has a
pacemaker, so she is a high-risk cardiac patient
and needs to be admitted to telemetry.”
Pacemaker interrogation can be performed
in the ED to rule out dysrhythmia and
pacing malfunction as underlying causes of
palpitations, syncope, and light-headedness.
Device interrogation may help to avoid
unnecessary hospital admission in some of these
patients.
3. “I thought electrical cardioversion was contraindicated in patients with permanent pacemakers.”
Electric direct-current cardioversion is safe as
long as the electrodes are placed in anteriorposterior orientation at least 8 cm away from
the pacemaker device. Device interrogation for
proper functioning should be performed after
cardioversion.
9. “I didn’t think that hiccoughs could be related
to the patient’s pacemaker.”
Direct stimulation of the diaphragm or the
phrenic nerve occurs with lead dislodgement
or with high output from a left ventricular lead
placed in the coronary sinus.
4. “Pacemaker-mediated tachycardia was on my
differential, but I was afraid to place a magnet
over the pacemaker.”
A pacemaker magnet only disables the sensing
function, not the pacing function, and it can be
effective in terminating pacemaker-mediated
tachycardia as well as for differentiating
among various types of potential pacemaker
malfunction.
10. “Ventricular tachycardia clearly wasn’t the
cause of his symptoms. If he had ventricular
tachycardia, his CRT-D device would have
shocked him.”
Ventricular tachycardia may occur at
rates below the programmed tachycardia
detection rate (TDR). Above the TDR, ICD
therapy is administered. A low TDR can be
programmed, with the risk of administering
therapy inappropriately to supraventricular
tachyarrhythmias. Antitachycardia pacing
and algorithms to improve the specificity of
VT detection have reduced the incidence of
inappropriate ICD therapy for supraventricular
arrhythmias.
5. “I thought all newer pacemakers were MRIcompatible.”
While advances in pacemaker design have
led to the development of pacing leads and
pulse generators that are safe for the magnetic
environment, safe MRI requires careful
screening, established protocols, and physician
supervision.
September 2014 • www.ebmedicine.net
15
Reprints: www.ebmedicine.net/empissues
of 3 or more appropriate shocks within a 24-hour
period is termed electrical storm), the patient should
be evaluated for possible electrolyte abnormalities
(potassium and magnesium), myocardial ischemia, proarrhythmic drug effect, or other causes
of QT prolongation. In cases of electrical storm,
amiodarone, intravenous beta-adrenergic receptor antagonists, and propofol are suggested drug
therapies.113-115 Refractory cases of electrical storm
may require general anesthesia, left ventricular assist devices, and emergent radiofrequency ablation.
The diagnosis of MI may be difficult in these patients, as transient postshock ST-segment deviation
is common and myocardial injury can be caused by
the shocks themselves.107,109,116,117
may fail to deliver appropriate therapy, as in situations
where rhythm sensing or shock delivery is compromised. For example, an ipsilateral tension pneumothorax may raise the defibrillation threshold, leading to
ineffective shocks.64 Antiarrhythmic agents that block
fast inward sodium channels (ie, lidocaine) may also
increase the threshold, but agents that prolong repolarization (ie, sotalol) may decrease the threshold.108
Keeping all of these in mind, if external electrical
therapy is required, transcutaneous pads should be
placed anterior-posteriorly if possible, and as far from
the pacemaker as possible to avoid damage to the
device.64,100,109 The rescuer may also consider magnet
placement to avoid unintentional device-mediated
therapies during resuscitation.109 After successful resuscitation, the device should be interrogated to ensure
proper status of its parameters.109
If central venous access is required, the femoral
vein is the safest approach in a patient with a pacemaker.64,110 Pacemaker wires in the subclavian vein
are often thrombosed, and may preclude normal
ipsilateral subclavian vein cannulation. In addition,
contact between a procedural guidewire and a lead
can trigger an inappropriate response.64
Disposition
The majority of patients presenting with implantrelated complications or pacemaker malfunction will
require consultation with a cardiologist and, potentially, hospital admission. Pacemaker interrogation
can be performed in the ED to rule out arrhythmia
and pacemaker malfunction, and to avoid unnecessary hospital admission in some of these patients.
Approach To The Pacemaker/Implantable
Cardioverter-Defibrillator Patient Who
Receives A Shock
Controversies And Cutting Edge
Many contemporary pacemakers include antitachycardia functions via combinations of overdrive
pacing, cardioversion, and/or defibrillation programmed to occur at designated detection zones.
