What is the pathophysiology of Ventricular Tachycardia (VTach)?

Pathophysiology of Ventricular Tachycardia (VTach)

Ventricular tachycardia is a serious cardiac arrhythmia originating from the ventricular myocardium or conduction system below the atrioventricular node, characterized by three or more consecutive ventricular beats at a rate greater than 100 beats per minute, which can lead to hemodynamic compromise and sudden cardiac death. 1

Definition and Classification

• VTach is defined as three or more consecutive ventricular complexes occurring at a rate greater than 100 beats per minute 1
• Sustained VTach lasts longer than 30 seconds or requires termination due to hemodynamic compromise in less than 30 seconds 1
• Nonsustained VTach terminates spontaneously in less than 30 seconds 1

Mechanisms of VTach

Reentry Mechanism

• Most common mechanism in structural heart disease, particularly in post-myocardial infarction scars 2
• Requires:
  • Anatomical or functional conduction block
  • Slow conduction pathway
  • Unidirectional block allowing retrograde conduction 2
• Creates a circuit where electrical impulses continuously propagate around a fixed or functional obstacle 2

Triggered Activity

• Common mechanism in outflow tract VTach (especially RVOT VT) 2
• Results from:
  • Delayed afterdepolarizations (DADs) dependent on intracellular calcium overload
  • Cyclic adenosine monophosphate (cAMP) elevation 2
• Often adenosine-sensitive and facilitated by catecholamines 2
• May terminate with vagal maneuvers 2

Abnormal Automaticity

• Enhanced automaticity can occur in ventricular tissue 2
• Results in spontaneous depolarization of ventricular cells at accelerated rates 2
• May be responsible for some forms of outflow tract VT 2

Anatomical Substrates

Structural Heart Disease

• Myocardial scarring (most common substrate in ischemic heart disease) 2
  • Creates heterogeneous tissue with areas of preserved myocardium within fibrotic scar
  • Slow conduction through these channels facilitates reentry 2
• Dilated cardiomyopathy creates substrate for VTach through:
  • Myocardial fibrosis
  • Myocyte disarray
  • Altered cellular electrophysiology 2

Accessory Pathways

• Can participate in VTach circuits when present 2
• Manifest pathways conduct in anterograde direction (visible as delta wave on ECG) 2
• Concealed pathways conduct only in retrograde direction 2
• Specialized pathways like atriofascicular fibers (Mahaim fibers) connect right atrium to distal right bundle branch 2

Outflow Tract VTach

• Originates from right or left ventricular outflow tracts 2
• RVOT VTach typically presents with left bundle-branch, inferior-axis morphology 2
• Often occurs in structurally normal hearts 2
• Mechanism usually involves triggered activity 2

Electrophysiological Characteristics

• VTach presents with wide QRS complexes (>120 ms) 2
• AV dissociation (ventricular rate faster than atrial rate) is diagnostic of VTach 2
• Fusion complexes represent merging of supraventricular and ventricular impulses 2
• Concordance of precordial QRS complexes (all positive or negative) suggests VTach 2

Clinical Significance

• VTach can present as hemodynamically stable (minimal symptoms) or unstable (syncope, cardiac arrest) 1
• Even brief episodes of VTach in patients with structural heart disease indicate increased risk for sudden cardiac death 1
• Sustained monomorphic VTach most commonly occurs due to myocardial scar from prior infarct 3
• Idiopathic VTach can occur in the absence of structural heart disease with generally better prognosis 2

Special Considerations

• Rapid anterograde conduction during atrial fibrillation over accessory pathways can lead to ventricular fibrillation and sudden cardiac death 2
• Incessant forms of VTach (like PJRT) may result in tachycardia-induced cardiomyopathy 2
• Polymorphic VTach has different pathophysiology than monomorphic VTach and often indicates acute ischemia or genetic channelopathies 4

Diagnostic Features

• Wide QRS complex tachycardia requires differentiation from supraventricular tachycardia with aberrancy 2
• ECG algorithms (Brugada criteria, Vereckei algorithm) help distinguish VTach from SVT with aberrancy 2
• Electrophysiological testing can confirm the diagnosis and mechanism when ECG is inconclusive 2

Understanding the pathophysiology of ventricular tachycardia is crucial for appropriate risk stratification, management decisions, and prevention of sudden cardiac death in affected patients.