fundamentals of pacemaker

IMPLANTATION OF PACEMAKER TIPS AND
TRICKS ESSENTIAL TESTING OF
PACEMAKER DURING AND AFTER
IMPLANTATION.
EARLY DIAGNOSIS OF PACEMAKER
RELATED PROBLEMS
implantationofpacemakertipsandtricks,essential
testingofpacemaker,earlydiagnosisofpacemaker
complications

INTRODUCTION
 Currently available permanent pacemakers contain a
pulse generator and one or more pacing leads.
 Early in the era of pacemaker implantation, this
procedure was only performed by the cardiac surgeons
because of the initial mandate for epicardial lead
implantation.
 Further advancements in the pacing hardware and
percutaneous venous catheterization simplified the
implantation technique and made it feasible to implant
the transvenous leads.
 Simultaneously, further innovations in the pulse
generator and its circuitry extended the utility of the
percutaneous technique even in the very young
patients.
implantationofpacemakertipsand
tricks,essentialtestingofpacemaker,early
diagnosisofpacemakercomplications

INCIDENCE
 Nearly 250 000 new cardiac pacemakers are
implanted annually in the United States, and an
additional 750 000 are implanted worldwide

HISTORY OF PACING
 Pacing and electrophysiology started with Luigi
Galvani (1737-1798) who studied animal electricity.
 Alesandro Giuseppe Anastasio Volta(1745-1827)
developed prototype of battery.
 Michael Faraday(1791-1867)pioneered in
electrochemistry,named electrodes,electrolytes,
and ions.
 Willem Einthoven (1870-1927) – ECG
 Arne Larsson- First pacemakerimplantation by
Dr.Senning and engineer Elmqvist.
 First implantable pacemaker was implanted by
Lillehei(1960) .

 Barouh Berkovits in 1964 first demand pacemaker.
 Doris Escher -1958-first transvenous pacemaker implant
 Seymour Furman first transvenous lead
 Wilson Greatbatch in 1970 lithium iodine battery
 Dual chamber pacing was pioneered in 1970
 Rate responsive pacing 1980s
 February 2014 during American Heart Month, Vivek
Reddy, MD, of Mount Sinai Heart at The Mount Sinai
Hospital implanted the United States' first miniature-
sized, leadless cardiac pacemaker directly inside a
patient's heart without surgery.

PACEMAKER TECHNOLOGY

The LCP is an entirely self-contained intracardiac device that
includes the pacemaker electronics, lithium battery, and electrodes.
The LCP length is 42 mm with maximum diameter of 5.99 mm.
A distal nonretractable, single-tur (screw-in) steroid-eluting
(dexamethasone sodium phosphate) helix affixes the LCP to the
endocardium.
The maximum depth of penetration of the fixation mechanism in tissue
is 1.3 mm.

Chest x-ray after LCP implant.
X-ray (posterior-anterior view) of the LCP
position, which was performed the day
after implantation.

LIMITATIONS
 The LCP is only a VVIR pacemaker and is not
appropriate for patients requiring dual-chamber sensing
and pacing
 There is a possibility of device dislodgment and
migration into the pulmonary vasculature
 LCP has a wider diameter than conventional pacing
leads, which raises the possibility of mechanically
induced proarrhythmia.
 The LCP system requires an 18F venous introducer
sheath, there is a possibility of vascular complications
 Safety profile within the context of cardiac pacemaker
implantation still requires further study

 Future studies will need to address the
safety/efficacy of alternate-site RV pacing (ie, base,
septum, and outflow tract), especially with regard to
minimizing the potential deleterious effects of
chronic RV apical pacing.

 There are other leadless cardiac pacing systems in
development,
 they require 2 components – a subcutaneous
energy transmitter (pulse generator) and a receiver
electrode in the cardiac chamber.
 These systems use energy delivery sources
ultrasound waves and alternating magnetic fields.
 Safety and efficiency these are still under
investigation, and
 the potential for interference from external sources
needs further investigation.

LEAD TECHNOLOGY

 Passive fixation leads distal end contains
extensions liketines,fins,helices and stabilizers
 Active fixation leads has distal screw,hook, or helix,
most popular is the extendible –retractable helix.
 Leads intended to pace the left ventricle have a
characteristic curve at the distal end and no
conventional right –heart type fixation mechanism.

