This document discusses emergency issues related to pacemakers and implantable cardioverter defibrillators (ICDs). It covers clinical cases, device components and functions, complications, and emergency department management strategies. Key points include descriptions of pacemaker modes and indications for pacemakers, cardiac resynchronization therapy, and ICDs. Common complications like infection, lead issues, and inappropriate shocks are reviewed. The document stresses the importance of obtaining a history, physical exam, ECG, and device interrogation in the ED. Magnet use and Sgarbossa criteria for diagnosing acute MI in paced patients are also summarized.

1. Emergency related Pacemaker and ICDs Issues
Anne-Marie de Vries, January 2015

2. Contents
1. Clinical case
2. Introduction pacemaker / Cardiac Resynchronisation Therapy
(CRT) / Implantable Cardiac Defibrillator (ICD)
3. Implant related complications
4. Pacing system malfunction
5. ED management
6. Magnet
7. Back to case
8. Demo-interrogation (by Medtronic)
9. Patient experience (ICD)

3. Clinical case

4. ECG
ECG

5. ECG

6. Introduction
• Components and lead position
• Pacemakers modes
• Pacemaker/CRT/ICD indications

7. Pacemaker components and lead position
• Basic components: pulse generator and lead(s)
• Pulse generator; hard and software, battery (5-10 years)
• Leads:conductor, electrode, fixation mechanism, terminal
connector pin, insulator

8. Lead position
• Atrial leads in the right atrial appendage
• Right atrial septum position to suppress AF
• Right ventricular leads are traditionally placed in the right
ventricular apex, however RVOT or inter-ventriculair position to
avoid dyssynchrony
• Left ventriculair lead via coronary sinus to free left lateral or
posterior left ventriculair wall
• Final position depends on venous cardiac anatomy, avoidance of
phrenic nerve stimulation, location of myocardial scar

9. Lead fixation

10. Pacemaker modes
5 Letter code:
I = Chambers paced
II = Chambers sensed
III = Response to sensing
IV = Programmability, rate modulation
V = Multi-site pacing
A= Atria T=Triggered
V=Ventricle I=Inhibited
D=Dual Chamber (A+V) R=rate modulation
O=none

11. Table 2 NASPE pacemaker code

12. Pacemaker modes
• ED physicians most likely deal with AAIR, VVIR, DDD
and DDDR
• Rate response modality detect physiological changes;
minute ventilation, QT interval, stroke volume

13. Indications
• Continuous amendments for pacemaker indications
several categories)
• Most recent guideline ACC/AHA/HRS guideline
pacemaker, ICD and CRT implantation 2008 (update
2012 on CRT)

14. Pacemaker indication
• Sinus node dysfunction;
Symptomatic SSS
DDDR*
• Acquired AV block;
- III and Mobitz II degree block
- Dual chamber pacing preferrable
• Chronic bifascicualr or trifascicular block
Syncope risk varies based on presence of AV block and
pacemaker indication depends of HV intervals (EP-study)

15. CRT
• Systolic heart failure due intra- and inter-ventriculair dyssynchrony
• Dyssynchrony occurs independent from QRS duration
• Dyssynchrony determined by Echocardiographic parameters; TDI
and speckle tracking imaging
• In patients with systolic heart failure significant reduction in NYHA
class*(PATH-HF, MUSTIC SR, MIRACLE, COMPANION,CARe-
HF,MIRACLE-ICD,CONTAK-CD,RHYTHM-ICD)
• Non-responders to CRT; 10-40% non LBBB (QRS <130 msec,
RBTB)

16. TDI (Tissue Dopler Imaging)

17. Speckle tracking imaging

18. ICD; indications 2012 ACCF/AHA/HRS guidelines
Level of Evidence: A:
LVEF<35% due to prior MI who are at least 40 days post MI (NYHA II-III)
LV dysfunction due to prior MI, LVEF < 30%, NYHA I
Survivors of Cardiac arrest due to VF or hemodynamically unstable sustained
VT after evaluation to define the cause of event and excluding any reversible
causes
Level B
Non-ischeamic DCM LVEF < 35%, NYHA II-III
Non sustained VT due to prior MI, LVEF < 35% or inducible VF/FT on EPS
Structural heart disease and spontaneous sustained VT
Syncope of undetermined origen with clinically relevant HD sign sustained VT
or VF induced at EPS
LQTS patients who experience syncope and/or VT while on b-Blockers

