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Permanent pacemakers: An overview

Article  in  British Journal of Cardiac Nursing · June 2009

DOI: 10.12968/bjca.2009.4.6.42422

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Clinical

Permanent pacemakers:
An overview
Alan Davies is Staff Nurse, Cardiac Catheterization Labs, Cardiology,
Royal Devon and Exeter Hospital, Barrack Rd, Exeter, EX2 5DW. Email: alan6386@hotmail.com

T
he permanent pacemaker (PPM) has increased in
use over recent years, with around 25 000 PPMs
implanted each year in the UK alone and rising
(National Institute for Health and Clinical Excellence
(NICE), 2005). Ector et al (2007) state that in 2005 there
were 603 pacemaker implants per million in the UK alone.
Many nurses who work in a variety of clinical areas are
exposed to patients with a PPM in situ. Nurses who care
for such patients should have a general awareness of
PPMs, as the presence of a PPM can impact on the
management of the patient in the clinical setting. This
article aims to provide an overview of the PPM, including
the insertion procedure, pre- and post-procedure care and
patient advice.

Left bundle
The intrinsic conduction system
Sinus branch Specialized conduction cells are distributed through the
node
heart in the form of an electrical pathway (Davies, 2007a)
Anterior
AV
fascicle
(Figure 1). These cells possess a quality known as automa-
node ticity, this is the ability of the cells in the heart to depolar-
ize spontaneously and initiate an action potential (impulse)
Right
atrium (Bowbrick and Borg, 2006).
Depolarization is a process whereby the myocardial cel-
Atrioventricular lular membrane switches from being more negatively-
region
Right bundle Posterior charged inside and positively-charged outside (polarized)
branch fascicle to the reverse (depolarized) (Khan, 2006). This is achieved
by the sudden influx of positively charged sodium (Na+)
and calcium ions (Ca2+) into the cell (Conover, 2003). The
sinoatrial node (SAN) activates the atria at a rate between
Figure 1. Conduction system of the heart 60 and 100 beats per minute in an adult patient. The wave
of depolarization, originating in the SAN spreads down
the conduction system to the atrioventricular (AV) node;
Abstract through the His bundle and into the left and right bundle
Many patients in many different clinical areas have a permanent branches, ending in the Purkinje fibers (Davies, 2007b). In
pacemaker (PPM) device implanted. Nurses are better equipped to some patients there is a problem with the intrinsic con-
deal with the unique needs of this patient group by understanding the duction system, leading to the need to insert a permanent
different types of pacemaker device available, how these devices pacemaker system (British Heart Foundation (BHF),
function, and how this impacts on the patient’s clinical care. An 2008).
understanding of the pacemaker device also helps to identify or
anticipate potential problems with the device, which may affect the Components of a permanent pacemaker
patient’s health. Certain clinical tests and equipment may also affect A PPM system is made up of a pulse generator (battery),
the functioning of a pacemaker device and it is important that nurses and one or more electrodes, known as leads (Johnson and
are aware of these effects so that steps can be taken to prevent or Rawlings-Anderson, 2007).
reduce these effects, and deliver the best possible care to patients All of the currently used pulse generators or pacemaker
with a permanent pacemaker. boxes are variations of lithium-iodine cells (Figure 2).
These cells work by generating electricity due to a chemi-
Key words cal reaction that takes place between the lithium and
w Pacemakers w PPM w Pulse generators w Leads iodine (Kenny, 2007). Pulse generators can last on average
Submitted for peer review 9 August 2008. Accepted for publication 18 May 2009. between 5 and 10 years (Kumar and Clark, 2003). Pulse
Conflict of interest: None
generators are usually about the size of a matchbox and
weigh around 20–50 grams (BHF, 2008).

