Ventricular Tachycardia

Basics

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)

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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