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STRATEGIES IN OUT-OF-HOSPITAL CARDIAC ARREST
145
Marenco JP, Wang PJ, Link MS, Homoud MK, Estes 6
NAM. Improving survival from sudden cardiac arrest:
The role of the automated external defi brillator. JAMA.
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Nichol G, Stiell IG, Laupacis A, et al. A cumulative 7
meta-analysis of the effectiveness of defi brillator-capable
emergency medical services for victims of out-of-hospital
cardiac arrest. Ann Emerg Med. 1999;34:517–525.
Weisfeldt ML, Kerber RE, McGoldrick RP, et al. Public 8
access defi brillation: a statement for health care pro-
fessionals from the American Heart Association Task
Force on Automatic External Defi brillation. Circulation.
1995;92:2763.
Eisenbert MS, Bergner L, Hallstrom AP, Cummins RO. 9
Sudden cardiac death. Sci Am. 1986;254:37–43.
Weaver WD, Cobb LA, Hallstrom AP. Factors infl uenc-10
ing survival after out-of-hospital cardiac arrest. J Am
Coll Cardiol. 1986;7:752–775.
Eisenberg MS, Hallstrom A, Bergner L. The ACLS score: 11
predicting survival from out-of-hospital cardiac arrest.
JAMA. 1981;246:50–52.
Kouwenhoven DR, Brady WJ. The development of the 12
defi brillator. Ann Intern Med. 1969;71:449–458.
Haskell WL. Cardiovascular complications dur-13
ing exercise training of cardiac patients. Circulation.
1978;57:920–924.
Hossack KF, Hartwig R. Cardiac arrest associated 14
with supervised cardiac rehabilitation. J Card Rehabil.
1982;2:402–08.
VanCamp SP, Peterson RA. Cardiovascular complica-15
tions of outpatient cardiac rehabilitation programs.
JAMA. 1986;256:1160–1163.
Weaver WD, Cobb LA, Dennis D, Ray R, Hallstrom 16
AP. Amplitude of ventricular fi brillation waveform
and outcome after cardiac arrest. Ann Intern Med.
1985;102:53–55.
Cummins RO, Eisenberg MS, Hallstrom AP, Litwin PE. 17
Survival of out-of-hospital cardiac arrest with early ini-
tiation of cardiopulmonary resuscitation Am J Emerg
Med. 1958;3:114–119.
Jakobsson J, Nyquist O, Rehnqvist N. Cardiac arrest in 18
Stockholm with special reference to the ambulance orga-
nization. Acta Med Scand. 1987;222:117–122.
Larsen MP, Eisenberg MS Cummins RO, Hallstrom 19
AP. Predicting survival from out-of-hospital cardiac
arrest: a graphic model. Ann Emerg Med. 1993;22:
1652–1658.
Eisenberg M, Bergner L, Hallstrom A. Paramedic pro-20
grams and out-of-hospital cardiac arrest: I. Factors asso-
ciated with successful resuscitation. Am J Public Health.
1979;69:30–38.
Bossaert L, VanHoeywghen R. Cerebral resuscitation 21
study group: Bystander cardiopulmonary resuscitation
made many people afraid of and adverse to providing
aid. Many organizations and individuals have voiced
safety concerns as well as liability issues in purchasing
and providing access to AEDs. Nevertheless, AEDs
are safe and effective even in untrained hands. Over
the past several years, as more and more evidence sup-
porting the safety and effi cacy of AED and PAD has
been published, state legislatures have promoted PAD
by writing legislation specifi cally to protect responders
using AEDs. Some states and the federal government
have gone further to even mandate AEDs be placed in
special environments, such as aboard commercial air-
craft, in health clubs, and in schools. There have even
been cases in which a business corporation has been
found negligent for not having AEDs available.
42
Section IV: Decision making
The “local site” personnel should consider the follow-
ing issues when deciding upon AED deployment:
Will the individual location is occupied by a good-•
sized number of persons for a signifi cant portion of
the 24-hour day?
Will the persons potentially present at the site are •
of the appropriate age and risk for sudden cardiac
death (middle-aged and older adults)?
Will EMS (and AED-equipped public safety offi cer) •
response times to the patient’s side likely be greater
than 4 minutes?
References
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cardiac death in the United States, 1989 to 1998.
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Nicol G, Hallstrom AP, Kerber R, et al. American 3
Heart Association Report on the Second Public
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Circulation. 1998;97:1309–1314.
