INTRODUCTION

A pacemaker (or artificial pacemaker) is a medical device which uses electrical impulses,
delivered by electrodes contracting the heart muscles, to regulate the beating of the heart.

HISTORY OF PACEMAKERS

In 1838 a Professor of Physics at the University of Pisa in Italy named Carlo Matteucci took
great interest in the work of Luigi Galvani. Using the Galvanometer he discovers that an electric
current accompanies each heartbeat. He also proves that nerves carry an electric current to the
muscles causing contraction. He proves this by building a device that uses a frogs leg with all
but one muscle removed and the nerve that connects to that muscle. Using a small amount of
electricity from a voltaic pile that is applied to the nerve he causes the muscle the contract. The
electrical impulse is measured using a galvanometer. The experiment proved that electricity
travels using nerves as a pathway and cause muscular contractions.

After that Several scientists other than medical profession discovered several inventions All
these discoveries did not go unnoticed by the world of medicine Many doctors and scientist
were looking for ways to apply their new found knowledge about electricity.

The first device that is documented to be effective was created in 1926. Dr. Albert Hyman
created an electromechanical instrument which many believe may be the first successful
pacemaker. The device was patented in 1931 and was first used in Sydney Australia. The hand
operated machine used a transthoracic needle that was inserted into the chest and then into the
heart. Within a year the device had been used 43 times with 14 successful outcomes.

The pacemaker made its big change in 1950 when a Canadian electrical engineer named
John Hopps paired with Dr. Wilfred Bigelow to create a pacemaker that could be used for long
periods and treat many of the new dysrhythmias that had been discovered. The new pacemaker
was a great advancement but still had some shortcomings. The device that sat on a tabletop was
large and heavy. The vacuum tube technology that was available at the time of development
was unreliable. The externally placed electrode patches sent electric impulses into the patient
resulting in a great deal of pain for the patient. The device worked, but its life would be short
because new technology that would change the world of electronics had just arrived

The Transistor makes a big impact in the medical field as well. The component allows all
things electronic to be smaller, lighter and more reliable.

Dr. Paul Zoll a cardiologist from Boston led the way in modern electronics with a pacemaker
that he created in 1951. The pacemaker used modern transistors but still was large, heavy and
relied on AC power. Despite these shortfalls the Zoll pacemaker remained a standard for
pacing patients for several years

The next advancement came from electrical engineer and part time TV repairmen Earl
Bakken. In 1957 he developed a smaller pacemaker that could be worn around the neck
allowing the patient to move as far as the extension cord would let them. This new pacemaker
was also less painful then those before because the leads were surgically attached to the
outside of the myocardium. The Bakken Pacemaker was well received by the medical
community and by the public but Earl Bakken was not satisfied. While the device was much
small then its predecessors it was still too heavy for many pediatric patients. Earl Bakken also
realized the need for a battery powered pacemaker after several patients died during a power
failure.

*y77y

While researching for a solution Bakken came across a 1956 issue of Popularp
Electronics. In it he found an article about how small amounts electricity could be amplified so
that sound could be projected to groups through loudspeakers. Pacemakers had always been
powered by a 110 volt AC circuit but Bakken thought of a way that power from a battery could
be amplified so that it could simulate the human heart. Bakken had to start from scratch. He
created a miniature mercury battery that supplied 9.4 volts and miniaturized his pacemaker
until it was 4 inches square 7 and only inch thick. Made of aluminum this pacemaker was light
enough to be carried around the neck of even the weakest child. The pacemaker was put into
clinical use within 4 weeks. Earl Bakken co-founded the company Medtronic and continued to
improve his pacemaker and Batteries.
 Up until now all pacemakers had external pulse generators. With the size of pacemakers and
the short battery life, the idea of implanting a pacemaker into a patient was unthinkable. In
1958 Wilson Greatbatch changed that thought process. Greatbatch was an electrical engineer
who was trying to create an implantable device that would monitor and record pulse rates.
Instead he created a device that would generate an electrical impulse.. He found Dr. William
Chardack and Dr. Andrew Gage of the Buffalo Veterans Hospital. They perfected the device and
implanted it into a dog for testing.

After two years of animal testing the pacemaker was implanted into a 77 year old man who
suffered from complete heart block. The patient went on to live two more years before
he died of unrelated causes. Greatbatch felt like the biggest limitation of his pacemaker was the
battery life. His battery would last 24 months before it needed to be replaced.

Wilson Greatbatch joined up with Medtronic and battery pioneer Earl Bakken and focused on
creating a better battery. Greatbatch and Bakken created and perfected the Lithium Iodine
battery that is still used to power pacemakers today. Greatbatch left Medtronic and created
his own company Wilson Greatbatch Ltd. Which concentrates on creating batteries to power
pacemakers. Earl Bakken and Medtronic turned there attention to perfecting and marketing the
Greatbatch Pacemaker

In Sweden. Dr. Ake Senning and engineer Rune Elmqvist made history when they implanted
the first pacemaker into a human but that was not always their plan.in October 8 1958 the first
implantable pacemaker was placed in Arne Larsson. The pacemaker that was placed in Larsson
was accidentally dropped and possibly damaged several times ,The team continued to work to
create a successful device and as a result Arne Larsson lived to be 86 years old dying in
December 28 2001 of cancer. In his lifetime he received 5 different lead systems
and 22 pulse generators of 11 different models. He outlived both of the doctors that saved his
life Leads proved to be point of failure in many of the pacemakers that were being developed in
the 1950s

Arne Larson

In the mid 1960s transvenous leads that could be easily placed inside the heart through the
subclavian vein replaced epicardial leads that required a thoracotomy so that the lead could be
placed on the outside of the heart. Also in the mid 1960s the demand pacer made its first
 appearance. Prior to the demand pacers creation all pacemakers fired at a preset rate regardless
of the hearts native rhythm. The power source was also an item that many tried to improve on.

During the 1970s, interest was directed towards using nuclear-energy fuelled cardiac
pacemakers. In these pacemakers, the energy of radioisotope decay (mostly plutonium-238) was
converted to electrical energy. Though these pacemakers assured impressive longevity (10-20
years) and reliability (99%) they had the inherent disadvantage of radiation exposure,
contamination of tissues with radioisotope in case of capsule leak, safety concerns of pacemaker
disposal after use, cost implications and a large size. As a result of these drawbacks, these
pacemakers could not attain widespread acceptance

TYPES OF PACEMAKERS

There are THREE TYPES of artificial cardiac pacemaker systems in common clinical use are:

1. Implantable pulse generators with endocardial or myocardial electrodes for long-term or

permanent use.

2. External, miniaturized, transistorized, patient portable, battery-powered, pulse generators with

exteriorized electrodes for temporary transvenous endocardial or transthoracic myocardial
pacing. (temporary)

3. Console battery- or AC-powered cardiovertors, defibrillators, or monitors with high-current

external transcutaneous for temporary pacing in asynchronous or demand modes, with manual
or triggered initiation of pacing

PERMENANT / IMPLANTABLE PACEMAKERS

A permenant pacemaker is an electronic device, approximately the size of a pocket watch,

that senses intrinsic heart rhythms and provides electrical stimulation when indicated.