262 British Journal of Cardiac Nursing June 2009 Vol 4 No 6

 Clinical

Table 1.
Indications for implantation of
a permanent pacemaker
w Heart block, including
Sinoatrial block
Mobitz type II block
Complete heart block
Trifascicular block
w Symptomatic bradycardia
w Sick sinus syndrome (sinus node disease)
w Ventricular standstill
w Hypertrophic cardiomyopathy
Figure 2. Pacemaker pulse generator
w Dilated cardiomyopathy
The leads are insulated wires that are implanted into the w Long QT syndromes
heart transvenously, attached at one end to the pulse gen- w Drug-refractory paroxysmal atrial fibrillation
erator and the other to the myocardium via active or pas- w Bradycardia–tachycardia syndrome
sive fixation (Figure 3). This in turn creates a two-way path
w Pause-dependent ventricular tachycardia
through which an impulse can be delivered to the myocar-
dium and received via the pulse generator (Kenny, 2007). w Ventricular pauses >3 seconds in length
The lead delivers an electrical impulse exciting myocardial w Recurrent syncope
cells causing a subsequent contraction (Johnson and Johnson and Rawlings-Anderson, 2007; Vardas et al,
Rawlings-Anderson, 2007). Once the lead(s) are in place, 2007; Timperley et al, 2008
a fibrotic capsule forms over the top of the lead fixing
them firmly in place (Kenny, 2007).
The choice of pacemaker used depends on many factors,
Indications for insertion including the underlying pathophysiology, patient’s age,
The most basic function of a PPM is to act as a safety net, activity level and underlying rhythm (Kumar and Clark,
to protect patients who are at risk from symptomatic 2003; Vardas et al, 2007).
bradycardia (Houghton and Grey, 2003). Permanent pace-
maker insertion is also indicated for patients with any of Pacemaker codes
the conditions summarized in Table 1. A generic shorthand method of referring to pacemakers
came into being in 1974 and has been revised several
Types of permanent pacemaker
There are several types of PPM available that pace the dif-
a) b)
ferent chambers of the heart, commonly known as:
w Atrial pacing
w Ventricular pacing
w Dual chamber/sequential A-V pacing
w Bi-ventricular pacing

c) d)

Figure 4. Lead positions for different types of pacing:

atrial (a), ventricular (b), dual chamber/sequential A-V
Figure 3. A single lead positioned in the right ventricle (c) and bi-ventricular (d)

British Journal of Cardiac Nursing June 2009 Vol 4 No 6 263

Clinical
Table 2.
NBG pacing codes
1 2 3 4
Chamber(s) paced Chamber(s) sensed Sensing response
O = None O = None O = None
A = Atrium A = Atrium T = Triggered
V = Ventricle V = Ventricle I = Inhibited
D = Dual (A+V) D = Dual (A+V) D = Dual (T+I)
Adapted from Kenny, 2007
times since by different organizations until the current
codes devised by the North American Society of Pacing
and Electrophysiology and British Pacing and
Electrophysiology Group came into use (usually referred
to as the NBG codes) (Kenny, 2007) (Table 2).
The first letter in the code corresponds to the chamber
being paced, this can be the atrium, ventricle or both. The
second letter corresponds to the chamber from which the
impulses are sensed. The third letter indicates the response
to the sensed signal. The fourth and fifth columns are
additional programmable features. For example a code
such as VVIR implies that the ventricle is paced, the ven-
tricle is sensed and the pacemaker will not active if it
detects the patients own intrinsic rhythm and the rate will
change depending on the needs of the patient (Mills,
2005). Rate response adjusts the rate of pacing based on
the activity level of the patient, pacemakers can sense this
increase in activity in a variety of ways, including; vibra-
tion, increase in respiration rate and changes in blood
temperature (Houghton and Grey, 2003).
Single chamber
Single chamber pacemakers will pace either the atrium or
the ventricle. For example an on-demand atrial pacemaker
(AAI) will pace and sense the atrium. Pacing is inhibited
when it detects the patient’s intrinsic rhythm (natural
Figure 5: Ventricular pacing with intrinsic rhythm showing loss of ‘atrial
kick’ when pacing.
264
5
Rate modulation Multisite pacing
O = None O = None
R = Rate modulation A = Atrium
V = Ventricle
D = Dual (A+V)
heart rhythm) (Mills, 2005). This type of pacemaker
requires the patient to have an intact conduction system
and functioning AV node (Mills, 2005).
Single chamber pacemakers that pace the ventricle (e.g.
VVI) work by pacing and sensing the ventricle. The pri-
mary benefits are for patients who require intermittent
pacing or those with complete heart block (Kenny, 2007).
This type of pacemaker does not affect atrial activity, so
the ‘atrial kick’ contribution to the cardiac output (an extra
15-30%) may be lost (Mills, 2005).
This is seen in Figure 5, which shows a patient with
intrinsic rhythm and ventricular pacing. The line below
the ECG is the pressure waveform, which is dampened
when the ventricles are paced, showing the effect of loss of
‘atrial kick’ on the patients pressure.
Another problem with this lack of synchronization is
that mitral or tricuspid insufficiency could develop. This
type of pacemaker is normally prescribed for patients who
lead a more sedentary lifestyle (Mills, 2005).
Dual chamber
Dual chamber pacing has been shown to produce small
but potentially significant benefits for patients with sick
sinus syndrome (SSS) and/or atrioventricular (AV) block,
when compared with single chamber ventricular pace-
makers (Castelnuovo et al, 2005). Dual chamber pacemak-
ers are often given to more active or younger patients
(Castelnuovo et al, 2005). A systematic review found a
significant statistical improvement in patients’ exercise
capacity when given dual chamber pacemakers as opposed
to single chamber pacemakers. (Castelnuovo et al, 2005).
Dual chamber pacemakers respond to each atrial stimu-
lation and activate the ventricle when this does not occur
naturally ensuring A-V synchrony (Mills, 2005).
Bi-ventricular pacing
Also known as cardiac resynchronization therapy (CRT) is
used for the treatment of heart failure when a patient ful-
fills the required criteria (Table 3). Underwood (2004)
describes heart failure as a relatively common condition
with a poor prognosis, characterized by reduced cardiac
output resulting in arterial under-filling, causing the body
to retain fluid, thus increasing fluid volume. This can lead
to systemic venous congestion and pulmonary oedema.
British Journal of Cardiac Nursing June 2009 Vol 4 No 6
 Clinical

