maka not on pacemakers or intracardiac devices from base to top at a cardiology residency or DM level

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Pacemakers and Intracardiac Devices

Cardiology Residency / DM Level Notes


1. CLASSIFICATION OF CARDIAC IMPLANTABLE ELECTRICAL DEVICES (CIEDs)

CIEDs deliver therapeutic electrical stimuli and encompass:
DeviceStimulus typePrimary purpose
Permanent pacemaker (PPM)Low voltage (1-5 V) pacing pulsesBradycardia
Implantable Cardioverter-Defibrillator (ICD)High voltage (500-1400 V) shocks + pacingVF/VT termination + backup pacing
CRT-P (biventricular pacemaker)LV + RV pacing pulsesCardiac resynchronization in HF
CRT-D (biventricular ICD)Same as above + defibrillationResynchronization + SCD prevention
Leadless pacemakerIntracardiac capsule, no leadSingle-chamber pacing, no pocket
Subcutaneous ICD (S-ICD)Subcutaneous coil + electrodeVF/VT termination without intravascular lead
Loop recorder (ILR)Passive sensing onlyLong-term arrhythmia monitoring
Source: Braunwald's Heart Disease, Chapter 69 (Mina K. Chung & James P. Daubert)

2. ANATOMY OF A PACING SYSTEM

Pulse Generator (PG)

  • Contains battery (lithium iodide; ~5-12 years lifespan) + circuitry
  • "End of life" (EOL) signaled by pacing rate or magnet response change (typically rate-responsive or VOO/DOO switch)
  • Programmable via telemetry (radiofrequency wand or Bluetooth)

Lead System

  • 1-3 leads depending on device type
  • Lead body: conducting wires + insulating material (polyurethane or silicone)
  • Fixation mechanisms:
    • Active fixation: extendable/retractable screw (helical tip) - can be placed anywhere, used in atrium, septum, His bundle, LV epicardium
    • Passive fixation: tines/fins (rely on trabecular entrapment) - most common in RV apex
  • Lead polarity:
    • Unipolar: distal tip (cathode) to generator can (anode) - larger pacing spike, more susceptible to EMI
    • Bipolar: distal tip (cathode) to proximal ring electrode (anode) - smaller spike, less EMI susceptibility

Electrode-Tissue Interface

  • Cathodal stimulation used for pacing (distal electrode = cathode)
  • Strength-duration curve: relates pulse voltage/current to pulse duration for capture
    • Rheobase: minimum voltage at infinitely long pulse duration (~1.5-2.0 msec)
    • Chronaxie: pulse duration at which threshold = 2x rheobase - this is the most energy-efficient pacing point
    • Energy formula: J = V²t(1/R), so optimizing near chronaxie balances safety and battery longevity
  • Pacing threshold increases transiently after implantation (acute injury from active fixation), peaks at ~1-2 weeks, then falls ("maturation")
  • Output typically programmed at 2x threshold voltage to maintain adequate safety margin

3. NASPE/BPEG PACEMAKER CODE (NBD CODE)

PositionIIIIIIIVV
MeaningChamber PacedChamber SensedResponse to SensingRate ModulationMultisite Pacing
OptionsO, A, V, DO, A, V, DO, T, I, DO, RO, A, V, D
  • O = None; A = Atrium; V = Ventricle; D = Dual (A+V)
  • T = Triggered; I = Inhibited; D = Dual (T+I)
  • R = Rate responsive
Common modes explained:
ModeMeaningWhen used
VVIVentricular pacing, ventricular sensing, inhibitedAF with bradycardia, single-chamber backup
VVIRAbove + rate adaptiveAF with chronotropic incompetence
DDDBoth paced/sensed, inhibited + triggeredNormal sinus rhythm, AV block
DDDRDDD + rate adaptiveSSS/AV block with activity
AAIAtrial pacing, atrial sensing, inhibitedSSS with intact AV conduction
VOO/DOOAsynchronous - no sensingMagnet application; EMI-prone setting
DDIDual sensing/pacing, inhibited only (no tracking)AF prevention when atrial tracking would be unsafe

DDD Timing Cycles (Key)

