7.1 Atrial Fibrillation, Narrow & Broad Complex Tachycardias

Arrhythmias and conduction abnormalities represent core high-yield clinical territories in MRCP(UK) Part 1. Candidates must master acute emergency stabilization algorithms, hemodynamic stratification, electrocardiographic criteria, pharmacotherapy via the Vaughan-Williams classification, and stroke risk stratification in atrial fibrillation.

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1. Atrial Fibrillation & Atrial Flutter

Atrial fibrillation (AF) is characterized by chaotic, uncoordinated atrial activation resulting in irregular ventricular response and loss of effective atrial systole. Atrial flutter arises from a macro-re-entrant circuit, most commonly around the tricuspid valve annulus within the right atrium (cavotricuspid isthmus), producing regular "sawtooth" flutter waves (typically negative in leads II, III, and aVF at an atrial rate of ~300 bpm with 2:1 AV block yielding a ventricular rate of ~150 bpm).

Acute Management & Hemodynamic Status

• Hemodynamically Unstable (Adverse Features): Shock (systolic BP <90 mmHg), syncope, ongoing myocardial ischaemia, or acute pulmonary oedema. Mandates immediate synchronized DC cardioversion (starting at 120–150 J biphasic, escalating as required) under sedation or general anaesthesia. Intravenous unfractionated heparin should be initiated promptly.
• Hemodynamically Stable: The therapeutic pathway branches into rate control versus rhythm control, coupled with systematic thromboembolic risk assessment.

Rate Control vs Rhythm Control Strategies

According to NICE and ESC guidelines, rate control is the preferred default initial strategy for most patients unless specific rhythm control indications are met:

• Rate Control First-Line: Suitable for patients >65 years, those with underlying coronary artery disease, patients who are sedentary, or those without significant heart failure symptoms. Monotherapy options include:
  • Standard Beta-Blockers: Bisoprolol (1.25–10 mg once daily) or metoprolol tartrate/succinate.
  • Rate-Limiting Calcium Channel Blockers: Diltiazem (60–120 mg TDS) or verapamil (40–120 mg TDS). Crucial contraindication: Never administer diltiazem or verapamil in patients with heart failure with reduced ejection fraction (HFrEF) or co-prescribed with beta-blockers due to risk of complete heart block and severe myocardial depression.
  • Digoxin: Indicated as monotherapy only in sedentary elderly patients or as an add-on agent in patients with concurrent heart failure. Digoxin acts by augmenting vagal tone to the AV node; it is ineffective during physical exertion or acute stress where sympathetic tone overrides vagal influence. Target serum concentration is 0.5–0.9 ng/mL.
  • Target Heart Rate: Initial resting heart rate <110 bpm (lenient rate control per RACE II trial); if symptoms persist, titrate toward strict rate control (<80 bpm at rest and <110 bpm during moderate exercise).
• Rhythm Control Indications: Preferred when there is a reversible precipitating trigger (e.g., chest infection, hyperthyroidism, acute alcohol excess), new-onset AF (<48 hours), heart failure clearly precipitated by AF, younger patients (<65 years), or patients who remain symptomatic despite optimal rate control.
  • Pharmacological Cardioversion: IV flecainide (Class Ic) is highly effective for rapid restoration of sinus rhythm. Strict absolute contraindication: Flecainide must never be given in structural heart disease, left ventricular systolic dysfunction, or coronary artery disease (ischaemic heart disease) due to high risk of fatal proarrhythmia demonstrated in the CAST trial. In structural heart disease or HFrEF, IV amiodarone (300 mg over 20–60 minutes, followed by 900 mg over 24 hours) is the antiarrhythmic of choice.

Thromboembolic Risk Assessment & Anticoagulation

Thromboembolic prophylaxis is guided by the validated CHA2DS2-VASc score:

• Treatment Thresholds:
  • Score 0 in males or 1 in females: No anticoagulation indicated.
  • Score 1 in males: Anticoagulation should be strongly considered.
  • Score >=2 in males or >=3 in females: Oral anticoagulation is mandatory.
• Direct Oral Anticoagulants (DOACs): First-line therapy over warfarin for non-valvular AF. Includes direct Factor Xa inhibitors (apixaban, rivaroxaban, edoxaban) and the direct thrombin inhibitor (dabigatran). DOACs offer superior or equivalent stroke prevention with significantly lower rates of intracranial haemorrhage and do not require routine INR monitoring.
• Valvular AF Exception: Patients with moderate-to-severe rheumatic mitral stenosis or mechanical prosthetic heart valves are categorized as "valvular AF". DOACs are contraindicated in these populations; warfarin (target INR 2.5–3.5 depending on valve prosthesis type and position) remains strictly required.
• Bleeding Risk Assessment: Assessed using the ORBIT score (preferred by NICE) or HAS-BLED score. A high bleeding score is not an automatic contraindication to anticoagulation; rather, it highlights modifiable risk factors (e.g., uncontrolled hypertension, concurrent NSAID/antiplatelet use, excess alcohol consumption) requiring clinical remediation.

Anticoagulation Timing Around Cardioversion

• AF Duration <48 Hours: Cardioversion can be performed immediately. Give therapeutic low-molecular-weight heparin (LMWH) or a DOAC at presentation. Post-cardioversion, patients with CHA2DS2-VASc >=1 (males) or >=2 (females) require long-term anticoagulation; those with score 0 (males) or 1 (females) require 4 weeks of anticoagulation.
• AF Duration >=48 Hours (or Unknown Duration): High risk of pre-existing left atrial appendage (LAA) thrombus. Requires either:
  1. Minimum of 3 weeks of continuous, therapeutic oral anticoagulation prior to elective cardioversion, followed by at least 4 weeks of therapeutic oral anticoagulation post-procedure (regardless of whether sinus rhythm is maintained).
  2. Transoesophageal Echocardiography (TOE) Guided Strategy: If early cardioversion is desired, a TOE is performed to definitively exclude LAA thrombus. If clear, cardioversion proceeds immediately under full anticoagulation coverage, followed by >=4 weeks of oral anticoagulation.

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2. Narrow Complex Tachycardias & Pre-Excitation

A narrow complex tachycardia exhibits a QRS duration <120 ms, indicating that ventricular depolarisation proceeds normally through the specialized His-Purkinje system. These originate at or above the AV junction.

Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)

AVNRT is the most common regular supraventricular tachycardia (~60% of cases), typically presenting in young women with sudden-onset palpitations, neck fluttering (due to right atrial contraction against a closed tricuspid valve creating cannon 'a' waves), and polyuria (atrial stretch triggering atrial natriuretic peptide release).

• Mechanism: Dual pathways within the AV node: a slow pathway (short refractory period) and a fast pathway (long refractory period). An atrial premature beat blocks down the fast pathway and conducts down the slow pathway, then re-enters retrogradely up the recovered fast pathway.
• ECG: Regular tachycardia, rate 140–220 bpm. P waves are either buried within the QRS complex or visible immediately after the QRS as a pseudo-r' in lead V1 or pseudo-S in leads II, III, and aVF.
• Acute Management Algorithm:
  1. Vagal Manoeuvres: Modified Valsalva manoeuvre (straining to 40 mmHg for 15 seconds supine, followed by immediate passive leg elevation to 45° for 15 seconds) achieves cardioversion in >40% of cases (REVERT trial). Carotid sinus massage (auscultate for bruits first; massage 5–10 seconds unilaterally).
  2. Intravenous Adenosine: First-line pharmacological intervention. Administered as a rapid bolus into a large antecubital vein followed by an immediate 20 mL saline flush. Initial dose 6 mg; if no conversion within 1–2 minutes, give 12 mg; if still unsuccessful, give a third dose of 18 mg. Adenosine activates A1 receptors on AV nodal myocytes, opening potassium channels and causing transient hyperpolarization and AV block (half-life <10 seconds).
  3. Adenosine Precautions: Causes transient flushing, bronchospasm, and severe chest tightness. Contraindicated in severe asthma and decompensated COPD (use IV verapamil 5–10 mg instead). Dipyridamole blocks adenosine reuptake (potentiates effect; reduce dose). Theophylline and caffeine are competitive adenosine receptor antagonists (diminish effect; higher doses required).

Atrioventricular Re-entrant Tachycardia (AVRT) & Wolff-Parkinson-White (WPW)

WPW syndrome involves an anomalous extranodal muscular connection between atria and ventricles: the bundle of Kent. Resting baseline ECG demonstrates the classic triad: short PR interval (<120 ms), slurred initial QRS upstroke (delta wave), and prolonged QRS duration (>120 ms) with secondary repolarization abnormalities.

