Cardiac Arrhythmia - Comprehensive Overview

1. Definition

2. Mechanisms of Arrhythmia

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

1. Two anatomically or functionally distinct pathways
2. Unidirectional block in one pathway
3. Sufficient conduction slowing in the other to allow recovery of the blocked pathway

3. Classification

Bradyarrhythmias (Rate <60 bpm)

Tachyarrhythmias - Supraventricular (SVT, QRS <120 ms)

Tachyarrhythmias - Ventricular (QRS ≥120 ms unless aberrant conduction)

4. ECG-Based Diagnostic Approach

1. Is the rate >100? → Tachyarrhythmia
2. Is QRS narrow (<120 ms) or wide (≥120 ms)?
3. Is the rhythm regular or irregular?
4. 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
5. 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)

• First occurrence
• Paroxysmal (<7 days, usually <48 hrs)
• Persistent (>7 days)
• Long-standing persistent (>1 year, amenable to cardioversion)
• Permanent (accepted; cardioversion not pursued)

• 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

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)

• Braunwald's Heart Disease, Ch. 64

7. Acute Management Summary

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.

Differentiating Ventricular Tachycardia (VT) vs. Ventricular Fibrillation (VF)

The Core Distinction at a Glance

1. Ventricular Tachycardia (VT)

ECG Characteristics

• Wide QRS (≥120 ms) at rate typically 100-250 bpm
• Regular rhythm (monomorphic VT) - complexes look the same beat to beat
• AV dissociation - P waves march through at a slower rate, independent of the QRS complexes. This is the single most specific sign of VT. It may be subtle - look for small bumps distorting the QRS/ST-T waves.
• Fusion beats - a hybrid complex formed when a sinus impulse partially activates the ventricle simultaneously with the VT focus (pathognomonic of VT)
• Capture beats - a normal narrow QRS occurring during the tachycardia when a sinus impulse briefly "captures" the ventricle (also pathognomonic of VT)

Types of VT

• Monomorphic VT: QRS morphology is identical beat to beat - most common; usually from re-entry around a scar
• Polymorphic VT: QRS morphology constantly changes - seen in ischemia, long QT
• Torsades de Pointes (TdP): A specific polymorphic VT where the QRS axis appears to "twist" around the isoelectric baseline. Associated with prolonged QT interval. Often self-terminating but can degenerate to VF.

Clinical Features

2. Ventricular Fibrillation (VF)

ECG Characteristics

• No identifiable QRS complexes - this is the defining feature
• Rapid, completely irregular, chaotic, dysmorphic deflections
• No organized waveforms - no P, QRS, or T waves
• Varying amplitude - subdivided into:
  • Coarse VF: higher amplitude waves (>0.2 mV) - more responsive to defibrillation, more likely to be recent
  • Fine VF: low amplitude, nearly flat - longer duration, harder to defibrillate; can be mistaken for asystole
• Mechanism: multiple simultaneously active functional reentrant wavelets traveling through the ventricles in non-stationary, rotating "spiral wave" patterns - the 3D complexity of ventricular geometry produces the chaotic ECG appearance

3. Key Differentiating ECG Signs in Detail

AV Dissociation (VT-specific)

Fusion and Capture Beats (VT-specific, pathognomonic)

• Fusion beat: Sinus impulse + VT complex activate the ventricles simultaneously → the QRS is intermediate in morphology between normal sinus QRS and VT QRS
• Capture beat: Rare moment where a sinus impulse fully activates the ventricle during VT → produces a normal, narrow QRS amid wide complexes

QRS Morphology (VT vs. SVT with aberrancy)

4. The Polymorphic VT - VF Spectrum

5. Clinical / Hemodynamic Differentiation

6. Emergency Management Based on the Distinction

WIDE COMPLEX TACHYCARDIA / NO PULSE
             ↓
Is there any organized QRS rhythm?
        ↙           ↘
      YES             NO
      VT             VF
       ↓               ↓
Pulseless VT      Immediate unsynchronized
Treat same as VF  defibrillation (200J biphasic)
                  + CPR immediately after shock

• Stable VT (pulse present): Synchronized cardioversion OR antiarrhythmics (amiodarone 150 mg IV over 10 min, then infusion; or lidocaine)
• Pulseless VT / VF: Immediate unsynchronized defibrillation. Every minute of delay = 7-10% decrease in survival. CPR continues between shocks. Epinephrine 1 mg IV q3-5 min. Amiodarone 300 mg IV push (then 150 mg) if VF/pVT persists after 2-3 shocks.

Key clinical rule: In any wide-complex tachycardia, assume VT until proven otherwise. Treating SVT with aberrancy as VT is safe; treating VT as SVT (e.g., giving verapamil) can be fatal.