Table 3.
Patient criteria for cardiac
resynchronization therapy
w New York Heart Association (NYHA) symptoms,
class III to IV
w Patients in sinus rhythm
With QRS on ECG ≥ 150 ms
Or QRS on ECG of 120–149 ms with mechanical
dyssyncrony confirmed by echocardiography
w Left ventricular ejection fraction (LVEF) ≤ 35%
w Currently receiving optimal pharmacological
therapy
National Institute for Health and Clinical Excellence, 2007

CRT uses three leads placed in the right atrium, the right
ventricle, and a third passed through the coronary sinus to
pace the left ventricle from behind (Johnson and Rawlings-
Anderson, 2007) (Figure 6). Leads are not passed directly
into the left ventricle as the risk of thromboembolism and/
or impairment to the aortic valve, pose an unacceptable
risk to the patient (Timperley et al, 2008). CRT attempts to
improve the efficiency of the pumping action of the heart
by ‘re-synchronizing’ the pumping action of the hearts
chambers (Fox et al, 2007). This works by improving ven-
tricular contraction by stimulating the right and left ventri-
cle, improving cardiac output, diastolic left ventricle filling
and ejection fraction (Timperley et al, 2008).
Recognizing pacemakers on the ECG
The main indicator of a pacemaker on an ECG is the pres-
ence of pacing spikes, otherwise known as pacing artifact.
These spikes occur as the pacemaker sends an electrical
impulse to the heart muscle (Mills, 2005). The location of
the pacing spike(s) shows which chambers are being
paced (Figure 7). Ventricular pacing causes broad QRS
Figure 6. Fluoroscopic image of bi-ventricular lead
positions
complexes on the ECG as the electrical impulse does not
travel down the normal fast conduction pathway
(Houghton and Grey, 2003).
Bi-polar/uni-polar leads
All electrical circuits have two poles: a positive pole called
an anode, and a negative pole called a cathode. Uni-polar
leads have a pole on the lead itself whereas bi-polar leads
have two poles on the lead. The large circuit made by the
uni-polar lead causes a large pacing spike on the surface
ECG, the smaller bi-polar circuit causes a smaller pacing
spike on the ECG (Kenny, 2007).
Preparation of the patient
The procedure should be fully explained to the patient and
any questions or concerns addressed. Timperley et al
(2008) state that before insertion of a PPM, patients
should be prepared for the procedure by taking bloods,

Pacing spike

a. Single chamber ventricular pacing, pacing spike located before QRS complex. The underlying
rhythm is complete heart block.

b. Dual chamber pacemaker, pacing spike located both before P wave and before QRS complex

