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Pacing and Defibrillation

Michael Eggen Ph.D.

Sr. Research Manager, Medtronic - Cardiac Rhythm Management

Adjunct Assistant Professor - University of Minnesota, Department of Surgery

January 7th, 2026

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Outline

Common Conduction System Abnormalities

What are we trying to fix with devices?
Assume familiarity with basic ECG waveform and conduction system

P, QRS, T wave

Pacing/Defibrillation Systems
Case Studies

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SA Nodal Pathologies

SA Node

Rate = 60 - 100 bpm

SA Nodal Pathologies

Sick Sinus Syndrome (unpredictable rate)
Chronotropic Incompetence (inadequate response to physiologic demand)
Block (complete dysfunction; congential/CAD/ablation)

Need to speed up the heart rate with a pacemaker

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AV Node Pathologies

AV Node

Rate = 40 - 55 bpm

AV Nodal Pathologies

1^st Degree Heart Block (AV > 200 msec)
2^nd Degree Heart Block (not 1:1)

Mobitz Type I: Wenckebach Phenomenon (dropped beat after progressive PR elongation)
Mobitz Type II (dropped beat w/no PR elongation)

3^rd Degree Heart Block (no conduction from atrium to ventricles)

Need to pace the ventricle to restore normal physiology

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Arrhythmia Definitions

Bradycardia – slow heart rate
Tachycardia – fast heart rate

These heart rates may or may not be appropriate. Pacing and defibrillation systems address inappropriate rhythms.

Fibrillation – chaotic depolarization of the atria or ventricles

Always inappropriate.

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Arrhythmias

Sinus bradycardia

Pacemaker

Atrial tachycardia/flutter (non-nodal)
Atrial fibrillation

Pacemaker to normalize ventricular rhythm sometimes combined with ablation

Ventricular tachycardia (reentrant, mono/polymorphic)

Shock to restore normal rhythm/Anti-tachycardia pacing

Ventricular fibrillation

Shock to restore normal rhythm

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Pacing/Defibrillation

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Basic System Function

Sense intracardiac signals by comparing the voltage between two electrodes
Determine therapy required to regulate arrhythmias/heart rate, if any…
Pace the heart (IPG)

Low voltage stimulation pulses (1-5V/0.5msec)

Cardiovert the heart (ICD)

High voltage/high frequency pacing or low voltage shocks

Defibrillate the heart (ICD)

High voltage shocks (up to 750V/10msec)

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Pacing/Defibrillation

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Implantable Pacing & Defibrillation Devices

Pacemaker (Implantable Pulse Generator, IPG)
Defibrillator (Implantable Cardioverter Defibrillator, ICD)
Lead(s)
Leadless Pacemaker (Transcatheter Pacing System (TPS), Leadless Cardiac Pacemaker (LCP)

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Pacing and Defibrillation Systems

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Lead

Pacing/Defibrillation System

IPG or ICD

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Pacing/Defibrillation Systems

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Endocardial Defibrillation Systems

Single Coil System

Dual Coil System

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Pacing System Nomenclature�(HRS/NASPE/BPEG Designation)

Roman numerals I-IV indicate the position in the coding. Adapted from Bernstein et al., (2002) PACE, 25, 260-4 (12).

AOO (Asynchronous atrial pacing)

AAI (A-pace, A-sense, A-inhibit)

VVI (V-pace, V-sense, V-inhibit)

DDD (Dual – pace, Dual – sense, Dual –inhibit)

VDD (V-pace, Dual – sense, V – inhibit)

DDDR (DDD + Rate response for chronotropic incompetence)

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CXRs of Pacemaker with Two Atrial Pacing Leads and One Ventricular Lead

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Pacemaker (IPG)

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Defibrillator (ICD)

209 cc

113 cc

80 cc

54 cc

33 cc

36 cc

39.5 cc

39 cc

49 cc

1989

2025

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Defibrillator (ICD)