  • AV delay (AVD): interval from atrial event to ventricular pacing (analog of PR interval)
  • Lower Rate Interval (LRI): max interval between paced beats = 60,000/LRL (msec)
  • Upper Rate Limit (URL): maximum tracking rate to prevent 1:1 atrial tracking at fast sinus rates
  • PVARP (Post-Ventricular Atrial Refractory Period): atrial channel blanked after V event - prevents sensing retrograde P waves as pacemaker-mediated tachycardia (PMT)
  • TARP = AVD + PVARP: Total Atrial Refractory Period - sets Wenckebach upper rate behavior
  • Rate-responsive AV delay: shortens AVD at faster rates to mimic physiology
  • Safety pacing: if crosstalk (atrial pulse sensed on ventricular channel), device paces ventricle ~100 ms after atrial pacing to prevent inhibition

4. SENSING AND CAPTURE PHYSIOLOGY

Capture

  • Successful depolarization of myocardium by pacing stimulus
  • Loss of capture on ECG: pacing spike not followed by P or QRS
  • Common causes: lead dislodgment, exit block (elevated threshold due to fibrosis, electrolyte abnormalities, drugs like flecainide/amiodarone), lead fracture, output programmed too low, battery depletion

Sensing

  • Device detects intrinsic cardiac activity via EGM (intracardiac electrogram)
  • Oversensing: device "sees" signals it should not (T waves, far-field R waves, myopotentials, EMI) - results in inappropriate inhibition of pacing (dangerous in pacing-dependent patients) or inappropriate ICD shocks
  • Undersensing: device fails to detect intrinsic events - results in asynchronous pacing (competitive rhythm risk), loss of rate-responsive behavior
  • Sensitivity setting is a voltage threshold: lower number = more sensitive (detects smaller signals)

5. RATE-RESPONSIVE PACING

  • Addresses chronotropic incompetence (heart rate fails to rise appropriately with exertion)
  • Sensors used:
    • Accelerometer (piezoelectric): detects body movement/vibration - most common
    • Minute ventilation: detects thoracic impedance changes with breathing
    • QT interval sensor: QT shortens with sympathetic stimulation
    • Dual-sensor devices combine above for more physiologic response
  • DDDR or VVIR modes; sensor gain/slope programmable

6. HEMODYNAMIC ASPECTS OF PACING

  • AV synchrony: atrial kick contributes ~20-30% of cardiac output; loss (ventricular pacing without atrial synchrony) reduces CO, raises atrial pressure -> "pacemaker syndrome" (retrograde VA conduction, neck vein pulsations, dizziness, dyspnea)
  • Pacing site matters:
    • RV apical pacing: causes dyssynchronous contraction (LBBB pattern) -> adverse remodeling over time, can cause pacing-induced cardiomyopathy
    • RV outflow tract (RVOT) / septal pacing: more physiologic
    • His bundle pacing (HBP): activates the native conduction system -> narrow QRS, most physiologic; technically challenging, higher thresholds
    • Left bundle branch area pacing (LBBAP): emerging technique, more reliable capture than HBP, captures LBB or LBB fascicles deep in septum

7. INDICATIONS FOR PERMANENT PACEMAKERS

Class I (Symptomatic Bradycardia / High-Degree Block)

Sinus Node Dysfunction (SND / SSS):
  • Symptomatic sinus bradycardia (including drug-induced when no alternative exists)
  • Symptomatic chronotropic incompetence
  • Symptomatic sinus pauses
  • Tachycardia-bradycardia syndrome with symptomatic bradycardia
AV Block:
  • Third-degree (complete) AV block - regardless of symptoms if rate <40 bpm or escape rhythm unreliable
  • Second-degree Mobitz II AV block - block below His, high risk of progression to complete block
  • Advanced second-degree block (2:1 or higher) with symptoms
  • Symptomatic second-degree Mobitz I (Wenckebach) - less common, usually AV nodal
  • Complete AV block after acute MI persisting >5-7 days
Bundle Branch Block / Bifascicular block:
  • Alternating LBBB and RBBB
  • RBBB + LAFB or LPFB with syncope when EP study shows HV ≥100 ms or infra-His block
Post-ablation:
  • Permanent AV block after AV node ablation
Hypersensitive Carotid Sinus Syndrome:
  • Symptomatic cardioinhibitory carotid sinus hypersensitivity (asystole >3 sec with symptoms)
Neurocardiogenic Syncope:
  • Recurrent reflex syncope with documented pauses (DDI or DDD with hysteresis)
Guidelines: 2018 ACC/AHA/HRS Guideline on Bradycardia and Cardiac Conduction Delay (Kusumoto FM et al., Circulation 2019)

