2.2 Tachyarrhythmias, Bradyarrhythmias & Channelopathies

2.2 Tachyarrhythmias, Bradyarrhythmias & Channelopathies

Cardiac electrophysiology represents a core domain of MRCPI Part I. Clinical competence requires systematic ECG interpretation, rapid differentiation of narrow versus wide complex tachycardias, evidence-based management of atrial fibrillation, clear criteria for cardiac pacing, and accurate identification of inherited channelopathies that predispose to sudden cardiac death (SCD).

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Approach to Tachyarrhythmias

The immediate clinical priority in any tachyarrhythmia is assessing hemodynamic stability:

• Adverse Features: Hypotension (systolic BP <90 mmHg), acute heart failure, syncope, or active myocardial ischemia.
• If Adverse Features Present: Immediate Synchronized DC Cardioversion under conscious sedation. Start at 120–150 J biphasic for atrial fibrillation/wide complex tachycardia, or 70–120 J for atrial flutter/SVT.
• If Hemodynamically Stable: Differentiate based on QRS width (<120 ms vs >=120 ms) and regularity.

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Narrow QRS Tachycardias (<120 ms)

1. Regular Narrow Complex Tachycardia

• Atrioventricular Nodal Re-entrant Tachycardia (AVNRT): Accounts for 60% of SVTs. Caused by functional re-entry within the AV node utilizing a slow anterograde pathway and fast retrograde pathway. P waves are buried within or immediately follow the QRS complex (pseudo-R' in V1, pseudo-S in II/III/aVF).
• Atrioventricular Re-entrant Tachycardia (AVRT): Re-entry utilizing an anatomical accessory pathway (e.g., Bundle of Kent in Wolff-Parkinson-White syndrome). Orthodromic AVRT conducts anterograde via the AV node and retrograde via the pathway (narrow QRS).
• Acute Management Algorithm:
  1. Vagal Maneuvers: Modified Valsalva maneuver (strain for 15 seconds followed by passive leg raise) converts ~43% of SVTs.
  2. Intravenous Adenosine: Purinergic A1 receptor agonist causing transient AV nodal block. Dose: 6 mg rapid IV push into a large peripheral vein followed by a 20 mL saline flush. If unconverted within 1–2 minutes, administer 12 mg, followed by a second 12 mg dose if required.
  3. Second-line Agents: Intravenous Verapamil (2.5–5 mg over 2 minutes) or Bisoprolol if adenosine fails or is contraindicated (e.g., severe asthma).

2. Irregular Narrow Complex Tachycardia

• Atrial Fibrillation (AF): Absence of P waves with irregular ventricular response.
• Atrial Flutter with Variable Block: Sawtooth flutter waves (leads II, III, aVF) at an atrial rate of 250–350 bpm with variable AV conduction.
• Multifocal Atrial Tachycardia (MAT): >=3 distinct P-wave morphologies with variable PR intervals, typically seen in severe COPD or exacerbations of pulmonary disease. Treated by correcting underlying hypoxia/hypercapnia and IV Diltiazem/Verapamil (avoid beta-blockers in severe bronchospasm).

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Wide QRS Tachycardias (>=120 ms)

Broad-complex tachycardia must be managed as Ventricular Tachycardia (VT) until proven otherwise (80–90% of cases). Differentiation from SVT with aberrant conduction (bundle branch block) is critical.

ECG Criteria Favoring VT (Brugada Criteria)

1. Absence of RS Complex in all precordial leads (V1–V6, regular concordant pattern).
2. RS Interval >100 ms in any precordial lead.
3. Atrioventricular Dissociation: P waves marching independently through QRS complexes, Capture beats (normal narrow QRS), or Fusion beats (hybrid QRS).
4. Morphology Criteria: QRS width >140 ms (LBBB-like) or >160 ms (RBBB-like), QR or monophasic R wave in V1.

Polymorphic VT & Torsades de Pointes

Torsades de Pointes is a specific form of polymorphic VT occurring in the context of QT prolongation (congenital or acquired secondary to hypokalemia, hypomagnesemia, or drugs like sotalol, erythromycin, haloperidol).