Indications (ACC/AHA/HRS Guidelines)

Class I - The procedure should be performed
Class IIa It is reasonable to perform the procedure, but additional studies with focused
objectives are needed
Class IIb - The procedure may be considered, but additional studies with broad objectives are
needed
Class III - The procedure should not be performed; it is not helpful and may be harmful
 In 2008, the American College of Cardiology (ACC), the AHA, and the Heart Rhythm
Society (HRS) jointly published guidelines.[5] For further details on the following indications, see
the ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm
Abnormalities.
Class I indications
Sinus node dysfunction
Acquired atrioventricular block in adults
Chronic bifascicular block
After acute myocardial infarction
Hypersensitive carotid sinus syndrome and neurocardiogenic syncope
After cardiac transplantation
Pacing to prevent tachycardia
Patients with congenital heart disease

Class IIa indications

Sinus node dysfunction
Acquired atrioventricular block in adults
Chronic bifascicular block
Hypersensitive carotid sinus syndrome and neurocardiogenic syncope
Patients with congenital heart disease
Pacing to prevent tachycardia
Permanent pacemakers that automatically detect and pace to terminate tachycardia

Class IIb indications

Sinus node dysfunction
Acquired atrioventricular block in adults
Chronic bifascicular block
After acute myocardial infarction
Hypersensitive carotid sinus syndrome and neurocardiogenic syncope
After cardiac transplantation
Pacing to prevent tachycardia
Patients with congenital heart disease

Class III indications

Asymptomatic first-degree AV block.
Asymptomatic type I second-degree AV block at the supra-His (AV node) level or
that which is not known to be intra- or infra-Hisian.
AV block that is expected to resolve and is unlikely to recur(e.g., drug toxicity, Lyme
disease, or transient increases in vagal tone or during hypoxia in sleep apnea
syndrome in the absence of symptoms
Parts of a pacemaker system

A pacemaker consists of a pulse generator and pacing leads.

PULSE GENERATOR

Battery cells power pulse generator. Lithium batteries lasting 6 years or more are used in
most pacemakers. Nuclear powered pacemakers (Plutonium238 source) can last 20 years or
more. Other pacemakers can have their batteries recharged; externally when the generator battery
fails the implantable unit that contains the batteries must be replaced surgically.

The Pulse generator has several controls. They are energy output, heart rate and pacing
node.

Energy output
It refers to the intensity of the electrical impulse delivered by the pulse generator to the
myocardium. The amount of out put is measured in milliampers(M.A).The MA setting is
regulated by the physician at the time of pacemaker incersion and is set at the lowest level that
will produce depolarization .A setting of 1.5 MA usually is sufficient to cause depolarization.

Heart rate

Heart rate is set according to the desired therapeutic aim and the clinical consideration of
the patient. heart rate is usually set at70-80 beats/minute. If the purpose of pacemaker is to
suppress dysarrythmias the rate is set higher often 100-200beat/minute.

PACEMAKER LEADS

Pacemaker leads are electrical conductors (wires), covered with insulation. They transmit the
electrical impulses from the pulse generator to the heart, and from the heart to the pulse
generator. Pacemaker leads are usually inserted into the subclavian vein or its tributaries, and
 positioned on the inner surface (endocardium) of the heart. They are attached to the endocardium
by a small screw mechanism, or are held in place by tines. If a screw (also known as a helix) is
used to fix the lead to the heart, the lead is called an active fixation lead (Figure

Active fixation lead Passive fixation lead. The white bar is 1

Cm

A passive fixation lead has tines ,which are designed to engage the trabeculae on the inner
surface of the heart. Pacemaker leads may also be placed on the outside of the heart (epicardium)
duringa surgical procedure. These leads are either sewn onto the heart, or fixed in place with a
small screw-in mechanism.

APPROACHES OF PACING
At present, 3 approaches to permanent cardiac pacing are in common use:
Single-chamber pacemaker With this device, 1 pacing lead is implanted in the right atrium
or ventricle
Dual-chamber pacemaker With this device, 2 pacing leads are implanted (1 in the right
ventricle and 1 in the right atrium); this is the most common type of implanted pacemaker
Biventricular pacing (cardiac resynchronization therapy [CRT]) With this approach, in
addition to single- or dual-chamber right heart pacing leads, a lead is advanced to the coronary
sinus for left ventricular epicardial pacing.
DUAL CHAMBER SINGLE

CRT (Cardiac resynchronization therapy)

CONCEPTUAL BUILDING BLOCKS OF PACEMAKER FUNCTION

Pacing
Pacing refers to the regular output of electrical current, for the purpose of depolarizing
the cardiac tissue in the immediate vicinity of the lead, with resulting propagation of a wave of
depolarization throughout that chamber. A pacemaker will pace at a certain frequency, or rate,
for example, 60 bpm. This rate is programmable. That is, it can be changed by using the
manufacturers programmer.

The pacing stimulus

Pacemakers function by delivering a small electrical current to myocardial cells. The electrical
activation spreads from cell to cell, throughout the heart. As each cell is electrically activated, it
contracts. The pacemaker delivers the electrical current between two points, called electrodes.
These two points may be either two electrodes on the pacemaker lead, or one electrode on the
pacemaker lead, and the metal coveringof the pacemaker pulse generator. Electrical current is
caused by the flow of electrons. This must occur in a circuit (i.e. a closed loop). A source of
current, such as the battery of a pacemaker, will have a negative end (from which electrons are
emitted) and a positive end (to which electrons are attracted). , pacingis more efficient when the
tip electrode of the pacinglead is the negative pole. The positive pole can either be a metallic
ring, about a centimeter back from the tip of the lead (Figure 1.6), or can be the body of the
pacemaker pulse generator itself

Sensing
The hearts intrinsic electrical activity (i.e. the P wave or QRS complex) transmits a small
electrical current (a few millivolts), through the pacemaker leads, to the pulse generator. This
current can be registered or sensed by the pacemaker circuitry. Pacemaker sensing describes the
response of a pacemaker to intrinsic heartbeats. The P waves, or atrial activity, are
transmitted through the atrial lead (if present) to the atrial channel of the pacemaker, and sensed
as atrial activity. Ventricular activity (the QRS complex) is transmitted through the ventricular
lead (if present) to the ventricular channel of the pacemaker, and this is sensed as ventricular
activity.
For electrical activity to be transmitted from the heart to the pacemaker, a closed electrical
circuit must be present, just the same as for an electrical impulse to be transmitted from the
pacemaker to the heart. Thus, just as with pacing, sensing can be unipolar or bipolar.

