Week 8 Advanced CIED Follow-Up - Advanced Follow Up

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Last updated 2:21 AM on 7/14/26
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Troubleshooting: Identifying Issues

  • Patient symptoms

    • Syncope/presyncope

    • Palpitations

    • Fatigue

    • Return of pre-implant symptoms

  • ECG abnormalities

    • Failure to capture

    • Failure to sense

    • Failure to output

    • Variations in pacing rate

    • Magnet rate indicates ERI/EOS

  • Remote monitoring

    • Arrhythmias

    • Device malfunctions

    • Heart failure

    • Advisory/recall

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Patient-Related

  • Underlying disease state

  • Electrolyte imbalance

  • Medications

  • Tissue substrate changes

  • Address patient-related issues first!

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System-Related

  • Generator

  • Header/connection

  • Lead integrity

  • Lead tissue interface (also a patient issue)

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Pacemaker Troubleshooting Process

  1. Gather information

  2. Run PUBLSTOP

  3. Review diagnostic data

  4. Simplify device settings

  5. Optional:

Evaluate chest x-ray

Invasive evaluation of the system

  1. Determine the cause - review

  2. Take corrective action

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Gather Information

  • Pulse generator

  • Leads

  • Implant data

  • Patient symptoms

  • Complete device check

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Gather Information: Pulse Generator

  • Manufacturer

  • Model #

  • Device capabilities

  • Advisory/recall

  • Chambers

  • Rate response

  • Special features

  • Date of implant

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Gather Information: Leads

  • Manufacturer

  • Model #

  • Date of implant

  • Capped leads

  • Leads may have different manufacturers/dates

  • Recalls/advisories

  • Unipolar/bipolar

  • Fixation

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Gather Information: Patient Information

  • Implant data

  • Medical records

  • CIED indication

  • May need to turn off alerts for known condition

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Gather Information: Patient Symptoms

  • Current symptoms?

  • Duration?

  • Past symptoms?

  • Correlation to activities/time of day?

  • Make differential diagnosis

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Differential Diagnosis: Palpitations

  • Palpitations: possible causes

    • Pacemaker mediated tachycardia - VA conduction test

    • DDD tracking of AF/Flutter - evaluate mode switching

    • Tracking EMI - unipolar leads?

    • VT - analyze episodes/alerts

    • PVCs - track frequency

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Differential Diagnosis: Weakness

  • Weakness/fatigue: possible causes

    • Failure to capture

    • Inappropriate base rate

    • Need for rate response

    • Pacemaker syndrome

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Differential Diagnosis: Dyspnea

  • Dyspnea/shortness of breath: possible causes

    • Pacemaker syndrome

    • Need for rate response

    • Underlying cardiac disease (eg. heart failure)

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Differential Diagnosis: Syncope

  • Syncope/presyncope: possible causes

    • Pacemaker syndrome

    • Underlying disease (Vascular disease, VT, etc.)

    • Crosstalk - check refractory periods/sensitivity

    • Loss of capture - threshold test

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Differential Diagnosis: Hiccups

  • Hiccups/coughing: possible causes

    • Diaphragmatic pacing

    • Phrenic nerve stimulation

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Differential Diagnosis: Muscle Twitching

  • Muscle twitching: possible causes

    • Lead insulation failure

    • Unipolar pacing

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Differential Diagnosis

Before running tests/making changes, note current programmed settings:

  • Mode

  • LRL

  • MTR/MSR

  • AV delays

  • Rate response

  • Lead polarity

  • Intervals

  • Algorithms

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Loss of Capture

Pacing that fails to lead to myocardial depolarization when it otherwise should have captured

  • Excludes functional non capture: pseudo malfunction

  • True loss of capture: identify underlying cause and correct

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Lead Dislodgement

  • Most likely in acute phase of lead implant (within 3 months)

  • Interview patient

  • Confirm lead type

  • Compare current data to implant data

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Macro vs. Micro Dislodgement

  • May recommend chest x-ray

  • Compare to post-implant x-ray

  • Macro dislodgement: can be seen on x-ray

  • Micro dislodgement: cannot be seen on x-ray

    • More common with passive fixation

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Lead Dislodgement Characteristics

  • Intermittent loss of capture

  • Different morphology when capturing

  • Sensing abnormalities

    • Far field oversensing

    • Undersensing

  • Normal impedance values

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Cross-Chamber Stimulation

  • Lead from one chamber stimulates the opposite chamber

  • Atrial lead dislodgement across tricuspid valve

  • Ventricular depolarization in response to atrial pacing

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Cross-Chamber Stimulation Testing