Active fixation lead Passive fixation lead
Lead diameter Smaller Larger
Introducer size Smaller Larger
Lead – tissue interface Trauma Atraumatic
Fibrotic ingrowth Slower Faster
Repositioning at
implant
Easy Easy
RV application Less common Very common
Atrial application Very common Very rarely
Proximal manipulation
to secure lead
Yes No
Chronic thresholds Slightly higher Slightly lower

STEROID ELUTION
 Clinical benefits of steroid eluting leads have been
established,but exact mechanism not clear.
 When steroid eluting lead is used, the fibrotic
capsule surrounding the lead-tissue interface tends
to be smaller and thinner, but not to the extent that
it would need to be to reduce the threshold by itself.

ELECTRODE CONFIGURATION
 Electrodes are typicallly made from platinum-
irridium, Eigiloy, platinum coated with titanium,
platinum and iridium oxide.
 These materials are biologically inert, resist
corrosion, and have excellent conduction
properties.
 Unipolar; with one electrode at each end, which as
the cathode and takes the metal outer casing of the
device as the anode.
 Bipolar ; with two electrodes at its distal end to form
anode and cathode.

Bipolar lead Unipolar lead
Pacing artifact Small Large
Pectoral stimulation Almost never Possible
Myopotential
interference
Almost never Possible
Size Larger diameter Smaller diameter
Flexibility Bulkier, stiffer Thinner, more flexible
Reliability record Excellent Near perfect

 Fig.7.9 and 7.10

INSULATION
 Tab. 7.3

PATIENT PREPARATION
informed consent
Routine pre-implant lab tests
 patients requiring a pacemaker may be on oral
anticoagulant
 standard practice was to discontinue warfarin 48
hours before the procedure, bridge with intravenous
heparin, and then reinitiate warfarin the day of the
procedure or even the night before.
 This practice has been associated with higher risk
of hematoma formation compared with that
encountered in unanticoagulated patients (up to
20%)

 Recently, there has been an increasing interest in
performing the pacemaker implantation without
reversal of the anticoagulant.
 This practice was associated with lower risk of
pocket bleeding and shorter hospital stay
Pacing Clin Electrophysiol. 2004 Mar;27(3):358-60.Giudici MC1, Paul DL, Bontu
P, Barold SS.

 Antibiotic prophylaxis is a controversial issue, but
most implanters prefer to give oral or intravenous
(IV) antibiotics to decrease the incidence of local or
systemic infections based on limited data available.
 Although there is a distinct lack of either national or
international guidance in this area, meta-analysis of
the randomized trials suggests a benefit from pre-
procedure intravenous antibiotics

INTRAOPERATIVE MEASUREMENTS
 Intrinsic signal from the heart should be measured first.
 If pacing threshold is tested before the intrinsic signal is
measured , the patient can become pacemaker
dependent, making it impossible to measure sensing.
 Sensing is tested by evaluating the signals that would
make an intracardiac electrogram using a device called
a pacing system analyzer(PSA).
 The intracardiac signal for the ventricle must be atleast
5mV and ideally between 6 and10mV in order to be
useful
 For the atrium, any signal >2mV Is considered desirable.
 If signals are inadequate, adjust the leads by mapping
correct position.

 Pacing thresholds in both chambers should be < 1V
 Thresholds depends largely on leads placement.
 Long-term performance depends on obtaining good
sensing and capture threshold values.

ELECTRICAL TESTING OF PACEMAKER
 Pacemaker components
 Battery
 Pacing impedance
 Pulse generator
1. Output circuit
2. Sensing circuit
3. Timing circuit
4. Rate adaptive sensor
5. Modes and mode switching

 Battery :
 Lithium iodine battery
 High energy density ,
 Long shelf life ,
 Predictable loss of
battery
 BOL (vol) – 2.8v
 BOL (res) - <1komhs
2.0 – 2.2V with 20,000-30,000Ω
impedence –battery is nearing
depletion
Electrical Testing Of Pacemaker

Pacing impedance :
 Pacing impedance refers to the opposition to current
flow. Two sources contribute to pacing impedance:
1. Pacing lead
2. Electrode - tissue
 Tissue of contact
 Electrode tip size
 Polarization
 Normal lead impedance vary from 250-1200ohms.
 Single impedance value may be of little use with out
previous values for comparison.