• Acute Treatment: Intravenous Magnesium Sulfate 2 g push regardless of serum magnesium level, correction of electrolytes, and overdrive cardiac pacing or isoprenaline infusion to shorten the QTc.

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Vaughan-Williams Classification of Antiarrhythmics

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Atrial Fibrillation Management Strategy

1. Stroke Risk & Anticoagulation (CHA2DS2-VASc Score)

• Congestive HF (1 point), Hypertension (1 point), Age >=75 (2 points), Diabetes (1 point), Stroke/TIA/Thromboembolism (2 points), Vascular Disease (1 point), Age 65–74 (1 point), Sex Category (Female) (1 point).
• Anticoagulation Threshold: Score >=1 in men or >=2 in women warrants Non-Vitamin K Antagonist Oral Anticoagulants (NOACs: Apixaban 5 mg bd, Rivaroxaban 20 mg daily, Dabigatran 150 mg bd, Edoxaban 60 mg daily) over Warfarin due to superior safety profiles and reduced intracranial hemorrhage rates.

2. Rate vs. Rhythm Control

• Rate Control: Target resting HR <110 bpm (lenient rate control per RACE II trial). First-line agents: Beta-blockers, Diltiazem/Verapamil, or Digoxin (especially in heart failure).
• Rhythm Control: Indicated in symptomatic AF despite rate control, young patients, or early AF (EAST-AFNET 4 trial). Modalities include electrical cardioversion, antiarrhythmic drugs (Flecainide if no structural heart disease; Amiodarone if heart failure present), and Catheter Ablation (pulmonary vein isolation).

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Bradyarrhythmias & Conduction System Disease

Classification of AV Block

• First-Degree AV Block: PR interval >200 ms (>5 small squares), all P waves conducted.
• Second-Degree AV Block - Mobitz Type I (Wenckebach): Progressive PR lengthening until a P wave fails to conduct. Benign, nodal site of block, usually responsive to atropine.
• Second-Degree AV Block - Mobitz Type II: Constant PR interval with intermittent unconducted P waves. Infra-Hisian block with high risk of progression to complete heart block.
• Third-Degree (Complete) AV Block: Total AV dissociation. P-P and R-R intervals are regular, but completely independent.

Emergency Management & Pacing Indications

• Acute Bradycardia Algorithm: Administer Atropine 500 mcg IV (repeat up to max 3 mg). If ineffective, initiate IV Isoprenaline or Adrenaline infusion, or proceed to Transcutaneous Pacing followed by transvenous wire placement.
• Permanent Pacemaker (PPM) Indications: Mobitz Type II AV block, 3rd-degree complete heart block, symptomatic sinus node dysfunction (Sick Sinus Syndrome), or trifascicular block with prolonged HV interval.

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Inherited Channelopathies

1. Long QT Syndrome (LQTS): QTc >480 ms (Bazett's formula: $QT_c = QT / \sqrt{RR}$). Mutation in ion channels.
   • LQTS Type 1 (KCNQ1): Triggers: Swimming, exercise. T-wave morphology: Broad-based.
   • LQTS Type 2 (KCNH2): Triggers: Auditory stimuli (alarm clocks), emotional stress. T-wave morphology: Notched/bifid.
   • LQTS Type 3 (SCN5A): Triggers: Rest, sleep. T-wave morphology: Late-appearing.
   • Management: Non-selective Beta-blockers (Nadolol or Propranolol), avoid QT-prolonging drugs, ICD for survivors of cardiac arrest.
2. Brugada Syndrome: Autosomal dominant mutation in SCN5A (cardiac sodium channel). Predominantly affects Southeast Asian males.
   • Type 1 Pattern: ST elevation >=2 mm in V1–V2 with coved appearance followed by negative T wave.
   • Diagnostic Provocation: Intravenous Ajmaline or Flecainide unmasks Type 1 pattern.
   • Management: ICD implantation is the only proven therapy for preventing SCD in high-risk patients; quinidine used for electrical storms.
3. Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT): Mutations in RYR2 (ryanodine receptor). Characterized by exercise/emotion-induced bidirectional VT in young patients with structurally normal hearts. Treated with high-dose Beta-blockers, Flecainide, and left cardiac sympathetic denervation.