8. PACEMAKER TROUBLESHOOTING

Failure to Pace (No Output)

  • Lead fracture, connector pin problem, oversensing (inhibition), battery depletion, "safety switch" to ERI mode

Loss of Capture (Output but No Response)

  • Lead dislodgment, elevated threshold (drug effect: flecainide, amiodarone; metabolic: hyperkalemia, hypothyroidism; fibrosis), output too low, insulation break

Oversensing

  • Causes: T-wave oversensing, far-field R-wave sensing (atrial channel sensing ventricular events), myopotentials (pectoral muscle in unipolar), EMI
  • Consequence: inappropriate pacing inhibition (if pacer dependent = syncope); inappropriate ICD shock
  • Fix: decrease sensitivity (raise threshold), switch to bipolar, reprogram refractory periods

Undersensing

  • Causes: inadequate EGM amplitude (scar, dislodgment), inappropriate sensitivity setting, intrinsic signal timing within blanking period
  • Consequence: competitive pacing, loss of inhibition, potential R-on-T phenomenon

Pacemaker-Mediated Tachycardia (PMT)

  • Mechanism: retrograde VA conduction after ventricular pacing -> retrograde P wave sensed outside PVARP -> triggers another V pace -> loop
  • Rate: upper tracking rate
  • Termination: magnet (asynchronous pacing), lengthen PVARP, enable PMT termination algorithm (most modern devices)

Pacemaker Syndrome

  • Retrograde VA conduction with VVI pacing -> no AV synchrony -> low CO, cannon A waves, dyspnea, dizziness
  • Treatment: upgrade to dual-chamber system

Runaway Pacemaker

  • Rare; device malfunction causing very rapid pacing (>200 bpm); battery end-of-life or component failure
  • Emergency: magnet application, device re-programming or emergent explant

9. IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS (ICDs)

Device Types

  1. Transvenous ICD (TV-ICD): lead in RV (sensing/pacing + shocking coil), ± SVC coil; generator in left pectoral pocket
    • Single-chamber (VR): RV only
    • Dual-chamber (DR): RA + RV leads - better discrimination of SVT vs VT
    • CRT-D: RA + RV + LV (CS) leads
  2. Subcutaneous ICD (S-ICD): no intravascular lead; generator at left axilla; subcutaneous coil + sensing electrode along sternum
    • Advantages: avoids transvenous lead complications; for patients with no pacing/CRT need
    • Disadvantages: no antibradycardia pacing, no ATP, larger device, inappropriate shocks from T-wave oversensing
  3. Extravascular ICD (EV-ICD, e.g., EMPOWER): lead tunneled substernally (no intravascular), generator left pectoral; can provide ATP
  4. Wearable cardioverter-defibrillator (WCD): external vest; temporary protection while deciding on ICD or bridge during waiting period (e.g., newly diagnosed LV dysfunction)

Shock Waveform

  • Biphasic waveform: 500-1400 V; reverses polarity mid-shock - reduces defibrillation energy requirement by ~30% vs monophasic
  • Defibrillation threshold (DFT): tested at implant (or not, as per contemporary practice); safety margin typically ≥10 J below maximum device output

ICD Therapies

  1. Antitachycardia Pacing (ATP): sequence of rapid pacing pulses (burst or ramp) to terminate VT without a shock - effective in up to 90% of VTs <250 bpm; painless; first-line therapy for VT
  2. Low-energy cardioversion: synchronized shock at lower energy; for organized VT
  3. High-energy shock: defibrillation; for VF or failed cardioversion
  4. Antibradycardia pacing: backup pacing (post-shock asystole, drug-induced bradycardia)

Detection Zones

  • VF zone (typically >200-220 bpm): shock therapy
  • VT zone (typically 150-200 bpm): ATP first, then shock if ATP fails
  • VT monitor zone (optional): detection + recording only, no therapy
  • Detection enhancements (SVT-VT discrimination):
    • Onset: sudden onset favors VT; gradual onset favors SVT
    • Stability: irregular RR intervals favor AF
    • Morphology: EGM morphology compared to template
    • AV relationship (dual-chamber): VA dissociation confirms VT