Bipolar sensing detects the intrinsic electrical activity occurring between the tip electrode and
the ring electrode of the lead. Unipolar sensing detects electrical activity occurring between the
tip of the lead, and the metal shell of the pulse generator. Because this is a much larger area,
other electrical signals, such as might be generated by the muscles of the diaphragm or sources
outside the body, are more likely to be detected (and therefore incorrectly interpreted by the
pacemaker as heart beats). It is important to note that the only way the pacemaker can determine
which chamber a signal originates from is by which lead transmits the signal to the pacemaker.
For example, the pacemaker will interpret any electrical signal transmitted through the atrial lead
to the atrial channel as a P wave, even if the signal is in fact a QRS complex large enough in
amplitude to be sensed by the atrial channel.

The sensitivity setting is measured in millivolts and is initially set at about 2 to 5 mV.
Failure to sense occurs when the generator does not recognize the hearts intrinsic
impulses(undersensing). The most common cause of failure to sense is displacement of the
electrode . Repositioning the patient on his or her left side may improve contact between the
electrode and the myocardium. If the response is still inadequate, then the sensitivity must be
increased. This increase is accomplished by turning down the millivoltage, allowing the
generator to detect beats that occur at lower millivolt levels. Conversely, if the pacemaker is
detecting beats that are not actually occurring (oversensing), then the sensitivity threshold must
be increased to block out artifact. This increase is accomplished by turning up the millivoltage.

Inhibition of output
A pacemaker can be programmed to inhibit pacing if it senses intrinsic activity, or it can be
programmed to ignore intrinsic activity and deliver a pacing stimulus anyway. If a pacemaker is
set so that it can be inhibited by intrinsic beats, then the pacemaker will not deliver a stimulus if
it senses an intrinsic beat at the proper time. For example, if a pacemaker is set to pace in this
was at 60 bpm, it will deliver a pacingstimulus only if an intrinsic beat does not occur.

Pacing Threshold
The threshold is the minimum amount of energy the pacemaker sends down the lead to
initiate a heart beat. Imagine a patient who had a pacing threshold of 0.75V (Volts). If the
pacemaker sent a pulse of 0.75V down the lead this would be enough to make the heart beat as
would any pulse larger/stronger than this. If the pacemaker in the same patient sent a pulse of
0.5V down the lead, this would not be enough and the pacemaker would fail to initiate a heart
beat (This would not be enough energy to push over the first domino) The minimum energy
needed to pace is called the pacing threshold.

Capture

Electrical capture, is Cardiac depolarization and resultant contraction (atrial or

ventricular) - Caused by pacemaker stimulus, is detected by examining an electrocardiogram.
Capture is both an electrical and a mechanical event. Electrical capture is indicated by a pacer
spike followed by a corresponding P wave or QRS complex, depending on which chamber is
being paced. If the atrium is paced, the spike appears before the P wave. If the ventricle is paced,
the spike occurs before the QRS complex

A pacer spike without a corresponding P wave or QRS complex indicates failure to capture
Electrical capture alone is inadequate. Adequacy of mechanical capture is assessed by feeling
for a pulse or checking blood pressure. Mechanical capture exists when the pacer spike and its
corresponding QRS complex are followed by a cardiac contraction
Rate response

Currently available pacemakers (and defibrillators) can be programmed to vary the pacing
rate in response to the patients level of activity. Various types of sensors have been developed to
allow the pacemaker to sense the patients level of activity. The parameters sensed include
patient movement, respiration, and changes in the T wave. Activation of the sensor by changes in
these factors, which are not related to exercise, might be a cause of more rapid than expected
pacingat rest. For example, hyperventilation or an activity that causes motion of the pacemaker
pulse generator (e.g. physical therapy of the chest or shoulder) may increase the activity of
pacemakers driven by minute ventilation and accelerometer sensors, respectively.

Triggered pacing
Pacemakers can be programmed to deliver a pacing stimulus whenever intrinsic activity is
sensed. This type of pacing is most often used in dual chamber pacemakers. Dual chamber
pacemakers can be programmed to sense activity in one chamber (usually the atrium) and
deliver a pacing stimulus in the other chamber (usually the ventricle) after a certain time delay.
This is known as triggered pacing. When referring to the appearance of this type of pacing on
telemetry or ECGs, it is commonly said that the ventricle is tracking the atrium, because if the
atrial rate becomes faster, the ventricular pacing rate will follow faster, in a 1 : 1 relationship.
Thus the exact rate of ventricular pacingwill not be determined by any setting on the pacemaker,
but by theccur within 1 second of the last sensed or paced beat.

PACING MODES
A standard pacemaker code has been developed jointly by the North American Society for
Pacing and Electrophysiology, and the British Pacing and Electrophysiology Group (the
NASPE/BPEG Generic Code, known as the NBG Code). The pacing function provided by a
pacemaker (or defibrillator) is usually given by a series of three or four letters. (There is a fifth
position in the code, which is not commonly used.) Each position denotes a different aspect of
pacemaker function. The identity of the letter in that position specifies the function. A given
combination of three or four letters is called a mode.

The positions and letters are as follows:

Position 1: chamber being paced
V = ventricle
A = atrium
D = atrium and ventricle (dual)
O = no pacing.

Position 2: chamber being sensed

V = ventricle
A = atrium
D = atrium and ventricle (dual)
O = no sensing.

Position 3: pacing response to a sensed beat

I = inhibited
T D = inhibited or triggered (dual) depending on the chamber
O = neither inhibited or triggered.

Position 4: rate response or absence

R = rate responsive
O = absence of rate response. (But this is usually just omitted

Examples:
The VVI mode paces and senses only in the ventricle.
Position 1 V indicates that it will pace only in the ventricle.
Position 2 V indicates that it senses intrinsic heartbeats only in the ventricle.
Position 3 I indicates that the response to a sensed heartbeat is inhibition of ventricular
pacing.
Position 4 blank, indicating that it is not rate responsive

PROCEDURE PACEMAKER IMPLANTATION

Approach Considerations
Permanent pacemaker insertion is considered a minimally invasive procedure. Transvenous
access to the heart chambers under local anesthesia is the favored technique, most commonly via
the subclavian vein, the cephalic vein, or (rarely) the internal jugular vein or the femoral
vein. The procedure is typically performed in a cardiac catheterization laboratory or in an
operating room (OR).
The pacing generator is typically placed subcutaneously in the infraclavicular region.
Occasionally, pacemaker leads are implanted surgically via a thoracotomy, and the pacing
generator is placed in the abdominal area. Single-chamber and dual-chamber pacer insertion can
be accomplished from either left or right pectoral sites. After appropriate sedation, the chest is
prepared with an antiseptic solution, and the area is covered with sterile drapes to keep the
incision area as clean as possible.
In current practice, antibiotic prophylaxis is standard for device implantation. Preoperative
antibiotic use reduces the risk of pacemaker-related infections by approximately 80%
Routinely, cefazolin 1 g is administered intravenously (IV) 1 hour before the procedure. If the
patient is allergic to penicillins or cephalosporins, vancomycin 1 g IV or another appropriate
antibiotic may be administered preoperatively

