(+)Ingrid T. Lim, MD
Senior Physician, The Permanente
Medical Group, Kaiser San Francisco,
Department of Emergency Medicine;
Chief of Continuing Medical Education,
Kaiser Permanente, San Francisco
Medical Center; Assistant Clinical
Professor, University of California, San
Francisco; Residency Site Director,
UCSF-SFGH Emergency Medicine
Residency, San Francisco, California
Pacemakers and AICDs:
Short Circuit of the Electronic Heart
The expanding use of technology for acute and chronic
electrical therapy of dysrhythmias is complex. Using a casebased approach, the presenter will review the identification
and management of normal and abnormal function of
implantable electronic devices.
• Discuss the normal and abnormal function of permanent
pacemakers.
• Discuss the normal and abnormal function of the
implanted cardioverter-defibrillator.
• Review potential non-electrical complications that can
occur with both pacemakers and ICDs.
WE-172
Wednesday, October 7, 2009
8:00 AM - 8:50 AM
Boston Convention & Exhibition Center
(+)No significant financial relationships to disclose
Pacemakers and AICDs: Short Circuit of the Electronic Heart
Ingrid Lim, MD
Pacemakers and AICDs: Short Circuit of the Electronic Heart
Ingrid Lim, MD, FACEP, FAAEM
Kaiser Permanente, San Francisco, CA
ACEP Scientific Assembly, Boston, MA
October 7, 2009
Course Objectives:
1. Describe the normal and abnormal function of permanent pacemakers.
2. Describe the normal and abnormal function of the implanted cardioverter-defibrillator (ICD).
3. Review potential non-electrical complications that can occur with both cardiac devices.
PACEMAKERS
The stats:
5 million people in the United States have permanent pacemakers.
Annually, 115,000-175,000 permanent pacemakers are placed in the United States.
Indications for pacemaker - usually because the heart rate is TOO SLOW (usually from sinus node
dysfunction -50%, and atrioventricular (AV) conduction abnormalities) and patient is symptomatic.
Guidelines by the American College of Cardiology and American Heart Association:
1. Acquired AV block (not associated with MI)
a. 2nd degree or greater atrioventricular (AV) block with symptomatic bradycardia
b. Intermittent or permanent complete heart block (associated with symptomatic
bradycardia, CHF, in asymptomatic patients: asystole > 3 seconds or escape rhythm <
40 bpm)
c. Atrial fibrillation, atrial flutter or SVT associated with complete heart block or
advanced AV block, bradycardia
2. AV blocks associated with acute myocardial infarction (AMI) - transient advanced AV block
with bundle branch block (BBB) or persistent advanced 2nd degree AV block or greater with
block in the His-Purkinje system
3. Chronic bifascicular and trifascicular blocks
4. Sinus node dysfunction (sick sinus syndrome or tachycardia-bradycardia syndrome)
5. Certain conditions: hypertrophic cardiomyopathy, hypersensitive carotid sinus syndrome,
dilated cardiomyopathy, long QT syndrome, congestive heart failure (CHF), prevention of
recurrent atrial fibrillation (afib)
Anatomy of a pacemaker:
What it does: 1-2 leads positioned in the right atrium and right ventricle via the subclavian or cephalic
vein with a pulse generator placed subcutaneously in the shoulder area. It delivers a small amount of
current (2-4 mA) to myocardial tissue that can initiate a propagating wave of depolarization. It can
also sense intrinsic cardiac activity or its absence.
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Kusumoto, F. M. et al. JAMA. 287:1848-1852. © 2002 American Medical
Association. All rights reserved.
Figure: Dual-Chamber Pacing
AV indicates atrioventricular; ECG, electrocardiogram. A, Schematic of a dual-chamber pacemaker. Leads are
usually placed in the right atrium and right ventricle. The leads are connected to a pulse generator usually
located in the shoulder area. The leads are used to transmit current from the pulse generator (pacing) and also
to transmit intrinsic electrical activity from the cardiac tissue (sensing). B, In sinus node dysfunction, loss of atrial
activity leads to a prolonged pause. When a pacemaker is implanted, atrial (pink asterisk) and ventricular (blue
circle) activity are sensed. If the low-rate timer expires without sensed atrial activity, an atrial pacing stimulus is
provided to maintain the heart rate. C, In complete AV block there is no relation between atrial and ventricular
activity. With dual-chamber pacing, atrial activity is sensed and the AV interval is initiated. When the interval
expires, a ventricular pacing stimulus is provided. In patients with sinus node dysfunction sensed ventricular
activity due to normal AV conduction inhibits the pacemaker. Using this set of timers (low-rate and AV interval),
dual-chamber pacemakers maintain AV synchrony regardless of the cause of bradycardia.
TWO components of the pacemaker:
1. Pulse generator: battery + electronic circuitry
o Battery – usually lithium, with life span of 5-15 yrs; battery depletion rarely cause of
sudden failure due to long life and gradual decrease in output that is detectable at
regular cardiology visits; the paced rate will decrease from prior visit.
o Electronic circuitry to detect and analyze the rhythm
 Asynchronous pacing: simplest circuit is one that paces the heart at fixed rate,
(no sensing)
 Synchronous or demand pacing: sensing circuit detects spontaneous intracardiac
electrical activity.
o Titanium based covering, hermetically sealed (airtight and fluid impermeable)
2. Leads
o Unipolar leads – most commonly used today
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
Distal (cathode = positive pole) electrode in contact with endocardium; proximal
(anode = negative pole) electrode is the casing of the pulse generator
 On EKG, there are large pacer spikes (>20 mm)
 These leads are more flexible, less likely to break or fracture
 More prone to complications affecting sensing function (because the electrodes
are distant to each other), prone to oversensing.
 Myopotential inhibition more frequently occurs in unipolar pacing (muscle
activity in the ipsilateral pectoral muscles can be interpreted by the pacer as
cardiac activity and result in the inhibition of pacing).
o Bipolar leads
 Both electrodes (anode and cathode) are distal, within the heart chamber
(negative electrode in contact with myocardium)
 On EKG, smaller pacer spikes (5 mm amplitude)
 Oversensing minimized, but leads more likely to break
o Endocardial contact: to fix the leads to the endocardium, they can be screwed in (active
fixation) or held in place by fins (passive fixation  more prone to complications such
as dislodgement or perforation)
NORMAL PACEMAKER FUNCTION:
Two basic functions:
1. Pace or stimulate the heart when necessary – can be asynchronous (fixed) or demand pacing
2. Recognize intrinsic (“native”) electrical activity
Basic terminology:
 Pacing = delivery of the signal to the heart
 Capture = actual event of heart responding to electrical signal
 Sensing = detection of intrinsic cardiac activity
Interpreting the alphabet soup - Pacemaker Nomenclature
North American Society of Pacing and Electrophysiology (NASPE) and British Pacing and
Electrophysiology Group (BPEG) created a 5 letter code to describe pacemakers, called the
NASPE/BPEG Generic Code:
• First three letters deal with anti-bradycardia functions (3 letter reference is most commonly
used to refer to mode of pacer)
o Position I: chambers being paced (A-atrium, V-ventricle, D-dual (both), or O-none) –
easiest to remember that first and foremost, the role of the pacemaker is to pace!
o Position II: location where the pacemaker senses native cardiac electrical activity (A, V,
D, or O) – the second function of the pacemaker is to sense.
o Position III: pacemaker’s response to sensing (T-triggering, I-inhibition, D-both, Onone).