10. INDICATIONS FOR ICD IMPLANTATION

Secondary Prevention (post VF/VT arrest - strongest evidence)

  • Survivors of cardiac arrest from VF or hemodynamically unstable VT not due to reversible causes
  • Sustained VT with structural heart disease
  • Meta-analysis: ICD vs amiodarone -> 50% reduction in arrhythmic death, 25% reduction in all-cause mortality

Primary Prevention

Ischemic cardiomyopathy:
  • MADIT-I / MADIT-II / SCD-HeFT trials established benefit
  • SCD-HeFT: EF ≤35%, NYHA II-III, optimal medical therapy -> amiodarone vs ICD vs placebo; ICD reduced all-cause mortality 23% vs placebo
  • MADIT-II: post-MI, EF ≤30% -> ICD reduced mortality 31%
  • Guideline: ICD for LVEF ≤35%, NYHA II-III, ischemic cardiomyopathy, on optimal medical therapy ≥3 months, expected survival >1 year with good functional status
Non-ischemic cardiomyopathy:
  • DEFINITE, SCD-HeFT: benefit also shown in NICM with EF ≤35%, NYHA II-III
  • DANISH trial (2016): ICD vs control in NICM - no significant reduction in all-cause mortality (HR 0.87, p=0.28), though significant reduction in SCD; contemporary HF therapy may have diluted benefit
  • Still indicated by guidelines for NICM, EF ≤35%, NYHA II-III after ≥3 months optimal therapy
Specific cardiomyopathies:
  • HCM: ICD for aborted cardiac arrest, spontaneous sustained VT, ≥2 major SCD risk factors (FHx SCD, NSVT, syncope, LV wall thickness ≥30 mm, abnormal BP response to exercise)
  • Arrhythmogenic right ventricular cardiomyopathy (ARVC): ICD for aborted arrest, sustained VT; consider for high-risk features
  • Brugada syndrome: ICD for aborted VF/VT; quinidine as adjunct; high-risk features (spontaneous type 1 pattern + syncope)
  • Long QT syndrome: ICD if aborted arrest or VT on beta-blockers; beta-blockers first line
  • Catecholaminergic polymorphic VT (CPVT): nadolol/flecainide first; ICD if VT/VF on therapy
  • Sarcoidosis with cardiac involvement: ICD often indicated with EF <35% or significant conduction disease
  • Chagas disease: ICD for VT/VF, high-risk features
Guideline threshold for primary prevention:
  • EF ≤35% after 3 months optimal medical therapy (regardless of etiology in most guidelines)
  • Note: Waiting period is critical - LVEF must be reassessed after 3-6 months of GDMT; early ICD implantation post-MI (within 40 days) has NOT shown benefit (DINAMIT trial)

11. CARDIAC RESYNCHRONIZATION THERAPY (CRT)

Mechanism

  • Patients with LBBB (or wide QRS) have dyssynchronous LV contraction (late lateral wall activation) -> reduced LV efficiency
  • CRT paces RV + LV simultaneously (biventricular pacing) to restore synchrony -> improved stroke volume, reduced MR, reverse remodeling over time

Indications (Class I)

  • LVEF ≤35% + LBBB morphology + QRS ≥150 ms + NYHA II-IV + on GDMT ≥3 months
  • NYHA II on GDMT: CRT-D (ICD + CRT) - MADIT-CRT, RAFT trials
  • NYHA III-IV: CRT-P or CRT-D - CARE-HF, COMPANION trials

Key Trials

TrialPopulationResult
CARE-HFNYHA III-IV, EF≤35%, QRS≥120msCRT reduced mortality 36%; CRT-P non-inferior to CRT-D for mortality
COMPANIONNYHA III-IV, EF≤35%, QRS≥120msCRT-P reduced HF hospitalization + death; CRT-D best
MADIT-CRTNYHA I-II, EF≤30%, QRS≥130msCRT-D reduced HF events 41% vs ICD alone; LBBB benefited most
RAFTNYHA II-III, EF≤30%, QRS≥120msCRT-D reduced death + HF hospitalization vs ICD
ECHO-CRTNYHA III-IV, EF≤35%, narrow QRS (<130ms)CRT harmful - increased mortality
Key teaching point: CRT is harmful in narrow QRS (<130 ms). QRS morphology matters: LBBB gets greatest benefit; RBBB/non-specific IVCD benefit is uncertain.

