ARYTHMYIA

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Arrhythmia: Mechanisms and Pathophysiology

Cardiac arrhythmias arise from abnormalities in the initiation and/or propagation of the cardiac electrical impulse. There are three core mechanisms: abnormal automaticity, triggered activity (afterdepolarizations), and reentry. - Harrison's Principles of Internal Medicine, 22E, p.1956

1. Normal Cardiac Impulse Propagation (Background)

The normal impulse originates in the sinoatrial (SA) node, travels across the atria via preferential pathways (including Bachmann's bundle), reaches the AV node - where conduction slows (reflected as the PR interval) - then propagates through the bundle of His, right and left bundle branches, and finally the Purkinje fiber network to activate the ventricular myocardium.

Key conduction velocities:

Purkinje fibers: 2-3 m/s
Ventricular myocardium: 0.3-0.4 m/s

Ionic basis of the action potential (AP):

Phase 0 (rapid upstroke): Na⁺ and Ca²⁺ inward currents
Phases 1-2 (plateau): K⁺ channels open slowly; Na/Ca channels inactivate
Phase 3 (repolarization): K⁺ outward currents dominate
Phase 4 (resting): quiet in atrial/ventricular myocytes; spontaneous depolarization ("funny current", I_f) in nodal tissues driven by a nonselective Na/Ca channel - the target of ivabradine
Harrison's Principles of Internal Medicine, 22E, p.1954-1956

2. Mechanism I: Abnormal Automaticity

Definition: Automaticity = spontaneous phase 4 depolarization. Normally this is a property of the SA node, AV node, and His-Purkinje system. When automaticity of a distal tissue exceeds the SA node rate, it takes over as pacemaker ("escape rhythm").

Pathologic enhanced automaticity occurs when:

The rate of phase 4 depolarization accelerates beyond normal in conduction tissues (SA node, AV node, His-Purkinje)
Non-nodal tissues acquire automaticity in disease states: border zones of infarcted myocardium, pulmonary veins (trigger for paroxysmal AF), coronary sinus, SVC, ventricular outflow tracts
Ischemia, reperfusion, or injury alters membrane properties to create new automatic foci

Clinical examples:

Accelerated junctional rhythm, accelerated idioventricular rhythm (AIVR)
Premature ventricular contractions (PVCs) from ischemic border zones
Atrial tachycardia (AT) from ectopic foci
Pulmonary vein ectopy triggering paroxysmal AF

Autonomic regulation is key: increased adrenergic tone accelerates phase 4 depolarization; vagal tone slows it. - Harrison's Principles of Internal Medicine, 22E, p.1956

3. Mechanism II: Triggered Activity (Afterdepolarizations)

Definition: Abnormal depolarizations occurring in the late phases of the AP that are "triggered" by a preceding AP and can initiate sustained arrhythmias.

A. Early Afterdepolarizations (EADs)

Occur during phases 2-3 of the AP
Facilitated by intracellular Ca²⁺ loading and AP prolongation
Heterogeneous QT prolongation across the ventricles allows EADs to trigger wavefronts
Result in Torsades de Pointes (TdP) - a polymorphic VT that can degenerate into VF

Precipitants of EADs:

QT-prolonging drugs (antiarrhythmics, antibiotics, antipsychotics)
Hypokalemia, hypomagnesemia
Bradycardia
Electrical remodeling in cardiomyopathies
Inherited Long QT syndrome (LQTS)

B. Delayed Afterdepolarizations (DADs)

Occur during phase 4 of the AP (after full repolarization)
Mechanism: excess intracellular Ca²⁺ drives repetitive spontaneous depolarizations via the Na/Ca exchanger
Can produce sustained arrhythmia including bidirectional VT

Precipitants of DADs:

Digitalis glycoside toxicity (classic cause)
Catecholamine excess
Ischemia/reperfusion
Heart failure with Ca²⁺ overload
Harrison's Principles of Internal Medicine, 22E, p.1957

4. Mechanism III: Reentry (Most Common Tachyarrhythmia Mechanism)

Definition: Circus movement of an electrical wavefront that perpetually re-excites the same tissue. This is the most common mechanism of tachyarrhythmias. - Washington Manual of Medical Therapeutics, p.231

Requirements for reentry (all three must be present):

An anatomic or functional circuit - a closed loop of conductive tissue
Unidirectional block - the wavefront can propagate in only one direction at the site of block (the other direction is refractory or blocked)
Slow conduction - within part of the circuit, conduction is slow enough that the rest of the circuit recovers excitability before the wavefront returns

Anatomic Reentry

Fixed barrier (scar, annulus fibrosus, accessory pathway) defines the circuit
Predictable, regular, and often terminable by pacing
Examples: AVNRT (AV nodal reentry tachycardia), AVRT (accessory pathway), atrial flutter (cavotricuspid isthmus), scar-based VT post-MI

Functional Reentry

No fixed anatomic barrier; instead, a region is functionally refractory
Circuit varies in size and location; frequency of depolarization varies
More complex; more difficult to terminate
Likely mechanism for: atrial fibrillation (multiple wavelets) and some forms of VF

Premature beat as a trigger: A premature impulse may find one pathway refractory (unidirectional block) while conducting through the other - if that pathway conducts slowly enough, the originally blocked pathway recovers and the impulse re-enters, establishing the circus loop.

Harrison's Principles of Internal Medicine, 22E, p.1957

Summary Diagram

Mechanisms of cardiac arrhythmia: abnormal automaticity (accelerated phase 4), reentry (circular wavefront around a barrier), early afterdepolarizations (EADs during plateau), and delayed afterdepolarizations (DADs in phase 4)

FIGURE 250-3 from Harrison's 22E: Schematic action potentials showing EADs, DADs, reentry circuit, and abnormal automaticity

Summary Table (Harrison's 22E, Table 250-1)

Category	Mechanism	Prototypical Arrhythmia
Abnormal automaticity	Enhanced phase 4 depolarization	Idiopathic VT, atrial tachycardia, AIVR
Triggered activity - EADs	Phase 2-3 afterdepolarizations	TdP in long QT syndrome, PVCs
Triggered activity - DADs	Phase 4 afterdepolarizations (Ca²⁺ overload)	Digitalis-induced VT/AT, reperfusion PVCs
Reentry	Unidirectional block + slow conduction	AVNRT, AVRT, atrial flutter, scar-related VT

Clinical Clues to Mechanism

Feature	Likely Mechanism
Sudden onset and abrupt termination of palpitations	Reentry
Terminates with Valsalva / carotid sinus massage	AV nodal reentry (AVNRT)
Gradual warm-up and cool-down	Enhanced automaticity
Long QT on baseline ECG	EAD-triggered TdP
Digitalis toxicity	DADs
Post-MI sustained VT	Scar-based anatomic reentry
Paroxysmal AF	Pulmonary vein automaticity triggering functional reentry

Washington Manual of Medical Therapeutics, p.231; Fuster and Hurst's The Heart, 15th Edition, p.1061

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