Mechanisms of Arrhythmia

Mechanisms of Arrhythmia

Normal Sinus Rhythm

Components of the Cardiac Conduction System:

  1. SA node - The primary pacemaker of the heart, located in the right atrium.
  2. AV node - Acts as a gateway that slows the conduction before the signal passes to the ventricles.
  3. Purkinje fibers - Spread the conduction throughout the ventricles.

Electrocardiogram (ECG) Phases:

  • P wave: Atrial excitation
  • PR interval: AV conduction
  • QRS complex: Ventricular excitation, Phase 0 (Na+ influx)
  • QT interval: Total Time of Ventricular Excitation & Recovery, Phase 3 (K+ efflux)
  • T wave: Ventricular repolarization

Types of Arrhythmia

  • Bradycardia (slow): Results from slow heart rates originating from the atria or AV node.
  • Tachycardia (fast): Results from fast heart rates originating from the ventricles.

Causes of Arrhythmias

Altered Impulse Formation:

  1. Altered Automaticity: Can be of the SA node or latent pathways influenced by the autonomic nervous system.

    • Sympathetic activation increases cAMP, enhancing pacemaker currents in nodal cells.
      • ↑ cAMP → ↑ pacemaker currents
    • Parasympathetic activation via ACh can suppress the SA node.
    • Ph4 slope, Threshold Potential (TP), and Maximum Diastolic Potential (MDP) determine cell firing rates.

  2. Abnormal Automaticity: Cells outside of the regular conduction system spontaneously depolarize, often due to injury-caused leaky membranes.

    • Can initiate ectopic beats or rhythms.

  3. Triggered Activity: Due to abnormal depolarizations triggered by previous action potentials.

    • Early Afterdepolarizations (EAD): Interrupt normal repolarization, often associated with Long QT syndrome.
    • Delayed Afterdepolarizations (DAD): Caused by high intracellular calcium levels.

Altered Impulse Conduction:

  1. Conduction Block: Impulse blocked by an unexcitable region. Can be transient or permanent, unidirectional or bidirectional.

    • Functional: During refractory periods.
    • Structural: Due to ischemia, fibrosis (scarring), or inflammation.
    • AV block: Most common type.

  2. Reentry Circuits: Electrical impulses circulate repeatedly around a reentry circuit, often associated with unidirectional conduction blocks.

    • Requires continuously excitable tissue, often seen with myocardial scars.
    • Usually leads to tachycardia.

AV nodal reentry: A specific type of reentry involving the AV node, which can generate a large reentry loop leading to tachycardia.

Specific Arrhythmia Examples:

Wolff-Parkinson-White Syndrome (WPW):

  • Abnormal accessory conduction pathway from atria to ventricles (Bundle of Kent) bypasses the rate-slowing AV node.
  • Characterized by a delta wave on ECG, with widened QRS complex and shortened PR interval.
  • Can lead to life-threatening tachycardia through reentry circuits.

Basis for Antiarrhythmic Therapy:

  1. Eliminate Increased Automaticity:
    • Decrease Phase 4 slope, increase Threshold Potential (TP), decrease Maximum Diastolic Potential (MDP).
  2. Eliminate Triggered Activity:
    • Shorten action potential duration (EAD) or reduce calcium overload (DAD).
  3. Interrupt Reentrant Circuits:
    • Increase refractory periods, reduce premature beats.

Mechanisms of Arrhythmia Development

Bradyarrhythmias (Decreased Firing Rate):

  • Decreased Automaticity: Often caused by parasympathetic stimulation or other factors reducing phase 4 depolarization.

Tachyarrhythmias (Increased Firing Rate):

  • Enhanced Automaticity: Can be due to sympathetic stimulation or ectopic foci acquiring pacemaker activity.
  • Triggered Activity: Due to prolonged action potential duration (EAD) or intracellular calcium overload (DAD).
  • Reentry Circuits: Unidirectional block with slowed conduction.
    • Functional: May involve atrial fibrillation, polymorphic VT, ventricular fibrillation.
    • Anatomical: Involves atrial flutter, AV nodal reentrant tachycardia, VT related to scar tissue.


Note: Treatment strategies for arrhythmias often involve addressing the underlying abnormality, be it enhanced automaticity, triggered activity, or reentry circuits.