1.Venous access
A central vein (ie, the subclavian, internal jugular, or axillary vein) is accessed via a
percutaneous approach..
The subclavian vein is typically accessed at the junction of the first rib and the clavicle. On
occasion, phlebography may be required to visualize the vein adequately or to confirm its
patency. Some centers employ the first rib approach under fluoroscopy, with no or minimal
incidence of pneumothorax.
After venous access is obtained, a guide wire is advanced through the access needle, and the
tip of the guide wire is positioned in the right atrium or the venacaval area under fluoroscopy.
The needle is then withdrawn, leaving the guide wire in place. If indicated, a second access will
be obtained in a similar fashion for positioning of a second guide wire.
2.Creation of pocket
A 1.5- to 2-inch incision is made in the infraclavicular area parallel to the middle third of the
clavicle, and a subcutaneous pocket is created with sharp and blunt dissection where the
pacemaker generator will be implanted. Some physicians prefer to make the pocket first and
obtain access later through the pocket or via venous cutdown; once access is obtained, they
position the guide wires as described above.
3.Placement of lead(s)
Over the guide wire, a special peel-away sheath and dilator are advanced. The guide wire and
dilator are withdrawn, leaving the sheath in place. A stylet (a thin wire) is inserted inside the
center channel of the pacemaker lead to make it more rigid, and the lead-stylet combination is
then inserted into the sheath and advanced under fluoroscopy to the appropriate heart chamber.
Usually, the ventricular lead is positioned before the atrial lead to prevent its dislodgment.
Making a small curve at the tip of the stylet renders the ventricular lead tip more
maneuverable, so that it can more easily be placed across the tricuspid valve and positioned at
the right ventricular apex
Once correct lead positioning is confirmed, the lead is affixed to the endocardium either
passively with tines (like a grappling hook) or actively via a helical screw located at the tip. The
screw at the tip of the pacemaker is extended or retracted by turning the outer end of the lead
 with the help of a torque device. Adequate extension of the screw is confirmed with fluoroscopy.
Each manufacturer has its own proprietary identification marks for confirming adequate
extension of the screw.
Once the lead is secured in position, the introducing sheath is carefully peeled away, leaving
the lead in place. After the pacing lead stylet is removed, pacing and sensing thresholds and lead
impedances are measured with a pacing system analyzer, and pacing is performed at 10 V to
make sure that it is not causing diaphragmatic stimulation. After confirmation of lead
position and thresholds, the proximal end of the lead is secured to the underlying tissue (ie,
pectoralis) with a nonabsorbable suture that is sewn to a sleeve located on the lead.
If a second lead is indicated, it is positioned in the right atrium via a second sheath, with the
lead tip typically positioned in the right atrial appendage with the help of a preformed J-shaped
stylet.
Positioning of pulse generator
When the leads have been properly positioned and tested and sutured to the underlying tissue,
the pacemaker pocket is irrigated with antimicrobial solution, and the pulse generator is
connected securely to the leads. Many physicians secure the pulse generator to underlying tissue
with a nonabsorbable suture to prevent migration or twiddler syndrome.
Typically, the pacemaker is positioned superficial to the pectoralis, but occasionally, a
subpectoral or inframammary position is required. After hemostasis is confirmed, a final look
under fluoroscopy before closure of the incision is recommended to confirm appropriate lead
positioning.
Completion and closure
The incision is closed in layers with absorbable sutures and adhesive strips. Sterile dressing
is applied to the incision surface. An arm restraint or immobilizer is applied to the unilateral arm
for 12-24 hours to limit movement.
A postoperative chest radiograph is usually obtained to confirm lead position and rule out
pneumothorax. Before discharge on the following day, posteroanterior and lateral chest
radiographs will be ordered again to confirm lead positions and exclude delayed pneumothorax.
Pain levels are typically low after the procedure, and the patient can be given pain medication
to manage breakthrough pain associated with the incision site.

Complications

Access-related complications
Early access-related complications include the following:
Bleeding
Hematoma
Phlebitis or thrombophlebitis of the vein
 Local infection
Arterial injury or puncture
Hemothorax
Pneumothorax
Catheter-related thrombosis (which may lead to pulmonary embolism)
Air embolism
Dysrhythmias
Atrial wall puncture from guide wire (which may lead to pericardial tamponade)
Lost guide wire
Anaphylaxis
Chylothorax (possible with left-side lead insertion)

Pocket-related complications
Early pocket-related complications include the following:
Swelling
Hematoma
Bruising and local pain
Infection

Lead-related complications
Early lead-related complications include the following:
Atrial or ventricular arrhythmias
Chamber perforation
Pneumothorax and pneumopericardium (with an atrial lead)
Intercostal or diaphragm pacing
Pectoral muscle stimulation
Lead dislodgement
Tricuspid valve laceration
Cardiac tamponade
Pericardial friction rub
Hypotension
Bleeding

Pacemaker generatorrelated complications

Early pacemaker generator related complications include the following:
Infection
Malfunction, including undersensing, oversensing, loss of capture, loss of output,
inappropriate rate, inappropriate mode, pulse generator failure, pacemaker-mediated
tachycardia, and pacemaker syndrome
 Cardiac Resynchronization Therapy
Cardiac resynchronization therapy (CRT), also referred to as biventricular pacing or multisite
ventricular pacing, is a component of modern heart failure therapy for qualified patients. In
CRT, there is a coronary sinus lead for left ventricular epicardial pacing in addition to a
conventional right ventricular endocardial lead. By simultaneously pacing the right and left
ventricles, CRT reduces the ventricular dyssynchrony that is frequently present in patients with
ventricular dilatation or conduction system defect.
CRT can involve either pacing (CRT-P) or defibrillation (CRT-D). The following discussion
focuses on CRT-P.
CRT is recommended for patients with
a left ventricular ejection fraction less than 35%,
a QRS duration longer than 120 msec, sinus rhythm,
New York Heart Association (NYHA) functional class III or ambulatory class IV heart
failure symptoms with optimal medical therapy.
Trials suggest that CRT may also reduce morbidity and mortality in patients with mildly
symptomatic heart failure. Consequently, the 2010 European guidelines and updated 2012
ACC/AHA/HRS guidelines now recommend CRT for the NYHA class II patient population. The
ACC/AHA/HRS guidelines also now indicate CRT for patients with left-bundle-branch block
with a QRS duration that is greater than or equal to 150 ms.
Biventricular pacing has been effective in improving symptoms and quality of life, reducing
heart failure hospitalizations, and reducing mortality because of its ability to achieve the
following results:
Reduction in ventricular electromechanical delay
Improved ventricular function
Reduced metabolic costs
Improved functional mitral regurgitation
Favorable remodeling
Reduction of cardiac chamber dimensions
Improved exercise capacity

Factors that influence the responsiveness of patients to CRT or that are used to identify
patients who will be responsive to CRT include the following:
QRS complex duration
Ventricular dyssynchrony (by echocardiography)
Successful lead placement
Physiologic atrioventricular delay

CRT requires left ventricular lateral wall pacing, which is achieved by placement of an
epicardial lead via the coronary sinus. Multiple-guide catheter systems are available for coronary
sinus cannulation, with most designs favoring a left pectoral approach. Coronary sinus
phlebography facilitates placement by demonstrating vessel size, position, and angulation. Left
anterior oblique and right anterior oblique projections are obtained with cine recording during
injection of 10-15 mL of contrast in the coronary sinus.
A guide wire is inserted through the catheter positioned in the coronary sinus and
maneuvered to the target venous branch. The coronary sinus lead is advanced over the guide wire
into the desired branch of the coronary venous system.
The guide wire and guide catheter are withdrawn, leaving the coronary sinus lead in place.
After acceptable thresholds and impedance are ensured, the lead is secured to the pectoralis with
a nonabsorbable suture.
Frequently encountered difficulties include problems in cannulating the coronary sinus, acute
angulation of the target venous vessels, and the absence of suitably sized veins in the left
ventricular pacing region of interest. Right pectoral positioning of the biventricular pacing leads
is more difficult in the presence of right subclaviansuperior venacaval angulation and frequently
requires the use of a deflectable guide catheter.