Figure 7. Pacing spikes on a rhythm strip

British Journal of Cardiac Nursing June 2009 Vol 4 No 6 265

Clinical
Subclavian
vein
Cephalic vein
Figure 8. The subclavian and cephalic veins are used for
transvenous access
including full blood count, urea and electrolytes and an
international normalized ratio (INR) if appropriate (i.e. if
the patient is on anticoagulants?)
The patient should also have a 12-lead ECG, a valid
consent form, and intravenous access for delivery of pro-
phylactic antibiotics and any sedation that may be required.
Prophylactic antibiotics (i.e. flucloxacillin/vancomycin 1g)
aid in the reduction and prevention of PPM infections
(Johnson and Rawlings-Anderson, 2007).
Swanton and Banerjee (2008) state that aspirin and/or
clopidogrel are also stopped if possible for around three
to four days before the implantation procedure. Warfarin
can be stopped four to five days prior to procedure. The
INR should be ≤1.5 to prevent a haematoma forming
around the pacemaker box. Warfarin is normally restart-
ed the same night as the procedure (Swanton and
Banerjee, 2008). The decision to stop warfarin or aspirin
Figure 9. Fluoroscopic image of dual chamber pacing
leads positioned in the right atrium and ventricle
266
may vary depending on the individual patient’s risk
assessment.
The PPM is normally positioned in the non-dominant
side. For example, if the patient is right-handed then the
PPM is positioned in the left upper chest and vice versa
(Johnson and Rawlings-Anderson, 2007).
Where cardiac monitoring is used before implantation,
the sticky residue left behind from the electrodes can be
removed with acetone. Alternatively the electrodes can be
repositioned away from the implant area to avoid the need
to do this.
The implantation procedure
PPMs are normally inserted in theatre or a cardiac cathe-
terization laboratory, with the patient being fully con-
scious, and optimal sterility maintained throughout the
procedure (Johnson and Rawlings, 2007). The implanta-
tion procedure normally lasts between 60 and 90 minutes
depending on the type of pacemaker inserted and indi-
vidual patient factors (Kumar and Clark, 2003).
During the procedure the patient’s ECG, blood pressure
and oxygen saturation are measured non-invasively (Johnson
and Rawlings-Anderson, 2007). The patient’s non dominant
side is used for implantation. Transvenous access is nor-
mally achieved via the subclavian or cephalic veins (Kenny,
2007), located just below the collar bone (Figure 8). The leads
are positioned using fluoroscopy to guide them into the cor-
rect position (Kumar and Clark, 2003) (Figure 9).
The permanent pacemaker pocket is made for the pulse
generator, usually located sub-cutaneously in front of the
pectoral muscle (Kumar and Clark, 2003) (Figure 9).
Sometimes for young and/or thin females, the pocket can
be located in the retro-mammary or axillary position
(Kenny, 2007).
Following the procedure patients should be monitored to
establish underlying rhythm and to highlight any pacing
irregularities. In addition the patient should also receive
regular observations (blood pressure, SpO2, heart rate, tem-
perature and respiratory rate) and regular checks of the
Pacemaker pocket
Figure 10. The permanent pacemaker pocker
British Journal of Cardiac Nursing June 2009 Vol 4 No 6