Eisenberg MS, Horwood BT, Cummings RO, Reynolds-4
Haertle R, Hearne TR. Cardiac arrest resuscitation: a
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Jermyn BD. Cost-effectiveness analysis of a rural/urban 38
fi rst-responder defi brillation program. Prehosp Emerg
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Nicholg, Hallstrom AP, Ornato JP, et al. Potential cost-39
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147
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
Pacemakers and AICDS in
emergency medicine
Theodore Chan
Medical Director, Department of Emergency Medicine, University of California, San Diego
Medical Center, Professor of Clinical Medicine, University of California, San Diego,
San Diego, California, USA
11
Section I: Case presentation
An 82-year-old woman with a history of Alzheimer’s
dementia was brought to the emergency department
(ED) from her nursing home by paramedics. She was
complaining of weakness and bilateral lower extrem-
ity swelling, but could not provide much history
beyond that. A review of records sent from the nurs-
ing home indicates that she had these complaints for
the prior 3 days. In addition, her appetite and intake
had been poor during this time, but she had no vomit-
ing, diarrhea, fevers, or other symptoms noted by the
nursing home staff. The staff became concerned when
they recorded a pulse rate of 48 beats/min, so they
called 911.
The nursing home records indicate the patient was
taking hydrochlorothiazide, diltiazem, potassium
supplementation, and thyroid hormone replacement,
with no recent changes to her medications. The past
medical history from the nursing record was notable
for hypertension, hypothyroidism, pacemaker place-
ment, and a remote history of breast cancer.
The triage vital signs were: blood pressure 106/52
mmHg, pulse rate 50 beats/min, respiratory rate 16
breaths/min, and temperature 37.2°C (98.9°F). On
initial evaluation, the patient was an elderly woman
in mild distress, lying on a gurney. Physical examina-
tion fi ndings were notable for a healed bilateral mas-
tectomy scar, a palpable pacemaker device along the
left upper chest wall, and clear breath sounds on chest
auscultation. Cardiac examination revealed a slow,
occasionally irregular heart beat with a faint systolic
murmur, best heard along the base. The abdomen was
soft and benign, and the extremities were nontender
with no edema.
The patient was placed on a cardiac monitor and a
12-lead EKG was obtained, which demonstrated pacer
spikes with intermittent QRS wave forms with T wave
inversions in the anterolateral leads (Figure 11-1).
There was no prior EKG available for comparison.
A complete blood count, serum electrolytes and TSH
level were unremarkable, and the cardiac troponin-I
level was ⬍ 0.02 ng/ml.
Section II: Case discussion
Dr Peter Rosen: Assuming that this is a patient capa-
ble of independent living, and we want to improve the
quality of her life, do you believe many of her symp-
toms can be explained by the pacemaker?
Dr David Brown: The description of the EKG doesn’t
specifi cally tell me whether each QRS is preceded by a
pacemaker spike, nor whether every pacemaker spike
is followed by a QRS. It doesn’t describe whether it
is atrioventricular (AV) pacing or ventricular pacing.
I think we need to know a little more about precisely
what the EKG showed. Is there evidence of pacemaker
CHAPTER 11
148
pacemaker dysfunction, we don’t need to immediately
reach for an external pacemaker. What would your
indications be for external pacing?
Dr Theodore Chan: If the nursing records note a sig-
nifi cant change in her mental status, or any suggestion
that she’s hemodynamically unstable, then external
pacing might be useful. It would be important to look
at the nursing records to see what her previous hemo-
dynamic status was. If she had a history of hyperten-
sion, then a blood pressure of 106 may be signifi cantly
low for her, and indicate hemodynamic instability.
PR: My experience with external pacing has been dis-
mal. I’ve had patients capture with it, but if they were
at all alert, they hated the experience, and required
heavy sedation. If the clinical circumstances were
forcing your hand, would you ever consider fl oating
another temporary transvenous pacemaker wire on
someone who has a nonfunctioning pacemaker?