19. Implant-related complications
1. Pocket hematoma
2. Infection
3. Lead dislodgement
4. Pneumothorax/hematothorax
5. Venous thrombosis
6. Pacemaker syndrome
7. Triscupid regurgitation
8. Twiddler syndrome
9. Pericardial effusion, perforation

20. Pocket hematoma
• Post procedural bleeding and pocket hematoma are relatively
common complications (on oac)
• Hematoma’s are generally treated conservatively unless large or
very painful they need surgical intervention (increased rate of
infection)

21. Infection
• About 0.2% (retrospective studie) of surgical site infection
(swelling, dehiscencion, erosion)
• However, fever of unknown origin an implanted device should
always be considered as a source of infection
• BC, Echogardiographic Dx
• Long term IVAB (Stahp A), device removal and lead extraction.
Re-insertion of device contralateral

22. Heamato- and pneumothorax
• About 1.5% pneumothorax (subclavian puncture)
• Hemothorax due to unintentional arterial puncture
• Avoidance with fluoroscopic insertion techniques or axillary
vein cannulation

23. Thrombosis
• Subclavian or brachio-chephalic venous thrombosis is a very
common event after pacemaker implantation with an
incidence of 2-22% from several days to up to 9 years after
implantation
• Often an asymptomatic occurrence shown on a venogram
during lead revision
• Symptomatic patients show typical manifestations of acute
DVT (swelling) or even vena cava superior syndrome
• PE is an uncommon event
• Therapy ranges from heparinisation/warfarin unto
percutaneous angioplasty or open surgery

24. Pacemaker syndrome
• Intolerance to ventricular pacing in the absence of
atrioventricular synchrony (“the AV dyssynchrony syndrome”)
• Ventricular pacing leads to suboptimal AV dyssynchrony
regardless of the pacing mode
• Symptoms result from the loss of physiological timing of atrial
and ventricular contractions
• Symptoms are a constellation of features due to decreased
cardiac output, loss of atrial contribution to ventricular filling,
loss of total peripheral resistance response, non physiological
pressure waves
• Patient needs adjustment of generator or lead to better
coordinate timing of atrial and ventricular contraction

25. Triscupid regurgitation
• Some patients present with R sided cardiac failure
• mechanism; impingement or adherence to leaflets,
perforation, impairment of valve closure due to entanglement,
, scar formation of thrombosis
• Or due to ventricular dyssynchrony
• Dx is made by 3D-TTE

26. Twiddler Syndrome
• Lead dislodgement due to a patient’s own compulsive
manipulation of generator causing the leads to become retracted
or coiled around the generator
• Dx ismade by radiographic appearance
• Dacron pouches
• Subpectoral pouches

27. Pacing system malfunction
• Generator malfunction in 4.6/1000 pacemakers and 20.7/1000
ICDs, most often due to battery malfunction
• Lead failure often due to insulation breaks, however this is a late
complication
• Pacemaker malfunction is a rare cause of syncope (8/162
patients in a retrospective study)
• An assesment of pacemaker malfunction should consist of ECG,
radiology, patients acid-base status (VBG), medication use and
interrogation (lead problems can result in very high impedance)

28. Lead dislodgement
• Usually after recent implantation, however up to 3 months after
implant is possible
• Undersensing, failure to capture or change in DFTs
• Telemetry, device interrogation
• Obtain a CXR in 2 directions (compare with previous CXR)
• Malposition near phrenic nerve or diaphragm may cause
hiccougs or muscle twitching
• Seldom leads may cause perforation and tamponade (TTE)

29. Pacing system malfunction
1. Failure to capture
2. Failure to sense
3. Failure to pace
4. Electromagnetic interference

30. Failure to capture
• Failure to deliver a pacing stimulus without subsequent
depolarisation
• Functional failure to capture when myocardial tissue is in
refractionary state
• Pathological failure to capture due to numerous conditions;
myocardial disease, electrolyte disturbances (Potassium !), anti-
arrhythmic drugs (Class Ic and QTc lengthening)
• Latency; might be confused with failure to capture; obtain a
multichannel recording recording (interrogation)
• Lead dislodgement, perforation and fracture, increasing DFT
may all lead to failure to capture