wound to monitor for signs of infection or haematoma
(Johnson and Rawlings-Anderson, 2007).
The implant wound can be closed in a variety of ways
including staples, glue, dissolvable or non-dissolvable
sutures. Local trust policy should always be followed. Any
non-dissolvable closure methods such as staples or non-
dissolvable sutures are usually removed at the local prac-
tice surgery around 7-10 days after the procedure.
Patients are usually followed up in pacing clinics once or
twice a year post-procedure (Stain, 2008). The frequency
of follow-up for each patient will depend on factors such
as his/her overall clinical condition and the type of pace-
maker implanted (more complex pacemakers may need
more frequent visits to adjust the PPM’s programming)
(Vardas et al, 2007).
Post-insertion complications associated
with permanent pacemakers
Pneumothorax and haemothorax
There is a small risk of pneumothorax (1–2%) when the
subclavian vein is used for lead access (Timperley et al,
2008). Breathlessness and increased pain on inspiration
may occur following pneumothorax/haemothorax. Other
symptoms can include an increase in respiratory rate and
cyanosis (Leach, 2004). This can lead to the need to insert
a chest drain (Johnson and Rawlings-Anderson, 2007).
The chest x-ray is used in addition to fluoroscopic imag-
ing—as it is hard to identify a pneumothorax/haemotho-
rax when the patient is lying down an upright x-ray should
be used (O’Grady, 2007).
Infection
Infection of the wound may occur. Many clinicians attempt
to further reduce the risk of infection by adding antibiotics
to the pacemaker pocket, such as gentamicin 80 mg
(Timperley et al, 2008). As a result of a low grade infection
or other mechanical means, a pacemaker may start to pro-
trude through the skin (termed erosion) (Kumar and Clark,
2003). Monitoring the patient’s vital signs including tem-
perature accompanied by regular checks of the wound site
for swelling, pain, redness, inflammation or weeping can
alert the nurse to signs of an infection.
Reentrant tachycardia
Pacemaker-mediated tachycardia (PMT) is a problem
associated with dual-chamber pacemaker systems. A retro-
grade (from ventricle to atrium) conduction triggers a loop
of events resulting in a sustained tachycardia (Bowbrick
and Borg, 2006) (Figure 11). This form of tachycardia is not
caused by the pacemaker but owing to the retrograde con-
duction (backward impulse) the pacemaker acts as a path
for reentry of the electrical impulse, generating a never-
ending loop of tachycardia. This is usually triggered by a
premature ventricular contraction (Kenny, 2007).
PMT can be seen on the ECG by closely grouped paced
complexes and can usually be prevented by prolonging the
atrial refractory (recovery) period. Many pacemakers can
detect PMT and automatically prolong the atrial refractory
British Journal of Cardiac Nursing June 2009 Vol 4 No 6
Clinical
Pacing in ventricle
P wave sensed Retrograde
in atrium conduction
Atrial contraction
Figure 11: Pacemaker-mediated tachycardia (adapted
from Bowbrick and Borg, 2006)
period for one cycle to interrupt the tachycardia (Bennett,
2006). PMT may cause haemodynamic instability.
Appropriately-trained staff can use a magnet to stop atrial
sensing, or alternatively the pacemaker can be repro-
grammed (Bowbrick and Borg, 2006).
Pacing of the diaphragm
In some cases the pacemaker may stimulate the patient’s
diaphragm due to the proximity of the electrical signal to
the phrenic nerve, causing hiccoughs (Mills, 2005).
Cardiac tamponade
Direct trauma inflicted during the implant procedure can
cause the pericardial sac to fill with fluid, causing elevated
pressure, which in turn prevents the ventricles filling
properly and can reduce the stroke volume. This is a
medical emergency and should be treated immediately,
usually via pericardiocentesis (passing a needle into the
pericardium and aspirating the fluid). Signs and symp-
toms include persistent hiccoughs, reduced pulse strength
during inspiration, reduced blood pressure, cyanosis, dis-
tended jugular veins, reduced urinary output and distant-
sounding heart sounds (O’Grady, 2007).
Pocket haematoma
Bleeding into the pacemaker pocket can occur. To reduce
the risk of this the patient’s INR should be less than 1.5
before implantation unless there are clinical reasons that
require a higher INR (e.g. mechanical valve) (Kumar and
Clark, 2003).
Lead displacement
Before the fibrotic capsule forms to better hold the lead in
place, the lead can become displaced, causing the pace-
maker not to function as intended. Most patients receive a
chest x-ray and pacing check to confirm lead position
before discharge (Kumar and Clark, 2003).
Pacing problems
There are also various problems associated with pace-
maker malfunction (Table 4). To this end the patient is
267
Clinical

Table 4.
Common pacemaker malfunctions

Problem Explanation Effect on patient Identification

Failure Pacemaker Can expose patient to Presence of a pacing spike on ECG without
to produces an the condition the appropriate atrial or ventricular response
capture impulse but pacemaker was inserted
fails to pace to treat
the myocardium

Failure No impulse is Can lead to reduced No pacing spike or subsequent P/QRS wave where
to pace generated by cardiac output and expected
the pacemaker subsequent drop in
blood pressure