• Position IV: programmability (of rate responsiveness)
o The code in this position is hierarchical.
o C – can communicate with external equipment (telemetry) and is assumed to have
multiprogrammable function
o R -- able to modulate rate, and is assumed to be able to communicate and be multiprogrammable
• Position V: anti-tachycardia functions (ICD)
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o Identifies the presence of anti-tachydysrhythmia functions, including pacing and
shocking.
** Nowadays, the majority of implanted pacemakers (70%) are dual chambers.
Examples: The emergency physician is likely to encounter: VVI, VVIR, DDD, DDDR
VVI:
• “Ventricular demand” pacer which prevents the ventricular rate from falling below a set rate
• Still the most common mode of pacing worldwide
• Position I (V): paces the ventricle
• Position II (V): senses the intrinsic ventricular depolarization
• Position III (I): inhibits pacer from firing when it detects firing of the ventricle faster than a
pre-set threshold.
• Disadvantage – fixed rate regardless of the patient’s physical activity, lack of AV synchrony,
risk of pacemaker syndrome.
• Good for the couch potato patient who does no exercise; the rate does not increase if you do
exertion.
VVIR: similar to VVI, except there are biosensors that increase the pacing rate in accordance with the
patient’s degree of physical exertion. The amount of increase in the pacing rate is programmable.
Note: Both VVI and VVIR cannot take advantage of the atrial blood transport, contributing up to 30%
of the cardiac output because the atrial contraction is asynchronous. Dual chamber pacing overcomes
this disadvantage.
DDD
• Position I (D): paces both atrium and ventricle
• Position II (D): senses both intrinsic atrial and ventricular depolarization
• Position III (D): sensed atrial signal inhibits atrial output and sensed ventricular signal inhibits
ventricular output. However, sensing an atrial event “triggers” the timing cycle of the AV
interval to see if a ventricular event follows. If no ventricular event follows, the pacemaker
will be triggered so that the ventricle is appropriately paced.
• Essentially demand atrial pacing (AAI)  programmed AV interval  demand ventricular
pacing (VVI)
DDDR: similar to DDD except it provides HR increases with exercise.
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AOO/VOO: asynchronously paces the atrium or ventricle without any sensing function (what happens
when you apply a magnet to the chest)
VAT: paces the ventricle in response to sensed atrial activity
DVI: paces both chambers but senses only the ventricle, and inhibits if there is sensed ventricular
activity. The pacer will pace both the atrium and ventricle, with an appropriate delay between the two,
unless it senses spontaneous ventricular depolarization, in which case the pacing activity of the
pacemaker will be inhibited.
Approach to a pacemaker EKG:
 Rate (if HR < 60 or > 120  think of a possible malfunction)
Rate is usually 60-100 bpm (varies depending on what rate was programmed)
 Each pacemaker is programmed to a minimal pacing rate, called the lower rate limiting
interval (LRLI) = the longest time the pacemaker will wait before firing the ventricle if
no ventricular complexes are detected.
 In DDD pacemakers – the interval between the atrial and ventricular pacing is the AV
interval (functions like the PR interval). The ventriculoatrial (VA) interval is the time
after the last ventricular spike that the pacemaker waits before firing the atrium.
Together, the AV interval + VA interval = LRLI.
 Rhythm: examine the pacemaker spikes
 Are they falling the right place.
 Is there a atrial pacemaker spike followed by a P wave (may be absent), then ventricular
spike followed by a wide QRS and T wave (also usually wide)?
1.
Pacemaker spike is usually 2 msec in duration, followed immediately by the
captured beat.
2.
Spike varies in height depending on whether the leads are unipolar (larger) or
bipolar. Pacing spikes are not always apparent in every lead (especially in bipolar
pacers),
3.
You may not be able to rely on hatch marks at the top of the EKG to indicate
pacer spikes.
 Axis: should be left-ward
 Intervals: QRS should be wide, resemble a LBBB pattern because the leads reside in the R atrium
or R ventricle, causing the R side of the heart to depolarize first
 ST segments: rule of appropriate discordance (QRS and ST segments pointing in opposite
directions), look for signs of ischemia
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VVI PM – single spike prior to QRS; after beat 5,
there is no native QRS sensed, PM fires
When assessing an EKG in a pacemaker patient, ask yourself these questions:
o Does the pacemaker have enough juice?
 If there are no spikes at all on the tracing despite a severe bradycardia or long
pauses, then the pulse generator might not be working.
o Does the pacemaker sense?
 Fast rate: find an area of the EKG where the HR is higher than the threshold of
the pacemaker. See if the pacemaker turns off. There should not be any
inappropriate spikes.
 Slow rate or pauses: If there are long pauses without QRS complexes, and there
aren’t any spikes during that pause, it might be oversensing.
o Does the pacemaker capture?
 Is there a wide QRS after the ventricular spike
Question:
Which one of these rhythm strips could be a dual-lead paced heart?
A.
B.
C.
or
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Answer: D (all of the above)
Pacemaker/ICD Radiology:
 CXR can distinguish the pacer from ICD (see ICD section): the ICD will be bigger; the leads of
an ICD include a thick coil of the shocking electrode
 Look for lead complications (fracture, breaks, migration by comparing to old films), insertion
complications (hemothorax, pneumothorax, pleural effusion, pericardial effusion, perforation,
arterial puncture) – see non-electrical complications section.
 Look for signs of CHF.
 Can easily identify if patient has a single or dual-chamber device.
 Plain films can also reveal the manufacturer of the device via a radio-opaque logo. You can
then plug that logo into a website to find out the manufacturer and model of the device:
http://www.sjm.com/devices/devicereferenceguide.aspx or download the key as a pdf:
http://www.bostonscientific.com/templatedata/imports/HTML/CRM/Product_Performance_Re
source_Center/pdf/M0-492-0807_MRG_Final.pdf
PACEMAKER on CXR:
NORMAL PA/LAT CXR

Normal appearance:
o Wires usually inserted the subclavian route, coursing along the inferior border of the
medial portion of the clavicle and turn downward toward the heart at the junction of the
medial segment of the clavicle and the right tracheal border.
o PA CXR: the pacing wire follows the right tracheal border and enters the right atrium
(RA), arriving at the right ventricle (RV). The wire will cross the midline (from R L)
to attach at the endocardium of the RV.
o Lateral CXR: should demonstrate the pacing wire’s distal tip coursing anteriorly toward
the lower portion of the sternum. If it’s facing toward the spine, the wire may be
incorrectly placed in the coronary sinus  clue on EKG: a RBBB pattern.