Implantable Cardioverter-Defibrillator( ICD)

An implantable cardioverter-defibrillator (ICD) is a specialized device designed to directly
treat a cardiac tachydysrhythmia. ICDs have revolutionized the treatment of patients at risk for
sudden cardiac death due to ventricular tachyarrhythmias
Indications for ICD placement
Indications for ICD implantation can be divided into 2 broad categories: secondary prophylaxis
against sudden cardiac death and primary prophylaxis. For secondary prophylaxis, ICD
placement is indicated as initial therapy in survivors of cardiac arrest due to VF or
hemodynamically unstable VT
Secondary prophylaxis
An ICD is recommended as initial therapy in survivors of cardiac arrest due to VF or
hemodynamically unstable VT. Published guidelines exclude cases in which there are
completely reversible causes
Primary prophylaxis
Indications for an ICD implant as primary prophylaxis against sudden cardiac death are listed
in the Table , below. The indications are listed as Class I or Class IIa, as classified by the
ACC/AHA 2008 guidelines.
Indication Classification Supporting Studies
Structural heart disease, sustained VT Class I AVID, CASH, CIDS
Syncope of undetermined origin, inducible VT or
Class I CIDS
VF at EPS
LVEF < 35% due to prior MI, at least 40 days
Class I SCD-HeFT
post-MI, NYHA Class II or III
LVEF 35%, NYHA Class II or III Class I SCD-HeFT
LVEF 30% due to prior MI, at least 40 days
Class I MADIT II
post-MI
LVEF < 40% due to prior MI, inducible VT or VF
Class I MADIT, MUSTT
at EPS
Unexplained syncope, significant LV dysfunction,
Class IIa Expert opinion
nonischemic CM
Sustained VT, normal or near-normal ventricular
Class IIa Expert opinion
function
Hypertrophic CM with 1 or more major risk
Class IIa Expert opinion
factors
Arrhythmogenic right ventricular
dysplasia/cardiomyopathy (ARVD/C) with 1 or Class IIa Expert opinion
more risk factors for sudden cardiac death (SCD)
Zareba et al , Viskin et al ,
Long QT syndrome, syncope or VT while Goel et al , Monnig et al ,
Class IIa
receiving beta blockers Goldenberg et al , Hobbs et
al
Nonhospitalized patients awaiting heart transplant Class IIa Expert opinion
Brugada syndrome, syncope Class IIa Expert opinion
Brugada syndrome, VT Class IIa Expert opinion
Catecholaminergic polymorphic VT, syncope or
Class IIa Expert opinion
VT while receiving beta blockers
Cardiac sarcoidosis, giant cell myocarditis, or
Class IIa Expert opinion
Chagas disease
TEMPORARY PACEMAKERS
Temporary cardiac pacing involves electrical cardiac stimulation to treat a bradyarrhythmia

or tachyarrhythmia until it resolves or until long-term therapy can be initiated. The purpose of

temporary pacing is to re-establish circulatory integrity and normal hemodynamics that are

acutely compromised by a slow or fast heart rate. In some situations, temporary pacing can be

lifesaving.

Temporary pacing can be divided into 2 types

1. Invasive approach

Transvenous pacing

Epicardial pacing

2. Non invasive

Transcutaneous pacing

1. Medtronics Single Chamber Temporary External Pacemaker Model 5348 can be used

for either atrial or ventricular pacing. It has a rapid rate pacing function for overdrive

pacing

2. .Medtronics Dual chamber Temporary External Pacemaker Model 5388 DDD used for

AV sequential pacing, i.e. the ability to pace either or both chambers of the heart in

sequence. It also has a rapid rate pacing function for overdrive pacing.
Connection

The connection between the pacemaker generator and the heart is made through either
unipolar or bipolar electrode wires. In a unipolar system, only the negative electrode is in direct
contact with the heart. In a bipolar system, both negative and positive electrodes lie within the
heart. Pacemakers can be either unipolar or bipolar. Distinguishing between the negative and
positive electrodes is important so that the wires are connected appropriately to the pulse
generator.6
The 2 types of invasive temporary pacing are epicardial and transvenous.3 The transvenous
category also includes devices that combine a specialized pulmonary artery catheter with a
pacemaker.1 Transvenous pacing involves a pulse generator, which is externally connected to 2
electrode wires, threaded through a large vein (generally the subclavian or internal jugular) into
either the right atrium or the right ventricle.1 These wires directly contact the endocardium
within the heart

Symptomatic abnormalities of the conduction system are the main indications for cardiac
pacing, a method by which a small pulsed electrical current is artificially delivered to the heart.
Of the several methods for temporary pacing of the heart (transcutaneous, transvenous,
transesophageal, transthoracic, and epicardial), transvenous and transcutaneous cardiac pacing
are the most commonly used. The main factor that dictates the use of one approach instead of
another is the urgency of the need for pacing.

In an emergency where a patient is experiencing cardiac symptoms or asystole,

transcutaneous pacing is the method of choice. Nevertheless, transvenous pacing has several
advantages over the transcutaneous method: enhanced patient comfort, greater reliability, and the
ability to pace the atrium. However, because transvenous pacing requires central venous access,
it cannot be initiated as fast as transcutaneous pacing can, and it is associated with several
complications that result from obtaining venous access.
A common scenario is one in which transcutaneous pacing is employed first in an emergency,
followed by transvenous placement of a lead that will enable a longer period of pacing and
evaluation in patients who may require permanent pacing later during their hospitalization.