Newer-generation devices employ algorithms to
distinguish ventricular from supraventricular tachycardia in order to reduce the risk of inappropriate
shocks. These devices use rhythm characteristics
such as onset, rate stability, electrogram morphology, and atrioventricular dissociation to differentiate
ventricular from supraventricular tachycardia.109,111
In one study, a dual-chamber algorithm reduced the
rate of inappropriate detection by 50%.112
The occurrence of a single shock in a patient
without preceding symptoms does not require immediate ED consultation with an electrophysiologist; referral within the week is generally appropriate.111 However, in the presence of symptoms such
as dyspnea, chest pain, or weakness, underlying
etiologies such as myocardial ischemia, decompensated heart failure, or electrolyte imbalance should
be considered. The patient who receives multiple
shocks should receive immediate attention and
cardiac monitoring in the ED until the device can
be interrogated. Multiple inappropriate shocks may
occur in response to supraventricular tachycardia
and may require reprogramming by an electrophysiologist or representative from the device
manufacturer. (See Figure 6, page 12.) If defibrillation therapy is found to be appropriate (delivery
Copyright © 2014 EB Medicine. All rights reserved.
Remote Monitoring
Some devices allow for remote monitoring of data,
including heart rate variability, tachyarrhythmia frequency and duration, intrathoracic impedance, and
percentage of time that the rhythm is paced. Integration of these data points can be clinically useful in
predicting heart failure hospitalizations.118-120 Future
research is required to define how remote monitoring might lead to improved clinical outcomes.
Leadless Pacing
As described above, many pacemaker complications
relate either to transvenous leads or the subcutaneous pulse generator. Leadless pacing systems are
currently under development and early experience
has demonstrated safety and efficacy in single-chamber ventricular pacing.121
Device Deactivation
Patients with terminal illness may request device
deactivation along with do not resuscitate (DNR)
status. The HRS has published a consensus statement that declares deactivation of an implanted
device as ethical and legally permissible.122 Emergency clinicians should engage patients in conversation about advance directives as they relate to
their cardiac device.
16
www.ebmedicine.net • September 2014
1. Summary
Emergency clinicians must be familiar with the
indications for pacemaker placement and aware of
the complications associated with implantation. A
systematic approach to evaluating the pacemaker is
key to expeditious diagnosis of device malfunction.
This includes careful history taking, a thorough
physical examination of the patient, and accurate
interpretation of the 12-lead ECG and chest radiographs. Device interrogation is a critical step in
troubleshooting with regard to both pacemaker and
antitachycardia functions.
2. 3. 4. Case Conclusions
Before reflexively calling the electrophysiologist to interrogate the pacemaker of the 78-year-old woman with widened
QRS complexes and bradycardia, you paused to consider
a life-threatening cause of both QRS widening and failure
to capture. You sent for a potassium level on a blood gas
sample and administered calcium gluconate before finding
out the lab result. You watched the QRS complexes on the
monitor narrow to their previous width as the heart rate
increased. After another dose of calcium gluconate, you
noticed that all pacing artifacts were captured. Lab results
returned, showing a serum potassium level of 8.7 mEq/L,
with prerenal azotemia. You consulted the nephrologist and
admitted the patient to the ICU.
You obtained a chest x-ray on the 38-year-old woman
with sarcoidosis and compared it to the x-ray obtained
shortly after implantation of her pacemaker. You noticed that both atrial and ventricular pacing leads were
retracted into the superior vena cava and wound around
the vertical axis of the pulse generator. The patient denied
manipulating the device, but the x-ray was consistent
with twiddler syndrome. The patient was admitted to the
cardiac ICU and later taken to the operating room for lead
revision and reinforcement of the pulse generator with a
Dacron® pouch.
5.* 6. 7.* 8. 9. References
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are
equally robust. The findings of a large, prospective,
random­ized, and blinded trial should carry more
weight than a case report.
To help the reader judge the strength of each
reference, pertinent information about the study
will be included in bold type following the ref­
erence, where available. In addition, the most informative references cited in this paper, as determined
by the authors, will be noted by an asterisk (*) next
to the number of the reference.