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Question: This 76 year old man with sinus disease received a single-chamber pacemaker through
the subclavian approach. Here are his CXR and EKG. What is the problem?
Harthorne J and Palacios I. NEJM
2002; 346:1878
Answer: the lead had
been passed by means of
the subclavian artery
(instead of the
subclavian vein)
through the ascending
aorta, across the aortic
valve, and into the left
ventricle (instead of the
right ventricle). If there
is RBBB pattern, you
should be concerned
about a migration of the
leads. Compare this
CXR with the normal
pacemaker CXR. The
leads do not cross the
midline and are too far
over to the left.
Pacemaker MAGNET
o How does the magnet work?
 Reed switch: every pacemaker has a reed switch which is comprised of two flat
ferromagnetic strips that will make contact when there is a magnetic field created by
externally applied magnet  inactivate the sensing system and allow testing of the
pacemaker’s pacing capacity by allowing the pacemaker to fire asynchronously at the
preprogrammed “magnet rate” (regardless of patient’s underlying rhythm). When the
magnet is removed, the ferromagnetic strips spring apart and sensing resumes.
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o Application of the magnet can diagnose battery depletion or component failure, failure to
generate output, failure to pace, or failure to capture.
EKG: DDD pacer (2
spikes), 1st half of EKG
with native rate; 2nd half –
after application of magnet
How do you apply the magnet?
 2 types of magnets: horseshoe and donut/ring magnets
 Apply it directly to the chest
 You may have to move it around and try different
orientations to engage the reed switch.
 Watch the monitor to see when it switches to asynchronous
firing
 You can do very little harm by applying the magnet – it
changes them from demand pacing to fixed pacing, and you
can always remove the magnet.
When to bust out the magnet?
3 situations:
1. HR is too slow. A patient with bradycardia (so slow that the pacer should have kicked in) or
patient with symptoms suggestive of bradycardia but is now in normal sinus rhythm and
asymptomatic. If applying the magnet causes the pacer to fire at its programmed rate (this is
the expected outcome), the pacer is likely oversensing (see below) and inhibiting spikes
inappropriately. If applying the magnet, there are no spikes, then there is likely component
failure. If there are spikes, but slower than the programmed rate, it’s a battery failure.
2. HR is too fast. A patient (usually with DDD pacer) presents with tachycardia (near upper limit
threshold of pacer) which might be due to pacemaker-mediated tachycardia (PMT) (see below).
Applying the magnet will suppress atrial sensing of the retrograde p waves and interrupt the
reentrant circuit between the atrial and ventricular chambers. Magnet application seems to
resolve the tachycardia.
3. ICD going wild! A patient that presents with recurrent shocks from his AICD.
Approach to the pacemaker patient:
⇒ Information you need to get from the patient:
• Pacemaker manufacturer
• Date of implant
• Indication for pacing
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⇒
⇒
⇒
⇒
• Cardiac meds
• Symptoms?
Exam: VS, CV exam, check the pacemaker pocket
Diagnostics: EKG, CXR, electrolytes (including Mg)
Magnet application
INTERROGATE!
PACEMAKER MALFUNCTION
FAILURE TO CAPTURE – the output is too low, resulting in failure to depolarize the ventricle or
atrium  no mechanical contraction  no QRS or p wave.
o EKG will show either complete absence of pacemaker spikes or a pacer spike without any
subsequent QRS. Or, a pacer spike without a subsequent p wave (failure to capture atrium)
o If constant (no capture at all) in a pacemaker-dependent patient, the patient can be pulseless (need
to treat as asystolic patient with ACLS algorithms).
o If the patient’s HR is above the threshold for pacing, the EKG will not have any pacer spikes. In
order for you to test the functioning of the pacemaker, there has to be spikes. Applying the
magnet will allow the pacer to fire at its programmed rate to confirm that the pacemaker can
pace.
o Causes [Sarko & Tiffany, 2000]:
 Lead dislodgment from endocardial surface (most common, usually within the 1st month
of insertion)
 Twiddler’s syndrome
 Lead fracture
 Cardiac perforation
 Battery failure
 Improperly programmed or inadequately programmed voltage
 Increased threshold for capture from
• Myocardial ischemia
• Fibrosis or scar tissue at contact site
• Metabolic (hyperkalemia, hypercarbia, hypoxemia, hypothyroidism)
• Drugs (beta-blockers, class 1A antdysrhythmics, flecanide, verapamil)
• Prolonged QT syndrome
Failure to capture: visible spike
without subsequent QRS; notice
how the underlying timing is
unaffected by the failure to capture
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FAILURE TO PACE (= failure to
output) – pacemaker does not fire when
expected.
o EKG will show a lack of spikes even
after LRLI has been exceeded.
o Causes of failure to generate output
[Sarko & Tiffany, 2000]:
 Lead fracture
 Loose connection
 Insulation defect
Marquette Electronics Copyright 1996
 Pulse generator defect
 Battery depletion
 Oversensing or “underpacing”
(myopotential sensing, large T or U waves, MRI, electrocautery, extracorporeal shock wave
lithotripsy, transcutaneous electrical nerve stimulation, succinylcholine induced muscle
fasciculations). Oversensing due to detection of skeletal muscle myopotentials has
decreased in prevalence due to the widespread use of bipolar pacing systems. Suspect this
if the patient has a HR that is lower than the target HR. To detect, place the magnet to shift
the pacer in asynchronous mode.
 Cross talk (seen in dual chambers – the pacing stimulus in one chamber is sensed by the
other chamber’s sensors as that chamber’s impulse and a spike is not generated)
FAILURE TO SENSE (also known as undersensing)
– pacer does not detect patient’s own intrinsic rhythm
and generates a pacer spike in the intrinsic rhythm,
during an intrinsic QRS or during the refractory period
of the T wave. QRS will be within the normal limits of
the intrinsic rhythm. EKG: appearance of pacemaker
spike occurring earlier than programmed rate.