TRANSVENOUS PACING

Transvenous cardiac pacing can be used as a bridge to permanent pacing when permanent
pacing is not available, when the pacing need is only temporary, or when further evaluation is
required. Therefore, all indications for permanent cardiac pacing are indications for transvenous
pacing as well. Temporary pacing is appropriate when a permanent pacemaker must be replaced,
repaired, or changed or when permanent pacing fails.
 INDICATIONS
Injury to the SA node or other parts of the conduction system after cardiac Chest and
cardiac
trauma associated with either temporary SA node or AV node dysfunction
Metabolic and electrolyte derangements (eg, hyperkalemia)
Drug-induced bradyarrhythmia (eg, digitalis toxicity); if treatment with the drug must be
continued and there is no alternative, permanent pacing should be considered
Other diseases (eg, Lyme disease, bacterial endocarditis) that may be associated with
temporary damage to the SA node or the AV node

PROCEDURE
In nonemergency situations, the first step is to explain the procedure to the patient and
obtain his or her baseline rate, rhythm, and vital signs. All equipment needed for the procedure
should be ready. Insertion of the pacing lead is then carried out as follows.
Venous access
The first step in transvenous pacing is obtaining venous access. Before venous access is
obtained, the subcutaneous tissue and area around the course of the needle should be
anesthetized with lidocaine 1% or 2%, with or without epinephrine.
The internal jugular vein and the subclavian vein are the most common sites of venous
access for temporary transvenous pacing. Femoral approach also using but , the increased chance
of thrombosis and infection, and the greater risk of complications associated with limb
movement.
Access via the internal jugular vein gives the pacing lead a straight route to the right atrium
(RA), reserves the subclavian vein for possible future permanent pacemaker implantation, and is
associated with fewer incidences of pneumothorax and hemothorax. Other obtaining venous
access, please see the following:
Central Venous Access, Internal Jugular Vein, Anterior Approach, Tunneled
Central Venous Access, Internal Jugular Vein, Posterior Approach
Central Venous Access, Subclavian Vein, Subclavian Approach
Central Venous Access, Subclavian Vein, Supraclavicular Approach
Femoral Central Venous Access

Placement of pacing lead

When fluoroscopy is available, a semirigid pacing lead may be used. The lead is advanced
until it reaches the RA. The desirable location for pacing the right ventricle (RV) is usually the
apex. To reach the RV, the catheter is passed through the tricuspid valve; this may be
accomplished more easily if the clinician forms a loop in the atrium and rotates the catheter.
Once in the RV, the catheter is advanced gradually toward the apex and septum. Some
clinicians may prefer RV outflow tract positioning for more stability.
The most desirable atrial pacing location is the right atrial appendage. A preformed J-shaped
catheter can be advanced anteriorly and medially in the low RA to reach the right atrial
appendage. It is then withdrawn to the superior vena cava (SVC) while being rotated anteriorly
to permit advancement into the right atrial appendage.

When the lead is in place, it is connected to the external generator, and the appropriate mode
is selected. The capture and sensing thresholds are also tested. In an emergency, the highest
output should be tried first; it should then be gradually reduced until the capture is lost.
If the situation is not an emergency, the rate is set 10-20 beats/min above the intrinsic
heart rate, and the output is initially set very low and then gradually increased until capture
occurs. The output should be set to a value at least 2-3 times higher than the threshold to
ensure a safe margin for any change that occurs in the capture threshold, which is usually less
than 1 mA. A slightly higher capture threshold is acceptable for atrial leads because they are less
stable than ventricular leads.
To check the sensing threshold (if it is needed in the demand pacing mode), the pacing rate
should be set lower than the intrinsic heart rate. The value of the sensing threshold should then
be gradually increased until the pacemaker fails to sense the intrinsic activity and consequently
begins firing. The sensing threshold is usually more than 5 mV in the ventricle and is much
lower in the atrium. The AV interval in AV sequential pacing is usually between 100 and 200
msec, which is comparable to a normal PR interval.
Confirmation of pacing lead position
Once the lead has been placed, its location should be confirmed by means of ECG and chest
radiography. On the electrocardiogram, a paced QRS should exhibit left bundle-branch block
(LBBB) morphology because the lead is located in the right ventricle.
The axis of the paced QRS may provide additional useful information. The axis may be
determined by checking leads I and aVF. A positive deflection in lead I indicates a leftward axis,
and a negative deflection in that lead indicates a rightward axis. A positive QRS deflection in
lead aVF indicates an inferior axis, and a negative QRS deflection in that lead indicates a
superior axis.
Accordingly, proper right ventricular lead placement in the apex should be associated with
LBBB morphology and a superior axis in the paced QRS complexes. If the pacing lead is in the
right ventricular outflow tract, the paced QRS complexes show LBBB morphology and an
inferior axis (which might also be rightward). Thus, on a surface ECG, lead V1 shows mainly a
positive QRS deflection and lead aVF a positive QRS deflection; lead I may show a negative
QRS deflection. A pacing lead in the coronary sinus will show right bundle-branch block
(RBBB) morphology.
 Unless RV outflow tract and left ventricular (LV) pacing are planned, the before mentioned
ECG characteristics are evidence of malpositioning, even if the malpositioning is not detected on
chest radiography. On an anteroposterior chest radiograph, the tip of a catheter in the RV should
be pointed slightly inferiorly and should be near the lateral border of the heart. On a lateral view,
it should point anteriorly a few centimeters behind the sternum. A J-shaped atrial pacing lead
should point cranially to the left and slightly anteriorly.

Complications
Transvenous cardiac pacing may be associated with a number of different complications, as
follows.
Sequelae of venous access
Depending on the site of venous access, a variety of adverse consequences may occur.
Pneumothorax and hemothorax develop more frequently when subclavian access is
performed. Infection and thrombus formation most often occur after femoral vein access but may
also develop when other access sites are used.
Loss of capture and undersensing
The causes of loss of capture during transvenous pacing can be divided into 2 groups: those
related to the patients condition and those related to the lead position and the pacing unit.
Hypoxia, acidosis, class I antiarrhythmic drugs, and electrolyte abnormalities are associated with
an increased threshold and may result in loss of capture.
Oversensing
Oversensing may be due to sensing P waves, T waves, or myopotentials. The location of the lead
should be checked because dislodgment and movement toward the tricuspid valve may result in
P-wave sensing by the pacemaker. In addition, the sensitivity of the generator can be reduced by
increasing the sensing threshold value to eliminate P-wave or T-wave oversensing.
Ventricular arrhythmia
Insertion of the catheter into the RV is associated with ventricular arrhythmia. Nonsustained
ventricular tachycardia (VT), a common finding during that procedure, is usually cured by
withdrawing the catheter. Sustained VT or ventricular fibrillation (VF) is a more serious
arrhythmic complication
Myocardial perforation
EPICARDIAL PACING

This type of pacing is initiated after cardiac surgery. Postoperatively, electrodes are lightly
sutured to the epicardium before the thorax is closed. These pacing wires are pulled through the
skin and secured to the external chest wall, ready for attachment to a temporary pacing generator
as needed.

Indications for temporary epicardial pacing

The main indication for insertion of epicardial pacing wires is perioperative arrhythmias
that may result in significant haemodynamic compromise. The most important arrhythmias
necessitating pacing include

bradycardia,
nodal or junctional arrhythmias
atrioventricular block.

Insertion

A patient may have a single set or a double set of electrodes, but each set of electrodes
includes 2 wires that protrude from a stab incision in the chest wall. When dual-wire sets are
used, one set or pair paces the ventricles and the other is attached to the atria.

