CardiologyTier 1Disease (DEADMAN)

Cardiac arrhythmias - atrioventricular node conduction block

Description

Delay or failure of conduction from atria to ventricles.

Grades

First degree - PR >200 ms, every P conducts
Second degree
- Mobitz I (Wenckebach) - progressive PR lengthening -> dropped QRS; RR intervals shorten, pause < 2x preceding RR
- Mobitz II - constant PR, sudden dropped QRS. Usually infranodal
- 2:1 block - unclassifiable by definition (no consecutive PRs to compare); level inferred from QRS width and response to manoeuvres
- High-grade / advanced - two or more consecutive P waves fail to conduct, with some conduction preserved
Third degree (complete) - AV dissociation with atrial rate > ventricular rate and a regular escape rhythm

The clinical question is always: nodal or infranodal?

	AV nodal (proximal)	Infranodal (His-Purkinje)
Typical grade	1st degree, Mobitz I	Mobitz II, 2:1 with wide QRS, complete with wide escape
Escape	Junctional 40-60, narrow, reliable	Ventricular 20-40, wide, unreliable
Atropine / exercise	Improves	Worsens (more P waves hit a refractory His-Purkinje system)
Carotid massage / vagal	Worsens	Improves
HV interval	<55 ms	>70 ms
Prognosis	Often benign, often reversible	Progresses to asystole - pace

Epidemiology

First-degree AV block ~1-2% of adults; up to 5% over 60
Mobitz I in ~2-3% of trained athletes and commonly during sleep (high vagal tone - benign)
Complete heart block incidence rises steeply with age; median age at pacing >75
Congenital complete heart block ~1 in 20,000 live births

Aetiopathogenesis

Causes

Degenerative (commonest) - idiopathic fibrosis of the conduction system
- Lev disease (fibrocalcific, from the aortic/mitral annulus, elderly), Lenegre disease (primary conduction system sclerosis, younger)
Ischaemic
- Inferior MI (RCA -> AV nodal artery): nodal, narrow escape, vagally mediated, atropine-responsive, usually resolves in days. Often does NOT need permanent pacing
- Anterior MI: infranodal, implies extensive septal infarction, wide escape, poor prognosis, needs pacing
Drugs - beta blockers, verapamil/diltiazem, digoxin, amiodarone, ivabradine, clonidine, lithium, donepezil/pyridostigmine, ticagrelor (ventricular pauses)
Electrolyte/metabolic - hyperkalaemia, hypothyroidism, hypothermia, hypoxia, acidosis
Infiltrative/inflammatory
- *Cardiac sarcoidosis - high-grade AV block in anyone under 60 is sarcoid until excluded*
- Amyloid, haemochromatosis, myocarditis (giant cell), Lyme carditis (reversible, days-weeks), Chagas, rheumatic fever, endocarditis with aortic root abscess (new AV block in IE = abscess until proven otherwise)
Iatrogenic - TAVI (esp. self-expanding valve with pre-existing RBBB), surgical AVR, septal myectomy/alcohol ablation, AVNRT ablation, catheter trauma
Genetic/neuromuscular - LMNA (lamin A/C: conduction disease + DCM + high SCD risk - low threshold for ICD not just pacemaker), SCN5A, myotonic dystrophy type 1, Emery-Dreifuss, Kearns-Sayre
Congenital - maternal anti-Ro/anti-La (neonatal lupus)
Vagal - athletes, sleep, OSA, vomiting, suctioning, pain

Diagnosis

Clinical

Asymptomatic, fatigue, exertional intolerance, presyncope, Stokes-Adams attacks (abrupt syncope, no warning, rapid full recovery, flushing on recovery)
Complete heart block signs
- Bradycardia ~30-40, variable intensity S1
- Cannon a waves in the JVP - atrium contracts against a closed tricuspid valve
  - Also in VT with AV dissociation, junctional rhythm, and paroxysmal nodal tachycardia with retrograde atrial activation
- Wide pulse pressure, systolic hypertension, occasional systolic murmur (inc stroke volume)
First-degree block with PR >300 ms can cause "pseudo-pacemaker syndrome" - atrial contraction against a closed valve