Failure to sense: pacer spikes are coming at the
wrong time; not sensing the intrinsic rhythm;
potentially dangerous: it can result in the
infamous R-on-T situation leading to VT or VF
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Causes of Failure to Sense
o Can be caused by sensitivity setting that is too low.
o Causes of failure to sense [Sarko & Tiffany, 2000]:
 Lead dislodgment
 Insulation defect in pacing lead
 Lead fracture
 Amplitude of P wave or QRS
complexes too low to be
sensed
 Magnet interrogation
 Complexes occurring during refractory
period
Failure to sense: notice beats 2, 7 and 8
have pacer spikes during the intrinsic
beat
 Myocardial fibrosis
 Acute myocardial infarction
 Severe electrolyte disturbance
 Antidysrhythmic drugs
 Myocardial perforation
 End of battery life
 Defibrillation
 MRI
KEY POINTS:
• Spikes without subsequent P or QRS  failure to capture
• No spikes + slow rate  failure to pace
• Inappropriate spikes  failure to sense
COMPLICATIONS UNIQUE TO CERTAIN PACEMAKER TYPES
Complications unique to single chamber pacemakers:
Pacemaker syndrome
• Occurs in pacemakers designed to pace the ventricle only (“ventricular demand”)
• Loss of AV synchrony (the “atrial kick”) and an inability to increase ventricular rate
adequately
• Elevated atrial pressures, due to atrial contraction when the mitral and tricuspid valves are
closed, and loss of properly timed AV depolarization and contraction
• Symptoms: lethargy, fatigue, weakness, dizziness, palpitations, dyspnea, syncope, CHF
• Treatment: dual chamber pacing
Complications unique to dual chamber pacers:
Pacemaker-mediated tachycardia
• Also known as endless loop tachycardia or pacemaker reentrant tachycardia
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• Develops in response to a premature ventricular complex (PVC) or premature atrial
complex (PAC) that is sensed by the pacemaker, leading to ventricular stimulation.
• Retrograde conduction through the AV node  atria; leads to the atrial sensing component
to sense it  ventricular component fires. Won’t fire at a rate faster than the upper
programmed limit.
• EKG: tachycardia in which each ventricular beat is preceded by a pacing spike, may see
retrograde P’s
• Treatment: magnet application will terminate the dysrhythmia; will need to be
reprogrammed (DDD VVI) to prevent atrial sensing of the retrograde impulse. Modern
pacemakers have algorithms to prevent/terminate PMT.
Pacemaker mediated tachycardia: PVC has retrograde
conduction through AV node, sensed by the atrial lead,
starting a reentrant endless loop
Twiddler’s Syndrome: occurs when the patient manipulates the generator and disturbs or
dislodges the leads, and the CXR shows a twisting and coiling of leads about the generator, lead
fracture, dislodgement or migration. Patients often present with malfunction of the device, or
symptoms of lead migration (hiccupping, pectoral or arm spasm, brachial plexus symptoms).
Runaway pacemaker: rapid tachycardia of up to 400
beats per minute. This is a true medical emergency!
Malfunction of the pacemaker generator (due to battery
failure, external damage, or another source). VF or VT
may develop. External magnet may help, but emergent
interrogation and reprogramming and surgical
intervention are often required. Treatment might require
disconnecting the generator and severing the pacemaker
leads in unstable patients. Fortunately, most modern
pacemakers are programmed to prevent discharges above
a set limit (usually 180 bpm); it is uncommon nowadays
Runaway pacemaker
How to diagnose AMI with a functioning pacemaker:
Criteria is similar to that of a patient with LBBB (Sgarbossa criteria, GUSTO-1 trial, 1996)
• Discordant ST elevation ≥ 5 mm in leads (sensitivity 53%, specificity 88%, positive
likelihood ratio (LR) 4.4) [discordant = ST-T wave complex points in the opposite
direction from the terminal portion of the QRS]
• Concordant ST elevation ≥ 1 mm (sens 18%, spec 94%)
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•
•
ST depression ≥ 1 mm V1-3 (sens 29%, spec 94%)
ST depression ≥ 1 mm in leads with concordant QRS polarity is 95% specific for AMI.
Note: many cardiologists will not rush to take the new LBBB patient to the cath lab. They prefer
to do a bedside echo looking for wall motion abnormalities (WMA) which would indicate an
acute transmural infarct. If WMA are present or +troponin, they will take them to cath
emergently. WMA develop before there is pain, EKG changes, or troponin leaks.
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IMPLANTABLE CARDIOVERTER DEFIBRILLATOR (ICD)
History of the ICD:
• 1947: first human defibrillation during cardiac surgery
• 1956: use of external transthoracic defibrillation for cardiac arrest
• 1980: Michel Mirowski (Johns Hopkins) implants the first automatic internal defibrillator
in a human
• 1985: FDA approves ICDs for widespread use. Initial device used epicardial patches for
defibrillation, generator placed in the abdomen, and a median sternotomy was required
for implantation.
• 1986: first nonthoracotomy system using a transvenous lead
Epidemiology:
Over 1 million patients currently have an ICD device, and numbers are increasing rapidly.
ICDs save lives!
 Approximately 450,000 people die annually from sudden cardiac death (SCD) – most
occur out-of-hospital. SCD accounts for nearly 50% of all cardiovascular mortality
worldwide.
 Ventricular tachycardia (VT) that degenerates to ventricular fibrillation (VF) accounts for
2/3 of SCDs.
 Purpose of the ICD: to prevent sudden cardiac death due to malignant dysrhythmias.
ICD recipients are usually survivors of VF or VT arrests, or they have conditions that
predispose them to life-threatening arrhythmias.
 Patients with ICDs have better survival rates compared to those patients on
antiarrhythmic drugs (AAD) – rate of sudden death is only 1-4% among ICD patients
versus 10-15% of those receiving AAD.
Indications [Arnsdorf and Ganz, 2008]:
While secondary prevention for patients surviving life-threatening ventricular arrhythmia has
long been the standard of care, more recent trials also demonstrate the survival benefit of the
ICD in patients at high risk for developing life-threatening arrhythmias (i.e. primary
prophylaxis).
Secondary prophylaxis:
 For secondary prevention in patients with prior episode of resuscitated VT/VF or
sustained hemodynamically unstable VT. This includes a variety of underlying heart
diseases and those with idiopathic VF and congenital long QT syndrome, but not patients
with VF within 24 hrs of an acute MI.
 For secondary prevention in patients with one or more episodes of spontaneous sustained
VT in the presence of structural heart disease and in selected other settings.
Primary prophylaxis:
 For primary prevention in selected patients with a prior documented myocardial
infarction and impaired LV systolic dysfunction.
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 For primary prevention in patients with an ischemic or non-ischemic cardiomyopathy,
New York Heart Association (NYHA) functional class II to III heart failure and a LV
ejection fraction (EF) < 35%
 For primary prevention in patients with syncope, structural heart disease, and inducible
VT/VF on electrophysiology study.
 For primary prevention in selected patients with certain underlying disorders who are
deemed to be at high risk for life-threatening VT/VF (including high risk patients with
hypertrophic cardiomyopathy, Brugada syndrome, or arrhythmogenic RV dysplasia)
 Heart failure patients with intraventricular conduction delay (as evidenced by a prolonged
QRS) may benefit from resynchronization therapy with biventricular pacemakers and
ICD.
