Approach to the Patient with Palpitation and Arrhythmia

1. Pathophysiology of Arrhythmia and Its Classification

Definition

Normal Cardiac Conduction

Mechanisms of Tachyarrhythmia

• Pathway A conducts slowly and recovers quickly
• Pathway B conducts rapidly and recovers slowly

Mechanism of Bradyarrhythmia

• Reduced automaticity of the SA node
• Impaired conduction through the AV node or His–Purkinje system

Classification of Arrhythmias

By Origin

Note: Occasionally, supraventricular tachycardia can mimic ventricular tachycardia and present as a broad-complex tachycardia due to coexisting bundle branch block or an accessory pathway.

By Rate

• Bradyarrhythmias (< 60/min): Sinus bradycardia, sinoatrial disease, AV block, bundle branch block
• Tachyarrhythmias (> 100/min): Divided into supraventricular and ventricular tachycardias

Supraventricular Arrhythmias

• Sinus arrhythmia / sinus tachycardia / sinus bradycardia
• Sinoatrial (sick sinus) disease
• Atrial ectopic beats
• Atrial tachycardia
• Atrial flutter
• Atrial fibrillation
• Supraventricular tachycardia (AVNRT, AVRT/WPW syndrome)

Ventricular Arrhythmias

• Ventricular premature beats (VPBs)
• Ventricular tachycardia (VT)
• Torsades de pointes
• Ventricular fibrillation (VF)

Conduction Defects / Bradyarrhythmias

• First-, second- (Mobitz I and II), and third-degree AV block
• Bundle branch block (RBBB, LBBB)
• Sinoatrial disease

2. Clinical Presentation and Approach to the Patient with Palpitation

Clinical Features

• Rapid palpitation
• Dizziness
• Chest discomfort or breathlessness
• Syncope (if extreme tachycardia prevents adequate cardiac filling)

• Fatigue
• Lightheadedness
• Syncope (Stokes–Adams attacks in complete AV block — sudden loss of consciousness without warning, brief anoxic seizure if prolonged asystole, pallor, followed by a characteristic flush on recovery)

• Palpitation, breathlessness and fatigue
• Lightheadedness (fall in BP)
• Chest pain (in underlying coronary artery disease)
• Systemic embolism/stroke (particularly in elderly, who may be asymptomatic from the AF itself)
• Cardiac failure (in patients with poor ventricular function or valve disease)

Specific Arrhythmia Presentations

Clinical Approach

• Character of palpitations: onset (sudden vs. gradual), termination, regularity, rate
• Associated symptoms: dizziness, chest pain, breathlessness, syncope
• Precipitating factors: exercise, emotion, alcohol, caffeine
• Past medical history: structural heart disease, previous MI, thyroid disease, drug use
• Family history: sudden cardiac death, inherited arrhythmia syndromes

• Pulse: rate, rhythm (regular/irregular/irregularly irregular)
• BP, JVP (cannon waves in complete AV block)
• Heart sounds (variable intensity of first heart sound in AV dissociation)
• Signs of heart failure

Investigations

• Identify structural heart disease (e.g., mitral valve disease in AF)
• Assess ventricular function
• Screen for cardiomyopathy

• Thyroid function tests (mandatory in new AF to exclude thyrotoxicosis)
• Electrolytes (hypokalaemia, hypomagnesaemia cause arrhythmias)
• Troponin (if acute coronary syndrome suspected)

3. ECG Findings in Common Arrhythmias

Sinus Arrhythmia

• Cyclical variation of rate: increases with inspiration, decreases with expiration
• Normal P wave morphology before each QRS

Sinus Bradycardia

• Rate < 60/min, otherwise normal ECG

Sinus Tachycardia

• Rate > 100/min, normal P waves preceding each QRS

Sinoatrial Disease (Sick Sinus Syndrome)

• Periods of sinus bradycardia, sinus arrest (no P waves), junctional escape beats, paroxysmal atrial fibrillation

First-Degree AV Block

• PR interval prolonged > 0.20 sec
• Every P wave is followed by a QRS complex

Second-Degree AV Block — Mobitz Type I (Wenckebach)