Under- The pacemaker The patient may be Pacing spikes seen on the ECG at various points in
sensing fails to detect aware of palpitations or the cardiac cycle not before P waves or QRS waves
the intrinsic missed beats. If pacing as would be expected
cardiac activity spikes fall on T waves
and paces this can be dangerous
anyway and cause ventricular
tachycardia or fibrillation
(VT/VF) requiring
emergency treatment
Adapted from Mills, 2005 and Kenny, 2007

usually placed on a cardiac monitor overnight and receives
regular observations (blood pressure, pulse etc) to ensure
the pacemaker is functioning as intended and identify any
potential haemodynamic compromise (O’Grady, 2007).
When presented with any of these problems it is impor-
tant to monitor the patient’s vital signs. A 12-lead ECG
should also be obtained.
Placing a magnet over the pulse generator reverts the
pacemaker to asynchronous mode and can be used by
appropriately-trained personnel to determine the battery
life of the pulse generator, to allow the use of emergency
pacing if the pacemaker is malfunctioning, identify which
chambers are being paced and assess capture. Magnet
application can also be used to pace a patient despite the
presence of electromagnetic interference (Mills, 2005).
Clinical considerations
Some clinical equipment and/or tests can affect the func-
tioning of PPMs. Health professionals caring for PPM
patients should be aware of these possible effects and take
steps to reduce risks to PPM patients (Table 5).
Advice to patients
Patients living with a PPM should receive health education
pertaining to the pacemaker. Current UK driving law states
that no driving is allowed for 1 week post-insertion (DVLA
need not be informed (DVLA, 2009)). Patients with a group
2 licence (formerly LGV/PCV licence) should not drive for
6 weeks following PPM insertion (the DVLA should be
informed (DVLA, 2009) (Timperly et al, 2008).
Patients should also be advised to keep the wound dry
for 5–7 days or until the wound is both dry and healed.
Table 5.
Clinical equipment affecting
permanent pacemakers
w Defibrillators (position defibrillator pads or
paddles away from pulse generator site, check
PPM post defibrillation)
w Diathermy (can cause inhibition of the PPM)
w Magnetic resonance imaging (MRI) (usually
contraindicated)
w Radiotherapy (can cause damage to PPM circuits)
w TENS (transcutaneous electrical nerve
stimulation)
Mills, 2005; Johnson and Rawlings-Anderson, 2007