31. Failure to sense
• On myocardial depolarisation a signal is send via the lead wire
and filtered by the generator
• Undersensing could be caused by a change in morphology or
vector of the depolarisation front
• PVC, BBB or VTs may need exceed the sensing threshold
(depending on the programming)
• Break in wire insulation or Battery depletion may cause under
sensing
• Undersensing immediate after implantation may be caused by
dislodgement or perforation
• Again; Class Ic or HYPERKALEMIA
• Long blanking and refractory periods of a pacemaker can lead to
relatively or functional undersensing

32. Failure to pace
• Failure to deliver a stimulus to the heart
• Absence of pacing artefacts on intrinsic rates lower than the lower rate
of the device
• Causes; oversensing, partial lead fracture or insulation defects,
crosstalk
• Oversensing could be caused by retrograde P waves, t waves,
ventricular EADs or DADs skeletal myo-potentials (pectoralis,
diaphragm, rectus abdomens)
• External electromagnetic interference
• Blunt trauma to pulse generator, lead fracture, dislodgement or loose
connection
• Pacing artefacts may not be visible on 12 lead ECG and give a false
impression of failure to pace
• PACs or PVCs on a single telemetry lead can give a false impression of
failure to pace

33. Pacemaker tachycardia
• 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)
• only in patients with dual chamber devices
• An intrinsic premature complex is sensed by an atrial lead of the
pacemaker which responds by generating a ventricular impulse. The
ventricular impuls 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
• Adenosine may not be effective where as magnet therapy will be
• NB ! pacemakers atrial sensing tresholds need to be adjusted
• NB ! Mode switch can cause the pacemaker to discontinue atrial
tracking when the atrial upper rate is exceeded

34. Pax

35. ED management
1. History
2. Physical examination
3. 12 lead ECG
4. VBG !!!
5. Radiology (CXR PA and lat)
6. Device interrogation/magnet function

36. ED Management
1. Hyperkalemia
2. Myocardial infarction (Sgarbossa)

37. Hyperkalemia
• Widened QRS complex (widened paced complexes)
• Severe hyperkalemia causes a sine wave following pacing
artefacts
• Elevation of pacing threshold; increased latency, intermittent
capture, or continuous loss of capture, loss of sensing
• Latency may be temporarily overcome by increasing the maximum
voltage of output HOWEVER treatment of hyperkaliema is a
priority

38. Acute myocardial infarction
• The depolarisation and depolarisation from ventricular paced
rhythms may complicate the diagnosis of acute MI (also in LBBB)
• ST and T waves shift in a discordant direction which can mask or
mimic AMI, “appropiate discordance”
• SERIAL ECGs show dynamic ST-segment changes
• 3 criteria used to Dx infarction in patients with LBBB are
• Concordant ST-elevation> 1 mm (score 5)
• Concordant ST-depression>1 mm in V1-V3 (score 3)
• Excessively discordant ST elevation > 5 mm (score 2) in leads
with a negative QRS complex

39. New or old LBBB ?
• “NEW developed LBBB” reflects AMI is NOT true ! Recognition goes
back to 1917 !
• New LBBB should be either due to a LARGE anterior or
anteroseptal infarction resulting in a large injury OR very focal lesion
just distal from the His bundel
• New or old, not always clearly visible in acute settings
• Patients with previous LBBB generally have underlying myocardial
or conduction system abnormalities predisposing to a larger risk
(older, hypertension, CHF)
• Historical studies do not make a fair differentiation in patients with
(L)BBB and ACS
• New studies show that in only 29% of new LBBB; ACS is present*
*Chang et al, Am J Emerg Med, 2009,; 27:916-21

40. The Ventriculair conduction system

41. Sgarbossa criteria
Criteria A Sgarbossa: (90% specifity): 5 point
Concordant ST-elevation> ANY 1mm in lead with a positive QRS
Criteria B Sgarbossa: (90% specifity): 3 point
Concordant ST- depression > 1 mm in ANY lead from V1-V3
Criteria C Sgarbossa: Excessively ST-elevation > 5mm score 2
(high sensivity, lower specifity, ratio of R vs > 20%)
> 3 points ; 90% specifity for ACS
Criteria from Sgarbossa based on a retrospective review from 17
patients from GUSTO-1