In each pair of wires, one lead is positive and the other (commonly the shorter of the 2 wires)
is negative; however, practice varies between institutions. Ventricular pacing wires exit through
the left side of the sternum; atrial pairs are placed on the right side. Having identifying labels on
the wires is helpful. If no labels are present, ascertaining which wire is which (and marking the
wires accordingly) can save precious time later in emergency situations.The wires are usually
sutured using 5/0 polypropylene sutures. The wires are passed percutaneously to the right of the
midline and are secured.

Insertion of ventricular pacing wires

Ventricular pacing wires are placed on the anterior or diaphragmatic surface of the right
ventricle. Wires should be inserted into the bare muscular portion of the ventricle to ensure
adequate myocardial contact

Left ventricular electrodes may be placed in the apex just to the left of the distal left
anterior descending artery or along the obtuse margin. The wires are then passed
percutaneously to the left of the midline and are secured.
+++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
+++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
+++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
+++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
++
+++++++++++++++++++++++++++++++++
+++++++++++++++++++++++++++++++++++++++++

Removal of pacing wires

Pacing wires are usually removed on the fourth postoperative day. If longer term pacing is
required, consideration should be given to permanent pacemaker insertion. Prior to removal, a
coagulation screen should be checked. Wires are removed with gentle transcutaneous retraction

Complications

Infrequent but serious complications have been described in association with temporary
epicardial pacing wires use. R

Bleeding from the site of insertion can occur necessitating insertion of additional sutures.
 Dislodgement and fracture of pacing wires can also occur and infection may complicate
prolonged use. A
Complications associated with wire removal Patients are at risk of ventricular
arrhythmias during epicardial pacing wire removal necessitating electrocardiographic
monitoring

TRANSCUTANEOUS PACING

Transcutaneous pacing (also called external pacing) is a temporary means of pacing a

patient's heart during a medical emergency. It is accomplished by delivering pulses of electric
current through the patient's chest, which stimulates the heart to contract

Indications

Transcutaneous cardiac pacing (the fastest method of cardiac pacing) can be used until
permanent pacing becomes available. Therefore, all indications for permanent cardiac pacing are
considered indications for transcutaneous pacing as well

Although transcutaneous cardiac pacing is indicated primarily for the treatment of bradycardia
and various types of heart block, intermittent overdrive pacing can also be used as an
antitachycardic treatment for various atrial and ventricular tachycardias (eg, postoperative atrial
flutter and monomorphic ventricular tachycardia). Pacing also may be used to prevent
bradycardia-dependent tachycardias (eg, torsades de pointes)

Transcutaneous pacing also becomes the pacing method of choice in patients who received
thrombolytic therapy for acute myocardial infarction when the risk of bleeding from surgical
incisions is high.

PROCEDURE

Patient Preparation
Anesthesia
Transcutaneous cardiac pacing may be associated with discomfort such as a burning
sensation of the skin, skeletal muscle contractions, or both. Because of this, patients who are
conscious and hemodynamically stable should be sedated with a drug, such as midazolam,
Positioning
 Before applying the pacing electrodes, wipe the patients skin with alcohol, and allow the
area to dry. Without abrading the skin, carefully shave excessive body hair, which can elevate
the pacing threshold and increase burning and discomfort
The anterior electrode should have negative polarity and should be placed either over the
cardiac apex or at the position of lead V3. If the positive electrode is placed anteriorly, the
pacing threshold may increase significantly; this, in turn, increases the patients discomfort and
may result in failure to capture

The posterior electrode, which should be of positive polarity, should be placed inferior to
the scapula or between the right or left scapula and the spine; it should not be placed over the
scapula or the spine. Alternatively, the positive electrode can be placed anteriorly on the right
upper part of the chest (see the image below). The latter configuration does not affect the pacing
threshold

Turn the pacemaker on, and choose the pacing mode. Most pacing units are capable of pacing
on either a demand mode or a fixed mode. The demand mode is usually preferable and should be
used initially. If capture In a healthy individual, the pacing threshold is usually less than 80
mA.cannot be obtained on that mode, then the fixed mode should be tried. In a healthy
individual, the pacing threshold is usually less than 80 mA.

Capture the heart rate. If the patient is in cardiac arrest with bradycardia or an asystolic
rhythm, the pacing should be initiated at the maximum current output to ensure that capture is
achieved as soon as possible, after which time the current can be gradually reduced to 5-10 mA
above the threshold.

NURSING MANAGEMENT OF THE PATIENT WITH A PACEMAKER

PREOPERATIVE CARE

Provide routine preoperative care

. Assess knowledge and understanding of the procedure, clarifying and expanding on existing

knowledge as needed. Clarifying knowledge, providing information, and conveying

emotional support reduces anxiety and fear and allows the client to develop a realistic

outlook regarding pacer therapy.

Place ECG monitor electrodes away from potential incision sites. This helps preserve skin
 integrity.

Teach range-of-motion (ROM) exercises for the affected side. ROM exercises of the affected

arm and shoulder prevent stiffness and impaired function following pacemaker insertion.

Prepare the area of pacemaker implantation shave the area,and wipe with antimicrobial
solution
Obtain an informed consent from the patient and relatives
Ask for any drug allergy / pencillin allergy

POSTOPERATIVE CARE

Provide postoperative monitoring, analgesia,

Obtain a chest X-ray as ordered. A postoperative chest X-ray is used to identify lead location

and detect possible complications, such as pneumothorax or pleural effusion.

Position for comfort. -Minimize movement of the affected arm and shoulder during the initial
postoperative period. Restricting movement minimizes discomfort on the operative side and
allows the leads to become anchored, reducing the risk of dislodging.

Assist with gentle ROM exercises at least three times daily, beginning 24 hours after
pacemaker implantation. ROM exercises help restore normal shoulder movement and prevent
contractures on the affected side.

Monitor pacemaker function with cardiac monitoring or intermittent ECGs. Report

pacemaker problems to the physician:

Failure to pace. This may indicate battery depletion, damage or dislodgement of pacer

wires, or inappropriate sensing.

Failure to capture (the pacemaker stimulus is not followed by ventricular

depolarization). The electrical output of the pacemaker may not be adequate, or the lead

may be dislodged.

Improper sensing (the pacemaker is firing or not firing, regardless of the intrinsic rate).

This increases the risk for decreased cardiac output and dysrhythmias.

Runaway pacemaker (a pacemaker firing at a rapid rate). This may by due to generator
 malfunction or problems with sensing.

Hiccups. A lead positioned near the diaphragm can stimulate it, causing hiccups. Hiccups

may occur in extremely thin clients or may indicate a medical emergency with

perforation of the right ventricle by the pacing electrode tip.

Assess for dysrhythmias and treat as indicated. Until the catheter is seated or adheres to the
myocardium, its movement may cause myocardial irritability and dysrhythmias. Fibrotic tissue
develops within 2 to 3 days.