• Progressive lengthening of successive PR intervals, culminating in a dropped beat (P wave not conducted)
• Cycle then repeats itself
• Usually due to impaired conduction in the AV node itself

Second-Degree AV Block — Mobitz Type II

• PR interval of conducted impulses remains constant
• Some P waves are not conducted
• Usually caused by disease of the His–Purkinje system; carries a risk of asystole

2:1 AV Block

• Alternate P waves are not conducted
• Impossible to distinguish between Mobitz type I and II

Third-Degree (Complete) AV Block

• Complete AV dissociation: atria and ventricles beat independently
• Atrial rate ~80/min; ventricular escape rate ~25–50/min
• Narrow QRS escape: block in AV node (His origin); Broad QRS escape: block below His (Purkinje origin)

Bundle Branch Block

• QRS ≥ 0.12 sec
• 'M'-shaped (rsR') configuration in leads V1 and V2
• Wide S wave in lead I

• QRS ≥ 0.12 sec
• Loss of Q wave (septal vector) in lead I
• 'M'-shaped QRS complexes in V5 and V6
• ST depression in left-sided leads

Atrial Ectopic Beats

• Premature but otherwise normal QRS complex
• Preceding P wave has different morphology (abnormal site of atrial activation)

Atrial Flutter

• Sawtooth flutter waves at approximately 300/min
• Usually associated with 2:1, 3:1 or 4:1 AV block (ventricular rates of 150, 100 or 75/min)
• Flutter waves visible in leads II, III and aVF
• Carotid sinus pressure or adenosine may temporarily increase AV block, revealing flutter waves

Atrial Fibrillation

• No P waves; baseline may show irregular fibrillation waves
• Normal but irregularly irregular QRS complexes ("irregularly irregular" pulse)
• Fast ventricular rate (120–160/min) at onset; may be slower with medication

Supraventricular Tachycardia (AVNRT)

• Regular tachycardia at rate 120–240/min
• Normal, narrow QRS complexes
• P waves usually not visible (buried in QRS) or seen immediately before or after QRS

Wolff–Parkinson–White Syndrome (AVRT — sinus rhythm)

• Short PR interval (pre-excitation via accessory pathway)
• Broad QRS with a slurred initial deflection — delta wave
• During orthodromic tachycardia: narrow-complex tachycardia indistinguishable from AVNRT
• During AF with WPW: irregular broad-complex tachycardia at extremely rapid rate

Ventricular Premature Beats

• Broad and bizarre QRS complexes (no preceding P wave in usual position)
• Complexes may be unifocal (identical) or multifocal (varying morphology)
• 'Couplet' = two successive ectopics; 'triplet' = three; bigeminy = alternating sinus and VPBs

Ventricular Tachycardia (VT)

• Rate > 120/min with broad, abnormal QRS complexes
• AV dissociation (pathognomonic)
• Capture beats (normal sinus beat in mid-tachycardia) and fusion beats (pathognomonic)
• Extreme left axis deviation
• Very broad QRS complexes (> 140 msec)
• No response to carotid sinus massage or intravenous adenosine

Torsades de Pointes

• Polymorphic VT: rapid irregular complexes that seem to twist around the baseline as the mean QRS axis changes
• Background ECG shows prolonged QT interval (> 0.44 sec in men; > 0.46 sec in women at 60/min)
• Often triggered by an R-on-T ectopic following bradycardia

4. Principles of Treatment of Common Arrhythmias

General Principles of Anti-Arrhythmic Drug Use

• Many arrhythmias are benign and do not require specific treatment
• Precipitating or causal factors should be corrected first (alcohol excess, myocardial ischaemia, hyperthyroidism, acidosis, hypokalaemia, hypomagnesaemia)
• If drug therapy is required, use as few drugs as possible
• Anti-arrhythmic drugs are potentially toxic and may be pro-arrhythmic
• Patients on long-term anti-arrhythmic drugs should be reviewed regularly

Anti-Arrhythmic Drug Classification (Vaughan Williams)

Class I drugs should be avoided in patients with heart failure (depress myocardial function). Class Ia and Ic drugs are often pro-arrhythmic.

