Arrythmias

Overview

An arrythmia refers to any disturbance in cardiac electrical activity that is not normal sinus rhythm with normal atrioventricular conduction. This may include changes in rate, rhythm or site of origin of the electrical signal for contraction.

Normal conduction of the heart

For the heart to pump normally:

SA node initiates an action potential spreading the current in to the right atrium (RA) and left atrium (LA) via Bachmann’s bundle
SA node → AV node
AV node delays conduction to ensure ventricles contract AFTER blood is emptied into the ventricles from the atria
AV node → Bundle of His
Bundle of His → Purkinje Fibres
Purkinje fibres → cardiomyocytes (contractile cells)

Classification of Arrythmias

Arrhythmias are classified clinically and electrophysiologically across three primary axes:

Heart rate and ECG morphology (the clinical/bedside framework)
Anatomical site of origin
Cellular electrophysiological mechanism.

Clinical & ECG Morphologic Classification

The primary bedside approach categorizes rhythms first by rate (<60 bpm vs. >100 bpm), then by QRS duration, and finally by rhythm regularity.

Arrhythmia
│
├── Bradyarrhythmias (< 60 bpm)
│   ├── Sinus Node Dysfunction (SND)
│   └── Atrioventricular (AV) Blocks
│
└── Tachyarrhythmias (> 100 bpm)
    ├── Narrow QRS Complex (≤ 120 ms) ── Supraventricular
    │   ├── Regular
    │   └── Irregular
    └── Wide QRS Complex (> 120 ms) ──── Ventricular or Aberrant SVT
        ├── Regular
        └── Irregular

Tachyarrhythmias (> 100 bpm)

Narrow-Complex Tachycardias (QRS ≤ 120 ms)

Conducted via the native His-Purkinje system; always supraventricular in origin (SVT).

Rhythm	Regularity	Characteristic P-Wave / Atrial Activity	Common Mechanism
Sinus Tachycardia	Regular	Normal upright P waves in II, III, aVF	Physiological / enhanced automaticity
AVNRT	Regular	Pseudo-r’ in V1, pseudo-S in inferior leads (or buried)	Dual AV nodal pathway micro-reentry
AVRT (Orthodromic)	Regular	Inverted P waves in inferior leads, RP interval > 70 ms	Macro-reentry via accessory pathway
Atrial Tachycardia	Regular	Ectopic P wave morphology distinct from sinus P	Enhanced automaticity or triggered activity
Atrial Flutter	Regular (variable block)	Typical “sawtooth” flutter waves (~300 bpm, leads II, III, aVF)	Macro-reentry around tricuspid annulus (cavotricuspid isthmus-dependent)
Atrial Fibrillation	Irregularly irregular	Disorganized baseline fibrillatory waves (400–600 bpm), no distinct P waves	Multiple chaotic wavelets / pulmonary vein micro-reentry
Multifocal Atrial Tachycardia (MAT)	Irregular	Distinct P-wave morphologies with isoelectric baseline	Multiple ectopic firing foci (often seen in COPD)

Wide-Complex Tachycardias (QRS > 120 ms)

Assumed to be Ventricular Tachycardia (VT) until proven otherwise (~80% of cases). The remaining ~20% represent SVT with aberrant conduction (bundle branch block) or antidromic AVRT.

Morphology	Rhythm	Key Distinguishing Features
Monomorphic Regular	Monomorphic VT	AV dissociation, capture/fusion beats, extreme right-axis deviation (“northwest axis”), positive/negative precordial concordance, Joseph/Brugada criteria
	SVT with Aberrancy	Typical RBBB or LBBB pattern with pre-existing or rate-dependent bundle branch block
	Antidromic AVRT	Anterograde conduction down accessory pathway; wide QRS with delta waves
Polymorphic / Irregular	Polymorphic VT	Continuously changing QRS axis and morphology (normal baseline QTc)
	Torsades de Pointes	Twisting of QRS axes around the isoelectric line; occurs in the setting of prolonged baseline QTc
	AF with WPW (Pre-excited AF)	Rapid, irregularly irregular wide complexes with varying QRS morphology and axis; high risk of degeneration to VF
	Ventricular Fibrillation (VF)	Chaotic, completely disorganized electrical deflection without discrete QRS, ST, or T waves

Bradyarrhythmias (< 60 bpm)

Bradyarrhythmias are classified anatomically based on where conduction fails along the conduction hierarchy:

Sinus Node Dysfunction (Sick Sinus Syndrome)

Sinus Bradycardia: Regular rhythm <60 bpm driven by normal SA node depolarisation.
Sinus Arrest / Pause: Transient failure of SA node impulse generation (pause not an exact multiple of the baseline P-P interval).
Sinoatrial Exit Block: Impulse is generated by the SA node but fails to exit into surrounding atrial myocardium.
Tachy-Brady Syndrome: Alternating paroxysms of SVTs (commonly atrial fibrillation or flutter) and prolonged sinus pauses.

Atrioventricular (AV) Blocks

First-Degree AV Block: PR interval > 200 ms with 1:1 AV conduction (every P wave is followed by a QRS). Conduction delay is typically nodal.
Second-Degree AV Block, Mobitz Type I (Wenckebach): Progressive PR interval prolongation culminating in a non-conducted P wave. Generally intranodal and benign.
Second-Degree AV Block, Mobitz Type II: Constant PR interval preceding a suddenly dropped QRS complex. Localises infraglobally (His-Purkinje system); carries high risk of progression to complete heart block.
High-Grade / Advanced AV Block:$\ge 2$ consecutive P waves fail to conduct to the ventricles at physiological atrial rates.
Third-Degree (Complete) AV Block: Complete absence of AV conduction; atria and ventricles beat independently (AV dissociation) with an escape rhythm (junctional narrow-complex at 40–60 bpm or idioventricular wide-complex at 20–40 bpm).

Electrophysiological Mechanism

At the cellular and tissue level, all arrhythmias stem from two fundamental abnormalities:

               Arrhythmogenic Mechanisms
                          │
         ┌────────────────┴────────────────┐
         ▼                                 ▼
Impulse Formation                 Impulse Conduction
  ├── Enhanced Automaticity         ├── Reentry (Micro & Macro)
  ├── Abnormal Automaticity         ├── Conduction Delay / Block
  └── Triggered Activity            └── Accessory Pathways
        ├── Early Afterdepolarisations (EAD)
        └── Delayed Afterdepolarisations (DAD)