Dr Shamai Grossman: I would always start with an
external pacemaker. The only real contraindication to
an external pacemaker, aside from failure to capture, is
patient discomfort. Patients often are very uncomfort-
able. The major problem with an external pacemaker
is it requires more amperage to pace someone than a
transvenous or an implanted pacemaker. We use far
more electricity externally to pace someone, and clini-
cally that causes discomfort. If the blood pressure can
tolerate it, you can concomitantly give analgesia and
that may help, but if you can’t get capture with an
external pacer or the patient is so uncomfortable he
or she refuses to allow you to externally pace him or
malfunction, or is she at a rate of 50 simply because
that is what the pacemaker is set at as a default for
when she goes into some other kind of bradycardia,
native bradyarrhythmia, for some other reason.
DB: Looking at her EKG with pacer spikes at a regular
rate of about 65, QRS waveforms at about 0.10 msec,
but with T wave inversions laterally and pacer spikes
that do not appear to be associated with the QRS
waveforms, I would think her bradycardia is at least in
part related to pacemaker malfunction. We have evi-
dence of a pacemaker that was set at 65, not capturing
the ventricles, and there’s what may be a junctionally-
derived escape rhythm at 50 beats/min that is main-
taining cardiac output. It is likely the bradycardia that
is causing her to be sick.
PR: In this situation would you recommend obtain-
ing a chest X-ray study immediately to look for a
pacemaker wire fracture, or do you just reach for a
magnet to defi ne whether or not there is pacemaker
function?
Dr Amal Mattu: I would probably do both simulta-
neously. Getting a quick chest X-ray study certainly
doesn’t take long, and might give you information
about whether there’s a break in the lead insulation
or dislodgement. In the meantime, I would be on the
phone with an electrophysiologist or a technician from
the pacemaker manufacturers who also might be able
to assess the pacer. I would place a magnet as well.
PR: This patient doesn’t sound like she’s in a great deal
of distress from the pacemaker dysfunction. Given
she’s functioning adequately in this case, despite the
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
V1
Figure 11.1 Presenting 12-lead EKG. Note the low amplitude pacing spikes not associated with the QRS complexes.
PACEMAKERS AND AICDS IN EMERGENCY MEDICINE
149
PR: So you’d see a series of spikes with or without a
QRS following.
TC: Correct.
SG: Application of a magnet can also determine if the
pacemaker’s battery needs to be replaced. Each pace-
maker type has a unique asynchronous rate for begin-
ning-of-life of the unit (BOL), elective replacement
indicator (ERI), and end-of-life of the unit (EOL).
PR: How can you tell if the pacemaker is single- or
dual-chambered, or what kind of pacemaker your
patient has?
TC: Dual-chamber pacemakers will often have both
atrial and ventricular spikes on the EKG.
SG: On chest X-ray study, if you see a lead going into
the atrium, and a lead going into the ventricle, then
clearly it’s a dual-chamber pacemaker. Often the spe-
cifi c type of pacemaker can be verifi ed by identifying
the generator on the chest X-ray study. In addition,
most patients carry a card with them verifying essential
pacemaker information, such as the model type and the
magnet rates. Patients who have atrial fi brillation gen-
erally don’t get DDD (atrial and ventricular lead) pace-
makers, because in atrial fi brillation the pacemaker
itself is not able to pace the atrium.
PR: Is it possible that the atrium can capture, but not
the ventricle, or vice versa with a dual chamber? What
would that look like?
TC: That depends on the underlying rhythm. If the
atrium were capturing and the ventricle not captur-
ing, and the native AV conduction intact, you would
see the atrial spike and subsequent P wave, followed
by the native QRS complex from conduction through
the intact AV pathway. If the native AV conduction
pathway is not intact or there is a block, you would
again see the atrial spike with P wave, followed by a
ventricular spike, but no corresponding paced QRS
complex due to the lack of ventricular capture.
PR: Would anybody set a pacemaker at a rate of 50?
DB: Perhaps not in an 82-year-old, but patients with
intermittent bradyarrhythmias who, for the most part,
are in sinus rhythm, might have a pacemaker placed
and set at a low rate to avoid competing with their
native sinus rhythm. The pacemaker would provide
a safety backup.
her, then you can try to fl oat a temporary transvenous
pacemaker wire in the ED.
PR: It’s been a long time since I’ve fl oated a wire, since
I’ve been lucky enough to work at places where many
resources are readily available, but if you’re in a more
remote community hospital, do you have any sugges-
tions for us in terms of fl oating a wire without fl uoro-
scopic guidance?