42. ECG ACS in LBTB

43. ICD trouble shooting
• Device and procedural complications (as with pacemakers)
• Arrhythmia related complications; inappropriate shocks,
appropriate shocks; ventricular storm and incessant tachycardia,
phantom shocks
• pro-arrhythmic effects
• Increased DFT (fibrosis, amiodarone),
• Heart-failure
• Phantom shocks
• Emotional and quality of life issues: anxiety, depression, fear for
Icd discharge, negative life style changes; unable to return to
work or to drive, decrease in physical activity

44. Inappropriate shocks in ICD patients
• Most often caused by SVTs or non sustained VTs
• Other causes; electromagnetic interference, inappropriate
sensing, ICD malfunction (lead fracture)
• Most inappropriate shocks are avoided with modern and
adequate ICD programming (high cut-off rates, arrhythmia
discrimination detection)

45. Appropriate shocks in ICD patients
• Increasing arrhythmia duration and ATP have diminished
delivered shocks (ATP terminates at least 90% of VTs)
• Electrical storm (definition in ICD carriers is 2 or more adequately
delivered shocks < 24 hours);
• Amiodarone loading, b Blockers (reduction of effects of sympatic
nerve system) and sometimes proceeding towards sedation. both
electrical storm and incessant VT indicate a worse prognosis due
to the underlying mechanism

46. Pro-arrhythmic effect of ICD
• Arrhythmogenic effect of implanted lead; irritation of local
myocardial tissue, fibrosis.
• Inserted in a prior scar site may induce reentry
• RV pacing causes interventricular and intraventricular
dyssynchrony
• “normal” bradycardia back up pacing may result in short-long
pacing sequence leading towards induction of VT
• Biventriculair pacing reduces SCD however may induce Vt due to
an abnormal sequence of depolarisation and depolarisation fronts

47. Magnet function
• Know where the magnet is located in your ED
• Know the effects of applying a magnet to a device
• Know the difference between a magnet application and
an electrical reset
• Most pacemakers and ICDs turn off the sensing mode
when a magnet is applied over the generator
• The pacemaker starts to pace in an asynchronous
mode in a fixed rate (Medtronic 65/min reflects EOL)
• Rarely a device may be programmed in a “magnet off”
setting

48. When to apply a magnet ?
1. To terminate a pacemaker mediated tachycardia
2. Inappropriate sensing (due to electromagnetic interference;
diathermy, MRI)
3. Over sensing due to lead problems
4. Stop ICD ATP or defibrillation shock therapy (backup
bradycardia pacing will still be provided).NB an alert sound will
be initiated when applying a magnet to a medtronic ICD (also on
lead and impedance problems or EOL)

49. ACLS in an ICD patient
• ICD and CRT-D patients should have same approach
• SHOCKS delivered are of NO risk for the MET-team
• If arrhythmia persists after a device defibrillation, attach patient to
anterior-posterior placed leads preferably 8 cm from generator
• Consider magnet placing to avoid unintentional device
defibrillation's
• Consider; increased DFTs due to ipsilateral pneumothorax
• `consider femoral access instead of subclavian due to often
thromboses veins (or in appropiate response of a pacemaker due
to wire interrogation)

50. More ?
go to: Medtronic Academy (for Physicians)
LIFTL Fellowship exam SAQ and SMACC 2014
Amal Mattu
ECG pedia

51. Back to clinical case
81 male
4/7 post dual chamber pacemaker insertion (pAF)
Re-currence of pre implantation dizziness, palpitations and
SOB
CXR: correct lead position
Interrogation: A not sensing, P wave in bipolar, re-programmed
to bipolar, treshold and impedence normal.
Loaded on amiodarone

52. Literature
1. Up to Date; Electrical storm and incessant ventricular tachycardia, Overview of
pacing in heart failure, implantable cardioverter defibrillators;
2. EMP: Managing Pacemaker related Complications and malfunctions in the ED
3. Cardiac Pacing and ICDs; 4th Edition, K.A Ellenbogen
4. A practical guide to cardiac pacing, 5th edition, H.Weston Moss
5. Electrofysiological Testing, 3d edition, R.N Fogoros
6. AHHF/AHA/HRS 2012 Guidelines for device based therapy
7. Medtronic Academy
8. LIFTL
9. Neeland et al, J am Coll Cardiol, 2012; 10;60 (2):96-105. “Evolving
considerations in the management of patients with LBTB and suspected AMI