  • Pace AAl or AOO to confirm ventricular activation

  • Verify with VVI

  • Differential diagnoses

    • Lead dislodgement

    • Unipolar pacing

    • Atypical lead placement

    • Leads reversed in header

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Perforation

  • Lead penetrates through cardiac tissue

  • Cathode no longer in contact with myocardium

  • Reported in 1-5% of patients

  • Chest x-ray or cardiac CT

  • Acute perforation: hemodynamically unstable due to tamponade

  • Late-occurring perforation: asymptomatic

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Perforation Signs and Symptoms

  • More likely in patients with weaker heart walls (apical MI)

  • Failure to sense

  • Loss of capture

  • Hematoma

  • Pneumonia

  • Muscle twitching

  • Liver perforation

  • Hiccups

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Loss of Lead Integrity

  • May cause change of impedance: systemic impedance determined by several factors

    • Conductor wires

    • Lead tip

    • Lead-header interface

  • Clavicular crush: common cause

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Lead Safety Switch

  • Automatically changes to unipolar in response to high impedance

  • Coaxial leads: eliminates outer conductor

  • Only in brady leads

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Loose Set Screw

  • Usually acute

  • Set screw can work loose over time

  • Manifests differently depending on degree of contact

    • Failure to output

    • Failure to sense

    • Intermittent loss of capture

    • Intermittent oversensing

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Loose Set Screw vs. Dislodgement

  • Dislodgement: no change in impedance

  • Loose set screw: impedance rises

    • Check unipolar vs. bipolar impedances

    • Loose anodal set screw: high bipolar, normal unipolar

    • Loose cathodal set screw: high bipolar, high unipolar

  • Manipulate pocket: may cause

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Electromyocardial Interface

  • Patient-related issues

    • Myocardial infarction

    • Infiltrative cardiomyopathy (ARVD)

    • Post-shock pacing threshold rise (cardioversion, defibrillation)

  • Pacemaker exit block: system-related issue

    • Virtual electrode: fibrous capsule that forms around lead tip

    • Excessive fibrous can cause chronic high thresholds

    • Reduced by steroid-eluting leads

    • Attributed to unknown causes

    • Difficult to differentiate from dislodgement: exit block usually more chronic (> 3 months)

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Other Causes of High Thresholds

  • Metabolic abnormalities

  • Electrolytes

  • Medications

  • Diabetes

  • Hemodialysis

  • Dehydration

  • Antiarrhythmics

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Pseudomalfunctions

  • Fusion

  • Pseudofusion

  • Functional non-capture

  • Latency

    • Pacing location (LV, His, epicardial)

    • Near loss of capture

  • Isoelectric lead

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Loss of Capture Troubleshooting Steps

  • Reestablish capture

    • Max outputs

    • Threshold test

    • Reprogram

  • Check bipolar impedance

    • High impedance: conductor fracture, loose set screw

    • Low impedance: insulation break

  • Check for normal unipolar impedance

    • Outer insulation break

    • Outer conductor fracture

    • Loose anodal set screw

  • Chest x-ray: look for macrodislodgement

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Undersensing

Device fails to sense and time off of intrinsic signals: any condition that causes change to intrinsic complex

  • Metabolics/medications

  • Abnormal rhythms

  • Myocardial infarction

  • Lead dislodgement

  • Magnet application

  • Battery depletion

  • Component failure

  • Header abnormalities

  • Functional undersensing

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Undersensing Effects

  • Overpacing: device fails to inhibit

  • Competitive pacing: shortly after intrinsic signal

  • Secondary effects

    • Functional non capture

    • PAV rather than SAV

    • Safety pacing off of intrinsic QRS

    • Mislabeling of intrinsic QRS as PVC

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Medications and Metabolics

  • Class IC antiarrhythmics (flecainide): most common medication causing undersensing

  • Hyperkalemia: most common metabolic issue causing undersensing

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Functional Undersensing

  • Intrinsic event falls within blanking/refractory period

  • Not sensed or tracked: may influence mode switch

  • Pseudomalfunction

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Undersensing Troubleshooting

