Pacemaker components include the battery, pacing impedance, pulse generator, and modes and mode switching. Pacing impedance refers to opposition to current flow and varies between 250-1200 ohms. The pulse generator includes output, sensing, and timing circuits. Capture threshold is the minimum energy for depolarization. Pacemaker follow up includes electrical testing and management of complications like pocket hematomas, infections, and device malfunctions such as failure to capture or output.

1. FOLLOW UP AND MANAGEMENT OF
PACEMAKER PROGRAMMING AND
TROUBLESHOOTING
SOUMYA KANTI DUTTA.

2.  Pacemaker components
 Battery(Lithium iodide or Vanadium silver)
 Pacing impedance
 Pulse generator
1. Output circuit
2. Sensing circuit
3. Timing circuit
4. Rate adaptive sensor
5. Modes and mode switching

3.  Pacing impedance :
 Pacing impedance refers to the opposition to
current flow.
 Sources that contribute to pacing impedance:
1. Pacing lead conductor coil
2. Electrode-tissue interface
 Normal lead impedance vary from 250-
1200ohms.
 Single impedance value may be of little use
with out previous values for comparison.

4. Pulse generator output circuit
 Capture threshold or Pacing threshold .
 Minimum amount of energy required to constantly
cause depolarization
 Voltage(mA) and pulse duration(mSec)
 V=IR

5. 2.0 v 1.5 v 1 v
1. Pulse generator output circuit

6. 1. Pulse generator output
circuit
 High Pacemaker Output can
cause
◦ Reduce longevity
◦ Diaphragmatic stimulation
◦ Muscle Sti. in Unipolar
pacemakers
◦ Patient may “feel” heart
beat
Electrical Testing Of Pacemaker

7. Electrical Testing Of Pacemaker
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)

8. 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 .
Electrical Testing Of Pacemaker

9. Pulse generator timing circuit :
 Lower rate interval - lowest rate that the pacemaker
will pace .
 Escape interval:sensed beat to next paced beat.
 A paced or non-refractory sensed event restarts the rate
timer at the programmed rate.

10. 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
Pulse generator timing circuit :

11. Pulse generator timing circuit :
 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

12.  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/adaptive AV delay :shorter AVI with increase in
heart rate,allow pacemaker to respond to exercise and
have better haemodynamics.
Pulse generator timing circuit :
sAVI – 150ms
pAVI – 200ms

13.  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
Pulse generator timing circuit :

14.  Refractory and
blanking
periods :
 Refractory
period –
sensing present
but no action
 Blanking period
- sensing
absent and
hence no action
Pulse generator timing circuit :

15. 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.

16. 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 .
Pulse generator timing circuit :

17. Pulse generator timing circuit :
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

18.  Rate responsive pacing refer to ability of pacemaker
to increase its lower rate in response to physiological
stimulus
 Upper rate limit:important to prevent tracking of
rapid atrial activity like in AF
 HRR should start with in 10s of exercise , peak at 90
– 120s and should return to baseline with in 60 –
120s after exercise.
 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)
 Rate smoothing: allows variation of R-R interval <6%
Pulse generator rate responsive pacing:

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

20. PACING MODES
 BEPG(British pacing and electrophysiology
group)
 NASPE(North American society of pacing
and electrophysiology)
 DD I/T R
 III-D(I+R) :dual tracking of atrial activity while
inhibited by ventricular activity
 5th position: antitachycardia function(pacing/shock)

21. 5. Pulse generator modes switching:
Electrical Testing Of Pacemaker
DDD / VDD
Atial tachyarrythmias
Sensed atrial events
Trigger fast ventricular rates
Palpitations. Dyspnoea. And Fatigue.
DDIR /
VVIR

22. 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.

23. Electrical Testing Of Pacemaker
Pacemaker follow up 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

25. 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

26. 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.

27. 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.

28. Device-related infections :
 The reported incidence of pacemaker-related
infection ranges from 0.5% to 6% in early series.
 The use of prophylactic antibiotics 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.