1. Pulse generator output circuit
 Capture threshold , Pacing threshold , stimulation threshold
 Minimum amount of energy required to constantly cause
depolarization
 Volts and pulse duration

2.0 v 1.5 v 1 v

 Rheobase ; point at
which the plateau
begins and roughly
establishes the
minimum voltage
requirements to
capture the heart.
 Chronaxie; the point at
which twice the
rheobase voltage value
meets the curve

Site At
implantation
Acute Chronic
Atrium <1.5mv 3-5 times
threshold
voltage
Twice the
Threshold
voltage
Ventricle <1mv With PW
0.5ms
With PW of
0.5ms

 High Pacemaker Output can cause
 Reduce longevity
 Diaphragmatic stimulation
 Muscle Sti. in Unipolar pacemakers
 Patient may “feel” heart beat
 Algorithm for checking pacemaker output
threshold every beat and maintaining threshold
just above it - Auto capture.

2. Pulse generator sensing circuit :
 Ability of the device to detect intrinsic beat of the heart
 Measured - peak to peak magnitude (mv) & slew rate(mv/ms)

2. Pulse generator sensing circuit :
 Reduce Lower Rate below intrinsic rate to inhibit pacing
and ensure intrinsic activity
 Increase sensitivity setting while observing EGM. The
sensitivity value at which sensing is lost on the EGM is
the sensing threshold.
 Sensitivity threshold safety is twice the attained valve.
Sensitivity Slew rate
Atrium 1-2mv(0.5mv) > 0.5 v/s
ventricle 2-3mv > 0.75 v/s

AUTOMATIC OPTIMIZATION OF OTHER PACEMAKER
FUNCTION BASED ON SENSING
 These include algorithms to prevent inhibition during
oversensing and loss of pacemaker capture.
 Ventricular safety pacing prevents inappropriate pacemaker
inhibition caused by ventricular oversensing of atrial pacing
stimuli.
 Safety pacing may be identified on ECGs by noting a shorter
than programmed AV delay, usually 80 to 130 milliseconds.
 Noise reversion to fixed-rate asynchronous pacing prevents
pacemaker inhibition during continuous ventricular
oversensing, including that occurring during electromagnetic
interference from sources such as electrocautery.
 Automatic assessment of the pacing capture threshold is
performed by closed-loop feedback algorithms that
periodically test capture and adjust the output based on test
results.

3. Pulse generator timing circuit :
a. Lower rate limit (LRL)
b. Hysteresis rate
c. Refractory and blanking periods
d. Ventricular safety pacing interval .
e. Upper rate response .

Pulse generator timing circuit
 Lower rate interval - lowest rate that the pacemaker will
pace .
 A paced or non-refractory sensed event restarts the rate
timer at the programmed rate.

Condition LRL (beats/mt)
Infrequent pauses 40-50
Chronic persistent bradycardia 60-70
Relative bradycardia detrimental
(long QT)
70-80
Detrimental fast heart rates
(angina)
50-60
VVI 60-70

 Hysteresis :
 Hysteresis allows the rate to drop below the programmed
pacing LRL.
 Advantages of hysteresis :
1. Encourages native rhythm – maintain AV sync in VVI , prolong
battery life
2. Prevent retrograde conduction – avoids pacemaker syndrome

 AV delay (AVI) – pacemaker equivalent of PR interval.
 Sensed vs paced AVI – paced AVI is programmed at 125-
200ms , sensed AV interval is programmed at 20-50ms shorter
than paced.
 Dynamic AV delay allow pacemaker to respond to exercise
sAVI – 150ms
pAVI – 200ms

 AV delay (AVI)
 Longer AVI :
 Good AV conduction – maintains AV synchrony , long battery life
 Achieved by following methods :Programming longer AVI , managed
ventricular pacing , AV delay hysteresis .
 Shorter AVI:
 HOCM – RV apical pacing decreases HOCM gradient
 CRT – usually 80-120ms , for 100%ventricular pacing and
optimize CO

 Refractory and
blanking periods :
 Refractory period
– sensing present
but no action
 Blanking period -
sensing absent
and hence no
action

 Blanking periods :3. Pulse generator timing circuit :
Blanking period Time Importance
Atrial blanking
period
50-100ms Non programmable ,
Avoid atrial sensing of its own
paced beat
Post ventricular
atrial blanking
period
220ms Avoid sensing of ventricular beat
Long PVAB decreases detection
of AF,AFL
Ventricular
blanking period
50-100ms Non programmable,
Avoid ventricular sensing of its
paced beat
Post atrial
ventricular
blanking period
28ms if the PAvB period is too long, R
on T - ventricular
tachyarrhythmia.