DB: When one is forced to proceed because of lack
of resources or instability of the patient, ideally, you
want to place the introducer in the right internal jugu-
lar vein since it’s a more direct route, straight down
through the superior vena cava and into the right
atrium and then into the right ventricle. Although
some EDs may have a portable c-arm, fl uoroscopy
is often unavailable to emergency physicians; how-
ever, ultrasound is very useful. A portable ultrasound
should be available in most EDs these days to watch
the wire progress to the right ventricle.
PR: Do you think that this patient, on a thiazide
diuretic, could have a metabolic abnormality, such as
hypokalemia, that’s interfering with the pacemaker
function? Could the pacemaker perhaps be in place,
but the heart can’t respond?
AM: Metabolic abnormalities would defi nitely be
in the differential when the pacemaker’s not being
sensed. Several electrolyte or metabolic abnormalities
are notorious for causing problems with pacemakers,
and are the most common cause of transcutaneous
pacemaker dysfunction that I’ve seen. Any patient
presenting with a pacemaker problem must have a set
of electrolytes and metabolic panel performed look-
ing for this relatively simple reversible cause.
PR: Could you take us through the use of a magnet?
What kind of magnet, where do you put it, what do
you expect to see, and how do you interpret the moni-
tor strip when the magnet is in place?
TC: We usually keep a donut-shaped magnet in the
ED. It should be placed directly on top of the pace-
maker generator where, once in place, the magnet
turns off sensing. This temporarily puts the pace-
maker into the asynchronous mode, where pacing is
initiated at a set rate. This may allow you to assess
whether capture is occurring, and helps assess func-
tion when the native heart rhythm is faster than the
rate the pacemaker is set at.
CHAPTER 11
150
effects may further compromise the patient’s current
status and hinder more than help.
PR: Do you ever see pacemaker dysfunction that
causes tachycardia rather than bradycardia?
AM: You can get a pacemaker-mediated tachycar-
dia, even from a normally functioning pacemaker.
Retrograde conduction of a ventricular beat may cause
the atrium to trigger a second ventricular contraction
that falls during the pacemaker’s refractory period.
Because this contraction is not sensed by the pace-
maker, the pulse generator fi res, initiating a reentry
tachycardia.
SG: Treatment consists of lengthening the atrioven-
tricular time by any of the following methods: (1) pro-
gramming an increase in the atrial refractory time,
(2) administering adenosine or verapamil, (3) increas-
ing atrial sensory threshold, and (4) applying a magnet
to stop atrial sensing by the pacemaker.
PR: There are patients who come to the ED to “have
their pacers interrogated.” I never know what they
mean by that, and I’m not sure what to do to help
them. Can you explain that for me?
TC: Interrogation is really a more in-depth assessment
of their pacemaker functioning, and usually requires the
technician or electrophysiologist to come in to assess the
sensing and the pacing functions, and also review prior
incidents. For example, in a pacemaker with an auto-
matic implantable cardioverter defi brillator (AICD),
they can look at the recent history of the device to see if
there were any shocks delivered to the patient.
PR: One of the problems with longstanding pace-
makers, like any other foreign body, is extrusion of
the pacemaker and infection at the site of the pace-
maker pocket. Obviously, you deal with the infection
the way you would with any localized abscess, but is
there any way to preserve the function while you’re
draining the abscess?
DB: If you have an infection generally, the pace-
maker, like any foreign body causing infection, needs
to be removed because it continues to be a nidus for
infection. As with most infections or abscesses, the
chances of it healing properly are diminished unless
you remove the foreign body.
PR: While we’re on the subject of internal defi bril-
lators, what do you do about patients who come in
SG: A trained athlete might also have the pacemaker
set at a slow rate.
PR: What would be your next step in evaluating this
person after getting an EKG, a chest X-ray study, and
a magnet strip?
DB: I think it’s clear that the pacemaker is not func-
tioning, and that’s why this patient is in a junctional
escape rhythm. Whether it’s not functioning because
the wire is broken, the battery has run out, or the
wire has become dislodged, almost doesn’t matter.
She needs to be admitted to the hospital to a mon-
itored bed, and to have this addressed by whoever
takes care of pacemakers in this hospital, whether
it’s general cardiology, or cardiac electrophysiology.
Particularly in this case, since her electrolytes and
renal function are normal, and the cardiac troponin
testing is negative, I don’t think we have to suspect
an underlying disease causing the heart muscle to
respond inappropriately to the pacemaker.
SG: I might consider in this case whether the brady-
dysrhythmia is related to an overdose of diltiazem.
