Ventricular Tachycardia

Ventricular Tachycardia is a topic covered in the 5-Minute Emergency Consult.

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Basics

Description

  • A wide complex tachydysrhythmia (WCT):
    • ≥3 consecutive QRS complexes with ventricular rate >100 bpm and QRS duration >120 ms
    • Rapid, regular depolarization of the ventricles independent of atria and normal conduction system
    • Considered sustained if lasts >30 s, produces syncope or arrest, or requires cardioversion/pacing
  • Monomorphic VT – single, stable QRS morphology
  • Polymorphic VT – changing QRS morphology:
    • Torsades de pointes:
      • Polymorphic form of VT
      • Alternating electrical polarity and amplitude
      • Long QT present on baseline ECG
      • Acquired or congenital
  • Bidirectional VT – beat-to-beat alternation in QRS frontal plane axis:
    • Digitalis toxicity
    • Catecholaminergic polymorphic VT (inherited, rare, highly lethal)

Etiology

  • Wide complex tachycardia:
    • 80% likelihood of being VT
    • 20% supraventricular tachycardia (SVT) with a baseline left bundle branch block (LBBB) or aberrancy
  • Wide complex tachycardia and a history of MI:
    • >98% likelihood of being VT
    • Age >35: 80% risk of VT
    • Age <35: 75% risk of SVT
  • Incidence of nonsustained VT:
    • 0–4% in the general population
    • Up to 60% of patients with dilated cardiomyopathy
  • Associated with increased risk for sudden cardiac death (SCD)
  • Mechanisms for VT:
    • Reentrant:
      • Occurs commonly in structural heart disease (dilated cardiomyopathy, ischemia, infiltrative heart disease, previous MI, scarring, prior surgery)
      • Unidirectional conduction
      • Fixed or functional conduction block
      • Region of “slow conduction”
    • Abnormal automaticity:
      • Abnormal impulse generated by region of ventricular cells at accelerated rate
    • Triggered activity:
      • Due to early or late after-depolarizations
  • Polymorphic VT causes:
    • Acquired (drug-induced or electrolyte abnormalities)
    • Congenital (long QT syndrome)
    • Ischemia
    • Organic heart disease
  • Regardless of the mechanism, all VT may degenerate to ventricular fibrillation (VF)

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Basics

Description

  • A wide complex tachydysrhythmia (WCT):
    • ≥3 consecutive QRS complexes with ventricular rate >100 bpm and QRS duration >120 ms
    • Rapid, regular depolarization of the ventricles independent of atria and normal conduction system
    • Considered sustained if lasts >30 s, produces syncope or arrest, or requires cardioversion/pacing
  • Monomorphic VT – single, stable QRS morphology
  • Polymorphic VT – changing QRS morphology:
    • Torsades de pointes:
      • Polymorphic form of VT
      • Alternating electrical polarity and amplitude
      • Long QT present on baseline ECG
      • Acquired or congenital
  • Bidirectional VT – beat-to-beat alternation in QRS frontal plane axis:
    • Digitalis toxicity
    • Catecholaminergic polymorphic VT (inherited, rare, highly lethal)

Etiology

  • Wide complex tachycardia:
    • 80% likelihood of being VT
    • 20% supraventricular tachycardia (SVT) with a baseline left bundle branch block (LBBB) or aberrancy
  • Wide complex tachycardia and a history of MI:
    • >98% likelihood of being VT
    • Age >35: 80% risk of VT
    • Age <35: 75% risk of SVT
  • Incidence of nonsustained VT:
    • 0–4% in the general population
    • Up to 60% of patients with dilated cardiomyopathy
  • Associated with increased risk for sudden cardiac death (SCD)
  • Mechanisms for VT:
    • Reentrant:
      • Occurs commonly in structural heart disease (dilated cardiomyopathy, ischemia, infiltrative heart disease, previous MI, scarring, prior surgery)
      • Unidirectional conduction
      • Fixed or functional conduction block
      • Region of “slow conduction”
    • Abnormal automaticity:
      • Abnormal impulse generated by region of ventricular cells at accelerated rate
    • Triggered activity:
      • Due to early or late after-depolarizations
  • Polymorphic VT causes:
    • Acquired (drug-induced or electrolyte abnormalities)
    • Congenital (long QT syndrome)
    • Ischemia
    • Organic heart disease
  • Regardless of the mechanism, all VT may degenerate to ventricular fibrillation (VF)

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