LV Lead Placement

  • LV lead placed via coronary sinus into a lateral or posterolateral branch
  • Problem in ~5-10%: cannot reach ideal vein; alternatives include surgical epicardial lead, LV endocardial pacing
  • Adequate biventricular pacing: must achieve >98% BiV pacing for optimal benefit

AV Node Ablation + CRT

  • When AF + rapid ventricular rate cannot be controlled medically and CRT device is implanted, AV node ablation ensures 100% biventricular pacing
  • Rate control alone + CRT: underperforms ablation + CRT in patients needing full resynchronization

12. LEADLESS AND NOVEL DEVICES

Leadless Pacemaker (Micra, Aveir)

  • Capsule implanted directly into RV via femoral venous approach; no subcutaneous pocket, no transvenous lead
  • Single-chamber: Micra VR (VVIR) - for AF + bradycardia
  • Dual-chamber: Micra AV (VDDR) - uses mechanical sensing of atrial contraction to trigger ventricular pacing; Aveir DR - two separate communicating capsules
  • Complications: cardiac perforation/tamponade (~1.5%), device embolization, vascular access issues; retrieval is possible but challenging
  • Advantages: no pocket (no pocket hematoma/infection), no lead (no lead failure)

Subcutaneous ICD (S-ICD) - Boston Scientific EMBLEM

  • No intravascular component; entirely subcutaneous
  • Sensing via 3 sensing vectors from subcutaneous electrode
  • Pre-implant screening ECG mandatory (SENSE screening) to ensure adequate T:R ratio to avoid T-wave oversensing
  • Cannot deliver ATP or chronic pacing - not suitable for pacing-dependent patients, VT requiring ATP, or patients needing CRT
  • Particularly preferred in: young patients (preserve vasculature), prior TV-ICD lead infections, no pacing need

Extravascular ICD (EV-ICD)

  • Lead tunneled under sternum; generator left pectorally
  • Combines benefits of S-ICD (no intravascular) with ability to deliver ATP
  • Emerging technology (EFFORTLESS EV-ICD registry)

Conduction System Pacing (CSP)

  • His bundle pacing (HBP): electrode placed at His bundle; corrects LBBB by capturing native conduction; narrow QRS
    • Challenges: higher threshold, risk of lead dislodgment, sensing issues
  • Left bundle branch area pacing (LBBAP) / Left bundle branch pacing (LBBP): electrode screwed deep into interventricular septum to capture LBB directly
    • More stable, lower thresholds than HBP, corrects LBBB
    • Increasingly used as alternative to biventricular CRT (CSP-CRT or His-optimized CRT)
    • LBBP-RESYNC trial: ongoing evaluation vs BVP-CRT

13. COMPLICATIONS OF CIEDs

Procedural

ComplicationNotes
Pneumothorax~1-2%; subclavian access > axillary > cephalic approach
HemothoraxVascular injury; may require drainage
Cardiac perforation/tamponade~0.5-1%; right ventricular perforation; presents with pleuritic pain, effusion
Lead dislodgmentEarly (within 24 hrs): most common with atrial lead; Late: fibrosis makes re-positioning difficult
Arterial punctureInadvertent subclavian artery; direct pressure or surgical repair
Air embolismVenous air entry via dilator; patient Trendelenburg, aspiration
Diaphragmatic pacingLV (CS) lead proximity to phrenic nerve; re-position or reduce output

Long-term

ComplicationManagement
CIED infectionMost serious; involves pocket or leads; TEE to rule out lead vegetation; explant entire system; IV antibiotics 6 weeks; reimplant on contralateral side after 72h negative cultures (if pacing-dependent, temporary pacing bridge)
Pocket hematomaDAPT/anticoagulation related; drain only if expanding/infected; avoid early drainage (increases infection risk)
Lead failureInsulation breach (impedance fall) or conductor fracture (impedance rise); oversensing / undersensing pattern; manage with lead abandonment + new lead
Subclavian crush syndromeLead fracture at clavicle-rib junction; switch to axillary vein approach
Twiddler's syndromePatient manipulates generator -> lead rotation -> dislodgment, retraction
Venous thrombosisSubclavian/axillary/SVC; anticoagulation if symptomatic; SVC syndrome rare
Tricuspid regurgitationRV lead interference with TV leaflet; mechanism: impingement, adhesion, perforation