• Orthodromic AVRT (95%): Antegrade conduction occurs through the AV node, and retrograde conduction travels via the accessory pathway. ECG shows a regular narrow complex tachycardia. Responds to vagal manoeuvres and IV adenosine.
• Antidromic AVRT (5%): Antegrade conduction travels via the accessory pathway, and retrograde conduction proceeds via the AV node. ECG demonstrates a wide complex regular tachycardia mimicking ventricular tachycardia.
• Pre-Excited Atrial Fibrillation (High-Yield Danger): Atrial fibrillation in a patient with WPW conducts impulses rapidly and directly down the non-decremental accessory pathway into the ventricles. ECG demonstrates an irregularly irregular, broad complex tachycardia with bizarre, polymorphous QRS morphology and varying delta waves at extremely rapid rates (often >250–300 bpm).
  • CRITICAL CONTRAINDICATION: AV nodal blocking agents (adenosine, verapamil, diltiazem, beta-blockers, digoxin) are strictly contraindicated. Blocking the AV node diverts all incoming fibrillatory wavefronts down the accessory pathway, accelerating ventricular response and directly triggering ventricular fibrillation and cardiac arrest.
  • Treatment: If hemodynamically compromised, immediate synchronized DC cardioversion. If stable, IV flecainide or IV procainamide (which prolong accessory pathway refractoriness). Definitive long-term cure is catheter radiofrequency ablation of the accessory pathway.

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3. Broad Complex Tachycardias

A broad complex tachycardia is defined by a QRS duration >=120 ms. In clinical practice, any broad complex tachycardia must be assumed to be Ventricular Tachycardia (VT) until proven otherwise (~85% of all broad complex tachycardias, and >95% in patients with prior myocardial infarction or structural heart disease). The alternative differential is supraventricular tachycardia with aberrant intraventricular conduction (pre-existing or rate-related bundle branch block).

Electrocardiographic Differentiation (Brugada Criteria)

Features supporting ventricular tachycardia over SVT with aberrancy include:

1. AV Dissociation: Independent atrial and ventricular activity (P waves marching through at a slower, unrelated rate). Highly specific.
2. Capture Beats: A normal sinus impulse momentarily "captures" the ventricles via the normal conduction system, producing an isolated narrow QRS complex in the midst of broad-complex tachycardia.
3. Fusion Beats (Dressler Beats): Hybrid QRS morphology produced when a supraventricular sinus impulse and a ventricular ectopic impulse depolarise the myocardium simultaneously.
4. Extreme Axis Deviation: QRS axis directed into the "northwest quadrant" (-90° to 180°).
5. Concordance Across Precordial Leads: Uniformly positive or uniformly negative QRS complexes across leads V1 through V6.
6. Marked QRS Width: QRS duration >140 ms with RBBB pattern, or >160 ms with LBBB pattern.

Management of Ventricular Tachycardia

• Pulseless / Unconscious: Follow Advanced Life Support (ALS) cardiac arrest algorithm: immediate CPR and unsynchronized high-energy defibrillation.
• Sustained Monomorphic VT with Adverse Features (Unstable): Synchronized DC cardioversion under sedation.
• Hemodynamically Stable Monomorphic VT: Intravenous Amiodarone (300 mg infused over 20–60 minutes via large vein, followed by 900 mg over the subsequent 24 hours). If pharmacological therapy fails, proceed to synchronized DC cardioversion.
• Polymorphic VT & Torsades de Pointes: Polymorphic VT with a baseline prolonged QT interval (QTc >480 ms) is termed Torsades de Pointes ("twisting of the points"), appearing as QRS complexes that periodically twist around the isoelectric line.
  • Causes: Congenital long QT syndromes (LQT1/LQT2/LQT3, Romano-Ward, Jervell and Lange-Nielsen), electrolyte depletion (severe hypokalaemia, hypomagnesaemia, hypocalcaemia), and drug-induced QT prolongation (macrolides, quinolones, psychotropics, Class Ia/III antiarrhythmics).
  • Management: Discontinue all QT-prolonging medications. Administer IV magnesium sulphate (2 g bolus over 10 minutes), even if serum magnesium levels are within normal limits. Correct hypokalaemia (target K+ 4.5–5.0 mmol/L). If recurrent, initiate overdrive transvenous pacing or isoprenaline infusion to accelerate basal heart rate and shorten ventricular repolarization.

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