Pacemakers (know indications for)

Pacing code (NBG, positions I-V)

I Paced	II Sensed	III Response	IV Rate	V Multisite
A / V / D / O	A / V / D / O	Trigger / Inhibit / Dual / O	R = rate response	A / V / D

DDDR - dual chamber, rate responsive. Default for sinus node disease or AV block in sinus rhythm
VVIR - single ventricular lead. Permanent AF with slow ventricular response
AAI - atrial only; rarely used - AV block develops in ~1-2%/yr
DDI / DDDR with mode switch - avoids tracking atrial tachyarrhythmia
VOO/DOO (asynchronous) - magnet mode, used intra-operatively with diathermy

Transvenous single/dual chamber
Leadless (Micra) - self-contained RV device; no pocket or leads; VVI(R), or AV-synchronous variants; for AF with slow VR, or no venous access
Epicardial - post-surgical, paediatric, no venous access
Temporary: transvenous wire, transcutaneous pads (bridge only, painful), isoprenaline infusion

~600-800 implants per million population per year in Australia; rising with age
Median age at implant >75 yr
Commonest indications: AV block and sinus node dysfunction (roughly equal)

Idiopathic fibrosis - Lev (fibrosis of conduction system) and Lenegre disease. Commonest
Ischaemic - inferior MI (AV nodal, usually transient, vagally mediated, atropine-responsive) vs anterior MI (infranodal, extensive infarct, poor prognosis)
Drugs - beta blockers, verapamil/diltiazem, digoxin, amiodarone, ivabradine, clonidine, lithium, anticholinesterases
Infiltrative/inflammatory - cardiac sarcoid (young patient with high-grade AV block until proven otherwise), amyloid, haemochromatosis, myocarditis, Lyme, Chagas
Post-procedural - TAVI (esp. self-expanding valve, pre-existing RBBB), surgical AVR, septal ablation, AV node ablation
Congenital complete heart block - maternal anti-Ro/La
Genetic - LMNA (lamin A/C: conduction disease + DCM + high SCD risk), SCN5A, myotonic dystrophy, Emery-Dreifuss
Metabolic - hyperkalaemia, hypothyroidism, hypothermia, hypoxia
Neurally mediated - carotid sinus hypersensitivity, vasovagal

Sinus bradycardia, sinus arrest, SA exit block, chronotropic incompetence
Tachy-brady syndrome - AF alternating with post-conversion pauses
- The pause on AF termination is the usual indication

The whole decision rests on whether the bradycardia causes symptoms, except where the block itself is dangerous
Tools: ECG, telemetry, Holter, external loop, implantable loop recorder, exercise test (chronotropic incompetence), EPS (HV interval)

Drugs (the commonest reversible cause), hyperkalaemia, hypothyroidism, Lyme, ischaemia, sepsis, post-operative state, hypothermia
A pacemaker for drug-induced bradycardia in a patient who needs the drug is legitimate - but say you considered stopping it first

	AV nodal (proximal)	Infranodal (distal)
ECG	Narrow escape, Wenckebach	Wide escape, Mobitz II, 2:1 with wide QRS
Escape rate	40-60, reliable	20-40, unreliable
Atropine/exercise	Improves	Worsens
Vagal manoeuvre	Worsens	Improves
HV interval	<55 ms	>70 ms = pace
Prognosis	Benign	Progresses to complete block

A. Sinus node dysfunction

Symptomatic sinus bradycardia, sinus pauses or chronotropic incompetence with documented symptom correlation
- Asymptomatic bradycardia, however slow, is not an indication
Symptomatic tachy-brady where the drug needed for the tachycardia causes the bradycardia

B. Acquired AV block

Third-degree (complete) AV block - irrespective of symptoms
Mobitz type II second-degree AV block - irrespective of symptoms
Advanced (high-grade) second-degree block, 2:1 block with wide QRS
Alternating bundle branch block
AV block after TAVI or cardiac surgery that does not resolve
These are paced regardless of symptoms because of unpredictable progression to asystole

C. Reflex

Carotid sinus syndrome with documented cardioinhibitory response and recurrent syncope
Severe recurrent reflex syncope, age >40, with documented spontaneous asystolic pause (DDD with closed-loop stimulation)

D. AF with bradycardia

Asymptomatic first-degree AV block (unless PR >300 ms with pacemaker-syndrome-like symptoms)
Asymptomatic Mobitz I (Wenckebach), especially nocturnal or in athletes
Asymptomatic bifascicular block
Reversible causes not yet corrected
Nocturnal pauses in a young athlete or in OSA - treat the OSA

Sinus rhythm -> dual chamber (DDD(R)), with algorithms to minimise unnecessary RV pacing (RV pacing burden drives pacing-induced cardiomyopathy and AF)
Permanent AF -> VVI(R) or leadless
AV block with EF <=40% -> CRT or conduction system pacing, not RV pacing
Chronotropic incompetence -> add rate response (R)

LBBAP increasingly used for AV block needing a high pacing burden - narrow paced QRS, physiological activation
In CRT for LBBB, biventricular pacing remains the default (LEFT-BUNDLE-CRT 2026)

Diathermy: use bipolar, or magnet -> asynchronous pacing. Magnet on an ICD suspends tachy therapy but does NOT change pacing mode
MRI: modern systems are MR-conditional; needs reprogramming and monitoring
Driving restriction after implant (Austroads: 2 weeks private, 4 weeks commercial - verify current edition)

Pacemaker syndrome - AV dyssynchrony in VVI pacing; fatigue, pulsation in neck, hypotension; cannon a waves. Treat by upgrading to dual chamber
Pacing-induced cardiomyopathy - ~10-20% with high RV pacing burden; upgrade to CRT/CSP
Twiddler syndrome - patient rotates generator -> lead dislodgement
Pacemaker-mediated (endless-loop) tachycardia - retrograde VA conduction re-triggers ventricular pacing; magnet or PVARP extension terminates
T-wave oversensing / crosstalk -> inappropriate inhibition
Subclavian crush (lead fracture), venous stenosis/thrombosis
Lead infection / endocarditis -> whole-system extraction, not antibiotics alone

RV apical pacing -> LBBB pattern with left axis deviation
- A paced RBBB pattern suggests lead perforation into the LV or coronary sinus - investigate
Sgarbossa criteria for diagnosing MI in paced/LBBB rhythm
- Concordant ST elevation >=1 mm (5 pts), concordant ST depression V1-V3 (3), excessively discordant ST elevation (modified Smith: ST/S ratio <= -0.25)

Problem	ECG	Causes
Failure to capture	Spike, no complex	Lead displacement, fibrosis, high threshold, hyperkalaemia, MI, flat battery
Failure to output	No spike when expected	Oversensing, lead fracture, battery depletion
Failure to sense (undersensing)	Spikes on intrinsic beats	Lead displacement, low signal amplitude, scar
Oversensing	Inappropriate inhibition	Myopotentials, EMI, T-wave

Generator longevity 5-15 yr depending on pacing burden and output
Follow-up: in-clinic or remote monitoring - battery, thresholds, impedance, pacing burden, AF episodes (device-detected AHRE has thromboembolic implications)

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