14. ELECTROMAGNETIC INTERFERENCE (EMI)

SourceRiskManagement
MRIMost CIEDs are now MRI-conditional (specific programming required)Programme to asynchronous mode (VOO/DOO); turn off tachyarrhythmia detection; 1.5T preferred; cardiologist + MRI team coordination
Electrosurgery (cautery)Oversensing -> inhibition or inappropriate shockProgram to asynchronous/suspend detection; use bipolar cautery when possible; donut/ring magnet over ICD inhibits detection during case
External defibrillationCan damage CIED; defibrillator pads placed as far from device as possible (anterior-posterior preferred)Check device post-shock
LithotripsyInhibition/shocks; trigger off R-waveSuspend ICD detection; lithotripter focus away from device
RadiotherapyCumulative radiation damage to CIED circuitryReposition device if in field; frequent device checks during treatment
Mobile phones, airport securityVery low risk with current devicesMaintain 15-cm separation from phone; walk through security without dwelling
Magnet behavior:
  • Over a pacemaker: applies asynchronous (VOO/DOO) pacing at magnet rate (~85 bpm typically; manufacturer-specific) - prevents oversensing inhibition
  • Over an ICD: suspends tachyarrhythmia detection (no shock); does NOT change pacing mode

15. ICD TROUBLESHOOTING

Appropriate Shocks

  • Delivery of shock for true VT/VF - desired
  • If recurrent: optimize anti-arrhythmic drugs (amiodarone, sotalol, mexiletine), catheter ablation for scar-related VT, reassess reversible causes

Inappropriate Shocks (IS)

  • Definition: ICD shock delivered for non-VT/VF rhythm
  • Most common cause: AF with rapid ventricular rate (most frequent overall), T-wave oversensing, SVT, lead fracture/noise
  • T-wave oversensing: more common with S-ICD; manage by adjusting sensing vectors, programming sensitivity
  • Lead noise (fracture): large-amplitude, non-physiologic signals; seen as very short RR intervals on EGM; reprogramming or lead replacement
  • Consequence of IS: significant psychological distress, possible proarrhythmia (shock on vulnerable period), increased mortality in some analyses
  • Management of IS: identify and eliminate cause; antiarrhythmics for AF; shock reduction algorithms; S-ICD screening

VT Storm

  • 3 separate episodes of VT requiring ICD intervention within 24 hours
  • Management:
    1. Correct reversible causes (ischemia, electrolytes, drugs)
    2. Amiodarone IV (150 mg bolus, then infusion)
    3. Beta-blockers IV (metoprolol, propranolol)
    4. Deep sedation (reduces sympathetic tone)
    5. Catheter ablation (urgent if storm persists)
    6. Temporary overdrive pacing if bradycardia-dependent VT
    7. Mechanical circulatory support (IABP, Impella) for cardiogenic shock

Failure to Shock / Detect VF

  • VF within detection programming (confirm detection turned ON)
  • Oversensing causing double-counting (VF detection criteria reached falsely); undersensing of VF
  • Elevated DFT (drug effect: amiodarone increases DFT; hypothyroidism)
  • Lead fracture, connector issue

16. REMOTE MONITORING

  • All modern CIEDs transmit data wirelessly to a base station (home monitor) -> manufacturer server -> clinician portal
  • Allows detection of: arrhythmias, lead problems (impedance change), battery status, fluid status (intrathoracic impedance as proxy for pulmonary congestion)
  • IN-TIME, CONNECT, TRUST trials: remote monitoring reduces mortality and hospitalization
  • Standard of care: remote monitoring + in-office device checks every 6-12 months

17. SPECIAL SITUATIONS

CIED in Pregnancy

  • Pacing is safe; lead implantation during pregnancy if urgently needed (use echocardiographic guidance to reduce radiation)
  • ICDs can deliver shocks safely to fetus without harm at standard energies

Perioperative CIED Management

  • If pacing-dependent: reprogram to asynchronous mode pre-op; have external pacing/defibrillation available
  • ICD detection: suspend via magnet or reprogramming; ensure magnet available throughout case
  • Postoperatively: restore original settings; check device interrogation

End of Life / CIED Deactivation

  • Ethically permissible to deactivate ICD at patient/family request (avoiding unwanted shocks at end of life)
  • Pacemaker deactivation more complex (patient may be pacemaker-dependent)
  • Requires advance care planning; palliative care team involvement