Treatment of Specific Arrhythmias

Sinus Bradycardia

• Asymptomatic: no treatment required
• Symptomatic (acute, e.g., MI): IV atropine (0.6–1.2 mg)
• Recurrent/persistent: permanent pacemaker implantation

Sinoatrial Disease

• Permanent pacemaker improves symptoms (but not prognosis)
• Indicated for symptomatic bradycardia including drug-induced bradycardia
• Dual-chamber pacemaker is normally used

AV Block

• First-degree / Mobitz type I: No treatment usually required; monitor
• Symptomatic second- or third-degree: IV atropine (0.6 mg); if fails → temporary pacemaker
• Asymptomatic Mobitz type II / third-degree: Permanent pacemaker (risk of asystole and sudden death; pacing improves prognosis)
• Complete AV block with asystole: IV atropine 3 mg or IV isoprenaline as bridge to temporary pacing

Atrial Ectopic Beats

• Treatment rarely necessary
• β-blockers if symptoms are intrusive

Atrial Tachycardia

• β-blockers (reduce automaticity), class I or III anti-arrhythmic drugs
• AV node-blocking drugs to control ventricular response
• Catheter ablation for recurrent cases (targets ectopic site)

Atrial Flutter

• DC cardioversion (high recurrence rate even with β-blockers or amiodarone)
• Catheter ablation — >90% chance of permanent cure; treatment of choice for persistent symptoms
• Class Ic drugs (flecainide) are contraindicated — can produce paradoxical extreme tachycardia

Atrial Fibrillation

• Well-tolerated occasional attacks: no treatment
• Symptomatic: β-blockers (first-line); reduce ectopic firing
• Class Ic drugs (propafenone, flecainide — not in CAD/LV dysfunction)
• Class III: amiodarone (most effective; side-effects restrict use); dronedarone (contraindicated in heart failure)
• Catheter ablation targeting pulmonary venous connections (~75% success)

• DC cardioversion or pharmacological cardioversion
• If AF < 48 hours: IV flecainide (stable, no structural disease) or IV amiodarone (structural heart disease)
• If AF ≥ 48 hours: anticoagulate for minimum 4 weeks before and 3 months after cardioversion
• Prophylaxis with amiodarone reduces recurrence

• β-blockers, rate-limiting calcium antagonists (verapamil, diltiazem), digoxin
• β-blockers and calcium antagonists are more effective than digoxin during exercise
• Digoxin + β-blocker combination helpful; calcium channel antagonists should NOT be combined with β-blockers (risk of bradycardia)
• 'Pace and ablate' strategy in exceptional cases

• Assessed using CHA₂DS₂-VASc score (maximum 9 points)
  • 0 points: no prophylaxis; 1 point: consider anticoagulation (males); ≥2 points: oral anticoagulant
• Bleeding risk assessed with HAS-BLED score (≥3 requires close monitoring)
• Direct oral anticoagulants (DOACs) — rivaroxaban, apixaban, edoxaban, dabigatran — have largely replaced warfarin; at least as effective with lower risk of intracranial haemorrhage
• Warfarin: target INR 2.0–3.0
• Aspirin should NOT be used — little/no effect on embolic stroke; significant bleeding risk
• Patients with AF secondary to mitral valve disease should always be anticoagulated

SVT (AVNRT / AVRT)

• Carotid sinus pressure or Valsalva manoeuvre
• Adenosine (3–12 mg IV in incremental doses) or verapamil (5 mg IV over 1 min)
• IV β-blocker or flecainide as alternatives
• DC cardioversion if severe haemodynamic compromise

• Catheter ablation — most effective (>90% permanent prevention); treatment of choice
• Alternatively: oral β-blocker, verapamil, or flecainide (commits young patients to long-term therapy)

WPW Syndrome (AVRT)

• Acute: carotid sinus pressure or adenosine; if AF with rapid conduction → emergency DC cardioversion
• Digoxin and verapamil are contraindicated (shorten refractory period of accessory pathway → may precipitate VF)
• Catheter ablation — first-line in symptomatic patients; nearly always curative
• Prophylactic drugs: flecainide or propafenone (slow conduction in accessory pathway)