Landmark study addressing secondary prevention that you should know:
Antiarrhythmics vs Implantable Defibrillators (AVID) trial (NEJM 1997)
 Largest and best designed trial (1066 patients)
 Enrollment criteria: survivors of VT/VF/cardiac arrest; VT with syncope, VT with LVEF
<40%
 Included nearly exclusive use of transvenous defibrillators, comparing them to the best
available antiarrhythmic drug therapies - amiodarone (97%) and sotalol (3%)
 Results: use of ICD improved survival regardless of underlying structural heart disease,
β-blockade, surgical revascularization or presenting arrhythmia
 Patients with the lowest left ventricular ejection fraction (LVEF) and those with advanced
CHF benefited the most.
Other trials you might hear about regarding primary prevention:
Multicenter Unsustained Tachycardia Trial (MUSTT - 1999)
 Hypothesis: electrophysiology guided (EP) therapy (with antiarrhythmic drugs or ICD)
could reduce arrhythmic and total mortality in high-risk patients who had arrhythmias
induced at EP study.
 704 patients were randomized to 2 arms: 1. EP guided therapy (received anti-arrhythmic
drugs and if failed, ICD therapy) or 2. no guided therapy
 Results: decrease in arrhythmic death/cardiac arrest with EP guided therapy. However,
the subgroup analysis revealed that the benefits were due entirely to the ICD: at 5 years,
there were absolute reductions in total mortality of 31% when compared with those
receiving pharmacologic therapy and 24% when compared with those receiving no
therapy (24% mortality in the ICD group, 55% in the pharmacologic group, 48% in the
group receiving no therapy).
 Number needed to treat (NNT)= 3 at 5 years
Multicenter Automatic Defibrillator Trial (MADIT II - 2002)
 Compared ICDs with conventional therapy in those patients with known CAD
 1232 patients, with prior MI, LVEF < 30%, randomized to receive ICD or not
 Endpoint – death from any cause, mean follow up – 20 months
 Results: mortality 20% without ICD vs 14% with ICD
 NNT = 18 over mean 20 months
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Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT – 2005)
 2521 patients
 Enrolled patients with either ischemic or non-ischemic cardiomyopathy, New York Heart
Association (NYHA) Class II or III heart failure, and LVEF < 35%.
 Results: reduction in mortality with ICD therapy for both the ischemic and non-ischemic
cardiomyopathy patients. ICD-treated patients lived longer than those treated with
amiodarone (which had no benefit). ICD benefit extended out to 5 years, independent of
heart failure etiology (ischemic or non-ischemic).
 Suggested that patients with LVEF < 35% should receive an ICD (especially if NYHA
class II-III, or class I, if history of MI or LVEF<35%). Caveat: neither MADIT II or
SCD-HeFT evaluated benefit of ICD in patients that were non-inducible during EP
study).
Defibrillator in acute Myocardial Infarction Trial (DINAMIT – Hohnsloser, et al, NEJM 2004)
• 674 patients, post MI, within the preceding 6-40 days (mean 18 days).
• Entry requirements: LVEF • 35 percent and reduced heart rate variability or elevated
resting heart rate (≥ 80 beats/min)
• Excluded: Patients with sustained VT >48 hours post-MI, NYHA class IV HF, or
coronary artery bypass grafting (CABG) or three-vessel PCI post-MI were excluded.
• Results: There was no difference in annual all-cause mortality between the ICD patients
and controls (7.5 versus 6.9 percent). Arrhythmic deaths were more frequent in the
control arm, while non-arrhythmic deaths were more frequent in the ICD arm. Possible
reasons why DINAMIT did not show the benefit from an ICD seen in the MADIT and
MUSTT trials include:
o Significant recovery of ventricular function may have occurred in some of the
study patients, which would dilute the long-term benefit of the ICD in this cohort.
o Some SCD events in the early postinfarction period may have been due to
recurrent ischemia, which would not be definitively treated by ICD discharge
o ICD implantation might impose additional risk in these patients immediately post
acute MI.
o The enrollment requirement for reduced heart rate variability could have selected
a group of patients with a high mortality from non-arrhythmic causes.
o This negative trial is the primary reason that current guidelines recommend that
ICD implantation should be deferred until at least 40 days after an MI.
The adjunctive role of antiarrhythmic (AAD) drugs:
 After several large randomized trials proved the superiority of ICD treatment over
therapy using antiarrhythmic medications for the prevention of sudden cardiac death
(SCD), AADs are generally considered 2nd line treatment, after ICD placement [AVID
Study, NEJM 1997].
 There is a role for AAD in patients with ICDs.
o Reduces the frequency of ICD shock by reducing the tendency for sustained VT
o Slows the episodes of VT to allow anti-tachycardia pacing to work
o Suppresses the atrial tachyarrhythmias that lead to inappropriate therapy or
trigger ventricular tachyarrhythmias.
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

Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients (OPTIC) study
[Connolly SJ, et al, JAMA 2006]
o 412 patients with ICDs randomized to receive treatment with β-blocker alone,
amiodarone + β-blocker, and sotalol
o At 1 yr follow up, shock rate were the following:
 β-blocker group: 38.5%
 Sotalol group: 24.3%
 Amiodarone + β-blocker group: 10.3%
Disadvantages of using AAD therapy:
o Potential risk with amiodarone (not sotalol) is the possibility of increasing the
ventricular defibrillation threshold (i.e. that an ICD shock is less likely to
successfully terminate an arrhythmia).
o Antiarrhythmic medications can be proarrhythmic  sotalol > amiodarone is
more prone to cause torsades de pointes
o Side effects of amiodarone: pulmonary and thyroid toxicity
Anatomy of an ICD – 3 components:
1. Sensing electrodes: usually placed transvenously via the axillary, subclavian, or cephalic
vein, onto the right ventricular apical endocardium. Dual chamber ICDs have an
additional electrode in the right atrium for atrial sensing and DDD pacing.
2. Defibrillation electrodes: relatively
JAMA. 296 (23): 2839-2847, © 2006, American
Medical Association. All rights reserved.
large surface area and are positioned to
maximize the density of current flow
through the ventricular myocardium.
Defibrillation coils are positioned on the
RV electrode and at the superior vena
cava/RV junction. The defibrillation
current passes from the coil, through the
myocardium and to the outside shell of
the defibrillation unit.
 In the past, a thoracotomy was done
to implant epicardial patches, which is
rarely performed nowadays due to the
increased risk of morbidity and
mortality. The metal housing of the ICD
(the “active can”) serves as one of the
shocking electrodes.
 The preferred waveform for internal
defibrillation is biphasic, which requires
lower energies than monophasic forms, requiring a smaller capacitor (reducing the
overall size of the ICD unit)
 Biventricular ICDs have a third electrode placed transcutaneously in a branch off of
the coronary sinus or surgically on the epicardium of the left ventricle.
3. Pulse generator: contains the sensing circuitry as well as the high voltage capacitors and
battery.
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 Although the ICDs used to be much larger and heavier, requiring implantation in the
abdomen, their small, lightweight build (e.g. mass <200 g (some weighing just little over
80 g), volume 30-50 ml, thickness 11 mm) allows for pectoral implantation (either
subcutaneously or submuscularly) in nearly all patients.