September 2014 • www.ebmedicine.net
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of pacemaker syndrome in patients with sinus node dysfunction treated with ventricular-based pacing in the Mode
Selection Trial (MOST). J Am Coll Cardiol. 2004;43(11):20662071. (Prospective cohort; 182 patients)
71.* Trohman RG, Kim MH, Pinski SL. Cardiac pacing: the state
of the art. Lancet. 2004;364(9446):1701-1719. (Review)
72. Mollazadeh R, Mohimi L, Zeighami M, et al. Hemodynamic
effect of atrioventricular and interventricular dyssynchrony
in patients with biventricular pacing: implications for the
pacemaker syndrome. J Cardiovasc Dis Res. 2012;3(3):200-203.
(Cross-sectional; 40 patients)
73.* Lamas GA, Lee KL, Sweeney MO, et al. Ventricular pacing
or dual-chamber pacing for sinus-node dysfunction. N Engl J
Med. 2002;346(24):1854-1862. (Randomized controlled trial;
2010 patients)
74. Maisel WH, Moynahan M, Zuckerman BD, et al. Pacemaker
and ICD generator malfunctions: analysis of Food and Drug
Administration annual reports. JAMA. 2006;295(16):19011906. (Retrospective observational)
75. Tracy CM, Epstein AE, Darbar D, et al. 2012 ACCF/AHA/
HRS focused update of the 2008 guidelines for devicebased therapy of cardiac rhythm abnormalities: a report of
the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines
and the Heart Rhythm Society. [corrected]. Circulation.
2012;126(14):1784-1800. (Guidelines)
76. Maisel WH. Pacemaker and ICD generator reliability: metaanalysis of device registries. JAMA. 2006;295(16):1929-1934.
(Meta-analysis; 3365 patients)
77. Hauser RG, Hayes DL, Kallinen LM, et al. Clinical experience with pacemaker pulse generators and transvenous
leads: an 8-year prospective multicenter study. Heart Rhythm.
19
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2007;4(2):154-160. (Prospective observational; 2652 pulse
generators, 615 leads)
78. Ofman P, Rahilly-Tierney C, Djousse L, et al. Pacing system
malfunction is a rare cause of hospital admission for syncope
in patients with a permanent pacemaker. Pacing Clin Electrophysiol. 2013;36(1):109-112. (Retrospective observational; 162
patients)
79. Emilsson K, Oddsson H, Allared M, et al. An unusual cause
of high threshold values at pacemaker implantation. Pacing
Clin Electrophysiol. 1997;20(2 Pt 1):366-367. (Case report)
80. Patton KK, Levy M, Viswanathan M. Atrial lead dysfunction: an unusual feature of hypothyroidism. Pacing Clin
Electrophysiol. 2008;31(12):1650-1652. (Case report)
81. Takasugi N, Kubota T, Kawamura I, et al. Sudden reversible pacemaker failure in a patient with cardiac sarcoidosis:
an unfortunate case of ventricular septal pacing. Europace.
2012;14(7):1061-1062. (Case report)
82. Montefoschi N, Boccadamo R. Propafenone induced acute
variation of chronic atrial pacing threshold: a case report.
Pacing Clin Electrophysiol. 1990;13(4):480-483. (Case report)
83. Barold SS, Herweg B. The effect of hyperkalaemia on cardiac
rhythm devices. Europace. 2014. (Review)
84. Santos KR, Adragao P, Cavaco D, et al. Diaphragmatic myopotential oversensing in pacemaker-dependent patients with
CRT-D devices. Europace. 2008;10(12):1381-1386. (Retrospective observational; 37 patients)
85. Gross JN, Platt S, Ritacco R, et al. The clinical relevance of
electromyopotential oversensing in current unipolar devices.
Pacing Clin Electrophysiol. 1992;15(11 Pt 2):2023-2027. (Prospective observational; 34 patients)
86. Brown KR, Carter W, Jr., Lombardi GE. Blunt traumainduced pacemaker failure. Ann Emerg Med. 1991;20(8):905907. (Case report)
87.* Misiri J, Kusumoto F, Goldschlager N. Electromagnetic
interference and implanted cardiac devices: the nonmedical environment (part I). Clin Cardiol. 2012;35(5):276-280.
(Review)
88. Misiri J, Kusumoto F, Goldschlager N. Electromagnetic interference and implanted cardiac devices: the medical environment (part II). Clin Cardiol. 2012;35(6):321-328. (Review)
89. Tandogan I, Temizhan A, Yetkin E, et al. The effects
of mobile phones on pacemaker function. Int J Cardiol.