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Pacing Lead

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Cathode

Anode

Fixation tines

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Defibrillation Lead

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Cathode

Anode

RV coil

SCV Coil

Connector

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Lead Implantation

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Defibrillator Check in EP Lab

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Pacing Lead Lifetime Activity

~ 70 bpm
~ 100,000 beats/day
~ 40,000,000 beats/year
~ 400,000,000 beats/10 years

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Lead Fixation Mechanisms

Fixation Mechanisms – Endocardial

Passive - Tined

Active - Helix

Passive - Shaped

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Passive fixation in relation to endocardial leads means that no part of the lead itself is actually embedded in the endocardium. Rather, the lead tip is trapped within the trabeculae and/or is held in position by its pre-formed shape (e.g., J-lead in atrium).

Passive fixation leads commonly use tines or fins to "catch" trabeculi in the heart, or the lead is canted or curved to help place and hold the lead tip in a certain position.

Passive anchoring devices, such as flanges or wedge tips, cages and balloons were early attempts to solve the dislodgment problems of early pacing leads. However, only after tined leads were introduced by Medtronic in 1976 did a true solution to dislodgment emerge with regard to passive fixation.

Today, there is approximately a 1-2% dislodgment rate ^{1, 2, 3, 4, 5, 6}with passive fixation leads:

1 - 2% in the atria,^{1, 2, 6}

1 - 2% in the ventricle^{.1, 3, 4, 5}

References:

1 Gammage MD, Marshall HJ, Harris JI. Five-year experience with polyurethane, passive fixation, steroid-eluting leads. PACE. 1998;(Pt II):842. Abstract.

2 Hua W, Mond HG, Strathmore N. Chronic steroid-eluting lead performance: a comparison of atrial and ventricular pacing. Pacing Clinical Electrophysiology. 1995;20(1 Pt 1):17-24.

3 Kazama S, Nishiyama K, Machii M, Tanaka K, Amano T, Nomura T, Ohuchi M, Kasahara S, Nie M, Ishihara A. Long-term follow-up of ventricular endocardial pacing leads. Jpn Heart J. 1993;34(2):193-200.

4 Mayer DA, Tsapogas MJ. Pacemakers: dual or single chamber implantation. Vasc Surg. 1992;26(5):400-7.

5 Miller GB, Leman RB, Kratz JM, Gillette PC. Comparison of lead dislodgment and pocket infection rates after pacemaker implantation in the operating room versus the catheterization laboratory. Am Heart J. 1998;115(5):1048-51.

6 Mond HG, Hua W, Wang CC. Atrial pacing leads: the clinical contribution of steroid elution. Pacing Clinical Electrophysiology. 1995;18(9 Pt 1):1601-8.

7 Glikson M, von Feldt LK, Suman VJ, Hayes DL. Short- and long-term results with an active fixation, bipolar, polyurethane-insulated atrial pacing lead. Pacing Clinical Electrophysiology. 1996;19(10):1469-73.

8 Stirbys P. Implantation of double screw-in leads. Pacing Clinical Electrophysiology. 1988;11(10):1482-4.

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Multi Pole LV Lead

Multipole poles to allow for flexibility in pacing locations

Quadripolar (4 electrodes)

Side Helix for stability in vein

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1:Basal

2: Mid

3: Apex

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The Visible Heart^®

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Canine - 33 weeks

Swine - Acute

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Electrodes - Steroid

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IMPLANT

CHRONIC

(8 weeks or longer)

Excitable

Cardiac

Tissue

Non-Excitable

Fibrotic

Tissue

Excitable

Cardiac

Tissue

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Electrodes - Steroid

Effect of Steroid on Stimulation Thresholds

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Pulse Width = 0.5 msec

Implant Time (Weeks)

Textured Metal Electrode

Smooth Metal Electrode

0

1

2

3

4

5

Steroid-Eluting Electrode

0

1

2

3

4

5

6

7

8

9

10

11

12

Volts

This graph compares the stimulation thresholds of contemporary pacing leads. Older electrodes exhibited higher threshold peaking than that of steroid leads shown on the slide.