DB: If she were living at home that would be a real
concern, but in a nursing home, where she has no con-
trol over her medications, this would be less likely.
PR: Even in nursing homes, there are dosage errors,
or even dosing changes that could be responsible;
for example, she also could have been given another
patient’s medication. If something can go wrong, it
certainly will. How would you test for this clinically?
Would you give her some glucagon?
DB: I would not. She’s maintaining a reasonable blood
pressure. Her mental status appears close to her base-
line, and giving her glucagon will often cause emesis and
make her miserable. Instead, I would simply observe her
on a monitor to assess whether the pacemaker works or
not. The diltiazem should wear off over 12–24 hours,
so she ought to be back in a paced rhythm by morning
if the pacemaker looks like it is intact.
SG: I might add that if the patient should deteriorate,
it should remain in the back of your mind, particu-
larly if you’re not fi nding success with external pac-
ing or transvenous pacing. I would give her glucagon
or perhaps some calcium. However, in a patient who
appears hemodynamically stable with normal cerebral
perfusion, trying medications that can have new side
PACEMAKERS AND AICDS IN EMERGENCY MEDICINE
151
back to the nursing home with a normally functioning
VVI pacemaker 2 days after admission. She was at her
baseline condition (Figure 11-2).
Section III: Concepts
Background
Nearly three million pacemakers or implantable car-
dioverter-defi brillators (ICDs) have been implanted
in the past decade (1990–2002) in the United States.
1
As a result, patients with pacemakers and ICDs are
now very commonly seen in the ED. The indications
for cardiac pacemakers have expanded broadly since
these devices were fi rst introduced in the 1950s to pre-
vent Stokes-Adams attacks. Recently revised guide-
lines from the American College of Cardiology and
American Heart Association now list a wide variety
of cardiac conditions as indications for pacemakers,
including sinus node and atrioventricular node dys-
function, atrioventricular block, chronic bifascicular
block, neurocardiogenic syncope and hypersensitivity
carotid sinus syndrome, hypertrophic cardiomyopa-
thy, and atrial fi brillation, to name a few.
2,3
Similarly,
the indications for ICDs have expanded to include
ventricular tachycardia (VT) and ventricular fi brilla-
tion (VF), familial or inherited conditions with high
risk for life-threatening ventricular tachydysrhythmias
(i.e., long QT syndrome), and syncope in patients
with advanced structural heart disease or Brugada
syndrome (RBBB pattern with ST-segment elevation
in lead V1).
4
complaining that they’re getting thumps all the time,
and it really bothers them?
TC: In the patient with a complaint that the device
is fi ring multiple times, and these are new events,
the question is whether or not the device is fi ring
appropriately. The device may be fi ring frequently,
but appropriately, if the patient’s underlying cardiac
rhythm is abnormal or life threatening. Alternatively,
the device may be malfunctioning and fi ring inap-
propriately when the patient has a normal or stable
baseline cardiac rhythm. In this case, I would have
the device interrogated to assess the patient’s underly-
ing rhythm when these shocks occurred, and to dis-
cern whether the device is fi ring appropriately. If it
is fi ring appropriately, I would treat the underlying
rhythm as appropriate; if not, I’d have the device set-
tings adjusted or replace the device.
Case resolution
Additional records were obtained from an outlying
hospital where the patient had formerly been admit-
ted. The prior EKG demonstrated that the T wave
inversions in the anterolateral distribution were old.
It was determined that she had a VVI pacemaker;
accordingly, the initial ED 12-lead EKG demonstrated
a failure to capture for the patient’s pacemaker. A chest
radiograph was obtained on this patient that revealed
a lead fracture in one of the pacemaker wires. The
patient was admitted to a telemetry bed on the elec-
trophysiology service, and underwent replacement of
her pacemaker the following day. She was discharged
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
V1
Figure 11.2 Follow-up 12-lead EKG after replacement of pacemaker and leads. Note the amplitude of the
ventricular pacing spikes followed by the typical paced QRS complexes.
CHAPTER 11
152
antitachycardia pacing takes place (O, A, V, or D); the
third letter the means of detection either by electro-
gram signal (E) or by other hemodynamic variables,
such as blood pressure or transthoracic impedance, in
addition to the electrogram signal (H); and the fourth
letter the chamber where antibradycardia pacing takes
place (O, A, V, or D). A short form of the NBD code
has been developed to signify the ICD function as one
of three types: shock capability only (ICD-S); shock
and bradycardia pacing (ICD-B); and shock, brady-
cardia pacing, and tachycardia pacing (ICD-T).