ECG

Measure PR, QRS width, P:QRS relationship, escape rate and width
Complete block: P waves march through independently; QRS regular (irregular ventricular rhythm argues against complete block)
Look for: wide QRS, bifascicular block, delta waves, epsilon waves, ischaemia
A long rhythm strip beats a 12-lead for intermittent block

Further

Telemetry / Holter / loop recorder for intermittent block
Exercise test - block worsening with exercise = infranodal
Bloods: K+, Ca2+, Mg2+, TSH, troponin, digoxin level, Lyme serology if exposure, ACE
TTE in all; cardiac MRI / FDG-PET if sarcoid or infiltrative disease suspected
EPS with HV interval measurement where the level is uncertain, or syncope with bifascicular block

Management

A. Acute symptomatic bradycardia / haemodynamic compromise

1. Atropine 600 mcg IV, repeat to 3 mg

Works for nodal block. May paradoxically worsen infranodal block - have pacing ready

2. Isoprenaline infusion or adrenaline infusion

3. Transcutaneous pacing - bridge only, painful, needs analgesia/sedation, confirm mechanical capture (pulse, not just spikes)

4. Temporary transvenous wire

5. Specific antidotes

Beta blocker overdose: glucagon (bypasses the receptor -> adenylate cyclase), high-dose insulin-euglycaemia
CCB overdose: calcium, high-dose insulin-euglycaemia
Digoxin toxicity: digoxin-specific Fab fragments
Hyperkalaemia: IV calcium first

B. Always correct the reversible cause before implanting

Cease the offending drug, correct K+, treat hypothyroidism, treat Lyme, revascularise, treat sarcoid with immunosuppression
Inferior MI block usually resolves within 7 days - do not pace early

C. Permanent pacing

Class I - pace irrespective of symptoms

Third-degree AV block (acquired, not reversible)
Mobitz II
Advanced/high-grade second-degree block, alternating BBB
AV block persisting after TAVI or cardiac surgery
Symptomatic AV block of any grade

Not an indication

Asymptomatic first-degree block, asymptomatic Mobitz I (especially nocturnal or in athletes), reversible causes not yet corrected

Mode

Sinus rhythm -> DDD(R)
Permanent AF -> VVI(R) or leadless
EF <=40% and a high pacing burden expected -> CRT or conduction system pacing, not RV apical pacing
Suspected LMNA or cardiac sarcoid needing a pacemaker -> consider an ICD instead (high SCD risk independent of the bradycardia)

D. Congenital complete heart block

Pace if: symptoms, ventricular rate <50, wide QRS escape, prolonged pauses, ventricular dysfunction or exercise intolerance

Associations

Aortic valve disease and aortic root abscess - anatomical proximity of the conduction system to the non-coronary cusp
TAVI - pre-existing RBBB is the strongest predictor of post-procedure pacing
Cardiac sarcoidosis - AV block often the first manifestation, before cardiomyopathy
Lyme disease - fluctuating high-grade block, reverses with antibiotics; temporary pacing only
Myotonic dystrophy type 1 - progressive conduction disease; prophylactic pacing with HV >70 ms
Anti-Ro/La in pregnancy - fetal heart block, irreversible
Obstructive sleep apnoea - nocturnal high-grade block resolving with CPAP
Hyperkalaemia - any conduction abnormality, with peaked T waves and QRS widening

Natural history & complications

First-degree: long thought benign; PR >200 ms is associated with inc AF, pacemaker implantation and mortality - not entirely innocent
Mobitz I: usually benign if narrow QRS and vagally modulated; wide QRS or symptoms change the calculus
Mobitz II: unpredictable progression to complete block and asystole - the reason it is paced regardless of symptoms
Complete heart block untreated: 1-year mortality historically ~50%; pacing restores near-normal survival
Bifascicular block: progresses to complete block at only 1-2%/yr, so is not paced alone - but syncope with bifascicular block warrants EPS or empirical pacing
Post-pacing: watch for pacing-induced cardiomyopathy with high RV pacing burden, and pacemaker syndrome with VVI pacing in sinus rhythm

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