 Cost: $30,000-45,000
 Battery lifespan: third generation ICDs are now lasting 6-8 years, which is a
tremendous advance compared to the first ICDs which depleted the battery within 18
months.
 Lifetime of ICD: usually 100 shocks can be delivered.
Modern ICD’s can perform all of the following functions:
1. ECG storage (unlike pacemakers which often have this function turned off to save
battery)
2. Antibradycardia pacing (dual chamber): may kick in during the 1st 5 seconds after a
shock because there is a brief asystolic period. Most modern ICDs have VVI pacing
capability for this purpose.
3. Tiered therapy for VT: current devices are programmed for tiered therapy, in which the
device will provide progressive anti-tachycardia pacing, cardioversion, and defibrillation,
as required. Helps to reduce the need for high-energy defibrillation (which depletes the
battery and causes discomfort to the patient).
 Antitachycardia pacing (ATP): tries to short-circuit the rapid ventricular rhythms
by sending brief bursts of impulses to the heart muscles at a pace faster than the
already accelerated ventricular rate. The aim is to depolarize the heart muscle at the
right moment, interrupting the abnormal rhythm and thereby avoiding an appropriate
ICD shock. Benefit: less drain on the power source, ideal for patients with frequent
ventricular tachycardias not controlled by medical therapy. Large-scale studies have
shown this to be 90-96% effective in terminating VT.
 Low energy cardioversion: mild shock to the heart (0.5-2 J), usually more effective
than anti-tachycardia pacing
 High energy defibrillation for VF (low energy shock won’t stop VF): 10-15 J at
minimum, but most devices deliver 35 J to allow a margin of safety. Devices can
typically give up to 5 shocks with a pause to analyze the rhythm.
Example of ICD multi-tiered programming algorithm for VT:
VT:
 If slow (160-180/min): ATP x 3  cardioversion @ 5 J, defib @ 35J
 If fast (>180-200/min): ATP x 1  defib @ 35 J  defib @ 35 J x 5
VF (not tiered – starting with low energy won’t convert VF):
 Defib @ 35 J  defib @ 35 J  defib @ 35 J x 4
4. Defibrillation if VF is detected.
Cardiac resynchronization therapy (CRT) = biventricular pacing
5. Abnormal chamber mechanics, where there is an interventricular conduction delay,
resulting in dyssynchronous contraction, contribute significantly to CHF.
6. A third electrode is placed through the coronary sinus into a venous branch along the free
wall of the left ventricle, or epicardially. It paces the LV restoring physiologic synchrony
of the ventricles.
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7. CRT improves the cardiac output, ejection fraction, and symptoms, quality of life, and
lowers hospitalization rates.
8. Current evidence shows that this CRT + ICD therapy is most beneficial in patients with
severe CHF.
Atrial ICDs
 Currently, only a very small percentage of ICD’s implanted (2%) are atrial defibrillators
[Goldberger, 2006]
 Recognizes and delivers shock for afib.
 Overall efficacy in terminating afib is 76-90% with no ventricular proarrhythmia and
good discrimination between atrial and ventricular tachyarrhythmias
 Rapid atrial pacing can terminate atrial tachycardias painlessly (often the precursor to
afib).
 Potential problem: atrial shocks are painful, and thus devices, programmed to be
triggered by the patient, may be underused.
KEY POINT: SHOCK HURTS! People generally describe it as feeling similar to being kicked
in the chest. Patients may lose consciousness for 15-20 seconds required for the device to charge
up and deliver the shock.
APPROACH to the ICD patient
History taking -- be sure to ask:

How many shocks?

Activity at the time of shock?

Antecedent or intercurrent symptoms such as chest pain, dyspnea, other ischemic
equivalents

What was the indication for the ICD placement?

Obtain a complete list of medications, with special attention to antiarrhythmics.
Physical exam: look for signs of trauma or infection over the generator site, CHF, new murmur
Diagnostics:
o 12 lead EKG
 Pay special attention to the intervals, especially the QT interval, as QT
prolongation may be seen in drug toxicity.
 Important note: after shock, most EKGs will show a transient ST elevation
or depression that normalizes within 5-15 minutes. If it does not revert to
baseline, worry about new ACS.
o CXR – look for lead fracture, lead displacement and CHF
o Labs:
 CBC
 Electrolytes, including potassium and magnesium (hypomagnesemia is a
common cause of arrhythmias in ICD patients)
 BUN/creatinine
 Drug levels of any anti-arrhythmics
 Cardiac enzymes only if there were multiple discharges, or symptoms
suggestive of cardiac ischemia (important note: 1/3 of patients will have
elevations in troponin T and 1/6 of patients in troponin I, lasts only up to 24
hrs after delivered shock).
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ICDs on CXR:
Notice how this is different from the pacemaker
CXR. There are thicker portions along the
leads (these are the superior vena cava coils and
the RV coils). The ICD box is bigger than the
pacemaker.
When ICDs go haywire!
Scenario #1: patient who presents after a single shock
 Most cardiologists tell their patients not to seek medical attention if they receive a single
shock and are otherwise asymptomatic. Workup should be pursued if they have
worrisome symptomatology: dyspnea, syncope or near syncope, chest pain, palpitations.
Many patients have home transmission systems – they can upload information to a
website for the cardiologist to interpret. Dispo: likely home if no other symptoms.
Scenario #2: patient who presents after multiple shocks
The multiple shock patient (> 2 shocks in 24 hrs)
 This is the most common ICD complaint – up to 20-25% ICD patients.
 This is a medical emergency and requires a cardiology consult for device
interrogation – although frequently it is later deemed to be inappropriate therapy.
 Put the patient on cardiac monitor and have external defibrillation immediately available.
First question to ask when a patient presents with repeated shocks: are they
appropriate or inappropriate?
 If the patient receives a shock in the ED, the EKG monitoring can
establish whether the shock was delivered appropriately for VT or VF.
Inappropriate shocks: occurs in 20-25% of patients, can be caused by…
 Most commonly: supraventricular tachyarrhythmias, afib with rapid ventricular
response, sinus tachycardia, as well as nonsustained VT.
 ICD malfunction (lead fracture, lead migration, insulation break, incorrect
programming of the device)
 Inappropriate sensing - double counting of signals from cardiac (T wave) or
extracardiac (respiratory motion) sources.
 Electromagnetic interference from small appliances can also cause spurious shocks:
electric razors, slot machines, antitheft detection devices, metal detectors, cell phones,
TV remotes, large speakers, electrical current leaks [McMullan, 2007]
 Clues in the history: patients with multiple repetitive shocks (occurring within
seconds or minutes of the previous shock) in the alert patient during intense physical
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activity, fever or pain prior to shock, may be getting inappropriate therapy for sinus
tachycardia. Shock associated with repetitive movements may suggest an
inappropriate therapy due to lead malfunction.