The different types of electrodes exhibit a wide range of threshold peaking.

Steroid-eluting electrodes continue to show lower chronic stimulation thresholds and no significant peaking.

Threshold changes are shown here over a 12-week period post-implant, where a comparison is made between:

• smooth metal electrode

• textured metal electrode

• steroid-eluting electrode

Traditionally, implant stimulation thresholds are relatively low.

Non-steroid-eluting electrodes exhibit a peaking phase from week 1 to approximately week 6, due to the maturation process at the electrode-tissue interface.

Steroid-eluting electrodes exhibit virtually no peaking.

The chronic phase of stimulation threshold occurs 8-12 weeks post-implant which is characterized by a plateau. This plateau is higher than the acute phase, due to fibrotic encapsulation of the electrode. Steroid-eluting lead chronic thresholds remain close to implant values.

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Pacing the Heart

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Bipolar Pacing Circuit

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Bipolar pacing circuit, including an implantable pulse generator and a pacing lead. Resistances: R_C = cathodic lead conductor, R_CT = cathode-tissue interface, R_T = tissue, R_AT = anode-tissue interface, and R_A = anodic lead conductor. Capacitances: C_CT = cathode-tissue interface and C_AT = anode-tissue interface.

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e^-

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Mechanism of Stimulation

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Must exceed the threshold potential for depolarization for a “critical mass” of cells (~ 1 V/cm gradient is required)

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Leadless Pacemakers

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Leadless Pacing

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Pocket Related Complications

Infection
Hematoma
Erosion

Lead Related Complications

Fractures
Insulation breaches
Venous thrombosis and obstruction
Tricuspid regurgitation

Reduce complications associated with traditional pacing technology¹

¹ Ritter P, et al. The rationale and design of the Micra Transcatheter Pacing Study: safety and efficacy of a novel miniaturized pacemaker. Europace. April 7, 2015

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Example - Micra

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Cathode

Size

Volume: 0.8cc
Mass: 2g
Length: 25.9mm
Width: 20Fr

Battery

Micra VR2 16 year longevity

18 mm

Anode

Active Fixation Nitinol Tines

Proximal Retrieval Feature

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Micra AV

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Transcatheter Pacing System with AV Synchrony (VDD)
Accelerometer based atrial sensing

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Implant Procedure in The Visible Heart^®

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Eggen MD, Bonner MD, Williams ER, Iaizzo PA. Multimodal Imaging of a Transcatheter Pacemaker Implantation within a Reanimated Human Heart. Heart Rhythm. 2014 Dec;11(12):2331-2

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Retrieval

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Vatterott P, Eggen M, Mattson A, Iaizzo P, et al. Retrieval of a Chronically Implanted Leadless Pacemaker within an Isolated Heart using Direct Visualization. Accepted for publication Heart Rhythm Case Reports

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Defibrillating the Heart

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Lead

Active Can Defibrillation

ICD

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e^-

Active Can Defibrillation

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Active Can Defibrillation

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Active Can Defibrillation

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Shocking Waveforms

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Mechanism of Defibrillation

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Must exceed the threshold potential for a “critical mass” of cells (~ 95% of the ventricular myocardium at a 5 V/cm gradient is required)

RV

LV

RV

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Extravascular Configurations

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EV ICD (Medtronic Aurora EV-ICD)

Advantages

Defibrillation and pacing without any intracardiac leads complications, preserves vasculature
Backup pacing/anti tachycardia pacing (ATP) options (currently does not support permanent RV pacing)
Lower risk/relative ease of extraction
Lower defibrillation thresholds than subcutaneous options (lead closer to the heart)

Mediastinal Space

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Subcutaneous Configurations

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Emblem S-ICD (Boston Scientific)

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Concomitant Systems

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Extravascular or Subcutaneous Defibrillator + Leadless Pacemaker (Currently under investigation by manufacturers)

Advantages: Permanent Pacing and Defibrillation without any intracardiac leads

Some patients develop a pacing indication after implantation of these systems and require either conversion to transvenous ICD therapy or addition of a transvenous pacemaker

Example: (A) S-ICD lead (Boston Scientific), (B) S-ICD, and (C) LP (Nanostim, Abbot) projected over right ventricular apex.

