What is the normal pathway of cardiac conduction and the pathophysiology of Ventricular tachycardia?

Normal Cardiac Conduction and Ventricular Tachycardia Pathophysiology

Normal Cardiac Conduction Pathway

The normal cardiac conduction pathway begins in the sinoatrial (SA) node, spreads through the atria to the atrioventricular (AV) node, then travels through the His-Purkinje system to activate both ventricles simultaneously from endocardium to epicardium. 1

• Electrical activation begins in the SA node, spreading through right and left atrial myocytes, reaching the AV node within 200 ms 1
• The impulse slows at the AV node, then rapidly travels down the His bundle and right and left bundle branches 1
• This specialized conduction system ensures near-simultaneous contraction of ventricular segments for optimal cardiac output 1
• A properly timed atrial contraction can increase cardiac output by 25-30% 1

Pathophysiology of Ventricular Tachycardia

Definition and Characteristics

• Ventricular tachycardia (VT) is a serious rhythm disturbance originating from any part of the myocardium or conduction system below the AV node 2
• VT presents with a wide QRS complex (>120 ms) and a heart rate greater than 120 beats per minute 2
• VT can be classified as monomorphic (consistent QRS morphology) or polymorphic (varying QRS morphology) 2

Mechanisms of Ventricular Tachycardia

• VT most commonly occurs through three primary mechanisms:
  • Reentry: The most common mechanism, involving circular movement of electrical impulses around a fixed anatomical or functional obstacle 3
  • Enhanced automaticity: Abnormal spontaneous depolarization of ventricular cells 3
  • Triggered activity: Abnormal depolarizations (early or delayed afterdepolarizations) that occur during or after normal action potentials 3

Structural and Functional Substrates

• Coronary artery disease and resulting myocardial scarring is the most common substrate for VT 2
• Other important substrates include:
  • Cardiomyopathies (dilated, hypertrophic, arrhythmogenic right ventricular) 3
  • Electrolyte disturbances (hypokalemia, hypomagnesemia) 2
  • Medication adverse effects (particularly those prolonging QT interval) 2
  • Congenital heart disease 3

Electrophysiological Consequences

• VT disrupts the normal cardiac conduction sequence, leading to:
  • Loss of coordinated atrial contribution to ventricular filling 3
  • Reduced diastolic filling time due to rapid rate 3
  • Asynchronous ventricular contraction reducing cardiac output 3
  • Risk of hemodynamic compromise depending on rate and underlying cardiac function 3

Clinical Significance

• VT can be hemodynamically stable or unstable depending on rate, duration, and underlying heart function 3
• Sustained VT can deteriorate into ventricular fibrillation, leading to sudden cardiac death 3
• VT is often the first manifestation of underlying cardiac disease, making prompt recognition critical 4
• The 12-lead ECG remains the primary diagnostic tool for identifying VT and distinguishing it from supraventricular tachycardias with aberrant conduction 2

Understanding these mechanisms is essential for appropriate management, which may include antiarrhythmic medications like amiodarone that affect sodium, potassium, and calcium channels to suppress abnormal ventricular activity 5.