2005;103(1):51- 58. (Cross-sectional; 679 patients)
90. Tandogan I, Ozin B, Bozbas H, et al. Effects of mobile
telephones on the function of implantable cardioverter defibrillators. Ann Noninvasive Electrocardiol. 2005;10(4):409-413.
(Cross-sectional; 43 patients)
91. Jilek C, Tzeis S, Vrazic H, et al. Safety of screening procedures with hand-held metal detectors among patients with
implanted cardiac rhythm devices: a cross-sectional analysis.
Ann Intern Med. 2011;155(9):587-592. (Cross-sectional; 388
patients)
92. Gimbel JR, Cox JW Jr. Electronic article surveillance systems
and interactions with implantable cardiac devices: risk of
adverse interactions in public and commercial spaces. Mayo
Clin Proc. 2007;82(3):318-322. (Case series; 2 patients)
93. Webster G, Jordao L, Martuscello M, et al. Digital music
players cause interference with interrogation telemetry
for pacemakers and implantable cardioverter-defibrillators without affecting device function. Heart Rhythm.
2008;5(4):545- 550. (Cross-sectional; 51 patients)
94. Wolber T, Ryf S, Binggeli C, et al. Potential interference
of small neodymium magnets with cardiac pacemakers
and implantable cardioverter-defibrillators. Heart Rhythm.
2007;4(1):1-4. (Cross-sectional; 70 patients)
95. Levine GN, Gomes AS, Arai AE, et al. Safety of magnetic
resonance imaging in patients with cardiovascular devices:
an American Heart Association scientific statement from
the Committee on Diagnostic and Interventional Cardiac
Catheterization, Council on Clinical Cardiology, and the
Copyright © 2014 EB Medicine. All rights reserved.
Council on Cardiovascular Radiology and Intervention: endorsed by the American College of Cardiology Foundation,
the North American Society for Cardiac Imaging, and the
Society for Cardiovascular Magnetic Resonance. Circulation.
2007;116(24):2878-2891. (Scientific statement)
96. Hayes DL, Holmes DR Jr, Gray JE. Effect of 1.5 tesla nuclear
magnetic resonance imaging scanner on implanted permanent pacemakers. J Am Coll Cardiol. 1987;10(4):782-786.
(Cross-sectional; 8 patients)
97. Nazarian S, Hansford R, Roguin A, et al. A prospective
evaluation of a protocol for magnetic resonance imaging of
patients with implanted cardiac devices. Ann Intern Med.
2011;155(7):415-424. (Prospective nonrandomized trial; 438
patients, 555 MRI studies)
98. Kanal E, Borgstede JP, Barkovich AJ, et al. ACR Blue Ribbon
Panel response to the AJR commentary by Shellock and
Crues on the ACR white paper on MR safety. AJR Am J
Roentgenol. 2003;180(1):31-35. (Comment)
99. Das G, Staffanson DB. Selective dysfunction of ventricular
electrode-endocardial junction following DC cardioversion
in a patient with a dual chamber pacemaker. Pacing Clin
Electrophysiol. 1997;20(2 Pt 1):364-365. (Case report)
100. Waller C, Callies F, Langenfeld H. Adverse effects of direct
current cardioversion on cardiac pacemakers and electrodes
Is external cardioversion contraindicated in patients with
permanent pacing systems? Europace. 2004;6(2):165-168.
(Case report; 3 cases)
101. Platonov MA, Gillis AM, Kavanagh KM. Pacemakers,
implantable cardioverter/defibrillators, and extracorporeal
shockwave lithotripsy: evidence-based guidelines for the
modern era. J Endourol. 2008;22(2):243-247. (Guideline)
102. Fishberger SB, Mehta D, Rossi AF, et al. Variable effects of
adenosine on retrograde conduction in patients with atrioventricular nodal reentry tachycardia. Pacing Clin Electrophysiol. 1998;21(6):1254-1257. (Prospective nonrandomized
trial; 13 patients)
103. Sarko JA, Tiffany BR. Cardiac pacemakers: evaluation
and management of malfunctions. Am J Emerg Med.