8
Initial workup: history and physical examination
Patients with pacemaker dysfunction can present to
the ED with a myriad of complaints. If the pacemaker
fails, the patient’s hemodynamic status is dependent
on the underlying native cardiac rhythm; as a result,
patients may present with symptoms similar to those
that precipitated the need for the pacemaker in the
fi rst place. Common presenting symptoms include
palpitations or “fl uttering” or “pounding” sensa-
tions, lightheadedness, dizziness, presyncope, actual
syncope, weakness, fatigue, and shortness of breath.
As with any ED patient, the initial step is to obtain
vital signs and determine the need for stabilization.
Pacemaker malfunction and reversion to an abnormal
underlying native cardiac rhythm has the potential to
result in signifi cant hemodynamic compromise and
instability. As such, the emergency physician must
determine if the clinical presentation and hemody-
namic status of the patient with device failure require
immediate intervention, such as with external pacing,
electrical cardioversion/defi brillation, or pharmaco-
logic pressor support.
Provided that the patient is stable, additional history
should be obtained to determine if the patient’s pace-
maker and its malfunction are the cause of the indi-
vidual’s clinical presentation. Does the patient know
the original indication for the pacemaker, the name of
the manufacturer, or the make and type (NPG code) of
the device? If they do not know this information, they
may have a pacemaker identifi cation card, which usu-
ally is provided when the pacemaker is implanted. This
card includes information on the manufacturer, make,
model, and type of pacemaker implanted (NPG code).
The patient should also be asked when the pace-
maker was implanted, as many complications, such as
a site infection, occur within a few weeks or months
Pacemakers and ICDs have become increasingly
complex, with memory requirements of less than
1 KB in the early 1990s up to more than 512 MB
today.
5
These sophisticated medical devices have very
low rates of malfunction, but when these failures
occur, the clinical impact on the patient can lead to
signifi cant morbidity and even death.
The specifi c actions, functions, and capabilities of a
given pacemaker are delineated by a letter code (NPG
code) developed by the North American Society of
Pacing and Electrophysiology (NASPE) and the
British Pacing and Electrophysiology Group (BPEG),
and revised in 2002.
6
The NASPE/BPEG pacemaker
code is often shortened to the fi rst three letter posi-
tions, such as DDD or VVI.
The fi rst letter position indicates the chamber of the
heart that is paced, such as the atrium (A), ventricle
(V), both or dual (D), or none (O).
The second letter position indicates where the pace-
maker senses native electrical activity of the heart
(again: A, V, D, or O).
The third letter position indicates the pacemaker’s
response to sensing native electrical activity, such as
triggering the pacemaker (T), inhibiting the pace-
maker (I), both (D), or none (O).
Commonly encountered pacemakers in the ED
include the VVI type (in which the pacemaker paces
the ventricle, senses native ventricular electrical
activity, and inhibits pacing when it does so), and
the DDD type (in which the pacemaker paces both
the atrium and ventricle, senses native and electrical
activity in both chambers, and both inhibits and trig-
gers pacing depending on the type of native activity
sensed).
The fourth and fi fth letter positions of the NPG
code are less commonly noted, but do indicate poten-
tially important functions.
The fourth letter position was used in the past to
indicate programmability of the pacemaker in a hier-
archical fashion, but now only indicates the presence
or absence of rate modulation (automatic adjustment
of the pacing rate), denoted as R or O respectively.
Similarly, the fi fth letter position was used in the
past to indicate any antitachydysrhythmic functions,
but now only specifi es the location or absence of mul-
tisite pacing (O, A, V, or D).
7
ICDs have a similar identifi cation code (NBD)
where the fi rst letter indicates the chamber shocked
(O, A, V, or D); the second letter the chamber where
PACEMAKERS AND AICDS IN EMERGENCY MEDICINE
153
In addition, patients may present to the ED with
pacemaker-mediated dysrhythmias, and the so-called
“pacemaker syndrome.”
Failure to pace, also known as output failure, occurs
when the pacemaker fails to deliver an electrical
stimulus to the heart. This can occur for a variety of
reasons, including battery or component failure, lead
fracture, dislodgement or disconnection, and oversens-
ing. Battery depletion is the most commonly reported
cause of pacemaker malfunction, and component or
generator failure has been reported with blunt trauma
to the chest wall.