Ventricular Premature Beats

• Treatment usually not necessary unless highly symptomatic
• β-blockers or catheter ablation if symptomatic
• Anti-arrhythmic drugs do not improve prognosis (may worsen in post-MI patients)
• Very frequent VPBs (> 10/hr) warrant echocardiography and exercise ECG

Ventricular Tachycardia

• If BP < 90 mmHg: synchronised DC cardioversion (treatment of choice)
• If well tolerated: IV amiodarone (bolus then continuous infusion)
• IV lidocaine (alternative; may depress LV function)
• Correct hypokalaemia, hypomagnesaemia, acidosis, hypoxia

• β-blockers (reduce ventricular automaticity)
• Amiodarone if additional control needed
• Class Ic drugs contraindicated in CAD or heart failure
• Implantable cardioverter-defibrillator (ICD) for poor LV function or haemodynamic compromise
• Catheter ablation for focal/infarct scar-mediated VT; treatment of choice for VT in normal heart

Torsades de Pointes

• IV magnesium (8 mmol over 15 min, then 72 mmol over 24 hrs) — in all cases
• If ineffective: atrial pacing (rate-dependent shortening of QT interval)
• IV isoprenaline as alternative to pacing (avoid in congenital long QT syndromes)
• Identify and treat underlying cause; stop QT-prolonging medications
• β-blockers effective for prevention in congenital long QT syndrome
• ICD for extreme QT prolongation (> 500 msec) or high-risk genotypes

Non-Pharmacological Treatments

DC Cardioversion (Electrical Cardioversion)

• Used for terminating organised rhythms (AF, VT)
• Shock delivered immediately after the R wave (if applied on T wave → may provoke VF)
• 100–150 Joule shock normally used
• Requires general anaesthesia/sedation (elective procedure)

Defibrillation

• For cardiac arrest due to VF and emergencies
• Unsynchronised shock (timing not critical in VF)
• Biphasic shock: first and second shocks 150 J; thereafter up to 200 J
• No anaesthetic needed (patient is unconscious)

Temporary Pacemakers

• Bipolar electrode via internal jugular/subclavian/femoral vein to RV apex
• Indicated for: transient AV block complicating MI, reversible bradycardia, bridge to permanent pacing
• Maximum 7 days to limit complication rates

Permanent Pacemakers

• Dual-chamber pacemakers (DDD) for second-/third-degree AV block — preserves AV synchrony
• Single-chamber for SA disease without AV block
• AAIR: atrial demand pacemaker with rate response function (for chronotropic incompetence)

Implantable Cardioverter-Defibrillators (ICD)

• Detects and terminates life-threatening ventricular tachyarrhythmias
• Treats via overdrive pacing, cardioversion or defibrillation
• Primary prevention: post-MI with LV ejection fraction < 30%; mild-moderate heart failure with LVEF < 35%; inherited conditions (long QT syndrome, cardiomyopathy)
• Secondary prevention: survivors of VF/VT cardiac arrest; VT with haemodynamic compromise or LVEF < 35%

Cardiac Resynchronisation Therapy (CRT)

• For selected patients with heart failure and LBBB (causes dyssynchronous LV contraction)
• Right atrial + right ventricular + LV lead (via coronary sinus)
• Improves symptoms, quality of life, and reduces mortality in NYHA class III–IV heart failure with LVEF ≤ 35%
• Most devices also include a defibrillator (CRT-D)

Catheter Ablation Therapy

• Treatment of choice for AVNRT, AVRT/accessory pathway tachycardias (>90% curative)
• Highly effective for atrial flutter (isthmus ablation), atrial tachycardia, normal heart VT
• Used for AF: targets pulmonary vein to left atrial connections (~70–80% success in paroxysmal AF in young patients with structurally normal hearts)
• Uses radiofrequency (heat) or cryoablation (freezing)
• Serious complications rare (<1%): complete heart block requiring pacemaker, cardiac tamponade