  • Determine underlying cause

  • Run sensing test: measure intrinsic amplitude

  • Fix underlying cause if possible

  • If not, make device more sensitive by lowering mV value

  • Be careful to avoid oversensing

  • Check unipolar sensing if needed

  • Check impedance and capture

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Oversensing

Device inappropriately senses and times off of signals other than intrinsic depolarizations

  • Inappropriate inhibition of pacing: underpacing

  • Inappropriate triggering of algorithms

  • Inappropriate triggering of ICD therapy

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Noise vs. Artifact

  • Noise: noncardiac signals sensed by CIED

  • Artifact: noncardiac signals seen on EGM by not sensed by CIED

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EMI

Electromagnetic interference

  • Usually in 30-300 Hz range

  • Commonly cyclical appearance

  • 60 Hz: standard frequency

  • Pacemakers: atrial channel more sensitive

  • ICDs: ventricular channel more sensitive

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Myopotentials

  • Extracardiac muscular activity

  • Typically only in one channel

  • Can be initiated by physical maneuvers: be careful with pacemaker dependent/ICD patients

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Conductor Fractures

usually on one channel

<p>usually on one channel</p>
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Sensing Conductor Fracture vs. Loose Set Screw

  • Loose set screw presents similarly:

    • More acute

    • Test with pocket manipulation

  • Check impedance to differentiate from dislodgement

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T Wave Oversensing

  • Sensing of ventricular repolarization as depolarization

    • Long QT syndrome

    • Hyperkalemia

    • Brugada syndrome

    • Inappropriate programming

  • Troubleshooting

    • Extend VREF

    • Adjust sensitivity value

    • Other sensing parameters

    • Switch to integrated bipolar

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R Wave Double Counting

  • Sensing ventricular depolarization twice

    • Delays in ventricular conduction

    • Bundle branch block

    • Class IC antiarrhythmics

    • Hyperkalemia

    • Loss of capture

  • Address underlying cause

  • Adjust blanking period if needed

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Farfield Oversensing

  • Intrinsic signals in one chamber sensed in opposite chamber

    • R wave/T wave oversensing on atrial channel: most common cause of inappropriate mode switching

    • P wave oversensing on ventricular channel: His bundle lead

  • Run sensing test

  • Decrease sensitivity by increasing mV value

  • Increase PVAB/PAVB if necessary

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Crosstalk

  • VA crosstalk: sensing V pacing pulse on atrial channel

  • AV crosstalk: sensing A pacing pulse on ventricular channel

  • Run sensing test

  • Decrease sensitivity

  • Increase blanking period

    • Increase PVAB to prevent VA crosstalk

    • Increase PAVB to prevent AV crosstalk

  • Lower outputs if possible

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ICD Leads

  • All leads vulnerable

    • Millions of cardiac cycles

    • Hostile environment

  • ICD leads: particularly vulnerable

    • More components

    • Higher voltages

    • Multilumen design

    • Single or dual coil

    • Dedicated or integrated bipolar

    • IS-1/DF-1 or DF4

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ICD Lead Recalls

  • Medtronic Sprint Fidelis

    • Highly flexible

    • Conductor fractures of tip electrode coil and ring electrode cable

  • St. Jude Riata Family

    • Large-diameter lumens

    • Inside-out insulation breach

    • Externalized cables

    • Connections between conductors

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Pace-Sense Failure

  • Seen with conductor fractures and insulation breaches

    • Oversensing of fast nonphysiologic signals

    • Inhibition of pacing

  • Inappropriate therapy

  • Loss of capture

  • Undersensing

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Shock Component Failure

  • Likely underreported

  • Failed defibrillation

  • Complete pulse generator failure

  • Hopefully catch beforehand

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Analyzing EGMs

  • Signals on sensing channel but not farfield: usually noncardiac

  • Look at stored episodes

  • Use real time EGMs

    • Pocket manipulation to rule out poor lead-header connection

    • Exercises to rule out myopotentials

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Insulation Breaches

  • EGMs less fully studied

  • Abnormal signals generated by secondary effects

    • Outside-in breach: myopotentials

    • Inside-out breach: spikes on sensing and shock channels from cables rubbing against each other

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Lead Impedance

Effective resistance of an electric component to alternating current, arising from combined effects of ohmic resistance and reactance

  • Higher impedance: lower current flow at same voltage

  • Ohm's law: V = IR

  • Pacing impedance: measured through subthreshold impulse

    • Lead-tissue interface (most of systemic impedance)