29. Device related infection :
2007;49;1851-1859 J. Am. Co

30. 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

31.  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:

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

33. 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. Inappropriate programming(low output /pulse
width)
6. Pseudo malfunction(pacing during refractory
period)
7. Functional non capture(oversensing).
8. Metabolic , drugs , cardiomyopathies

34. Medication effect on Capture
Drugs that increase
capture threshold
Drugs that decrease
capture threshold
Amiodarone
Flecainide
Propafenone
Sotalol
Procainamide
lidocaine
Atropine
Epinephrine
Isoproterenol
corticosteroids

35. 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:

36. 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

37. 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 .
3. Open circuit - lead fracture , loose screw ,
incompatible lead .
4. Battery depletion
5. Recording artifact.

38.  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.

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

40. Battery depletion :
 Elective replacement indicators (ERI)
1. Low voltage(2.1-2.4V)
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)

41. Pacemaker undersensing :
 Pulse artifact or intrinsic complex present but no
sensing(sensed beat doesn’t reset escape interval or
cycle).
 Causes are
1. Defect in signal production – scar /fibrosis
following MI , 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.

42. Pacemaker over sensing :
 Inappropriate inhibition as
failure to pace
 Causes
1. EMI
2. T , P , R over sensing .
3. Far field R wave
sensing(atrial).
4. Cross talk
5. Myopotential
(unipolar)
6. Make break signals
Cross talk :
High atrial output
High ventricular sensitivity
Low VBP
Ventricular sensing of paced
atrial impulse
Ventricular Asystole

43. Pacemaker Syndrome
“An assortment of symptoms
related to the adverse
hemodynamic impact from the
loss of AV synchrony.”

44. Pacemaker Syndrome
Symptoms include:
 Dizziness
 Presyncope
 Chest tightness
 Shortness of breath
 Neck pulsations(cannon A wave)
 Apprehension/malaise
 Fatigue

45. Pacemaker Syndrome May Be Caused By:
 Loss of capture, sensing
 A-V intervals of long duration
 Onset of 2:1 block
 Single chamber system(VVI)
 Absence of rate increase with exercise
 ECG:Retrogradely conducted inverted P over T
 CORRECTIVE ACTION:
◦ Reduce pacing rate.
◦ Hysteresis on to allow more sinus rhythm
◦ Shift to dual chamber pacing.

46. Pacemaker-Mediated Tachycardia
(PMT)
 A rapid paced rhythm that can occur
with atrial tracking pacemakers

47. PMT is the Result of:
 Also known as pacemaker re-entry
tachycardia or endless-loop tachycardia
(like other re-entry dysrhythmias,
pacemaker is now a part of the re-entry
circuit,Mostly anterograde limb of
reentrant tachycardia)
 Retrograde conduction
 PVARP
 Tracking fast atrial rates (physiologic or
non-physiologic)

48.  only in patients with dual chamber devices
 The ventricular impulse is retrogradely
conducted via the AV node to the atria, now the
atrial lead senses the atrial impulse and
generates a ventriculair pulse (completed loop)
 This pacemaker re-entry tachycardia will not
exceed the programmed upper rate, however
can be significant enough to cause symptoms
 magnet therapy.
 Pacemakers atrial sensing tresholds need to be
adjusted
 Mode switch can cause the pacemaker to
discontinue atrial tracking when the atrial upper
rate is exceeded

49. Rate Drop Response
 Delivers pacing at high rate when
episodic drop in rate occurs
 Pacing therapy indicated for patients
with neurocardiogenic syncope
Rate Drop Response

50. 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 ).

51. 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.

53. PERIOPERATIVE MANAGEMENT
 Require perioperative determination of pacemaker
dependency.
 An external defibrillator should be close by.
 Intraoperative management:
Application of magnet.
Perioperative reprogramming to
assynchronous mode.
Rate adaptive sensors should be disabled.
Oversensing of electrocautery is more common with
unipolar leads.
 When external cardioversion is required ,defibrillation pads
should be placed at least 8 inches from the pulse
generator.

54. THANK YOU