Arrhythmia
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Cardiac Arrhythmia - Comprehensive Overview
Sources: Braunwald's Heart Disease, Washington Manual of Medical Therapeutics, Miller's Anesthesia
1. Definition
An arrhythmia is any disturbance of the normal cardiac rate, rhythm, or conduction. The term encompasses bradycardias (rate <60 bpm), tachycardias (rate >100 bpm), and abnormalities of conduction (heart blocks). The normal sinus rhythm originates in the sinoatrial (SA) node and propagates through the AV node, His bundle, and Purkinje fibers.
2. Mechanisms of Arrhythmia
All arrhythmias arise through one or more of three fundamental electrophysiologic mechanisms:
A. Abnormal Automaticity
- Normal enhanced automaticity: Increased phase-4 depolarization rate of pacemaker cells beyond normal (e.g., inappropriate sinus tachycardia). Treated with beta-blockers or I₁ (funny current) blockers like ivabradine.
- Abnormal automaticity: Non-pacemaker cells (atrial, ventricular) develop spontaneous depolarization, seen in ischemia, metabolic disturbances, or digoxin toxicity (e.g., ectopic atrial tachycardia).
B. Triggered Activity
- Early afterdepolarizations (EADs): Occur during phases 2-3 of the action potential, associated with prolonged QT (hypokalaemia, drug effects). Mechanism of Torsades de Pointes (TdP).
- Delayed afterdepolarizations (DADs): Occur during phase 4, driven by calcium overload. Seen in digitalis toxicity, catecholaminergic states.
C. Re-entry
The most common arrhythmia mechanism. Requires:
- Two anatomically or functionally distinct pathways
- Unidirectional block in one pathway
- Sufficient conduction slowing in the other to allow recovery of the blocked pathway
Examples: AVNRT, AVRT (WPW), atrial flutter, ventricular tachycardia in scar tissue.
3. Classification
Bradyarrhythmias (Rate <60 bpm)
| Arrhythmia | Key Feature | Common Cause |
|---|---|---|
| Sinus bradycardia | Rate <60, normal P-QRS | Vagal tone, beta-blockers, inferior MI, hypothyroidism |
| Sick sinus syndrome | Sinus pauses, SA exit block, tachycardia-bradycardia | SA nodal degeneration, post-cardiac surgery |
| 1st degree AV block | PR >200 ms, all P waves conduct | Vagal tone, medications |
| 2nd degree - Mobitz I (Wenckebach) | Progressive PR lengthening → dropped beat | AV node disease; usually benign |
| 2nd degree - Mobitz II | Fixed PR, sudden dropped beat | His-Purkinje disease; risk of progression to complete block |
| 3rd degree (complete) AV block | P waves and QRS dissociated | Ischemia, fibrosis, medications; urgent pacing needed |
Tachyarrhythmias - Supraventricular (SVT, QRS <120 ms)
Tachycardias requiring atrial or AV nodal tissue for initiation/maintenance. Prevalence of paroxysmal SVT is ~2.25/1000, with women affected twice as often as men.
| Arrhythmia | ECG Feature | Mechanism |
|---|---|---|
| Sinus tachycardia | Rate 100-180, normal P-QRS | Physiologic (fever, pain, hypovolemia, anemia) |
| Inappropriate sinus tachycardia | Persistent elevated rate at rest >100 | Enhanced SA node automaticity |
| AVNRT | "Absent P waves" - P buried in QRS; pseudo-r' in V1 | Re-entry in dual AV nodal pathways (short RP) |
| AVRT (WPW) | Delta wave, short PR in sinus; may see narrow or wide tachycardia | Accessory pathway re-entry |
| Atrial fibrillation | Absent P waves, irregularly irregular, fibrillatory baseline (V1, II, III, aVF) | Ectopic foci in pulmonary veins + multiple reentrant circuits |
| Atrial flutter | Sawtooth pattern leads II, III, aVF; atrial rate 250-350 bpm, usually 2:1 conduction (ventricular rate ~150) | Macroreentrant circuit around tricuspid annulus (typical) |
| MAT | Irregularly irregular; ≥3 distinct P-wave morphologies | Enhanced automaticity; associated with COPD, CHF |
| EAT | Long RP tachycardia, abnormal P-wave axis | Automaticity, triggered activity, micro-reentry |
| Junctional tachycardia | P retrograde or absent; uncommon in adults | Automaticity; common post-cardiac surgery in children |
Tachyarrhythmias - Ventricular (QRS ≥120 ms unless aberrant conduction)
| Arrhythmia | ECG Feature | Notes |
|---|---|---|
| PVCs | Wide QRS, no preceding P; compensatory pause | Common; benign unless frequent/in structural disease |
| Ventricular tachycardia (VT) | Wide regular QRS tachycardia, AV dissociation, fusion/capture beats | Re-entry around scar; hemodynamically unstable VT = immediate cardioversion |
| Torsades de Pointes | Polymorphic VT, twisting QRS axis around baseline | Long QT (drug-induced, electrolyte, congenital); treat with IV magnesium |
| Ventricular fibrillation | Chaotic, no organized QRS | Cardiac arrest; immediate defibrillation required |
4. ECG-Based Diagnostic Approach
The diagram below (from Washington Manual) provides a systematic algorithm:
Step-by-step logic:
- Is the rate >100? → Tachyarrhythmia
- Is QRS narrow (<120 ms) or wide (≥120 ms)?