    • Conductors

    • Lead-header interface

  • Normal range: 300-1800 ohms

  • Changes to impedance more indicative of failure

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Shock Impedance

  • Measured through low-energy shock

  • Shock circuit:

    • Lead-header connection

    • High-voltage conductors

    • Shocking coils

    • Anatomical features

  • Single coil leads: 30-110 ohms

  • Dual coil leads: 20-70 ohms

  • Low-voltage measurement not very accurate

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High Voltage Failure

  • High voltage conductor fracture

    • Abrupt impedance increase

    • Absolute value > 100 ohms

  • High voltage insulation breach

    • May cause impedance decrease

    • Difficult to diagnose with low voltage pulses

    • Can cause catastrophic short-circuit

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Lead Failure Algorithms

  • Rapid oversensing

  • Impedance changes

  • Lead safety switch: change to unipolar

    • Cathodal conductor only

    • Works best with coaxial brady leads

  • Lead integrity alert: ICD leads

    • Impedance changes

    • Frequent isolated rapid intervals

    • Nonsustained VT with rapid intervals

    • Audible tone, RM alert, extends detection durations

    • Some algorithms withhold shocks for nearfield-only signals

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Impedance Troubleshooting

  • Impedance not very sensitive or specific, especially low-voltage shock impedance

  • Monitor single out of range impedance or gradual rise over time

  • Reprogram to unipolar/integrated bipolar

  • Assess time frame

  • Chest x-ray if needed

  • Patients with at-risk leads

    • Education

    • Remote monitoring

    • Programming changes

    • Often replace during gen. change

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Pacemaker Syndrome Definition

  • Initially associated with RV pacing

  • Later associated with several factors:

    • Loss of AV synchrony

    • Loss of V-V synchrony

    • Retrograde VA conduction

    • Lack of rate response

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Loss of AV Synchrony

  • Atrial systole: 10-30% cardiac output

  • Ventricles contract too late: blood flows backward

  • Ventricles contract too early: atria contract against closed valve

  • Symptoms:

    • Dizziness

    • Syncope

    • Dyspnea

    • Fatigue

    • Palpitations

    • Distended neck veins

    • Hypotension

    • Heart failure

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Pacemaker Syndrome Causes

  • VVI devices

    • No AV synchrony

    • Retrograde VA conduction

    • Only indicated for permanent AF w/SVR or ICD patients with no pacing indications

  • DDD devices

    • Chronotropic incompetence with no rate response

    • RV pacing: V-V dyssynchrony

    • Algorithms to promote intrinsic conduction: AV dyssynchrony

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Pacemaker Syndrome Symptoms

  • Dyspnea on exertion

    • Decreased CO

    • Chronotropic incompetence

    • Worsening heart failure

  • Heart failure:

    • Nocturnal dyspnea

    • Orthopnea

    • Edema

    • Weight gain

    • Lung sounds

  • Vascular symptoms

    • Hypotension

    • Syncope/presyncope

    • Related to decreased CO

  • Fatigue

  • Headache

  • Dizziness

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Physical Examination

  • Palpitations

  • Drop in systolic BP of > 20 mmHg when turning pacing on

  • Cannon A waves

    • Atria contract against closed AV valves

    • Blood regurgitates backward

    • Pulsation in neck/abdomen

    • Waveform on central venous pressure tracing

    • Seen with RVAC, CHB, pulmonary HTN, VT

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Pacemaker Syndrome at Follow Up

  • Run tests in a way that feels best for patients

  • DDD maintains AV synchrony

  • Be careful when coming on pacing

  • Monitor patient for symptoms

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Programming Considerations

  • VVI: reduce pacing

    • Decrease rate

    • Rate hysteresis

    • Rate response off

  • Permanent AF: compensate for loss of atrial kick

    • Increase base rate

    • Turn rate response on

  • DDD: balancing act

    • Algorithms that promote intrinsic conduction reduce RV pacing, can cause AV dyssynchrony