 Refractory period:
Refractory period Importance
Ventricular refractory period
(VRP)
Prevent sensing of T wave .
Atrial refractory period (ARP) AVI (120-200ms) .
Post ventricular atrial refractory
period
Avoid sensing retrograde P
waves (PMT) , far field R
waves .

Ventricular safety pacing/ventricular
triggered period/cross talk sensing
window :
Atrial pacing in DDD
Trigger ventricular sensing
PAVB - pAVI
False inhibition of
ventricular pacing circuit
Asystole

 Rate responsive pacing refer to ability of pacemaker to increase its
lower rate in response to physiological stimulus
 Sinus node dysfunction .
 HRR should start with in 10s of exercise , peak at 90 – 120s and
should return to baseline with in 60 – 120s after exercise.
 Fastest rate at which pacemaker will pace upper rate response.
 If intrinsic atrial rate exceeds URR then wenckebach or 2:1 AVB
 Choosing URR : young patients (150b/mt) , old angina (<110b/mt).
 Various sensors (activity , minute ventilation , QT)
4. Pulse generator rate responsive pacing:

4. Pulse generator rate responsive pacing:
Wenckebach
2:1 AVB

4. Pulse generator modes:

 VVI mode it is the basic single-chamber ventricular
pacing mode; it allows pacing to occur when the
ventricular rate slows below the programmed lower rate
limit..
 There is no atrial sensing, so AV synchrony is not
preserved. This mode is indicated for patients with
permanent AF.
 AAI mode is the corresponding single-chamber atrial
pacing mode.
 It is appropriate for patients with sinus node
dysfunction and normal AV conduction.
 Because it does not provide ventricular pacing, it should
not be used in patients at risk for AV block

 DDD pacing mode is most commonly used in the patients
whose rhythm is not permanent AF .
 In this mode the atrial rate cannot go lower than the
programmed lower rate.
 In the setting of AV block, all ventricular events are paced. A
special characteristic of the DDD pacing mode is the ability to
“track” intrinsic atrial activity to maintain AV synchrony.
 The DDD mode has an upper rate limit, the maximum rate that
intrinsic atrial activity will be tracked.
 The maximum rate is selected to exceed the maximum sinus
rate that the patient is capable of achieving.
 The upper rate limit is predominantly of importance to prevent
tracking of rapid atrial activity in spontaneous atrial
arrhythmias such as AF.

 Automatic Mode Switching
 Automatic mode switching in the DDD pacing mode
initiates a temporary change in mode to a nontracking
one (usually DDI or DDIR) during paroxysmal atrial
tachyarrhythmias.
 This prevents the adverse consequences of rapid
ventricular pacing as a result of tracking nonphysiologic
high atrial rates.
 Most mode-switching algorithms use the atrial rate as an
indicator for the onset of an atrial tachyarrhythmia.
 When the atrial rhythm again meets the defined criteria
for a physiologic rhythm, the mode switches back to an
atrial tracking mode

5. Pulse generator modes switching:
DDD / VDD
Atrial tachyarrythmias
Sensed atrial events
Trigger fast ventricular rates
Palpitations. Dyspnoea. And Fatigue.
DDIR /
VVIR

Pacemaker follow up guidelines:
NASPE guidelines
Single or dual pacing
1st visit 6 – 8 week post implant , if symptomatic prior
to this
5th month
From 6th month q 3month
Battery wear present q 1month

PACEMAKER COMPLICATIONS

Pocket
complications
Pocket hematoma
Infection
Erosion
Wound pain
Allergic reactions
Pacemaker
complications
Lead dislodgement
Pneumothorax /air
embolism
Cardiac perforation
Extracardiac stimulation
Venous thrombosis
Coronary sinus dissection
Twidller syndrome
Pacemaker malfunction

Pocket hematoma :
 The risk of haematoma is increased in patients taking
antithrombotic or anticoagulant drugs (Goldstein et al., 1998).
 Most small hematomas can be managed conservatively with
cold compress and withdrawal of antiplatelet or antithrombotic
agents.
 Occasionally, large hematomas that compromise the suture
line or skin integrity may have to be surgically evacuated.
 Needle aspiration increases risk of infection and should not
be done.
Pacemaker complications

Pocket hematoma :
 In patients requiring oral anticoagulants (warfarin), to take INR
of about 2.0 at the time of implantation is safe (Belott &
Reynolds, 2000).
 Unfractionated heparin or low-molecular-weight heparin are
always discontinued prior to device implant and ideally avoided
for a minimum of 24 hours post implantation.
 Administration of anticoagulants can be resumed within 48-72
h after implantation if there is no evidence of substantial
hematoma formation.

