7.2 Bradyarrhythmias, Conduction Block & Antiarrhythmic Drugs
Key Takeaways
- Mobitz II block and complete heart block are infranodal, produce an unreliable escape rhythm and are indications for permanent pacing; Mobitz I rarely needs a pacemaker.
- Amiodarone is a class III agent causing thyroid dysfunction, pulmonary fibrosis, hepatitis, corneal microdeposits and slate-grey skin, and it potentiates warfarin and digoxin.
- Flecainide is a class Ic agent contraindicated after myocardial infarction and in structural heart disease because of proarrhythmic mortality demonstrated in the CAST trial.
4. Bradyarrhythmias & Conduction Blocks
Sick Sinus Syndrome (Sinus Node Dysfunction)
Intrinsic dysfunction of the sinoatrial node, commonly due to fibrodegenerative changes in elderly individuals. Manifests as inappropriate sinus bradycardia, sinus pauses (>3 seconds), sinoatrial exit block, or the tachycardia-bradycardia syndrome (paroxysmal atrial tachyarrhythmias alternating with profound sinus pauses). Definitive management requires a permanent pacemaker (dual-chamber, DDDR) combined with antiarrhythmic/rate-controlling medication for the tachycardic episodes.
Atrioventricular (AV) Blocks
- First-Degree AV Block: Constant, prolonged PR interval >200 ms (5 small squares). Every P wave is conducted to the ventricles. Anatomical site is almost always intra-nodal. Usually benign, asymptomatic, and does not require pacing unless accompanied by bifascicular block.
- Second-Degree AV Block - Mobitz Type I (Wenckebach): Progressive PR interval prolongation from beat to beat until a single P wave fails to conduct (dropped QRS). The cycle then resets. The greatest increment in PR prolongation occurs between the first and second conducted beats of the cycle. Occurs at the level of the AV node itself. Commonly seen during high vagal tone (athletes, sleep) or in acute inferior myocardial infarction. Generally carries a benign prognosis; pacemaker is rarely indicated unless severely symptomatic.
- Second-Degree AV Block - Mobitz Type II: Constant, fixed PR intervals with intermittent, non-conducted P waves (e.g., 2:1, 3:1, or 4:1 conduction). The defect lies distal to the AV node within the His bundle or bundle branches (infranodal). Carries an ominous prognosis with high risk of sudden progression to complete heart block, syncope (Adams-Stokes attacks), and sudden cardiac death. Absolute indication for permanent pacemaker insertion, regardless of symptoms.
- Third-Degree (Complete) AV Block: Complete absence of AV conduction; atria and ventricles depolarise independently (complete AV dissociation with regular P-P intervals and regular, slower R-R intervals). If the escape rhythm originates high in the junction, QRS is narrow (40–55 bpm); if infranodal/ventricular, QRS is broad and slow (20–40 bpm). Clinical examination reveals variable intensity of the first heart sound (S1) and intermittent, prominent cannon 'a' waves in the jugular venous pulse (caused by right atrial systole against a closed tricuspid valve). Requires urgent temporary pacing followed by definitive dual-chamber permanent pacemaker insertion.
5. Vaughan-Williams Classification of Antiarrhythmic Drugs
| Class | Mechanism of Action | Exemplar Drugs | Electrophysiological Effects | Key Clinical Indications & Caveats |
|---|---|---|---|---|
| Ia | Fast Na+ channel blockade (moderate) + K+ channel blockade | Procainamide, Disopyramide, Quinidine | Prolongs action potential duration (APD) and QTc interval; slows phase 0 | Pre-excited AF, ventricular arrhythmias. Risk of Torsades de Pointes. Disopyramide has marked anticholinergic and negative inotropic effects. |
| Ib | Fast Na+ channel blockade (mild/rapid kinetics) | Lidocaine, Mexiletine | Shortens APD; preferentially binds ischaemic tissue | Acute ventricular tachyarrhythmias post-MI. Ineffective in supraventricular arrhythmias. CNS toxicity (tremor, seizures). |
| Ic | Fast Na+ channel blockade (potent, slow kinetics) | Flecainide, Propafenone | Marked slowing of conduction velocity; no effect on APD; widens QRS | Paroxysmal AF cardioversion/pill-in-the-pocket, WPW. Strictly contraindicated in ischaemic or structural heart disease (CAST trial proarrhythmia). |
| II | Competitive beta-adrenergic receptor antagonism | Bisoprolol, Metoprolol, Atenolol, Esmolol | Blunts Phase 4 spontaneous depolarisation; slows SA/AV node conduction | Rate control in AF, post-MI mortality reduction, suppression of ventricular ectopy. Contraindicated in acute decompensated heart failure, severe asthma, AV block. |