2000;18(4):435-440. (Review)
104. Lewalter T, Schimpf R, Kulik D, et al. Comparison of spontaneous atrial fibrillation electrogram potentials with the
P-wave electrogram amplitude in dual chamber pacing with
unipolar atrial sensing. Europace. 2000;2(2):136-140. (Prospective observational; 42 patients)
105. Jacob S, Panaich SS, Maheshwari R, et al. Clinical applications of magnets on cardiac rhythm management devices.
Europace. 2011;13(9):1222-1230. (Review)
106. Becker R, Ruf-Richter J, Senges-Becker JC, et al. Patient
alert in implantable cardioverter defibrillators: toy or tool?
J Am Coll Cardiol. 2004;44(1):95-98. (Prospective cohort; 240
patients)
107. Stevenson WG, Chaitman BR, Ellenbogen KA, et al. Clinical
assessment and management of patients with implanted
cardioverter-defibrillators presenting to nonelectrophysiologists. Circulation. 2004;110(25):3866-3869. (Review)
108. Glikson M, Friedman PA. The implantable cardioverter
defibrillator. Lancet. 2001;357(9262):1107-1117. (Review)
109. Pinski SL. Emergencies related to implantable cardioverterdefibrillators. Crit Care Med. 2000;28(10 Suppl):N174-N180.
(Review)
110. McPherson CA, Manthous C. Permanent pacemakers and
implantable defibrillators: considerations for intensivists. Am
J Respir Crit Care Med. 2004;170(9):933-940. (Review)
111.* Gehi AK, Mehta D, Gomes JA. Evaluation and management
of patients after implantable cardioverter-defibrillator shock.
JAMA. 2006;296(23):2839-2847. (Review)
112. Friedman PA, McClelland RL, Bamlet WR, et al. Dualchamber versus single-chamber detection enhancements for
implantable defibrillator rhythm diagnosis: the detect supraventricular tachycardia study. Circulation. 2006;113(25):2871-
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2879. (Randomized controlled trial; 400 patients)
113. Credner SC, Klingenheben T, Mauss O, et al. Electrical storm
in patients with transvenous implantable cardioverter-defibrillators: incidence, management and prognostic implications. J Am Coll Cardiol. 1998;32(7):1909-1915. (Prospective
cohort; 136 patients)
114. Nademanee K, Taylor R, Bailey WE, et al. Treating electrical
storm: sympathetic blockade versus advanced cardiac life
support-guided therapy. Circulation. 2000;102(7):742-747.
(Prospective nonrandomized trial; 49 patients)
115. Mulpuru SK, Patel DV, Wilbur SL, et al. Electrical storm
and termination with propofol therapy: a case report. Int J
Cardiol. 2008;128(1):e6-e8. (Case report)
116. Sham’a RA, Nery P, Sadek M, et al. Myocardial injury
secondary to ICD shocks: insights from patients with lead
fracture. Pacing Clin Electrophysiol. 2014;37(2):237-241. (Prospective observational; 22 patients)
117. Gurevitz O, Lipchenca I, Yaacoby E, et al. ST-segment deviation following implantable cardioverter defibrillator shocks:
incidence, timing, and clinical significance. Pacing Clin Electrophysiol. 2002;25(10):1429-1432. (Prospective observational;
28 patients)
118. Cowie MR, Sarkar S, Koehler J, et al. Development and validation of an integrated diagnostic algorithm derived from
parameters monitored in implantable devices for identifying
patients at risk for heart failure hospitalization in an ambulatory setting. Eur Heart J. 2013;34(31):2472-2480. (Retrospective observational; 2231 patients)
119. Sack S, Wende CM, Nagele H, et al. Potential value of automated daily screening of cardiac resynchronization therapy
defibrillator diagnostics for prediction of major cardiovascular events: results from Home-CARE (Home Monitoring in
Cardiac Resynchronization Therapy) study. Eur J Heart Fail.
2011;13(9):1019-1027. (Prospective cohort; 377 patients)
120. Whellan DJ, Ousdigian KT, Al-Khatib SM, et al. Combined
heart failure device diagnostics identify patients at higher
risk of subsequent heart failure hospitalizations: results from
PARTNERS HF (Program to Access and Review Trending Information and Evaluate Correlation to Symptoms
in Patients With Heart Failure) study. J Am Coll Cardiol.
2010;55(17):1803- 1810. (Retrospective observational trial;
694 patients)
121. Reddy VY, Knops RE, Sperzel J, et al. Permanent leadless
cardiac Pacing: results of the LEADLESS trial. Circulation.