Device-related infections :
 The reported incidence of pacemaker-related infection ranges
from 0.5% to 6% in early series
 The use of prophylactic antibiotics and pocket irrigation with
antibiotic solutions has decreased the rate of acute infections
following pacemaker implantations to <1 to 2 percent in most
series
 The mortality of persistent infection when infected leads are not
removed can be as high as 66%.
 DM, malignancy, operator inexperience, advanced age,
corticosteroid use, anticoagulation, recent device manipulation,
CRF, and bacteremia from a distant focus of infection.

Device related infection :
 Device infection is defined as either:
 (a) deep infection - infection involving the generator pocket
and/or the intravenous portion of the leads, with bacteremia,
requiring device extraction or
 (b) superficial infection - characterized by local
inflammation, involving the skin but not the generator pocket,
and treated with oral antibiotics.

2007;49;1851-1859 J. Am. Coll. Cardiol.

2007;49;1851-1859 J. Am. Coll. C

Wound pain :
 Infection , Pacemaker implanted too superficially ,
Pacemaker implanted too laterally , Pacemaker allergy .
Skin erosion :
 Incidence has been estimated around 0.8% .Old age ,
infection.
 Surgical revision of pocket and reimplantation .
Allergic reactions :
 Always rule out infection before coming to diagnosis of allergy

Lead dislodgement:
 Relatively common – 5-10%
of patients(ICD database
2001)
 Atrial more common than
ventricular(2-3% vs. 1%)
 Micro dislodgement , macro
dislodgement
 Increased pacing threshold ,
failure to pace and sense
 Active fixation (decreases risk)

Pneumothorax , :
 Uncommon complication – 1.6-
2.6%
 During or 48 hrs after procedure
 Inadvent puncture and laceration
of subclavian vein , artery or lung
 Related to operator experience
and underlying anatomy
 Avoided by
1. Venogram – flouroscpic puncture
2. Axillary venous access (Martin
etal’96)

Cardiac Perforation :
 Uncommon but potentially serious complication - lower
than 1%.
 Acute (<5 days) ,
 subacute(5d-1month) ,
 chronic (>1month)
 Increasing stimulation threshold , RBBB pattern for RV
pacing, intercostal muscle or diaphragmatic contraction,
friction rub, and pericarditis, pericardial effusion, or
cardiac tamponade.

CARDIAC
PERFORATION
 CXR ,
 ECHO ,
 CT
 Management;
 Lead withdrawal and
repositioning.
 Surgical back up

Extracardiac stimulation
 The diaphragm or pectoral or intercostal muscles
 Diaphragmatic stimulation - direct stimulation of the diaphragm
(left) or stimulation of the phrenic nerve (right).
 Early postimplantation period , dislodgment of the pacing lead.
 MC in patients with LV coronary vein branch lead placement
for CRT
 Output pacing importance (testing and treatment)
 Pectoral stimulation - incorrect orientation of the pacemaker or
a current leak from a lead insulation failure or exposed
connector.

Venous thrombosis :
 Venous thrombosis occurs in 30% to 50% of patients and only
1-3% of patients become symptomatic.
 Manifestations vary from usually asymptomatic, acute
symptomatic thrombosis, and even SVCS .
 Early or late after pacemaker implantation.
 Predictors of severe stenosis are multiple pacemaker leads,
previous pacing , double coils , hormone therapy .
 Asymptomatic (no treatment) , symptomatic (anticoagulants –
endovascular stents – surgical correction).