    • CHB and CRT patients should have shorter AV delays

    • Rate response drives pacing in the atrium: physiologic

    • CRT: algorithms to promote BIV pacing

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P Wave Abnormalities

  • Right atrial abnormality: change to beginning of P wave

    • Tall, peaked P wave

    • COPD

    • Pulmonary HTN

    • Congenital heart disease

    • RVHF

  • Left atrial abnormality: change to end of P wave

    • Wide, notched P wave

    • CAD

    • Cardiomyopathy

    • HTN

    • Valvular heart disease

<ul><li><p>Right atrial abnormality: change to beginning of P wave</p><ul><li><p>Tall, peaked P wave</p></li><li><p>COPD</p></li><li><p>Pulmonary HTN</p></li><li><p>Congenital heart disease</p></li><li><p>RVHF</p></li></ul></li></ul><ul><li><p>Left atrial abnormality: change to end of P wave</p><ul><li><p>Wide, notched P wave</p></li><li><p>CAD</p></li><li><p>Cardiomyopathy</p></li><li><p>HTN</p></li><li><p>Valvular heart disease</p></li></ul></li></ul><p></p>
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Aberrancy

  • Abnormal intraventricular conduction of a supraventricular impulse

  • One or more components of distal conduction system refractory when impulse arrives

    • Different conduction pathway

    • Any supraventricular impulse that is early enough

<ul><li><p>Abnormal intraventricular conduction of a supraventricular impulse</p></li><li><p>One or more components of distal conduction system refractory when impulse arrives</p><ul><li><p>Different conduction pathway</p></li><li><p>Any supraventricular impulse that is early enough</p></li></ul></li></ul><p></p>
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PACs: Three Possible Outcomes

A: Nonconducted PAC

B: Aberrant RBBB Pattern

C: Normal QRS Complex

<p>A: Nonconducted PAC</p><p>B: Aberrant RBBB Pattern</p><p>C: Normal QRS Complex</p>
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Importance of Underlying Rate

  • Refractory periods determined by heart rate

    • Slower rate: longer

    • Faster rate: shorter

  • Longer PAC intervals will cause aberrancy at slower rates

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Atrial Extrastimulus Pacing

Mimics PAC: can cause aberrancy

<p>Mimics PAC: can cause aberrancy</p>
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Drug Toxicity and Electrolytes

Anything that alters the action potential can cause aberrancy:

  • Electrolyte abnormalities

    • Hypocalcemia

    • Hypercalcemia

    • Hyperkalemia

  • Medications

    • Class IC antiarrhythmics (flecainide)

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Rate Related Aberrancy

  • Aberrancy can result from rapid acceleration and deceleration as well as high overall rates

  • Rate related bundle branch block:

    • Every beat falls within bundle branch refractory period

    • Usually RBBB pattern

    • Occurs at critical rate: similar to Wenckebach

    • Rate is lower in diseased hearts

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Aberrancy in ICDS

  • Transvenous ICD: morphology discriminator

    • Patient exercising: sinus rate reaches VT zone

    • Morphology discriminator will label aberrancy as VT

    • Turn morphology off or turn on other discriminators

  • SICD: subcutaneous ECG

    • Aberrancy can cause R wave double-counting

    • Changes to T wave can cause T wave oversensing

    • Rate appears double

    • Change sensing vector

<ul><li><p>Transvenous ICD: morphology discriminator</p><ul><li><p>Patient exercising: sinus rate reaches VT zone</p></li><li><p>Morphology discriminator will label aberrancy as VT</p></li><li><p>Turn morphology off or turn on other discriminators</p></li></ul></li><li><p>SICD: subcutaneous ECG</p><ul><li><p>Aberrancy can cause R wave double-counting</p></li><li><p>Changes to T wave can cause T wave oversensing</p></li><li><p>Rate appears double</p></li><li><p>Change sensing vector</p></li></ul></li></ul><p></p>
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Ashman Phenomenon

Aberrant ventricular conduction due to changes in QRS cycle length

  • Associated with AF: irregularly irregular conduction

  • Long-short rule: the earlier in the cycle the PAC occurs and the longer the preceding cycle, the more likely the PAC will be conducted aberrantly

<p><strong>Aberrant ventricular conduction due to changes in QRS cycle length</strong></p><ul><li><p>Associated with AF: irregularly irregular conduction</p></li><li><p><strong>Long-short rule</strong>: the earlier in the cycle the PAC occurs and the longer the preceding cycle, the more likely the PAC will be conducted aberrantly</p></li></ul><p></p>
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Rhythm Differentiation

  • VT, SVT with aberrancy, or antidromic AVRT?