10,11
However, abrupt failure is rare
with today’s lithium-iodine batteries.
12
Typically, a
gradual deterioration occurs over weeks to months
as the battery is depleted, initially manifesting as a
decrease in programmed pacing rate, and subsequent
decrease in stimulus voltage. These changes may be
noted on regularly scheduled checks of the pacemaker
and, as a result, emergent replacement is uncommon.
Complete lead fracture or disconnection can cause
failure to pace by preventing delivery of the pacing
impulse to the myocardium. Lead fractures typically
occur at the attachment to the generator, or at various
lead stress points, particularly abrupt angulations. In
addition, poor contact between the pulse generator and
lead can also result in failure to pace.
Oversensing occurs when the pacemaker senses
other electrical activity and misinterprets that activity
as native cardiac depolarizations, causing the device
to initiate its programmed activity—triggering or
inhibiting pacing. For pacemakers that inhibit upon
sensing native cardiac activity, oversensing can result
in a failure to pace. Common non-cardiac activi-
ties that can result in pacing inhibition include chest
wall and skeletal muscle myopotentials, particularly
from the pectoralis and rectus abdominis muscula-
ture.
13
In fact, succinylcholine has been reported to
cause pacemaker malfunction from oversensing of
skeletal muscle fasciculations.
14
Intermittent contact
from lead disconnections, also known as “make-
break” signals, can also generate electrical activity
resulting in pacing inhibition.
15
In addition, normal
native cardiac signals may be misinterpreted by the
pacemaker, resulting in pacing failure. For example,
a VVI pacemaker may oversense T wave activity as a
QRS complex and thus inhibit the ventricular pacing
stimulus.
Environmental electrical activity can also result in
oversensing and pacemaker malfunction. Wireless
of implantation. In addition, if the patient has knowl-
edge of any recent changes to the pacemaker settings
or other device interventions or interrogations, this
information may be useful in determining the poten-
tial for any complications or malfunction. Knowing
the age of the battery and the date its function was
last checked would be similarly useful.
Careful physical examination is important in the
assessment of the device. The implantation site should
be inspected for any signs of infection or migration,
as well as evidence of a mechanical problem with the
device generator. The chest wall should be examined
for any extracardiac stimulation by the pacemaker,
such as chest wall twitching or diaphragmatic irrita-
tion (manifesting as hiccups).
The examination should focus, in particular, on
an assessment of cardiac status and functioning.
Abnormally slow, fast, or irregular pulse rates may
indicate a malfunction has occurred. Inspection of the
neck veins may reveal distension and the presence of
so-called “cannon” A-waves, indicating asynchrony
of the atria and ventricles. Cardiac auscultation may
reveal abnormal fi rst and second heart sounds (i.e.,
paradoxical splitting), which could indicate abnormal
pacing. In addition, a pericardial friction rub may be
present if the pacemaker lead has perforated the myo-
cardium. Evidence of heart failure, such as rales on
chest examination or lower extremity edema that is
new, may also indicate pacemaker failure.
The approach to the history and examination of
patient with an ICD should be similar to that of a
patient with a pacemaker, though the clinical presen-
tation is more limited in scope. The most common
complaint of patients with ICDs is an increase in shock
frequency.
9
This presentation may represent a normally
functioning ICD responding to increased episodes of
triggering dysrhythmias (such as VT or VF), or an
abnormally functioning ICD fi ring inappropriately.
Alternatively, malfunction may occur when the ICD
does not shock when it should. In this case, patients
will present with clinical manifestations of the under-
lying abnormal cardiac rhythm (VT or VF), includ-
ing syncope, pre-syncope, lightheadedness, weakness,
shortness of breath, chest pain, and cardiac arrest.
Etiologies and differential diagnosis
Pacemaker malfunction can occur as a result of a fail-
ure to pace, failure to capture, and failure to sense.
CHAPTER 11
154
depending on changes in the amplitude, vector, and
frequency of myocardial potentials. Thus, changes in
the myocardium that cause an impact upon intracar-
diac electrical signals, such as from acute infarction
(especially right ventricular infarction), bundle branch
blocks, or other rhythm disturbances, can cause
undersensing. In addition, changes in the electrode-
myocardium interface, from infl ammation or exter-
nal defi brillation, can also result in failure to sense
native activity. As with failure to pace or capture,
lead fracture, dislodgement, insulation defects, or dis-
connections can result in a failure to sense. Finally,
undersensing can be caused by simple programming
errors where the pacemaker-sensing threshold is set
well above normal baseline cardiac activity.