2014. (Prospective nonrandomized trial; 33 patients)
122. Lampert R, Hayes DL, Annas GJ, et al. HRS expert consensus statement on the management of cardiovascular implantable electronic devices (CIEDs) in patients nearing end of
life or requesting withdrawal of therapy. Heart Rhythm.
2010;7(7):1008-1026. (Consensus statement)
CME Questions
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CME credits for this issue, scan the QR code
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www.ebmedicine.net/E0914.
1. Cardiac resynchronization therapy is indicated
for patients with heart failure and:
a. Recurrent ischemic events
b. Ventricular dysrhythmias
c. A left bundle branch block
d. Atrioventricular nodal conduction delay
2. Electrocardiographic findings indicative of
severe hyperkalemia in a patient with a paced
rhythm include:
a. QRS widening
b. Failure to capture
c. Sine wave QRS morphology
d. All of the above
3. Acute myocardial infarction in a paced rhythm:
a. Is always electrocardiographically silent
b. Can be detected by elevated ST segments in a pattern of exaggerated discordance
c. Is the most common cause of failure to sense
d. Can be detected by applying a magnet
4. The manufacturer of a pacemaker can be identified by:
a. The amplitude of pacing artifacts on the 12- lead ECG
b. The size of the pulse generator
c. Placing a magnet over the pulse generator
d. None of the above
September 2014 • www.ebmedicine.net
21
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5. Management of an infected device usually
involves:
a. Intravenous antibiotics and device removal
b. Needle aspiration of the infected pocket and intravenous antibiotics
c. A prolonged course of oral antibiotics
d. Incision and drainage of the pocket followed by wound care
Get 4 Hours Stroke CME Credit From
The July and August 2013 Issues Of
EM Practice Guidelines Update
6. What is the most common cause of failure to
pace?
a. Lead fracture
b. Oversensing
c. Lead dislodgement
d. Battery depletion
The July and August 2013 issues of our online
journal supplement, EM Practice Guidelines
Update, are devoted to stroke topics, and each
offers 2 hours of Stroke CME credit. All subscribers to Emergency Medicine Practice automatically
receive free subscriptions to EM Practice Guidelines Update; to access the articles, simply log in
to your www.ebmedicine.net account (or give us
a call and we’ll help you get your account set up).
The July 2013 issue reviews the 2009 guideline on transient ischemic attack (TIA) and the
revised American Heart Association/American
Stroke Association (AHA/ASA) “tissue-based” diagnosis of TIA. Jonathan Edlow, MD, of Harvard
Medical School, offers a guest editorial on the
evolution of effective emergency care options
for TIA patients, and Editor-in-Chief Sigrid Hahn,
MD reviews and comments on portions of the
guideline relevant to emergency clinicians. Read
the issue online at: www.ebmedicine.net/TIA.
7. MRI in patients with pacemakers:
a. Is uniformly contraindicated
b. Can be performed without complications as long as the pacemaker was manufactured after 2002
c. Can be performed, as long as a magnet is placed over the implanted device
d. Can be performed in some cases, but only if specific guidelines are met
8. What is the mechanism of pacemaker-mediated
tachycardia?
a. A re-entrant circuit
b. Increased automaticity at the site of the ventricular electrode tip
c. Cardiac remodeling
d. Delayed afterdepolarizations
9. Placing a magnet on a pacemaker effectively:
a. Switches the pacemaker into an asynchronous mode
b. Turns pacing off
c. Turns sensing on
d. Switches the pacemaker into a demand pacing mode
The August 2013 issue reviews 2 different
guidelines published in 2013 on acute ischemic
stroke and the use of intravenous t-PA (tissue
plasminogen activator) from: (1) the American
College of Emergency Physicians jointly with
the American Academy of Neurology, and (2)
the AHA/ASA. Christopher Hopkins, MD of the
University of Florida College of Medicine-Jacksonville, the guest editor, provides an assessment of
these controversial new guidelines, which have
been 8 years in development. Read this issue
online at: www.ebmedicine.net/Stroke.
10. External defibrillation in a patient with an
implanted cardiac device:
a. Is contraindicated
b. Is not necessary if the device has anti-
tachycardia function (ICD)
c. Can be performed if pads are placed a safe distance away from the device
d. Can be performed, but only at 50 joules
Copyright © 2014 EB Medicine. All rights reserved.
22
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