  • 12 lead: AV relationship, axis, R wave progression, durations

  • EGMs: more difficult

    • Don't assume one or the other

    • Physician may want additional testing

<ul><li><p>VT, SVT with aberrancy, or antidromic AVRT?</p></li><li><p>12 lead: AV relationship, axis, R wave progression, durations</p></li><li><p>EGMs: more difficult</p><ul><li><p>Don't assume one or the other</p></li><li><p>Physician may want additional testing</p></li></ul></li></ul><p></p>
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Rhythm vs. Rate Control

  • Rhythm control:

    • Prevent arrhythmias

    • Terminate arrhythmias

    • Restore normal sinus rhythm

  • Rate control:

    • Slow conduction through the AV node

    • Reduce ventricular rate during supraventricular arrhythmias

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Mechanisms of Tachycardia

Antiarrhythmics target different mechanisms: most commonly reentrant circuit by altering conductivity/refractoriness

  • Reentry: electrical impulse caught in self-propagating loop

  • Abnormal automaticity: non-pacemaker cells display automaticity

  • Triggered activity: afterdepolarizations trigger new action potential

<p>Antiarrhythmics target different mechanisms: most commonly reentrant circuit by altering conductivity/refractoriness</p><ul><li><p>Reentry: electrical impulse caught in self-propagating loop</p></li><li><p>Abnormal automaticity: non-pacemaker cells display automaticity</p></li><li><p>Triggered activity: afterdepolarizations trigger new action potential</p></li></ul><p></p>
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Antiarrhythmic Actions

  • Phase 0: increase/decrease conduction velocity

  • Phase 3: change duration of ERP

  • Phase 4: suppress abnormal automaticity and triggered activity

  • Autonomic tone: chronotropy, inotropy, dromotropy

<ul><li><p>Phase 0: increase/decrease conduction velocity</p></li><li><p>Phase 3: change duration of ERP</p></li><li><p>Phase 4: suppress abnormal automaticity and triggered activity</p></li><li><p>Autonomic tone: chronotropy, inotropy, dromotropy</p></li></ul><p></p>
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Vaughan-Williams Classification

  • Class I: sodium channel blockers

  • Class II: beta blockers

  • Class III: potassium channel blockers

  • Class IV: calcium channel blockers

  • Class V: parasympathetic stimulation

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Class I: Sodium Channel Blockers

Divided into three subclasses:

  • Class IA: moderate influence on phase 0

  • Slow conduction velocity

  • Prolong repolarization

  • Extend AP duration

  • Procainamide, quinidine, disopyramide

  • Risk of Torsades de Pointes, GI upset, enhanced AV conduction, hypotension

  • Class IB: weak influence on phase 0

  • Little impact on conduction velocity

  • Shorten repolarization

  • Decrease AP duration

  • Lidocaine, mexiletine, phenytoin, tocainide

Class IC: strong influence on phase 0

  • Repolarization unchanged

  • No effect on AP duration

  • Slow conduction to break or prevent arrhythmias

  • Flecainide, propafenone, encainide, moricizine

<p>Divided into three subclasses:</p><ul><li><p><strong>Class IA: moderate influence on phase 0</strong></p></li><li><p>Slow conduction velocity</p></li><li><p>Prolong repolarization</p></li><li><p>Extend AP duration</p></li><li><p>Procainamide, quinidine, disopyramide</p></li><li><p>Risk of Torsades de Pointes, GI upset, enhanced AV conduction, hypotension</p></li></ul><p></p><ul><li><p><strong>Class IB: weak influence on phase 0</strong></p></li><li><p>Little impact on conduction velocity</p></li><li><p>Shorten repolarization</p></li><li><p>Decrease AP duration</p></li><li><p>Lidocaine, mexiletine, phenytoin, tocainide</p></li></ul><p></p><p><strong>Class IC: strong influence on phase 0</strong></p><ul><li><p>Repolarization unchanged</p></li><li><p>No effect on AP duration</p></li><li><p>Slow conduction to break or prevent arrhythmias</p></li><li><p>Flecainide, propafenone, encainide, moricizine</p></li></ul><p></p>
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Class IC Risks

  • Flecainide: contraindicated for CAD/SHD patients

  • Flecainide/propafenone: VT, CHF, enhanced AV conduction

  • Flecainide: most documented impact on pacing thresholds

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Classes Subclasses Explained

Class 1a: A affects all

Class 1b: B brings the Back end in

Class 1c: C changes conduction and capture

<p>Class 1a: A affects all</p><p>Class 1b: B brings the Back end in</p><p>Class 1c: C changes conduction and capture</p>
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Class II: Beta Blockers

  • Decrease sympathetic tone

  • Block myocardial beta-adrenergic receptors

  • Prevent binding of norepinephrine/epinephrine

  • Impact SA node, AV node, blood pressure

  • "Lol" drugs: esmolol, metoprolol, propranolol...