Appropriate shocks: for VT/VF.

Electrical storm:
 High number of successive shocks in a short period (>3 distinct episodes of VT/VF
requiring shock within 24 hr period)  portends high mortality.
 Up to 30% of ICD patients will experience a storm, often during their first ICD
discharge experience, usually within first 9 months of implantation.
 Patients with electrical storm need admission for aggressive monitoring and often
need to be started on AAD.

Clues in the history: shocks that occur hours apart while the patient is at rest usually
signify recurrent successfully treated ventricular arrhythmias – likely appropriate therapy;
shock preceded by chest pain, shortness of breath, or syncope is more likely appropriate.

Modern ICDs now have strategies to minimize the number of appropriate shocks without
compromising patient safety: by increasing duration of the arrhythmia necessary to
trigger therapy (e.g. from 16 20 beats), anti-tachycardia pacing (ATP) which should
terminate at least 90% of persistent VT. See earlier section, page 20.

Other adjunctive therapies include antiarrhythmic drugs (amiodarone or sotalol) or
catheter ablation.
KEY POINT: Formal interrogation is the only way to discern between the
appropriate and inappropriate shocks.
Treatment:
 Use standard medications to control the underlying arrhythmias – β-blockers,
amiodarone, calcium channel blockers, while potentially reversible causes are being
addressed. Patient might benefit from anxiolytics.
 Magnet: only place over the ICD if it appears that the repeated shocks were not
appropriate (e.g. an alert patient with rapid afib); make sure the external defib/pacer pads
are in place.
Magnets use with ICDs
 In the ED, in a patient getting frequent inappropriate shocks, a magnet can be taped over
the generator to inhibit further shocks.
 What it does: disables the tachyarrhythmia detection/treatment, cardioversion and
defibrillation functions, without altering its backup bradycardia sensing and pacing (but it
does not cause the ICD to go into asynchronous pacing)
 To apply: Place magnet on ICD x 30 seconds  continuous beep; may continue to beep
while the magnet rests on the ICD
 Don’t forget to apply the external defib pads to the patient before using the magnet.
 Caveat: not all ICDs will resume their actions once the magnet is removed (unlike
pacemakers); this is manufacturer dependent.
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
Caveat in obese patients: if using a single donut magnet, it may not be powerful enough
to deactivate the ICD; solution: stack two magnets on top of each other [McMullan,
2007]
Scenario #3: Patient is in VT/VF without any ICD therapy delivered
 Several possible causes: VT is slower than the device threshold for delivering therapy,
the morphology may not meet recognition criteria, or the device is malfunctioning.
 Treatment: If the patient is stable, chemical or electrical cardioversion. If unconscious or
unstable, follow ACLS guidelines as if the device is not there. If the ICD is working, let
it shock, and deliver the ACLS meds.
Cardiopulmonary resuscitation (CPR) and defibrillation:
 There are no contraindications for CPR in the ICD patient.
 The rescuer is not endangered by an ICD shock (it might feel like a little tingle which
might be prevented if wearing gloves)
 Consider deactivating the ICD once external monitoring is in place to avoid unintentional
therapies.
 Pad/Paddle placement: preferable to place them in the anterior-posterior configuration (to
avoid damage to the device [McMullan, 2007] (Note: external shocks may fail in patients
with epicardial patch electrodes (i.e. those with thoracotomy implantation), because of
the electrical shielding from the insulator material on the patches. Just move the external
paddles if initially unsuccessful in the routine position), at least 10 cm (5 inches) away
from generator.
 Most ICD’s will deliver a maximum of 5 successive shocks to conserve battery life and
turn off if it’s unsuccessful.
 Resuscitative medications (lidocaine and amiodarone) can increase the defibrillation
threshold, rendering ICD therapies ineffective.
KEY point: External shocks near the ICD can damage the ICD circuitry –
thus, after external cardioversion or defibrillation, the ICD must be interrogated
to confirm that the parameters have not been reset by the shocking.
NON-ELECTRICAL COMPLICATIONS: Pacemakers and ICDs


In the U.S., complication rate for device implantation is 8-9%
Since the first routine follow-up after implantation is usually 10-14 days later, the EP
may be the first physician to evaluate the patient post-implantation.
Lead complications:
• Complications from lead placement:
o Hemothorax or pneumothorax (1% clinically significant ) – usually present
within 48 hr of the procedure. SC emphysema may be present and may cause
pacemaker malfunction by insulating unipolar leads [Cardall, 1999]. Diagnosis
on CXR. Placement of chest tube is required if pneumothorax is > 10%.
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o Venous thrombosis: incidence in subclavian or brachiocephalic veins in patients
with pacemakers may be as high as 44% although they may not all be clinically
significant [Cardall, 1999]. Suspect if patient presents with pain and swelling of
the ipsilateral arm following pacemaker lead procedure (implantation, lead
extraction, replacement). Thrombus can extend to superior vena cava (SVC) and
cause SVC syndrome. Diagnose with B-mode ultrasonography and compression
US. Treatment is similar to other cases of venous thrombosis (heparin, low
molecular weight heparins, and eventually warfarin).
o Subclavian arterial puncture
o Chylothorax
o Brachial plexus injuries
o Cardiac perforation – when the lead actually penetrates through the heart into
the pericardial space. Usually an acute complication, during implantation (less
likely due to lead dislodgement and migration). Perforation may be unrecognized
if the patient is hemodynamically stable. Clinical presentation can vary from
pericarditis to hemodynamic collapse. CXR can show the electrode extending
just beyond the heart border. US can rapidly detect pericardial fluid or
tamponade. Treatment: pericardial drainage, possible emergent cardiac surgery.
•
Lead infection:
o Often in chronic device patients
o Very serious complication with extremely high mortality (66% if leads not
removed, and 26.9% even if aggressively treated with systemic antibiotics and
lead removal).
o Can involve infected vegetations on the lead.
o Staphyloccoci - 93.5% of the time
o Symptoms: fever, chills, signs of septicemia, and pulmonary involvement.
o Dx: blood cultures, transesophageal echo (TEE). TEE showed abnormal
formations on pacemaker leads 94% of cases of lead infection [Cardall, 1999].
o Treatment: because of the high mortality  absolute indication for lead removal.
Role of the emergency physician: immediate antibiotics (vancomycin),
blood cultures, CXR, admit and consult appropriate subspecialty for
definitive treatment.
KEY POINT: Think about lead infection in a patient with a fever + cardiac device.
Always get blood cultures before giving any cardiac device patient antibiotics.
•
Lead dislodgment
o Clues on H&P: hiccups (phrenic nerve stimulation), arm twitching, RBBB on
EKG, pacemaker malfunction (failure to capture or pace), CXR (be sure to get AP
and lateral views and compare to prior films)
o Relatively common problem (5-10% of patients)
o Displacement usually occurs early (within the first few weeks post-procedure
because fibrinous adherence of the pacing leads tends to safeguard against late
displacement)
o Can be displacement within the chamber or out of the chamber.