72 year-old patient

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https://www.nejm.org/do/10.1056/NEJMdo006737/full/?requestType=popUp&relatedArticle=10.1056%2FNEJMoa2206485

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Sensing

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Electrodes – Lead Sensing

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True Bipolar

Integrated Bipolar

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At the most fundamental level,

sensing algorithms count

atrial and ventricular contractions

and their timing. This information

is then used to assess the rhythmic state

of the heart.

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Electrodes - Sensing

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Induction-Defibrillation Sequence

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Signal Processing

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Signal Processing

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Signal Processing

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Pace/Sense Example

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An electrocardiogram (above) and pacemaker marker channel (below) printed from a programmer. Note the loss of capture on the atrial channel (indicated by the arrow); notice that no P-wave follows the pacing pulse.

Marker Channel

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Pace/Sense Example

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An electrocardiogram (above) and pacemaker marker channel (below) printed from a programmer. Note the ventricular oversensing (indicated by the arrow); notice that no QRS complex is associated with the detected event.

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Indications for Pacing

Class I - Conditions for which there is evidence and/or general agreement that a given procedure or treatment is beneficial, useful, and effective.

Class II/III…

1. Third-degree AV block at any anatomic level, associated with any one of the following conditions:

a. Bradycardia with symptoms presumed to be due to AV block. (Level of evidence: C)
b. Arrhythmias and other medical conditions that require drugs that result in symptomatic bradycardia. (Level of evidence: C)
c. Documented periods of asystole >23.0 seconds or any escape rate <40 beats per minute (bpm) in awake, symptom-free patients. (Level of evidence: B, C)
d. After catheter ablation of the AV junction. (Level of evidence: B, C) There are no trials to assess outcome without pacing, and pacing is virtually always planned in this situation unless the operative procedure is AV junction modification.
e. Postoperative AV block that is not expected to resolve. (Level of evidence: C)
f. Neuromuscular diseases with AV block such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb’s dystrophy (limb-girdle), and peroneal muscular atrophy. (Level of evidence: B)

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Many and very complex

(see ACC/AHA/HRS Guidelines on www.hrsonline.org)

See Handbook

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Conduction System Pacing

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HIS BUNDLE or

LBBAP

Left bundle branch area pacing, includes:

Left bundle branch pacing (both non-selective and selective)
Left fascicular pacing
Left ventricular septal pacing (without clear evidence for LBB capture)

HIS

LBB

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CSP Targets

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1

2

3

Click to view:

Septogram

TVA summit

All landmarks

2

1

3

2

LBB

LAF

LSF

AV node

HB

RBB

⦿

TVA summit

LPF

Target

10cc RV angiography in RAO 30° view

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https://med.umn.edu/iem/events/advanced-cardiac-electrophysiology-clinical-and-preclinical-experiences

May, 2026

Day 1: Lectures on cardiac anatomy, conduction system, alternate site pacing, cardiac pacing timing, physiology, ablation. Lab tour and study cardiac specimens in the human heart library.

Day 2: Preclinical EP studies including cardiac hemodynamics, cardiac pacing. Students will learn how to test pacing parameters and outcomes in an acute setting.

Day 3: Clinical EP immersion with Dr. Roukoz

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Case Studies

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S-A Node:

80 bpm

A-V Node:

Healthy

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Heart Rate = 80 bpm

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A-V Node:

40 - 60 bpm

S-A Node:

Sick

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Heart Rate = 40 - 60 bpm

Cardiac Output is Too Low

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A-V Node:

Blocked

S-A Node:

Sick

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Heart Rate = <30 bpm escape

Marginal Cardiac Output (fainting)

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A-V Node:

Sick

S-A Node:

Healthy

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Ventricular Rate = 40-60 bpm