| III | Potassium channel blockade (I_Kr inhibition) | Amiodarone, Sotalol, Dronedarone | Prolongs repolarization, APD, and effective refractory period; lengthens QTc | Broad-spectrum (AF rhythm control, stable VT/VF). Amiodarone exhibits Class I–IV actions. Monitoring required: LFTs, TFTs (hypo/hyperthyroidism), CXR (pulmonary fibrosis), corneal microdeposits, slate-grey skin discoloration. |
| IV | Non-dihydropyridine L-type Ca2+ channel blockade | Verapamil, Diltiazem | Slows AV nodal conduction velocity and prolongs refractory period | Paroxysmal SVT termination, rate control in AF with preserved LVEF. Contraindicated in HFrEF, WPW with AF, and co-administration with beta-blockers. |
| Misc | Adenosine A1 receptor agonism / Na+/K+ ATPase inhibition | Adenosine, Digoxin, Magnesium sulphate | Adenosine hyperpolarizes AV node; Digoxin augments central vagal tone | Adenosine: first-line acute termination of AVNRT/orthodromic AVRT. Digoxin: AF rate control in sedentary/HFrEF. Magnesium: Torsades de Pointes. |
Sinus Node Disease and Reversible Bradycardia
Sick sinus syndrome (sinus node dysfunction) covers inappropriate sinus bradycardia, sinus pauses, sinoatrial exit block and the tachy-brady syndrome, in which paroxysmal atrial fibrillation alternates with symptomatic pauses on termination. It is a disease of fibrotic degeneration in older patients, and the tachy-brady variant is the classic reason a patient needs both a pacemaker and rate-controlling or anticoagulant therapy — the pacemaker permits drug treatment of the tachycardia that would otherwise be limited by the pauses.
Before committing any patient to a permanent device, exclude reversible causes:
| Reversible cause | Clue |
|---|---|
| Drugs (beta blockers, verapamil, diltiazem, digoxin, ivabradine, donepezil) | Recent initiation or dose increase; renal impairment |
| Hypothyroidism | Bradycardia with slow-relaxing reflexes, raised TSH |
| Hyperkalaemia | Tented T waves, broad QRS, sine wave |
| Raised intracranial pressure | Cushing reflex: bradycardia with hypertension |
| Inferior myocardial infarction | Vagally mediated, usually atropine-responsive, often transient |
| Hypothermia, obstructive sleep apnoea, athletic training | Context |
| Infiltration: sarcoidosis, amyloidosis, Lyme carditis | Young patient with unexplained high-grade block |
Unexplained complete heart block in a patient under 60 should prompt consideration of cardiac sarcoidosis or Lyme carditis, both of which can be reversible with treatment and are commonly missed.
Acute Management and Pacing
Acute symptomatic bradycardia with adverse features (shock, syncope, myocardial ischaemia, heart failure) is treated with atropine 500 micrograms intravenously, repeated to a maximum of 3 mg, then second-line measures such as isoprenaline, adrenaline infusion or transcutaneous pacing while transvenous pacing is arranged. Atropine is ineffective in infranodal block, because the lesion is below the level of vagal influence — a Mobitz II or complete heart block with a broad escape rhythm should go straight to pacing rather than repeated atropine.
Digoxin Toxicity
Digoxin is not in the Vaughan-Williams classification but generates a disproportionate number of examination questions. Toxicity causes nausea, confusion, xanthopsia (yellow-green visual haloes), and almost any arrhythmia, classically atrial tachycardia with block or bidirectional ventricular tachycardia. Hypokalaemia, hypomagnesaemia and hypercalcaemia potentiate it, as does renal impairment and co-prescription of amiodarone, verapamil, spironolactone or macrolides. The reverse-tick ST depression of digoxin effect is a normal therapeutic finding and does not indicate toxicity. Treatment is digoxin-specific antibody fragments (DigiFab) for life-threatening arrhythmia or a potassium above 5.0 mmol/L in acute poisoning; calcium should be avoided in digoxin-associated hyperkalaemia.
A 74-year-old woman is admitted to the medical assessment unit following two episodes of unheralded syncope while shopping. She regained consciousness promptly within one minute on both occasions, with no post-ictal confusion or involuntary movements. She takes no regular medications. On examination, her pulse is 44 bpm and regular, blood pressure is 126/74 mmHg, and systemic examination is unremarkable. Her 12-lead ECG demonstrates regular sinus rhythm at 88 bpm with intermittent non-conducted P waves occurring at a regular 2:1 ratio. The PR intervals of all conducted beats are completely normal and constant (160 ms) without preceding progressive prolongation. Which of the following is the definitive management of choice for this patient?