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Lead fracture
•
Exit block: Occurs when there is excessive inflammation
at the electrode-myocardium interface. Because the
electrode threshold potential is elevated  failure to
capture or output. If it occurs in a sensing lead, will
result in undersensing. Can be from ischemia or infarct
of the endocardium, systemic hyperkalemia, use of class
III antiarrhythmic drugs. Less common today with
steroid-eluting leads.
• Lead fracture:
o Leads usually have a lifespan of 20-30 yrs.
o Incidence of lead fractures: 2.6%
o May occur any time after insertion and may be
associated with tight fixation of the lead
o Less common now with polyurethane lead coating, produces an insulation break
that allows the current to leak out
o Best seen on an overpenetrated PA CXR
o Common sites of fracture:
 subclavian vein between the clavicle and first rib (the “subclavian crush”),
where the wire is in the form of a loop and excessive flexing may occur
 the connection point to the generator
Pocket Complications
• Pocket hematoma: hematomas can occur soon after
AICD erosion
implantation because of dissection of fascial planes
through the skin
by residual arterial and venous bleeding. Bleeding
can also track into the chest along pacemaker leads.
Hematomas large enough to be palpated require
treatment and surgical exploration. Aspiration to
decompress the pocket is usually not effective, and
often leaves a clot that can become infected. Needles
in the pocket can encounter leads and compromise
lead insulation. RESIST the temptation to put
needles or scalpels into the hematoma – they need to be drained in the OR or the cath lab.
• Pocket infection: soon after implantation, local inflammation and fluctuance, purulent
discharge. If later infection, pain may be the only complaint without obvious cellulitis
overlying the generator. Usual culprit: Staphyloccoccus aureus (acute infections),
Staphylococcus epidermidis (late or chronic infections). Empiric vancomycin should be
initiated in the ED. Blood cultures and pocket cultures (ask the surgeon or cardiologist to
do this). Often replacement of the entire pacemaker or ICD is necessary.
• Wound dehiscence – rare occurrence, usually within days of implantation, usually from
excessive stress on the wound suture line as a result of insufficient pocket size, pocket
hematoma, patient manipulation or trauma. Tx: surgical debridement and
reapproximation of wound edges.
• Migration of the pacemaker within the pocket & erosion: erosion of the pocket wall
superficial to the pacemaker from migration as a result of trauma hematoma or local
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tissue ischemia. Skin may erode, and lead to infection. Debridement and relocation of
the pacer is necessary.
Of note:
 Prophylactic antibiotics are not required for pacemaker or ICD patients undergoing
procedures that may cause transient bacteremia.
Central venous catheters
 If you have to place a central line, go for the groin (femoral) or the contralateral IJ or
subvclavian.
 Risk of dislodging a thrombosis along the lead system (with complete occlusion nearing
20% at 2 years), causing artifact that induces an inappropriate shock, dislodging a newly
implanted lead (within first 2 months), entanglement, and it may be technically difficult
because subclavian stenosis is common.
Other considerations:
 Patients with intractable hiccups or pectoral spasm can be signs of lead dislodgement
and migration causing diaphragmatic stimulation. Especially in the biventricular pacing
(diaphragmatic pacing is more likely to occur due to the phrenic nerve stimulation by the
LV lead). Check a CXR!
 Sudden right heart failure: can be a sign of severe tricuspid regurgitation after
adhesion, perforation, or impairment of the valve leaflets by the ICD leads. EP’s need to
have a high suspicion for this and order an echocardiogram.
 Succinylcholine: oversensing muscle fasciculations  inappropriate shocks. Consider
using one of the nondepolarizing agents or a defasciculating dose.
 Electrocautery: can be misinterpreted as tachydysrhythmia and cause discharges, also
inhibits pacemaker function. ICDs should be disabled before use of electrocautery.
Bipolar devices (like Bovies) are generally considered safe. Single use, battery powered
units that directly heat a metal tip (like for nail trephination) are theoretically safe.
 MRIs: absolute contraindication – magnetic fields can cause burns, spurious discharges,
disable or reprogram the device.
Patient information about Pacemakers:
1. Household Appliances: Although it has not been systematically studied, it is generally
accepted that pacemakers are adequately shielded from microwave energy produced by
common household appliances like microwaves, television, radios and toasters.
2. Cellular Phones: Cell phones are safe if used normally, but if the phone is placed
directly over the implant site (i.e. phone is in the shirt pocket and left on) it can cause
interference. Temporary transvenous pacemakers are susceptible to cell phones and
walkie-talkies within 200 cm of the pacemaker. For this reason, most ICU's (where
temporary transvenous pacemakers are often used) do not allow cell phones or walkietalkies.
3. Security Systems: Electromagnetic systems have been shown to cause interference at
times, but proximity and duration seem to be the key factors in causing problems. Advice
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is to move through the security system at a normal pace and not to linger around the
device for an extended period of time.
4. External Electrical Equipment: Welding tools and motor-generator systems can
interfere with pacemaker programming. In general, stay at least two feet away from such
equipment. Electrocautery during surgery is okay as long as bipolar coagulation systems
are used. Bipolar systems localize the follow of current and usually do not cause
interference if kept more than 6 inches from the generator.
5. Diagnostic Procedures: Magnetic Resonance Imaging is dangerous because the strong
magnetic field can dislodge the electrodes from the heart causing myocardial damage,
and it can also interfere with the programming of the pacemaker. If MRI is necessary,
cardiology can be consulted to switch it to asynchronous pacing mode.
Patient information about ICDs:
1. Movement restrictions post-implantation: patients are instructed to avoid excessive
movements (raising arm above shoulder height or reaching behind the back) for 2 weeks
post-implantation to prevent lead dislodgment; no sudden, vigorous pulling or chopping
movements with affected arm for 4 weeks (includes most sports activities). No heavy
lifting > 10 lbs for 2 weeks or >20 lbs for 4 weeks.
2. Precautions:
 Household appliances (including microwave ovens), but do not lean on it or stand
close during operation
 Cellular or cordless phone: keep at least 6 inches away from ICD, try to use on the
opposite side. Store cell phones opposite the side of the ICD. Don’t place in the shirt
pocket.
 Power tools: keep properly grounded. Chain saw use should be avoided.
 Do not hold or carry magnets near ICD.
 Do not perform electrical arc welding.
 Security devices: walking through slowly should not harm the ICD. It might set off
the security devices. You might need to ask for a hand search, but the hand held
metal detector wand contains a magnet and should not be placed near ICD.
ACEP Scientific Assembly
Boston, Oct 2009
27
Pacemakers and AICDs: Short Circuit of the Electronic Heart
Ingrid Lim, MD
References
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ACEP Scientific Assembly
Boston, Oct 2009
28