Electrical testing of pacemaker

Electrical Testing Of Pacemaker
& Pacemaker Complications
Msn Pavan Kumar,DM,NIMS.

Pacemaker complications

 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

 Pacing impedance :
 Pacing impedance refers to the opposition to current flow. Three
sources contribute to pacing impedance:
1. Pacing lead conductor coil
2. Electrode-tissue interface
 Electrode resistance
 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

1. Pulse generator output circuit

2.0 v 1.5 v 1v

1. Pulse generator output circuit

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

1.Pulse generator output circuit
 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

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 .

3.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
 Physiological response to faster heart rates can be answered


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

3. Pulse generator timing circuit :  Blanking periods :

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

3. Pulse generator timing circuit :  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

4. Pulse generator rate responsive pacing:

 Rate responsive pacing refer to ability of pacemaker to increase its
lower rate in response to physiological stimulus
 Sinus node dysfunction , AF patients – fail to increase heart rates
 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:

Wenckebach

2:1 AVB

4. Pulse generator modes:

5. Pulse generator modes switching:

DDD / VDD
Atrial tachyarrythmias

Sensed atrial events

DDIR /
Trigger fast ventricular rates VVIR

Palpitations. Dyspnoea. And Fatigue.

5. Pulse generator modes switching:

Programming mode switching Mode switching occurs when
the sensed atrial rate exceeds a programmed atrial tachycardia
detection rate. By definition, this value must be faster than the URL
(maximum tracking rate). Atrial tachycardia detection is typically
programmed to 175-l88bpm or thereabouts.AMS base rate is higher
than LRI.

Pacemaker follow up guidelines: Transtelephonic monitoring guidelines
Medicare guidelines
Single chambered pacing Dual chambered pacing
1st month q 2 week 1st month q 2 weeks
2nd -48th month q 12 week 2nd – 30th month q 12weeks
49th – 72nd month q 8 week 31st – 48th month q 8 weeks
73rd month and later q 4 weeks 49th month and later q 4week
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


Pocket complications Lead dislodgement
Pocket hematoma Pneumothorax /air embolism
Infection Cardiac perforation
Erosion Extracardiac stimulation
Wound pain Venous thrombosis
Allergic reactions 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.


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.

Device related infection :

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

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)
3. One way mechanism sheath

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.
 CXR , ECHO , CT
 Lead withdrawal and repositioning ; surgical back up

Cardiac Perforation :

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

Twiddler syndrome:
 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


 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

Failure to capture:

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:

Pacing threshold

Normal Increased
Dislodgement
Normal Exit block
Battery depletion
Functional non capture
Impedance Insulation
Decreased failure/break

Lead fracture
Increased 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.

Failure to
output:
Application of magnet

Eliminates pauses Pauses persistent

Over sensing Normal Battery
depletion
Pseudo malfunction
Impedance Insulation
Decreased failure/break

Lead fracture
Increased Loose screw

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

 Electromagnetic interference :

Source Pacer Inhibition Rate Asynchronous Uni/
damage increase noise bipolar
Cardioversion/ Y N N N U/B
Defibrillation
Anit theft devices / N Y N N U
Weapon detector
Phone (cell/cordless) N Y Y Y U/B
Ablation Y Y Y N U/B
Diathermy/ Y Y Y Y U/B
lithotripsy
FM radio N Y N Y U
TV transmitter
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

Electrical testing of pacemaker

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