Ventricular Tachycardia
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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
- Torsades de pointes:
- 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
- Reentrant:
- 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
- Torsades de pointes:
- 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
- Reentrant:
- 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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