- Is the rhythm regular or irregular?
- Are P waves present? What is the RP relationship?
- Short RP (<50% of RR): Typical AVNRT, orthodromic AVRT, junctional tachycardia
- Long RP (>50% of RR): Sinus tachycardia, atypical AVNRT, EAT, SANRT
- Wide-complex regular: VT vs. SVT with aberrancy (VT is more common and should be assumed until proven otherwise)
5. Common Arrhythmias In Depth
Atrial Fibrillation (AF)
The most common sustained tachyarrhythmia. Affects >10% of those aged >75 years.
Classification (5 forms):
- First occurrence
- Paroxysmal (<7 days, usually <48 hrs)
- Persistent (>7 days)
- Long-standing persistent (>1 year, amenable to cardioversion)
- Permanent (accepted; cardioversion not pursued)
Risk factors: Advanced age, male sex, HTN, CHF, DM, valvular disease, previous MI, obesity, OSA. Post-cardiothoracic surgery AF occurs in 20-50% of patients.
Pathophysiology: Initiated by rapid ectopic firing from pulmonary vein foci; maintained by multiple reentrant circuits. Structural and electrical remodeling (fibrosis, inflammation) perpetuates the arrhythmia. CRP and IL-6 are elevated and correlate with duration.
Management principles:
- Rate control: beta-blockers, non-dihydropyridine CCBs, digoxin
- Rhythm control: cardioversion (electrical or pharmacologic) + antiarrhythmics (amiodarone, flecainide, propafenone, sotalol)
- Anticoagulation: CHA₂DS₂-VASc score guides DOAC or warfarin use for stroke prevention
- Ablation: pulmonary vein isolation for symptomatic drug-refractory AF
Sinus Bradycardia
Benign in most cases (athletes, vagal tone, sleep). Treat only if symptomatic or hemodynamically unstable. Acute: atropine 0.5 mg IV. Chronic: pacing.
AV Blocks
- Mobitz I: usually AV nodal; benign; may resolve with atropine
- Mobitz II: His-Purkinje; high risk of complete block; requires pacemaker
- Complete AV block: pacing is definitive therapy
6. Antiarrhythmic Drug Classes (Vaughan Williams)
| Class | Mechanism | Key Drugs | Use |
|---|---|---|---|
| IA | Na⁺ channel block (moderate, ↑APD) | Quinidine, procainamide, disopyramide | AF, VT |
| IB | Na⁺ channel block (fast on-off, ↓APD) | Lidocaine, mexiletine | Ventricular arrhythmias |
| IC | Na⁺ channel block (slow on-off, no APD change) | Flecainide, propafenone | SVT, AF (no structural disease) |
| ID | Late Na⁺ current block | Ranolazine | Reduces EAD-triggered activity |
| II | Beta-adrenergic blockade | Metoprolol, carvedilol, propranolol | Rate control, post-MI, VT |
| III | K⁺ channel block (↑APD, ↑refractoriness) | Amiodarone, sotalol, dronedarone, ibutilide | AF, VT/VF |
| IV | L-type Ca²⁺ channel block | Verapamil, diltiazem | Rate control (SVT, AF) |
- Braunwald's Heart Disease, Ch. 64
7. Acute Management Summary
| Presentation | Immediate Action |
|---|---|
| Hemodynamically unstable tachyarrhythmia (any type) | Synchronized cardioversion (or defibrillation for VF/pVT) |
| VF / pulseless VT | Immediate defibrillation + ACLS |
| Stable narrow-complex regular SVT | Vagal maneuvers → IV adenosine |
| Stable AF with rapid ventricular response | Rate control (IV beta-blocker or CCB) |
| TdP | IV magnesium sulfate, correct electrolytes, remove offending drugs |
| Symptomatic bradycardia | IV atropine → temporary pacing |
8. Chronic / Invasive Options
- Catheter ablation: Curative for most SVTs (AVNRT ~96%, AVRT ~95%, typical AFL ~90%). Also increasingly used for AF (pulmonary vein isolation) and scar-related VT.
- Implantable cardioverter-defibrillator (ICD): Primary/secondary prevention of sudden cardiac death in patients with VT/VF or high risk (EF <35%).
- Permanent pacemaker: Sick sinus syndrome, high-degree AV block, symptomatic bradycardia.
Sources: Braunwald's Heart Disease (2 Vol Set), Washington Manual of Medical Therapeutics, Miller's Anesthesia 10e, Fuster and Hurst's The Heart 15e.
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