268 British Journal of Cardiac Nursing June 2009 Vol 4 No 6


Patients should also be advised to see a relevant health
professional if there are any signs of fever, infection or
pain/swelling/heat at the wound site (Timperley et al,
2008). Vigorous activity and contact sports should also be
avoided following insertion of a PPM (Swanton and
Banerjee, 2008).
If non-dissolvable stitches or staples are used to close
the wound the patient should be advised to have them
removed (usually by a GP or practice nurse/district nurse)
in 7–10 days (Timperley at al, 2008).
Patients should carry their pacemaker card detailing the
type of pacemaker they have. This card should be pre-
sented to doctors and/or dentists prior to any procedure
(Johnson and Rawlings-Anderson, 2007).
Sources of electromagnetic interference can cause the
pacemaker to revert to asynchronous pacing mode, prompt
unnecessary pacing, or even mimic cardiac activity (Mills,
2005; Schoenfeld, 2007). Patients exposed to any sources
of electromagnetic interference that could affect the func-
tioning of the PPM should not linger near these sources or
expose themselves without due reason (Table 6). Pacemaker
patients should also be advised to avoid areas displaying a
‘no pacemakers’ sign.
Conclusions
There are a number of arrhythmic conditions that may
mean a patient is prescribed a permanent pacemaker, and
the specific type of PPM, functionality and position of the
leads will vary. However, the cautions and considerations
that apply to all patients with a PPM implanted should be
kept in mind in order to provide effective care. BJCardN
Acknowledgments
The author would like to thank Dr M Ghandi and Jenny Tagney, and
Medtronic for the image of the pulse generator in Figure 2.
Table 6.
Potential sources of electromagnetic
interference to be avoided
w Airport weapons detectors
w CB radio-transmitting systems
w Some (ultrasonic) dental drills
w Shop anti-theft systems
w Mains-driven electric motors
(especially if sparking/faulty)
w Magnets
w Vibrations (helicopters/hovercrafts)
w High-powered radar stations
w Mobile phones—patients normally advised to use
on opposite side to pulse generator (i.e. if
implanted on right side would use left arm/ear)
and to keep phones at least 6 inches/15 cm
away from the pulse generator
Mills, 2005; Schoenfeld, 2007
British Journal of Cardiac Nursing June 2009 Vol 4 No 6
View publication stats
Clinical
Key Points
w Many nurses in a variety of clinical areas are exposed to patients
with a permanent pacemaker
w A working knowledge of the different types of PPM device can help
the nurse to care for a patient more effectively
w An awareness of what affects a PPM can help health professionals
to take steps to prevent or reduce risks to patients with a PPM, both
in and out of the clinical environment
w ECG recognition of pacemakers can help to identify pacing problems
Bennet DH (2006) Cardiac Arrhythmias: Practical Notes on Interpretation
and Treatment. 7th edn. Hodder Arnold, London
British Heart Foundation (2008) Living with a heart condition:
Pacemakers. http://tinyurl.com/qsh737(accessed 19 May 2009)
Bowbrick S, Borg A (2006) ECG complete. Churchill Livingstone, Edinburgh
Castelnuovo E, Stein K, Pitt M, Garside R, Payne E (2005) The effective-
ness and cost-effectiveness of dual-chamber pacemakers compared with
single-chamber pacemakers for bradycardia due to atrioventricular
block or sick sinus syndrome: systematic review and economic evalua-
tion. Health Technol Assess 9(43)
Conover MB (2003) Understanding Electrocardiography. 8th edn. Mosby, St
Louis
Davies A (2007a) Recognizing and reducing interference on 12-lead elec-
trocardiograms. Br J Nurs 16(13): 800-4
Davies A (2007b) Calculating cardiac axis on a 12-lead ECG. British
Journal of Cardiac Nursing 2(11): 513–7
Driver and Vehicle Licensing Agency (2009) About Medical Standards for
Drivers http://tinyurl.com/olvppq (accessed 19 May 2009)
Ector H and Vardas P for European Heart Rhythm Association, European
Society of Cardiology (2007) Current use of pacemakers, implantable
Cardioverter defibrillators and resynchronization devices: data from the
registry of the European Heart Rhythm Association. Eur Heart J
9(suppl 1): 144–9
Fox M, Mealing S, Anderson R et al (2007) The clinical effectiveness of
cardiac resynchronization (biventricular pacing) for heart failure: sys-
tematic review and economic model. Health Technol Assess 11(47)
Kenny T (2007) The Nuts and Bolts of Cardiac Pacing. Blackwell Futura,
Oxford
Khan E (2006) The pathological origins of arrhythmias. British Journal of
Cardiac Nursing 1(9): 408–17
Kumar P, Clark M (2003) Clinical Medicine. 5th edn. WB Saunders,
Edinburgh
Leach R (2004) Critical Care Medicine at a Glance. Blackwell Publishing,
Oxford
National Institute for Health and Clinical Excellence (2005) Dual-chamber
Pacemakers for Symptomatic Bradycardia due to Sick Sinus Syndrome and/
or Atrioventricular Block [Technology appraisal 88]. NICE, London
National Institute for Health and Clinical Excellence (2007) Cardiac
Resynchronization Therapy for the treatment of Heart Failure.
[Technology appraisal 120]. NICE, London
O’Grady E (2007) A Nurse’s Guide to Caring for Cardiac Intervention
Patients. John Wiley & sons Ltd, Sussex
Mills EJ (2005) ECG Interpretation: A 2-in-1 Reference for Nurses.
Lippincott, Williams and Wilkins, Philadelphia
Schoenfeld MH (2007) Contemporary pacemaker and defibrillator device
therapy: Challenges confronting the general cardiologist. Circulation
115: 638-653
Stain N (2008) Home monitoring for ICDs and Pacemakers. Coronary
Heart 10: 24–7
Swanton RH, Banerjee S (2008) Swanton’s Cardiology. 6th edn. Blackwell
Publishing, Massachusetts
Timperley J, Leeson P, Mitchell RJ, Betts T (2008) Pacemakers and ICDs.
Oxford University Press, Oxford
Underwood JCE (2004) General and Systematic Pathology. 4th edn.
Churchill Livingstone, Edinburgh
Vardas PE, Auricchio A, Blanc JJ et al for European Society of Cardiology;
European Heart Rhythm Association (2007) Guidelines for cardiac pac-
ing and cardiac resynchronization therapy: The Task Force for Cardiac
Pacing and Cardiac Resynchronization Therapy of the European Society
of Cardiology. Developed in collaboration with the European Heart
Rhythm Association. Eur Heart J 28(18): 2256-95
269