While initially designed to treat abnormal brady-
dyshrythmias, pacemakers themselves can actually
cause heart rhythm disturbances. These pacemaker-
mediated dysrhythmias include pacemaker-mediated
tachycardias (PMTs), runaway pacemakers, sensor-
induced tachycardias, and dyshrhythmias due to
lead dislodgement. PMT can occur in dual-chamber
pacemakers with atrial sensing where the pacemaker
itself acts as part of a large reentry “endless loop”
circuit. PMT is usually initiated by a premature ven-
tricular contraction conducted retrograde through the
AV node, causing atrial depolarization that is sensed
by the pacemaker as native atrial activity, and results
in a pacing stimulus to the ventricle, thus complet-
ing the circuit loop. In PMT, the rate does not exceed
the pacemaker’s programmed upper limit.
23
Similarly,
atrial tachycardias, such as atrial fl utter, can be sensed
by these pacemakers, and result in a ventricular tachy-
cardia that does not exceed the upper limit.
Pacemakers with rate modulation usually vary the
pacing rate on specifi c sensors that detect vibration,
temperature, or even minute ventilation as a measure
of physiologic activity. Sensor-induced tachycardias
occur when these sensors are stimulated by other
stimuli, such as vibrations from external factors (i.e.,
loud noises, machinery, helicopters), febrile illness, or
arm or chest movement.
24,25
Runaway pacemaker is
an uncommon, but life-threatening, malfunction in
which the pacemaker fi res inappropriately rapid dis-
charges, potentially inducing VT or VF. Fortunately,
modern pacemakers are programmed to prevent such
rapid discharges, and this complication is exceedingly
rare today.
26
Another pacemaker malfunction that
can cause abnormal cardiac rhythms occurs when a
cellular phone signals and electrical cautery have been
reported to cause abnormal pacemaker function from
oversensing; in the case of cellular phones, malfunc-
tion is seen most commonly when the device is held to
the ear on the same side of the pacemaker pocket.
16,17
Failure to capture occurs when the pacemaker
generates a pacing impulse, but the stimulus fails to
trigger or “capture” the myocardium to cause car-
diac depolarization. This failure can occur because
the pacemaker is unable to generate a suffi cient cur-
rent to trigger depolarization, or the voltage thresh-
old required for capture at the electrode-myocardial
interface has changed. As noted above, a failing bat-
tery can manifest gradually with decreasing impulse
voltage that can result in pacer activity, but is insuf-
fi cient to capture the myocardium. Similarly, partial
lead fractures, or breaks in the electrode insulation,
can result in current leakage and inability to capture
despite delivery of the pulsing stimulus.
Exit block occurs when a pacing stimulus at an
appropriate voltage current fails to trigger depolariza-
tion, commonly from electrode-myocardium interface
alterations changing the pacing threshold. An elevated
threshold can be seen soon after initial implantation
because of tissue changes and infl ammation at the
lead insertion sites, resulting in a failure to capture
within weeks of implantation. However, advances in
steroid-eluting leads and initial pacemaker program-
ming voltage outputs set signifi cantly higher than
threshold levels have reduced this risk.
18
Ischemia and infarction can also alter the electrode-
myocardium interface, elevate pacing thresholds, and
result in failure to capture. External defi brillation on
patients with pacemakers has been well documented
to increase the risk of failure to capture, presumably
from tissue damage at the electrode-myocardial inter-
face.
19
Similarly, metabolic and electrolyte derange-
ments, including systemic hyperkalemia, hypoxemia,
hypothyroidism, and acidemia, can result in a fail-
ure to capture.
20,21
Antidysrhythmic agents, such as
fl ecainide and amiadarone, have been reported to
elevated pacing thresholds and result in failure to
capture.
22
Underlying prolonged myocardial refracto-
riness, such as in long QT syndrome, may also result
in failure to capture if pacing impulses are delivered
during the longer native refractory periods.
Failure to sense, or undersensing, occur when the
pacemaker fails to sense underlying native cardiac
activity. Undersensing can be complete or intermittent,