CIED Extraction (Transvenous Lead Removal - TLE)

  • Indications: infection (Class I), lead malfunction affecting clinical management, lead recalled for safety
  • Techniques: simple traction, locking stylets, laser sheaths (Spectranetics), mechanical dilator sheaths, femoral workstation
  • Risks: vascular/cardiac tear (~1% major complications at high-volume centers), hemothorax, tamponade; requires cardiac surgical backup

18. KEY EXAM/CLINICAL PEARLS

PointDetail
Wenckebach (Mobitz I) siteUsually AV node; QRS narrow; usually benign; Atropine helps
Mobitz II siteBelow His bundle (His-Purkinje); wide QRS; pacemaker mandatory
Complete heart block with wide escapeInfranodal; unreliable; pacemaker urgently
2018 guidelines landmarkBradycardia: Kusumoto et al., Circulation 2019
Waiting 40 days post-MI for ICDDINAMIT showed no benefit from early ICD (day 6-40 post-MI)
S-ICD prerequisiteSENSE screening mandatory pre-implant
CRT harmNarrow QRS <130 ms (ECHO-CRT); always check QRS width
CRT best respondersLBBB + QRS ≥150 ms + ischemic CM + women
Most common IS causeAF with rapid rate; then T-wave oversensing
Magnet on pacemakerAsynchronous pacing at magnet rate (device-dependent, ~85 bpm)
Magnet on ICDSuspends detection only; does NOT pace asynchronously (unless also bradycardic)
PMT terminationLengthen PVARP; PMT algorithm delivers AV refractory extension
Pacemaker syndromeVVI mode + retrograde VA conduction; upgrade to DDD
Tricuspid regurgitation from leadLead removal + TV repair if severe
Most feared CIED complicationCIED infection; needs complete system removal
DFT increaseAmiodarone, hypothyroidism, hyper/hypokalemia, antiarrhythmic drugs

Sources

  • Braunwald's Heart Disease, Chapter 69 - Mina K. Chung & James P. Daubert (CIEDs)
  • Braunwald's Heart Disease, Chapter 68 (Bradyarrhythmias and Conduction Disorders)
  • Fuster and Hurst's The Heart, 15th Edition, Chapter 37 (Ventricular Arrhythmias/SCD) and Chapter 36 (AF)
  • Referenced guidelines: ACC/AHA/HRS 2018 Bradycardia Guideline; AHA/ACC/HRS 2017 VT/SCD Guideline; ESC 2021 Pacing GuidelinesThese are complete, residency/DM-level notes built from base to top. Here's a quick orientation to the structure:
The 18 sections progress logically:
  1. Device classification (what each CIED is)
  2. Hardware anatomy (PG, leads, electrodes)
  3. NBD pacing code (understand any programmed mode)
  4. Sensing & capture physics (strength-duration curve, chronaxie, threshold maturation)
  5. Rate-responsive pacing (sensors, chronotropic incompetence)
  6. Hemodynamics of pacing (AV synchrony, pacing site effects, His/LBBAP)
  7. Pacemaker indications (SND, AV block, bifascicular, hypersensitive carotid - Class I/II)
  8. Pacemaker troubleshooting (failure to pace, loss of capture, over/undersensing, PMT, runaway pacemaker)
  9. ICD types (TV-ICD, S-ICD, EV-ICD, WCD) + shock physics
  10. ICD therapy zones (ATP, cardioversion, defibrillation, detection zones)
  11. ICD indications (secondary prevention meta-analysis; primary prevention trials: MADIT, SCD-HeFT, DANISH, with key LVEF/QRS thresholds)
  12. CRT (mechanism, indications, key trials with data: CARE-HF, COMPANION, MADIT-CRT, RAFT, ECHO-CRT)
  13. Leadless, S-ICD, CSP/HBP/LBBP (emerging tech)
  14. Complications (procedural + long-term including infection management)
  15. EMI (MRI, cautery, magnet behavior)
  16. ICD troubleshooting (inappropriate shocks, VT storm algorithm)
  17. Remote monitoring, special situations (pregnancy, perioperative, end-of-life, TLE)
  18. High-yield exam pearls (table format)
All content sourced from Braunwald's Heart Disease (9th ed.) and Fuster & Hurst's The Heart (15th ed.).
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