What is the pathophysiology of ventricular tachycardia (VT)?

Pathophysiology of Ventricular Tachycardia

Ventricular tachycardia (VT) is primarily caused by three major pathophysiological mechanisms: reentry (most common in structural heart disease), triggered activity (common in outflow tract VT), and abnormal automaticity, with each mechanism requiring specific substrate conditions and creating distinct electrophysiological characteristics. 1

Definition and Classification

• VT is defined as three or more consecutive ventricular complexes occurring at a rate greater than 100 beats per minute 1
• Sustained VT lasts longer than 30 seconds or requires termination due to hemodynamic compromise in less than 30 seconds 2
• Nonsustained VT terminates spontaneously in less than 30 seconds 2

Primary Pathophysiological Mechanisms

1. Reentry Mechanism

• Most common mechanism in structural heart disease, particularly in post-myocardial infarction scars 1
• Requires:
  • Anatomical or functional conduction block
  • Slow conduction pathway
  • Unidirectional block allowing retrograde conduction 1
• Myocardial scarring creates heterogeneous tissue with areas of preserved myocardium within fibrotic scar, forming the ideal substrate 1

2. Triggered Activity

• Common mechanism in outflow tract VT, especially right ventricular outflow tract (RVOT) VT 3
• Results from delayed afterdepolarizations (DADs) and is dependent on:
  • Intracellular calcium overload
  • Cyclic adenosine monophosphate elevation 3
• Often adenosine-sensitive and facilitated by catecholamines 3
• May not be easily inducible at baseline electrophysiological testing and may require rapid burst pacing or isoproterenol stimulation 3

3. Abnormal Automaticity

• Results from spontaneous depolarization of ventricular cells at accelerated rates 1
• Less common than reentry or triggered activity 1
• Can occur in various conditions including electrolyte abnormalities, drug toxicity, and myocardial inflammation 1

Anatomical Substrates

• Ischemic heart disease: Most common substrate through myocardial scarring 1
• Dilated cardiomyopathy: Creates substrate through myocardial fibrosis, myocyte disarray, and altered cellular electrophysiology 1
• Right ventricular outflow tract: Common site for idiopathic VT 3
• Left ventricular outflow tract: Can be classified by site of origin (endocardial, coronary cusp, or epicardial) 3

Special Considerations in Different Populations

Pediatric Considerations

• Arrhythmias are common in children after surgical repair of congenital heart disease 3
• VT in pediatric patients may result from surgical incisions, coronary manipulation, electrolyte imbalance, or infusion of vasoactive medication 3
• In infants, VT is defined as three or more consecutive complexes at a rate greater than 100 bpm 2

Idiopathic VT

• VT arising from the right ventricle is the most common form in apparently healthy people 3
• Usually has left bundle-branch, inferior-axis morphology 3
• Often presents as non-ischemic exercise-induced and/or repetitive monomorphic VT 3
• Symptoms tend to be mild and syncope is rare 3

Electrophysiological Characteristics

• VT presents with wide QRS complexes (>120 ms) and AV dissociation 1
• Fusion complexes represent merging of supraventricular and ventricular impulses 1
• Concordance of precordial QRS complexes suggests VT 1
• QRS morphology differs from the patient's normal QRS during sinus rhythm 4

Clinical Significance

• VT can present as hemodynamically stable or unstable 2
• Even brief episodes of VT in patients with structural heart disease indicate increased risk for sudden cardiac death 2
• Incessant forms of VT may result in tachycardia-induced cardiomyopathy 1
• Idiopathic VT generally has a better prognosis than VT associated with structural heart disease 1

Diagnostic Features

• Wide QRS complex tachycardia requires differentiation from supraventricular tachycardia with aberrancy 1
• Electrophysiological testing can confirm the diagnosis and mechanism when ECG is inconclusive 1
• R-S interval >100 ms in any precordial lead implies VT 4
• Presence of AV dissociation is pathognomonic of VT 4

Understanding these pathophysiological mechanisms is crucial for appropriate diagnosis and management of ventricular tachycardia, as different mechanisms may respond to different therapeutic approaches.