Bradyarrhythmias and Pacemakers
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Direct answer
Bradyarrhythmias arise from sinus node dysfunction or atrioventricular conduction disease, and the first task is localisation: Mobitz I (Wenckebach) block with a narrow QRS is usually AV-nodal, often transient and managed conservatively, whereas Mobitz II and third-degree block with a wide QRS are infranodal, carry Stokes-Adams risk and need pacing. Exclude reversible causes first — rate-limiting drugs, hyperkalaemia, ischaemia (AV-nodal in inferior infarction, infranodal with poor prognosis in anterior infarction), hypothyroidism and Lyme disease. Pacemaker nomenclature (NBG code) describes the chamber paced, sensed, the response and rate modulation.
What you must remember
- ECG localisation: Mobitz I shows progressive PR prolongation before a dropped beat (usually AV-nodal, benign); Mobitz II shows sudden dropped beats without PR change (infranodal, dangerous); complete heart block shows AV dissociation with a narrow junctional escape of 40–50 beats per minute (often congenital, better tolerated) or a wide ventricular escape of 20–40 (syncope-prone).
- Pacing indications: symptomatic sinus node dysfunction including tachy-brady syndrome; Mobitz II and third-degree atrioventricular block regardless of symptoms; alternating bundle branch block; symptomatic pauses.
- Reversible causes and their acute care: withhold offending drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone); intravenous atropine 1 mg repeated — unreliable below the AV node and in transplanted hearts; transcutaneous pacing as a bridge; chronotropic infusions; glucagon for beta-blocker toxicity; calcium and insulin-dextrose for hyperkalaemia.
- Infarction context: inferior infarction causes AV-nodal block that is usually transient (atropine, temporary wire if needed); anterior infarction causes infranodal block with wide complexes — temporary pacing, frequently progressing to permanent implantation.
- NBG code: first letter — chamber paced (A, V, D); second — chamber sensed; third — response; fourth — rate modulation; in practice VVI for atrial fibrillation with slow rates, DDD for sinus rhythm, biventricular for resynchronisation.
- Device follow-up and complications: regular threshold, sensing and impedance checks; pneumothorax, lead dislodgement and pocket infection; pacemaker syndrome from VVI pacing in sinus rhythm; MRI-conditional protocols; leadless pacemakers in selected patients.
Common confusion
Physiological bradycardia is over-treated: asymptomatic pauses in trained athletes and sleep-related slowing need no device. Candidates mislabel Wenckebach as dangerous — with a narrow QRS it rarely is — while under-calling Mobitz II, which is paced regardless of symptoms. Atropine is another trap: it can worsen infranodal block by accelerating the sinus rate against a fixed distal substrate; below the node, pacing is the answer.
Exam-focused takeaway
Stems pair an ECG with a symptom and ask for disposition: asymptomatic Wenckebach (observe), syncope with wide-complex complete block (permanent pacemaker), bradycardia after inferior infarction (atropine and observation), or beta-blocker toxicity with a potassium of 7 (calcium first). NBG-code questions ask you to expand VVIR or DDD. Anchor each block type to its escape rhythm and prognosis.
Frequently asked questions
How are Mobitz I and Mobitz II blocks managed differently?
Mobitz I with a narrow QRS is usually AV-nodal and observed if asymptomatic; Mobitz II and third-degree block are infranodal and merit pacemaker implantation regardless of symptoms.
Why does atropine sometimes fail in complete heart block?
Atropine acts at the AV node; infranodal block with a wide ventricular escape does not respond and may worsen — transcutaneous or transvenous pacing is required.
What does the NBG pacemaker code describe?
Chamber paced, chamber sensed, sensing response, and rate modulation — for example, DDDR paces and senses both chambers with dual response and rate adaptation.
Which bradycardic patterns need no pacemaker?
Asymptomatic sinus bradycardia in athletes, sleep-related pauses, and asymptomatic Mobitz I with a narrow QRS.
How does infarct location predict block behaviour?
Inferior infarction produces transient AV-nodal block; anterior infarction produces infranodal, wide-complex block needing temporary then often permanent pacing.