Twiddler syndrome:
Obese women with loose, fatty subcutaneous tissue
Small size of the implanted generator with a large pocket
Twisting of pulse generator in long axis
Lead dislodgement and lead fracture
Failure to capture

 The prevelance of this
syndrome is 0.07% (Gungor et
al., 2009)
 Rotated along the transverse
axis it is referred by us as the
reel syndrome.
 Pocket should be revised.
 Avoid by
 Limit the pocket size,
 Suture the device to the fascia
 The patients not to manipulate
their device pocket
Twiddler syndrome:

 Failure to capture
 Failure to output
 Sensing abnormalities(under and over
sensing)
 Specific mode complications
1. Pacemaker related tachycardia
2. Pacemaker syndrome

Failure to capture:
 Pacing artifact present but no evoked potential .
 Causes
1. Lead dislodgement or perforation
2. Lead maturation(inflammation/fibrosis)(exit block)
3. Battery depletion
4. Circuit failure(coil fracture , insulation defect)
5. Capture management algorithm failure
6. Inappropriate programming
7. Pseudo malfunction
8. Functional non capture
9. Metabolic , drugs , cardiomyopathies

Electrocardiographic tracing from a patient with a DDDR pacemaker. All ventricular
pacing artifacts but one failed to result in ventricular depolarization—
that is, failure to capture
Failure to capture:

Failure to capture:
Pacing threshold
Normal
Increased
Battery depletion
Functional non capture
Impedance
Normal
Dislodgement
Exit block
Decreased
Insulation
failure/break
Increased
Lead fracture
Loose screw

Failure to output:
 Absence of pacing stimuli and hence no capture .
 Causes
1. Pseudo malfunction - hysteresis , PMT termination ,
sleep rate
2. Over sensing - EMI ; T P R over sensing ;
Myopotential/diaphragmatic ; Cross talk ; Make break
signals
3. Open circuit - lead fracture , loose screw , air in the
pocket , incompatible lead .
4. Battery depletion
5. Recording artifact.

 Failure to output:
VVIR pacemaker This patient had a pacemaker programmed to
a unipolar sensing configuration. The sensing of myopotentials
led to symptomatic pauses, and reprogramming the pacemaker
to a bipolar sensing configuration prevented subsequent
myopotential over sensing.

Application of magnet
Failure to output:
Eliminates pauses
Pauses persistent
Impedance
Normal
Decreased
Insulation
failure/break
Increased
Lead fracture
Loose screw
Battery
depletion
Over sensing
Pseudo malfunction

Battery depletion :
 Elective replacement indicators (ERI)
1. Low voltage(2.1-2.4)
2. Low pacing rate on magnet application
3. Elevated battery impedance
4. Increased pulse width duration
5. Restricted programmability
6. Change to simpler pacing mode
 End of life (EOL)
1. Low voltage(≤2.1vol)

Pacemaker undersensing :
 Pacing artifact present but no sensing(sensed beat
doesn’t reset cycle)
 Causes are
1. Defect in signal production – scar /fibrosis , BBB , ectopic ,
cardioversion , defibrillation , metabolic.
2. Defect in signal transmission – lead fracture/dislodgement,
insulation failure , partial open circuit.
3. Defect in pacemaker – battery depletion , sensing circuit
abnormalities , committed DVI.

Pacemaker undersensing :
VVI pacemaker

Pacemaker over
sensing :
 Present as failure to pace
 Causes
1. EMI
2. T , P , R over sensing .
3. Cross talk
4. Myopotential (unipolar)
5. Make break signals
Cross talk :
High atrial output
High ventricular sensitivity
Low VBP
Ventricular sensing of
paced atrial impulse
Pts with Poor AV conduction –
Ventricular Asystole

 Electromagnetic interference :
Source Pacer
damage
Inhibition Rate
increase
Asynchronou
s noise
Uni/
bipola
r
Cardioversion/
Defibrillation
Y N N N U/B
Anti theft devices /
Weapon detector
N Y N N U
Phone
(cell/cordless)
N Y Y Y U/B
Ablation Y Y Y N U/B
Diathermy/
lithotripsy
Y Y Y Y U/B
FM radio
TV transmitter
N Y N Y U
MRI/PET Y Y(N) Y(N) Y(N) U/B

Pacemaker syndrome :
 Seen in 20% of PPI (5%
severe symptomatic)
 VVI/DDD/AAI
 Pulsations in neck , fatigue
, cough ,chest fullness ,
headache , chocking
sensation , PND, confusion
, syncope , pulmonary
edema.
 Rx : VVI – program
hysteresis , or change to
DDD ; DDD –atrial lead
reprogrammed or changed

 Pacemaker mediated tachycardia :
 Dual chamber
 VPC , intact retrograde
conduction , PVARP<VA .
 Px , Rx :
1. PVARP > VA
2. Long PVARP after VPC
3. Absent atrial sensing after
VPC

Thank you

fundamentals of pacemaker

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