<ul><li><p><strong>Decrease sympathetic tone</strong></p></li><li><p>Block myocardial beta-adrenergic receptors</p></li><li><p>Prevent binding of norepinephrine/epinephrine</p></li><li><p>Impact SA node, AV node, blood pressure</p></li><li><p>"Lol" drugs: esmolol, metoprolol, propranolol...</p></li></ul><p></p>
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Class III: Potassium Channel Blockers

  • Prolong repolarization

  • Increase AP duration

  • Longer refractory periods, no effect on conduction velocity

  • Blocks reentry

  • Amiodarone, sotalol, dronedarone, ibutilide, dofetilide

<ul><li><p><strong>Prolong repolarization</strong></p></li><li><p>Increase AP duration</p></li><li><p>Longer refractory periods, no effect on conduction velocity</p></li><li><p>Blocks reentry</p></li><li><p>Amiodarone, sotalol, dronedarone, ibutilide, dofetilide</p></li></ul><p></p>
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Class III Risks

  • Lengthen QT interval: risk of Torsades de Pointes

  • Monitor during initial dosing

  • Sotalol: Torsades, CHF, bradycardia, bronchospasms, lowers DFTs

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Aminodarone

  • Low risk of Torsades

  • Most commonly used antiarrhythmic

    • Stable monomorphic VT

    • Hemodynamically unstable AF

    • AF refractory to electrical cardioversion

  • Cross-class characteristics

  • Side effects: lung toxicity, pulmonary fibrosis, hepatic upset, vision problems, hyperthyroidism, neurologic toxicity, blue-gray skin, AV block, hypotension, GI upset, bradycardia, photosensitivity, arrhythmias, death

  • Raises DFTs

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Class IV: Calcium Channel Blockers

  • Influence SA and AV nodes

  • Affect transition from phase 4 to phase 0 of slow AP

  • Depress automaticity

  • Slow heart rate

  • Decrease contractility

  • Diltiazem, verapamil

<ul><li><p>Influence SA and AV nodes</p></li><li><p><strong>Affect transition from phase 4 to phase 0 of slow AP</strong></p></li><li><p>Depress automaticity</p></li><li><p>Slow heart rate</p></li><li><p>Decrease contractility</p></li><li><p>Diltiazem, verapamil</p></li></ul><p></p>
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Class V: Parasympathetic Stimulation

  • Increased parasympathetic stimulation

  • Similar effect to beta blockers

  • Rhythm and rate control

  • Digitalis/digoxin, adenosine, magnesium sulfate

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Digitalis

  • Activates vagal nerves

  • Slows signals from SA node

  • Slows AV conduction

  • Prolongs AV node refractory period

  • Positive inotrope: used to treat heart failure

  • Toxicity: nausea/vomiting, neurological effects, tachyarrhythmia

<ul><li><p>Activates vagal nerves</p></li><li><p>Slows signals from SA node</p></li><li><p>Slows AV conduction</p></li><li><p>Prolongs AV node refractory period</p></li><li><p><strong>Positive inotrope: used to treat heart failure</strong></p></li><li><p>Toxicity: nausea/vomiting, neurological effects, tachyarrhythmia</p></li></ul><p></p>
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Adenosine

  • Transient depression of SA node and AV node

  • Temporary AV nodal block

  • Cardioversion of AV nodal dependent SVTs (AVRT, AVNRT)

  • Diagnosis of non AV nodal dependent SVTs (AT, AFlutter)

<ul><li><p>Transient depression of SA node and AV node</p></li><li><p>Temporary AV nodal block</p></li><li><p><strong>Cardioversion of AV nodal dependent SVTs (AVRT, AVNRT)</strong></p></li><li><p>Diagnosis of non AV nodal dependent SVTs (AT, AFlutter)</p></li></ul><p></p>
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Antiarrythmics Drawbacks

  • Only moderately effective:

    • 40-50% during initial usage

    • 30% during prolonged usage

    • 10% discontinue due to side effects

  • Many physicians seek nonpharmacologic treatments

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Antiarrhythmics Effect on CIEDs

  • AF burden

  • PVC count

  • Episodes

  • Beta blockers: brady indication

  • Flecainide: increased pacing thresholds

  • Amiodarone: increased DFTs