Document the date of pacemaker insertion, the model and type, and settings. This
information is important for future reference.

Immediately report signs of potential complications, including myocardial perforation,

cardiac tamponade, pneumothorax or hemothorax, emboli, skin breakdown, bleeding, infection,
endocarditis, or poor wound healing , Early identification of complications allows for aggressive
intervention.

Provide a pacemaker identification card including the manufacturers name, model number,
mode of operation, rate parameters, and expected battery life. This card provides a reference for
the client and future health care providers.

Assessment
After a temporary or a permanent pacemaker is inserted, the patients
heart rate and rhythm are monitored by ECG. The pacemakers
settings are noted and compared with the ECG recordings
to assess pacemaker function. Pacemaker malfunction is detected
by examining the pacemaker spike and its relationship to the
surrounding ECG complexes (Fig. 27-28). In addition, cardiac
output and hemodynamic stability are assessed to identify the patients
response to pacing and the adequacy of pacing. The appearance

appearance
or increasing frequency of dysrhythmia is observed and
reported to the physician.
The incision site where the pulse generator was implanted (or
the entry site for the pacing electrode, if the pacemaker is a temporary
transvenous pacemaker) is observed for bleeding, hematoma
formation, or infection, which may be evidenced by swelling, unusual
tenderness, unusual drainage, and increased heat. The patient
may complain of continuous throbbing or pain. These symptoms
are reported to the physician.
The patient with a temporary pacemaker is also assessed for
electrical interference and the development of microshock. The
nurse observes for potential sources of electrical hazards. All electrical
equipment used in the vicinity of the patient should be
grounded. Improperly grounded equipment can generate leakage
of current capable of producing ventricular fibrillation. Exposed
wires must be carefully covered with nonconductive material to
prevent accidental ventricular fibrillation from stray currents.
The nurse, working with a biomedical engineer or electrician,
should make certain that the patient is in an electrically safe
environment.
Patients, especially those receiving a permanent pacemaker,
should be assessed for anxiety. In addition, for those receiving
permanent pacemakers, the level of knowledge and learning needs
of the patient and the family and the history of adherence to the
therapeutic regimen should be identified.

Diagnosis
NURSING DIAGNOSES
Based on assessment data, major nursing diagnoses of the patient
may include the following:
Risk for infection related to pacemaker lead or generator insertion

Nursing Interventions
PREVENTING INFECTION
The nurse changes the dressing regularly and inspects the insertion
site for redness, swelling, soreness, or any unusual drainage. An increase
in temperature should be reported to the physician. Changes
in wound appearance are also reported to the physician.

Promote safety and avoid infection.

Wear loose-fitting clothing around the area of the pacemaker.
State the reason for the slight bulge over the pacemaker implant.
Notify physician if the pacemaker area becomes red or painful.
Avoid trauma to the area of the pacemaker generator.
Study the manufacturers instructions and become familiar with the pacemaker.
Recognize that physical activity does not usually have to be curtailed, with the exception of
contact sports.
Carry medical identification indicating physicians name, type and model number of
pacemaker,
manufacturers name, pacemaker rate, and hospital where pacemaker was inserted

Risk for ineffective coping

PROMOTING EFFECTIVE COPING
The patient treated with a pacemaker experiences not only lifestyle
and physical changes but also emotional changes. At different times
during the healing process, the patient may feel angry, depressed,
fearful, anxious, or a combination of these emotions. Although
each patient uses individual coping strategies (eg, humor, prayer,
communication with a significant other) to manage emotional distress,
some strategies may work better than others. Signs that may
indicate ineffective coping include social isolation, increased or
prolonged irritability or depression, and difficulty in relationships.
To promote effective coping strategies, the nurse must recognize
the patients emotional state and assist the patient to explore
his or her feelings. The nurse may help the patient to identify perceived
changes (eg, loss of ability to participate in contact sports),
the emotional response to the change (eg, anger), and how the patient
responded to that emotion (eg, quickly became angry when
talking with spouse). The nurse reassures the patient that the responses
are normal, then assists the patient to identify realistic
goals (eg, develop interest in another activity) and to develop a
plan to attain those goals. The nurse may also teach the patient
easy-to-use stress reduction techniques (eg, deep-breathing exercises)
to facilitate coping. Education (Chart 27-3) may assist a patient
to cope with changes that occur with pacemaker treatment

Deficient knowledge regarding self-care program

Teaching Patients Self-Care

After pacemaker insertion, the patients hospital stay may be less
than 1 day, and follow-up in an outpatient clinic or office is common.
The patients anxiety and feelings of vulnerability may interfere
with the ability to learn information provided. Nurses
often need to include home caregivers in the teaching and provide
printed materials for use by the patient and caregiver. Priorities
for learning are established with the patient and caregiver.
Teaching may include the importance of periodic pacemaker
monitoring, promoting safety, avoiding infection, and sources of
electromagnetic interference

Electromagnetic interference: Describe the importance of the following:

Avoid large magnetic fields such as those surrounding magnetic resonance imaging, large
motors, arc welding,
electrical substations. Magnetic fields can deactivate the pacemaker.
Some electrical and small motor devices, as well as cellular phones, may interfere with
pacemaker function if
placed very close to the generator. Avoid leaning directly over devices, or ensure that contact is
brief; place
cellular phone on opposite side of generator.
Household items, such as microwave ovens, should not cause any concern.
When going through security gates (eg, at airports, government buildings) show identification
card and request
hand search.
Hospitalization may be necessary periodically to change battery or replace pacemaker unit.

HOME CARE Provide appropriate teaching for the client and family about: Placement of the
pacemaker generator and leads in relation to the heart. How the pacemaker works and the rate
at which it is set. Battery replacement. Most pacemaker batteries last 6 to 12 years.
Replacement requires a outpatient surgery to open the subcutaneous pocket and replace the
battery. How to take and record the pulse rate. Instruct to assess pulse daily before arising and
notify the physician if 5 or more BPM slower than the preset pacemaker rate. Incision care and
signs of infection. Bruising may be present following surgery. Signs of pacemaker malfunction
to report, including dizziness, fainting, fatigue, weakness, chest pain, or palpitations. Activity
restrictions as ordered.This usually is limited to contact sports (which may damage the generator)
and avoiding heavy lifting for 2 months after surgery. Resume sexual activity as recommended
by the physician. Avoid positions that cause pressure on the site. Avoid tight-fitting clothing
over the pacemaker site to reduce irritation and avoid skin breakdown. Carry the pacemaker
identification card at all times, and wear a MedicAlert bracelet or tag. Notify all care providers
of the pacemaker. Do not hold or use certain electrical devices over the pacemaker site,
including household appliances or tools, garage door openers, antitheft devices, or burglar
alarms. Pacemakers will set off airport security detectors; notify security officials of its presence.
Maintain follow-up care with the physician as recommended.

COLLABORATIVE PROBLEMS/
POTENTIAL COMPLICATIONS
Based on the assessment findings, potential complications that
may develop include decreased cardiac output related to pacemaker
malfunction.